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Internal Medicine study notes

Elevated intracranial pressure/ intracranial HTN
o ICP>20 mm Hg
o Causes: trauma, space-occupying lesions, hydrocephalus, impaired CNS venous outflow
o Dx: diffuse headaches (worse in morning), N/V early in the day, vision changes, papilledema, CN deficit, somnolence, confusion,
unsteadiness, cushings reflex (HTN and bradycardia)
o Dx: CT or MRI
Cavernous sinus thrombosis
o Secondary to infection of the medial aspect of the face around the eyes and nose (can also be ethmoid or sphenoid sinus infections)
o Sx: headache, low grade fever, periorbital edema, cranial nerve palsies
CN 3,4,5 (V1,V2, V3) all pass through the cavernous sinus and can be affected
Headache d/t neuropathic pain d/t irritation of V1 and V2
Dx: MRI or CT w/ contrast of the orbits
Tx: IV broad=spectrum antibiotic; anticoagulation, glucocorticoid, or surgery may be indicated
Acoustic neuroma/ vestibular schwannoma
o Typically unilateral
o Sx: sensorineural hearing loss
o Tumor of the sella and suprasellar space
o Sx: headache, focal neurologic changes, visual problems; can cause central diabetes insipidus (decreased ADH)
o Dx: CT or MRI to exclude an intracranial mass lesion if the dx is unclear or the syndrome has recently started
o Tension headache
Most common type
Dx of exclusion
Tx: NSAIDs or other analgesics
o Migraine headache
Precipitants: emotions, food (chocolate, red wine, cheese), menses
Sx: visual disturbance (flashes, sparks, stars, luminous hallucinations), photophobia, aura, N/V, headaches lasting 4-72 hrs (usually
unilateral, pulsating quality)
Other possible sx: aphasia, numbness, dysarthria, weakness
Tx: IV antiemetics (chlorpromazine, Prochlorperazine, or metoclopramide) +/- NSAIDS or triptans for acute migraine headaches;
triptans or ergotamine
Triptans must be started early in the course of the migraine before sx become severe in order to be of benefit
Prophylactic (preventative) tx: propanolol (#1), calcium channel blockers, tricyclic antidepressants (amitriptyline),
SSRIs, botulinum toxin injections
o for pts with >3 migraine headaches/month
o cluster headaches
Sx: frequent short duration high intensity headaches
Other possible sx: red tearing eye with rhinorrhea, horner syndrome
Tx: triptans, ergotamine, 100% oxygen, prednisone, or lithium
o giant cell (temporal) arteritis
sx: visual sx (irreversible blindness), jaw claudication, scalp tenderness, headache; sx in other arteries (decreases arm pulses,
bruits near clavicles, aortic regurgitation); systemic sx (muscle pain, fatigue, weakness)
dx: elevated ESR and CRP; biopsy of artery (most accurate)
tx: high dose prednisone (started before biopsy)
o pseudotumor cerebri (benign/idiopathic intracranial HTN)
communicating hydrocephalus; diagnosis of exclusion
a/w obesity, venous sinus thrombosis, vitamin A toxicity, medications (corticosteroids, OCPs), trauma
sx: headache (pulsatile, wake pt from sleep, a/w pulsatile tinnitus; worse lying flat/ better standing up); mimics a brain tumor d/t
elevated ICP (N/V, transient visual obscurations, blurry vision), papilledema w/ diplopia from 6
cranial nerve (abducens) palsy
vision loss, sluggish pupillary reflexes to light, papilledema,
dx: CT or MRI to exclude an intracranial mass lesion (empty sella d/t downward herniation of archnocele d/t high CSF pressure,
slit like ventricles), lumbar puncture showing increased pressure (w/o CSF disturbances)
note: papilledema is not a contraindication to an LP unless the pt has evidence of obstructive to noncommunicating
hydrocephalus and/or space-occupying lesion +/- mass effect or midline shift
tx: weight loss, acetazolamide (decreased CSF production), steroids, repeated lumbar puncture (rapidly lower ICP);
ventriculoperitoneal shunt if medical therapy not sufficient
Transient ischemic attack (TIA)/ stroke
o #3 cause of death
o Causes: carotid stenosis, cardioembolism, lipohyalinosis, small-vessel disease, atheroembolism from carotid artery
Ischemia (85%), bleeding (15%)
Embolic sources: carotid stenosis, heart (atrial fibrillation, valvular heart disease, DVT through patent foramen ovale)
o Risk factors: HTN, diabetes, hyperlipidemia, smoking
Hypertensive stroke is most common in the putamen and adjacent internal capsule hemiparesis, semi-sensory loss,
homonymous hemianopsia
o Sx: acute focal neuro deficits, amaurosis fugax
Amaurosis fugax: transient monocular blindness; gray shade being pulled down over the eye d/t ischemia to the retinal artery
TIA: transient neuro deficit secondary to ischemia in a defined vascular territory that lasts <24 hr
MCA stroke (90%)
Sx: contralateral weakness/sensory loss, homonymous hemianopsia (loss of visual field on opposite side of stroke), eye
deviation to side of lesion, aphasia, if speech center effected
o Speech center on same side as handedness (if right handed L. side dominant Left sided speech center)
Anterior cerebral artery (ACA) stroke
Sx: personality/cognitive defects, urinary incontinence, weakness leg>arm
Posterior cerebral artery (PCA) stroke
Sx: ipsilateral sensory loss of face & CN 9/10, contralateral sensory loss of limbs, limb ataxia
Cerebellar hemorrhage: ataxia, vomiting, occipital headache, gaze palsy (towards the lesion), facial weakness (opposite
Lacunar stroke
Occurs d/t microatheroma and lipohyalinosis (small vessel hyalinosis); type of ischemic stroke
o RF: HTN, diabetes
o Most common in the posterior internal capsule pure motor stroke
Putamen hemorrhage: most common site of HTN hemorrhage; internal capsule lies adjacent to the putamen and is almost always
involved hemiparesis; hemisensory loss, homonymous hemianopsia, stupor, coma; eye are deviated away form the paralytic
o Dx: CT w/o contrast (best initial; differentiate ischemic from hemorrhagic stroke), MRI (most accurate)
Determine etiology
carotid duplex U/S or MRA to evaluate for carotid artery stenosis
o tx: >70% stenosis + symptomatic cerebrovascular disease carotid endarterectomy > angioplasty w/
>80% stenosis, asymptomatic, good surgical candidates carotid endarterectomy
o consider carotid surgery for 50-60% stenosis
o medical management with aspirin and statins <50% stenosis
echocardiogram: damaged valves or thrombi
o tx: surgically repair/replace damaged valves; heparin warfarin to INR of 2-3 for thrombi
EKG: assess for atrial arrhythmia (fibrillation or flutter)
o Holter monitoring if initial EKG is normal to r/o arrhythmia
o Tx: warfarin to INR of 2-3 as long as arrhythmia persists
o Tx:
Non-hemorrhagic stroke (ischemic stroke)
<3hr since onset thrombolytics (IV tPA)
>3hr since onset aspirin; if pt was already on aspirin add dipyridamole or change to clopidogrel
hemorrhagic stroke: no treatment
control RFs: HbA1c<7%, control BP, LDL<100, smoking cessation
Rankin score system for stroke
o Measures the degree of disability or dependence n the daily activities of stroke pts (or other neuro disability)
o 0= no sx
o 1 - No significant disability. Able to carry out all usual activities, despite some symptoms.
o 2 - Slight disability. Able to look after own affairs without assistance, but unable to carry out all previous activities.
o 3 - Moderate disability. Requires some help, but able to walk unassisted.
o 4 - Moderately severe disability. Unable to attend to own bodily needs without assistance, and unable to walk unassisted.
o 5 - Severe disability. Requires constant nursing care and attention, bedridden, incontinent.
o 6 - Dead.
hypertensive encephalopathy
o Sx: altered mental status (confusion), severe HTN, increased ICP, and/or seizures
o Diff dx: drugs (cocaine, amphetamines), stroke, subarachnoid hemorrhage, meningitis, mass lesion, rebound HTN from meds (clonidine),
o Tx: decreased BP in ICU (goal 100-110 mmHg systolic)
o Note: hemorrhages appear as hyperdense areas on CT scan, whereas infarcts are hypodense parenchymal areas
o Subarachnoid hemorrhage
d/t rupture of an aneurysm (usually anterior circle of Willis)
RFs of aneurysm: polycystic kidney diseases, smoking, HTN, hyperlipemia, high alcohol consumption
Sx: worst headache of my life; sudden onset severe headache, meningeal irritation (stiff neck, photophobia), fever, loss of
consciousness (sudden increase in ICP), focal neurological complications
Dx: CT w/o contrast, LP (blood, xanthochromic CSF; may have elevated WBC)
WBC count should not exceed the normal ratio of 1 WBC for every 500-1000 RBCs; if elevated above this, consider
EKG: may have large or inverted T waves (d/t excessive sympathetic activity)
Angiography to determine the site of aneurysm (CT angiography, catheter angiography, or MRA)
Tx: nimodipine (calcium channel blocker; prevents future ischemic stroke), embolization (coiling)> surgical clipping,
ventriculoperitoneal shunt if hydrocephalus occurs, seizure prophylaxis with phenytoin
o Transient LOC and postural tone w/ spontaneous recovery
d/t transient global decrease in cerebral perfusion (not regional hypoperfusion like TIA)
o causes:
vasovagal: fainting d/t excessive vagal tone hypotension w/o reflex increase in HR or vasomotor tone; #1 cause of syncope
prodromal sx: nausea, yawning, diaphoresis
triggers: micturition, defecation, coughing, emotion (stress or fear), pain
tx: if young pt w/no PMhx then just reassurance & D/C home
carotid sinus hypersensitivity
occurs in old men; triggers (pressure on carotic sinus)= turning head, tight collar, shaving neck over area
dx: carotid massage to reproduce sx (auscultate 1
to ensure no bruits)
orthostatic hypotension: decrease >20mm Hg with postural changes
causes: diabetic neuropathy (autonomic insufficiency), other peripheral neuropathy (alcoholic, nutritional,
amyloid), parkinsonism, idiopathic dysautonomia, hypovolemia, anti-HTN/ vasodilator drugs, neuro disorder (Shy-
Drager syndrome) physical deconditioning, sympathectomy, acute dysautonomia (guillain-barre syndrome variant)
cardiac disease: arrhythmias or outflow obstruction (aortic stenosis, hypertrophic obstructive cardiomyopathy)
arrhythmias #1 cause of cardiac induced syncope (usually bradycardia)
bradyarrhythmias: sinus bradycardia, sinoatrial block, sinus arrest, sinus syndrome, AV block
tachyarrhythmias: supraventricular tachycardia, with structural cardiac disease, atrial fibrillation a/w the wolf-
Parkinson-white syndrome, atrial flutter with 1:1 AV conduction
cardiopulmonary disease: PE, pulmonary HTN, atrial myxoma, myocardial disease (massive MI), LV myocardial
restriction or constriction, pericardial constriction/tamponade, aortic outflow tract obstruction (aortic valve stenosis,
hypertrophic obstructive cardiomyopathy)
vascular disease (TIA, carotid stenosis): r/o with carotid artery U/S or duplex scanning
neurologic disorder (seizures, intracranial lesions); consider EEG or CT/MRI is hx suggest seizures or intracranial lesions
o epilepsy: seizure of unclear etiology
o partial seizures: focal to one part of the body
simple=intact consciousness, complex= loss of consciousness
o absence (petit-mal) seizures
occurs in children
consciousness only briefly impaired; appears as if the person is staring into space
tx: ethosuximide
o generalized tonic-clonic seizures
causes: electrolyte disturbances (hypo/hypernatremia, hypomagnesemia, hypocalcemia), uremia, hypoxia, hypoglycemia, CNS
infection (encephalitis, meningitis, abscess), CNS anatomic abnormalities (trauma, stroke, tumor), hepatic failure, drug withdrawal
(alcohol, barbiturate, benzodiazepine), cocaine toxicity
sx: phases of muscular rigidity (tonic) followed by muscle jerking (clonic)
dx: BMP (r/o metabolic disturbance), toxin screen, CT or MRI of head (r/o anatomic defect), electroencephalogram (EEG)
EEG is only done if there is no other clear etiology of the seizure
o Status epilepticus
Tx: IV benzodiazepine (Lorazepam, diazepam) fosphenytoin> phenytoin phenobarbital neuromuscular blocking agent
(succinylcholine, vecuronium, or pancuronium) + intubation+ general anesthesia (midazolam or propafol)
Phenytoin SE: hypotension & AV block (b/c also a class Ib antiarrhythmic)
o Treatment
Treatment is not always necessary following a single seizures
Treatment indications: status epilepticus, abnormal EEG, family hx of seizures
choice= phenytoin, valproic acid, or carbamazepine; alternatives= gabapentin, topiramate, lamotrigine, oxcarbazepine,
if single agent not effective, try an alternative drug; if still not effective 2 drugs; if still not effective surgical
correction of a seizure focus
treat until pt is seizure-free for 2 yrs, then test if discontinuation can be done via a sleep deprivation EEG
driving restrictions: recommend that the patient find an alternate means of transportation
o Physiologic
Causes: fear, anxiety, fatigue, metabolic (hypoglycemia, hyperthyroid, pheochromocytoma), toxic (alcohol withdrawal, valproic
acid, lithium, methylxanthines=caffeine or theophylline)
o Essential tremor
Autosomal dominant (~1/3 of cases)
Tremor occurs at rest and with intention
Exacerbated by intentional activity and caffeine, decreased by alcohol use
Tx: propanolol
o Neurologic diseases: Parkinsons, cerebellar disease, Wilsons disease
o Causes: infectious, medications, SLE, sarcoidosis, carcinomatosis
o Sx: headache, fever, N/V, stiff painful neck, malaise, photophobia, altered mental status (confusion, lethargy, coma), myalgias, seizures
Increased ICP, kernings sign (unable to extend knees with hips flexed), brudzinskis sign (passive flexion of neck causes thigh/leg
N. meningitidis: Maculopapular rash w/ petechiae or purpura
Varicella or HSV: vesicular lesions
Complications: seizures, coma, brain abscess, subdural empyema, DIC, respiratory arrest; deafness, brain damage, hydrocephalus
o Acute: onset w/in hrs-days
Neonates (<3mo): GBS> E.coli >listeria monocytogenes; klebsiella spp.
Kids (3mo-18yrs): Neisseria meningitidis > strep pneumoniae >H. influenzae
Adults (18-50): Strep pneumo > N. meningitidis > H. influenzae
Elderly (>50 yo): Strep pneumo > N. meningitidis > listeria monocytogenes
Immunocompromised: L. monocytogenes > gram (-) bacilli > strep pneumo
Aseptic meningitis
Enterovirus, HSV, certain bacteria, parasites, fungi
o chronic: onset w/in wks-months
mycobacteria, fungi, lyme dz, parasites
o differential diagnosis: meningitis, brain or epidural abscess, subarachnoid hemorrhage
bugs that cause meningitis: strep pneumo (#1), N. meningitidis (#2), GBS/strep agalactiae, listeria monocytogenes, H. influenzae;
staph aureus or staph epidermidis following neuro procedures; enteroviruses, HSV 1 or 2, cryptococcus (HIV pts), TB, rocky
mountain spotted fever
o dx: CSF exam (lumbar puncture), blood cultures
CT scan before lumbar puncture if focal neurologic signs or abnormal level of consciousness, papilledema
Normal LP: WBC <5 (all lymphocytes or monocytes), glucose 50-75, protein <60
bacterial: elevated opening pressure, elevated WBC (PMNs) & protein, low glucose, gram stain usually positive
aseptic/viral meningitis: increased lymphocytes, protein normal, glucose normal
HSV: normal/increased opening pressure, elevated WBC (lymphocytes), normal/elevated protein, normal
glucose, high RBC count
o If HSV meningitis is suspected MRI (enhancement of the temporal lobes), HSV polymerase chain reaction
TB: normal/increased opening pressure, increased WBC (monocytes), low glucose, high protein
Repeat LP in 48 hrs shows decreased glucose from last value; AFB culture takes 6-8 wks; MRI (enhancement of the
basal region)
o tx: empiric antibiotics, steroids if cerebral edema (glucocorticoids decreased inflammation), vaccination; prophylaxis for close contacts
(rifampin or ceftriaxone)
start antibiotics after LP &blood cx unless there are anticipated delays such as need for CT, then start immediately
infants <3mo: cefotaxime + ampicillin + vancomycin (aminoglycoside if <4 wk old)
3mo-50 yo: (ceftriaxone or cefotaxime) + vancomycin
>50 yo: (ceftriaxone or cefotazime) + vancomycin + ampicillin
immunocompromised: ceftazidime + ampicillin+ vancomycin
o cryptococcal meningitis tx: IV amphotericin B + flucytosine, followed by chronic suppression with oral
lumbar puncture is still diagnostic if done 30min-2hrs after antibiotics
If neisseria meningitidis is suspected, start antibiotics immediately
Pneumococcus or meningococcus: 3
gen cephalosporin + vancomycin
Listeria (gram (+) rod): ampicillin
HSV: acyclovir + bacterial coverage until cx results are back
TB: 4 drug treatment (isoniazid+ rifampin + pyrazinamide + ethambutol or streptomycin)
all pt >65 yo :strep pneumo
Asplenic pt against encapsulated organisms: strep pneumo, n. meningitidis, H. influenzae
meningococcus (n. meningitidis) vaccine: immunocompromised, dorm/military
o household & close contacts: rifampin (2x/day for 2 days) or 1x ciprofloxacin
Supportive tx (analgesics, fever reduction) for aseptic meningitis; self-limited
Brain tumors
o Cerebellar tumor
Sx: ipsilateral ataxia (pt fall towards the side of the lesion), nystagmus, intention tremor, ipsilateral muscular hypotonia,
marked difficulty in coordination and performing rapid alternating movements; obstruction of CSF flow ICP headaches, N/V,
Brain abscess
o Can be d/t distant infections (lung, teeth, heart, GI, bone) or d/t contiguous spread of infection (middle ear, mastoids, paranasal sinuses)
o Agents: aerobic and anaerobic streptococci (69-70%) and bacteroides spp. 9anaerobes; 20-40%) are the most common; staph
aureus (10-15%)
o Sx: headaches, focal neurologic deficit
o Dx: CT scan (solitary/isolated ring-enhancing lesions)
Neurologic lesions
o Upper motor neurons: weakness, spasticity/ clonus/ increased muscle tone, hyperreflexia, extensor plantar responses
o Lower motor neurons: weakness, wasting, fasciculations
o Front lobe damage: apathy, inattention, disinhibition, labile affect
Dominant front lobe: Broca (motor) aphasia
o Parietal lobe damage
Dominant parietal lobe damage: inability to read, write, name, or do math
Nondominant parietal lobe damage: ignoring one side of body, trouble with dressing
o Temporal lobe damage: memory impairment, hyperaggression, hypersexuality
Dominant temporal lobe damage: Wernicke (sensory) aphasia
o Occipital lobe damage: visual hallucinations/ illusions
o Signs of cerebellar dysfunction: intention tremor, ataxia, broad-based gait, dysmetria, difficulty with rapid alternating movements,
nystagmus, dysarthria, scanning speech; muscle hypotonia can be seen pendular knee reflex
Cranial nerves
o Locations
Midbrain: CN 3,4
Pons: CN 5,6,7,8
Medulla: 9,10,11,12
o Trigeminal neuralgia
cranial nerve dysfunction
sx: severe pain in the face (stabbing)
pain precipitated by: chewing, touching the face, speaking words where the tongue strikes the back of the front teeth
tx: carbamazepine or oxcarbazepine; baclofen, lamotrigine; surgical decompression if not controlled by meds
postherpetic neuralgia
o d/t singles (herpes zoster reactivation); pain syndrome after resolution of the vesicular lesions
o tx:
shingles prevention: zoster vaccine to all pt >60yo
incidence prevention following shingles: antherpetic meds (acyclovir, famciclovir, valganciclovir)
pain control: tricyclic antidepressants, gabapentin, pregabalin, carbamazepine, phenytoin, or antiepileptic meds; topical capsaicin
disk herniation
o sx: pain at the site of compression, signs of nerve compression (if radiculopathy)
o dx: x-ray, MRI
cervical fracture
o sx: can compromise innervation to the diaphragm if phrenic nerve interrupted
o dx: tender to palpation, x-ray
o fluid filled dilated central canal in the spinal cord; d/t tumor or severe trauma
o sx: capelike distribution of loss (across upper back and both arms); loss of pain/temp, reflexes; muscle atrophy
o dx: MRI (most accurate)
o tx: surgical removal of tumor if present; drainage of fluid from the cavity
anterior spinal artery infarction
o sx: loss of all function except for posterior column (positional and vibratory sensation intact); flaccid paralysis below lesion, loss of deep
tendon reflexes at the level of lesion; spastic paraplegia several wks later, loss of pain & temp sensation, extensor plantar response
subacute combined degeneration of the cord
o d/t vit B12 deficiency or neurosyphilis
o sx: loss of positional and vibratory sensation
spinal trauma
o sx: acute onset of limb weakness and/or sensory disturbance; sphincter function impaired; loss od DTRs at the level of injury, hyperreflexia
below the level of injury
o tx: glucocorticoids
brown sequard syndrome
o unilateral hemisection fothe spinal cord
o sx: loss of pain & temp on the contralateral side; ipsilateral loss of motor function & positional/vibratory sensation
cauda equina syndrome
o sx: low back pain, saddle anesthesia, bowel or bladder dysfunction; possible lower extremity weakness & loss of reflexes d/t compression
of multiple sacral nerve roots
o tx: surgical emergency
brain abscess
o can spread from contiguous infection (sinuses, mastoid air cells, otitis media) or from any source of bacteremia
o sx: headache, N/V, fever, seizures, focal neurological findings
o dx: MRI or CT (best initial; ring, contrast enhancing lesion with surrounding edema and mass effect), brain biopsy (most accurate)
LP is contraindicated d/t risk of herniation
o Tx: empiric tx with penicillin + metronidazole+ (ceftriaxone or cefepime); vancomycin can be used instead of penicillin if pt has recent
neurosurgery (increased risk of staph)
Treat 6-8 wks IV, followed by 2-3 mo orally
o Most common CNS mass lesion in AIDs pt
o Sx: headache, seizures, focal neurologic deficits
o Dx: CT or MRI (multiple enhancing lesions often in basal ganglia)
o Tx: sulfadiazine + pyrimethamine
#1 causes of altered mental status in elderly= dehydration
Normal pressure hydrocephalus
o d/t decreased CSF absorption at the arachnoid villi or obstructive hydrocephalus
o Sx: gait disturbance (broad-based shuffling gait, bradykinetic), dementia, urinary incontinence
o Dx: CT or MRI (dilated ventricles)
o Tx: if repeated spinal taps cause improvement ventriculo-peritoneal shunts for definitive treatment
Frontotemporal dementia
o Causes: Picks disease
May have a family hx of frontotemporal dementia
o Sx: prominent personality changes (euphoria, disinhibition, apathy), compulsive behaviors (peculiar eating habits, hyperorality), impaired
Intact visuospatial functions
o Dx: MRI (symmetrical frontal or temporal lobe atrophy)
Multi-infarct dementia
o Sx: rapid onset dementia
o Dx: MRI (multiple areas of increased T-2 weighted density in the periventricular areas)
Alzheimers disease
o Sx: visuospatial problems early (getting lost while driving), anterograde memory dysfunctionpersonality and behavioral changes
hallucinations, changes in alertness
o Dx: MRI (normal or diffuse cerebral cortex atrophy)
o Tx: donepezil (anticholinesterase inhibitor increases Ach)
Dementia with lewy body
o Sx: fluctuating cognitive impairment with pronounced variation in attention and alertness, and bizarre visual hallucinations; motor
features of parkinsonism (with poor response to dopaminergic agonist therapy); prominent or persistent memory impairment; deficits in
attention, frontal-subcortical skills, and visuospatial ability
Progressive cognitive decline that interferes with normal social or occupational functions
Other features: repeated falls, syncope, transient LOC, neuroleptic sensitivity, systematized delusions
Creutzfeldt-jakob disease
o Fatal neurodegenerative disease d/t prions
Occurs on older pts (500-70 yo); most case sporadic, other familial or iatrogenic
o Sx: rapidly progressive dementia, myoclonus
o Dx: EEG (periodic high voltage complexes; periodic synchronous bi or triphasic sharp wave complexes), brain biopsy (cortical spongiform
o Tx: none; death usually occurs within 12 months
Parkinson disease (paralysis agitans)
o Progressive neurodegenerative disease; mean age 70.5yo (pt >50-60 yo)
d/t dopamine depletion in the substantia nigra (basal ganglia) and in the nigrostriatal pathway to the caudate & putamen
increased inhibition of the thalamus & reduced excitatory input to the motor cortex
o Secondary parkinsonism: antipsychotics (metoclopramide, prochlorperazine, reserpine, thorazine) & antiemetics are most common causes;
repeated head trauma, encephalitis
o Sx: tremor (pill rolling, at rest & decreased with purposeful action, 5-7 Hz frequency, may be a sensation of internal tremulousness),
bradykinesia, rigidity (asymmetric, increased resistance to passive movement; cogwheel rigidity d/t tremor superimposed on increased
tone), postural instability (orthostatic hypotension d/t inability of pulse and BP to reset appropriately with movement), micrographia (small
writing), limited facial expression (hypomimia)
Shy-Drager syndrome (multiple system atrophy): parkinsonism predominantly with orthostasis
Sx: parkinsonism, autonomic dysfunction (postural hypotension, abnormal sweating, dry mouth, dry skin,
disturbance of bowel/bladder control, abnormal salivation or lacrimation, impotence, gastroparesis), widespread
neuro signs (cerebella, pyramidal, or lower motor neuron)
Tx: intravascular volume expansion (fludrocortisone, salt supplementation, alpha-adrenergic agonists, application of
constrictive garments to the lower body); note that anti-parkinson drugs are generally ineffective
Motor sx
Craniofacial: hypomimia (masked facial expression), decreased spontaneous eye blink rate, speech impairment
(hypokinetic dysarthria, hypophonia, palilalia= involuntary repetition of syllables/words/phrases), dysphagia,
sialorrhea= drooling
Visual: blurred vision, impaired contrast sensitivity, hypometric saccades, impaired vestibuloocular reflex, impaired
upward gaze & convergence, eyelid opening apraxia
Musculoskeletal: micrographia (small handwriting), dystonia, myoclonus, stooped posture, camptocormia (severe
anterior flexion of the thoracolumbar spine), kyphosis, scoliosis, difficulty turning in bed
Gait: shuffling, short stepped gait, freezing, festination (involuntary quickening of the gait)
Nonmotor sx
Cognitive dysfunction and dementia, psychosis and hallucinations (paranoid psychosis; visual hallucinations most
common), mood disorders (depression, anxiety, apathy/abulia), sleep disturbances (insomnia sleep initiation
problems, frequent awakening, and early morning awakening), fatigue, autonomic dysfunction, olfactory dysfunction,
pain and sensory disturbances, dermatologic findings (seborrheic dermatitis)
o Ambulia= loss of impulse/will/motivation to think, speak, and act
Dementia: subcortical; psychomotor retardation, memory difficulty, altered personality, problems with executive
function (decision making or multi-tasking), memory retrieval, visuospatial misperception
o Cortical neuronal Lewy inclusion bodies filled with alpha synuclein+ amyloid plaques & neurofibrillary
tangles (more common to Alzheimers disease)
o Dx: Based on clinical impression
Brain MRI to r/o structural lesions
Striatal dopamine transporter imaging (DaTscan) may be useful for pts where clinical diagnosis is unclear
o Treatment

Dopamine agonists (pramipexole, ropinirole): best initial tx for severe parkinsonism
Pergolide and cabergoline should NOT be used d/t risk of valvular heart disease
Bromocriptine is also not frequently used d/t SE
Levodopa + peripheral decarboxylase inhibitor (carbidopa) is most effective for symptomatic treatment
Carbidopa inhibits aromatic AA decarboxylation; inhibits metabolism of levodopa in the peripheral circulation
SE: on/off phenomena (episodes of too much dopamine and insufficient dopamine)
COMT inhibitor (Entacapone, tolcapone): extend the duration of levodopa/carbidopa by blocking the metabolism of dopamine
MAO B inhibitors (Selegiline, rasagiline): block metabolism of dopamine; only MAO-B inhibitors are a/w the possibility of
retarding the progression of parkinsonism
mild symptomatic benefit; only used for early disease
Avoid tyramine-containing foods (wine, cheese); they precipitate HTN
Anticholinergic drugs (benztropine, trihexyphenidyl): used for young pts when tremor or rigidity is the predominant sx (mild
SE: dry mouth, worsening prostatic hypertrophy, constipation
Amantadine: used for early or mild PD or for problematic dyskinesia
Increases release of dopamine & NE from nerve endings; weak NMDA receptor antagonist; anticholinergic
Psychosis: quetiapine or clozapine (atypical neuroleptics); stop or reduce drugs causing psychosis in reverse order of potency
(anticholinergic, amantadine, COMT inhibitors, and lastly dopamine agonists)
Choose antipsychotics with the least extrapyramidal sx (antidopaminergic)
Note: clozapine requires weekly or bi-weekly blood counts d/t risk of granulocytopenia (risk exponentially decreased
with time; almost nothing >6mo)
Daytime sleepiness: sleep hygiene, modafinil, methylphenidate, or judicious use of coffee during the day
Fatigue: amantadine, stimulants (methylphenidate, pemoline)
Depression: SSRI (SE possibly aggravates motor sx, adverse interaction with selegiline causing serotonin syndrome)
Deep brain stimulation (electrical stimulation)
Dopamine agonist for pt <65, levodopa for pt >65
Multiple sclerosis
o Multiple neurologic deficits of the CNS; presents in 20-40s; insidious onset of intermittent neurologic deficits
o Sx: scattered motor & sensory deficits (paresthesias and numbness, weakness, gait disturbance, visual disturbances); optic neuritis
blurry vision or visual disturbances (most common), painless loss of vision; diplopia, internuclear ophthalmoplegia; b/l trigeminal
neuralgia; cognitive defects, mental status changes, emotional lability, dementia; spasticity (painful contracted muscles), hyperreflexia,
fatigue, cerebellar deficits; scanning speech
Internuclear ophthalmoplegia: inability to adduct 1 eye with nystagmus in the other eye
o Dx: MRI ( demyelination plaques= white matter lesions surrounding the ventricles, corpus callosum, basal ganglia); lumbar puncture of
CSF (elevated protein, <50-100 WBCs, oligoclonal bands/ elevated IgG, elevated myelin basic protein)
o Tx:
high dose steroids (glucocorticoids) for acute exacerbation (shorten duration)
prevent relapse & progression: 1
choice glatiramer acetate (copolymer 1) or interferon-beta; natalizumab (alpha-4 integrin
inhibitor), mitoxantrone, azathioprine, cyclophosphamide, cyclophosphamide, methotrexate
glatiramer acetate: synthetic mixture of polypeptides containing random combinations of 4 AA found in myelin basic
protein; induces suppressor T-cells to down regulate the T-cell mediated immune response to myelin antigens
natalizumab SE: progressive multifocal leukoencephalopathy (PML; new multiple white matter hypodense lesions)
interferon beta is best for the relapsing-remitting form of MS
immunosuppressive agents (cyclosporine, methotrexate, mitoxantrone, etc) can be used for the progressive form of MS
(downhill course w/o clear-cut remissions)
Spasticity: baclofen, dantrolene, or tizanidine (central acting alpha agonist)
Amyotrophic lateral sclerosis (ALS)
o Loss of upper and lower motor neurons
o Onset age 20-40
o Sx: weakness starting distally & asymmetrically, difficulty chewing & swallowing, difficulty speaking, decrease in gag reflex; pooling
of saliva in pharynx aspiration, weak cough, respiratory difficulties
Upper motor neurons: weakness, spasticity, hyperreflexia, extensor plantar responses
Lower motor neurons: weakness, wasting, fasciculations
o Dx: electromyography (loss of neural innervation in multiple muscle groups), elevated CPK
o Tx: riluzole (reduces glutamate buildup in neurons; may prevent progression)
Spasticity: baclofen
Respiratory distress/failure: CPAP, BiPAP, tracheostomy & ventilator maintenance
Most common cause of death is respiratory failure
Charcot-marie-tooth disease
o Genetic; loss of motor and sensory innervation
o Sx: distal weakness & sensory loss, wasting in the legs (legs look like inverted champagne bottles), decreased DTRs, tremor foot drop
o Dx: electromyography (most accurate)
Foot drop
o d/t damage in the common peroneal nerve or radiculopathy of any of the spinal roots that contribute to the peroneal nerve (L4-S2)
o sx: high-stopping or Steppage gait d/t the inability to dorsiflex the foot
Restless leg syndrome
o More common middle age-older pt; pt with chronic kidney disease and/or iron deficiency anemia
o Sx: uncomfortable sensation or urge to move the legs (creepy and crawly sensation)
worse at night or at rest; Worsened by caffeine
relieved by moving the legs, massage, warming
bed partner may complain of being kicked at night
o Tx: dopamine agonists (pramipexole, ropinerole)
Huntington disease
o Autosomal dominant; Hereditary CAG trinucleotide repeat on Chr. 4; onset age 30-50 yo
o Sx: choreaform movement disorder (dyskinesia), dementia, behavior changes (irritability, moodiness, antisocial behavior), mood
disturbances (depression, apathy)
Movement disorder progression: fidgetiness /restlessness, dystonic posturing, rigidity, akinesia
Choreiform movements: facial grimacing, ataxia, dystonia, tongue protrusion, writhing movement of the extremities
o Dx: clinical (movement, memory, mood changes); head CT or MRI (caudate nucleus atrophy enlargement of the lateral ventricles)
o Tx: dyskinesia tetrabenazine; psychosis haloperidol or quetiapine
Tourette disorder
o Sx: vocal tics, grunts, coprolalia (involuntary swearing); motor tics (sniffing, blinking, frowning), obsessive-compulse behavior
o Tx: neuroleptics (haloperidol, clonazepam, pimozide)
Facial (7
CN) nerve palsy/ bell palsy
o Causes: idiopathic, lyme disease, sarcoidosis, herpes zoster, tumors, stroke
o Sx: paralysis of the entire side of the face (except stroke will only have lower face paralysis b/c upper face innervated from both
hemispheres); difficulty eating, hyperacusis (sounds are extra loud d/t loss of stapedius muscle innervation), taste disturbances (CN7 detects
taste in anterior 2/3 of tongue), difficulty closing the eye (especially at night) dryness corneal ulceration
Central facial paresis will still have forehead furrowing; bells palsy (peripheral 7
nerve palsy) will have absence of
forehead furrows
o Dx: clinical; electromyography and nerve conduction studies (most accurate)
o Tx: self-resolving (60%); prednisone; taping eye shut & lubricants at night to prevent corneal ulcers
Peripheral neuropathies
o Causes: diabetes mellitus (most common), uremia, alcoholism, paraproteinemia (monoclonal gammopathy of unknown significance=MGUS)
o Sx:
Ulnar: wasting of hypothenal eminence, pain in 4
Radial: wrist drop
Median n: thenar wasting, pain/numbness in first 3 fingers
Lateral cutaneous nerve of thigh: pain/numbness of outer aspect of 1 thigh
Occurs with pregnancy, obesity, sitting with crossed legs
Tarsal tunnel (tibial nerve): pain/numbness in ankle and sole of foot; worse with walking
Peroneal: weak foot with decreased dorsiflexion and eversion
o Tx: 1
choice=pregabalin or gabapentin; TCA antidepressants, seizure meds (phenytoin, carbamazepine, lamotrigine)
Acute inflammatory polyneuropathy (Guillain-barre syndrome)
o Autoimmune attack of myelin sheath in multiple peripheral nerves; no CNS involvement
a/w infections, recent immunization, or pt with lymphoma, sarcoidosis, or SLE
associated infections: campylobacter jejuni (#1), herpes viruses, mycoplasma, hemophilus influenzae, HIV
o Sx: weakness/ parestheisas in the legs that ascends toward the chest (ascending paralysis), loss of DTRs; respiratory muscle
weakness, autonomic dysfunction possible (hypo/hypertension, tachycardia)
Note: sensation remains intact or is only slightly diminished
o Dx: clinical diagnosis; nerve conduction studies/electromyography (decrease in propagation/velocity of electrical impulses d/t
demyelination), CSF (increased protein, normal cell count)
PFTs: decrease forced vital capacity and peak inspiratory pressure if diaphragm involved; earliest way to detect impending
respiratory failure
Serial measurement of bedside vital capacity is used to monitor respiratory function
o Tx: self-resoling; IVIG (children) or plasmapheresis (adults) to reduce severity and length of disease
Myasthenia gravis
o Antibodies against Ach receptors at the neuromuscular junction muscle weakness
o Sx: double vision, difficulty swallowing; ptosis, weakness with sustained activity, normal pupillary responses
o Dx: acetylcholine rector antibodies (best initial), edrophonium test (short acting acetylcholinesterase inhibitor; improvement in motor
function that lasts a few minutes), electromyography (most accurate; decreased strength with repetitive stimulation); CXR/CT/MRI (look for
thymoma or thymic hyperplasia)
o Tx: neostigmine or pyridostigmine (long acting acetylcholinesterase inhibitors)
Acute exacerbation: IVIG or plasmapheresis
If not controlled: <60 yo thymectomy, >60 yo prednisone
Weaning off steroids: azathioprine, cyclophosphamide, or mycophenolate
o Sx: hallucinations (auditory)
Mini mental status exam for dementia
o <9 severe cognitive impairment, 10-20 moderate impairment, 21-24 mild impairment, 25-30= normal cognition
o orientation to time (5), orientation to place (5), registration (3), attention and calculation (5), recall (3), language (2), repetition (10),
complex commands (6)
attention and calculation: serial sevens or sell world backwards
language: naming a pencil and watch
neurocutaneous diseases
o tuberous sclerosis
sx: neuro sx (seizures, progressive psychomotor retardation, slowly progressive mental deterioration), skin sx (adenoma
sebaceum, shagreen patches, ash leaf patches), retinal lesions, cardiac rhabdomyomas
adenoma sebaceum: reddened facial nodules
shagreen patches: leathery plaques on the trunk
ash lead patches: hypopigmented areas
tx: seizure control
o neurofibromatosis (von Recklinghausen disease)
sx: neurofibromas, 8
CN tumors, caf au lait spots (cutaneous hyperpigmented lesions), meningioma and gliomas
neurofibromas: soft, flesh colored lesions attached to peripheral nerves
tx: 8
CN lesions may need surgical decompression to help preserve hearing
o sturg-weber syndrome
sx: port-wine stain of face, seizures, CNS (homonymous hemianopsia, hemiparesis, mental subnormality)
dx: skull x-ray (calcification of angiomas)
tx: control seizures
Lhermitte Test (barber chair phenomenon): electrical sensation that runs down the back and into the limbs; d/t lesion of the posterior column or
caudal medulla
o The patient is sitting or standing and the examiner is behind them and introduces lower cervical flexion
A positive test results in production of an electrical type response or a pins and needles sensation near the end range of flexion
o Diff dx: multiple sclerosis, vit B12 deficiency, behcets disease, transverse myelitis, radiation myelopathy, compression of the spinal cord
(cervical spondylosis, disc herniation, tumor, Arnold-chiari malformation)
Spurlings test: assess nerve root pain (radicular pain) in the neck
o Downward pressure on the top of the patients head in the neutral position, in neck extension, and with neck extended and tipped to the
affected side
Lumbar puncture
o Contraindications: acute head trauma, signs of elevated ICP, suspected subarachnoid hemorrhage
Near a clear CT/MRI in these settings; risk of uncal herniation death
o CSF analysis
Condition Cells Glucose (mg/dL) Protein (mg/dL) Pressure (mmHg)
Normal CSF 0-3 lymphocytes 50-100 20-45 100-200
Bacterial meningitis >1000 PMNs <50 ~100 >200
Viral/aseptic meningitis >100 lymphocytes Normal Normal/slightly increased Normal/ slightly increased
Pseudotumor cerebri Normal Normal Normal >200
Guillain-barre syndrome 0-100 lymphocytes Normal >100 Normal
Cerebral hemorrhage Blood (RBC) Normal >45 >200
Multiple sclerosis Normal/ slightly increased lymphocytes Normal Normal/slightly increased normal
Sleep disorders
o Circadian rhythm disorders
Delayed sleep phase syndrome: inability to fall asleep at normal bedtimes such as 10pm-midnight; pt cannot fall asleep
until 4-5am but have normal sleep if they are allowed to sleep until late morning; pt c/o insomnia and excessive daytime
Dx: sleep hx and sleep diary
Advanced sleep phase disorder: inability to stay awake in the evening (usually after 7pm) making social functioning difficult; c/o
early morning insomnia d/t early bedtime
Head and neck
Menieres disease
o Distention of the endolymphatic compartment of the inner ear
Triggers: alcohol, caffeine, nicotine, food high in salt
o Sx: sense of ear fullness, vertigo (20 min-24 hr), low-frequency sensorineural hearing loss, tinnitus; vertigo can cause N/V and postural
instability; symptoms wax & wane; nystagmus during an acute attack
o Tx: salt restricted diet (2-3g /day); if persistant diuretics, antihistamines, anticholinergics
o Abnormal remodeling of the otic capsule (bony overgrowth of the stapes) stapes footplate becomes fixed to the oval window causing loss
of piston action
Age 20-30, F>M, possible autoimmune
o Sx: Conductive hearing loss
o Dx: PE, CT (may show lucent or sclerotic focus in the temporal bone near the oval window)
Rinne test (bone conduction> air conduction), Weber test (sound lateralizes to the affected ear; sound is perceived as louder b/c
ambient noise of the room is perceived less on that side, so bone conduction seems louder)
o Tx: hearing amplification or surgical stapedectomy
o Elderly pts (>50yo)
o Sx: sensorineural hearing loss (starts as symmetric high-frequency hearing loss)
Difficulty hearing in corwsed or noisy environments; trouble hearing high-pitched noises or voices
Medication induced ototoxicity
o Sx: bilateral sensorineural hearing loss (reversible or permanent), and/or tinnitus
o Drugs: aminoglycosides, loop diuretics (furosemide), chemotherapeutic agents, aspirin
Serous otitis media (non-infectious effusion)
o Most common middle ear pathology in pts with HIV
o Auditory tube disfunction d/t HIV lymphadenopathy or obstructing lymphomas
o Sx: middle ear effusion w/o signs of inflammation dull tympanic membrane that is hypomobile, conductive hearing loss
o Dx: pneumatic otoscopy
Ramsay Hunt syndrome
o Herpes zoster infection in the ear
o Sx: facial nerve palsy (bells palsy), vesicles in the auditory canal and auricle
Malignant otitis externa
o Elderly pts w/poorly controlled diabetes; pseudomonas aeruginosa infection
o Sx: ear pain & drainage, granulation tissue seen w/in the ear canal
Complications: osteomyelitis of the skull base, destruction of the facial nerve
o Dx: CT or MRI
o Tx: ciprofloxacin
o normal aging (starts age 40, peaks age 60)
o loss of elasticity in the lens lack of accommodation of the lens difficulty focusing in near objects
Optic neuritis
o Age 20-45 yo; F>M; a/w multiple sclerosis
o Sx: rapid impairment of vision in 1 eye (rarely b/l) and pain on eye movement (retrobulbar pain); marked changes in color
perception; afferent pupillary defect and filed loss (usually with central scotoma)
o d/t increased ICP
o Sx: transient loss of vision that lasts a few seconds with changes in head position, morning headaches
Central retinal vein occlusion
o RFs: coagulopathy, hyperviscosity, chronic glaucoma, atherosclerotic RFs (age, HTN, diabetes)
o Sx: sudden painless unilateral loss of vision
o Dx: disk swelling, venous dilation and tortuosity, retinal hemorrhages, cotton wool spots
Central retinal artery occlusions
o d/t embolism ischemia of the inner retina
RFs: carotid artery disease, endocarditis, cardiac valvular disease, long bone fracture, hypercoagulable conditions, vasculitis, atrial
Recall ophthalmic artery is the first intracranial branch of the internal carotid artery; supplies blood to eye via central retinal
artery (supplies inner retina) and ciliary branches (supplies choroids and anterior portion of globe)
o Sx: sudden painless loss of vision in 1 eye; commonly a/w amaurosis fugax before the occlusion
o Dx: ophthalmoscopy (pallor of the optic disc, cherry red fovea, boxcar segmentation of blood in the retinal veins; diffuse ischemia retinal
whitening and cherry red spots)
o Tx: ocular massage and high flow oxygen
Amaurosis fugax
o Retinal emboli
a/w atherosclerosis, CV disease, HTN
o Sx: monocular transient visual loss; like a curtain falling down
o Dx: ophthalmoscopy (zones of whitened edematous retina following the distribution of the retinal arterioles)
Choroidal rupture
o d/t blunt ocular trauma
o dx: ophthalmoscopy (central scotoma, retinal edema, hemorrhagic detachment of the macula, subretinal hemorrhage, crescent-shaped streak
concentric to the optic nerve)
Vitreous hemorrhage`
o Causes: diabetic retinopathy (#1)
o Sx: sudden loss of vision and onset of floaters
o Dx: fundus is hard to visualize
o Tx: conservative (upright position during sleep which enhances settling of hemorrhage)
Retinal detachment
o Most common age 40-70 yo; usually the inciting event is months before retinal detachment (myopia or trauma retinal breaks fluid seeps
in an separates the retinal layers)
o Separation of the inner layers of the retina
May be a/w metabolic disorder (DM), trauma (including ocular surgery), vascular disease, myopia, or degeneration
o Sx: loss of vision, photopsia (flashes of light) with showers of floaters (spots in the visual field); a curtain coming down over my eyes
o Dx: fundoscopy (elevated retina with folds and/or a tear)
o Tx: laser therapy and cryotherapy (create permanent adhesions between the neurosensory retina, retinal pigment epithelium, and choroid)
Diabetic retinopathy
o Diabetic retinopathy occurs before nephropathy
o Background/simple retinopathy: microaneurysm, dot and blot hemorrhages, hard exudates, retinal edema
o Per-proliferative retinopathy: cotton wool spots
o Proliferative/malignant retinopathy: neovascularization
o Eventual blindness
o Tx: argon laser photocoagulation to prevent complications
Hypertensive retinopathy
o initally focal spasm of arterioles then progressive sclerosis and narrowing
o Dx: fundoscopy (AV nicking, copper wiring or silver wiring, exudates and hemorrhages)
Acute angle-closure glaucoma
o Seen in elderly pts (age 55-70); usually occurs following pupillary dilation (ex. In a dark movie theatre, during times of stress, or due to
drug intake)
o Sx: acute onset of sever eye pain, visual loss, halos around lights, headache, N/V
Eye is red with a hazy/steamy cornea; fixed dilated pupil that is nonreactive to light; anterior chamber is shallow ith
inflammatory changes; tonometry (increased intraocular pressure)
o Dx: tonometry (elevated intraocular pressure)
o Tx: medical emergency; narcotics for pain control, decrease intraocular pressure (mannitol, acetazolamide, timolol, or pilocarpine);
laser peripheral iridotomy for permanent cure
Avoid atropine (dilates the pupil and worsen the glaucoma)
Timolol (topical beta blocker) and acetazolamide (carbonic anhydrase inhibitor) reduce the production of aqueous humor
Pilocarpine opens the canals os Schlemm to allow drainage of aqueous humor
Open angle glaucoma
o Sx: gradual loss of peripheral vision (over years) tunnel vision; central vision is spared
o Dx: elevated intraocular pressure, cupping of the optic disk
o Tx: beta-blocker (timolol eye drops), laser trabeculoplasty, surgical trabeculectomy
Sympathetic ophthalmia/ spared eye injury
o Immune mediated inflammation of ene eye (the sympathetic eye) after a penetrating injury to the other eye
d/t the uncovering of hidden antigens (some antigens are contained w/in the eye are protected from immunologic
recognition by natural barrier; breaking the barrier results in release of these antigens autoantibodies and cell mediated
o Sx: anterior uveitis, panuveitis, papillary edema, or blindness
o Progressive thickening of the lens
Caused by oxidative damage that occurs with aging
o Sx: gradual blurred vision and glare
o Tx: lens extraction (phacoemulsification, extracapsular or intracapsular cataract extraction)
o a/w HLA B27-related conditions
o Sx: blurred vision, moderate pain, conjunctival injection, constricted pupils; hypopyon in severe anterior uveitis; keratic precipitates
(mutton fat) and iris nodules may be present
macular degeneration
o RF: Pt >50 yo (age related), smoking
o Degeneration and atrophy of the outer retina, retinal pigment epithelium, bruchs membrane, and choriocapillaries
o Sx: painless progressive and unilateral or bilateral loss of central vision (burring of central vision); intact peripheral fields and
navigational vision; distortion of straight lines (lines appear wavy)
o Dx: drusen deposits in the macula
intraocular foreign body
o RF: high-velocity injuries (drilling, grinding, etc)
o Dx: pen light exam with topical anesthetic; if no gross abnormalities fluorescein application followed by a slit lamp> woods lamp
exam; if no abrasion or foreign body seen with high suspicion CT or ultrasonography of orbit
MRI contraindicated! (can dislodge the foreign body d/t strong magnetic field)
Allergic conjunctivitis
o Acute HSR reaction d/t environmental exposure to allergens
a/w personal/family hx of asthmas, seasonal rhinitis, atopic ermatitis, food allergies, urticaria
o Sx: intense itching, hyperemia, tearing, and conjunctival edema and eyelid edema; photophobia, burning sensation
o Tx: self-limited w/in 24hrs, decrease exposure to allergens, avoid rubbing eyes, topical antihistamines, artificial tears, cool compresses
Atopic keratoconjunctivitis
o Severe form of ocular allergy
o Sx: itching, tearing, thick mucus discharge, photophobia, blurred vision
Toxic conjunctivitis
o d/t direct damage to ocular tissues from drugs after prolonged use (aminoglycosides, glaucoma drops, artificial tears, contact lens solution)
Herpes simplex keratitis
o RF: excessive sun exposure, outdoor occupation, fever, immunodeficiency (HIV)
o Sx: pain, photophobia, blurred vision, tearing, redness; can cause corneal blindness
Corneal vesicles and dendritic ulcers
o Dx: clinical; epithelial scrapings (multi-nucleated giant cells)
o T: oral or topical antiviral tx
Bacterial keratitis
o RF: contact lenses, corneal trauma, foreign body
o Sx: cornea appears hazy with a central ulcer and adjacent stromal abscess; hypopyon may be present
Herpes simplex retinitis
o Occurs in HIV pts
o Sx: rapidly progressing b/l necrotizing retinitis (acute retinal necrosis syndrome); starts as keratitis and conjunctivitis with eye pain
rapidly progressive visual loss & blindness
o Dx: fundoscopy (widespread pale peripheral lesions and central necrosis of the retina)
CMV retinitis
o Occurs in HIV pts
o Sx: painless loss of vision
o Dx: fundoscopy (fluffy or granular retinal lesions located near the retinal vessels and associated hemorrhages)
Herpes zoster ophthalmicus
o d/t varicella-zoster virus reactivation in the trigeminal ganglion travels to the ophthalmic branch to the forehead and eye
mostly in elderly or immunosuppressed
o sx: fever, malaise, burning/itching sensation in the periorbital region; vesicular rash in the distribution of the cutaneous branch of
the 1
division of the trigeminal nerve
o dx: conjunctivity and dendriform corneal ulcers
o tx: high dose acyclovir (started w/in 72hrs after eruption) to recues the development of complications
Postoperative endophthalmitis
o Occurs w/in 6 wks of surgery; infection within the vitreous of the eye
o Sx: eye pain, decreased visual acuity; swollen eyelids and conjunctiva, hypopyon (pus in the eye), corneal edema and infection
o Dx: sent vitreous for gram stain and culture
o Tx: intravitreal antibiotics or vitrectomy
o a/w primary biliary cirrhosis
o bilateral cholesterol-filled soft yellow plaques on the medial aspects of the eyelids; benign; lipid-filled macrophages in the dermis
o agent: staphlococci
o purulent infection of one of the glands of the eyelids (abscess located over the upper or lower eyelid)
stye=small external hordeolum involving Zeiss or Molls glands
o tx: frequent hot compresses, incision and drainage if unresolved within 48 hrs after starting tx; antibiotics against staph
o chronic sterile granulomatous inflammatory lesion of the meibomian glands
painful swelling that progresses to a nodular rubbery lesion (hard painless lid nodule)
persistent or recurrent chalazion can be d/t meibomian gland carcinoma (sebaceous carcinoma)
basal cell carcinoma=most common malignancy of the lid margin & may appear similar to chalazion
o dx: histopathologic exam to r/o malignancy
o tx: incision and drainage
o choric inflammatory condition involving b/l lid margins
o sx:
anterior blepharitis: crusty discharge clinging to the lashes
posterior blepharitis: hyperemic lid margins with telangiectasias
o infection of the episcleral tissue between the conjunctiva and sclera
o sx: acute onset mild-moderate discomfort, photophobia, watery discharge; diffuse or localized bulbar conjunctival injection
o usually pt >40 yo
o infection of the lacrimal sac d/t obstruction of the nasolacrimal duct
agents: staph aureus, beta-hemolytic strep
o sx: pain, swelling, tenderness, redness in the tear sac area (medial canthal region); mucous or pus can be expressed; may have fever or
Nasal polyp
o a/w chronic rhinitis, post-nasal drainage, asthma, aspirin (or NSAID) exacerbated respiratory disease (bronchospasm)
o sx: bilateral nasal obstruction & discharge, anosmia (decreased smell decreased taste); bilateral grey glistening mucoid masses in the nasal
o Whitish patch or plaque that can not be scraped off; cant be characterized as any other disease (dx of exclusion)
a/w chronic irritation to the oral mucosa d/t smoking, alcohol, or ill-fitting dentures
complications: squamous cell carcinoma
Oral ulcers
o Gingivostomatitis d/t HSV1
Multiple vesicular intraoral lesions that have a red border
Oral candidiasis
o Risk factors: diabetes
o Whitish plaques that can be scraped off with a tongue depressor
Temporomandibular joint (TMJ) dysfunction
o Hx of nocturnal teeth grinding
o Sx: ear pain (d/t proximity of joint; pain worse with chewing), audible clocks or crepitus with jaw movement
o Tx: nighttime bit guard, surgery
Thyroid cancer
o Papillary thyroid cancer
Most common thyroid malignancy; epithelial origin
Slow infiltrative local spread to other parts of the thyroid and lymp nodes
Dx: histology (psammoma bodies; large cells with ground glass cytoplasm and pale nuclei with inclusion bodies and central
grooving; hurthle cells may be present)
o Follicular thyroid cancer
Epithelial origin
Encapsulated; invasion of tumor capsule and blood vessels distinguishes it from follicular adenoma
Early hematogenous spread to lung, brain, and bone
Dx: histology (hurthle cells may be present)
o Medullary cancer of the thyroid
C-cell origin; Secretion of calcitonin
o Lymphoma of the thyroid
Increased risk from hashimotos thyroiditis
Sx: rapid enlargement of the thyroid gland, compressive sx (dysphagia, voice change)
Dx: CT scan of neck (enlargement of the thyroid gland around the trachea; doughnut sign), thyroid U/S (pseudocystic pattern),
reduced radioactive iodine uptake; core needle biopsy
o d/t infection with Haemophilus influenzae or steptococcus pyogenes
o sx: high grade fever, severe sore throat, odynophagia (painful swallowing), droolin, progressive airway obstruction
o tx: prevention with Hib vaccine;
Peritonsillar abscess
o Complication from tosillitis
o Sx: fever, chills, sore throat; hot potato voice, deviation of the uvula; unilateral lymphadenopathy
Complications: airway obstruction, spear to the parapharyngeal space involvement of the carotid sheath
o Tx: aspiration of the abscess, IV antibiotics
Retropharyngeal abscess
o Sx: sore throat, fever, difficulty swallowing (dysphagia), pain with swallowing (odynophagia), pain with certain neck movements (extension),
trismus (inability ot open the mouth normally)
o Complication: spread of infection to mediastinum acute necrotizing mediastinitis
danger space of infection is between the alar and prevertebral fasciae
o dx: CT or lateral x-ray of neck
o tx; IV broad-spectrum antibiotics, urgent drainage of the abscess
infectious mononucleosis
o sx: fever, pharyngitis, posterior cervical lymphadenopathy, malaise, splenomegaly; risk of splenic rupture (avoid contact sports until the
physical exam is normal no splenomegaly)
o dx: atypical lymphocytosis, positive heterophile antibody test
o sx: pseudomembranous pharyngitis, low grade fever, unilateral nasal discharge, pharyngitis, cervical lymphadenopathy
ECG interpretation
o Inferior surface: Leads II, III, aVF; supplied by right coronary artery
o Anterior surface: leads V2-V4; supplied by left anterior descending coronary artery (LAD)
o Lateral surface: leads I, aVL, V5 & V6; supplied by left circumflex artery
o Posterior surface: R waves in leads V1 & V2
o Horizontally: 1 small box= 0.04 sec , each large box=0.2 sec (200 ms) if paper speed is 25 mm/sec
o Vertically: 1 small box=10mm=1mV
o Steps: rate, rhythm, axis, intervals, P wave, QRS complex, ST segment, T wave, overall interpretation
o Heart rate
Counting boxes from R-R interval (300/ # big boxes): 300, 150, 100, 75, 60, 50
If irregular rhythm: count # QRS complexes x 6
Divide by 6 b/c standard ECG displays 10 sec of time to get 60 sec (bpm)
o Rhythm:
Sinus rhythm:
P wave upright in leads I, II, aVF, and V4-V6; negative in aVR. Negative or biphasic in III and V1
o Most important: up in I & aVF, down in aVR
P waves before every QRS complex
If QRS <0.12 sec, then rhythm is supraventricular
If the QRS is wide (ie, >0.12 sec), then the rhythm is either supraventricular with aberrant conduction, pre-excitation, or
ventricular pacing, or it is of ventricular origin
o Axis: direction and magnitude of various complexes
Normal between -30 to 90 degrees (directed downward/ inferior and to the left)
Left axis deviation: between -30 to -90
Right axis deviation: between 90 and 180
Between -90 and -180 is either extreme L or R deviation
Determining axis
If the QRS complex is positive (upright) in both leads I and II, then the axis falls between -30 and 90o, and the axis is
If the QRS complex is positive in lead I but negative in lead II, then the axis is leftward (-30 to -90o).
If the complexes are negative in lead I and positive in aVF, then the axis is rightward (90 to 180o).
If the complexes are negative in both I and II, then the axis is extreme (180 to -90o).
Another method of axis determination is to find the lead in which the complex is most isoelectric; the axis is directed
perpendicular to this lead. As an example, if the QRS is isoelectric in lead 3 which is directed at 120o, then the electrical
axis is either 30o or -150o.
A third method is to determine the frontal lead in which the QRS is of the greatest positive amplitude. The axis is
parallel to this lead.
o P wave: atrial depolarization
duration <0.12 sec (3 small boxes) and amplitude <0.25 (2.5 small boxes)
Right atrial depolarization before L atrium Notched in limb leads & biphasic in V1
o PR interval: measured from the beginning of the P wave to the first part of the QRS complex; represent atrial depolarization and conduction
through the AV node and the His-Purkinje system
Normally 0.12-0.2 sec (3-5 small boxes)
Short PR interval: wolff-parkinson-white syndrome
Long PR interval: 1
degree AV block
Shorter at faster HR d/t sympathetic enhancement of AV node conduction
o QRS: ventricular depolarization
Total time <0.06-0.10 sec (1.5-2.5 small boxes)
Long QRS interval: bundle branch block, ventricul preexcitation, ventricul pacing, ventricular tachycardia
Q wave: initial negative deflection (septal depolarization); seen in leads I, aVL, V4-V6
R wave (L. ventricle myocardium depolarization): first positive deflection
Small R wave in V1= initial septal depolarization
Should progress in size across V1-V4/V6 (precordial leads)
S wave (terminal depolarization of the high lateral wall): negative deflection following the R wave
R wave: second positive deflection
Lower case letters are used for small amplitude waves <0.5mV
Atrial repolarization is hidden within QRS complex
o ST segment
J point: initial part of the ST segment; intersection of the end of the QRS complex and the beginning of the ST segment
Normally isoelectric
o T wave: ventricular repolarization; begins at the epicardial surface and spreads to the endocardium (opposite of depolarization; last to
depolarize is 1
to repolarize)
Slow upstroke with rapid downstroke; in same direction as the major deflection of the QRS
o QT interval: measure of ventricular repolarization
Corrected for heart rate (QTc) using Bazetts formula: QTc= QT interval/ (square root of RR interval in sec)
Normal <0.44 sec (M), <0.45-0.46 sec (F)
Note that QRS prolongation will increase QT time and therefor does not signify problems with ventricular repolarization, but with
o U wave: may be repolarization of the His-Purkinje system, or late repolarization of the mid-myocardial M cells
May be seen, esp V2-V4
Amplitude usually <0.2 mV
more evident during hypokalemia or bradycardia; occurs with QT interval prolongation or QT or JT interval shortening (digoxin,
o hypertrophy
right atrial hypertrophy: large diphasic P wave with a tall initial component in V1
Left atrial hypertrophy: large diphasic P wave with a wide terminal component in V1 (2
part of wave going down is larger than
the first upward wave)
Right ventricular hypertrophy
R wave >s wave in V1; R wave gets progressively smaller from V1-V6
S wave persists in V5 & V6
Right axis deviation with slightly widened QRS
Left Ventricular Hypertrophy
Hypertrophy of the L. ventricle produces QRS complexes that are exaggerated in amplitude (both height and depth),
especially in the chest leads
o Larger S (downward) in V1, large R in V5 (more excessive depolarization away from V1, towards V5 which
lies over the L. ventricle)
o Sokolow + Lyon
S V1+ R (V5 or V6) > 35 mm
o Cornell criteria
SV3 + R avl > 28 mm in men
SV3 + R avl > 20 mm in women
o Framingham criteria
R avl > 11mm, R V4-6 > 25mm
S V1-3 > 25 mm, S V1 or V2 +
R V5 or V6 > 35 mm, R I + S III > 25 mm
o Any precordial lead (V1-V6) >35 mm
Dysrhythmias/ conduction disturbances
o Premature atrial complexes (PACs)
Premature activation of the atria originating form a site other than the SA node
RFs: tobacco, alcohol, caffeine, stress
Dx: EKG (early P wave)
Asymptomatic: avoid reversible risk factors
Symptomatic: beta-blocker
o Premature ventricular contractions (PVCs)
Wide QRS (>120 ms), bizarre morphology, compensatory pause
More common in pt with cardiac pathology; increased frequency after MI
Tx: observation
not treated with antiarrhythmic agents unless they occur very frequently, are sustained, or induce hemodynamic
o beta blockers (#1) for symptomatic patients; amiodarone 2
check magnesium and phosphate levels
o Supraventricular tachycardia
Tx: direct current (DC) cardioversion if sx or hemodynamic instability; antiarrhythmics (adenosine, metoprolol, procainamide)
Ventricular tachycardia/fibrillation
Tx: immediate defibrillation; antiarrhythmics (lidocaine, procainamide, amiodarone); maintain K+>4 mEq/L and Mg >2 mEq/L
o atrial fibrillation
abnormal irregular heart rhythm with chaotic generation of electrical signals in the atria of the heart; disordered atrial
rapid ventricular response w/ HR>110
paroxysmal is self-limiting; persistent >7 days, permanent >1 yr
impulses come from the pulmonary veins
complications: myocardial ischemia, exacerbation of heart failure, thrombus formation in the noncontractile atria systemic
embolization stroke
AF >48 hrs increases risk of intraatrial thrombus formation
causes: anything that causes atrial dilation or excessive sympathetic tone
Most common: HTN, coronary atherosclerosis
Inflammatory disease (pericarditis, myocarditis), surgery (post-bypass surgery, post-valvular surgery), drugs
(theophylline, caffeine, digitalis, amphetamines), atherosclerotic coronary artery disease, rheumatic heart disease (esp
w/ mitral stenosis), hyperthyroidism/thyrotoxicosis, congenital heart disease (ASD, Ebstein anomaly), HTN heart
disease, alcohol consumption (holiday heart syndrome, alcoholic cardiomyopathy), pulmonary disease (esp pulmonary
embolus), CHF, MI, infections (urosepsis), hypoxia, anxiety
CHAD 2 score: predictor for risk of stroke in pt with non-rheumatic atrial fibrillation
CHF (1 pt), HTN >140/90 or on meds (1 pt), age >75 yo (1pt), DM, (1pt), prior stroke/tia/thromboembolism (2 pts)
o Stroke risk: 0=1.9%, 1=2.8%, 2= 4%, 3= 5.9%, 4=8.5%, 5=12.5%, 6=18.2%
CHA2DS2-VASc score: additional non-major stroke risk factors include age 65-74, female gender and vascular disease. In
the CHA2DS2-VASc score score, 'age 75 and above' also has extra weight, with 2 points.
Anticoagulation: 0= non or aspirin daily, 1= aspirin daily or warfarin, >2= warfarin
dx: ECG (absence of discrete P waves, irregularly irregular ventricular response), CXR (dilated L. atrium), echo (increased left
atrial size, thrombus, ejection fraction), CMP, cardiac markers, TSH level to r/o thyroid etiology
if hemodynamically unstable (hypotension, angina pectoris, pulmonary edema) DC cardioversion
hemodynamically stable ventricular rate control (IV beta-blocker, calcium channel blocker, or digoxin)
if >48 hr AF 3-4 wks of warfarin therapy
o monitor warfarin with INR levels; goal 2-3
elevated INR but asymptomatic hold warfarin until INR reach acceptable range
Elevated INR & excessive bleeding vit K & fresh frozen plasma
o low-dose aspirin is alternative for pt w/o any structural heart disease/HTN/or other factors for
stroke (lone atrial fibrillation); doesnt require anticoagulation meds
pharmacologic cardioverting agents: procainamide, sotalol, amiodarone
o if a-fib present <48 hrs you can start cardioversion right away
o If a-fib present >48 hrs, first do TEE to check for presence of thrombus
If no thrombus cardioversion; if thrombus present anticoagulate for 3-4 wks then cardiovert
o Atrial flutter
Macro re-entry narrow complex tachycardia; re-entry around tricuspid valve (250-300 bpm possible; 1:1 every circle around
valve stimulates AV node conduction)
Dx: adenosine challenge (rhythm does not break with adenosine), Cardizem challenge (rhythm slows with Cardizem= diltiazem)
Tx: AV node blocking agents to decrease electrical conduction; ablation at isthmus to stop re-entrant circuit
o Bradycardia/atrioventricular block
Sinus bradycardia is seen after inferior MI (b/c R. coronary artery also supplies the sinoatrial node)
Dx: ECG, echo
First-degree AV block: PR interval prolongation (>200 ms=1 large box); d/t conduction delay in AV node
Tx: pacing only if symptomatic (bradycardia, syncope, heart failure, asystole >3 sec)
Second degree heart block
Mobitz I second degree AV block (wenkebach): gradual prolongation of the PR interval before a nonconducted P wave/ drop
beat (P wave w/o QRS); d/t abnormal AV node conduction (can be d/t inferior MI)
Mobitz II second degree AV block: nonconducted P waves not preceded by PR prolongation
Tx: atropine 0.5-1.0mg or isoproterenol used if block @ AV node w/ severe bradycardia
o Stand-by pacemaker if risk of complete heart block, new L bundle branch block w/ primary atrioventricular
block, new bifascicular block
Third-degree AV block: complete AV dissociated with no P-wave conduction; SA & AV node fire at independent waves; complete
independence of P waves and QRS complexes
Tx: temporary transcutaneous or transvenous pacemaker & evaluate for permanent pacemaker
o Ventricular fibrillation
Causes: MI, electrolyte imbalance, myocarditis, cardiomyopathy, drug side effect
Dx: EKG (fibrillary waves, absence of regular QRS complexes)
Tx: early defibrillation
o Ventricular tachycardia
Regular wide complex tachycardia
If not hemodynamically compromised IV amiodarone>lidocaine
If hemodynamically compromised cardioversion
o torsades de pointes
polymorphic ventricular tachycardia a/w prolonged QT interval
risk factors: familial long QT syndrome, malnourished pts (hypomagnesemia), drugs (TCAs, moxifloxacin, fluconazole)
tx: magnesium sulfate
o wolff-parkinson-white syndrome
accessory pathway between atria and ventricles Preexcitation (early ventricular depolarization; delta wave= early up-slurring
of the R wave; widens QRS complex >0.12 sec, shortens PR interval <0.12 sec)
can cause tachyarrhythmias (atrial fibrillation, paroxysmal supraventricular tahcycardia)
if hemodynamically unstable DC cardioversion
If hemodynamically stable procainamide or ibutilide
WPW pts with AF: avoid digoxin, verapamil, and other AV nodal blocking agents
o calcium gluconate is cardio-protective during hyperkalemia (peak T waves, lengthened PR and QRS interval)
antiarrhythmic medications
o class I: Na+ channel blockers; elongate the period of depolarization (prolonged QRS)
Ia: quinidine, procainamide
Ib: lidocaine
Ic: flecainide (use-dependent; more effective at higher HR)
Tx: ventricular arrhythmias and SVTs
o Class II: beta blockers
o Class III: K+ channel blockers; QT prolongation
o Class IV: calcium channel blockers
chest pain: ischemic vs non-ischemic; cardiac vs non-cardiac
o ischemic chest pain: dull or sore, squeezing or pressure-like
pleuritic, positional, or tender pain make ischemia unlikely
o non-cardiac chest pain diff dx: costochondritis (chest wall tenderness), pericarditis, aortic dissection , duodenal ulcers, GERD, pneumonia, PE,
coronary artery disease (atherosclerotic heart disease, ischemic heart disease)
o major risk factors for CAD: DM, smoking, HTN, hyperlipidemia (LDL most dangerous), age (>45 M, >55 F), 1
degree family hx of premature
(<55 M, C65 F) CAD
other RF: physical inactivity, alcohol abuse, low fruits/veggies in diet, emotional stress, elevated electron-beam CT scan calcium
scores, PET scanning
smoking cessation= greatest immediate improvement in pt outcomes for CAD
CAD equivalents: peripheral artery disease, carotid disease, aortic artery disease, DM
o differential dx: GI disorder w/ chest pain (GERD, ulcer disease, cholelithiasis, duodenitis, gastritis)
o dx: ECG (best initial), f/u with cardiac enzymes (CK-MB and troponin)
cardiac enzymes are only ordered if in the ED with acute chest pain; if in the office transfer to ED
exercise tolerance testing if pt is stable and ECG is not diagnostic and pt able to exercise up tot 80% max HR (220-pt age)
if pt unable to exercise chemically increase oxygen consumption in the myocardium via [persantine (dipyridamole)
or adenosine] + nuclear isotope testing; or dobutamine + echo
if ECG is not readable d/t baseline abnormality detect ischemia via nuclear isotope uptake (thalium or sestamibi; decreased
uptake with abnormalities) or echo (wall motion abnormalities)
holter monitoring detects rhythm disorders; continuous 24-72 hr ambulatory EKG monitoring
angiography detects eh anatomical location of CAD to determine if revascularization with bypass or angioplasty is indicated; <50%
stenosis is insignificant; consider surgery >70% stenosis
angiography=most accurate test for CAD; used if ECG and stress testing are equivocal
o treatment
chronic angina: aspirin and beta blocker (greatest mortality benefit), nitroglycerin (oral or transdermal patch for chronic;
sublingual, paste, or IV for acute)
thienopyridine (antiplatelet) meds if intolerance to aspirin: clopidogrel > prasugrel or ticlopidine
o clopidogrel or prasugrel used following angioplasty w/ stenting
o side effects: clopidogrel (TPP), prasugrel (risk of hemorrhagic stroke dont use in pt >75 yo), ticlopidine
ranolazine for refractor/persistent angina
ACE inhibitors/ARBs: used for low EF/systolic dysfucntion or regurgitant valve disease
o SE: cough (not ARB), hyperkalemia (d/t aldosterone inhibition)
If hyperkalemia switch to hydralazine (arterial vasodilator decreased afterload) + nitrate
(coronary a. dilator)
Calcium channel blockers (verapamil, diltiazem) only used if: severe asthmas or cocaine-induced chest pain (cant
tolerate beta-blockers), Prinzmetal variant angina
o SE: edema, constipation, heart block
o Dihydropyridine CCBs (-dipine) are contraindicated d/t reflex tachycardia (increased oxygen consumption,
increased mortality)
Lipid management
o Statin (HMG-CoA reductase inhibitor) to keep LDL <100 in pt with CAD or equivalent; antioxidant effects on
endothelial lining of coronary arteries
Keep LDL< 70 in pt with CAD + DM
SE: liver dysfunction (#1, f/u AST & ALT routinely), myositis, increased CPK, rhabdomyolysis
o Niacin: add to statin if lipid control inadequate; increases HDL best
SE: glucose intolerance, increased uric acid, pruritus (histamine release)
o Gemfibrozil: decreases triglyceride level best
SE: increased risk of myositis when used with statin
o Cholestyramine: bile acid sequestrant
SE: GI sx (constipation, flatus)
o Ezetimibe: lowers LDL with any clear benefit
o CABG (coronary artery bypass grafting) used for: 3 vessel disease (each vessel >70% stenosis), 2 vessel
disease + DM, L. main coronary a. occlusion, persistent sx despite medical therapy
Internal mammary a. lasts ~10 yrs > saphenous vein last ~5 yrs
o Percutaneous coronary intervention (PCI; angioplasty) is best for acute coronary syndromes (esp. ST
segment elevation)
Medical tx (aspirin, beta blocker, ACEi/ARB, statin) is greater than or equal to PCI for stable CAD
acute coronary syndrome: spectrum of acute cardiac ischemia ranging from unstable angina to acute MI
o usually d/t thrombus formation in a coronary artery with an atherosclerotic plaque; other causes are embolic occlusion, coronary
vasospasm, vasculitis, aortic root or coronary artery dissection, cocaine use (vasospasm & thrombosis)
o risk factors: same as CAD
o sx: crushing substernal chest pain (sore/dull, radiates to L. arm), anxiety, diaphoresis, nausea; s4 gallop (during atrial systole; d/t ischemia
LV noncompliance)
o complications of acute MI (hypotension a/w all)
bradycardia: sinus bradycardia (d/t vascular insufficiency of SA node) vs third degree (complete) AV block
third degree heart block: cannon a waves (atrial systole against a closed tricuspid valve b/c atria and ventricle are
contracting out of coordination with each other; bounding jugulovenous wave bouncing up into the neck)
o tx: atropine; if refractory pacemaker
tachycardia: R. ventricular infarct, tamponade/free wall rupture, V. tach or V. fibrillation, valve or septal rupture, extension of the
infarction/reinfarction, aneurysm/mural thrombus
R. ventricular infarct a/w new inferior MI
o R. coronary a. supplies the RV, AV node, and inferior wall of heart
o Dx: flip EKG leads to right side (ST elevation in RV4 most specific)
Lungs clear to auscultation
o Tx: high volume fluid replacement; avoid nitrates (worsen cardiac filling)
Tamponade/free wall rupture
o Several days after infarct; sudden loss of pulse, jugulovenous distention
o Dx: emergency echo
Lungs clear to auscultation
o Tx: emergency pericardiocentesis on the way to OR for repair
Ventricular tachycardia or fibrillation can cause sudden death; loss of pulse
o Dx: EKG
o Tx: emergency electrical shock (cardioversion/defibrillation)
Valve or septal defect
o Sx: new onset murmur, pulmonary congestion
o Dx: echo; step-up in O2 sat from right atria to right ventricle indicates septal rupture
Extension of the infarction/reinfarction
o Sx: recurrence of pain, new rales, new increase in CK-MBs, sudden onset pulmonary edema
o Dx: EKG
o Tx: same meds as acute MI: re-treat with angioplasty or thrombolytics
Aneurysm/mural thrombus
o Dx: echo
o Tx: heparin followed by warfarin for mural thrombi
o dx: ECG, cardiac enzymes
ECG changes: ST changes become Q waves over days-1wk
ST elevation in V2-V4= anterior wall LV MI; worst mortality of left untreated
ST elevation in II, III, aVF= inferior wall MI
ST depression in V1 & V2= posterior wall MI
Cardiac enzymes
Enzyme Time to become abnormal Duration of abnormality
Myoglobin 1-4 hrs 1-2 days
CK-MB 4-6 hrs 1-2 days
Troponin 4-6 hrs 10-14 days

CM-MB is best to detect a new ischemic event a few days after a previous one
Troponin can have false (+) results in renal insufficiency b/c its excreted through kidney
o Tx: aspirin (#1; decreases mortality), morphine, oxygen, nitroglycerin, thrombolytics or angioplasty (greatest decrease in mortality); transfer
to ICU; beta-blocker (metoprolol), statin, ACE inhibitor/ARB
Stable angina: aspirin, beta-blocker, nitrates
Unstable angina/NON-STEMI: aspirin, beta blocker, nitrates, heparin, GPIIb/IIIa inhibitors
Non-STEMI refractory to med tx urgent angiography & possible PCI
o Indications of medical failure: persistent pain, S3 or CHF developing, worse EKG changes, rising troponin
STEMI: aspirin, beta blocker, nitrates, heparin (only after thrombolytics); PCI> thrombolytics
Decrease mortality; not time dependent: beta-blocker (metoprolol), statin, ACE inhibitor/ARB
Prasugrel> clopidogrel if intolerance to aspirin or angioplasty w/ stenting in the past year
Monitor in ICU w/ continuous rhythm monitoring; #1 cause of death w/in days post-MI= ventricular arrhythmia (v. tach or V. Fib)
PCI> thrombolytics; done w/in 90 min of pt arriving to ED w/chest pain
Heparin is used at the time of the procedure
Complications of PCI: rupture of coronary a., restenosis of the vessel, hematoma at entry site (femoral area)
o Drug eluting stent (paclitaxel, sirolimus) that inhibits local T cell response decreases risk of restenosis
Thrombolytics (tPA)
Absolute contraindications: major bleeding in GI (melena) or CNS, recent surgery (2 wks), severe HTN (>180/110),
nonhemorrhagic stroke w/in last 6 mo
Should be started w/in 30 min of arriving to ED if pt unable to get PCI; can be given w/in 12 hrs of chest pain (best
relative risk reduction w/in 2 hrs)
ACE inhibitor/ARB: benefit best in pt w/ ejection fraction <40%
Calcium channel blockers: when beta blocker cant be used, cocaine-induced pain, Prinzmetal or vasospastic variant angina
Heparin: used for ST depression or other NON-STEMI and unstable angina
LMWH >unfractionated heparin
No benefit of thrombolytic tx if no ST elevation
Heparin prevent clot from forming/growing further
Glycoprotein IIb/IIIa inhibitors (abciximab, tirofiban, eptifibatide): inhibits aggregation of platelets
Decreases mortality in ST depression; used for pt going for angioplasty & stenting
Hospital discharge planning
Post-MI stress test to asses if angiography is needed--> assess if angioplasty or CABG needed
o Do not do stress test is symptomatic
o Do not do angiography if no signs of reversible myocardial ischemia
Home meds: aspirin, beta blocker, statin, ACE inhibitor
o Clopidogrel if intolerant to aspirin or post-stent; ticlopidine if intolerant to both
o ACE inhibitor is best for anterior wall infarcts; use ARB if cough
Post-MI sex: no wait time needed; erectile dysfunction may occur d/t anxiety or beta-blocker; do no combine nitrates
with sildenafil (both vasodilators hypotension)
Re-start any exercise as tolerated
o stable: flow-limiting stenosis by an atherosclerotic plaque; ischemia during exercise
o unstable: ischemic pain at rest or at lower threshold of exertion or new onset of chest pain
occurs if thrombotic occlusion is complete or undergoes spontaneous lysis
complete occlusion >30 min ischemia
o variant angina (prinzmetals angina)
d/t temporary spasm of the coronary arteries
RF: smoking (#1)
Episodes often occur in the middle of the night; precipitated by exercise, hyperventilation, emotional stress, cold exposure, cocaine
Dx: holter monitor (transient ST elevations with return of ST segments to baseline upon resolution of sx)
Tx: calcium channel blockers or nitrates
tako-tsubo cardiomyopathy
o acute myocardial damage following an emotionally stressful event (loss of loved one, natural disaster) or hypoglycemia
o ballooning and L. ventricular dyskinesis chest pain; can cause sudden death
o tx: beta blocker and ACE inhibitor
acute myocardial infarction
o risk factors: smoking, hypercholesterolemia
Non-ST segment elevation MI (NSTEMI): partial occlusion of vessel
STEMI: full vessel occlusion
TIMI risk score
1 pt each: >65 yo, >3 RF for CAD, prior coronary stenosis >50%, ST deviation >1mm (up or down), > anginal events in
prior 24hrs, use of aspirin in prior 7 days, increased cardiac biomarkers
o risk factors for CAD: Hypertension > 140/90 or on antihypertensives, Cigarette smoking, HDL < 40, Diabetes,
Family history of premature CAD (CAD in male first-degree relative, or father less than 55, or female first-
degree relative or mother less than 65).
% risk at 14 days of: all-cause mortality, new or recurrent MI, or severe recurrent ischemia requiring urgent
o Score of 0-1 = 4.7% risk
o Score of 2 = 8.3% risk
o Score of 3 = 13.2% risk
o Score of 4 = 19.9% risk
o Score of 5 = 26.2% risk
o Score of 6-7 = at least 40.9% risk
GRACE risk score
Variables: Age, HR, systolic BP, creatinine, Killip class, cardiac arrest at admission, elevated cardiac markers, ST segment
o sx: retrosternal or epigastric pressure sensation/pain (heavy, squeezing, crushing); tachycardia, HTN, and diaphoresis d/t sympathetic
activation; N/V, sense of impending doom; S4 gallop may be seen d/t noncompliance of ischemic heart
pain may radiate to the arm, lower jaw, or neck; persists >30 min an is not relieved by rest
diabetic pts: sudden onset of dyspnea, pulmonary edema, or ventricular arrhythmias
myocardial pump failurecardiogenic shock or ventricular arrhythmias (V tach or V fib.);
papillary muscle dysfunction or papillary muscle rupture
ventricular septal rupture
rupture of ventricular free wall cardiac tamponade
ventricular aneurysm
o occurs days-months after MI
o complications: sx of CHF, ventricular arrhythmias, mitral regurg, and/or thrombus formation
o dx: ST-segment elevations persists weeks after acute event; echo (kyskinetic wall motion of a portion of
the L. ventricle)
Dressler syndrome: immune pericarditis, pleuritis, and fever
o Occurs weeks after an MI
o pericarditis: pain worse with deep inspiration, improved by leaning forward
EKG: diffuse ST elevation (reciprocal depression in aVR), elevated ESR
o Tx: NSAIDs or prednisone
Avoid anticoagulation to prevent development of hemorrhagic pericardial effusion
o dx: ECG, cardiac enzymes; submaximal exercise stress testing (stable pts before hospital discharge), LV systolic function via echo
initial ECG findings and cardiac enzymes may be normal, so serial studies are necessary
Creatine phosphokinase-myocardial band (CK-MB) rises within 4-8 hrs, returns to normal by 48-72 hrs
Better marker for reinfarction following a recent MI
Cardiac-specific troponin I (cTnI), cardiac-specific troponin T (CTnT): rise ~6 hrs after infact; cTNI remain elevated for 7-10
days, cTnT for 10-14 days
NSTEMI (subendocardial): ST segment depression
STEMI (transmural): ST segment elevation >0.1mV in 2+ contiguous leads and/or new L. bundle branch block
Tall, positive, hyperacute T waves in the ischemic vascular territory elevation of the ST segments T-wave inversion
(hrs to days later) diminished R wave amplitude or Q waves (signified significant myocardial necrosis and
replacement by scar tissue)

o tx: for any acute coronary event (oxygen, nitroglycerin, aspirin)
(beta-blocker, ACE inhibitors, nitroglycerin, aspirin, heparin, lipid lowering agent)
Ca2+ channel blockers if beta-blocker contraindicated
Morphine if nitroglycerin does not control pain
Clopidogrel, prasurgrel, or ticagrelor if pt cant be on aspirin or in addition to aspirin following stent placement
o Clopidogrel is used for pt with unstable angina/non-ST elevation MI, or post-PCI
Used for 1 mo with bare metal stents, or 1 yr if drug eluting stents to prevent subacute stent
Abciximab only for pts where invasive procedures planned (PCI catheter)
Percutaneous coronary intervention (PCI) vs coronary artery bypass surgery (CABG)
CABG: pts with multivessels atherosclerotic stenosis and impaired systolic function
Implantable cardioverter-defibrillator
Used for post-mi pts with severe LV dysfunction (ejection fraction <30-35%) d/t increased risk of sudden cardiac death
from ventricular arrhythmias
Lifestyle changes: smoking cessation (most important RF)
ST-segment elevation MI (STEMI): aspirin, beta blocker, anticoagulation (heparin), nitrates (increase coronary blood flow),
morphine (decreases pain & HR), supplemental oxygen; thrombolytics (tPA, streptokinase, reteplase) or percutaneous coronary
intervention (angioplasty and/or stenting)
Indications for thrombolytic therapy (must meet all): ischemic type chest pain, ST-segment elevation >1mm in 2+
anatomically contiguous leads, no contraindications to thrombolytic therapy, pt <75 yo
o Thrombolytics are used ideally w/in 1-3 hrs, max 12 hrs after event
o Absolute contraindications: major surgery/trauma w/in past 2 wks, aortic dissection, active internal bleeding
(excluding menses), pericarditis, hx of cerebral tumor/hemorrhage/arteriovenous malformation, prolonged
traumatic cardiopulmonary resuscitation, bleeding diathesis, allergy to agent/ prior reaction, CVA w/in past
12 months, pregnancy, hx of uncontrolled HTN, recent hepatic/renal biopsy
o Relative contraindications: BP >180/110 on >2 readings, bacterial endocarditis, diabetic retinopathy
w/recent bleed, severe renal/liver disease, chronic warfarin therapy, stroke/TIA within 12 months
PCI is used for pts with acute STEMI w/in 2-3 hr of sx onset, ideally w/in 90 min; also used for pts when thrombolytics
are contraindicated, are hypotensive, or in cardiogenic shock
Non-ST segment elevation MI (NSTEMI)
Acute heart failure
o Acute= over hours-days; cardiac decompensation with pulmonary edema & low cardiac output; can cause cardiogenic shock
Chronic heart failure (CHF)
o Chronic= months-years; hear it unable to meet the metabolic needs of the body while maintaining normal ventricular filling pressures
o Causes: ischemia, HTN, valvular disease, alcohol abuse, cocaine, thyrotoxicosis
Myocardial injury: Adriamycin, alcohol use, cocaine, ischemic cardiomyopathy (atherosclerotic coronoary artery disease),
rheumatic fever, viral myocarditis
Chronic pressure overload: aortic stenosis, HTN
Chronic volume overload: mitral regurgitation
Infiltrative diseases: amyloidosis, hemochromatosis
Chronic tachyarrhythmia or bradyarrhythmia
o Sx: dyspnea, orthopnea, paroxysmal nocturnal dyspnea, peripheral/pedal edema, elevated jugular venous pressure, crackles/rales in lungs
pulmonary edema
NYHA functional classification (best predictor of mortality)
Class I: no limitation during ordinary physical activity
Class II: slight limitation of physical activity. Develops fatigue or dyspnea with moderate exertion
Class III: marked limitation of physical activity. Even light activity produces sx
Class IV: sx at rest. Any activity causes worsening
o Dx: clinical diagnosis; BNP level (normal level excludes CHF as cause of dyspnea); echocardiography (transthoracic best initial; assess
ejection fraction distinguishes systolic from diastolic dysfunction, valvular function), most accurate=multiple-gated acquisition scan
(MUGA) or nuclear ventriculography;
Determining etiology: EKG, cardiac stress testing, CXR, holter monitor, cardiac catheterization (coronary angiography), CBC
(anemia), thyroid function, endomyocardial biopsy (infiltrative disease or infection), swan-ganz right heart cath (distinguish CHF
from ARDS)
TEE best at evaluating heart valve function and diameter
Nuclear ventriculography best for wall motion abnormalities
important to assess in pt on doxorubicin chemotherapy
o Tx (general): salt restriction, diuretics, digoxin, vasodilators; ACE inhibitors, beta-blockers
f/u echo yearly
o Diastolic dysfunction (backward failure)= impaired diastolic relaxation and decreased ventricular compliance
Sx: dyspnea, peripheral edema, ascites
Dx: EF>40%
Tx: beta blockers, diuretics; ACE inhibitors/ARB, hydralazine
NOT helpful: digoxin, spironolactone
o Systolic dysfunction (forward failure)= low CO d/t impaired heart contraction (low ejection fraction)
#1 cause of CHF with systolic dysfunction is ischemic cardiomyopathy d/t coronary atherosclerosis or HTN, valve disease;
alcohol, postviral (idiopathic) myocarditis, radiation, Adriamycin (doxorubicin), chagas disease, hemochromatosis (also restrictive
cardiomyopathy), thyroid disease, peripartum cardiomyopathy, thiamine deficiency
Sx: fatigue, lethargy, hypotension
Dx: EF <40%; S3 gallop
Tx: ACE inhibitors or ARBs, spironolactone, beta-blocker (carvedilol, metoprolol, bisoprolol); digoxin (symptom relief; improves
cardiac contractility), diuretics (sx control; furosemide, torsemide, or bumetanide); implantable defibrillator, biventricular
pacemaker, cardiac transplant
Mortality benefit: ACE inhibitors/ARB, beta blockers, spironolactone, hydralazine/nitrates, implantable defibrillator
If ACE inhibitors not tolerated or less beneficial hydralazine w/ nitrates (decrease preload & clear pulmonary
#1 cause of death is arrhythmias/sudden death
carvedilol is a nonspecific beta blocker with alph-1 receptor blocking activity
do not give beta blockers in acute CHF
spironolactone: aldosterone inhibition used for class 3 and 4 CHF
o spironolactone SE: hyperkalemia, gynecomastia
no antiandrogenic effects with eplerenone
implantable defibrillator for pt with ischemic cardiomyopathy and EF<35%
biventricular pacemaker for pt with dilated cardiomyopathy, EF<35%, QRS>120 ms, and persistent sx
o Left sided
Low CO & pulmonary edema
Tx: dietary salt restriction, loop diuretics
o Right sided
Sx: elevated jugular venous pressure, hepatomegaly d/t hepatic congestion, peripheral edema
Cor pulmonale: R. sided heart failure d/t pulmonary HTN
Tx: diuretics
Tx: volume replacement with saline or colloid solution (increase preload to prevent hypotension)
Dilated cardiomyopathy
o Causes: viral myocarditis, beriberi (thiamine deficiency), doxorubicin therapy
Restrictive cardiomyopathy
o Impaired diastolic filling w/ preserved systolic function
d/t Myocardial fibrosis, hypertrophy, or infiltration
o Causes: amyloidosis, fibrosis following radiation tx or open heart surgery, endomyocardial fibrosis (Africa; fever & eosinophilia)
o Sx: progressive exertional dyspnea, dependent edema, elevated JVP during inspiration distention of neck veins (Kussmaul sign)
o Dx: endomyocardial biopsy may be necessary
Diff dx: constrictive pericarditis
o Tx: no effective therapy
Hypertrophic obstructive cardiomyopathy (HOCM)
o Congenital asymmetric enlarged septum obstruction of L. ventricle outflow tract
o Sx: syncope, dyspnea, chest pain
o Dx: crescendo-decrescendo systolic murmur along the L. sternal border w/o carotid radiation
o Tx:
Diuretics are contraindicated
Mitral stenosis
o Causes: rheumatic heart disease
o Loud S1, opening snap following S2, low pitch diastolic rumble @ apex, ruddy cheeks
Distance between s2 & opening snap narrows as severity of stenosis increases
L. atrial dilation pulmonary HTN hemoptysis & R. sided heart failure atrial fibrillation
Mitral regurgitation
o Holosystolic murmur at the apex
Aortic stenosis
o In pts <30 yo d/t congenital bicuspid valve; age 30-70 d/t congenital stenosis or acquired rheumatic heart disease; >70 yo d/t degenerative
calcific stenosis
o Late systolic murmur radiating to the carotid, paradoxical splitting of the 2
heart sound, diminished carotid upstrokes (delayed slow-rising
carotid upstroke =pulsus parvus et tardus), narrow pulse pressure
Progress of the stenosis causes angina & presyncopal sx syncopal episodes (precipitated by exertion) heart failure (d/t low
CO and high diastolic filling pressures)
angina pectoris: retrosternal chest pain precipitated by exercise and relieved by rest
Left ventricular hypertrophy
o Dx: echocardiogram
Severe aortic stenosis has valve area <1cm2 (normal 3-4 cm2) and mean pressure gradient >40 mmHg
o Tx: aortic valve replacement or balloon valvuloplasty
Preoperative cardiac catheterization (assess aortic valve area, pressure gradient, coronary arteries for stenosis)
Balloon valvuloplasty used for pts that are not good candidates for valve replacement
Aortic regurgitation
o Early diastolic decrescendo murmur, widened pulse pressure
Infectious endocarditis
o Causative agents: staph aureus (IV drugs or catheters; acute infx), strep viridans (dental procedures; subacute infection), coagulase negative
staph (neonates, prosthetic valvue), enterococci (GI disease or instrumentation), strep bovis (elderly pt w/GI mucosal lesion like cancer)
Culture negative organisms: fungus, Abiotrophia spp., Bartonella spp., coxiella burnetii, legionella spp., chlamydia; HACEK
organisms= Haemophilus aphrophilus/paraphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis,
Eikenella corrodens, Kingella kingae
Negative culture can also be d/t prior antibiotic use
Risk factors: IV drugs use, dental procedures, previously damaged heart valves, prosthetic heart valves
o Sx: fevers, new or changed heart murmer, chills, LUQ pain, Janeway lesions (painless hemorrhagic macules on palms & soles), roth spots
(hemorrhagic retinal lesions w/ white centers)
Subacute infection: anorexia, weight loss, night sweats, septic vasculitis (petechiae, splenomegaly, GN, osler nodes= tender nodules
on finger/toe pads, Janeway lesions, roth spots, splinter hemorrhages)
Vegetations on heart valves= platelets, fibrin, bacteria
R sided cause septic pulmonary emboli
More common with IV drug users
Tricuspid regurg: holosystolic murmur, increases with inspiration
Pulmonary emboli: pleuritic chest pain, purulent sputum, hemoptysis
L sided causes septic emboli to region with a rich blood supply (brain, kidneys, liver, spleen)
CT showing Splenic fluid collection indicates septic emboli to spleen
o Complications: CHF d/t valve damage, intracardiac abscess, conduction disturbances if septal wall involvement; emboli causes spleen or
renal infarction or abscess, MI or stroke; aneurysms d/t infection of vaso-vasorum weak artery walls , brain mycotic aneurysms, kidney
dysfucntion (hematuria, GN), conjunctival petechiae, splenomegaly, septic emboli to lungs
o Dx: 2 major criteria, 1 major + 3 minor, or 5 minor criteria; serial blood cultures (bacteremia), TEE>transthoracic echo to assess vegetations
Major criteria: isolation of typical organism (viridans strep, staph aureus, enterococci, strep bovis, or HACEK) from 2 separate
blood cx, or persistently positive blood cultures with other organisms; evidence of endocardial invovlemnt (oscillating intracardial
mass, or new valvular regurg)
Minor criteria: predisposing valvular lesion or IV drug use, fever >100,4, vascular phenomena (arterial or septic pulmonary
emboli, mycotic aneurysm, Janeway lesions), immunologic phenomena (GN, osler nodes, roth spots, positive rheumatoid factor),
positive blood cultures not meeting major criteria
o Tx: antibiotics for 4-6 wks
Best empiric: vancomycin + gentamicin
Vanco trough goal 15-20
Specific bugs
Strep penicillin G
staph aureus nafcillin + gentamicin; oxacillin, nafcillin, or cefazolin
staph epi or resistant staph vancomycin + gentamicin
MRSA or coagulase negative staph vancomycin
Viridans strep ceftriazone 4 wks
Enterococci ampicillin + gentamicin
HACEK organisms ceftriaxone
Fungal amphotericin + valve replacement
if prosthetic valve with staph infection add rifampin
If bugs resistant to treatment add aminoglycoside and increase duration of treatment
Valve excisions & replacement as needed: persistent infection, recurrent emboli, refractory to medical treatment
Fungal endocarditis: large friable vegetations w/ high risk of embolization
Dental prophylaxis: If heart defect + risk of bacteremia
Heart defects: prosthetic heart valve, previous infectious endocarditis, unrepaired cyanotic heart disease, heart
transplant with abnormal valves causing regurg
Risk of bacteremia: dental work with blood, respiratory tract surgery
Amoxicillin; alternatives are ampicillin, cephalosporin, clindamycin, azithromycin, clarithromycin
Colonoscopy for strep bovis endocarditis d/t high risk of colon cancer or polyp allowing seeding of organism
Surgery if: CHF, ruptured valve, chordae tendinae, prosthetic vavle, fungal infections, abscess, AV block, recurrent emboli while on
acute pericarditis
o acute inflammation of the parietal pericardium and superficial myocardium
o causes: idiopathic, infectious, vasculitis (autoimmune, post-radiation), HSR/immune (dressler syndrome), disease of surrounding structure
(ex. Transmural MI), metabolic (uremic, gaucher), trauma, neoplasm (breast, lung, lymph)
o sx: nonexertional pleuritic chest pain (sharp, substernal, worse with inspiration & lying down; relieved by sitting forward; not relieved by
pericardial friction rub (harsh, high pitched, scratchy; best @ L. sternal border, variable intensity)
ECG: diffuse ST-segment elevation & PR depression (opposite in aVR and V1), low voltage diffusely
o Complications: pericardial effusion, bleeding, tamponade, constrictive pericarditis
o Tx:
Viral or inflammatory: aspirin or NSAIDs (indomethacin) for pain relief or ibuprofen+ colchicine; steroids for refractory sx
Dialysis for uremic pericarditis
constrictive pericarditis
o inflammation w/ granulation tissue forms a thickened fibrotic adherent sac that gradually contracts impairs diastolic filling
o causes: radiation tx, cardiac surgery, or any cause of acute pericarditis (viral, uremia)
o sx: chronic & slowly progressive weakness, fatigue, exertional dyspnea, pericardial knock (high-pitch early diastolic sound just after aortic
valve closure), elevated JVP during inspiration distention of neck veins (Kussmaul sign)
appears like R. sided heart failure: chronic lower-extremity edema, hepatomegaly, ascites
ECG: low voltage
o dx: CXR (cardiomegaly, calcified pericardium), MRI (shows thickening of pericardium), endomyocardial biopsy may be necessary
o tx: resection of the pericardium
Cardiac effusion/ tamponade
o Tamponade: increased pressure w/in the pericardial space d/t accumulating effusion Impedes diastolic filling of the heart decreased
CO cardiovascular collapse
If the fluid accumulates slowly, the sac can hold up to 2000 mL before causing problems; if it accumulates rapidly <200 mL can
produce tamponade
Causes: malignancy or infection causing pericardial effusion, trauma, ventricular rupture
o Sx: pulsus paradoxus (fall in systolic BP >10 mmHg with inspiration), hypotension, chest pain, dyspnea, jugular venous distention,
distant cardiac sounds
Beck Triad (acute tamponade): hypotension, elevated JVP, small quiet heart
ECG: low voltage diffusely, electrical alternans
o Diff dx: pericardial effusion causing cardiac tamponade, constrictive pericarditis, restrictive cardiomyopathy
o dx: CXR (cardiac enlargement)
o Tx: echo-guided pericardiocentesis or surgical pericardial window
Give IV fluids for supportive care while waiting for procedure (pts are preload dependent)
aortic dissection
o tear of the intima that allows longitudinal dissection false lumen or channel for blood flow
type A: involves ascending aorta or proximal aorta
type B: involves anything but the ascending aorta, usually starts distal to the L. subclavian artery branch
2/3 start in the ascending aorta a few cm above the aortic valve
intraluminal flap can occlude branch arteries; retrograde rupture into the pericardial sac cardiac tamponade; rupture into
pleural space exsanguination; acute aortic regurg fulminant heart failure
o risk factors: cystic degenerative of elastic media (Marfan, Ehlers-Danlos), HTN, aortic valve abnormalities (stenosis, bicuspid valve),
coarctation of the aorta, pregnancy, atherosclerotic disease, cardiac sx or cath.
o sx: sudden severe chest pain (sharp/tearing/ripping, radiates to back, not relieved by nitroglycerin)
complications: horner syndrome (compression of superior cervical ganglion), superior vena cava syndrome (d/t compression),
hemopericardium, pericardial tamponade, aortic regurg, bowel ischemia, hematuria, HTN, hemiplegia (carotid a. dissection)
o dx: CXR (widened mediastinum), unequal pulses or BP in the arms (d/t dissection along brachiocephalic artery), a new murmur of aortic
insufficiency (early diastolic murmur; if the dissection near the aortic valve); confirm with TEE/CT with contrast/CTA/MRI
o tx:
type A urgent surgery
type B medical management 1
(decrease MAP via vasodilation with sodium nitroprusside + beta blocker; or labetalol)
note: anticoagulation & thrombolytic therapy are contraindicated
aortic aneurysm (dissecting hematoma)
o risk factors: smoking, atherosclerosis/peripheral vascular disease, HTN
o thoracic
o abdominal aortic aneurysm (AAA)
dilation >1.5x normal (>3cm diameter); most occur below the renal a.
sx: midline pulsatile mass
dx: 1x screening via ultrasound is recommended for men 65-75 yo who have ever smoked
<5.5 cm serial noninvasive monitoring every 3-12 mo (MRI, CT, or ultrasound)
>5.5 cm surgical excision of affected aorta with ducron graft replacement
o cardiogenic shock: hypotension (<80 systolic), reduced cardiac index (<1.8 L/min/m2), elevated LV filling pressure (PCWP >18mm Hg)
cold extremities, pulmonary edema, elevated jugular venous pressure
tx: reduce afterload (nitroglycerin or nitroprusside)
o septic shock: hypotension, tachypnea, low urine output, fever, metabolic acidosis (lactic acidosis d/t hypoxemia & hypotension)
tx: IV 0.9% saline, IV antibiotics, supplemental oxygen; vasopressors if hypotension not responsive to fluids
o hypovolemic/hemorrhagic shock: decreased CO, decreased PCWP, increased SVR, decreased BP, increased HR
o mixed venous oxygen saturation helps differentiate between shock types
measure with swan gatz catheter
insertion locations (Right internal jugular #1, L. subclavian #2)
high Sv02 + high CO: septic shock, excessive blood flow (hypervolemia, vasoactive therapy)
low SvO2 with low CO: cardiogenic shock, PE
o prehypertension (120-139/80-89), stage 1 (140-159/90-99), stage 2 (>160/100)
o essential HTN (no identifiable cause)
o causes of secondary HTN: renal/renovascular disease, endocrine (hyperaldosteronism, thyroid or parathyroid dz, cushings syndrome,
pheochromocytoma, hyperthyroidism, acromegaly), drugs (OCPs, decongestants, estrogen, appetite suppressants, chronic steroids, TCAs,
NSAIDs), coractation of the aorta, cocaine & other stimulants, sleep apnea
o hypertensive emergency: HTN a/w acute end-organ damage (encephalopathy, MI, aortic dissection, pulmonary edema secondary to acute LV
o hypertensive urgency: asymptomatic severe HTN
tx: start anti-HTN tx, then recheck BP in 24-48 hrs (outpt tx for asymptomatic HTN); goal is to decrease BP in 24-48 hrs
o increased systemic vascular resistance (afterload) concentric LVH; HTN also accelerates atherosclerosis
most damaging to the heart, eyes, CNS, kidneys
LVH w/ S4, MI, CHF, aortic dissection
retinal changes: arteriovenous necking, cotton wool spots=infarction of the nerve fiber layer in the retina, papilledema
intracranial hemorrhage, other types of stroke
nephrosclerosis (arteriosclerosis of afferent and efferent arterioles and glomerulus), decreased GFR
o Dx: at least 2 readings >4 wks apart; evaluate for end-organ damage & cardiovascular risk factors
Assess for end organ damage & cardiovascular RFs: UA (protein, blood, glucose, microscopic exam), Hgb or HCT, WBC, serum K+,
Ca2+, PO4, creatinine BUN, fasting glucose, lipid panel, ECG, TSH
PE: auscultate for bruits, fundoscopic exam, palpitation for kidney masses or enlarged aorta, look for edema & perfusion
of legs, neuro exam
A cuff that is too small will falsely elevate BP
If pt is diabetic also check for microalbuminuria
o Tx: pre-HTN (lifestyle changes), stage 1 (thiazide diuretic #1 choice, beta blocker next best; ACE inhibitor best for diabetes or CHF),
stage 2 (2 drug tx; thiazide + beta blocker first choice)
Modify lifestyle: reduce salt intake, lose weight, avoid excessive alcohol consumption (has pressor action), exercise regularly, low-
saturated fat diet, stress management
Drug options: diuretic, antiadrenergic, vasodilator, ACE inhibitor, angiotensin receptor antagonist, Calcium channel antagonist
Beta blockers and thiazide diuretics decrease M &M, so they are 1
line agents
o Thiazide diuretics (best for black pts w/o diabetes)
o beta-blockers (decrease HR, CO, renin release)
o avoid beta-blockers in hypertensive pts with CHF +volume overload (use ACE inhibitor instead to
decrease afterload)
Ace inhibitors (#1 for diabetic pts), angiotensin II receptor blockers (also good for diabetics)
vasodilators are used with beta-blockers and diuretics in pts with refractory HTN
Goals: <135/85 BP with 130/80 minimum goal in pt with diabetes or renal insufficiency; ideal goal <120/80
Prognosis depends on cardiovascular RFs and end-organ effects of HTN
post-op pain can cause HTN; lower pain & monitor BP before starting other BP lowering drugs
note: HTN (unless markedly elevated) should not be acutely decreased in a pt w/suspected stroke d/t risk of
hypoperfusion and worsening brain ischemia
o normal levels: total cholesterol <200 mg/dL, LDL <100 mg/dL, HDL >45 mg/dL
LDL= total cholesterol- HDL- (triglycerides/5)
o Secondary causes of lipid disorders: diabetes, hypothyroidism, obstructive liver disease, chronic renal failure/nephrotic syndrome,
medications (progestins, anabolic steroids, corticosteroids), familial hypercholesterolemia
o risk of atherosclerotic CAD= #1 cause of death in US
Risk factors for CAD (10 yr risk of CV events): smoking, HTN, low HDL (<40 mg/dL), family hx of premature CAD (<55yo
M, <65 yo F), age of pt (>45 yo M, >55 yo F)
HDL>60 negates 1 RF
high risk pt: known CHD or other atherosclerotic vascular disease (stroke, peripheral vascular disease, abdominal aortic
aneurysm), diabetes (CHD risk equivalent);
o Very high risk: goal LDL<70 mg/dL; CHD + (diabetes or smoking or recent acute coronary event)
Risk LDL goal Start lifestyle modification Start drug tx
high risk pt

<100 >100 >130
Intermediate risk (2+ RFs)

<130dL >130 >160
Low risk pt (<3 RFs) <160 mg >160 >190

o dx: routine screening of average risk pt every 5 yrs (starting 35 yo M, 45 yo F; or age 20 if multiple CAD risk factors or DM)
o tx: lifestyle changes (diet low in saturation fat & cholesterol, exercise), lipid lowering drugs
diet: saturated fat <7% of total daily calories; cholesterol <200 mg/day
statins: HMG-CoA reductase inhibitor
Best at lowering LDL; also lowers TG and raises HDL
SE: myopathy rhabdomyolysis, elevated liver enzymes hepatitis
o Monitor LRTs & creatine kinase
Nicotinic acid (niacin)
Lowers triglycerides & LDL, raises HDL
SE: flushing & pruritus (d/t prostaglandin-related vasodilation and histamine release; relieved by aspirin taken
30 min before niacin), tachycardia
Bile acid resins (cholestyramine)
Lowers LDL & raises HDL
SE: constipation, nausea, GI discomfort; binds fat-soluble vitamins
Fibric acid derivatives (gemfibrozil)
Best at lowering triglycerides; also raised HDL
SE: gallstones, nausea, increased LRTs (caution if used with statins)
o Familial hypercholesterolemia
Defective or absent LDL surface receptors
Family hx of hypercholesterolemia & premature atherosclerotic CAD
Dx: Lipid panel (elevated total & LDL cholesterol & triglycerides, low HDL)
Tx: lifestyle modification (low fat diet, exercise), HMG-CoA reductase inhibitor (statin)
peripheral vascular disease
o causes: thrombotic arterial occlusion or embolism most common; Buerger disease, fibromuscular dysplasia, Takayasu arteritis
emboli typically from heart (A. fib., dilated cardiomyopathy, endocarditis); can also occur following vascular procedures
o Risk factors: smoking #1, diabetes, HTN, dyslipidemia, increased homocysteine
o Sx: claudication (pain with walking that resolves with rest) rest pain (vascular insufficiency), Pallor with elevation of limb, rubor on
dependency (ex. Hanging legs over bed)
Limb ischemia: pain, pallor, pulselessness, paresthesias, poikilothermic, paralysis
If sudden onset acute arterial occlusion from embolus
Chronic arterial insufficiency hair loss, thick & brittle nails, shiny atrophic skin ulcers or gangrene
o Dx: angiogram of lower extremity, MRA, or doppler ultrasound if pain at rest, nonhealing ulcer, or critical leg ischemia
Doppler ultrasound measure ankle-brachial index (ABI): normal >1, claudication 0.41-0.90, ischemia <0.4
Bruit indicates accelerated blood flow velocity and turbulence at sites of stenosis
Treadmill test: determine severity of disease by how far pt can walk
o Tx: change modifiable cardiovascular RFs (exercise, aspirin or clopidogrel, stop smoking #1, LDL <100, BP <135/85, ACE inhibitor),
pentoxyphylline or cilostazole (antiplatelet & vasodilation), anticoagulation w/ heparin for acute ischemia; angioplasty or bypass grafting
Supervised exercise programs help build strength and collateral circulation
Angioplasty or bypass grafting used if ABI<0.4, if severely debilitating, rest pain, non-healing ulcer
Only good for large vessel stenosis; not useful for diffuse atherosclerotic disease or small vessel disease
Buerger disease (thromboangiitis obliterans)
o Inflammation of small & medium arteries (legs or arms)
Most common in male smokers <40 yo
Fibromuscular dysplasia
o Hyperplastic vascular disorder; most common in renal or carotid arteries of females
Takayasu arteritis
o Inflammatory vascular disorder; usually branches of the aorta (subclavian a.)
Most common in young females
o Sx: arm claudication (unequal BPs), Raynaud phenomenon, fever, weight loss,
Renal artery stenosis
o In young pt fibromuscular dysplasia, in older pt atherosclerotic plaque
o Tx:
Young pt: angioplasty with stent placement
Intra-arterial monitoring
o Safe locations: femoral, radial, dorsalis pedis
Kids: brachial artery is also safe
Allen test: compression of the radial & ulnar arteries, then release of the ulnar to see if collateral circulation for the hand is
o Indications: monitor BP in hypotensive or HTN pt that requires meds to control it, or for pt that requires multiple blood draws
o Mean arterial pressure= 2/3 diastolic + 1/3 systolic= Diastolic + 1/3 pulse pressure

Dichroitic notch: closure of the aortic valve; located farther down if seen from femoral line monitor (doppler effect)
Area under the curve correlates to intravascular volume
Decreased: tamponade, hypovolemia, cardiogenic shock (MI, PE), tension pneumothorax
Central line
o Safe locations; subclavian v, femoral v, internal jugular v, PICC line
Subclavian vein is the 1
choice b/c its the site of least infection
o Systemic vascular resistance (SVR)= [(MAP-R atrial P)/CO] x80; normal is 800-1200 dynes/s/cm-3

cannon a-wave: elevated a-wave d/t tricuspid stenosis or AV dissociation (ventricular tachycardia or congenital heart block)
steep y descent: RV infarct, constrictive pericarditis, constrictive hypertrophy
Hemoglobin binding curve for oxygen

Right shift: increased tissue perfusion b/c looser binding of oxygen
Causes: acidosis, increased temp, increased 2,3, BPG, increased PCO2
Blood products
o Packed RBCs: HCT 70-80%; each unit should increase HCT by 3 points
o Fresh frozen plasma: replaces clotting factors; not indicated for hemophilia A /B or vWD
o Cryoprecipitate: replaces fibrinogen (some use for DIC)
o Decreased RBC mass decreased O2 carrying capacity; Hgb <13 g/dL for men, <12 g/dL for women
Microcytic (MCV <80): iron deficiency, thalassemia, sideroblastic anemia, lead poisoning
Normocytic: acute blood loss, hemolysis, anemia of chronic disease, anemia of renal failure, myelodysplastic syndrome
Macrocytic (MCV >100): folate deficiency, vit B12 deficiency, drug toxicity (zidovudine)
Folate deficiency occurs before B12 deficiency (B12 stores last ~10 yrs)
o Sx: fatigue, exercise intolerance (SOB; dyspnea), pale conjunctiva/skin/palms, dizziness, palpitations, impaired concentration, light
headedness, angina, syncope, chest pain (cardiac ischemia)
o Dx: CBC (best initial test); possible iron studies, electrophoresis; if suspected GI bleeding upper & lower endoscopy
Microcytic (MCV<80): iron deficiency, thalassemia, sideroblastic, anemia of chronic disease
Low retic count d/t production problems (except alpha that 3 gene deletion), hypochromic, target cells (most common
with thalassemia)
Macrocytic (MCV >100): B12 or folate deficiency, sideroblastic anemia, alcoholism, antimetabolite meds (azathioprine, 6-MP,
hydroxyurea), meds (zidovudine, phenytoin), liver disease or hypothyroidism, myelodysplastic syndrome
Peripheral smear best initial test to determine cause of macrocytic anemia; hypersegmented neutrophils in B12/folate
deficiency, or antimetabolite meds
Normocytic: acute blood loss or hemolysis before MCV compensation
Hemolysis will eventually increase retic count elevated MCV (retic cells are larger)
Blood loss iron deficiency anemia
TIBC is inversely related to the transferrin saturation
Ferritin= stored iron; increases with chronic inflammatory diseases, malignancy, or liver injury
Corrected retic count
actual retic+ (HCT/45); normally 1%
retic/RBC count; normally 50,000-70,000
low retic count in macrocytic & microcytic anemia (except alpha thal 3 gene deletion, which has high retic count)
o tx: PRBCs indicated if: symptomatic (SOB< lightheaded, confused, syncope, hypotension + tachycardia, chest pain), decreased HCT (25-30) in
elderly pt or pt with heart disease
o Iron deficiency
Blood loss: GI blood loss (esophageal varices, PUD, gastritis, small-bowel polyp or carcinoma, colonic angiodysplasia,
colon cancer, IBD, hookworm infestation), uterine blood loss (menstruation/menorrhagia, uterine fibroids), other blood
loss (chronic hemodialysis, surgical blood loss, repeated blood donation or phlebotomy, paroxysmal nocturnal
Malabsorption: gastrectomy, celiac disease, IBD
Inadequate dietary intake/increased physiologic demands: infancy/adolescence, pregnancy, vegetarian diet
o Pregnancy causes expanded blood volume & acute transport of iron to the fetus
Sx: anemia sx + PICA or pagophagia (ice craving), glossitis, cheilosis, koilonychia, dysphagia a/w plummer-vinson syndrome=
esophageal web
Dx: low iron, increased TIBC, low ferritin; microcytic hypochromic; increased RDW (normal if d/t chronic disease; cells
are smaller d/t less Hgb), increased PLT, bone marrow biopsy for stainable iron low (most accurate)
Tx: oral iron sulfate 325 mg 2-3x/day for 6 months; if insufficient IM iron
Note: normal iron requirement is 1-2 mg, menstruating 2-3 mg, pregnant 5-6 mg; duodenum can only absorb
o Sideroblastic anemia
Causes: lead poisoning, isoniazid, vit B6 def., alcohol (suppressive to bone marrow)
Dx: increased iron & ferritin, decreased TIBC, basophilic stippling of RBCs, Prussian blue stain for ringed sideroblasts (enlarged
mitochondria in RBC; most accurate)
Normally microcytic, macrocytic when a/w myelodysplasia
Tx: correct cause; vit B6 (pyridoxine) replacement may help
o Thalassemia
Dx: electrophoresis (most accurate); decreased MCV, increased ferritin, normal TIBC & RDW; genetic testing most accurate for
alpha thallasemia
Usually asymptomatic with normal iron studies
o 1 gene deletion: asymptomatic
o 2 gene deletion: mild anemia, normal electrophoresis
o 3 gene deletion: moderate anemia, hemoglobin H (beta-4 tetrads), increased retic count
beta thalassemia
o 1 gene deletion: increased Hgb F and A2
o 3 gene deletion: normal Hgb F, no transfusion dependence
tx: beta-thalassemia major (cooley anemia) with chronic transfusions lifelong
tx iron overload from transfusions with either oral deferasirox or parenteral defereoxamine
o Anemia of chronic disease
Causes: cancer, chronic infection, rheumatoid arthritis, renal failure (d/t decreased erythropoietin)
Iron is trapped in storage, trapped in macrophages or ferritin
Dx: normal MCV, TIBC (normal or decreased), and RDW; increased ferritin (acute phase reactant), decreased iron
Tx: correct underlying cause; erythropoietin for renal failure pt
o Vit B12 or folate deficiency
Causes of vit B12 deficiency: pernicious anemia (a/w other autoimmune disease), pancreatic insufficiency, diet deficiency
(vegan, vegetarian), Crohn diseases (damage to terminal ileum), blind loop syndrome (gastrectomy or gastric bypass),
diphyllobothrium latum, celiac diseases
Sx: neuro changes (peripheral neuropathy, posterior column damage loss of position and vibratory sense, ataxia)
Recall: pancreatic enzymes are needed to remove B12 from R-protein to bind intrinsic factor
Transcobalamin= B12 carrier, acute phase reactant
Causes of folate deficiency: dietary deficiency (goat milk), psoriasis and skin loss/turnover, drugs (phenytoin, sulfa, methotrexate),
celiac diseas
Dx: peripheral smear (hypersegmented neutrophils) f/u with folate and B12 level; increased LDH, indirect bili, and
homocysteine levels; decreased retic count (d/t destruction while leaving bone marrow), hypercellular bone marrow,
Only B12 deficiency increases methylmalonic acid level
Pernicious anemia: anti-intrinsic factor and anti-parietal cell antibodies
Pancytopenia possible (not just macrocytic anemia)
Tx: replace B12 or folate as needed (folate will fix anemia d/t B12 deficiency but not neuro sx)
SE: hypokalemia from cell production
o Hemolytic anemia
Dx: decreased HCT and haptoglobin level, decreased folate from increased cell production, increased MCV, increased K+ from cell
Bilirubin gallstones can occur
o Hereditary spherocytosis
Defect in cytoskeleton of RBCs loss of normal flexibility hemolysis
Sx: hemolytic anemia, intermittent jaundice, splenomegaly, bilirubin gallstones
Dx: low MCV, high MCHC (mean corpuscular hemoglobin concentration), negative coombs, osmotic fragility (most accurate)
Loss of central pallor of normal RBCs
Tx: folic acid, splenectomy
o Autoimmune (warm/IgG) hemolysis
RBC destruction in spleen or liver
Causes: CLL, lymphoma, SLE, drugs (penicillin, alpha- methyldopa, rifampin, phenytoin)
Dx: coombs test, microspherocytes on smear
Tx: glucocorticoids (prednisone); if not responsive IVIG
Recurrent episodes splenectomy; if not responsive rituximab
Alternatives to steroids: cyclophosphamide, cyclosporine, azathioprine, mycophenolate, mofetil
o Cryoglobulinemia vs Cold agglutinin disease
Both d/t IgM antibodies

o G6PD (glucose 6 phosphate dehydrogenase) deficiency
X-linked recessive inability to generate glutathione reductase
Sx: sudden anemia, and jaundice following oxidative stress (infection, dapsone, quinidine, sulfa drugs, primaquine, nitrofurantoin,
fava beans)
Dx: peripheral smear (Heinz bodies, bite cells), G6PD level 1-2 mo after an acute episode (most accurate; level normal right after
hemolytic event)
Tx: avoid oxidant stress
o Hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP)
HUS a/w E.coli 0157:H7
TTP a/w ticlopidine, clopidogrel, cyclosporine, AIDs
Sx: intravascular hemolysis, thrombocytopenia, renal insufficiency
TTP: neuro disorders (confusion, seizures), and fever
Dx: negative coombs, normal PT/aPTT
Tx: plasmapheresis or plasma exchanges; if delay in plasmapheresis expected FFP
Avoid giving platelets
o Paroxysmal nocturnal hemoglobinuria
Stem cell defect; defective phosphatidylinositol class A gene (PIG-A) deficiency of CD 55 & 59 (decay accelerating factor)
Increased RBC hemolysis & thrombosis during acidosis d/t increased complement activation
o large vessel thrombosis of mesenteric and hepatic veins most common; #1 cause of death
o sleep relative hypoxia increased PCO2 acidosis
sx: episodic dark morning urine
complications: aplastic anemia, myelodysplasia, acute leukemia; pancytopenia, iron deficiency anemia
dx: flow cytometry to detect low CD 55 & 59 (most accurate); ham test or sucrose hemolysis test to detect complement pathway
tx: prednisone, eculizumab (inactivates C5 in complement pathway), folic acid and transfusion as needed; bone marrow transplant
o aplastic anemia
pancytopenia of unclear etiology; autoimmune destruction of bone marrow by T cells
causes of pancytopenia: infection (HIV, hepatitis, CMV, EBV), cancer, radiation, toxins (toluene, insecticides=DDT,
benzene), drugs (sulfa, phenytoin, carbamazepine, chloramphenicol, alcohol, chemotherapy), SLE, paroxysmal nocturnal
hemoglobinuria, B12 and folate deficiency, thyroid inhibiting meds (propylthiouracil, methimazole)
dx: dx of exclusion; bone marrow biopsy (most accurate)
tx: blood transfusion, antibiotics, platelets; allogeneic bone marrow transplant if pt <50 yo; if pt >50yo antithymocyte globulin +
(cyclosporine or tacrolimus)
Cryoglobulinemia Cold agglutinin disease
a/w hep C a/w EBC, Waldenstrom macroglobulinemia, mycoplasma pneumoniae,
Sx: joint pain, glomerulonephritis, purpuric skin lesions, neuropathy sx: hemolysis
Dx: rheumatoid factor (+), cold precipitable immune complexes; SLE C3
decreased, Hep B C4 decreased
dx: direct coombs (positive only for complement), peripheral smear (normal
or spherocytes)

Tx: treat Hep C with ribavirin and interferon tx: stay warm, rituximab, immunosuppressants (cyclophosphamide,
*NOT responsive to steroids or splenectomy

Sickle cell disease
o Autosomal recessive point mutation; glutamine valine @ 6
AA of beta-hemoglobin chain
Sickle cell trait: heterozygous for sickle gene
Sx: defect in ability to concentrate urine (osothenuria); hematuria
o Clinically asymptomatic; normal CBC & smear
Tx: none needed
o Sickling triggered by hypoxia, acidosis, dehydration, infection, or variations in body temp
Hemolytic anemia with increased retic count
o Complications: acute painful crisis, autosplenectomy, aplastic crisis, hemorrhagic or ischemic stroke d/t thrombosis, pigmented or bilirubin
gallstones, papillary necrosis of the kidney, priapism, CHF, osteomyelitis with salmonella, retinopathy, skin ulcers, avascular necrosis of the
femoral head
Acute painful crisis d/t microvascular occlusion of bone (long bones of arm/legs, vertebral column, sternum); lasts 2-7 days
Precipitated by: infection, cold, dehydration, venous stasis, acidosis
Tx: hydration, pain control (NSAIDs, narcotics), O2, transfusion as needed
Acute chest syndrome
Vaso-occlusive crisis w/in the lungs a/w infection or pulmonary infarction (pneumonia, vaso-occlusion, PE)
Sx: fever, tachypnea, tachycardia, hypoxia, chest pain worse on inspiration, pulmonary infiltrates bronchial breath
sounds & egophony
o Increased WBC, increased retic count, decreased Hgb & HCT; sickle & target cells on peripheral smear
o Complications: respiratory failure
Tx: empiric antibiotic tx, oxygen, analgesia
Autoinfarction of the spleen increases risk of infection with encapsulated organisms, also increases risk of osteomyelitis d/
salmonella spp., pneumonia d/t strep pneum or H. influenzae
Encapsulated organisms: Strep pneumo, H. influenzae, klebsiella, pseudomonas aeruginosa, Neisseria meningitidis,
cryptococcus neoformans
Aplastic crisis: viral suppression of RBC precursors; a/w parvo B19 virus
Dx: decreased retic count (best initial test), PCR for parvo B19 DNA (most accurate)
o Bone marrow will have giant pronormoblasts (not required to dx)
Tx: IVIG, erythropoietin, transfusion
o Dx: peripheral smear (best initial; sickle cells, target cells, howell jolly bodies of asplenia), hemoglobin electrophoresis (most accurate)
Howell jolly bodies: remnants of nuclear material in RBCs
o Tx: oxygen, hydration, analgesia, folic acid replacement, vaccines (pneumococcal), hydroxyurea
hydroxyurea or 5-deoxyazacytidine (decitabine): increases HbF production; decreases # of sickle cell crisis
PCN prophylaxis & vaccination against pneumococcus
Blood transfusion indications: aplastic crisis, severe hypoxemia in acute chest syndrome, to decrease viscosity & cerebral
thrombosis in pt w/ stroke, priapism, visual changes from retinal infarction
If fever or elevated WBC ceftriaxone, levofloxacin, or moxifloxacin
Polycythemia vera
o Mutation in JAK2 protein Overproduction of all 3 cells lines; RBC line increases the most
o Sx: hyperviscosity (headache, blurred vision, tinnitus, HTN, fatigue, splenomegaly, thrombosis, bleeding from engorged BVs), pruritis (d/t
elevated basophils histamine release), gout (increased cell turnover)
Can convert to AML
o Dx: JAK2 mutation (most accurate), low erythropoietin, HCT>60%, low iron low MCV, elevated B12, increased basophils, normal oxygen
o Tx: phlebotomy, hydroxyurea (lowers cell count)
Essential thrombocytosis
o Platelet count >1 million thrombosis and bleeding; a/w JAK 2 mutation in 50%
o Tx:
<60 yo, asymptomatic, platelet<1.5 million no treatment
>60 yo, thromboses or platelet >1.5 million hydroxyurea
if RBC suppression anagrelide
aspirin for erythromelalgia (red painful hands)
idiopathic thrombocytopenic purpura (ITP)
o isolated thrombocytopenic purpura
o dx: diagnosis of exlucsion; antiplatelet antibody, increased megakaryocytes, U/S or CT of spleen (r/o splenomegaly)
o tx:
no bleeding, >30,000 PLT no tx
mild bleeding, <30,000 PLT glucocorticoids (prednisone)
severe bleeding (GI/CNS), PLT <10,000 IVIG, anti-rho (Anti-D)
recurrent episodes, steroid dependent splenectomy
vaccinate against N. meningitidis, H. influenzae, and pneumococcus before spleen removal
splenectomy or steroids not effective rituximab, azathioprine, cyclosporine, mycophenolate
romiplostim and eltrombopag when splenectomy fails
von Willebrand disease (vWD)
o autosomal dominant; decreased level or functioning of vWF
o sx: epistaxis, gingival/gum bleeding; worse after aspirin use
o dx: normal PLT count, increased aPTT, increased bleeding time, decreased vWF, ristocetin cofactor assay to detect vWF dysfunction
o tx: DDAVP (desmopressin; releases subendothelial stores of vWF); if no response factor 8 or vWF replacement
o x-linked recessive deficiency of factor 8 or 9
o sx: delayed joint or muscle bleeding
o dx: PT normal, increased aPTT; mixing study w/ normal plasma will correct aPTT; assay for factor 8 or 9 (most accurate)
o tx: mild DDAVP (desmopressin); severe replacement of specific factor
factor 11 deficiency
o sx: increased bleeding after trauma/surgery
o dx: increased aPTT (corrected in mixing study)
o tx: FFP to stop bleeding
factor 12 deficiency
o usually asymptomatic; elevated aPTT
o no tx needed
disseminated intravascular coagulation (DIC)
o RF: sepsis, burns, abruptio placentae or amniotic fluid embolus, snake bites, trauma tissue factor release, cancer
o Dx: low platelets and fibrinogen, increased D-dimer and fibrin split products, elevated PT and aPTT
o Tx: if PLT<50,000 FFP; if bleeding not controlled cryoprecipitate (replaces fibrinogen)
o Factor V Leiden mutation (#1)
o Tx: warfarin (INR 2-3 for 6 mo)
Heparin induced thrombocytopenia (HIT)
o Unfractionated heparin> LMWH; 5-10 days after starting tx, platelet count drop >30%
o Venous>arterial clots
o Dx: ELISA for platelet factor 4 Ab or serotonin release assay
o Tx: stop heparin, direct thrombin inhibitor (argatroban, lepirudin, bivalirudin), warfarin (only after starting thrombin inhibitor)
Avoid giving platelets
Antiphospholipid syndromes thrombosis (arteries and veins)
o IgG or IgM antibodies against the (-) charged phospholipids
Lupus anticoagulant: abnormal aPTT
Anticardiolipin antibody: multiple spontaneous abortions (need to r/o antiphospholipid syndrome after two 1
trimester or one
trimester abortion)
o Dx: mixing study (best initial; aPTT remains elevated b/c not d/t a clotting factor deficiency); normal PT & INR; false (+) VDRL or RPR
lupus anticoagulant russel viper venous test (most accurate; prolonged, doesnt correct after mixing with normal plasma)
o Tx:
heparin & warfarin (as for DVT/PE); lifelong anticoagulation may be needed if recurrent thrombotic episodes
prevent recurrence of abortion with heparin and aspirin (warfarin contraindicated b/c teratogenic)
o pancytopenia d/t bone marrow fibrosis; usually in older pts
o dx: peripheral smear (tear drop shaped cells, nucleated RBCs)
o tx: TNF inhibitors (thalidomide, lenalidomide); allogeneic bone marrow transplant if pt <50-55 yo
o Myelodysplastic syndrome
Preleukemic; pancytopenia despite hypercellular bone marrow; pt >60 yo; a/w 5 q deletion
Sx: infection, bleeding, fatigue & weight loss, splenomegaly possible
Dx: CBC (anemia, low MCV), nucleated red cells, Prussian blue stain (ringed sideroblasts), Pelger-Huet cells (bilobed nucleus),
hypercellular bone marrow
Severity is based on % blasts
Tx: transfusion, erythropoietin, lenalidomide (decreased transfusion dependence for pt with 5q deletion)
Azacitidine decreased transfusion dependence w/o increased survival
o acute leukemia (ALL & AML)
pancytopenia; normal or elevated WBC count but blasts are nonfunctional
sx: fatigue, infection, bleeding
M3 (promyelocytic leukemia) a/w DIC
Dx: blood smear (best initial; shows blasts), flow cytometry (most accurate)
myeloperoxidase a/w acute myelocytic leukemia (AML)
M3 (promyelocytic) AML: auer rods, translocation btwn chr 15 & 17
Cytogenetics is the best indicator of prognosis
Tx: chemotherapy to remove blasts from peripheral blood smear (inducing remission); If poor prognosis BMT, if good
prognosis continue more chemotherapy
M3 AML: add all-trans-retinoic acid (ATRA)
ALL: add intrathecal chemotherapy (methotrexate) to prevent relapse in CNS
o Chronic myelogenous leukemia (CML)
BCR-ABL (9:22 translocation, Philadelphia chromosome); elevated WBC count (all neutrophils)
Sx: pruritis (basophils releasing histamine), splenomegaly (early satiety, abdominal fullness, LUQ pain); hypermetabolic syndrome
(fatigue, night sweats, fever)
Highest risk to transform into acute leukemia (blast crisis)
Dx: leukocyte alkaline phosphatase score (low in CML, high in Leukemoid reaction; best initial), PCR on peripheral blood for BCR-
ABL (most accurate)
Tx: tyrosine kinase inhibitors (imatinib=gleevec, dasatinib, or nilotinib); BMT curative
Acute leukostasis reaction leukopheresis to remove excess WBCs
o Sx d/t blocked delivery of O2 to tissues (RBCs cant get to tissues) blurry vision, confusion, priapism
o Chronic lymphocytic leukemia
Clonal proliferation of B-lymphocytes that are abnormal functioning attack normal RBCs and platelets, hypogammabulemia);
>50 yo
Sx: fatigue (#1), lymphadenopathy, spleen or liver enlargement, infection
Richter phenomenon: conversion of CLL into high grade lymphoma
Dx: WBC >20,000 (mostly lymphocytes), anemia and thrombocytopenia (marrow infiltration or auto-immune warm IgG Ab),
smudge cells on peripheral smear (d/t fragile nucleus)
Stage 0 (elevated WBC), stage 1 (lymphadenopathy) no tx
Stage 2 (hepatosplenomegaly), stage 3 (anemia), stage 4 (thrombocytopena) fludarabine + rituximab
o Also give if symptomatic (severe fatigue, painful nodes)
PCP prophylaxis
Refractory cases cyclophosphamide
Mild cases chlorambucil
Severe infection IVIG
Autoimmune thrombocytopenia or hemolysis prednisone
o Hairy cell leukemia
B-cells with filamentous projections on smear; middle aged men
Sx: massive splenomegaly, sx of pancytopenia
Dx: pancytopenia, monocytopenia, dry tap (non-aspirable) despite hypercellularity of the marrow; most accurate tartrate
resistant acid phosphatase (TRAP) or CD 11
Tx: cladribine
o Mucosal associated lymphoid tissue
Lymphoma of the stomach a/w Helicobacter pylori
tx: PPI + clarithromycin and amoxicillin
o Hodgkin vs Non-hodgkin lymphoma
Proliferation of lymphocytes in lymph nodes and spleen;
Hodgkin typically presents as low grade disease; Non-hodgkin typically presents as disseminated disease
Hodgkin centers around cervical area
Sx: painless lymphadenopathy; B symptoms (fever, weight loss, night sweats)
Dx: excisional biopsy (best initial), high LDH level= worse severity
Reed sternberg cells seen in hodgkin lymphoma
Staging: CT scan ab/pelvis/chest, bone marrow biopsy
o Stage I: 1 lymph node group
o Stage 2: 2+ lymph node groups on the same side of the diaphragm
o Stage 3: both sides of the diaphragm
o Stage 4: widespread disease
Hodgkin: Lymphocyte predominance has the best prognosis; lymphocyte depleted has the worst prognosis
Non-hodgkin: Burkitt and immunoblastic have the worst prognosis
Stage Ia or IIa: local radiation
o Relapses chemotherapy
o Radiation SE: increased risk of solid tumors (breast, lung), increased risk of premature coronary artery
breast screening 8 yr after starting tx
Stage III or IV, any B sx: combo chemotherapy + rituximab (anti-CD 20)
o Non-hodgkin Chemo: cyclophosphamide, Adriamycin (doxorubicin/ hydroxydaunorubicin), vincristine,
o Hodkin Chemo: Adriamycin (doxorubicin), bleomycin, vinblastine, dacarbazine
Determine Adriamycin dosing using MUGA or nuclear ventriculogram (MUGA assesses for cardiac
toxicity, nuclear ventriculogram to assess LV ejection fraction) d/t risk of cardiotoxicity
o Chemotherapy SE: risk of acute leukemia, myelodysplastic syndrome, and non-hodgkin lymphoma
Cardiomyopathy (doxorubicin), neuropathy (vincristine), lung fibrosis (bleomycin), hemorrhagic
cystitis (cyclophosphamide), renal and ototoxicity (cisplatin)
o Relapses extra high dose chemo + bone marrow transplant
Multiple myeloma
o Plasma cell proliferation that produced monoclonal immunoglobulin (IgG or IgA)
o Sx: back pain (osteolytic lesions, fractures, vertebral collapse), renal dysfunction, anemia (d/t marrow infiltration), sx of hypercalcemia
(constipation, anorexia, weakness, increased urination, or neuro abnormalities), recurrent infections, amyloidosis
Neoplastic cells produce osteoclast activating factors lytic bone lesions & hypercalcemia
hypercalcemia, pancytopenia (anemia= normocytic normochromic, leucopenia, thrombocytopenia)
smoldering myeloma: myeloma w/o bone lesions or other end-organ damage, indolent course
observe w/o treatment; symptomatic tx (lower calcium, reverse anemia)
o dx: >10% abnormal plasma cells in bone marrow biopsy (most accurate); serum protein electrophoresis (M spike of IgG or IgA); plain
radiographs (lytic lesions in bone); low hemoglobin, RBCs in rouleaux formation, elevated ESR, high calcium, high serum protein w/ normal
albumin level; poor renal function (elevated BUN and creatinine), tubular casts of bence jones protein (light chain Ig; seen on urine
immunoelectrophoresis), hyperuricemia (d/t increased turnover of nuclear material of plasma cells); decreased anion gap
beta2 microglobulin levels correspond to severity of disease
decreased anion gap b/c IgG is a cation that causes compensatory increased chloride and bicarbonate
radionuclide bone scan is normal (b/c lytic lesions do not pick up the nuclear isotope)
bence jones protein is detected by urine immunoelectrophoresis; urine dipstick will detect only albumin
o tx: systemic chemotherapy (alkylating agents; dexamethasone + lenalidomide and/or bortezomib; if no response radiation therapy; if <70
yo transplantation afer induction chemo (autologous peripheral blood stem cell transplantation > bone marrow transplant)
median survival of only 2-4 yrs w/treatment
renal failure or infection is the most common cause of death
lower calcium: IV normal saline, bisphosphonates
Increased renal excretion with normal saline if hypercalcemia related to dehydration and increased Cr
Bisphosphonates inhibit osteoclastic bone reabsorption
decrease anemia: erythropoietin
monoclonal gammopathy of undetermined significance (MGUS)
o pt usually >75 yo
o dx: asymptomatic IgG or IgA spike <3.5 g; <10% plasma cells in bone marrow; bence jones proteinuria <1g/24 hrs
o tx: close observation for possible multiple myeloma development in 10-15 yrs
waldenstoms macroglobulinemia
o malignant proliferation of plasmacytoid lymphocytes (elevated IgM)
o sx: lymphadenopathy, splenomegaly, anemia, abnormal bleeding, hyperviscosity syndrome (d/t increased IgM)
sx of hyperviscosity: lethargy, blurry vision & vertigo, engorged BVs in eyes, mucosal bleeding, Raynaud phenomenon
NO lytic bone lesions
o dx: IgM >5g/dL; Bence Jones proteinuria
o tx: chemotherapy + plasmapheresis
chemo: (chlorambucil or fludarabine) + prednisone
o sx: fever, malaise/fatigue, weight loss, arthralgia/myalgia
o polyarteritis nodosa (PAN)
vasculitis of small and medium vessels; spares the lungs
a/w Hep B
sx: glomerulonephritis, peripheral neuropathy (peroneal nerve foot drop most common; mononeuritis multiplex), stroke,
abdominal pain with eating, GI bleeding, N/V, skin sx (lower extremity ulcers, livedo reticularis, purpura, nodules; rarely
mononeuritis multiplex: multiple peripheral neuropathies of nerves large enough to have a name
dx: biopsy of sx site (most accurate), angiography (beading); anemia, leukocytosis, elevated ESR & CRP, P-ANCA (20%)
test for Hep B
tx: prednisone + cyclophosphamide
o polymyalgia rheumatica (PMR)
pt >50 yo; affects shoulders and hips
sx: pain and stiffness in shoulder and pelvic girdle muscles (difficulty combing hair and rising from a chair)
dx: elevated ESR, anemia (normochromic normocytic); normal CPK and aldolase
tx: steroids
o giant cell (temporal) arteritis
sx: visual sx (irreversible blindness), jaw claudication, scalp tenderness, headache, muscle fatigue, decreased temporal artery
pulse; sx in other arteries (decreases arm pulses, bruits near clavicles, aortic regurgitation, aortic aneurysm)
dx: elevated ESR and CRP; biopsy of artery (most accurate)
tx: high dose prednisone; f/u with serial CXR to f/u aortic aneurysm
o Wegener granulomatosis
affects respiratory tract, kidneys (renal insufficiency), eyes, joints, skin
upper respiratory sx: sinusitis, otitis media, mastoiditis, oral and gingival involvement
dx: C-ANCA (best initial; cytoplasmic antineutrophil cytoplasmic antibody= anti-proteinase-3 antibody), biopsy (most accurate;
Lung>renal> sinuses)
tx: prednisone + cyclophosphamide
o Churg-Strauss syndrome
involves lungs an kidneys; asthma
dx: eosinophila, P-ANCA (anti-myeloperoxidase antibody; antineutrophil cytoplasmic antibody); biopsy (most accurate)
tx: prednisone + cyclophosphamide
o microscopic polyangiitis
dx: P-ANCA
o Henoch-Schonlein purpura
Affects children
Sx: GI pain & bleeding, purpura o skin (leukocytoclastic reaction= painless palpable purpura on butt & legs), arthralgia, hematuria
(renal involvement)
Dx: clinical; biopsy (most accurate; leukoclastic vasculitis)
Tx: self-resolving; steroids for severe extrarenal sx with renal insufficiency (renal damage not helped by steroids)
Kawasaki disease (mucocutaneous lymph node syndrome)
o Usually seen kids <10 yo
o Sx: high fever, bilateral conjunctivitis, injected pharynx, cracked lips strawberry tongue, edema, desquamation of the extremities,
polymorphic rash, cervical lymphadenopathy
Scleroderma (systemic sclerosis)
o fibrosis of skin and internal organs
Most common in young (20-40 yo) F
o sx: raynaud syndrome, skin (fibrosis, telangiectasia, abnormalities in pigment), esophageal dysmotility w/ GERD, diverticuli, renal (sudden
HTN crisis), restrictive lung disease, pulmonary HTN right ventricular hypertrophy, myocardial fibrosis, pericarditis, heart block
limited scleroderma= CREST syndrome: calcinosis, Raynaud phenomenon, esophageal dysmotility, Sclerodactyly (thickened
& thick skin of fingers/toes), telangiectasia
Raynaud syndrome: pain and pallor (or cyanosis) followed by reactive hyperemia (red); precipitated by cold or emotional stress
o Dx: ANA (+), SCL-70 (anti-topoisomerase; most specific), anticentromere (CREST syndrome)
o Tx:
Renal crisis: ACE inhibitors (even if elevated Cr)
Esophageal dysmotility: PPIs for GERD
Raynaud: calcium channel blockers
Pulmonary fibrosis: cyclophosphamide
Pulmonary HTN: bosentan (endothelin antagonist)
Systemic lupus erythematosis (SLE)
o Autoimmune connective tissue disease
o Sx: symmetric arthritis, pericarditis, nephritis, pleuritis, skin disorders
Other possible sx: alopecia, pneumonia, alveolar hemorrhage, restrictive lung disease, ocular sx (photophobia, retinal lesions like
cotton wool spots, blindness), mesenteric vasculitis, Raynaud phenomenon, antiphospholipid syndrome
Pancytopenia, urinary sediment; anemia of chronic disease, lymphopenia, leukopenia, thrombocytopenia; anti-SSA or anti-SSB also
decreased complement levels and elevated anti-dsDNA during acute exacerbation (markers of disease activity)
o Diagnostic criteria (4/11): malar rash, discoid rash, photosensitivity, oral or vaginal ulcers (usually painless), arthritis, Serositis
(inflammation of pleura or pericardium +/- effusions), renal disease, heme disorder, immune disorder, ANA, neuro disorder
Malar rash: fixed erythema, flat or raised over the malar area, that tends to spare the nasolabial folds
Discoid rash: erythematous raised patches with adherent keratotic scaling and follicular plugging
Arthritis: nonerosive/nondeforming, involving >2 peripheral joints with tenderness, swelling and effusion
Renal: persistent proteinuria or cellular casts; membranous glomerulonephritis
Kidney damage d/t immune complex-mediated damage; activates complement low C3
Neuro: seizure, psychosis, stroke d/t vasculitis
Hematologic: hemolytic anemia or leukopenia (<4000) on >2 occasions, or lymphopenia (<1500) on >2 occasions, or
thrombocytopenia (<100,000)
Immune disorders: positive LE cell preparation, positive anti-dsDNA, anti-Sm, False (+) VDRL or RPR test, positive ANA
o Tx:
Acute flare: high dose boluses of steroids
Hydroxychloroquine for mild disease limited to skin and joints
Lupus nephritis: steroids +/- (cyclophosphamide or mycophenolate)
Kidney biopsy is needed to determine severity of disease; simple glomerulosclerosis will not respond to tx
Cyclophosphamide SE: acute hemorrhagic cystitis, bladder cancer, sterility, myelosuppression
o MESNA and increased fluid intake help to avoid bladder SE (d/t acrolein)
Young pts dies of infection; old pts die of MI (d/t accelerated atherosclerosis)
o Most common in AA female 20-30 yo
o d/t Inflammatory non-caseating granulomas
o Sx: new cough, dyspnea, myalgias, erythema nodosum, weight loss, fever, anterior uveitis, arthritis
Erythema nodosum: bilateral pretibial tender erythematous raised nodules
o Dx: CXR (bilateral hilar lymphadenopathy +/- interstitial infiltrates; reticular opacities), hypercalcemia, elevated angiotensin converting
Hypercalcemia d/t increased 1,25-vit D production in macrophages in granuloma
o Tx: steroids
Sjogren syndrome
o Autoimmune; antibodies to lacrimal and salivary glands; F>M onset 40-50 yo
a/w rheumatoid arthritis, SLE, primary biliary cirrhosis, polymyositis, hashimoto thyroiditis
lymphocytic infiltration of salivary glands (enlarged and firm glands); dry mucous membranes
o sx: dryness of mouth and eyes, burning & itching of eyes (keratoconjunctivitis sicca), need to constantly drink water, difficulty swallowing,
dental caries; dyspareunia d/t loss of vaginal secretions
other possible sx: vasculitis, lung disease, pancreatitis, renal tubular acidosis, lymphoma
o dx: Schirmer test (filter paper on eye to observe amount of tears produced), lip or parotid gland biopsy (most accurate); SS-A & SS-B (Ro
and La)
possible ANA, RF, anemia, leukopenia, eosinophilia
o tx: water the mouth (frequent sips of water, sugar-free gum, fluoride treatments), artificial tears, pilocarpine and cevimeline (increase Ach to
produce saliva)
Behcet syndrome
o Sx: painful oral and genital ulcers, erythema-nodosum like skin lesion; ocular lesions uveitis & blindness, arthritis, CNS lesions mimicking
multiple sclerosis; pathergy (sterile skin pustules from minor trauma such as a needle stick)
o Tx: corticosteroids; to wear off steroids azathioprine, cyclophosphamide, colchicine, thalidomide
o Immediate HSR; pt was already sensitized to antigen; IgE binds mast cells release of histamine prostaglandins, leukotrienes
o Causes: insect bites/stings, meds (PCN, phenytoin, lamotrigine, quinidine, rifamipin, sulfa), foods
o Sx: rash (urticaria= wheel and flare), hypotension, tachycardia, respiratory distress (SOB, wheezing, swelling of lips/tongue/face; stridor)
o Tx: airway protection; epinephrine, antihistamine (diphenhydramine=H1 blocker, ranitidine=H2 blocker), glucocorticoids
(methylprednisolone, hydrocortisone)
o Sudden swelling of face, tongue, eyes, airway
o Dx: decreased C2 and C4 levels; deficiency of C1 esterase inhibitor
o Tx:
acute airway protection, FFP
chronic androgens (danazol, stanozol)
o causes: insects, meds, pressure (dermatographism), cold, vibration
o tx: antihistamines (hydroxyzine, diphenhydramine, fexofenadine, loratadine, cetirizine, ranitidine), leukotriene receptor antagonists
(montelukast, zafirlukast)
allergic rhinitis (seasonal allergies, hay fever)
o IgE dependent
o Sx: watery eyes, sneezing, itchy nose, itchy eyes, inflamed boggy nasal mucosa, pale or violaceous turbinates, nasal polyps
o Dx: clinical dx
o Tx: avoidance of precipitating allergen, intranasal corticosteroid, antihistamine (loratadine, clemastine, fexofenadine, brompheniramine),
intranasal anticholinergic (ipratropium), desensitization
Common variable immunodeficiency
o B cells present but immunoglobulins are deficient (all subtypes; IgG, IgM, IgA)
o Sx: recurrent sinopulmonary infections (bronchitis, pneumonia, sinusitis, otitis media), giardiasis, spruelike intestinal malabsorption;
increase in autoimmune diseases (pernicious anemia, seronegative rheumatic diseases)
Increased risk of lymphoma
o Dx: decreased immunoglobulin levels, decreased response to antigen stimulation of B cells
o Tx: antibiotics for infections; chronic IVIG
X-linked (bruton) agammaglobulinemia
o Males; decreased B cells and lymphoid tissue; decrease/absence of tonsils, adenoid, lymph nodes, and spleen
o Sx: recurrent sinopulmonary infections
o Tx: antibiotics for infections; chronic IVIG
Severe combined immunodeficiency
o Deficiency in B and T cells
o Sx: recurrent sinopulmonary infections; infections with opportunistic organism (PCP, varicella, candida)
o Tx: bone marrow transplant
IgA deficiency
o Sx: recurrent sinopulmonary infections, atopic diseases, anaphylaxis to blood transfusion, spruelike condition with fat malabsorption;
increased riks of vitiligo, thyroiditis, and RH
Hyper IgE syndrome (Job syndrome)
o Sx: recurrent skin infections with staphylococcus
o Tx: prophylactic antibiotics with dicloxacillin or cephalexin
Wiskott-Aldrich syndrome
o T cell deficiency
o Sx: immunodeficiency, thrombocytopenia, eczema
o Tx: bone marrow transplant
Chronic granulomatous disease
o Sx: aphthous ulcers, inflammation of the nares, granulomas
Infections with staph, Burkholderia, nocardia, Aspergillus
o Dx: nitroblue tetrazolium testing (decrease in respiratory burst that produced hydrogen peroxide)
neutropenic fever
o sx: fever, neutropenia
fever: 1x oral temp >101 F or >100.4 for >1hr
neutropenia: Abs neutrophil count <500cells/mm3
increased risk of infection (esp. gram (+) on skin and oral cavity or gram (-) from bowel)
any neutropenic pt w/ signs of clinical deterioration should be suspected of having sepsis
may not be febrile if elderly or on corticosteroids
o risk factors: chemotherapy
nadir of WBC count occurs 7-14 days after chemotherapy
mucositis: breakdown of skin & mucosal barriers d/t chemotherapy or radiation; vulnerable to gram (+) infection; if present, add
vancomycin to treatment as well as anti-pseudomonal tx (cefepime, ciprofloxacin, imipenem, or beta-lactam + aminoglycoside)
o tx:
if no obvious source of infection, assume gram (-) and add in anti-pseudomonal tx: cefepime, ciprofloxacin, imipenem, or beta-
lactam + aminoglycoside
if fever lasts >3 days add in vancomycin
if fever persists 5-7 days after vanco add antifungal (fluconazole or amphotericin B)
cancer pt should be immunized against pneumococcus and influenza
MMR and varicella zoster vaccines are contraindicated b/c they contain live virus
G-CSF (granulocyte colony stimulating factor) stimulates bone marrow to produce neutrophils; given
prophylactically after chemo to reduce neutropenia
o VE=VT * f
Minute ventilation depends on tidal volume and respiratory frequency
Restrictive lung diseases decrease tidal volume compensatory increased frequency
Ex: idiopathic pulmonary fibrosis, obesity, kyphoscoliosis, pleural effusion, neuromuscular disease (myasthenia gravis,
ALS, myopathy)
o Oxygen/hemoglobin curve
P90%=60 mmHg, P75= 40 mmHg, P50=26 mmHg
Mental status changes occur below the P50 level
o Hypoxemia= PaO2/FiO2 <200
Brain becomes ischemic after 4 min of hypoexmia
o RR>30 #1 sign of impending lung failure
Other signs of lung failure: use of accessory muscles (oblique mm. during exhalation; scalene, intercostals)
o Pt needs to be on supplemental oxygen if PO2 <55 or SpO2 <88 on room air
Check O2 sat or ABG on room air after mild exertion (walking 20 steps)
Tachypnea indicates at least mild respiratory distress
o Ventilation settings
Compliance= change in volume/change in pressure
Peak pressure= inspiratory/dynamic
Plateau pressure= expiratory/ static
Controlled mandatory ventilation: pt not taking any breaths (plateau pressure never goes negative)
Ex: brain death, narcotics, paralysis
Ventilator setting= assist-control mode
o start with FiO2 with100% oxygen
o tidal volume: 6cc/kg ideal body weight for ARDS, 8-10 cc/kg all other respiratory failure
ideal body weight based on height & sex
men: 50+ 0.91 (Ht-152.4)
women: 45.5+ 091 (Ht-152.4)
o RR: 10-14 normal range
Synchronized IMV: combines helped & natural breathing
Pressure support: helps pts spontaneous breaths to achieve a desired tidal volume
o Acute cough <3 wks
Causes: URI, CHF, pneumonia, PE
o Chronic cough >3-8 wks
Causes: COPD, bronchogenic carcinoma; irritants (ACE inhibitors, post-nasal drip, GERD), asthma
Dx: CXR (normal in GERD, asthma, and post-nasal drip), trials of treatment; CT thorax or bronchoscopy if suspicious for carcinoma
Tx: stop irritating drugs (ACE inhibitor), avoid irritants
o Massive hemoptysis >100-600 mL coughed up in 24 hr
Complication: asphyxiation
o Diff dx: malignancy, bronchitis (blood streaked purulent sputum), TB, lung abscess, bronchiectasis (chronic copious sputum production), PE
o Dx: CXR, fiberoptic bronchoscopy
o Tx: intubation if massive hemoptysis
Postnasal drip syndrome
o d/t sinusitis, rhinitis (nonallergic, allergic, postinfectious, vasomotor, drug-induced, environmental irritant induced)
o sx: frequent throat clearing, nasal discharge, sensation of liquid in the throat
o tx: 1
generation antihistamine + decongestant for 3wks
allergic rhinitis: newer generation antihistamine + nasal corticosteroid
if sx do not improve sinus radiographs (sinusitis shows opacification, air-fluid levels, or mucosal thickening)
o diff dx: PE, asthma, pneumonia, panic attack, anemia, tamponade, arrhythmia, pleural effusion, COPD, methemoglobinemia, carbon monoxide
obstructive lung diseases
o progressive airflow obstruction; may include airway hyperreactivity
o causes: bronchiectasis (cystic fibrosis), asthma, chronic bronchitis, emphysema
o sx: progressively worse dyspnea (exertional mild activity at rest), expiratory wheezing
blue bloater: chronic bronchitis, overweight, edema, cyanotic
pink puffer: emphysema, thin, ruddy cheeks
acute exacerbation: respiratory distress, labored respirations, cyanosis, wheezing
dx: CXR (hyperinflated lungs), ABG (assess oxygenation and acid-base status)
tx: oxygen, bronchodilators, steroids
signs of acute respiratory failure: RR>40, inability to speak d/t dyspnea, accessory muscle use with fatigue despite maximal
treatment, confusion, restlessness, agitation, lethargy, rising PaCO2, extreme hypoxemia
tx: intubation with ventilatory support
o complications of chronic hypoxemia: pulmonary HTN, secondary erythrocytosis, exercise limitation, impaired mental functioning
o dx: spirometry (FEV1<80% of expected, FEV1/FVC<0.7 (mild), <0.3-0.5 (moderate), or <0.3 (severe); increased TLC), ABG (hypoxia, CO2
retention, respiratory acidosis)
o tx: bronchodilators (beta agonist, anticholinergics), high dose glucocorticoids, antibiotics if infection suspected, supplemental oxygen,
smoking cessation
oxygen and smoking cessation decrease mortality
supplemental home oxygen needed if PaO2<55 mmHg; continuous use >18hr/day
use oxygen with caution in pt w/chronic respiratory difficulty b/c respiratory drive may depend on relative hypoxia
o COPD (chronic obstructive lung disease)= chronic bronchitis or emphysema
Lung destruction decreasing the elastic recoil of the lungs
chronic bronchitis: excessive secretion of bronchial mucus
sx: productive cough for >3 mo in >2 consecutive years
dx: clinical dx in the absence of any other disease that could cause these sx
emphysema: abnormal permanent dilation of air spaces distal to the terminal bronchiole, with destruction of their walls and w/o
obvious fibrosis
RFs: tobacco (destroys elastin fibers); alpha-1 antitrypsin deficiency
Sx: shortness of breath (worse w/ exertion), intermittent exacerbations (increased cough, sputum, SOB), barrel chest from
increased air trapping, muscle wasting and cachexia
Dx: CXR (best initial; increased AP diameter, air trapping and flattened diaphragms); pulmonary function testing (most accurate;
decreased FEV1 & FVC, decreased FEV1/FVC ration (<70%); increased total lung capacity); plethysmography (increase in residual
volume); CBC: increase in HCT from chronic hypoxia
Acute exacerbation: ABG (increased PCO2, hypoxia, respiratory acidosis)
Possible EKG changes: right atrial/ventricle hypertrophy, atrial fibrillation of multifocal atrial tachycardia
Possible echo changes: right atrial/ventricle hypertrophy, pulmonary HTN
Tx: albuterol anticholinergics inhaled steroids
Improves mortality: smoking cessation, oxygen, vaccines (influenza, pneumococcal)
o Criteria for oxygen use:
P02<55 mmHg or Oxygen sat <88%
(signs of right heart failure or elevated HCT) + (PO2 <60mmHg or O2 sat <90%)
Symptom improvement: short acting beta agonists (albuterol), anticholinergic agents (tiotropium, ipratropium),
inhaled steroids, long acting beta agonists (salmeterol), pulmonary rehabilitation
o inhaled bronchodilators have variable response
o anticholinergics work better for COPD than for asthma
o possible improvement with theophylline or lung volume reduction surgery
o lung transplant when all medical therapy is insufficient
acute bronchitis exacerbations of chronic bronchitis: bronchodilators, systemic corticosteroid
(methylprednisolone), antibiotics
o antibiotics against strep pneumo, H. flu, and Moraxella catarrhalis
macrolides (azithromycin, clarithromycin), cephalosporins (cefuroxime, cefixime, cefaclor,
ceftibuten), amoxicillin/clavulanic acid, quinolones (levofloxacin, moxifloxacin, gemifloxacin)
line: doxycycline, TMP/SMX
o Asthma (reactive airway disease)
Bronchial hyperactivity , smooth muscle hypertrophy; bronchospasm that is reversible
Sx: chronic nonproductive cough that is worse at night, nasal polyps, exercise intolerance, acute onset SOB, cough, chest tightness
PE: wheezing, eczema or atopic dermatitis, increased length of expiratory phase of respiration, increased use of
accessory respiratory muscles
Respiratory rate is the best indicator of severity of asthma (normal RR 10-16)
exacerbated by: URI/other infections, allergies, cold air, exercise, emotional stress, catamenial (related to menstrual
cycle), meds (aspirin, NSAIDs, beta blockers, histamine, nebulized meds, tobacco smoke), GERD
signs of severe attack: normal to increased PCO2 levels, speech difficulty, diaphoresis, altered sensorium, cyanosis,
silent lungs
o hyperventilation normally causes decreased PCO2; elevated PCO2 indicated CO2 retention d/t severe airway
obstruction 9air trapping) and/or respiratory muscle fatigue
Classification Days with
with sx
Daily meds Quick relief
<2 days/wk <2/mo no daily meds needed short acting inhaled
beta2 agonists PRN;
possibly oral steroids
Mild persistent >2/wk but
>2 /mo low-dose inhaled steroids or cromolyn,
leukotriene modifier or nedocromil, or sustained-
short acting inhaled
beta2 agonists PRN;
release theophylline possibly oral steroids
Daily >1/wk Low-medium dose inhaled steroids+ long-acting
beta2 agonist or medium dose inhaled steroid +
leukotriene modifier or theophylline
short acting inhaled
beta2 agonists PRN;
possibly oral steroids
continual frequent High dose inhaled steroids + long-acting inhaled
beta2 agonist; if needed add oral steroids
short acting inhaled
beta2 agonists PRN;
possibly oral steroids

acute exacerbation: best initial=ABG (increased A-a gradient) or decreased peak expiratory flow; CXR (r/o other
pathology; may show hyperinflation from asthma), pulmonary function tests (most accurate)
o peak expiratory flow is based on height and age; compared to pts usual PEF when stable
o pulmonary function testing: decreased FEV1> FVC; decreased FEV1/FVC
increase in FEV1 >12% after bronchodilator treatment
o CBC may show increased eosinophils
o Skin testing may ID a specific allergen
o Increased IgE level increased with allergic etiology
asymptomatic pt w/ hx of sx: pulmonary function testing using methacholine (Ach analog) or histamine challenge
(decreased FEV1 >20% during challenge)
Tx: bronchodilators, inhaled or oral corticosteroids
Acute exacerbation: oxygen, albuterol, corticosteroids (take 4-6 hrs for onset), ipratropium; magnesium
(bronchodilator; used if not responsive to albuterol while waiting for steroids to take effect), epinephrine (last resort)
Vaccinate: influenza and pneumococcal
Omalizumab (anti-IgE) used for allergic etiology
Inhaled short acting beta agonists: albuterol, pirbuterol, levalbuterol
Long-acting beta agonists: salmeterol, formoterol
Low dose inhaled corticosteroids (long-term control): beclomethasone, budesonide, flunisolide, fluticasone,
mometasone, triamcinolone
o SE: dysphonia, oral candidiasis
Oral corticosteroids (prednisone)
o SE: osteoporosis, cataracts, adrenal suppression, fat redistribution, hyperlipidemia, hyperglycemia, acne,
hirsutism, thinning of skin, striae, easy bruising
Cromolyn, nedocromil: inhibit mast cell mediator release and eosinophil recruitment
o Best for pt with extrinsic allergies (like hay fever)
Leukotriene modifiers: montelukast, zafirleukast, zileuton
o Zafirleukast: hepatotoxic, a/w Churg-Strauss syndrome
Anticholinergics: ipratropium, tiotropium
o permanent abnormal dilation and destruction of bronchial walls; chronic dilation of the large bronchi
o causes: cystic fibrosis, infections (TB, pneumonia, abscess), panhypogammaglobulinemia and immune deficiency, foreign body or tumors,
allergic bronchopulmonary aspergillosis, collagen-vascular disease (RA)
disease precipitated by: infection, airway obstruction, impaired defense or drainage mechanism
o sx: recurrent/chronic cough, high volume mucopurulent foul smelling sputum, dyspnea, wheezing, hemoptysis, weight loss, anemia of hornic
disease, crackles on lung exam, clubbing (uncommon)
o dx: CXR (best initial; dilated thickened bronchi= tram-tracks), CT scan (most accurate), sputum culture, pulmonary function tests
(obstructive pattern)
o tx: antibiotics for acute exacerbations, hydration, chest physiotherapy & postural drainage (dislodging plugs in bronchi), inhaled
same antibiotics used as for COPD exacerbation; sputum culture to r/o mycobacterium avium intracellulare (MAI)
surgical resection of focal lesions may be indicated
allergic bronchopulmonary aspergillosis (ABPA)
o hypersensitivity of the lungs to fungal antigens; occurs in pts with asthma and hx of atopic disorders
o sx: recurrent episodes of brown-flecked sputum; cough, wheezing, hemoptysis, and bronchiectasis can occur
o dx: CXR (transient infiltrates), peripheral eosinophilia, skin test reactivity to Aspergillus antigens, precipitating antibodies to Aspergillus on
blood test, elevated serum IgE
o tx: oral steroids (prednisone) for severe cases; oral itraconazole for recurrent episodes
restrictive lung disease
o low lung volumes d/t alteration of lung parenchyma (intrinsic) or chest wall, pleura, respiratory muscles (extrinsic)
poor breathing mechanics or lung expansion
o causes: poliomyelitis, myasthenia gravis, scoliosis; pneumonia, ARDS, pulmonary edema, interstitial fibrosis, pneumoconiosis (interstial lung
pneumoconiosis d/t occupational exposures (asbestos): can cause pleural calcifications
normal or high FEV1/FCD (low VC), low DL(CO)
o dx: spirometry
reduced FVC & total lung capacity, normal/increased FEV1, normal FEV1/FVC
pulmonary embolism (PE)
o risk factors: local trauma to vessel, hypercoagulability, venous stasis
hypercoagulable states: factor V leiden mutation (most common hereditary thrombophilia), prothrombin gene mutations
neoplasms, surgery
o physio
obstruction of pulmonary artery-> platelets release vasoactive substances (serotonin) increased pulmonary vascular
resistance increased R. sided heart tension
progressive right sided heart failure is the most common cause of death d/t PE
increased alveolar dead space, V/Q mismatch reflex bronchoconstriction pulmonary edema, hemorrhage, loss of surfactant
(decreased lung compliance)
most common sources of PE: proximal deep veins (#1; iliac, femoral, or popliteal), right heart, pelvic veins, upper extremity
veins, calf veins, renal veins
o SE: acute onset dyspnea, increased RR (most common sign), pleuritic chest pain, tachycardia, hypoxemia (SaO2 <92%); possible rales, 4

heart sound, fever, diaphoresis
signs of R. ventricular dysfunction: bulging neck veins, L. parasternal lift, accentuated 2
heart sound, systolic murmur that
increases with respiration
Massive PE: severe dyspnea, syncope, hypotension, or cyanosis
Smaller more peripheral PE causing infarction of lung tissue: pleuritic pain, cough, or hemoptysis
o Wells score estimates pretest probability of PE
clinically suspected DVT 3.0 points
alternative diagnosis is less likely than PE 3.0 points
tachycardia (heart rate > 100) 1.5 points
immobilization ( 3d)/surgery in previous four weeks 1.5 points
history of DVT or PE 1.5 points
hemoptysis 1.0 points
malignancy (with treatment within 6 months) or palliative 1.0 points
Score interpretation
2-6 pt moderate probability
o <4 + (-) D-dimer low probability
>7 pt high probability
o Dx: ECG, CXR (typically normal), spiral(helical) CT with contrast, D-Dimer, V/Q study, lower extremity venous U/S, MRI, TEE
(echocardiogram), invasive pulmonary angiogram
ECG changes: T-wave inversion in anterior leads (V1-V4), sinus tachycardia, new a.fib; S wave in lead I, Q wave in lead III, inverted
T wave in lead III (S1,Q3,T3)
CXR signs: Westermark sign (nonspecific prominence of central pulmonary a. + decreased pulmonary vascularity), Hampton hump
(peripheral wedge shaped density above diaphragm), palla sign (enlargement of R. descending pulmonary artery)
D-Dimer is used to r/o PE for pts with low probability of having a PE
Lower extremity venous U/S to demonstrate acute DVT + clinical signs of PE is sufficient to dx PE when CT and V/Q are
MRI, TEE, or pulmonary angiogram can be helpful if other studies are nondiagnostic
o Tx: oxygen, anticoagulants or IVC filter, thrombolysis or surgical embolectomy
Thrombolysis or surgical embolectomy is used for pt with r.sided heart failure or hypotension d/t PE
Anticoagulants prevent recurrence
Start with: IV unfractionated heparin, SubQ LMWH (enoxaparin, tinzaparin), or direct factor 10a inhibitor
o Unfractionated heparin requires continuous infusion and coag studies q4-6hrs
Transition into use of warfarin (vit K antagonist)
o Requires PT & INR monitoring; target INR ~2.5
o Overlap treatment for >5 days until INR is therapeutic for 2 consecutive days
For provoked (trauma or surgery) DVT of calf or upper extremity treat 3 mo
For provoked DVT of proximal leg or PE treat 6 mo
For idiopathic or unprovoked DVT/PE or with ongoing RFs (malignancy, antiphospholipid syndrome) indefinite
anticoagulation may be required
IVC filter if active bleeding or other contraindication to anticoagulation or recurrent DVT/PE despite anticoagulation
Pleural effusion
o Exudate: d/t inflammatory or malignant causes; usually with high protein or LDH levels
Causes: parapneumonic (complication of pneumonia), infectious, connective tissue diseases (rheumatoid pleurisy, lupus pleuritis),
impaired lymphatic drainage, PE, pancreatitis, chylothorax, asbestos exposure
Light criteria for exudative pleural fluid: pleural fluid: serum protein >0.5, pleural fluid: serum LDH >0.6, pleural fluid
LDH >2/3 upper limit of normal for serum LDH
Pleural fluid LDH correlates with degree of pleural inflammation
o Transudate: d/t alteration of oncotic forces; usually with low protein and LDH levels
increased hydrostatic pressure: CHF or constrictive pericarditis
decreased oncotic pressure: nephrotic syndrome, cirrhosis w/ ascites (hepatic hydrothorax), malignancy, PE,
hypothyroidism (myxedema)
decreased intrapleural pressure: atelectasis
o Sx: diminished breath sound, dullness to percussion
o Dx: CXR, diagnostic thoracentesis
Indications for thoracentesis: uneven pleural effusion or unilateral pleural effusion, evidence of infection (productive cough, fever,
pleurisy), alarming signs (significant weight loss, hemoptysis, hypoxia), need to evaluate underlying lung parenchyma
Thoracentesis not done for pt with known CHF with B/L effusions (unless resistant to diuretics) or if effusion <10mm
on lateral decubitus film
~50 mL fluid is needed to be visible on lateral decubitus film; fluid >500ml usually obscures the whole hemidiaphragm
Fluid appearance Causes
Clear yellow Transudative; CHF, cirrhosis, nephrotic syndrome
Frank pus Infectious process, empyema
Bloody Cause depends on HCT level in fluid
*<1%: blood d/t traumatic tap
*1-20%: cancer, PE, TB
*>50% hemothorax (trauma, malignancy, PE w/infarction)
Milky, turbid Chylothorax; triglycerides >110 mg/dL d/t disruption of thoracic duct, cholesterol effusion
Dark green biliothorax
o tx: therapeutic thoracentesis for effusion that is significant in size w/ pt dyspneic at rest (safely remove up to 1500 mL), tube drainage for
complicated parapneumonic effusion to prevent fibrous peels; 1 wk trial of antibiotics if pt does not meet criteria for immediate drainage
indications for chest tube drainage (fluid characteristics): empyema, positive gram stain of fluid, presence of loculations,
pH<7.10, glucose <40 mg/dL, LDH >1000 U/L
chest tube left in place until drainage is <50mL/day
empyema: chest tube, antibiotics 4-6 wks; if multiloculated, give fibrinolytic agents (streptokinase, urokinase) through the chest
tube, VATS (video-assisted thorascopic surgery) is an option to break up fibrinous adhesions
hepatic hydrothorax: diuretics and salt restricted diet transjugular intrahepatic portosystemic shunt (TIPS) liver
chest tube is not recommended
if TIPS is contraindicated, you can consider pleurodesis
acute respiratory distress syndrome (ARDS)
o non-cardiogenic pulmonary edema acute dyspnea
o causes: sepsis, severe bleeding, pneumonia, toxic ingestion, burns
release of inflammatory mediators increased alveolar capillary permeability, alveolar damage, leakage of proteinaceous fluid
into the alveoli pulmonary edema
o sx: acute onset of tachypanea, tachycardia, fever, and dyspnea
o dx: CXR(bilateral alveolar infiltrates) , PCWP<18mmHg (normal), PaO2/FiO2 <200; elevated A-a gradient, decreased lung compliance
PCWP>18mmHg suggest cardiogenic pulmonary edema
o Tx: mechanical ventilation (increased positive end expiratory pressure (PEEP), low tidal volume <6mL/kg)
PEEP improves oxygenation by preventing alveolar collapse at the end of expiration increases functional residual capacity &
decreases the work of breathing
Aspiration pneumonitis
o Chemical injury to lungs d/t aspiration of acidic gastric contents inflammation, respiratory distress, pulmonary infiltrate that is apparent
in 4-6 hr
o Typically resolves w/in 48 hrs; observation with f/u CXR
o Dx: CXR, sputum gram stain & culture, blood cultures; serology as needed, fiberoptic bronchoscopy with bronchoalveolar lavage if specimen
needed from lower respiratory tract
Diffuse interstitial infiltrates P carinii or viral; bilateral apical infiltrate TB, cavitation necrotizing infx (staph aureus, TB, or
gram negatives such as klebsiella pneumoniae)
Sputum culture is helpful if purulent & minimally contaminated (<10 epithelial cells & >25 PMNs per low-power field)
Organisms that require serology (not easily cultured): legionella, mycoplasma, C. pneumoniae
o Risk stratification for pneumonia
History: >50 yo, hx of cancer, CHF, cerebrovascular disease, renal or liver disease
Clinical: altered mental status, HR >125, RR >30, hypotension <90 systolic, temp <95 or >104
o Tx: depends on risk stratification
Low risk: out-pt oral antibiotics
High risk, hypoxemic, hemodynamically unstable in-pt
o Community acquired pneumonia: infection of alveoli, distal airways, and interstitium of the lungs; occurs outside the hospital setting
Agents: Strep pneumo, Moraxella catarrhalis, H. influenzae; influenza or adenovirus
Sx: chills, fever, productive cough, pleuritic chest pain
Rust colored sputum is more likely strep pneumo
Bronchial breath sounds, inspiratory crackles
CURB 65: used to predict mortality in community acquired pneumonia
1 pt each: confusion of new onset, urea >7 mmol/L (19 mg/dL), RR >30, BP <90 systolic or <60 diastolic, >65 yo
risk of death at 30 days: 00.7%, 13.2%, 23.0%, 317.0%, 441.5%, 557.0%
Dx: CXR (lobe consolidation)
Tx: oral antibiotics, pain reliever, antipyretic, cough suppressant, f/u 1-2 wks
Empiric antibotics: macrolides (azithromycin) or antipneumococcal quinolones (gatifloxacin, levofloxacin)
o if hospitalized IV 3
gen cephalosporin + (macrolide or antipneumococcal quinolone)
o Atypical pneumonia
Agents: mycoplasma pneumoniae, legionella (preceded by GI sx), chlamydia pneumoniae, chlamydia psittaci (bird droppings),
coccidiomycosis (SW US), histoplasmosis (Mississippi river valley), pneumocystis carinii (AIDs pt), TB
Sx: insidious onset, dry cough, headache, sore throat, myalgias
Dx: CXR (findings worse than clinical exam)
o Aspiration pneumonia
Agents: strep pneumoniae, H. influenzae, gram (-) organisms, oral anaerobes
RF: altered consciousness (seizures, alcoholism, drug overdose, CBA), dysphagia (esophageal reflux, diverticula, obstruction),
neuro disorder (advanced dementia, parkinsonism, myasthenia), sedation to procedures (bronchoscopy, intubation, endoscopy)
impaired epiglottic reflex
Dx: CXR (right lower lobe pneumonia), foul smelling sputum
Tx: antibiotics
o Nosocomial/ hospital acquired pneumonia (includes nursing homes)
Agents: gram (-) organisms; E.coli, pseudomonas aeruginosa, staph aureus
Tx: antipseudomonal beta-lactam (piperacillin, cefepime) + aminoglycoside +/- clindamycin
o Legionella pneumonia
Sx: GI sx before lung sx; myalgias, abdominal pain, diarrhea, severe pneumonia
o Disseminated pulmonary histoplasmosis
Occurs in HIV pts (CD<100); endemic in ohio river valley
Sx: fever, weight loss, night sweats, N/V, cough, SOB, diffuse lymphadenopathy, hepatosplenomegaly
Pancytopenia (if bone marrow involved), elevated LRTs, elevated ferritin
Dx: serum or urine antigen (most sensitive and rapid)
Mild-moderate disease: itraconazole
Severe disease: IV liposomal amphotericin B for 2wks, followed by itraconazole for 1 yr
o Pneumocystis carinii/jirovecii pneumonia (PCP)
Sx: fever, dry cough, worsening dyspnea; increased RR, hypoxemia
Dx: CXR (diffuse bilateral pulmonary infiltrates), ABG, increased LDH, CD4<200
Giemsa or silver stain: large cysts/blebs on lungs rupture pneumothorax
Differential dx: PCP, TB, atypical myocobacteria, cryptococcus, disseminated histoplasmosis, community acquired
pneumonia (strep pneumo, mycoplasma, influenzae)
Prednisone (corticosteroid) used of PO2 <70 or A-a gradient >35 mm Hg
If allergic to sulfa: pentamidine, or clindamycin + primaquine
o Mycobacterium tuberculosis= acid fast bacilli
o High risk background (prison, homeless, immigrant, HIV); transmission via inhalation ingest by alveolar macrophages
Note: people with primary TB are not contagious, only active (secondary) TB contagious
o Sx:
Primary TB is usually asymptomatic, may have pleural effusion; affects middle and lower lung zones; granulomatous lesion w/
center that can be necrotic (caseous necrosis) cavity; healed lesion= ghon complex
Secondary TB: chronic cough (dry purulent sputum; may be streaked with blood), weight loss, fever, night sweats, malaise,
apical rales
Reactivation TB: apical & posterior segment of upper lobes, or superior segment of lower lobes
Miliary tB: hematogenous dissemination of the tubercle bacilli; 1-2mm granulomas
Rasmussen aneurysm: rupture of a dilated vessel in a cavity
Sx: fever, wasting, rales & rhonchi if partial bronchial obstruction, pallor, finger clubbing d/t hypoxia
Extrapulmonary TB: lymph nodes (painless lymphadenopathy), pleura, GU tract, bones & joints, minges, peritoneum
sterile pyuria: WBCs in urine, hematuria, dysuria, frequency
pott disease in spine
adrenal insufficiency d/t adrenal TB
o Dx: CXR (if CD4>200 then bilateral apical infiltrate with cavitation, pleural effusions, ghon or ranke complex), PPD (dx latent/primary TB),
serial sputum culture, PCR for mycobacterial DNA, AFB on microscopic exam
PPD does not r/o TB in immunocompromised host; PPD in low risk pop >15 mm, high risk (health care workers or
immunocompromised other than HIV) >10 mm, close contacts of TB pt or HIV pt >5mm is positive
Primary TB: ghon complex= calcified primary focus, Rankes complex= ghon complex+ calcified hilar lymph node
Secondary TB (reactivation) occurs in the most oxygenated portion of the lungs (apical/posterior segments)
AFB culture takes 4-8 wks on regular medium or 2-3 wks on liquid medium
Report to health department
o Tx: 4 drug antibiotics (isoniazid+ rifampin + pyrazinamide + pyridoxine; alternatives include amikacin, ethambutol or streptomycin) for 2
mo, then 2 drug antibiotics for 4 more months (isoniazid + rifampin)
use pyridoxine (Vit B6) to prevent peripheral neuropathy
SE of treatment: hepatitis, hyperuricemia, thrombocytopenia
Note: oral OCPs decrease drug levels use barrier contraceptive during TB treatment
First 2 wks of treatment in respiratory isolation in hospital; then AFB every 8hrs until 3x (-), then d/c home to continue treatment
for 6 mo
Prophylaxis for latent (primary) TB: 6-9 months of isoniazid +/- pyridoxine
Lung cancer
o #1 cause of cancer death in US
o risk factors: smoking, radiation, environmental toxins (asbestos, radon)
asbestos can cause squamous cell, adenocarcinoma, or mesothelioma
o sx: chronic nonproductive cough, hemoptysis, fatigue, decreased appetite, unintentional weight loss
scattered rhonchi, finger clubbing
phrenic nerve invasion diaphragmatic paralysis
laryngeal nerve invasion hoarseness
horner syndrome: ptosis, miosis, anhidrosis
occurs with apical/Pancoast tumor compression of superior cervical ganglion lack of sympathetic innervation
superior vena cava syndrome: obstruction of venous drainage edema of face and arm, formation of collateral veins in upper
o small cell (oat cell) cancer
neuroendocrine origin; central location; early metastasis
causes paraneoplastic syndromes: SIADH, ectopic production of ACTH, Cushing syndrome, Eaton-lambert syndrome, peripheral
lambert-eaton syndrome: d/t autoantibodies against voltage gated calcium channels in the presynaptic motor
nerve terminal defective release of acetylcholine proximal muscle weakness, absent reflexes
o tx: plasmapheresis, immunosuppressive drug therapy
o non-small cell cancer: squamous, adenocarcinoma, large cell
squamous cell
central/hilar location, local extension instead of metastasis bronchial obstruction atelectasis, pneumonia
most likely to cavitate
can produce PTH-like hormone hypercalcemia
peripheral location; metastasis early to bone/adrenal/CNS
o a/w pulmonary scars/fibrosis & less related to smoking (most common pt is young female nonsmoker)
o can cause thrombophlebitis
large cell
peripheral location; metastasis to CNS & mediastinum Superior vena cava syndrome, laryngeal n. paralysis
o dx: CXR, tissue dx, staging
popcorn or bulls eye calcification of a solitary pulmonary nodule suggests a benign process; lack of calcification increases risk
of malignancy
risk of malignancy increases with size (>2.5 is highly suspicious)
solitary nodules
in low risk pt (<35 yo, nonsmoker): f/u calcified nodule w/ serial chest CT; considered benign if no growth in 2 yrs
in high risk pt bronchoscopy w/ biopsy
o staging
stage I: tumor is w/o nodal involvement or distant metastasis
IA: tumor <3cm w/o extension to adjacent tissues
o tumor >3cm
o invades visceral pleura, causes atelectasis of less than entire lung or extends at least 2cm from carina
stage II: tumor is w/o distant metastasis
IIA: tumor <3cm with ipsilateral hilar and/or ipsilateral bronchial node involvement
o stage IB + involvement of ipsilateral hilar and/or ipsilateral bronchial node
o tumor invading chest wall, diaphragm, mediastinal pleura, or pericardium
o tumor with atelectasis of entire lung or extending w/in 2 cm of carina
stage III: tumor is w/o distant metastasis
o Tumor invading chest wall, diaphragm, mediastinal pleura, pericardium or tumor with atelectasis of entire
lung, or tumor extending w/in 2 cm of carina + ipsilateral hilar or ipsilateral bronchial node
o Tumor with involvement of ipsilateral mediastinal and/or subcarinal nodes
o Involvement of contralateral nodes or of scalene or supraclavicular nodes (either side)
o Tumor invading mediastinum, heart or great vessels, trachea/esophagus, vertebral body or carina
o Tumor with malignant pleural or pericardial effusion
o Satellite tumor nodules w/in same lobe as primary tumor
stage IV: distant metastasis (including tumor nodules in different lobe from primary tumor)
o tx:
small cell: chemo, radiation; 20-30% curative if limited disease (limited to 1 hemithorax), otherwise poor prognosis
stage I, II, IIIa curative resection & radiotherapy
pulmonary function tests before surgery to predict if pt has sufficient pulmonary reserve
surgery is not possible if: bilateral disease, malignant pleural effusion, involvement of heart/carina/aorta/vena cava
breast pathology
breast cancer
o RFs: BRCA mutation (risk of breast and ovarian cancer)
o sx: breast mass, retraction of the nipple if breast ligament involvement
o dx: palpable breast mass or screening mammography; biopsy (FNA, core needle, or open biopsy)
ultrasound is used to distinguish cystic from solid breast mass; used if lesion is painful or varies in size/pan with menstruation
screening mammography age 50-74 every 2 yrs; mammography is needed before biopsy to look for bilateral disease and to
determine if there is a single lesion or multiple lesions within the same breast
FNA cant screen for receptors; core needle biopsy can screen for estrogen receptor, progesterone receptor, and HER2/neu
(estrogen receptor) status
PET scan is used to determine the content of abnormal lymph nodes that are not easily accessible to biopsy; cancer has increased
o Tx: lumpectomy+ radiation or modified radical mastectomy; sentinel node biopsy; hormonal therapy for receptor positive cancer;
Contrast or dye is used to detect the first node from the surgical resection
Negative sentinel node eliminates the need for axillary lymph node dissection
All ER or PR positive pts aromatase inhibitors (anastrozole, letrozole, exemestane)> Tamoxifen or raloxifene
o Tamoxifen SE: endometrial cancer, clots
o Aromatase inhibitor SE: osteoporosis
HER2/neu receptor positive trastuzumab
Adjuvant chemotherapy indicated: lesions >1cm, positive axillary lymph nodes
Tamoxifen prophylaxis for pts with multiple 1
degree relative with breast cancer

GI pathology
Oral candidiasis
o Tx: nystatin
Zenker diverticulum
o Outpouching of pharyngeal constrictor mm.
o Sx: dysphagia, halitosis, regurg of food particles aspiration pneumonia
o Dx: barium study
avoid endoscopy or NG tube d/t risk of perforation
o tx: surgical repair
Vascular rings & webs
o Dx: barium study
o Congenital anomaly; aortic arch vessels encircle the trachea and/or esophagus
o Schatzk ring: peptic stricture of distal esophagus
Intermittent dysphagia to solids
Tx: pneumatic dilation
o Plummer-vinson syndrome: located in proximal esophagus
a/w iron deficiency anemia; can transform to SCC
Sx: dysphagia
Tx: iron replacement
o Sx: reflux sx, progressive systemic sclerosis
o Dx: manometry (inability to close LES)
o Tx: PPI
Diffuse esophageal spasm or nutcracker esophagus
o a/w emotional factors, functional GI disorders; may be precipitated by cold liquids
o Sx: intermittent chest pain not related to exertion & dysphagia
o Dx: manometric studies (high amplitude peristaltic contractions; normal LES response; most accurate), esophagogram (corkscrew
esophagus during spasm); r/o atypical coronary a. spasm or unstable angina (ECG, stress testing)
o Tx: antispasmodics (calcium channel blockers, nitrates), dietary modulation, psychiatric counseling
o Esophageal motility disorder; high lower esophageal sphincter tone
o Sx: dysphagia to solids & liquids
o Dx: barium swallow (bird beak sign at GE junction, dilation of the proximal esophagus), manometry (absent peristalsis; most accurate), CXR
(widening of esophagus), upper endoscopy if alarming sx for cancer (weight loss anemia, blood in stool)
Histology: hypertrophied inner circular muscles with absent or degenerating neurons (ganglion cells( in the myenteric plexuses
air-fluid level seen on CT (incidental finding)
o tx: mechanical dilations: pneumatic dilation, botulinum toxin injection (goof for 3-6mo), surgical sectional or myotomy
esophageal varices
o d/t portal HTN
o sx: signs of liver disease (spider angioma, caput medusa, palmar erythema, asterixis), splenomegaly; vomiting blood +/- black stool
o Dx: check vitals, hematocrit, platelet count, coag panel
Orthostasis: >10 increase in HR or >20 drop in BP from lying down to sitting up/standing
o Tx: fluid resuscitation (#1), NG tube, octreotide, FFP, PRBCs, platelets, IV PPI, endoscopy (cautery, variceal band ligation or sclerotherapy),
if hemorrhage: IV fluid resuscitation, consider intubation if ongoing hematemesis, prophylactic antibiotics, type & screen for
possible transfusion, Somatostatin analog (octreotide)
Octreotide used when melena w/o hematemesis, with NG tube showing red blood
Decreases portal HTN
PRBCs if HCT <30 in an older pt or pt with coronary artery disease
FFP for active bleeding with altered coag panel
Platelets if <50,000 with active bleeding
Banding is better than sclerotherapy
Transjugular intrahepatic portosystemic shunting (TIPS) is used to decrease portal pressure
Propanolol prevents subsequent episodes
Mallory-weiss tear
o Tears at the GE junction d/t repeated retching or vomiting; bleeding d/t rupture of submucosal arteries of the distal esophagus &
proximal stomach
o Sx: Hematemesis of bright red blood or black stools
o Tx: self-resolving; if persistent bleeding epinephrine injection or electrocautery
Drug induced esophagitis
o Causes: tetracyclines, aspirin, NSAIDs, alendronate, potassium chloride, quinidine, iron
Direct mucosal injury d/t caustic nature of there drugs
o Sx: odynophagia, retrosternal pain, difficulty swallowing
Infectious esophagitis
o Agents: candida (#1), CMV, herpes
Occurs in AIDS pt
o Tx: empiric fluconazole
if no improvement upper endoscopy
if confirmed candida not responding to fluconazole IV amphotericin
Laryngopharyngeal reflux (silent reflux)
o Acid reflux into the pharynx, larynx, or the back of the nasal airway inflammation
o Sx: hoarseness, barking or chronic cough, excessive throat clearing, reactive airway disease (asthma), apnea, trouble feeding/spitting
up/inhaling food, trouble gaining weight; bitter taste or burning sensation in the back of throat may be present, feeling like there is a lump
in the throat that doesnt go away with repeated swallowing, sensation of postnasal drip or excess throat mucus
Lacks typical sx of GERD (no heart burn sensation)
Kids: narrowing of area below vocal cords, contact ulcers, recurrent ear infections d/t eustachian tube dysfunction,
lasting buildup of middle ear fluid
Adults: scarring of throat & larynx, increased risk of cancer
o Dx: endoscopy, pH monitoring
o Tx: weight loss, smoking cessation, avoid alcohol, food restrictions, avoid eating 3 hr before bed, chew gum to increase saliva & neutralize
acid; PPI, H2 blockers, or prokinetic agents; sucralfate to protect injured mucous membranes, antacids if heartburn; fundoplication
Foods to avoid: chocolate, mints, fats, citrus fruits, carbonated beverages, spicy or tomato-based products, red wine, caffeine
GERD (gastroesophageal reflux disease)
o Sx: burning chest pain after meals or lying down (not precipitated by exertion; heartburn=pyrosis), regurgitation, sour/bitter taste
(metallic), sore throat, hoarseness, cough
Complication: barretts esophagus (columnar metaplasia; increased risk of adenocarcinoma), dysphagia, odnynophagia, weight
loss, overt or occult bleeding, iron deficiency anemia, chronic cough (aspiration causing vagal stimulation)
Alarming sx: obstruction, anemia, weight loss, heme positive stools, >5 yr sx
Precipitants: nicotine, alcohol, chocolate, peppermint, caffeine, late night meals, obesity
Pain responds to PPI, aluminum hydroxide, magnesium hydroxide, or viscous lidocaine
o Dx: clinical dx; esophagoscopy (endoscopy) for complicated GERD or if refractory to tx; esophageal pH monitoring if endoscopy is negative
or if atypical sx
o Tx: H2 blocker (famotidine) or antacid if mild or intermittent sx, proton pump inhibitor (omeprazole), lifestyle modification,
metoclopramide (gastric motility stimulant); surgical increase of LES tone if refractory to meds
Lifestyle modifications: low fat diet, elevation of the head of bed (6-8 inches), avoid caffeine/alcohol/peppermint/ chocolate,
smoking cessation, weight reduction, avoid eating 3 hr before bed
24 hr pH monitoring if treatment not working to confirm dx
surgical options: nissen fundoplication (wrapping stomach around LES), endocinch (suture around LES), heat or radiation of LES
to promote scarring
Peptic stricture (benign peptic esophageal strictures)
o RF: chronic GERD, radiation, scleroderma, caustic ingestion
o Sx: slowly progressive dysphagia to solid food w/o anorexia or weight loss; as strictures progress they can block reflux (improvement of
heartburn sx)
o Dx: endoscopy (symmetric circumferential narrowings)
Hiatal hernia
o Protrusion of the stomach above the diaphragm; can cause GERD
o Dx: barium swallow (gastric folds protruding above the diaphragm)
Barrett esophagus
o Columnar metaplasia d/t >5 yrs GERD
o Dx: biopsy
o Tx:
Barrett (metaplasia) w/o dysphagia: PPI; f/u endoscopy every 2-3 yo
Low grade dysplasia: PPI; f/u endoscopy every 6-12 mo
High grade dysplasia: ablation via endoscopy (photodynamic therapy, radiofrequency ablation)
esophageal cancer
o squamous cell CA
usually occurs in the upper & middle esophagus
RF: alcohol, tobacco use, diet (nitrosamine, betel nuts, hot food/drinks, pickled foods), HPV, achalasia, Plummer-Vinson syndrome,
caustic ingestions, nasopharyngeal carcinoma, dietary deficiency of beta-carotene/b1/zinc/zeleinum
o Adenocarcinoma
Usually occurs in the distal 1/3 of the esophagus
RF: GERD (>20 yrs), Barretts esophagus (intestinal metaplasia of the lower esophagus), obesity, high dietary calorie & fat intake,
o Sx: dysphagia (solids liquids), weight loss, anorexia, odynophagia (mediastinal invasin), hematemesis, hoarse voice (recurrent laryngeal N.
involvement), aspiration pneumonia, respiratory sx (involves tracheobronchial tree), tracheoesophageal or bronchoesophageal fistula, chest
o Dx: barium swallow, upper endoscopy w/ biopsy, transesophageal u/s to determine penetration (staging), metastatic work-up (CT
chest/abdomen, CXR, bone scan)
o Staging
I: invades lamina propria or submucosa; nodes (-)
IIa: invades muscularis propria or adventitia; nodes (-)
IIb: invades up to muscularis propria; regional nodes (+)
III: invades adventitia (positive regional nodes) or tumor invades adjacent structures (positive or negative nodes)
IV: distant metastasis
o Tx: neoadjuvant chemo+ radiation, esophagectomy (stage 0,1,2a), otherwise palliative tx (stent placement for dysphagia)
Epigastric pain (general info)
o Causes: non-ulcer dyspepsia (#1), gastric ulcer (worse with food; weight loss), duodenal ulcer (pain better with food), cancer (weight loss),
pancreatitis (tenderness in PE), GERD (bad taste, cough, hoarse), gastroparesis (DM, bloating)
o Dx: endoscopy
o Tx: PPI (-prazole) >H2 blocker (-tidine), liquid antacids; misoprostol (prostaglandin analog; good for NSAID induced gastric damage, obsolete
d/t PPI efficacy)
o Pain in the upper abdomen (esp. midline); can be a/w fullness, early satiety, bloating, nausea
o Functional (non-ulcer) dyspepsia: sx >12 wks w/o evidence of ulcer on endoscopy
Dx of exclusion
If <45 yo and no alarming sx start with trial of PPI & lactose free diet
If no response endoscopy
Indications for endoscopy: pt >55 yo or >45 yo with new dyspepsia, pt with cancer sx (weight loss, anemia, obstructive sx,
dysphagia, etc.), pt that failed to respond to tx for PUD
o gastritis= inflammation or erosion of gastric lining
o causes: alcohol, NSAIDs, H.pylori, protal HTN, stress (burns, trauma, sepsis, multiorgan failure, mechanical ventilation, coagulopathy)
atropic gastritis a/w B12 deficiency
o sx: painless GI bleeding (coffee ground emesis or Heme positive stool=5-10 mL blood, melena= 50-100 mL blood)
acute erosive gastritis: severe hemorrhagic erosive lesion after exposure to injurious agents (aspirin, NSAIDs, alcohol)
hematemesis & abdominal pain
o dx: upper endoscopy, H. Pylori testing (endoscopic biopsy, serology, urea breath test, or stool antigen)
o tx: PPI, misoprostol for NSAID-induced (rarely used)
Peptic ulcer disease (gastric or duodenal ulcers)
o Causes: H. pylori infection (gram (-) bacteria; #1), NSAIDs (#2), zollinger Ellison syndrome (gastrinoma), stress (burns, head trauma),
crohn disease, gastric CA
H. Pylori increases risk of: gastric adenocarcinoma, MALToma, chronic active gastritis
Zollinger Ellison syndrome: gastrin secreting tumor (usually pancreatic; >1000 pg/mL) increased acid production
Alcohol and tobacco delay healing
o Sx: recurrent epigastric pain (dull, sore, gnawing)
Gastric ulcers
Sx: pain worse with food weight loss
Duodenal ulcers
Sx: burning pain that occurs on an empty stomach (b/c acid stimulation lasts 2-5 hrs after meal); pain relieved by
antacids or eating
o Complications: cancer, hemorrhage, perforation, gastric outlet obstruction
o Dx: endoscopy (most accurate; biopsy for H. Pylori and cancer), or upper GI barium study; dx H.pylori (urease breath test, biopsy, stool
H.pylori antigen test, or H. Pylori antibody test)
o Tx:
If NSAID induced H2 blocker or PPI
H. Pylori PPI + clarithromycin + amoxicillin; f/u in 4-8 wks
If no response to tx, repeat H. pylori testing; if still (+) PPI+ 2 new antibiotics (metronidazole + tetracycline) +
If gastric ulcer, routinely repeat endoscopy to confirm healing
If not healing biopsy to r/o cancer
Determine if tx failure d/t nonadherence to meds, alcohol, tobacco, or NSAID use
Gastric cancer
o Sx: dysphagia (cardiac region), persistent vomiting (blocking pyloric channel), early satiety (mass effect), pain d/t ulcer formation,
bleeding anemia, weight loss
o Dx: endoscopy
o Causes: alcohol, biliary tract disease (gallstones, biliary sludge=microlithiasis, sphincter of oddi dysfunction, ductal obstruction), ERCP,
increased triglycerides >1000 mg/dL, hypercalcemia, infection (mumps, CMV), abdominal trauma, drugs (thiazides, pentamine,
furosemide, sulfonamides, azathioprine, L-asparaginase, didanosine), cystic fibrosis, scorpion sting
o Sx: acute epigastric abdominal pain radiating to the back, N/V; severe disease has hypotension & fever
Complications: phlegmon (solid mass of inflamed pancreas w/ patchy areas of necrosis), pancreatic necrosis, pancreatic abscess
(2-3 wk later), pancreatic pseudocyst (inflammatory fluid + pancreatic secretions w/o an epithelial lining), vitamin B12
deficiency (anemia, hypersegmented neutrophils, neuropathy)
Suspect complications if peristent increased amylase, abdominal pain, mass, or fever
Pseudocyst spontaneously resolves w/in 6 wks if <6cm otherwise drained if painful or enlarging
o Dx: increased serum amylase & lipase (more specific), abdominal CT scan with PO and IV contrast or MRI (necrosis, calcified pancreas), x-ray
(calcified pancreas, sentinel loops of bowel= air filled piece of small bowel in LUQ), ERCP to determine etiology (stones, stricture, tumor);
secretin stimulation test (normal pancreas releases bicarb-rich fluids after IV injection of secretin)
Possible lab abnormalities: elevated WBC, LDH, AST, amylase & lipase, urine trypsinogen activation peptide; low HCT, calcium;
Low calcium indicates a worse prognosis; severe pancreatic damage low lipase fat malabsorption; calcium bind fat
in GI (saponification) Calcium malabsorption
Ranson criteria for severity; >3 increases mortality
Initial: age >55, WBC >16, glucose >200, LDH >350, AST >250
w/in 48 hrs of admit: HCT decrease >10 pts, BUN increase >5mg/dL after IV hydration, arterial PO2 <60, Ca2+ <8
mg/dL, base deficit >5, estimated fluid sequestration >6L
o tx: pancreatic rest (NPO, NG suction if ileus & bowel distention or protracted vomiting), narcotic analgesia (meperidine), IV fluids, enzyme
replacement, PPI
if >30% necrosis on CT or MRI antibiotics (imipenem) + needle biopsy to determine if infected
if infected surgical debridement
ERCP as need to place stents, remove obstructing stones and dilate strictures
most common cause of early death = hypovolemic shock
Pancreatic cancer
o 5
leading cause of cancer death; peak incidence 60 yo, 2/3 cases >65 yo
o risk factors: male sex, age >50, black, smoking (#1), chronic pancreatitis, long standing diabetes, obesity, familial pancreatitis, family hx of
pancreatic cancer
o tx: neoadjuvant chemotherapy + pancreaticoduodenectomy (Whipple procedure); or palliative care (includes pancreatic & common bile duct
stenting to relieve obstruction)
mean survival ~9 mo
o adenocarcinoma
sx: painless jaundice d/t biliary obstruction (if tumor at head of pancreas)
Sx: painless jaundice, pruritus, weight loss, light-colored stools
Dx: CT scan, LRTs (cholestasis elevated alkaline phosphatase with elevated total & conjugated bilirubin)
o Zollinger Ellison syndrome (gastrinoma)
Sx: ulcers (large >1-2cm, multiple, distal in the duodenum, recurrent after H.pylori eradication), diarrhea d/t acid inactivating
Hypercalcemia if a/w MEN
Dx: endoscopy (confirm ulcers), fasting serum gastrin level (>1000 pg/mL); if inconclusive secretin stimulation test; if still
inconclusive-> calcium infusion study (increases serum gastrin in pt with gastrinoma), serum chromogranin A (marker of
neuroendocrine tumor) can confirm in difficult cases
Elevated gastrin level despite already high gastric acid output; persistent despite injecting secretin
Measure gastri pH to exclude the possibility of secondary hypergastrinemia d/t achlorhydria
r/o metastatic disease with Somatostatin receptor scintigraphy (nuclear octreotide scan) + endoscopic U/S
tx: surgical resection if focal; lifelong PPI if metastatic
Tropical sprue
o Hx of livingin in endemic areas (peurto rico) for ?1month
o Sx: chronic fatty diarrhea, malabsorption of nutrients (vit B-12 & folic acid megaloblastic anemia, glossitis, cheilosis, proterberant
abdomen, allor, pedal edema), cramps, gas, fatigue, progressive weight loss
Hyperactive bowel sounds, borborygmi
o Dx: small intestinal mucosal biopsy (blunting of villi, infiltration of chronic inflammatory celling including lymphocytes, plasma cella, and
Celiac disease/sprue
o Autoimmune intolerance to gluten; Intestinal villous atrophy
o Sx: weight loss, bloating, flatulence, malnutrition (steatorrhea, deficiency of fat soluble vitamins A,D,E,K), dermatitis herpetiformis, iron
deficiency anemia
Vit d deficiency calcium deficiency, osteoporosis
Vit K deficiency bleeding, easy bruising
o Dx: anti-tissue transglutaminase, IgA antigliadin Ab, anti-endomysial Ab; small bowel biopsy (most accurate; flattening of villi), D-xylose test
(measure urine excretion of sugar after 5 hrs; tests the gut absorption of this simple sugar)
o Tx: gluten-free diet (wheat, oat, rye, barley)
Lactose intolerance
o Sx: increased stool osmolality
No weight loss or vitamin malabsorption
o Dx: clinical after removing milk products for 1 days
o Tx: avoid milk products except yogurt; oral lactase replacement
Whipple disease
o Sx: arthralgias, ocular findings, neuro changes (dementia, seizures), fever, lymphadenopathy
o Tx: ceftriaxone, TMP/SMX
Inflammatory bowel disease (IBD)
o Bimodal age distribution of presentation onset (20-30, 60)
o Sx: anemia d/t iron deficiency or chronic GI blood loss; fatigue, weight loss, chronic ab pain, diarrhea, decreased weight, blood in stool,
Extraintestinal manifestations: arthralgias, uveitis, iritis, erythema nodosum, pyoderma gangrenosum, sclerosing cholangitis,
increased risk of colon cancer, anemia
o Dx: endoscopy, barium studies for small bowel
Screen for colon cancer after 8-10 yrs of colonic involvement with colonoscopy every 1-2 yrs
o Tx:
acute exacerbaction steroids
chronic: 5-ASA derivatives (mesalamine) Asacol of UC, Rowasa fo UC limited to rectum, Pentasa for crohn
azathioprine and 6-MP (mercaptopurine) to wean pt off steroids
perianal disease ciprofloxacin and metronidazole
fistulae unresponsive to other treatment anti-TNF (infliximab); no response surgery
UC surgical resection curative
Crohn surgical resection only for obstruction
o Crohns disease
Sx: transmural, skip lesions anywhere from mouth to anus; granulomatous; aphthous ulcers in mouth, weight loss, vague
abdominal pain, linear ulcers with a cobblestone pattern
Complications: fistulas, abscess, obstruction (d/t stricture), non-healing ulcers
Extraintestinal sx: erythema nodosum, arthritis (polyarticular, asymmetric), ankylosing spondylitis, uveitis
(photophobia, blurred vision, headache), cholelithiasis, fatty liver, nephrolithiasis (after small bowel resection or
o Cholelithiasis d/t ileal bile salt malabsorption cholesterol rich lithogenic bile
Dx: abdominal CT, small bowel fluoroscopic study (string sign on barium x-ray), or endoscopy
Antisaccharomyces cerevesiae antibody (ASCA)
Tx: surgery used only for complications
o Ulcerative colitis
Colitis=inflammation of the intestines (typically large bowel)
Diff dx: ischemic, infectious, radiation, IBD
Sx: lesions start in the rectum and proceed proximally; continuous only in the submucosa or mucosa; crypt abscesses, crampy
abdominal pain, weight loss, low volume bloody mucoid diarrhea, tenesmus; hx of similar sx
Complication: toxic megacolon, hemorrhage
o Toxica megacolon: >6cm diameter dilation, fever, increased WBCs, tachycardia, hypotension or altered
mental status
Extraintestinal sx: erythema nodosum, pyoderma gangrenosum, uveitis, fatty liver, primary sclerosing cholangitis
Dx: stool samples to r/o infectious causes, colonoscopy w/ biopsy; lead pipe colon on barium x-ray
Infectious causes of bloody diarrhea: entamoeba histolytica, salmonella, shigella, camplobacter, c. diff, e.coli
Annual or biennial colonoscopy starting 8 yr after dx of pancolitis
Antineutrophil cytoplasmic antibody (ANCA)
Mild-moderate & maintenance: sulfasalazine & other ASA compounds (mesalamine)
Moderate-severe: corticosteroids (only used until remission, then tapered down over 6-8 wks)
Refractory disease;: immune modulators (6-MP, azathioprine, methotrexate, TNF antibody (infliximab))
o Infliximab SE: increased risk of infection (esp. TB reactivation)
Total colectomy is curative; done for carcinoma or dysplasia, toxic megacolon, perforation
Toxic megacolon: NPO, NG suction, IV fluids, IV antibiotics, IV corticosteroids, surgical consult; total colectomy if
refractory to medical tx
Irritable bowel syndrome (IBS)
o Sx: chronic dysmotility (bloating, cramping), pain (relieved by defecation or change in bowel movement, decreased at night), looser and
more frequent stool with the onset of pain (intermittent diarrhea), constipation, passage of mucus, sense of incomplete emptying;
extraintestinal sx (depression, sexual dysfunction, urinary changes)
o Dx of exclusion
o Tx: antispasmodic (dicyclomine=Bentyl, or hyoscyamine), TCA antidepressant (amitriptyline), lubiprostone (chloride channel activator to
increase bowel movement frequency), protonix (pantoprazole), colase; stress reduction techniques (meditation), maintain food journal of
irritants/relievers and for nutritional intake; increase fiber in diet
Constipation: Linaclotide (linzess; guanylate cyclase-C agonist)
diarrhea: antimotility agent (loperamide)
Bowel ischemia
o RFs: severe atherosclerotic disease, atrial fibrillation, hypotension
o Sx: anion gap metabolic acidosis, acute onset abdominal pain, nausea, hypoactive bowel sounds, abdominal tenderness; blood diarrhea
w/in 12-24 hrs
ischemic colitis
o Splenic flexure most commonly involved (watershed areas)
o The most common cause of acute abdomen at any age is appendicitis
o Herniation of mucosa and submucosa through a weakness in the muscle lining of the colon (a/w meat-filled diet); pseudodiverticula b/c not
all layers
Complications: acute diverticulitis, hemorrhage, obstruction; may have chronic sx similar to IBS (pain aggravated by eating, relief
with defecation; bloating, constipation or diarrhea), LLQ pain
Dx: colonoscopy (most accurate) or barium studies
o Diverticular hemorrhage is one of the most common causes of lower GI bleeding in pt>40 yo
Sx: painless passage of bright red blood; abrupt in onset & resolution
Tx: usually self-limited; give IV fluids and transufion as needed; if recurrent or chornic bleeding resection of affected colon
o Diverticulitis
Hx of constipation and low fiber diet; d/t inspissated stool particles (fecalith) obstructing diverticula bacterial overgrowth
Sx: LLQ pain (or RLQ if cecum), fever, N/V, hypoactive bowel sounds, constipation; may have peritoneal irritation
Abscess: tender mass on exam, persistent fever & leukocytosis after treatment
o Tx: conservative management if small, CT-guided percutaneous drainage or surgical drainage for large
Fistulas: majority are colovesical w/ male predominance; others are colovaginal, coloenteric, colouterine, coloureteral;
rarely colocutaneous
o Tx: single stage surgery with fistula closure and primary anastomosis
o If colovesical fistula pneumaturia or fecaluria
Obstruction: ileus or pseudo-obstruction more likely than complete
Strictures: d/t recurrent diverticulitis; slow onset obstruction
o Tx: trial of endoscopic therapy (bougienage, balloon, laser, electrocautery, or blunt dilating endoscope)
I: small confined pericolic abscess
II: distant abscess (retroperitoneal or pelvic)
III: generalized suppurative peritonitis from rupture of abscess (non-communication w/ bowel lumen)
IV: fecal peritonitis d/t free communicating perforation
Differential dx: diverticulitis, painful diverticular disease w/o diverticulitis, acute appendicitis, Crohn disease, colon cancer,
ischemic colitis, irritable bowel syndrome, GYN issues (ruptured ovarian cyst, endometriosis, ectopic pregnancy, PID)
Dx: CXR & ab x-ray (ID pneumoperitoneum, assess cardiopulmonary status), CBC (increased WBCs), CT scan (evaluate for abscess,
fistula, perforation; pericolic fat stranding, bowel wall thickening >4mm)
Contrast enema is contraindicated; Endoscopy contraindicated during the acute phase
o Endoscopy should be done >6wk after resolution of acute attack to exclude neoplasm
Out-pt: broad spectrum antibiotics (TMP-SMX ,or ciprofloxacin + metronidazole, or clindamycin + gentamicin), clear
liquid diet
In-pt: IV fluids, electrolyte balance, NPO, gradually advance diet, IV broad spectrum antibiotics (ampicillin+
aminoglycoside + metronidazole, or ampicillin-sulbactam, or ticarcillin-clavulanate; imipenem or meropenem used for
severe/complicated case)
o In-patient if: narcotics needed for pain, peritoneal signs, comorbid illness, inability to tolerate PO intake,
complications that may require surgery
Emergent surgery: generalized peritonitis, uncontrolled sepsis, perforation, clinical deterioration
Elective resection: fistula, recurrent diverticulitis (>2 episodes requiring hospitalization)
Polyposis syndromes
o Familial adenomatous polyposis: defect in APC gene; thousands of polyps
o Peutz-Jeghers syndrome
Multiple hamartomatous polyps, melanotic spots on lips & skin; increased frequency of breast/gonadal/pancreatic CA
o Gardener syndrome: colon CA + (osteomas, desmoid tumors, other soft tissue tumors)
o Turcot syndrome: colon CA + CNS malignancy
o Juvenile polyposis: colon CA + multiple hamartomatous polyps
Colon cancer
o Screening: colonoscopy > barium enema, CT colonoscopy, capsule endoscopy > fecal occult blood testing
Routine every 10 yrs starting age 50
1 family hx: start 10 yrs before age of onset of family members cancer or by age 40
HNPCC: start age 25 with colonoscopy every 1-2 yrs
FAP: start sigmoidoscopy age 12 every year
Previous single adenomatous polyp: colonoscopy every 3-5 yrs
Previous hx of colon cancer: coloscopy at 1 yr and 3 yr post-resection, then every 5 years
o Infectious causes of bloody diarrhea: entamoeba histolytica, salmonella, shigella, camplobacter, c. diff, e.coli
o Clostridium difficile
Gram (+) spore forming
Pseudomembranous colitis; a/w antibiotic use (days-2ks after antibiotics use: clindamycin, cephalosporins, ampicillin)
Prominent in the sigmoid/rectal area
Sx: diffuse watery diarrhea, cramps, fever, abdominal tenderness
Dx: cytotoxin assay in the stool; stool C. diff antigen; endoscopy will show pseudomembranes (not required for dx)
Tx: IV/oral metronidazole or oral vancomycin
Recurrences: Metronidazole is used for 1
recurrence, oral vancomycin used for 2
o Cryptosporidium parvum
Can cause diarrhea in immunocompetent and immunocompromised pt; pt with CD4<180 tend to have a more persistent clinical
Dx: modified acid-fast stain showing oocysts
GI bleeding
o Upper GI bleeding: ulcer disease (#1), gastritis, esophagitis, duodenitis, cancer, varices
o Lower GI bleeding: diverticulosis (#1), angiodysplasia (AV malformation), polyps or cancer, IBD, hemorrhoids, rapid upper GI bleeding
Iron in stool can be confused for melena
o Dx: check vitals, hematocrit, platelet count, coag panel
Orthostasis: >10 increase in HR or >20 drop in BP from lying down to sitting up/standing
Nuclear bleeding scan, angiography, capsule endoscopy
EKG to assess heart function in severe bleeding (may cause heart ischemia)
o Tx: fluid resuscitation (#1), blood products
PRBCs if HCT <30 in an older pt or pt with coronary artery disease
FFP for active bleeding with altered coag panel
Platelets if <50,000 with active bleeding
o Causes: cirrhosis, cancer (hepatocellular CA, peritoneal carcinomatosis), heart failure, TB, dialysis, pancreatic disease, alcoholic hepatitis,
viral hepatitis
o Sx: fluid wave, abdominal swelling & discomfort; accumulation >25 mL of fluid; intolerance of distension, early satiety, shortness of breath,
shifting dullness (>1500 mL of fluid needs to be present to present with flank dullness)
Signs of cirrhosis: spider telangiectasias, palmar erythema, gynecomastia, portal HTN esophageal varices, caput medusae,
hemorrhoids; jaundice
Cancer: sister mary joseph nodule (umbilical nodule; indicated in gastric ca, colon ca, hepatocellular ca, lymphoma)
o Dx:
History: alcohol use, needle drug use, sexual hx, family hx of liver disease
Abdominal paracentesis: Cell count & differential, [albumin], [total protein], culture; optional= [glucose], [LDH], gram stain,
[amylase]; other tests= TB smear & culture, cytology, [triglyceride], [bilirubin]
Indication for paracentesis: new onset ascites, abdominal pain and tenderness, fever
Fluid appearance:
Clear Uncomplicated ascites; if clear yellow cirrhosis
Turbid/cloudy Spontaneously infected fluid
Opalescent Cirrhosis + elevated triglyceride
Milky chylous ascites; Triglyceride >200-1000mg/dL d/t cirrhosis or cancer
Pink or bloody *requires corrected neutrophil count: -1 neutrophils from absolute neutrophil count for every 250 RBCs; start empiric antibiotics if >250
*d/t traumatic tap, punctured collateral (from previous tap), cirrhosis, or cancer
Brown Bilirubin in fluid; if ascetic bilirubin>serum, consider ruptured gallbladder or perforated duodenal ulcer
o SAAG (serum albumin-ascites gradient)
High gradient >1.1 g/dL (indicates portal HTN): cirrhosis, alcoholic hepatitis, massive hepatic metastases, heart
failure/constrictive pericarditis, Budd-Chiari syndrome, portal vein thrombosis
Low gradient <1.1 g/dL: peritoneal carcinomatosis, infections (except SBP), peritoneal TB, pancreatitis, Serositis, nephrotic
syndrome, bowel obstruction/infarct
o Protein: ascetic fluid is exudate if total protein >2.5-3 g/dL
low protein (transudative) ascites has a higher risk of spontaneous bacterial peritonitis
o glucose: normally the same as serum; if low used up by WBCs, bacteria, malignant cells, gut perforation
o LDH ascetic fluid/serum ratio: >1 indicates infection or tumor
o Amylase: elevated from pancreatitis or gut perforation
o If suspected heart failure: CXR and echocardiogram
o Suspected cancer: FNA of palpable nodules
o Gut perforation into ascites: neutrophil count >250 cells/mm3, total protein >1g/dL, glucose <50 mg/dL, LDH greater than the upper limit of
normal for serum
o Spontaneous bacterial peritonitis
Infection w/o perforation of the bowel
Agents: E.coli (#1), anaerobes, pneumococcus
Dx: paracentesis (neutrophil cell count >250); fluid cultures (most accurate)
Tx: cefotaxime
d/t recurrences, when ascites fluid albumin is low prophylactic norfloxacin or TMP/SMX
o Treatment
Cirrhosis: d/x alcohol, consider baclofen treatment, tx underlying liver dz when possible, salt-restricted diet, diuretics
(spironolactone + furosemide)
Liver transplant for irreversible cirrhosis
Surgical options: serial therapeutic paracentesis, transjugular intrahepatic portosystemic shunts (TIPS)
Autoimmune hepatitis: glucocorticoid (prednisone) and/or azathioprine
Avoid: NSAIDs, ACE inhibitors/ARBs
o Caution: beta blockers (increase risk of diuretic resistant ascites) but helps prevent variceal hemorrhage
(must weigh benefits & risks)

Diuretic-resistant ascites in pt w/ cirrhosis
o Usual tx for ascites: salt restricted diet, diuretics (spironolactone & furosemide)
o Differentiate from malignant ascites (peritoneal carcinomatosis), budd-chiari syndrome (hepatic vein thrombosis), chylous malignant
ascites, nephrogenic ascites (tx renal transplant)
o Dx: doppler U/s or CT scan ov liver & spleen + alpha-fetoprotein (r/o hepatocellular carcinoma or portal vein thrombosis)
o Tx:
Repeat education about diet compliance (salt restricted)
Oral midodrine=vasopressorincreased renal perfusion, increase renal sodium excretion reduce ascites
5mg 3x/day; adjust dose every 24 hr to increase systolic BP 10-15 mmHg
Oral midodrine + parenteral octreotide is used to reverse type I hepatorenal syndrome
Serial paracentesis + salt restricted diet (2g/day) as a bridge to transplant or TIPS procedure
Replace albumin (6-8g albumin/L fluid removed) when >5 liters are removed
SE: protein & complement deficiency
TIPS (transjugular intrahepatic portosystemic shunt) procedure + diuretics
Relative contraindications to TIPS: spontaneous or problematic hepatic encephalopathy, alcoholic hepatitis, MELD score
>18, advanced age, parenchymal renal disease
liver transplant is the only definitive therapeutic option if d/t portal HTN
AVOID/STOP: Beta blockers (reduce survival), NSAIDs (renal vasoconstriction), ACE inhibitors/ARBs
GI tract anatomy/physiology review
o Layers: mucosa (surface epithelium, basal lamina, lamina propria= fibroblasts, nerves, BVs, connective tissue, immune cells), muscularis
mucosa, submucosa (Meissners nerve plexus), muscularis externa/propria (muscularis inner circular, Auerbachs myenteric nerve plexus,
muscularis outer longitudinal), serosa (fat & BVs)
o Esophagus: keratinized stratified squamous epithelium, submucosal mucous glands; upper 1/3 striated muscle, lower 1/3 smoothm.
o Stomach: body= columnar mucous cells, antrum= cuboidal
o Small bowel: columnar cells w/ brush border (microvilli)
Duodenum: brunners glands
Ligament of Treitz separates duodenum from jejunum
Jejunum: wider (4cm), thicker, more vascular, larer villi, thick circular folds
Ileum: prominent lymphoid (peyers patches), less circular folds
o Colon: goblet & absorptive columnar cells
o L. Colon: oval ringed lumen; transvers & right colon triangular shaped lumen; crescent moon shape for appendix opening
Liver & gallbladder
Liver related tests
o Bilirubin
Biliary stasis jaundice, pruritus, light-colored stools
Jaundice is clinically noticeable when serum bilirubin >2-2.5 mg/dL
Dx: cholestasis elevated alkaline phosphatase with elevated total & conjugated bilirubin; U/S of biliary system;
extrahepatic dilatation w/o evidence of stones CT scan or ERCP to detect occult stones or structures and r/o
malignant causes (cholangiocarcinoma, pancreatic CA, ampullary of vater cancer)
Conjugated (direct) bilirubin: enzymatically bound to glucuronic acid
Only conjugated bilirubin can be filtered & renally excreted
Elevated: hepatocellular disease (elevated ALT & AST, abnormal clotting factor & albumin synthesis) or biliary
obstruction (elevated alkaline phosphatase)
o Acute hepatocellular necrosis (viral and drug hepatis, hepatotoxins, acute heart failure)
o Obstruction: primary sclerosing cholangitis
Unconjugated (indirect) bilirubin: reversibly & noncovalently bound to albumin
Causes of elevation: hemolysis, Gilbert syndrome
Normal levels ~30 (M) or ~20 (F)
Elevated: liver failure, hepatitis, rhabdomyolysis, MI
Note: level of LRTs do not correlate to the severity of the disease; liver biopsy is needed to assess severity
Primary Sclerosing cholangitis
o Autoimmune intrahepatic & extrahepatic large bile duct obstruction
occurs in younger males; a/w inflammatory bowel disease (esp ulcerative colitis)
o sx: jaundice or sx of biliary obstruction (pruritus)
complications: stricture, infection (cholangitis), cholangiocarcinoma, cirrhosis
o dx: elevated alkaline phosphatase, bilirubin, and GGTP; ERCP (most accurate; beading, narrowing, or strictures), beading of bile ducts
biopsy is not essential to dx
o tx: cholestyramine or ursodeoxycholic acid
Primary biliary cirrhosis
o Autoimmune destruction of intrahepatic bile ducts (small & medium sized) bile stasis, cirrhosis
Most common in 35-60 yo F; a/w other autoimmune diseases (rheumatoid arthritis)
Decreased ability to absorb and store fat-soluble vitamins
o Sx: pruritus, fatigue, jaundice, steatorrhea, hepatosplenomegaly; xanthomas and xanthelasmas; osteoporosis
Complications: cirrhosis
o Dx: increased alkaline phosphatase (2-5x), serum bilirubin (normal), anti-mitochondrial antibodies; liver biopsy (most accurate)
o Tx: ursodiol (ursodeoxycholic acid; reduces cholesterol absorption, reduces cholestasis), cholestyramine (bile acid Sequestrant; relieves
Biliary colic
o Usually a/w cholelithiasis
Risk factors: fat, female, 40s (fertile)
o Sx: acute onset severe RUQ pain (precipitated by fatty meal, ~30-60 min), N/V
o Dx: elevated bilirubin & alkaline phosphatase (mild if non obstructive, bilirubin >3g/dL if obstruction), RUQ ultrasound
Acute cholecystitis
o Stone impacted in the cystic duct; infection with enteric flora (e.coli, klebsiella)
o Sx: fever, increased WBC, peristent RUQ pain
o Dx: ultrasound (gallbladder wall thickening, pericholecystic fluid); scintigraphy via HIDA (hepatobiliary iminodiacetic acid) scan if
questionable dx (nonvisualization of gallbladder indicates obstruction)
o Tx: NPO, IV fluids, IV antibiotics, cholecystectomy w/in 48-72 hrs
o Intermittent obstruction w/reflux of bacteria up the biliary tree
o Tx: if septic urgent decompression w/ surgery or ERCP
o Hepatic vein thrombosis
o Causes: viral (hepatitis, CMV, EBV, HSV 1), toxic, autoimmune (ANA, anti-LKM=liver kidney microsome), hemochromatosis, Wilsons disease,
alpha-1 antitrypsin disease
o Sx: N/V, diffuse abdominal pain, fever, myalgias, fatigue, arthralgias, jaundice, dark urine
Chronic if sx >6mo
transaminase >1000 IU/L viral or toxic hepatitis or ischemia (shock liver)
alcoholic hepatitis: transaminase <500 IU/L, AST:ALT =2:1, conjugated hyperbilirubinemia, signs of hepatocellular
disease (hypoalbuminemia, ascites)
o Autoimmune hepatitis
Occurs in young women
Dx: (+) ANA, anti-smooth muscle antibodies, liver-kidney-microsomal antibodies; liver biopsy (most accurate)
Tx: glucocorticoid (prednisone) and/or azathioprine
o Non-alcoholic steatohepatitis/ nonalcoholic fatty liver disease
a/w obesity, diabetes, hyperlipidemia, corticosteroid use
Dx: Microvesicular fatty deposits found on liver biopsy w/o a hx of alcohol use
o Acetaminophen hepatitis
d/t 1 massive dose (>10 g) or chronic use
drug is normally metabolized by liver P450 toxic metabolite that is bound by glutathione
dx: nomogram (plot serum acetaminophen level against time of last ingestion) to determine if N-acetylcysteine is needed
tx: oral activated charcoal, N-acetylcysteine (started w/in 10 hrs & continued for 72 hrs)
observation only if nomogram shows levels below the danger zone
o Hep A
Fecal-oral transmission
Sx: arthritis, vasculitis, cryoglobulinemia
Dx: anti-hep A IgM
Tx: self-limited in weeks
prevention: Hep A vaccine (2 doses 6 mo apart) if traveling to an endemic area or pt with chronic liver disease; HAIg
w/in 2 wks post-exposure + vaccine; vaccinate close contacts
o Hep E
Fecal-oral transmission
Pregnancy women have an increased risk of severe hepatic necrosis and liver failure
Tx: self-limited w/in weeks
o Hep B
Complications: cirrhosis, hepatocellular CA, polyarteritis nodosa
Dx: HBsAg, HBeAg (indicates viral replication/infectious)
Chronic hep B: surface antigen positive for >6 mo; e-antigen often positive; hepatitis B DNA level by PCR is the best way
to determine viral replication activity
o Liver biopsy determines the degree of inflammation and fibrosis
Tx: interferon (acute infection), lamivudine (chronic infection)
Prevention: hep B vaccine (3 doses w/in 6 mo), HBIg post-exposure + vaccine
o Anti-HBsAg w/o IgG indicates vaccination induced immunity no Ig needed post-exposure
Chronic hep B (any 1 of the following): adefovir, lamivudine, telbivudine, entecavir, tenofovir, interferon
o Interferon SE: arthralgias, thrombocytopenia, depression, leukopenia
o Adefovir SE: renal dysfunction
o Hep D
Defective RNA virus that requires Hep B to replicate (either co-infection or later superinfection)
o Hep C
Transmission: blood transfusion, IV drug use
Complications: cirrhosis, hepatocellular CA, polyarteritis nodosa, cryoglobulinemia, membranoproliferative
glomerulonephritis (secondary to cryoglobulinemia), B-cell lymphoma, plasmacytoma, autoimmune diseases (Sjogrens
syndrome, thyroiditis), lichen planus, porphyria cutanea tarda, idiopathic thrombocytopenic purpura
Dx: anti-hep C Ab (ELISA), hep C RNA assay (PCR)
Hep C PCR RNA viral load is the most accurate way of determining disease activity
Liver biopsy determines the degree of inflammation and fibrosis
Tx: ribavirin, pegylated interferon alpha, proteases (Telaprevir, boceprevir); vaccinate against hep A & B
wait 3-4 months post-exposure before starting treatment to see if there is spontaneous clearance; goal is to reduce viral
load to prevent complications
o note: start treatment if elevated ALT, detectable HCV RNA and histologic evidence of chronic hepatitis
of at least moderate grade
If pregnant w/ hepatitis: Test newborn @12-18 mo for hep C RNA
Protease inhibitors
o check viral load at 4,8, and 12 wk & 6mo after tx.
If 0 viral load then treatment is only needed 24 wks total (only 12 of which is with protease
inhibitor), if higher then treat for 36-48 wks
o Telaprevir requires eating w/ 2g fat to slow absorption
Started with IFN & ribavirin
o Bocepravir is started 4 wks after starting IFN & ribavirin
Interferon SE: flu-like sx, depression, psychosis, pancytopenia
Ribavirin SE: hemolysis anemia
Note: no longer required to f/u LRTs as part of tx
Chronic hep C: interferon + ribavirin
o Vaginal birth and breast feeding are both fine for pts with hepatitis virus
Alcoholic liver disease
o Dx of exclusion; liver biopsy (most accurate); AST>ALT; binge drinking gives a sudden rise in GGTP
Non-alcoholic fatty liver disease
o Range: steatosis, steato-hepatitis, advanced fibrosis in non-alcoholic pts
o a/w obesity and DM2
MOA most likely insulin resistance increased fat accumulation in the hepatocytes (increased rate of lipolysis and elevating
circulating insulin levels); intrahepatic fatty acid oxidation increase in oxidative stress local incrase in Proinflammatory
cytokines TNF-alpha liver inflammation, fibrosis, cirrhosis
o Dx: liver biopsy (macrovesicular fat deposition with displacement of the nucleus to the periphery)
Alpha-1 antitrypsin deficiency
o Occurs in young (<40 yo) non-smoker
o Sx: liver disease + emphysema (COPD)
o Tx: replace enzyme
wilsons disease
o autosomal recessive; presents age 5-35
o decreased copper excretion d/t decreased ceruloplasmin; copper accumulation in liver, kidney, RBCs, nervous system
o sx: Kayser-fleisher rings in eyes, dysarthria, spasticity, chronic liver disease cirrhosis, neuro sx (psychosis, tremor, ataxia, seizures;
parkinsonian sx d/t copper deposition in basal ganglia), coombs negative hemolytic anemia, renal disease (aminoaciduria, renal tubular
acidosis, nephrocalcinosis, nephrolithiasis)
o dx: decreased serum ceruloplasmin, slit lamp exam for Kayser-Fleisher rings (best initial test), liver biopsy, increased copper excretion in
urine after giving penicillamine (24 hr urine; most accurate), LRTs (elevated aminotransferases, impaired synthesis of coagulation factors
and albumin); MRI (atrophy of the lenticular nucleus)
coombs (-) hemolytic anemia
o tx: copper chelator (penicillamine or trientine), zinc (inhibits intestinal copper absorption), liver transplant
o Autosomal recessive mutation in C282y gene; excessive iron absorption in the duodenum; iron accumulation in organs hydroxyl free
radicals fibrosis
Secondary hemochromatosis (iron overload) d/t multiple transfusion or chronic hemolytic anemia
Affected organs: liver, pancreas, heart, joints, skin, thyroid, gonads, hypothalamus
o Sx: Diabetes mellitus, Bronze skin, cirrhosis, cardiomyopathy (arrhythmias, CHF), hypogonadotropic hypogonadism (impotence,
amenorrhea, decreased libido), arthropathy/arthritis (pseudogout), fatigue, abdominal pain, hypothyroidism
Increased risk of infection with organisms that feed on iron (vibrio vulnificus, Yersinia, listeria)
o Dx: increased serum iron & ferritin, increased transferrin saturation (>50%), decreased TIBC, liver biopsy (determines iron concentration;
most accurate); mildly elevated AST and alkaline phosphatase
EKG may show conduction defects; echocardiogram may show dilated or restrictive cardiomyopathy
Abdominal MRI and HFE (C282y) gene testing can be used to confirm the diagnosis instead of liver biopsy
Prussian blue= stain for RBC cell iron
o Tx: phlebotomy, iron chelation (deferoxamine, deferasirox), liver transplant, treat complications
Iron chelators are used for pt that cant be managed with phlebotomy or are anemic w/ hemochromatosis from overtransfusion
Acute liver failure
o Tx: transplant or self-resolution
Mucomyst (acetylcysteine) is sometimes used although no research evidence of its benefit
Fulminant liver failure
o Sx: rapidly progressive encephalopathy, coagulopathy, elevated bilirubin, ascites, peripheral edema, hypoglycemia, hyperammonemia, lactic
o Tx: fatal w/o emergency liver transplant
Chronic liver disease/ cirrhosis
o Sx: ascites, elevated estrogen (gynecomastia, testicular atrophy, palmar erythema, spider angiomas); portal HTN varices
(esophageal/gastric), hemorrhoids, caput medusae (distended abdominal wall veins); hypoglycemia (liver stores glycogen),
hyperbilirubinemia, jaundice, coagulopathy (decreased clotting factors), hypoalbuminemia edema, leukonychia (white nails); asterixis,
encephalopathy; thrombocytopenia d/t splenic sequestration
Elevated estrogen is d/t decreased production of steroid hormone binding globulin
Coagulopathy: liver produces all clotting factors (except factor 8)
Tx: FFP and platelets if bleeding occurs
Esophageal varices
Tx: propranolol, banding via endoscopy
Hepatic encephalopathy
d/t increased ammonia inhibitory neurotransmission via GABA receptors in CNS
o precipitated by alkalosis, hypokalemia, hypovolemia, GI bleeding, constipation, dehydration, large protein
loads, hypoxia, sedatives, hypoglycemia, infection
Sx: decreased mental function, asterixis (flapping tremor), rigidity, hyperreflexia, fetor hepaticus (musty breath)
Tx: lactulose or lactitol (nonabsorbable disaccharides); neomycin or rifaximin (antibiotics), ornithine-aspartate
infusion, or oral sodium benzoate; diet changes (decrease protein intake (<70g/day), high glucose), laxatives
o Lactulose is broken down by GI bacteria acidic colon converts absorbable ammonia into nonabsorbable
o If no response to disaccharides ornithine-aspartate infusion or oral sodium benzoate (decrease absorption
of ammonia in GI tract) or neomycin (nonabsorbable antibiotic that destroys ammonia-producing colonic
bacteria; SE ototoxic and nephrotoxic)
Hepatopulmonary syndrome: lung disease and hypoxia; orthodeoxia (hypoxia upon sitting up)
Hepatorenal syndrome: renal failure d/t renal hypoperfusion from advanced liver disease (constriction of renal vessels)
Sx: azotemia, oliguria, hyponatremia, hypotension, low urine sodium (<10mEq/L)
Tx: octreotide (somatostatin analog), midodrine
Ascites & edema
Tx: spironolactone & other diuretics, serial paracentesis
Spontaneous bacterial peritonitis
Agents: E.coli, klebsiella, strep pneumo
Sx: abdominal pain, fever, vomiting, rebound tenderness
o Cirrhosis: Permanent fibrosis & regenerative nodules in liver decreased blood flow portal HTN (>10mm Hg increase in pressure
gradient) ascites, peripheral edema, splenomegaly, gastric/esophageal varices, hemorrhoids
Decreased albumin & clotting factor synthesis
Causes: alcoholic liver disease, chronic Hep B or C, drugs (acetaminophen, methotrexate), autoimmune, biliary cirrhosis,
hemochromatosis, wilsons disease, hepatic congestion (R. side heart failure, constrictive pericarditis), alpha-1 antitrypsin
deficiency, hepatic veno-occlusive dz, nonalcoholic steatohepatitis (NASH)
o Dx: portal HTN detected via doppler ultrasound
Childs classification: estimates hepatic reserve in liver failure; predicts M &M
f/u labs every 3-4 mo: CBC, renal function tests, electrolytes, LFTs, coagulation tests
endoscopy to determine presence of esophageal varices
if hepatocellular CA suspected CT guided biopsy
o Tx: transjugular intrahepatic portal-systemic shunt (TIPS) to lower portal pressure, liver transplant
Vaccines for pt with chronic liver disease: Td/TDaP, flu, pneumococcal, Hep A & B
Varices: hemodynamic stabilization, emergent upper GI endoscopy if hematemesis, beta-blockers to prevent rebleeding; variceal
ligation/banding, endoscopic sclerotherapy, IV vasopressin (vasoconstriction of mesenteric vessels reduces portal pressure; given
with nitroglycerin to prevent SE), IV octreotide infusion (splanchnic vasoconstriction, decreases portal pressure), esophageal
balloon tamponade, TIPS procedure
beta blockers decrease portal HTN
Sandostatin or octreotide cause splanchnic vasoconstriction
Ascites: bed rest, low NaCl diet, diuretics (furosemide, spironolactone), paracentesis
Hepatic encephalopathy: lactulose (prevents ammonia absorption), neomycin (kills bowel flora to decrease ammonia production),
limit protein in diet to 30-40 mg/day
Spontaneous bacterial peritonitis: broad spectrum antibiotics; repeat paracentesis in 2-3 days to document decrease in ascitic
fluid PMN (<250)
IV cefotaxime or ampicillin/sulbactam
Empiric tx used for PMN>250 in ascities: ampicillin + gentamicin or 3
generation cephalosporin or quinolone
FFP for any coagulopathy
Abstinence from alcohol for >6 mo required before pt eligible for transplant
MELD score (modified end-stage liver disease): patients risk of dying while waiting for a liver transplant
o Based on INR, bilirubin, creatinine, if pt has dialysis >2x/wk
kidney & other urology
o fractional excretion of sodium: ratio of sodium excreted vs filtered in the kidneys
FeNa= 100x(UNa/PNa)/(UCr/PCr)
=100x [(urinary sodium x plasma creatinine)/ (plasma sodium x urinary creatinine)]
Creatinine represents the GFR
o Normal urine output 1.0ml/kg/hr (kg of ideal body weight)
o Glomerular filtration rate (GFR): inversely related to serum creatinine (increased creatinine indicates a decreased GFR)
o Glomerular arteriole control
Afferent: Prostaglandin dilates
Efferent: angiotensin II constricts
o Kidney filter= fenestrated capillary, glomerular basement membrane, podocytes
Best initial test for any kidney disorder is urinalysis, BUN, and creatinine
o Urine analysis/ microscopy: protein, white cells (direct microscopy exam) or leukocyte esterase (dipstick), RBCs, specific gravity, pH, nitrites
Proteinuria >300 mg/day; nephrotic level proteinuria >3g/day
normally 30-50 mg/24 hrs of Tamm-Horsfall protein is excreted; standing and increased physical activity increase
urinary protein excretion
Microalbuminuria: 50-300 mg/day
o >300 mg/D is detectable on urine dipstick; urine dipstick only detects albumin (not other proteins; other
proteins detected with immunoelectrophoresis)
o ACE inhibitor/ARB should be started for any degree of proteinuria in a diabetic pt (delays development of
renal insufficiency)
f/u persistent proteinuria with a kidney biopsy; severe proteinuria indicated glomerular damage
determining total protein excretion in a day: UA (best initial), protein: creatinine ratio> 24 hr urine collection
o 1+ protein ~ 1 g/24 hr in UA (2+=2g/24 hr, etc.)
o protein: creatinine is faster and technically easier to perform
ratio indicates g protein/24 hrs (ratio of 1.2 indicates 1.2 g protein/24 hrs)
Protein(tam Horsfall protein) based casts indicate tubular injury (intrinsic renal damage)
RBC casts glomerular nephritis, WBC casts renal parenchymal inflammation/infection, fatty casts nephrotic
syndrome, granular (muddy brown) casts ATN; broad waxy casts CKD
Hyaline casts (only tam Horsfall protein) are physiologic; d/t dehydration, extreme exercise, low flow state, etc.
>5 squamous cells indicates a poor sample (not clean catch)
nitrites: indicates presence of gram (-) bacteria on dipstick
o Hematuria
Diff dx:
Intrarenal: kidney trauma, renal stones/crystals, pyelonephritis, renal cell CA, vascular injury (vasculitis, renal
Extrarenal: trauma (foley placement), infectious (urethritis, prostatitis, cystitis), nephrolithiasis, neoplasm (prostate,
Dx: distinguish hematuria from hemoglobinuria/myoglobinuria (rhabdomyolysis)
Polycystic kidney disease
o Autosomal dominant
o Sx: bilateral flank masses, flank pain, HTN, hematuria
Bartters syndrome
o Autosomal recessive: defect in salt reabsorption in the thick ascending limb of the loop of Henle hyperplasia of the juxtaglomerular
apparatus increased renin increased aldosterone hypokalemia
Acute glomerulonephritis/ nephritic syndrome
o Inflammatory renal diseases
o Causes
Primary renal disorders: membranoproliferative GN types 1&2, mesangioproliferative GN, crescentic GN (anti-GBM, ANCA),
fibrillary GN, proliferative GN (IgA nephropathy)
Secondary renal disorders: SLE, postinfectious/poststrep, hep C or B related GN (cryoglobulin-induced), vasculitis related
(wegner, Churg-Strauss, polyarteritis nodosa, microscopic polyangiitis, Henoch-Schonlein purpura), infective endocarditis related
o Sx: HTN & edema (d/t volume retention), hematuria, renal failure, low proteinuria (<3.5 g/24 hr),renal failure ( oliguria, azotemia)
o Dx: UA w/ microscopic appearance, biopsy of kidney (histology & immunofluorescence), serum markers for suspected disease (C3,C4, ANCA,
anti-GBM ASO, hepatitis panel, blood cx, cryoglobulin)
Biopsy needed to determine primary histiopathic injury to the nephron
Dysmorphic/fragmented RBCs or RBC casts indicate a glomerular origin to disease
active sediment indicates and inflammatory process
Pts with nonglomular hematuria & no evidence of infection should have an ultrasound, IVP, or cystoscopy to assess for
stones or malignancy
Decreased C3,C4 (complement mediated disease): SLE, MPGN, infective endocarditis, post-strep/postinfectious GN, cryoglobulin-
induced GN
Cryoglobulin induced GN: get cryoglobulin titers; Hep C & B testing
Post-strep GN: ASO titer; occurs 10-20 days after strep throat or skin infection
Infectious endocarditis: get blood cx
Anti-glomerular BM: goodpasture, anti-GBM GN
Goodpasture: renal & lung involvement (hemoptysis); antibody against type 4 collagen
Pacui-immune (antineutrophil cytoplasmic antibody): C-ANCA (wegner), P-ANCA (churg-strauss, microscopic polyangiitis)
Churg strauss: granulomas, asthma, eosinophilia
GN following a URI IgA nephropathy or post-strep GN
o Tx: supportive (dialysis for renal failure, anti-HNT & diuretics for edema) +/- immunosuppressive drugs
ANCA-induced GN: steroids + cyclophosphamide
Antibody induced GN: plasmaphoresis
Nephrotic syndrome
o Noninflammatory renal disease; benign sediment instead of active inflammatory sediment in urine
o Causes
Primary nephrotic syndrome: minimal change disease, membranous nephropathy, focal segmental glomerulonephrosis (FSGS),
membranoproliferative GN (MPGN)
Membranous glomerulonephritis is a/w Hep B infection in children
Secondary nephrotic syndrome: DM, SLE, multiple myeloma or amyloidosis, viral (HIV, Hepatitis), cancer, meds (NSAIDs), heavy
metals (mercury), hereditary renal conditions
o Sx: proteinuria (>3.5 g/24 hr), hypoalbuminemia (<3g/dL), edema (starts in dependent areas like feet), hyperlipidemia
Complications d/t hypoprotein state
hypercoagulable state d/t decreased antithrombic 3 & proteins C & S
hypogammaglobulinemia increased infection risk (esp pneumococcal infection)
iron deficiency anemia d/t hypotransferrinemia
vit D deficiency d/t loss of vitamin D-binding protein
Increased lipids d/t decreased oncotic pressure triggering liver to start lipoprotein synthesis
Albumin crosses the glomerular basement membrane d/t loss of (-) charge of the BM
o Dx: UA w/microscopy, renal biopsy (unless diabetic nephropathy)
If hyperlipidemia present: waxy casts, oval fat bodies seen on microscope
DM: glucose, HBA1c; microalbuminuria in early stage (urine albumin 30-300; albumin/creatinine ratio of 30-300; >300 is
detectable on urine dipstick)
multiple myeloma or amyloidosis: serum & urine electrophoresis
viral: HIV, Hepatitis testing
o Tx: diet changes (strict salt restriction, low protein diet), diuretics (thiazide, loop; ACE or ARB if diabetes),
Diabetic nephropathy: ACE inhibitor, tight glycemia control (goal AbA1c= 6.5-7.0), BP control (goal <130/80, or <125/75 if
heavy proteinuria >1g/d), maintain LDL<100 mg/dL
Lower CV risk factors since diabetic pts with nephropathy are categorized as highest risk
Acute kidney disease (acute renal failure)
o Increased serum creatinine >50% or 0.5-1.0 mg/dL
Acute on chronic renal failure is indicated by an increase of creatinine >25% w/in 3 months
Risk factors: acute drop in BP, ACE inhibitor, radio-contrast, atheroemboli following catheter procedure
o Sx: weight gain, edema
Uremia: fatigue, weakness, nausea & early morning vomiting, itchiness, confusion, pericarditis, coma
Azotemia: increased BUN w/o sx
oliguria: <400 mL urine /24 hrs; poor prognostic sign
anuria: <50 mL urine/24 hr
diff dx: acute obstruction, cortical necrosis, vascular catastrophes (aortic dissection)
complications: pulmonary edema (tx furosemide), hyperkalemia, anion gap metabolic acidosis (if <16mEq/L tx w/sodium bicarb),
hypocalcemia, hyponatremia, hyperphosphatemia, hyperuricemia, uremia, infection (uremia impairs immune functions)
o dx: H&P, baseline Cr, urine output, urinalysis, urine chem (FENa, osmolality, urine Na+, urine Cr), renal ultrasound & bladder catheter to r/o
obstruction, medication review, CMP (Na, K, Ca,PO4; albumin, BUN, Cr), CBC w/diff, dipstick for protein
renal failure index= (UNa/ [UCr/PCr[)/100
<1% prerenal failure, >1% ATN
o prerenal failure: decrease in systemic arterial blood volume or renal perfusion
causes: hypovolemia (GI losses, diuretics), reduced effective artieral blood volume (cirrhosis w/ portal HTN, severe burns, sepsis,
SIRS, nephrotic syndrome hypoalbuminemia), decreased CO (CHF, pericardial tamponade), peripheral vasodilation, renal a.
obstruction, hepatorenal syndrome, ACE inhibitors, NSAIDs
decreased GFR decreased clearance of metabolites (BUN, Cr, uremic toxins)
dx: oliguria, urine osmolarity >500, urine Na+ <20, FENa <1%, increased BUN:Cr >20:1, increased urine/plasma Cr ratio >40:1;
hyaline casts, increased urine specific gravity
o intrinsic renal failure: unable to concentrate urine effectively
causes: tubular disease (ATN; d/t ischemia or nephrotoxins), glomerular disease, vascular disease, interstitial disease (allergic
interstitial nephritis d/t meds)
nephrotoxic drugs (ATN): aminoglycosides, radiocontrast, chemotherapy
drugs causing tubulointerstitial nephritis: cephalosporins, methicillin, rifampin
dx: decreased urine osmolality <350 mOsm/kg, increased urine Na+>40 mEq/L, FENa >2-3%, decreased BUN: Cr <20:1, decreased
urine-plasma Cr ratio <20:1; dipstick positive for protein 3-4+
RBC casts glomerular nephritis, WBC casts renal parenchymal inflammation/infection, fatty casts nephrotic
syndrome, granular (muddy brown) casts ATN
ATN: isothenuric, muddy brown grandular casts (cellular debri), proteinuria; FENa>1%, urine Na+>20 mEq/L
Glomerulonephritis: proteinuria, microhematuria, RBC casts
Tubulointerstitial nephritis: isothenuric, mild proteinuria, WBCs, WBC casts, urinary eosinophils
o post-renal failure: obstruction of the urinary tract increased tubular pressure decreased GFR
causes: BPH, post-op urinary retention (d/t anesthesia), cervical cancer commonly metastasizes to the ureters
dx: hydronephrosis on renal ultrasound; unable to concentrate urine so isosthenuria (urine osmolality=serum), specific gravity
1.010, microscopic (hematuria crystals or stones; WBCs BPH; normal external compression (ex. Tumor))
tx: foley catheter insertion
o tx
avoid meds that decrease renal blood flow (NSAIDs) or nephrotoxic (aminoglycosides, radiocontrast)
adjust med dosages for level of renal function
correct fluid imbalance & electrolyte disturbances; optimize CO
failure with medical tx dialysis
indications for dialysis (if refractory to med tx): fluid overload, metabolic acidosis, hyperkalemia, uremic pericarditis (dialysis
right away!), severe hyperphosphatemia, uremic sx
Chronic kidney disease (chronic renal failure)
o Kidneys tend to be smaller
o Staging based on GFR
1=elevated GFR >90 + proteinuria, 2= 90-60, 3= 30-60, 4=15-30, 5=<15
HTN & edema d/t inability to excrete Na+; hyperkalemia, metabolic acidosis
osteodystrophy starts at stage 2; increased phosphorous increase in PTH increased Ca2+ from bone to plasma
anemia starts at stage 3 (d/t decreased erythropoietin & decreased RBC survival)
o increases mortality risk from cardiovascular event 5-30x; albuminuria is an independent RF for mortality
Hepatorenal syndrome
o Acute prerenal renal failure in a pt with advanced liver disease (cirrhosis, sever alcoholic hepatitis, metastatic tumor, any cause of fulminant
hepatic failure)
Arterial vasodilation in the splanchnic circulation d/t portal HTN causing increased production of nitric oxide decreased renal
perfusion decreased GFR & sodium excretion (increased renin/angiotensin system)
o Type I (more severe): >50% lowing of creatinine clearance (<20mL/min) in <2wk or at least a 2x increase in serum creatinine (>2.5 mg/dL).
May or may not be oliguric (<500 mL/day)
o Type II: less severe than type I; ascites that is resistant to diuretics
o Triggers: GI bleed or infection (ex. spontaneous bacterial peritonitis); more likely if pre-existing renal insufficiency
Note: rapid diuresis azotemia but NOT hepatorenal syndrome
o Differential dx: ATN & other causes of prerenal disease
o Diagnostic criteria (dx of exclusion): chronic or acute liver disease w/ failure & portal HTN, plasma [creatinine] >1.5 mg/dL that progresses
over days-wks, absence of other causes for renal diseases (shock, ongoing bacterial infection, obstruction, parenchymal renal disease,
nephrotoxic drugs), urine red cell excretion <50 cells/high power filed, protein excretion <500 mg/da, lack of improvement in renal function
after volume expansion with IV albumin for at least 2 days & withdrawal of diuretics
oliguria, benign urine sediment, low rate of sodium excretion, progressive rise in the plasma [creatinine]
Sx may be masked d/t decreased urea & creatinine production (d/t liver disease and decreased muscle mass, decreased protein &
meat intake)
estimate GFR via creatinine clearance in 24hr urine
o treatment
IV clonidine decreases renal sympathetic tone & renal vascular resistance increase GFR in early stage disease
Midodrine (alpha-1 agonist) & octreotide (Somatostatin analog): systemic vasoconstriction & inhibition of endogenous vasodilator
Norepinephrine + albumin (NE only used in ICU setting)
Under research:
Ornipressin or terlipressin (ADH/arginine vasopressin analog splanchnic vasoconstriction)+/- albumin (1 g/kg/day;
100 g max)
Misoprostol (prostaglandin analog), N-acetylcysteine (decreased splanchnic vasodilation & NO production via
decreased formation of reactive O2 species), ACE inhibitor
Transjugular intrahepatic portosystemic shunt (TIPS): do not do if MELD score >18
Dialysis: for pts w/ renal failure waiting liver transplant or if possibility of improvement in liver function
Treat underlying liver disease: abstinence from alcohol, lamivudine for hep B, etc.
Most pts die w/in wks of onset of renal failure unless liver transplant
renal tubular acidosis
o type 4: d/t aldosterone deficiency or insensitivity to aldosterone failure to secrete acid as NH4+, retention of K+; non-anion gap metabolic
acidosis with primary decreased bicarbonate
o dx: CT scan abdomen
if recurrent stones 24 hr urine collection to ID underlying metabolic disorder (measure calcium, citrate, creatinine, uric acid,
oxalate, pH, and Na)
o tx: pain relief (NSAIDs>narcotics), <5mm Allow spontaneous passage using conservative management (fluid intake >2L daily)
o Removal or fluid and toxins when the kidney cannot do so efficiently
o Absolute indications: intractable metabolic acidosis, severe persistent electrolyte elevation (hyperkalemia, hypermagnesemia), intoxication
(methanol, ethylene glycol, lithium, aspirin= salicylic acid, magnesium-containing laxatives), fluid overload (hypervolemia not controlled by
meds pulmonary edema, HTN emergency), severe uremia (uremic pericarditis or encephalitis)
Sx of uremia: N/V, lethargy/deterioration in mental status, encephalopathy, seizures, pericarditis
Other indications: chronic renal failure (while waiting for transplant or for poor transplant candidates), acute renal failure
o It takes ~12 hrs for electrolytes to stabilize after dialysis; many procedures that require anesthesia are best done 24 hrs after dialysis to
prevent hemodynamic instability
o Hemodialysis
Blood interfaces w/an artificial solution resembling human plasma (dialysate); dialysate flows outside the capillary network while
the fluid & solutes flow through the semipermeable membrane
Usually 3-5 hrs, 3x/wk
Blood must be heparinized to prevent clotting
Access sites: central catheter in femoral or internal jugular vein (temporary), arteriovenous fistula (permanent; radial artery to
forearm veins; audible bruit indicates patency), implantable graft, PermaCath in internal jugular vein
Hemodynamically unstable pts: continuous arteriovenous or venovenous hemodialysis
Shiley catheter is the temporary catheter used; avoid the subclavian vein
A-V fistula needs to mature 3-4 months before it can be used for dialysis
Pros: More efficient/quicker than peritoneal dialysis & can be initiated quicker with temporary access
Cons: Less physiologically similar to kidney function than peritoneal dialysis; vascular access required
Complications: hypotension, hypo-osmolarity of ECF compared to brain N/V, headache, seizures, coma; first use
syndrome (chest pain, back pain, or anaphylaxis after a pt uses a brand new machine), infection of vascular access site,
amyloidosis of beta-2 microglobulin in bones & joints
o Peritoneal dialysis
Dialysate fluid is infused into peritoneal cavity, then fluids and solutes from peritoneal capillaries diffuse into dialysate fluid, which
is drained from abdomen
Hyperosmolar (high glucose) solution is used to remove water from blood via osmosis
Chronic ambulatory peritoneal dialysis (CAPD); implanted catheter; dialysate fluid drained & replaced every 4-8 hrs
Acute peritoneal dialysis: temporary catheter is used to drain & replace dialysate fluid every hour
Pros: pt can perform dialysis on their own; closer to normal kidney physiology
Cons/complications: high glucose load ( hyperglycemia & hypertriglyceridemia), peritonitis, pt must be highly motivated to self-
dialyze, increased abdominal girth (increased abdominal pressure risk of abdominal/inguinal hernia), protein malnutrition
o Sx: dysuria, suprapubic pain, +/- fever
o Dx: urinalysis (best initial; >10 WBCs), urine culture (most accurate)
No further dx is needed when symptomatic with WBCs in urine
Urine culture and imaging studies are done for frequent episodes or failure to respond to tx
o Tx: TMP/SMZ, ciprofloxacin, cephalexin, or nitrofurantoins (esp pregnant pt)
treat for 3 days in uncomplicated cases; treat 7 days if anatomical abnormality
genital pathology
o chlamydia trachomatis screening in sexually active women <24 yo and women at increased risk for STDs (new sexual partner, multiple
o ovarian cancer
dx: ultrasound or CT scan (best initial); biopsy (most accurate)
tx: surgical resection (all visible tumor and pelvic organs), chemotherapy
o cervical cancer
dx: pap smear screening (starting age 21, every 2-3 yrs, screen until age 65); colposcopy
atypical squamous cells of undetermined significance (ASCUS) HPV testing
o if (+) colposcopy
o if (-) repeat pap in 6 mo
tx: hysterectomy for advanced cervical cancer
prevention with HPV vaccine
o testicular cancer
sx: painless lump in the scrotum that does not transilluminate
metastasizes along lymphatic channels
dx: inguinal orchiectomy
staging with CT scan of abdomen, pelvis, chest
tx: orchiectomy; radiation for local disease, chemotherapy for widespread disease
o prostate cancer
sx: urinary obstructive symptoms, palpable lesion on exam
dx: rectal exam for palpable mass, prostate specific antigen, biopsy (best initial, most accurate)
PSA corresponds to the volume of cancer
ultrasound can be used to localize lesions to biopsy when PSA is high
gleason grading: measure of aggressiveness or malignant potential
tx: prostatectomy >radiation; hormonal therapy
complications of prostatectomy: erectile dysfunction, urinary incontinence
hormonal therapy shrinks current lesions (not preventative for recurrences); flutamide, GNRH agonists, ketoconazole,
o condylomata acuminata (anogenital warts)
d/t human papilloma virus (HPV)
sx: verrucous, papilliform, skin colored or pink lesions in the anogenital region
tx: chemical or physical agents (trichloroacetic acid, 5-florouracil epinephrine gel, podophyllin), immune therapy (imiquimod,
interferon alpha), surgery (cryosurgery, excisional procedures, laser treatment)
podophyllin: topical antimitotic agent that causes cell death; teratogenic
Adrenal insufficiency
o Acute sx: orthostatic hypotension, chronic abdominal pain, weakness
Hyponatremia, hyperkalemia, acidosis, hypoglycemia, fever, tachycardia, azotemia (d/t volume depletion from decreased
aldosterone), eosinophilia (d/t decreased cortisol)
o Chronic sx: malaise, weight loss, chronic fatigue, anorexia, N/V, hypoglycemia, hypotension, hyperpigmentation if primary disease
o Dx: cortisol level, ACTH stimulation test with cosyntropin (ACTH analog) if abnormal, get ACTH level; CT scan for primary dz, MRI for
secondary dx
Cortisol levels are normally highest in the morning, then lower throughout the day; elevated during illness, or after
Morning cortisol <5 microgram/dL insufficiency; >20 microgram/dL intact function
ACTH stimulation test: 250 microgram ACTH given, then measure cortisol at time 1,30 min, 60 min; normal if >7 microgram/dL
increase or max level >18 microgram cortisol
Insulin-glucose tolerance test= gold standard for testing the hypothalamic-pituitary axis
Chronic adrenal insufficiency: cosyntropin stimulation test with cortisol and ACTH levels (#1)
Cortisol low, ACTH high primary adrenal insufficiency
Cortisol and ACTH low secondary or tertiary adrenal insufficiency
Increase in cortisol level >20 mcg/dL 30-60 min after the administration of 250 mcg of cosyntropin r/o primary
adrenocortical insufficiency (addisons disease)
o Tx:
Acute tx: IV saline + glucose, corticosteroids (hydrocortisone 100 mg q6-8 hr; at high dose it provides both corticosteroid &
mineralocorticoid activity)
Long term tx: glucocorticoids (hydrocortisone 25-30 mg/day) +/- mineralocorticoids (fludrocortisone 0.1-0.2 mg/day; needed if
primary insufficiency)
Glucocorticoid SE: diabetes, HTN, obesity, osteoporosis, cataracts
Note: if pt on steroids chronically and is having surgery hydrocortisone IV before surgery & q6hr for 24 hr after
(stress dose of corticosteroids to prevent acute primary adrenal insufficiency)
o Addisons disease (primary adrenal failure)
Low cortisol & aldosterone
Causes: autoimmune destruction (#1), TB adrenalitis, chronic granulomatous infection (Histoplasma, Coccidioides), B/L adrenal
hemorrhage (sepsis, DIC), metastases (lung, breast, stomach), x-linked adrenoleukodystrophy; CMV or MAI infection in AIDs pt
Sx: N/V, abdominal pain, diarrhea or constipation, weight loss, hyperpigmentation, decreased BP, vitiligo
Hyponatremia (d/t mineralocorticoid deficiency & increased vasopressin d/t lack of cortisol), hyperkalemia
(a/w mild hyperchloremic acidosis)
o Secondary adrenal insufficiency
Low ACTH secretion from pituitary; low cortisol but normal aldosterone
Causes: chronic exogenous use of corticosteroids (#1), autoimmune, metastatic cancer, infiltrative disease
o primary amenorrhea (no menses by age 16)
differential dx: pregnancy, mullerian or vaginal agenesis, androgen insensitivity, turner syndrome
o secondary amenorrhea/ oligomenorrhea:
amenorrhea: 3mo w/o menses in a women with previously regular menses
oligomenorrhea: infrequent interval >40 days or <9 menses/yr
differential dx: pregnancy, hypothyroid, hyperprolactin, sheenhan syndrome, premature ovarian failure
prolactin is inhibited by dopamine, stimulated by serotonin and TRH
dx: pregnancy test (beta-hCG), prolactin and TSH levels which would alter GnRH pulsations, and FSH and LH assessing ovarian
Progesterone challenge test (7-10 days of 10 mg medroxyprogesterone acetate=provera) looking for withdrawal
bleed is a test for estrogenization
carcinoid syndrome
o increased serotonin from enterochromaffin cells in GI tract
o sx: cutaneous flushing, headache, intermittent diarrhea, bronchial constriction wheezing, HTN, cardiac changes in right side of heart
o dx: urine 5-hydroxyindoleacetic acid (5 HIAA)
o tx: octreotide (somatostatin analog)
Cushing syndrome
o Excessive systemic corticosteroid levels (iatrogenic or intrinsic)
Causes: ectopic ACTH production (small cell lung CA, pancreatic CA, neuroendocrine tumors, bronchial corinoids), pituitary
adenoma (elevated ACTH)
o Sx: fatigue, weight gain (thin extremities with truncal obesity, moon face, supraclavicular fat pad), proximal muscle weakness, easy
bruising, hirsutism, purple striae, hyperglycemia, osteopenia, osteoporosis, HTN, acne, cataracts, susceptibility to infections,
hypokalemia (d/t corticosteroid having some mineralocorticoid action; occasional hypervolemia hypernatremia)
o Dx: screen with low dose dexamethasone suppression test or 24 hr urinary free cortisol; plasma ACTH level
Elevated ACTH: cushings disease or ectopic ACTH (distinguish with high dose dexamethasone suppression test)
Failure to suppress 24 hr urinary cortisol or serum cortisol level by 50% ectopic ACTH syndrome
o Tx: spironolactone (for severe hypokalemia)
Conn syndrome (increased aldosterone)
o Aldosterone acts on the late distal tubules to increase Na+ reabsorption with K+ loss
o Sx: HTN, hypokalemia
o Type 1: autoimmune destruction of pancreatic beta cells complete loss of insulin production
o Type 2: insulin resistance and relative insulin deficiency
o Risk factors: obesity or overweight (BMI >25), signs of metabolic syndrome (HTN, low HDL, triglyceride >250 mg/dL), 1
degree relative
with diabetes, hx of gestational diabetes
Start screening 45yo and repeat every 3 yrs; kids with risk factors screening at 19yo and every 2 yrs
o Sx: polyuria, polydipsia, nocturia; Macrovascular complications (coronary artery disease, stroke, peripheral vascular disease), microvascular
complications (retinopathy, nephropathy, neuropathy)
Diabetic retinopathy: dot hemorrhages, hard exudates; eventual blindness
Diabetic retinopathy occurs before nephropathy
Diabetic neuropathy
Sx: peripheral sensory problems; loss of proprioception imbalance; numbness and tingling
Increased risk of epidural abscesses cord compression
Dx: spine MRI
Diabetic nephropathy
Tx: ACE inhibitor or ARB
Occurs >10 yrs after onset of diabetes; anatomic neuropathy dysmotility; inability to sense stretch of the GI tract
Sx: chronic abdominal discomfort, bloating, constipation, anorexia, N/V, early satiety
Dx: clinical; nuclear gastric emptying study if no response to treatment
Tx: erythromycin, domperidone, or metoclopramide to increased GI motility; improve glycemic control, small
frequent meals, bethanechol
Diabetic ketoacidosis
Precipitants: infection, pregnancy, MI
Glucagon stimulates hepatic gluconeogenesis and glycogenolysis; lipolysis is enhances release of free fatty acids
oxidation causes ketones
Sx: polyuria, polydipsia, weight loss, mental status changes, vision blurring; kussmaul breathing (deep & rapid to
compensate for metabolic acidosis), N/V, abdominal pain, fatigue, malaise; signs of dehydration
o Complications: cerebral edema (d/t rapid correction of hyperglycemia or rapid hypotonic fluid
administration), ARDS, thromboembolism, fluid overload, acute gastric dilatation
o Cardiovascular collapse= most common cause of death in DKA
d/t acidosis, hypovolemia & electrolyte deficiencies
Anion gap metabolic acidosis, hyperglycemia, hypovolemia (d/t osmotic diuresis), ketone bodies in serum; depletion
of total body K+, Mg2+, and phosphate
o may appear as hyperkalemia b/c K+ moving out of cell as H+ moves in, but urinary losses cause overall
Tx: hydration, insulin, potassium, bicarbonate (only used if pH <6.9, cardiac instability, or severe hyperkalemia)
o Hydration: 1-2 L normal saline bolus, followed by 250-500 ml/hr
o Insulin: bolus of 0.1-0.15 U/kg, followed by continuous 0.1 U/kg/hr; decrease infusion rate to 0.05 U/kg/hr
when blood glucose decreases to 250-300 mg/dL
If glucose falls too low, give sugar with the insulin; insulins main role during DKA is to resolve the
ketosis (monitored with anion gap; goal is bicarb >18, anion gap <12)
Give subQ insulin 30 min before stopping insulin infusion to avoid rebound acidosis
o Goal drop in glucose 80-100 mg/dL/hr
Nonketotic hyperosmolar hyperglycemia
Sx: Dehydration d/t osmotic diuresis, metabolic disturbances altered consciousness, blurred vision (d/t myopic
increase in les thickness and intraocular hypotension secondary to hyperosmolarity)
Elevated glucose (>100 mg/dL), serum osmolarity >320-370 osm, neuro sx (seizures, coma)
Tx: fluid resuscitation with normal saline, insulin
Nontraumatic amputations of the lower extremities
o Dx: fasting serum glucose >126 (2x; most specific), glucose tolerance testing (>200 mg/dL; most sensitive), random glucose >200 mg/dL + sx
of diabetes
Impaired fasting glucose/impaired glucose tolerance tests (prediabetes): fasting glucose 100-126 mg/dL, oral glucose tolerance
test (75 g load) 140-200
HbA1c to monitor glycemic control
o Tx: lifestyle modification, glucose control with meds, office visits every 3-6 mo (with HbA1c check), yearly ophthalmologic exam, semi-annual
dental visits, yearly urine screens to detect microalbuminuria, yearly foot exams (if neuropathy present, every 3 mo)
Lifestyle modification: low sugar & fat diet, exercise, strict glycemic control, smoking cessation, target Bp <130/80 (<120/75 if
proteinuria >1-2g/day or renal insufficiency), LDL<100 mg/dL
Some changes are for highest risk for cardiovascular disease
SE: weight gain, injection instead of oral med
Sulfonylureas (glipizide, glyburide): augments pts insulin production in the pancreatic beta cells
best for young pts with fasting plasma glucose <300 mg/dL
SE: hypoglycemia if not eating (long-half life; increased risk if elderly or renal insufficiency)
Repaglinide: non-sulfonylurea with similar MOA; rapid onset of action
Caution in elderly and pt with renal or hepatic insufficiency
Januvia (sitagliptin)
SE: pancreatitis
Metformin (biguanide): decreases gluconeogenesis in the liver; decreases insulin resistance
Good for young obese pts
Avoid in pts with renal insufficiency or liver dysfunction d/t risk of lactic acidosis
TZDs (-glitazone): promote skeletal muscle glucose uptake; decrease insulin resistance
Void in pt with liver failure or CHF
SE: hepatotoxicity, edema
GLP-1 (glucagon-like peptide) agonist (direct or by decreased degradation with DDP-4 antagonist)
GLP-1 agonists: Exenatide, liraglutide
DDP-4 antagonists (-gliptin)
Alpha-glucosidase inhibitors (acarbose): inhibits breakdown of complex carbohydrates in the GI tract
Se: GI distress, dose-dependent hepatotoxicity
o Causes: lymphocytic (hashimoto) thyroiditis, surgical or radioactive idodine treatment for hyperthyroid (graves disease), iodine
Hashimoto thyroiditis: #1 cause of hypothyroid in US; middle aged F most common
Increased risk of thyroid lymphoma
Dx: anti-thyroperoxidase antibodies (TPO)
Iodine deficiency is the most common worldwide cause of goitrous hypothyroid
o Sx: increased weight, fatigue, thinning of hair, coarse skin, constipation, hoarseness, memory changes
Complications: oligomenorrhea, galactorrhea, carpal tunnel syndrome, myxedema (dull facies, swollen eyes, doughy extremities,
sparse hair, thickened tongue), proximal muscle weakness in shoulders/hips
o Dx: beta-hCG (r/o pregnancy as cause of oligomenorrhea), serum TSH, free T4 (direct measure or estimated via T3 uptake= measure of
available protein binding)
Pregnancy & OCP use increase thyroid-binding globulin (TBG) increased total T4, decreased T3 uptake
Hypoprotein states (nephrotic syndrome) decrease TBG decreased total T4, increased T3 uptake
Subclinical hypothyroidism: increased TSH, normal free T4 with mild sx + some derangement of cholesterol metabolism
(increased total or LDL cholesterol)
o Tx: levothyroxine (T 6-7 days allows daily dosing), goal 1.7-2.1 ug/kG; titrate to handle sx and normalize TSH level
TSH level take 6-8 wks to readjust to new dosing level
With old pt & those with CV disease, start low & build up dosing slowing to dosing goal (increased dose every 4-6 wks)
Note: other vitamins & meds (esp iron containing) should be taken separately to avoid interfering w/ absorption
Hyperthyroidism (thyrotoxicosis)
o Causes: graves disease (#1; autoantibodies that stimulate TSH receptors), toxic multinodular goiter, autonomous hyperfunctioning
adenoma (hot nodule/plummer disease), thyroiditis (subacute/dequervain thyroiditis, post-radiation, postpartum, amiodarone-induced),
malignancies (TSH secreting pituitary adenoma, hydatiform mole, choriocarcinomas that secretes hCG, ovarian teratomas, metastatic
follicular thyroid carcinomas)
o Sx: weight loss, tachycardia, HTN, smooth nontender goiter, warm skin, loose stools
Neuromuscular: nervousness, anxiety, action tremors, brisk reflexes (hyperreflexia); inability to concentrate, proximal m.
weakness (hips and shoulders), emotional lability, insomnia, fatigue
Cardiac: wide pulse pressure, flow heart murmurs, tachycardia, atrial fibrillation, cardiomegalyhigh output heart failure
GI: weight loss, hyperdefecation (increased GI motility)
Eyes: retraction of upper eyelid (d/t increases sympathetic tone), lid lag, exophthalmos (graves disease)
Skin: warm, moist, velvety; fine hair texture/alopecia, sweating
Reproductive: oligomenorrhea; decreased sperm count, impotence, and gynecomastia
Elderly: depression/apathy, weight loss, atrial fibrillation, worse angina pectoris, CHF
Increased risk of rapid bone loss (d/t thyroid hormones cause increased osteoclastic bone resorption)
o Graves disease: goiter, thyroid bruit, hyperthyroid sx, ophthalmopathy, dermopathy
Ophthalmopathy: inflammation of extraocular mm, orbital fat, and CT proptosis (exophthalmos), diplopia, periorbital edema
Dermopathy: raised hyperpigmented orange peel texture papules; most common over shins (pretibial myxedema)
o Thyroid storm: tachycardia >140 bpm, fever (104-106), agitation, delirium, restlessness or psychosis, vomiting, diarrhea
Tx: IV fluids, antibiotics if needed, propanolol, glucocorticoids to decrease T4 T3 conversion, antithyroid meds to block
production or iodine solution to block release of thyroid hormone
o Dx: low serum TSH, increased free T4; thyroid-stimulating Ig, diffusely elevated uptake of radioactive iodine on thyroid scan
o Tx: antithyroid drugs (methimazole, propylthiouracil), radioactive iodine ablation (#1), surgical ablation of thyroid
Surgery indicated if goiter is causing obstructive sx or pregnant woman
Exophthalmos may persist despite treatment
Most pts are hypothyroid after radioactive iodine ablation or surgical resection; so lifelong replacement of hormones is
needed (levothyroxine)
Immediate SE of radioactive iodine: thyrotoxicosis as dying thyroid cells release excess thyroid hormone
new-onset atrial fibrillation, hand tremor
o Pretreat with antithyroid meds (methimazole) to deplete thyroid hormone stores before beginning
radioactive iodine therapy
o Prednisone helps to prevent exacerbation of hyperthyroid ophthalmopathy that can occur with radioactive
iodine treatment
o Catecholamine secreting tumor; originates in chromaffin cells of adrenal medulla
MEN 2a: pheochromocytoma, medullary thyroid CA, hyperparathyroidism
MEN 2b: pheochromocytoma, medullary thyroid CA, mucosal neuromas
o Sx are paroxysmal (intermittent): HTN, tachycardia, headache, palpitations, flushing, diaphoresis, dilated pupils, chest pain;
anxiety/nervousness, tremor, pallor, malaise, N/V, orthostatic hypotension
o Dx: 24 hr urine for metanephrine, VMA (vanillylmandelic acid) & free catacholamines; CT or MRI to locate tumor; if not found scintigraphic
localization w/MIBG or octreotide (Somatostatin analog)
Consider screening for RET or VHL
o Tx: surgical resection
1 wk before surgery: alpha-blocker (phenoxybenzamine) to prevent HTN exacerbation; liberal salt diet (prevent volume
contraction); beta blockers can also be used but only after starting the alpha blocker
SIADH (syndrome of inappropriate antidiuretic hormone release)
o ADH/arginine vasopressin is released from the posterior pituitary
Causes of excess ADH release: Small cell lung cancer (paraneoplastic syndrome), post-op pain
o Sx: lethargy, seizures, confusion, coma
o Dx criteria: serum osm <270, urine osm >serum osm, urine Na >20 mEq/L, absence of hypovolemia, normal renal/adrenal/thyroid
function, no obvious surgical/traumatic/painful stimulus known to activate the neuroendocrine stress response (includes ADH release),
absence of other known causes of hyponatremia
o tx:
hypertonic saline along with furosemide (prevent volume overload)
used up to target Na+ 120-125 mmol/L (only used for severely decreased Na+, or when Na+ was rapidly decreased);
dont correct Na+ faster than 0.5-1.0 mEq/L
complication: osmotic cerebral demyelination (central pontine myelinolysis) quadriplegia, pseudobulbar palsies,
locked-in syndrome, coma, or death
mild or chronic cases: water restriction
wilsons disease
o autosomal recessive; presents age 5-35
o decreased copper excretion d/t decreased ceruloplasmin; copper accumulation in liver, kidney, RBCs, nervous system
o sx: Kayser-fleisher rings in eyes, dysarthria, spasticity, chronic liver disease cirrhosis, neuro sx (psychosis, tremor, ataxia, seizures;
parkinsonian sx d/t copper deposition in basal ganglia), coombs negative hemolytic anemia, renal disease (aminoaciduria, renal tubular
acidosis, nephrocalcinosis, nephrolithiasis)
o dx: decreased serum ceruloplasmin, slit lamp exam for Kayser-Fleisher rings, liver biopsy, increased copper excretion in urine after giving
penicillamine (24 hr urine; most accurate), LRTs (elevated aminotransferases, impaired synthesis fo coagulation factors and albumin)
o tx: copper chelator (penicillamine or trientine), zinc (inhibits intestinal copper absorption), liver transplant
o Autosomal recessive mutation in C282y gene; excessive iron absorption in the duodenum; iron accumulation in organs hydroxyl free
radicals fibrosis
Secondary hemochromatosis (iron overload) d/t multiple transfusion or chronic hemolytic anemia
Affected organs: liver, pancreas, heart, joints, skin, thyroid, gonads, hypothalamus
o Sx: Diabetes mellitus, Bronze skin, cirrhosis, cardiomyopathy (arrhythmias, CHF), hypogonadotropic hypogonadism (impotence,
amenorrhea, decreased libido), arthropathy/arthritis, fatigue, abdominal pain, hypothyroidism
o Dx: increased serum iron & ferritin, increased transferrin saturation (>50%), decreased TIBC, liver biopsy (determines iron concentration;
required for dx)
Abdominal MRI and HFE (C282y) gene testing can be used to confirm the diagnosis instead of liver biopsy
Prussian blue= stain for RBC cell iron
o Tx: phlebotomy, iron chelation (deferoxamine, deferasirox), liver transplant, treat complications
Iron chelators are used for pt that cant be managed with phlebotomy or are anemic w/ hemochromatosis from overtransfusion
Vitamin excess/deficiencies
Vitamin Excess deficiency
D *decreased Ca2+ & phosphate
Thiamine *seen in alcoholics & fad diets
*sx: poor short term memory, lower extremity paresthesias, decreased vibratory position sense; tachycardia, hypotension
Fluid balance in body
o Water deficit= Total body water x [(serum Na/140)-1]
Total body water= cofactor *weight
cofactor 0.6 for men, 0.5 for women & elderly men, 0.45 for elderly women
TBW decreases with age & obesity (fat is low on water content)
Water distribution: 2/3 ICF, 1/3 EFC (1/4 plasma 85% venous, 15% arterial, interstitial fluid)
Hours to correct= (serum Na-140)/0.5
Infusion rate= water deficit/hours to correct
o Calculating maintenance fluids
100 mL/kg for 1
10 kg, 50 mL/kg for next 10 kg, 20 mL/kg for every 1 kg remaining
divide total by 24 for hourly rate
4mL/kg for 1
10 kg, 2 mL/kg for next 10 kg, 1 mL/kg for every 1 kg remaining
gives hourly maintenance level
give fluid to maintain urine output at 0.5-1 mL/kg/hr
o Fluid replacement therapy
Normal saline (0.9%; 154 mOsm/L): used for dehydration, blood loss
Replace blood loss with crystalloid at a 3:1 ratio (either NS or LR)
D5 NS: maintenance fluid (often given with 20mEq of KCl/L of fluid)
D5W: used to dilute powered medications, sometimes for correcting hypernatremia
Lactated ringers solution: replacement of intravascular volume
Do not use if hyperkalemia (solution contains K+)
Serum osmolarity= (2*Na) + (BUN/2.8)+ (glucose/18)
o Normal 280-295 mOsm/kg
o plasma hypertonicity (>295 mOsm/kg): stimulates Osmoreceptors in the hypothalamus produces thirst; also stimulates posterior pituitary
to release ADH (act on V2 receptors in kidney collecting ducts to increase water absorption)
o Serum Na+ <130-135 mEq/L
o Sx
Neuro d/t brain cell welling or cerebral edema: headache, delirium, irritability, muscle twitching, weakness, hyperactive deep
tendon reflexes, increased ICP, seizures, coma
GI: NV, ileus, watery diarrhea
CV: HTN d/t increased ICP
Increased salivation & lacrimation
Oliguria anuria
o Normal serum osmolarity (280-295 mOsm/kg; pseudohyponatremia): hyperproteinemia, hyperlipidemia, post-transurethral resection of
prostate/bladder tumor (d/t mannitol containing irrigation fluid)
o High serum osmolarity (>295 mOsm/kg): hyperglycemia, exogenous solutes (radiocontrast, mannitol)
Corrected [Na]: for every 100 glucose over 100, add 1.6 Na+
Osmotic shift of water out of cells
o Low serum osmolarity (<280 mOsm/kg)
Hypovolemia + urine Na <10 mEq/L: dehydration, vomiting, diarrhea, diaphoresis, third spacing
Signs of dehydration: flat neck veins, dry mucous membranes, decreased urine output
Hypovolemia increased renin & angiotensin levels increased aldosterone increased Na+ absorption, K+ & H+
o Increased plasma osmolality ADH release water reabsorption
Hypovolemia+ urine Na >20 mEq/L: renal salt loss (diuretics, ACE inhibitor, mineralocorticoid deficiency, ATN)
Euvolemic + urine Na >20 mEq/L + urine osm <300: psychogenic/primary polydipsia, beer potomania, hypothyroid,
glucocorticoid deficiency, inappropriate fluid resuscitation (D5W or water alone after insensible losses), post-op hyponatremia
Primary polydipsia: Both the urine and the blood are diluted d/t excessive water ingestion
Thyroid hormone and cortisol are both permissive for free water excretion; deficiency water retention
Euvolemic + urine Na >20 mEq/L + urine osm >300: SIADH
Hypervolemic: CHF, hepatic failure, nephrotic syndrome (renal failure)
o Tx:
normal saline used for mild or slowly developed hypovolemic hyponatremia
water restriction for asymptomatic euvolemic pt
hypotonic hyponatremia
mild (Na+ 120-130): withhold free water
moderate (Na+ 110-120): loop diuretics given with saline
severe (Na+ <110 or asymptomatic): hypertonic saline to increase serum sodium by 1-2 mEq/L/hr until sx improve
o rapidly developed hyponatremia with severe sx (seizures, coma) requires rapid correction with 3%
o do not increase Na+ >8mmol/L during the first 24 hrs d/t risk of central pontine demyelination
o Na+ >145 mmol/L
o Sx: altered mental status, restlessness, weakness, focal neuro deficit, dry mucous membranes, decreased salivation
o Hypovolemic
Causes (water loss>Na+ loss): dehydration, diaphoresis, diarrhea, respiratory losses, diuretics, osmotic diuresis d/t glycosuria,
renal failure
Tx: IV normal saline (0.9%) until volume deficit is restored, then 5% dextrose in half-normal saline (0.45%)
Correct no more than 1mEq/L/hr
Mild cases can be started with D5W 0.45% saline
o Euvolemic
Causes: diabetes insipidus, insensible respiratory (tachypnea)
Diabetes insipidus: complete (urine osmolality <300) vs partial (urine osmolality 300-600 mOsm/kg); elevated serum
o Causes: decreased ADH, renal ADH resistance (hypercalcemia, hypokalemia, tubulointerstitial disease, drugs)
Drugs: lithium, demeclocycline, foscarnet, cidofovir, amphotericin
Dx: desmopressin differentiates nephrogenic from central diabetes insipidus
Tx: salt restriction, vasopressin, D5W or oral fluids, discontinue drug/treat underlying imbalance
Tx: IV 5% dextrose in water
o Hypervolemia
Causes: iatrogenic (NaHCO3 or TPN), exogenous glucocorticoids, Cushings syndrome, primary hyperaldosteronism , saltwater
Tx: diuretics (furosemide) and D5W
o Normal K+ level 3.5-5.0
o Causes: chronic alcoholism (hypomagnesemia, hypokalemia, hypophosphatemia), GI losses (vomiting, NG suction, diarrhea, laxatives, enema,
intestinal fistulae, decreases absorption), renal losses (diuretics, hyperaldosteronism, excessive glucocorticoids, Mg 2+ deficiency, bartters
syndrome), dietary deficiency, some antibiotics, profuse sweating
Shift K+ into cells: alkalosis, insulin, beta-2 agonists (epinephrine)
o Sx: arrhythmias (prolongs cardiac conduction), muscle weakness, fatigue, muscle cramps, paralytic ileus, polyuria & polydipsia, N/V
If k+ <2.5: decreased deep tendon reflexes, flaccid paralysis, tetany, rhabdomyolysis
exacerbates digitalis toxicity
ECG changes: T wave flattens out/broadens or inverted T-wave, U wave, ST depression, premature ventricular beats
o Tx: potassium (oral KCl; IV only if K+ <2.5 or arrhythmias d/t K+), magnesium if low
magnesium is a cofactor for potassium uptake
o K+ >5.0 mEq/L
o Causes: renal failure, hyporeninemic hypoaldosteronism, blood transfusion, medications, addisons disease
Releases K+ from cells: Acidosis, cell lysis (rhabdomyolysis, hemolysis, burns), GI bleeding, insulin deficiency, beta-blocker
Pseudohyperkalemia (spurious); K+ movement out of cells immediately before or after venipuncture d/t prolonged use of a
tourniquet +/- repeated fist clenching (causes acidosis)
Drugs: drugs that block aldosterone synthesis/action (ACE inhibitors, angiotensin receptor blockers, spironolactone,
amiloride, cyclosporine, heparin), trimethoprim, pentamidine, nonselective beta blockers (blocks b2 intracellular K+ uptake),
digitalis (blocks Na-K-ATPase pump), NSAIDs (decrease renal perfusion), succinylcholine (extracellular leakage of K+ through Ach
receptors), iatrogenic overdose from giving K+ to pt
Addisons disease (primary adrenal failure)
o Sx: muscle weakness, flaccid paralysis, respiratory insufficiency, cardiac toxicity (sine wave on ECG, ventricular fibrillation), decreased deep
tendon reflexes, N/V, intestinal colic, diarrhea
ECG changes (K+ >6): peaked T waves, prolonged PR interval, widening of QRS & merging of QRS with T wave; ventricular
fibrillation and cardiac arrest can occur
o Tx:
membrane stabilization with calcium gluconate (cardioprotective)
Shift K+ into cells: insulin w/ glucose (quickest correction of hyperkalemia ~15-30 min), albuterol (beta-2 agonist), sodium
Decrease total body K+: sodium polystyrene sulfonate (Kayexalate; K+ binding resin; takes ~1-2 hrs), furosemide, dialysis
o normal serum calcium 8.5-10.5 mg/dL
most of calcium is bound to albumin
hypoalbuminemia low total calcium but normal ionized calcium
Corrected calcium levels for when albumin is abnormal
o Corrected calcium= 0.8 (4-serum albumin g/dL) + measured total calcium mg/dL
Increased pH increases the binding of calcium to albumin total calcium is normal, but ionized Ca2+ is low
Hormonal control of calcium levels
PTH: increases Ca2+, decreases PO4
o Increases one resorption, in kidney increases calcium reabsorption while wasting phosphorous, in gut it
activates Vit D
Calcitonin: decreases plasma Ca2+ and PO4
o Decreases bone resorption, in kidney wastes calcium while increasing reabsorption of phosphorous, in gut is
decreases postprandial Ca2+ absorption
Vit D: increases both plasma Ca2+ and PO4
o increases bone resorption, in kidney increases calcium reabsorption while wasting phosphorous, in gut
increases absorption of both calcium & phosphorous
o Causes: malabsorption (chronic pancreatitis, vit D deficiency, short bowel syndrome), renal failure (decreased production of 1,25-
dihydroxy vit D), primary hypoparathyroidism, post-op after transfusions (calcium binds citrate in blood transfusions), acute
pancreatitis (calcium deposits), hyperphosphatemia (PO4 precipitates with Ca2+), pseudohypoparathyroidism (end organ resistance to
PTH), hypomagnesemia (decreases PTH secretion), osteoblastic metastases
o Sx:
Bone: rickets and osteomalacia
Neuro: neuromuscular irritability (hyperactive deep tendon reflexes, chvosteks sign= facial n twitching when tapped,
trousseaus sign= carpal spasms after BP cuff inflation, numbness/tingling in circumoral/fingers/toes, muscle crams, convulsions,
grand mal seizures), basal ganglia calcifications
Cardiac: arrhythmias, prolonged QT interval
o Dx: BUN, Cr, magnesium, albumin, ionized calcium; amylase, lipase, LFTs if suspected causes
o Tx: if symptomatic IV calcium gluconate w/ magnesium if low; long term oral calcium supplements (calcium carbonate) + vit D
If PTH deficiency VIt D (or calcitriol) + high oral calcium intake+ thiazide diuretics (lower urinary calcium to prevent
o Causes: Most common are malignancies and hyperparathryoidism
primary hyperparathyroidism, MEN syndrome, familial hypocalciuric hypercalcemia (AD), vit D or A intoxication, multiple
myeloma, metastatic cancer to bone, Pagets disease of the bone, renal cell carcinoma (osteolytic when metastatic), squamous cell
lung CA (releases PTH like hormone), renal failure (usually hypocalcemia, but may elevate PTH enough to cause hypercalcemia),
acromegaly, Addisons disease (chronic adrenal insufficiency), thiazide diuretics, lithium (increases PTH levels in some pt), milk-
alkali syndrome (excessive intake of calcium and certain absorbable antacids), granulomatous disease (sarcoidosis, TB),
primary hyperparathyroidism: stimulates PTH increased bone turnover
o solitary parathyroid adenoma or part of MEN
o usually found as abnormal lab in asymptomatic pt
o hypercalcemia, hypophosphatemia, elevated PTH
o tx: parathyroidectomy if Ca >15mg/dL or <50 yo with significant decreased bone mineral density
lithium: stimulation of PTH
malignancy-related hypercalcemia: local destruction of bone (multiple myeloma, leukemia, lymphoma) or
humoral release of PTHrP (breast, renal, or lung CA), increased IL-6
o stimulate osteoclast activity through direct bone marrow invasion: multiple myeloma, leukemia, breast
o excess 1,25-vit D: lymphomas
o dx: CBC, peripheral smear, imaging of bones (x-ray or CT), PTH and PTHrP level, bone marrow biopsy
o tx: treat tumor, bisphosphonates, calcitonin
sarcoidosis (and other granulomatous diseases): excess 1,25 (OH2)D synthesized in macrophages and lymphocytes
o tx: avoid sunlight, decreased vit D & calcium intake, glucocorticoids if needed
paget disease of the bone: d/t osteoclast hyperfunction
o increased bone turnover; increased bone breakdown and compensatory increase in bone formation; mosaic
pattern of lamellar p=bone; most commonly involves pelvis, skull, spine, and long bones
o sx: skeletal deformities, bone or joint pain, fractures, never entrapment, or osteosarcoma; enlarging cranial
bones increased hat size or entrapment of CN8 hearing loss
o dx: elevated alkaline phosphatase, x-ray
excessive vit D intake: increased calcium intestinal absorption, and if severe bone resorption
o low PTH, elevated 25(OH)2D, normal 1,25 (OH)2D
o tx: glucocorticoids
renal insufficiency: secondary hyperparathyroidism d/t partial resistance to PTH effects
o tx: limited dietary phosphate, IV calcitriol
o Sx : stones, bones, grunt/groans, psychiatric overtones
<12 mEq/L: polyuria, dehydration
occur >12 mEq/L: GI sx (anorexia, constipation, N/V, abdominal pain, peptic ulcer disease), kidney problems (polyuria,
nephrolithiasis, prerenal azotemia), musculoskeletal sx (arthralgias, myalgias, weakness), neuropsychiatric disturbances (fatigue,
confusion, lethargy, stupor, coma, mental status changes, psychosis)
nephrolithiasis, nephrocalcinosis, bones aches & pains, osteitis fibrosa cystica (brown tumors; von Recklinghausen disease
of bone; increase risk of fractures), muscle pain & weakness, pancreatitis, peptic ulcer disease, gout, constipation, depression,
fatigue, anorexia, sleep disturbances, anxiety, lethargy, polydipsia & polyuria, HTN, weight loss, shortened QT interval
osteitis fibrosa cystica isd/t osteoclastic resorption of bone replacement w/ fibrous tissue
can also cause secondary hypertension
o Dx: BUN, Cr, magnesium, albumin, ionized calcium; amylase, lipase, LFTs if suspected causes
24hr urinary calcium excretion and creatinine clearance
Familial hypocalciuric hypercalemia: decreased urinary calcium excretion despite increased serum calcium
Radioimmunoassay of PTH or PTH-related protein; bone scar or bone survey for lytic lesions, urinary cAMP (high in primary
Elevated PTH: primary/secondary/tertiary hyperparathyroidism, MEN syndrome
o Tx
Increase urinary excretion of calcium: IV 0.9% saline, loop diuretics (furosemide)
Effects seen w/in hrs
SE: volume overload, electrolyte disturbances
Inhibit bone resorption: bisphosphonates (-dronate), calcitonin
Bisphosphonates work w/in 1-2 days
o SE: hypophosphatemia, hypomagnesemia, hypocalcemia, osteonecrosis of jaw
Calcitonin works w/in hours
o SE: efficacy short lived (tachyphylaxis)
Glucocorticoids if vit D-related mechanisms (intoxication, granulomatous disorders) or multiple myeloma
SE: hyperglycemia, osteoporosis, immune suppression
Hemodialysis if renal failure
o Sx: weakness, rhabdomyolysis, paresthesias, respiratory failure
o Causes: poor nutrition, diuretic use, malabsorption, alcohol abuse
Acid/base disorders
o Dx: pH, serum HCO3 & pCO2
pH=pK+ log ([conjugate base]/[acid])= 6.1 + log ([HCO3]/(0.03*PaCO2))
normal: PH (7.35-7.45), HCO3 (22-26 mEq/L), PCO2 (35-45 mm Hg)
delta gap: calculated anion gap-12= expected bicarb depletion/excess
o Respiratory acidosis
pH <7.35, PaCO2 >40 mmHg
Causes: hypoventilation
Hypoventilation: obesity (pickwickian syndrome), pulmonary/thoracic dz (COPD, sleep apnea, CF, scoliosis, ankylosis),
neuromuscular dz (myasthenia gravis, lambert-eaton, poliomyelitis, muscular dystrophies, Guillain-barre, ALS), drug
induced (anesthetics, narcotics, sedatives), primary CNS dysfunction (brainstem lesion, infection, stroke)
o Respiratory alkalosis
Causes: hyperventilation (tachypnea)
Hyperventilation: PE, atelectasis, pulmonary edema, pleural effusion, pneumonia, high altitude, salicylate intoxication
o Metabolic acidosis
pH <7.35, serum HCO3 <24
Winters formula for Expected compensatory pCO2= 1.5 (HCO3)+8
o If PCO2 is drastically different, then its a mixed acid-base disorder
anion gap= [Na]- [HCO3+ Cl]; normal 6-12 mEq/L
corrected anion gap for depleted albumin: for every -1 of albumin from 4, then add 3 Na+ to the anion gap
serum osmolality= (2*Na)+ (glucose/18)+ (BUN/2.8)
osmolar gap= observed osmolarity-calculated osmolarity; normal <10
Anion gap acidosis
Causes: lactic acidosis (hypoxia, poor perfusion, mitochondrial dysfunction), ketoacidosis (DM1, starvation,
alcoholism), methanol ingestion (formic acid), ethylene glycol ingestion (glycolic & oxalic acid), salicylate poisoning,
Uremia (H+ and NH4+)
o High osmolar gap: acute methanol, ethanol, or ethylene glycol poisoning
o Hypoxia/poor perfusion: carbon monoxide poisoning, shock (circulatory failure)
o MUDPILES: methanol, uremia (renal failure), DKA, paraldehyde, INH, lactic acidosis, ethylene glycol,
o Post-ictal (seizure) lactic acidosis is transient and typically resolves w/in 60-90 min; observe &
repeat CMP after 2 hrs
Non-anion gap acidosis
Causes: diarrhea, renal tubular acidosis, acute renal failure, addison disease (aldosterone deficiency)
o Metabolic alkalosis
Alkaline pH (>7.45), increase in serum bicarbonate (>24)
Expected compensatory pCO2= 0.9 (bicarb)+ 16 +/-2
Chloride-sensitive (hypochloremic, saline-responsive): urinary chloride <20 mE/day & signs of volume depletion
o d/t ECG volume contraction: increased mineralocorticoid action bicarb retention, H+ loss, K+ loss
o causes: thiazide or loop diuretics, loss of gastric secretions (vomitinghyperemesis gravidarum, bulimia)
vomiting: hypochloremic hypokalemic metabolic acidosis
o tx: saline infusion + potassium if depleted
chloride resistant
o urine chloride >20 mEq/day & ECF volume expansion
o causes: primary hyperaldosteronism, barter syndrome Gitelmans syndrome, excessive black licorice
o most common in elderly women
o risk factors: low calcium/vit D intake, smoking, corticosteroid use, lack of weight bearing exercise, alcohol ingestion, lower body mass
o sx: spontaneous fractures of weight bearing bones, vertebral compression fractures loss of height, wrist fracture
vertebral fracture: sudden onset of pain, local tenderness to palpation; normal neuro exam (note that age related decreased ankle
reflex is normal)
o dx: dual energy x-ray absorptiometry (DEXA; bone densitometry) of spine & pelvis to used to screen for osteoporosis in women >65 yo or
>60 yo+ RF
T-score compares bone density with the normal density of a young woman
Osteopenia: T score 1.5-2 SD below
Osteoporosis: T score >2 SD below
o Tx: calcium & Vit D (best initial); bisphosphonate (-dronate), estrogen or raloxifene for postmenopausal women, teriparatide (PTH analog),
calcitonin nasal spray
Bisphosphonate SE: osteonecrosis of the jaw, pill esophagitis
Teriparatide SE: osteosarcoma, hypercalcemia
o general info
sx: joint swelling, redness, warmth, tender to palpation, limited rand of motion in all planes (active & passive)
diff dx: infectious (staph aureus, N. gonorrhea, TB, lyme, fungal), crystal (gout, pseudogout), trauma, osteoarthritis, rheumatoid
arthritis, hemochromatosis
non-inflammatory arthritis diff dx: osteoarthritis, fibromyalgia, hypothyroidism, neuropathic pain, depression
viral causes are acute (<6wks): hep B or C, rubella, parvo B19
o tx: NSAIDs PRN for pain; self-limited
SLE & psoriatic arthritis are usually asymmetric
o Psoriatic: peripheral joint (>5), pauciarticular asymmetric arthritis or DIP joints only; inflammation of joints,
periosteum, along tendons, and bone insertion points sausage digits (also seen with Reiter syndrome)
Rheumatic fever: symmetric polyarthritis, 6-8 wks
Reactive arthritis: follows a GI or GU infection w/ salmonella, shigella, campylobacter, Yersinia, or chlamydia
Reiter syndrome: arthritis, uveitis, urethritis
o Can follow chlamydia infection; a/w HLA-B27
Ankylosing spondylitis: occurs in young men; morning stiffness, worse w/rest; sacroiliitis w/sclerosis around
sacroiliac joints
dx: aspiration of joint fluid for gram stain, culture, cell count, crystal analysis; radiograph, possible biopsy
non-inflammatory exudate: WBC <1000-2000, <25-50% PMNs
synovial fluid WBC: normal (0-200), OA (200-2000), inflammatory (2000-50,000), septic (>50,000)
tx: start empiric antibiotics until diagnostic results are back
infections: drainage of fluid, IV antibiotics (started for all inflammatory arthritis)
o steroids cant be used until infection is r/o
o gonorrhea IV ceftriaxone; staph aureus nafcillin or vancomycin
crystals: colchicine, NSAIDs, or corticosteroids
open surgical drainage or arthroscopy if joint fluid is loculated, or if located in shoulders/ hips/ sacroiliac joints
o gout
d/t accumulation of monosodium urate crystals from a defect in urate metabolism
overproduction: increased cell turnover (myeloproliferative disorders (polycythemia vera); cancer, hemolysis,
psoriasis, chemo), enzyme deficiency (lesch-nyhan syndrome, glycogen storage disease); alcohol
decreased excretion: renal insufficiency, ketoacidosis/lactic acidosis, drugs (thiazides, asprin, niacin)
sx: podogra (arthritis of the 1
metatarsophalangeal joint= big toe); pain, redness, tenderness of joint; +/- fever
tophi= tissue deposits of urate crystals
uric acid kidney stones
dx: aspiration of joint (negative birefringent needle shaped crystals (yellow), crystals intracellular in PMNs, increased WBCs of
neutrophils); elevated uric acid level, elevate ESR and WBC in acute attack; x-ray of joint (normal or erosion; punched out erosion
with a rim of cortical bone)
1: asymptomatic hyperuricemia
2: gouty arthritis: often at night in 1
MTP joint, ankle, or knee w/ rapid progression, lasts hrs-wks
o tx: NSAID (indomethacin; #1); oral colchicine, steroids if other tx contraindicated (renal insufficiency)
Colchicine SE: diarrhea, bone marrow suppression neutropenia; contraindicated in renal
steroids: injection for single joint, oral for multiple joints
3: intercritical gout (period between attacks): asymptomatic
o tx: decrease uric acid levels: avoid organ rich foods & alcohol, avoid thiazides, Probenecid or sulfinpyrazone
to increase urine excretion (uricosuric), allopurinol to decreased production; weight loss
low dose colchicine during treatment initiation to prevent an acute attack
uricosuric drug SE: HSR, contraindicated in renal insufficiency
allopurinol SE: HSR, TEN, steven johnson syndrome
4: chronic tophaceous gout; usually >10 yr after acute intermittent gout; chronic swelling & discomfort ath increases in
time, subcutaneous tophaceous deposits of monosodium urate
o tx: acute tx + allopurinol; surgery if nerve compression, joint deformity, or chronic skin ulceration + infection
o pseudogout (calcium pyrophosphate deposition disease)
d/t accumulation of calcium pyrophosphate dehydrate crystals
risk factors: hemochromatosis, hyperparathyroidism
a/w DM, hypothyroidism, Wilson disease
sx: affects large joints (knees, wrists)
dx: joint aspiration=arthrocentesis (short & rhomboid weakly positive birefringent crystals (blue in polarized light), elevated
WBC count); x-ray (calcification of cartilaginous structures and degenerative joint disease); chondrocalcinosis or linear calcium
deposits in joint
acute attack: NSAIDs; if no response intraarticular steroids (triamcinolone)
if recurrent attacks colchicine prophylaxis
o rheumatoid arthritis
autoimmune; inflammatory; a/w HLA types; joint deformity d/t chronic synovitis pannus formation damage to all structures
surrounding the joint (cartilage destruction and erosion of periarticular bone, damage to ligament & tendons)
more common in young women; onset age 30-50 yo
sx: bilateral symmetric erosive polyarticular arthritis (multiple small enflamed joints; PIP, MCP, wrist, knee, ankle), morning
stiffness that gets better with use (>30 min stiffness), ulnar deviation of MCP joints, radial deviation of wrist, swan-neck
deformities, boutonniere deformity, rheumatoid nodules, Bouchard nodes (PIP enlargement)
extraarticular sx: vasculitis lesions ischemic ulcers, keratoconjunctivitis sicca (Sjogren syndrome), sicca syndrome
(dry mucous membranes), episcleritis, interstitial lung disease (pleural effusion, nodules of lung parenchyma), cardiac
(pericarditis), neuro (myelopathy, spinal cord compression from subluxation of disk), carpal tunnel syndrome, anemia
of chronic disease, baker cyst (d/t inflamed synovial fluid excess fluid production), cervical joint involvement
(esp C1/C2 subluxation; neck pain, stiffness, hyperreflexia), fatigue, fever, increased risk of developing osteopenia
& osteoporosis
felty syndrome: RA, splenomegaly, neutropenia; leucopenia, lymphadenopathy, thrombocytopenia
Caplan syndrome: RA, pneumoconiosis (restrictive lung disease), lung nodules
arthritis affects >3 joints: elbow, wrists, MCP or PIP joints (DIP spared), knee, ankle, or MTP
rheumatoid nodules: subcutaneous nodules on extensor surface of proximal ulna or other pressure points
(juxtaarticular regions)
dx: increased ESR, rheumatoid factor (IgM anti-IgG), ANA titer, x-ray; arthrocentesis to obtain synovial fluid if dx unclear (r/o
infection or crystal disease); anti-cyclic citrulinated peptide (anti-CCP), normocytic anemia
diagnostic criteria (6+ = RA): joint involvement (up to 5 pts), elevated ESR or CRP (1 pt), duration >6 wks (1 pt), RF for
anti-CCP (1pt)
x-ray: periarticular bone & cartilage destruction (periarticular osteopenia) w/loss of joint space & joint margin
erosions; joint space narrowing, subchondral polysclerosis, marginal osteophyte formation, cyst formation
o obtain cervical x-ray before any surgery to assess for cervical subluxation (intubation risk)
acute sx (pain control): NSAIDS or COX-2 inhibitors (celecoxib), low dose corticosteroids (if NSAIDs not effective before
DMARDS onset of action)
disease modifying anti-rheumatic drugs (DMARDs):
Drug Side effects
methotrexate (#1) Toxic to liver, bone marrow, lungs
hydroxychloroquine (for mild disease) Toxic to retina (screen with dilated eye exam)
sulfasalazine Bone marrow toxic, hemolysis with G6PD
deficiency, rash, oligospermia
TNF antagonists (etanercept, infliximab, adalimumab) Reactivation of TB, infection
Rituximab (removes CD20 lymphocytes) Infection
Gold salts (oral or parenteral gold) Nephrotic syndrome
o other DMARDs: leflunomide, abatacept, penicillamine
If refractory to other tx immunosuppressives (azathioprine, leflunomide, cyclosporine, cyclophosphamide)
o Juvenile rheumatoid arthritis or adult still disease
Sx: high spiking fever (>104F) in a young pt + rash (salmon colored, chest & abdomen); splenomegaly, pericardial effusion, mild
joint sx
Dx: clinical; anemia, leukocytosis
Tx: aspirin or NSAIDs; if no response steroids
o Osteoarthritis (degenerative joint disease)
Loss of articular cartilage in weight bearing joints; noninflammatory
sx: arthritis (pain worsens with activity), mild morning stiffness (<15-30 min; relieved with rest), Heberden nodes (DIP
enlargement); crepitations in involved joint
involves DIP joints & large weight bearing joints(knee, hip, ankle)
complications: lumbar spinal stenosis, baker cyst
dx: x-ray of joint(degenerative joint space narrowing, osteophytes, dense subchondral bone d/t subchondral sclerosis, bone
tx: weight loss, moderate exercise, acetaminophen for pain (if not effective NSAIDs; if not effective intraarticular steroids);
joint replacement if severe disease
o septic arthritis
agents: staph (#1), strep, gram (-) rods
most common post-op organism following artificial joint placement=staph epidermidis
RF: damaged joint (prosthetic joint> RA> osteoarthritis
synovial lining has no BM, so bacteria and antibiotics easily cross
sx: warm, red, immobile joint, often palpable effusion; if bacteremia fever & chills
dx: arthrocentesis (WBC>50,000 cells, neutrophils predominant; gram stain, fluid culture), blood cultures; get x-ray or CT scan for
possible prosthetic joint infection
tx: empiric tx with ceftriaxone + vancomycin
gram (-) bacilli: quinolones, aztreonam, cefotaxime, piperacillin, aminoglycosides
gram (+) cocci: oxacillin, nafcillin, cefazolin, piperacillin + tazobactam
o resistant gram (+) cocci: linezolid, daptomycin, tigecycline
prosthetic joint infection: remove the joint, treat for 6-8 wks with antibiotics, then replace the joint
o gonococcal arthritis
#1 infectious arthralgia in pt <40yo (young sexually active person); more frequent during menses
sx: asymmetric polyarthritis=migratory arthralgias & tenosynovitis (wrist/hands 1
), pustular skin lesions, petechial rash; can
also be purulent monoarthritis
joint is warm, tender; a/w mild fever
dx: culture of urethra, cervix, rectum, or pharynx (joints are often sterile); also culture/ gram stain the joint fluid, blood
cultures; inflammatory exudate in joint (WBC >50,000)
tx: IV ceftriaxone, cefotaxime, or ceftizoxime as empiric tx; quinolones only if sensitive
if recurrent gonorrhea infection test for terminal complement deficiency
seronegative spondyloarthropathies
o usual onset in male <40 yo; a/w HLA-B27
(-) rheumatoid factor
o sx: joint pain (involving spine and large joints), enthesopathy (inflammation where tendons and ligaments attach to bones), uveitis
o ankylosing spondylitis
M>F 20-30 yo
sx: low back pain and stiffness that radiates down the buttocks (pain relieved by activity), flattening of normal lumbar curvature
(eventually fusion of vertebral joint via bridging syndesmophytes; bamboo spine), decreased chest expansion, enthesopathy of
achilles tendon
other possible sx: transient arthritis, of knee/hip/shoulders, anterior uveitis, AV block, aortic insufficiency, increased
risk of aortic regurg (secondary to scarring of aortic valve cusps, increased risk of vertebral fracture with minor
trauma (d/t decreased bone mineral density)
dx: x-ray of sacroiliac joint (best initial; narrowing of sacroiliac joints, bilateral sacroilitis), MRI (most accurate); elevated ESR
tx: exercise, NSAIDs; if ineffective anti-TNF (etanercept, adalimumab, infliximab)
o psoriatic arthritis
sx: preceding psoriasis, sacroiliac joint involvement, sausage digits from enthesopathy, nail pitting
dx: elevated ESR, x-ray of joint (pencil in a cup deformity, bony erosion, irregular bone destruction), elevated uric acid (d/t
increased skin turnover)
tx: NSAIDs methotrexate (severe dz or if NSAIDs not effective) anti-TNF
o reactive arthritis (Reiter syndrome)
secondary to IBD, sexually transmitted infection, GI infection (Yersinia, campylobacter, salmonella)
sx: joint pain, ocular sx (uveitis, conjunctivitis), genital sx (urethritis, balanitis); keratoderma blennorrhagicum (looks like pustular
cant pee, cant see, cant climb a tree
dx: clinical; tap hot swollen joints to r/o infections
tx: NSAIDs; if ineffective sulfasalazine
o soft tissue swelling & tenderness; joint movement limited by active movement but not passive movement
o young women with chronic musculoskeletal pain and tenderness with trigger points of focal tenderness at trapezius, medial fat pad of the
knee, and lateral epicondyle
o sx: pain at many sites (neck, shoulders, back, hips); stiffness, numbness, fatigue, headaches, sleep disorder
o dx: clinical
o tx: amitriptyline (best initial), milnacipran, pregabalin; trigger point injections with local anesthetic
milnacipran: inhibitor of Serotonin and NE reuptake
polymyositis and dermatomyositis
o polymyositis: proximal muscle weakness (esp getting up, walking up stairs); some have pain & tenderness
o dermatomyositis: malar involvement, shawl sign (erythema of face, neck, shoulders, upper chest, and back), heliotrope rash (swollen purple
eyelids), gottron papules (scaly patches on the back of hands, esp PIP and MCP joints), proximal muscle weakness w/ normal
sensation and reflexes
a/w cancer in 25% (ovary, lung, GI, lymphoma)
muscle involvement d/t damage of muscle fibers (inflammation, necrosis, fiber atrophy, or antibody-mediated damage)
o dx: CPK and aldolase (best initial), muscle biopsy (most accurate); anti-Jo antibody a/w lung fibrosis
possible positive/elevated: ANA, rheumatoid factor, ESR, CRP
MRI show patchy muscle involvement; electromyography is often abnormal
o Tx: steroids; if not responsive methotrexate, azathioprine, IV immunoglobulin, or mycophenolate
Hydroxychloroquine helps with skin lesions
carpal tunnel syndrome
o compression of the median nerve as it passes under the flexor retinaculum
a/w overuse of the hand/wrist, pregnancy, DM, rheumatoid arthritis, acromegaly, amyloidosis, hypothyroidism
o sx: pain along the median nerve distribution in hand (palmar side of thumb, index finger, half of ring finger; pain worse at night), atrophy of
the thenar eminence
tinel sign: tapping median nerve reproduces sx
phalen sign: flexion of the wrists at 90 degrees reproduces sx
o dx: clinical; electromyography or nerve conduction testing
o tx: wrist splints, avoid manual activity, NSAIDs; steroid injection if splints & NSAIDs not effective; surgical decompression curative
dupuytren contracture
o hyperplasia of palmar fascia contracture of 4
& 5
o RFs: genetic, alcoholism, cirrhosis
o Tx: triamcinolone injection; surgical release
Rotator cuff injury
o Rotator cuff tendonitis/ impingement
d/t repetitive activity above shoulder height
Sx: shoulder pain aggravated by activities such as reaching or lifting the arm over the head
Dx: neer test (passive motion of the arm above the head pain and guarding), improvement of ROM after lidocaine
injection into the joint
o Rotator cuff tear
d/t trauma (falling on an oustreated hand) or as the end result of chronic impingement and tendonitis
Sx: inability to flex or abduct the shoulder; limited mid arc abduction and external rotation;, pain in shoulder when lying
on it, tenderness at supraspinatus insertion
o Dx: MRI
o Tx: NSAIDs, rest, physical therapy; if ineffective steroids; if ineffective or complete tear surgery
Patellofemoral syndrome
o Anterior knee pain secondary to trauma, imbalance of quadriceps strength, or meniscal tear
o Sx: pain walking up/down stairs, pain worse when walking after sitting a prolonged period but decreases after walking
Crepitus, joint locking, instability
o Dx: clinical
o Tx: physical therapy and strength training with cycling
No knee brace or surgery
Achilles tendonitis
o Sx: posterior heel pain on the achilles tendon insertion site or on the tendon itself; pain with palpation and passive dorsiflexion of the ankle
o Tx; rest, analgesics, stretching/strengthening exercises
Retrocalcaneal bursitis
o Bursae are located between the posterior calcaneus and the achilles tendon, and between the achilles tendon and the skin
o Sx: posterior heel pain secondary to chronic irritation of the underlying bursae
Plantar fasciitis
o d/t repetitive use or excessive loading (ex. Training for marathon)
o Sx: gradual onset pain at the bottom of the foot near calcaneus (point tenderness at fascia insertion on the calcaneus; worse in the morning
and after prolonged sitting, improves with walking)
o Dx: clinical (marked tenderness over the medial calcaneal tuberosity, increased pain with passive dorsiflexion of the toes)
o Tx: stretching exercises, arch supports (orthotics), NSAIDs, night splinting; if ineffective steroids; surgical release (rarely needed)
Calcaneal stress fracture
o Occur in athletes in running or jumping sports; pt with RF for osteopenia
o Sx: diffuse heal pain that is worse by medial and lateral compression
Tarsal tunnel syndrome
o Tarsal tunnel is on the medial aspect of the help; formed by the flexor retinaculum traversing over the talus and calcaneus
o Sx: pain that worsens with use; pain, burning, tingling, or numbness that can radiate to the plantar heel or to the distal sole and toes
Sx exacerbated by percussion of the tarsal tunnor or with dorsiflexion and eversion of the foot
low back pain
o differential dx:
musculoskeletal low back or leg pain: lumbar sprain or strain, degenerative disk disease, herniated disk, spinal stenosis, trauma,
congenital disease (kyphoscoliosis), spondylitis
referred or visceral pain: pelvic disease, renal disease, aortic aneurysm, GI disease
non-mechanical low back pain: neoplasia, infection, inflammatory arthritis, paget disease, cauda equina syndrome
o dx: H& P (test strength, sensation, refluxes), Patrick maneuver (hip external rotation + knee flexion over the other leg making a 4 while
examiner pushes on flexed knee & opposite side of pelvis helps distinguish pain from sacroiliac joint), x-ray, CT scan or MRI
red flags to indicate imaging: >50 yo, hx of cancer, unexplained weight loss, pain >1mo, nighttime pain causing difficulty
sleeping, no response to previous tx, neuro sx
1) x-ray: assess lytic lesions and compression fractures
2) MRI>CT: assess for cancer, infection, disc disease
o tx:
any acute mechanical back pain w/o neuro deficit 4-6 wks of early mobilization, NSAIDs, muscle relaxants
MRI or CT if not responsive or sudden neuro deficit
o musculoskeletal pain
lumbosacral strain #1 cause of back pain; starts after physical exertion
sx: local tenderness & contraction of the paraspinal muscles
pain doesnt radiate, normal neuro exam, (-) straight leg test
tx: encourage continuing usual activities, avoid twisting motions or heavy lifting, NSAIDs or other non-narcotic analgesics,
narcotics only if severe pain & only use short term, muscle relaxant, massage, acupuncture, weight loss, back strengthening
exercises; f/u in 4 wks
if symptoms do not improve in 6 wks, consider imaging studies, referral to surgeon
prevention: keep the back straight while lifting an object, bend at the knees, avoid sleeping on stomach, regular
exercises that avoid repetitive twisting and bending
o cauda equina syndrome
sx: low back pain, saddle anesthesia, bowel or bladder dysfunction; erectile dysfunction, possible lower extremity weakness &
loss of reflexes d/t compression of multiple sacral nerve roots
tx: surgical emergency; surgical decompression
o sciatica
d/t herniated disk, usually L4-L5 or L5-S1
sx: pain in distribution of lumbar or sacral nerve roots +/- motor or sensory deficits; back pain w/radiation down the back of the
leg or lateral foreleg
L4: dorsiflexion of foot, knee reflex, inner calf sensation
L5: dorsiflexion of toe, inner foot sensation
S1: eversion of foot, ankle reflex, outer foot sensation
dx: straight leg test to 45-60 degrees
tx: encourage continuing usual activities, avoid twisting motions or heavy lifting, NSAIDs or other non-narcotic analgesics,
narcotics only if severe pain & only use short term, muscle relaxant, massage, acupuncture, weight loss, back strengthening
exercises; f/u in 4 wks
steroid injection can be tried if no response to conservative management
if symptoms do not improve in 6 wks, consider imaging studies, referral to surgeon
o spondylolysis
defect in part interarticularis (congenital or secondary to stress fracture)
ankylosing spondylitis: occurs in young (<40 yo) males; pain worse at rest/improves with movement, decreased chest mobility
o cord compression (d/t tumor or infection)
sx: vertebral tenderness, decreased sensory level, hyperreflexia below level of compression
dx: spinal imaging (x-ray best initial; MRI > CT with intrathecal contrast)
give glucocorticoids first before dx testing if obvious cord compression in order to decrease cord pressure
cancers that metastasize to bone: lung, breast, prostate, lymphoma, GI, melanoma
multiple myeloma: increased calcium, mild renal failure (increased Cr), anemia
sx: systemic complaints (fever, decreased weight), pain at night or that is not relieved by lying supine; new onset of
pain in pt >50yo
dx: lateral and AP x-ray of spine, ESR, CBC
tx: chemo for lymphoma, radiation for solid tumors
TB osteomyelitis of spine (Pott disease)
Sx: chronic and slowly progressive pain, fever, night sweats
Epidural abscess
Usually d/t staph aureus
Dx: elevated ESR, fever
Tx: steroids, anti-staph antibiotic (vancomycin or linezolid empiric tx; if sensitive, change to beta lactam (oxacillin,
nafcillin, cefazolin) + gentamicin; surgical drainage for large collections
o Lumbar spinal stenosis (neuropathic claudication)
Narrowing of the spinal canal pressure on the cord (esp in back extension d/t cord compression on ligamentum flavum); pt >60
yo; a/w degenerative joint disease (degenerative central canal stenosis)
Enlarging osteophytes at facet joints and hypertrophy of the ligamentum flavum
Sx: pain with walking (esp downhill= back extension; radiates to butt and lateral thighs), may have unsteady gait & leg
weakness when walking
Tx: weight loss, steroid injections; surgical correction to dilate the spinal canal
o Agents: staph aureus (#1), salmonella (sickle cell pt)
Risk factors: IV drug use, sickle cell, immunocompromised
Children obtain infection via hematogenous spread
adults obtain infection via contiguous (nearby) infection (often a/w vascular insufficiency and diabetes)
o diabetes ulcer from peripheral neuropathy or vascular disease; may have a draining purulent sinus tract
in the lesion
o sx:
vertebral osteomyelitis: tenderness to gentle percussion over the spinous process; back pain. Low grade fever, elevated
o dx: x-ray (best initial), biopsy (most accurate); MRI if initial x-ray is normal (bone scan if MRI contraindicated); ESR can be used to f/u
response to therapy, elevated platelets (inflammatory marker); +/- fever or elevated WBC
use MRI 1st for vertebral osteomyelitis
o tx: wait for cultures and treat appropriately; long-term IV antibiotics +/- surgery
staph: oxacillin, cefazolin, nafcillin, or ceftriaxone if sensitive; vancomycin or linezolid if resistant
gram (-) bacilli such as E.coli: fluoroquinolones (ciprofloxacin)
SE: interfere with bone growth (contraindicated in pregnancy and kids), achilles tendon rupture
acanthosis dermatosis (grover disease)
o pruritus, erythematous-brown keratotic papules over the anterior chest, upper back, and lower rib cage
acanthosis nigricans
o symmetrical hyperpigmented velvety plaques in the axilla, groin, and neck
a/w insulin resistance (diabetes mellitus, addisons disease, polycystic ovarian syndrome, obesity); GI malignancy in older pts
acrochordons (skin tags)
o multiple skin tags a/w insulin resistance, pregnancy, or crohns disease (perianal)
actinic keratosis
o pre-malignant lesion (predisposes to SCC); occur in sun-exposed areas
o dry scaly flat papules with an erythematous base; sandpaper-like texture; hyperkeratosis can become prominent cutaneous horns
o dx: acanthosis (thickening of epidermis), parakeratosis (retention of nuclei in stratum corneum), dyskeratosis (abnormal keratinization),
hyperkeratosis (thickening of stratum corneum)
o d/t C1 esterase inhibitor deficiency increased C2b and bradykinin
hereditary or d/t ACE inhibitor use (-pril); C1q normal in hereditary and low in acquired, C4 down in all forms
o sx: rapid onset of non-inflammatory edema of the face/limbs/genitals, laryngeal edema, edema of the bowel colicky abdominal pain
episodes usually follow an infection, dental procedure, or trauma
atopic dermatitis
o usually in infancy; involves cheeks, forehead, limbs
o sx: pruritus is usually the only sx
basal cell carcinoma
o most common malignant tumor of the eyelid (thinning or loss of eyelashes in the region of the tumor; bleeding and ulceration can occur)
tx: surgical excision using microscopically controlled margins (Mohs technique)
spread from a periocular BCC into the orbit can occur tx= enucleation of the eye
o slow-growing papule with pearly rolled border, and overlying telangiectasia
o dx: invasive clusters of spindle cells surrounded by palisaded basal cells
blue nevi
o smooth-surfaced, dome-shaped melanocytic papules that develop from macules; <1cm diameter
blue color d/t the depth of the melanin in the skin
bullous pemphigoid
o pt usually >60 yo
triggers: furosemide, NSAIDs, captopril, penicillamine, antibiotics
o pruritic disease; tense blisters in flexural areas; urticarial plaques
does NOT involve mucous membranes
o dx: IgG and C3 deposits at the dermal-epidermal junction (against the hemidesmosomes); subepidermal bulla with eosinophils
capillary hemangioma
o can be found in deep tissues and the viscer (sp. Liver)
thin walled BVs with narrow lumens willed with blood and separated by connective tissue; vessels are lined by endothelium that
rapidly proliferates during the growth phase of the tumor
o strawberry (infantile, capillary) hemangioma
variant of capillary hemangioma=most common benign vascular tumor in children; appear w/in the first few days-weeks of birth
and grow rapidly during the first 1-2 yrs of life
superficial: bright red compressible plaques with sharply demarcated borders
deeper: duskier blue appearance
tx: reassurance; most self-resolve by 5-8 yo
cavernous hemangiomas
o soft blue compressible masses up to a few cm in size
large dilated vascular spaces; can appear on skin, mucosa, deep tissues, and viscera
a/w with von Hippel-Lindau disease when in the brain or viscera
cherry hemangioma/ senile hemangiomas
o most common benign vascular proliferation in adults; appear 30-40 yo
o small bright red cutaneous papules
dilated capillaries and post-capillary venules in the papillary dermis that do not repress spontaneously
cold injuries
o frostbite
tx: rapid rewarming with warm water
contact (irritant, allergic) dermatitis
o type 4 HSR: a/w hx of exposure to irritant substance (plant uroshiol (poison ivy/oak/sumac=woody scrub, ginko fruit, mango skin),
cosmetics, formaldehyde, fragrances, preservatives, rubber, nickel)
initial sensitization occurs w/in 10-14 days of exposure
o pruritus, erythema, edema, vesicles & bullae; can be secondarily infected (impetiginized by staph or strep)
o tx: avoid exposure, calamine lotion, topical antihistamines, topical corticosteroids, oral steroids
dermatitis herpetiformis
o a/w gluten sensitive enteropathy (celiac sprue or celiac disease), HLA B8/DR3/DQw2
o pruritic papules and vesicles on elbows, knees, buttocks, posterior neck, scalp
o dx: anti-endomysial antibodies
o tx: dapsone
erythema multiforme
o a/w recent herpes simplex infection
o most acral in distribution
hypersensitivity reactions
o antibody mediated (type 2): immune hemolytic anemia, Rh hemolytic disease of the newborn
o immune complex- mediated (type 3): serum sickness
o cell-mediated (type 4): tuberculin skin test, allergic contact dermatitis
latent period of 1-2 days before dermal inflammation
ichthyosis vulgaris
o normal skin at birth with gradual progression ot dry scaly skin; skin is dry & rough with horny plates of the extensor surfaces of the limbs;
condition worsens in the winter d/t dryness; lizard skin
Kaposi sarcoma
o a/w HHV8 infection
o Reddish purple dark vascular plaques or nodules on cutaneous or mucosal surfaces
o low-grade malignancy; pathologically resembles SCC
o solitary, firm, round, skin colored or reddish plaque nodule with central keratin plug (vocano-like nodule)
lentigo simplex
o round or oval macule with even pigmentation; d/t intraepidermal melanocyte hyperplasia
lichen planus
o inflammatory; pruritic violaceous flat-topped papules with fine white streaks on the surface (wickhams striae)
lichen simplex chronicum
o d/t chronic scratching, picking, or rubbing of the skin
o thickened plaques on the skin with increased skin markings and hyperpigmentation, or thickened papules with excoriated centers
o most common malignancy in women 25-29 yo
o risk factors: fair skin, hx of blistering sunburns, family hx, dysplastic nevus syndrome, atypical nevi and >100 typical nevi
o solitary lesion; mole that has changed in size or color, and becomes symptomatic (pruritic, painful, bleeding)
asymmetry, border irregularities, color variations, diameter >6mm, enlargement
o dx: excisional biopsy w/ narrow margins
o tx: if depth <1mm excision with a 1cm free margin; >1mm sentinel lymph node study
miliaria (heat rash)
o superficial aggregated small vesicles, papules, or pustules over the trunk; burning & itching
neurocutaneous diseases
o tuberous sclerosis
sx: neuro sx (seizures, progressive psychomotor retardation, slowly progressive mental deterioration), skin sx (adenoma
sebaceum, shagreen patches, ash leaf patches), retinal lesions, cardiac rhabdomyomas
adenoma sebaceum: reddened facial nodules
shagreen patches: leathery plaques on the trunk
ash lead patches: hypopigmented areas
tx: seizure control
o neurofibromatosis (von Recklinghausen disease)
sx: neurofibromas, 8
CN tumors, caf au lait spots (cutaneous hyperpigmented lesions), meningioma and gliomas
neurofibromas: soft, flesh colored lesions attached to peripheral nerves
tx: 8
CN lesions may need surgical decompression to help preserve hearing
o sturg-weber syndrome
sx: port-wine stain of face, seizures, CNS (homonymous hemianopsia, hemiparesis, mental subnormality)
dx: skull x-ray (calcification of angiomas)
tx: control seizures
o d/t niacin deficiency
o sx: dermatitis, diarrhea, dementia
pemphigus vulgaris
o blistering of skin & mucous membranes; (+) nikolskys sign
o dx: IgG deposits intercellularly in the epidermis (autoantibodies against desmoglein)
o tx: steroids, immunosuppressive agents (azathioprine, prednisone, methotrexate)
o porphyria cutanea tarda
deficiency of uroporphyrinogen decarboxylase (in heme synthesis pathway)
painless blisters, increased skin fragility on the dorsal surfaces of the hands, facial hypertrichosis & hyperpigmentation
triggers: ethanol, estrogens, hep C infection
dx: elevated urinary porphyrin
tx: phlebotomy, hydroxychloroquine, interferon alpha
o salmon colored patches, silvery scales over the extensor surfaces of the elbows, knees, scalp, and trunk
pyoderma gangrenosum: a/w inflammatory bowel disease
o most common 30-60 yo
o rosy hue (flushed skin) with telangiectasia over the cheeks, nose, and chin; papules and pustules may be present
flushing precipitated by hot drinks, heat, emotion
o tx: topical metronidazole for the papules/pustules
seborrheic dermatitis
o a/w parkinsons disease, HIV
o acute or chronic papulosquamous dermatitis; dry/waxy scales and underlying erythema
usually involves: scalp, central face, presternal, interscapular area, umbilicus, and body folds
o tx: topical antifungal agents
seborrheic keratosis
o seen in elderly pts
o greasy brown crust-like lesions with a stuck on appearance
spider angiomas
o a/w pregnancy, liver disease, pt with estrogen supplements (OCPs)
o dilated cutaneous arterioles; central papule with radiating blanching capillaries
squamous cell carcinoma
o aggressive, metastasizes frequently
risk factors: exposure to sunlight (#1), arsenic, aromatic hydrocarbons, chronic osteomyelitis, chronic scars
o total depigmentation d/t autoimmune destruction of melanocytes
a/w other autoimmune diseases: pernicious anemia, autoimmune thyroid disease such as graves or chronic autoimmune
thyroiditis, type 1 DM, primary adrenal insufficiency, hypopituitarism, alopecia areata
peak age 20-30
o macular depigmentat that involves acral and peri-orifical areas
drug induced rashes/reactions
o agents: PCNs, sulfa drugs (thiazides, furosemide, sulfonylureas), allopurinol, phenytoin, lamotrigine, NSAIDs
o morbilliform rash=mild
o erythema multiforme: multiple target lesions that can be confluent; can also be d/t herpes or mycoplasma
tx: prednisone
o phototoxic drugs: tetracyclines (esp. doxycyline)
exaggerated sunburn reaction with erythema, edema, and vesicles over sun-exposed areas
o >30% of the body surface area is involved
o steven johnson syndrome (erythema multiforme major) & toxic epidermal necrolysis (TEN)
immune complex mediated HSR
drugs: sulfonamides (TXM-SMX), NSAIDs, anticonvulsants (phenytoin), barbiturates
Steven johnson syndrome
sudden onset mucocutaneous lesions over 2 sites (usually oral and conjunctival); epidermal necrolysis syndrome;
includes mucosal surfaces; target appearance of lesions; fever, tachycardia, hypotension, altered consciousness,
conjunctivitis, seizures, coma can occur
o respiratory epithelium involvement respiratory therapy
<10% of body surface is involved
tx: supportive, IVIg
toxic epidermal necrolysis (TEN)
rash of skin & mucous membranes; severe mucocutaneous exfoliate disease; erythematous morbilliform eruption that
rapidly evolves into exfoliation of the skin; positive nikolskys sign; painful blisters in oral mucosa
tx: IVIg
warfarin-induced skin necrosis
o a/w protein C deficiency
o sx: pain, bullae formation, skin necrosis
breast, buttocks, thighs, and abdomen commonly involved
o tx: vitamin k; d/c warfarin if lesion progress & replace with heparin
soft tissue infections general info
o Sx:
Signs of systemic toxicity: fever or hypothermia, HR>100, systolic BP <90 or 20 mmHg below baseline
Necrotizing infections: pain disproportionate to PE, violaceous bullae, cutaneous hemorrhage, skin sloughing, skin anesthesia,
rapid progression, gas in tissue
o Dx: clinical assessment
if signs of systemic toxicity blood cx, drug susceptibility, CBC w/ diff, creatinine, bicarb, creatine phosphokinase, CRP
f/u with gram stain & cx of needle aspiration or punch biopsy
plain film or MRI if suspicion of deeper infection
o Tx:
Hospitalization: hypotension and/or an elevated creatinine level, low serum bicarbonate level, elevated creatine phosphokinase
level (2 3 times the upper limit of normal), marked left shift, or a C-reactive protein level 113 mg/L
Surgery consult for possible I & D
Staph covering agents: Penicillins (ox-clox-diclox-naf), 2
gen cephalosporins (cefoxitin, cefotetan, cefuroxime), beta lactam-beta
lactamase inhibitor combo (amoxicillin or ticaracillin/clavulanate, ampicillin/sulbactam, piperacillin/tazobactam), Carbapenem
(imipenem, meropenem)
Erysipelas, cellulitis, hair follicle infections (folliculitis, furuncle, carbuncle)
Mild: oral dicloxacillin, cephalexin, cefadroxyl
o If PCN allergy: erythromycin, clarithromycin, clindamycin
o If MRSA: doxycycline, clindamycin, or TMP/SMZ
Severe (systemic sx): IV oxacillin, nafcillin, or cefazolin
o If PCN allergy: clindamycin, vancomycin
o If MRSA: vancomycin, linezolid, daptomycin, tigecycline
f/u 24-48 hrs to assess clinical response
o erysipelas
deeper skin infection, can invade dermal lymphatics & cause bacteremia; cellulitis confined to the dermis and lymphatics
agents: Strep (s.pyogenes)> staph
risk factors: lymphatic obstruction, local trauma or abscess, fungal infections, DM, alcoholism
sx: bright red hot swollen lesion (fiery red tender painful plaque w/ well demarcated edges); leukocytosis, fever, chills if
complications: sepsis, local spread, necrotizing fasciitis
tx: uncomplicated IM or oral PCN or erythromycin, otherwise same as cellulitis
o cellulitis
infection of dermis & subcutaneous tissue
agents: staph>strep (group A=beta hemolytic=pyogenes)
chronic fungal foot infection can serve as a nidus for bacterial cellulitis (should be eradicated in recurrent cellulitis)

Means of bacterial invasion Likely pathogen
wounds, abscesses staph aureus
local trauma, breaks in skin step pyogenes (group A strep)
acute sinusitis haemophilus influenzae
immersion in water pseudomonas aeruginosa, aormonas hydrophila, vibrio vulnificus
risk factors: breaks in skin venous stasis diseases, lymphedema, diabetic ulcers
sx: warm red swollen tender skin, +/- fever
orbital involvement= medical emergency
signs of toxicity: high grade fever w/ rigors & chills, malaise, fatigue, confusion
Tx: staph PCN or cephalosporin; start IV antibiotics until signs of infection improvement, then follow up oral antibiotics for 2
if signs of toxicity IV nafcillin or cefazolin; oral dicloxacillin for mild cellulitis
o hair follicle infections: folliculitis, furuncles, carbuncles
agents: staph aureus
folliculitis: pus is limited to the epidermis
furuncle (boil): small abscess
carbuncles: collection of furuncles; diabetic pt at increased risk
o comedones (blackheads & whiteheads) nodulocystic & scarring
o tx:
mild: topical retinoids or topical benzyl peroxide
if ineffective topical erythromycin or clindamycin
mild-moderate: topical vit A (tretinoid, adapalene, tazarotene) or benzyl peroxide + topical antibiotic (erythromycin, clindamycin,
if ineffective oral antibiotic (minocycline or doxycycline)
moderate-severe: oral doxycycline against Propionibacterium acnes + oral vit A (isotretinoin)
vit A SE: teratogenic (oral or topical), hyperlipidemia (oral)
nodulcystic & scarring acne (oral isotretinoin)
cutaneous abscesses
o collection of pus w/in the dermis and deeper skin tissues; painful, tender, fluctuant red nodules (start as pustule surrounded bya rim of
erythematous swelling)
o agents: usually polymicrobial of skin & adjacent mucous membrane flora
o tx: incision & drainage with dry dressing
Gram stain, culture, and systemic antibiotics are rarely necessary
herpes zoster (shingles)
o d/t varicella zoster virus latent infection (initial infection=chicken pox); latent infection in the sensory dorsal root ganglia
o sx: pain precedes vesicular eruption by ~48 hrs; eruption along the affected dermatome; eruption lasts 2-3 wks
o tx: acyclovir
herpetic whitlow
o infection of the hand with HSV1 or 2
o sx: throbbing pain in distal pulp space; non-purulent vesicles on the volar surface; systemic sx (fever, lymphadenopathy) can occur
o dx: multinucleated giant cells seen on Tzanck smear
o tx: self-limiting; oral acyclovir and topical bacitracin to prevent secondary infection
o Superficial skin infection
o Agents: staph aureus, strep pyogenes (group A beta-hemolytic strep)
o Sx: weeping, crusting, oozing, draining of skin; pruritis honey colored macules, vesicles, and bullae (skin blisters that enlarge and rupture)
o Tx:
Mild: topical mupirocin, bacitracin, or repatamulin
Severe: oral dicloxacillin or cephalexin
molluscum contagiosum
o agent: poxvirus
a/w cell-mediated immunodeficiency (HIV, corticosteroid use, chemotherapy)
o multiple dome shaped lesions with central umbilication; pink translucent quality and may be arranged in a linear fashion d/t spread of
virus to adjacent skin by scratching (can cause conjunctivitis if lid margins infected)
kids (trunk & extremities), adults (face, lower abdomen, genitals), STD (penis, pubis, inner thighs)
o tx: curettage or liquid nitrogen
pityriasis rosea
o a/w human herpesvirus 7 (HHV7)
o oval fawn colored plaques <2cm in diameter; initial herald patch, followed by general eruption in 1-2 wks; Christmas tree pattern; cigarette-
paper like appearance (crinkled)
o sx: generalized itching, pruritic vesicles & pustules in runs over the finger webs, heels of palms, and wrist creases
o tx: 5% permethrin cream (applied to neck down & left on overnight), topical steroids call be added for dermatitis; 1% lindane solution,
bedding & clothing should be cleared or set aside for 2 weeks
staph scalded skin syndrome
o d/t staph aureus toxins
usually seen in children <6yo
o sx: exfoliation of skin; skin is tender & warm w/ a diffuse erythematous rash that is sandpaper-like; bullae, (+) nikolskys sign, facial edema,
perioral crusting, dehydration
similar presentation to toxic epidermal necrolysis (TEN)
o tx: supportive care, anti-staph meds (oxacillin or nafcillin best; cefazolin)
toxic shock syndrome
o acute febrile illness d/t exotoxin-producing staph aureus
tampon use or other foreign body (ex. Nasal packing ) can predispose to infection
o sx: generalized skin eruption, fever hypotension, vomiting, diarrhea, multi-organ involvement (renal, liver, CNS); diffuse erythema that
starts on the trunk, erythema of palms & soles, strawberry tongue, conjunctival hyperemia; desquamation of palms & soles 1-2 wks later
o tx: supportive care, anti-staph meds (oxacillin or nafcillin best; cefazolin)
o superficial fungal infection; corpis=body, manus=hand, pedis=foot, cruris=groin, capitis=hair, unguium=nail
tinea corporis (body ringworm)
agents: dermatophyte (trichophyton rubrum)
ring-shaped lesions with advancing scaly distinct border and central clearing, or scaly patches over the trunk;
dx: KOH prep (hyphae)
tx: topical 2% antifungal lotions (terbinafine) or systemic griseofulvin
tinea versicolor (malassezia furfur)
superficial fungal infection of the skin; pale velvety pink or white hypopigmented macules that do not tan (someimtes
hyperpigmented macules that are velvety-tan or brownish); do not appear scaly but scale on scraping
dx: KOH microscope prep (large blunt hypae and thick walled budding spores; spaghetti and meatballs)
tx: topical selenium sulfide lotion + ketoconazole shampoo
o dx: KOH prep (best initial), fungal cx (most accurate)
o tx:
if not in hair or nails topical antifungal (clotrimazole, ketoconazole, econazole, miconazole, nystatin for yeast only, ciclopirox)
if hair or nails terbinafine or itraconazole
o Inflammation of a lyph node
o Sx: fever, tender lymphadenopathy of regional lymph nodes, red streaking of skin from the wound or area of cellulitis
Complications: thrombosis of adjacent veins, sepsis
o Dx: blood and wound cultures
o Tx: warm compresses, antibiotics (penicillin G, antistaph penicillin, or cephalosporin), wound drainage may be needed
necrotizing infections
o infection of deep soft tissues
o agents: s. pyogenes, clostridium perfringens (gas gangrene), vibrio vulnificus, Aeromonas hydrophila
o risk factors: surgery, diabetes, trauma, IV drug use
o Sx: pain disproportionate to PE, skin discoloration, violaceous bullae, cutaneous hemorrhage, skin sloughing, skin anesthesia, rapid
progression, gas in tissue (crepitus)
Complications: sepsis, toxic shock syndrome, multiorgan failure
o tx: surgical consult for rapid surgical exploration and excision of devitalized tissue; borad-spectrum parenteral antimicrobial therapy
group A strep or clostridium spp: parenteral clindamycin + penicillin
o Community associated MRSA (CA-MRSA) skin & soft tissue infections
Cutaneous abscess incision and drainage
Antibiotics if severe or extensive disease or rapid progression in presence of cellulitis, sx of systemic dz, associated comorbidities
or immunosuppression, extremes of age, abscess in an area difficult to drain, a/w septic phlebitis, lack of response to I&D alone
Out-pt with nonpuruelent cellulitis: empiric tx for GBS for 5-10 days (beta lactam)
Empiric coverage for CA-MRSA: oral clindamycin, trimethoprim-sulfamethoxazole (TMP-SMX), tetracycline
(doxycycline or minocycline), linezolid
To cover both CA-MRSA and GBS: clindamycin, TMP-SMX, tetracycline + beta lactam (amoxicillin), or linezolid
Hospitalized pt with complicated infection (deeper infection, surgical/traumatic wound infx, major abscesses, cellulitis, infected
ulcers & burns)
Surgical debridement, broad-spectrum antibiotics, empirical tx for MRSA (IV vancomycin, or or IV linezolid, IV
daptomycin, IV televancin, oral clindamycin; beta lactam (cefazolin) can be considered with nonpurulent cellulitis
o Tx 7-14 days
o Recurrence MRSA skin & soft tissue infections
Educate pt on hygiene (personal & close contacts) and wound care
Decolonization may be considered in selected cases if despite optimizing wound care and hygiene measures patient develops a
recurrent SSTI, or ongoing transmission is occurring among household members or other close contacts
Nasal decolonization with mupirocin twice daily for 510 days +/- topical body decolonization regimens with a skin
antiseptic solution (eg, chlorhexidine) for 514 days or dilute bleach baths. (For dilute bleach baths, 1 teaspoon per
gallon of water [or 14 cup per 14 tub or 13 gallons of water] given for 15 min twice weekly for 3 months can be
considered.) (C-III).
Oral antimicrobial therapy is recommended for the treatment of active infection only and is not routinely recommended
for decolonization
o An oral agent in combination with rifampin, if the strain is susceptible, may be considered for decolonization
if infections recur despite above measures
Screening cultures prior to decolonization are not routinely recommended if at least 1 of the prior infections was documented as
due to MRSA
Surveillance cultures following a decolonization regimen are not routinely recommended in the absence of an active infection
oral or vaginal candidiasis
o dx: clinical; KOH prep, fungal dx
o tx: topical antifungal
o animal bites: mix of aerobic & anaerobic spp; Pasteurella spp (#1), staph aureus, bacteroides tectum, fusobacterium, Capnocytophaga,
tx: oral amoxicillin-clavulanate or IV ampicillin-sulbactam, or ertapenem
If mild PCN allergy: cefoxitin or cabapenem
If Severe PCN allergy: oral or IV doxycycline, TMP-SMZ, or fluoroquinolone + clindamycin
o Human bites: mix of aerobic & anaerobic; streptococci, staph aureus, Eikenella corrodens, Fusobacterium peptostreptococcus, prevotella,
Porphyromonas spp
Tx: IV ampicillin-sulbactam or cefoxitin
Animal associated infections
o Bacillus anthracis, Francisella tularensis, Yersinia pestis
o Tx: doxycycline or ciprofloxacin
If tularemia: aminoglycoside (streptomycin or gentamicin) for 7-10 days; if mild doxycyline or tetracycline for 14 days
If bubonic plaque: streptomycin, tetracycline, or chloramphenicol for 10-14 days
Isolated for 48 hrs after starting tx b/c they may develop pneumonic plague
Cat scratch disease (Bartonella henselae)
o Tx: azithromycin
Cutaneous bacillary angiomatosis
o d/t Bartonella (gram (-) bacillus)
o Bright red firm friable exophytic nodules in an HIV infected pt
o Tx: oral erythromycin or doxycycline for 4 wks
Genetic disease/syndromes
Cystic fibrosis
o Autosomal recessive defect in chloride channel protein (CFTR=cystic fibrosis transmembrane conductance regulator) thick viscous
Thick mucous in lung, pancreas, liver, sinuses, intestines, genitourinary tract
Neutrophils cause DNA plugging in airway secretions
o Sx:
Lung: chronic lung disease (cough, sputum, hemoptysis, bronchiectasis, wheezing, dyspnea), recurrent episodes of infection, sinus
pain, polyps
Infections: H. influenzae, Pseudomonas aeruginosa, staph aureus, Burkholderia cepacia
GI: meconium ileus as infant, distal intestinal obstruction, biliary cirrhosis, pancreatic insufficiency (steatorrhea, vit A/D/E/K
malabsorption), recurrent pancreatitis
GU: men (azoospermia, vas deferens missing), women (infertile)
o Dx: increased sweat chloride test (most accurate; chloride >60meq/L; pilocarpine increases Ach increased sweat production)
Possible CXR or CT findings: bronchiectasis, pneumothorax scarring, atelectasis, hyperinflation
o Tx:
Lung disease: antibiotics (inhaled aminoglycosides for CF pt), inhaled recombinant human deoxyribonuclease (rhDNase; breaks
down DNA in mucus plugs), inhaled bronchodilators (albuterol), vaccines (influenza, pneumococcal), lung transplant in advanced
disease not responsive to tx
Other med micro
Actinomyces israelli
o Gram (+) branching bacteria
o Sx:
Cervicofacial actinomycosis: slowly progressive non tender indurated mass multiple abscesses, fistulae, draining sinus tracts
o Dx: yellow sulfur granules in fluid
o Tx: IV penicillin for 6-12 wks
o Tick-borne illness d/t gram (-) bacteria
Endemic in SE, S-central, mid-atlantic, and Midwest reagions of the US; incubation 1-3 ks
o Sx: fever, malaise, myalgias, headache, N/V
Usually no rash; spotless rocky mountain spotted fever
o Dx: leukopenia and/or thrombocytopenia, elevated aminotransferases
o Tx: doxycyline (#1; also covers rocky mountain spotted fever and lyme disease)
HIV infection
o Exposure prophylaxis: draw blood for HIV serology, start antiretroviral therapy with 2-3 drugs while awaiting the results
Prophylaxis usually started with 2 nucleoside reverse transcriptase inhibitors; if a 3
drug is used it is a protease inhibitor
Repeat testing after 6 wks, 3 mo, and 6 mo
o HAART therapy
2 nucleoside analog reverse transcription inhibitors + (nonnucleoside analog reverse transcriptase inhibitor or protease inhibitor)
should not be started during an acute illness
o vaccination
upon diagnosis, pt should receive the following vaccines (as long as CD4 >200 and no AIDS defining illness): influenza,
hep B, Hep A (if men who has sex with men), pneumococcus; Td booster every 10 yrs
if not vaccinated as a child, pt should also receive: MMR, varicella (zoster once >60 yo)
avoid live vaccines (except MMR and varicella/zoster): BCG, anthrax, oral typhoid, intranasal flu, oral polio, yellow fever
o Normal CD4 count is 600-2500 cells/mm3
CD4 <500: recurrent pneumonia, TB, vaginal candidiasis, herpes zoster
CD4 <200: PCP (pneumocystitis jiroveci pneumonia), toxoplasma, cryptococcus, Histoplasma, cryptosporidia
Start prophylactic TMP-SMX (bactrim)
CD4<100 screen for toxoplasmosis (if positive then increased TMP-SMX dose)
CD4< 50: disseminated Histoplasma, MAC (mycobacterium avium-intracellulare), CM retinitis/colitis/esophagitis, CNS lymphoma
Prophylaxis with clarithromycin or azithromycin against MAC
o Lung disease
Community-acquired pneumonia is still most common type in HIV pts (ex. Strep pneumoniae); immunodeficiency just
opens them up to other possible pathogens
Diffuse interstitial infiltrates: PCP, disseminated histoplasmosis, mycobacterium tuberculosis, mycobacterium kansassi
Patchy infiltrates & pleural-based infiltrates: TB, cryptococcal lung disease
Cavitary lesions: TB, PCP, coccidiomycosis
o AIDS defining illness
PCP pneumonias is the most common opportunistic infection in AIDS
Cerebral toxoplasmosis is the most common CNS mass lesion in AIDS

Lyme disease (Borrelia burgdorferi)
o Transmitted via tick bite
o Sx:
Stage 1= early localized (~1 mo after tick bite): flu-like illness (arthralgias, myalgias, fever, headache, headache, fatigue),
erythema migrans
Erythema migrans: annular rash 5-7cm, bulls eye appearance, may have burning/itching/pain
Stage 2= early disseminated (days-months after infection); cardiac (conduction disturbances, myocarditis, pericarditis),
neuro problems (wks-months after primary infection; bilateral facial nerve palsy, fluctuating sx of meningitis w/lymphocytic
pleocytosis and increased protein, mild encephalitis, sensory radiculoneuropathy)
Bennwarth syndrome= radicular pain followed by CSF pleocytosis
Stage 3= late or persistent infection (months-yrs after primary infection); generalized musculoskeletal pain, migratory
polyarthritis, intermittent oligoarthritis of knee (lasts wks-months); tertiary borreliosis subtle encephalitis, neurocognitive
dysfunction, or peripheral neuropathy
o Differential dx: lyme dz, meningitis, Guillain-barre syndrome
o Dx: lumbar puncture to r/o meningitis, serologic tests for antibodies against Borrelia burgdorferi
Serologic tests not (+) until >6 wks after infection
o Tx: 14 days for local skin infection, 21 days for early disseminated, 1 month for arthritis, neuro, or cardiac sx
Stage 1: oral doxycycline (#1); alternatives are amoxicillin, cefuroxime, erythromycin
If pregnant amoxicillin
Stage 2 or 3: IV antibiotics (ceftriaxone, cefotaxime, or penicillin G) if tertiary heart block/other severe heart disease or neuro
o d/t the fungus Rhizopus
o Tx: surgical debridement, IV amphotericin
Rheumatic fever
o d/t group A streptococcus
o sx: erythema marginatum (nonpruritic erythematous papules occurring in polycyclic waves over the trunk sparing the face), strep
pharyngitis migratory polyarthritis, carditis, rheumatic heart disease (10-20 yrs later), chorea, subcutaneous nodules
o tx: aspirin (for inflammation), corticosteroids if carditis, penicillin for pharyngitis
rocky mountain spotted fever
o d/t rickettsia rickettsii
o sx: rash that begins on wrists and ankles and spreads centripetally, appears on palms & soles later; headache, myalgias, abomdinal pain
o tx: doxycycline (#1), tetracycline
if pregnant chloramphenicol
rubella (german measles)
o RNA togavirus
o Fever, malaise, tender suboccipital adenitis after 14-21 days; rash 1-5 days later (maculopapular rash initially on facetrunk &
extremities; lasts <3 days)
maculopapular rash, posterior cervical and posterior auricular lymphadenopathies, polyarthralgia
pt is infectious 1 wk prior to onset of rash to 15 days after
o prevention (live attenuated rubella vaccine), acetaminophen for symptomatic relief
rubeola (measles)
o Paramyxovirus
o Sx: rash that starts head down, cough, coryza, conjunctivitis, Koplik spots
Koplik spots: 1-2mm bluish lesions with an erythematous halo on buccal mucosa
o Tx: supportive; antibiotics for otitis and pneumonia
Staph aureus
o Gram (+) cocci in clusters, coagulase (+)
Strep pneumo
o Gram (+) cocci in pairs (lancet shaped)
Syphilis (treponema pallidum)
o Primary: chancre (nontender ulcer that is nonerythematous with rolled borders and a clean base; nontender inguinal lymph nodes
1wk-3 mo after inocluation
Diff dx of genial ulcers: chancre, chancroid, herpes virus, superficially infected skin lesions
Chancroid: painful exudative ulcer with ragged borders and necrotic base
Herpes: painful grouped vesicles on a red base that eventually ulcerate
o Secondary: local or diffuse pruritic mucocutaneous rash (includes palms & soles), generalize tender lymphadenopathy, condylomata lata (flat
or velvety warts), mucous patches in mouth, patchy hair loss
o Late-stage syphilis (tertiary): proliferative obliterative endarteritis over chronic infection (vasa vasorum in aorta necrosis of the media of
the arterial wall saccular aneurysmal dilations of the aorta); granulomas in skin/liver/bone; gummas if granulomas develop amorphous or
coagulated center; neurosyphilis (tabes dorsalis, Argyll Robertson pupil= accommodates but doesnt react to light)
o Dx: RPR or VDRL to screen; confirm with FTA-ABS (fluorescent treponemal antibody absorption) or MHA-TP (microhemagglutination assay
for Treponema Pallidum); darkfield microscopy if serology (-) but high suspicion (or start empiric tx with penicillin if darkfield not
False (+) RPR and VDRL tests in pts with SLE or during pregnancy
o Tx: IM benzathine penicillin G (1x if infection <1yr, 3 weekly injections if >1yr or cardio involvement); IV penicillin for 10-14 days if
Pregnant women that are allergic to penicillin should be desensitized and still given penicillin to prevent congenital
Consider giving IM penicillin to child after birth
Titers should decreases at least 4x with treatment
Toxic shock syndrome
o Staph aureus
o Sx: diffuse erythema involving the palms followed by desquamation after 7-10 days, fever >102, hypotension
o Tx: penicillin or oxacillin + clindamycin
SIRS: systemic inflammatory response syndrome
o 2/5 of the criteria qualifies for SIRS
o HR >90, WBC >12 or <4 or 10% bands, temp >100.4 (38 C) or < 96.8 (36 C), RR> 20 or PaCO2 <32 mmHg
o Sepsis= SIRS + bacterial infection
Note: w/o the SIRS criteria, a systemic bacterial infection= bacteremia
Severe sepsis includes end organ damage
Septic shock add in severe drop in BP
o Dx: lactate level, blood & urine cx
o Tx: IV fluids, antibiotics, oxygen
IV fluids is important to prevent high-output heart failure from septic shock
line sepsis
o Staph epidermidis (coagulase negative staph) is the most common cause of line sepsis
o sx: fever, chills, hypotension, increased WBC; redness, purulence, or induration along the catheter tract or at exit site
o dx: blood culture (2 locations; usually peripheral and at central line to compare growth)
o tx: empiric broad spectrum IV antibiotics, remove catheter if indicated
catheter should be removed if: non-tunneled or implanted; is redness over the subcutaneous tract of the catheter; remove if
infection is d/t staph aureus, gram (-), or fungus
if infection is limited to the catheter exit site and is d/t staph epidermidis (coagulase negative staph), then a trail of
vancomycin through the central venous catheter to stop the infection can be done w/o removing the line
if no obvious source of infection for sepsis, assume gram (-) and add in anti-pseudomonal tx: cefepime, ciprofloxacin, imipenem, or
beta-lactam + aminoglycoside
if fever lasts >3 days add in vancomycin
if fever persists 5-7 days after vanco add antifungal (fluconazole or amphotericin B)
other vaccination
o all pt >18 yo should receive 1x TDaP booster instead of the Td booster (every 10 yrs)
o pneumococcal vaccine is administered 1x @65 yo, or for pt with chronic condition (lung/CV, renal, asplenia, immunocompromised, DM) as a
vaccine with booster 5 yrs later if given before age 65
+ -
+ A B
- C D
negative predictive value (NPV): the probability of being free of a disease if the test result is negative
o a pt with a high probability of having a disease will have a low NPV; the prevalence of the disease is directly related to the pre-test
probability of having the disease
normal (bell-shaped) distribution: 68%=1SD from the mean, 95%=2 SD, 99.7%=3 SD
case-control study
o used to compare the exposure of people with the disease (cases) to the exposure of the people without the disease (controls)
o compare results using an exposure odds ratio
if the prevalence of the disease is low, the odds ratio approximates the relative risk
cohort study
o people are followed over time for the occurrence of the disease
o measure: relative risk or relative rate, median survival
RR>1 indicates a positive association between the risk factor and the outcome, RR<1 means there is a negative
clinical trial
o type of parallel study: randomized one treatment to one group and a different treatment to the other group (ex drug vs placebo)
o measure: median survival
cross-sectional study/ prevalence study
o simultaneous measurement of exposure and outcome (snapshot study)
o measure: prevalence odds ratio to compare the prevalence of disease between different populations
factorial design
o involves 2 or more experimental interventions (each with 2 or more variables that are studies independently)
cluster analysis: grouping of different date point into similar categories
o randomization at the level of groups rather than at the level of individuals
effect modification: occurs when the effect of the main exposure on the outcome is modified by the level of another variable
o ex: effect of OCPs on breast cancer is effected by family history; effect of estrogen on venous thrombosis (modified by smoking); risk fo lung
cancer exposed to asbestos (modified by smoking)
o it is NOT a bias
hazard ratio: ratio of an event occurring in the treatment arm vs the non-treatment arm
o ratio <1 indicates that the treatment arm had a lower event rate
o ratio> 1 indicate the treatment arm had a higher rate of events
P-value/ confidence interval
o a small sample size can lead to lack of statistical significance from insufficient power to detect the difference between exposed and
unexposed subjects (narrow he confidence interval surrounding the point estimate)
95% confidence interval 99% confidence interval
Null value (1) outside confidence interval P value <0.05 P value <0.01
Null value (1) inside confidence interval P value >0.05 P value >0.01
types of bias
o lead time bias: occurs when 2 interventions are compared to diagnose a disease, and 1 intervention diagnoses the disease earlier than the
other without an effect on the outcome (such as survival)
it makes it appear that the intervention prolonged survival when it really just diagnosed the disease sooner
o susceptibility bias (subgroup of selection bias): occurs when the treatment regimen selected for a patient depends on the severity of the
patients condition without taking into account other possible confounding variables
o measurement bias: occurs from poor data collection with inaccurate results

Poison Overdose Withdrawal Treatment
Acetaminophen *N/V, anorexia
*liver damage, acute renal
failure can occur
*activated charcoal if w/in 4 hrs
of ingestion (decreases
*obtain serum acetaminophen
levels starting at 4 hrs of
ingestion (not earlier)
*N-acetylcysteine if w/in 8 hrs of

*Slurred speech, sedation,
unsteady gait, nystagmus
*risk of subdural hematoma
from falling

*anxiety, insomnia, tremors,
diaphoresis (first 6-24 rhs),
hallucinations or withdrawal
seizures (first 48 hrs), delirium
tremins (48-96 hrs; HTN,
agitation, tachycardia,
hallucinations=tactile & visual,
*CIWA score to determine
severity of withdrawal: N/V,
anxiety, agitation, paroxysmal
sweats, tremors, orientation &
clouding of sensorium, tactile/
auditors/ visual disturbances,

Lorazepam/ Atovan)
Anticholinergic *hyperthermia, mydriasis,
delirium, urinary retention,
decreased bowel sounds, dry
*atropine, pralidoxime
Aspirin (salicylate) *tinnitus, fever,
hyperventilation, N/V
*anion gap metabolic acidosis
& respiratory alkalosis with
an almost normal pH (7.39-
*sodium bicarbonate
Barbiturate *drowsiness, incoordination,
slurred speech

Benzodiazepine Slurred speech, unsteady gait,
drowsiness, mild respiratory
Beta-blocker *bradycardia, AV block,
hypotension, diffuse wheezing;
can cause cardiogenic shock
*#1: atropine, IV fluids
Caustic substance (lye=drain
*damages GI tract (necrosis,
edema, scarring, severe pain;
white tongue, heavy salivation,
dysphagia; esophageal and
stomach ulcers)
*if ulcers perforate peritonitis
or mediastinitis
*if perforation suspected
Gastrografin study
*upper GI endoscopy
Carbon monoxide *Headache, N/V, abdominal
discomfort, confusion, coma;
pinkish-red skin
*anion gap metabolic acidosis
*test carboxyhemoglobin level
*hyperbaric oxygen
Cocaine HTN, tachycardia, feelings of
euphoria, increased alertness,
mydriasis; cardiac ischemia,
intracranial hemorrhage
Increased appetitive
Cyanide *headache, vomiting, abdominal
pain, flushed skin
*if inhaled bitter almond odor

Digoxin Bradycardia, blurred vision,
disturbed color perception,
fatigue, headache, abdominal
pain (anorexia, N/V);
bidirectional ventricular
tachycardia, accelerated
junctional rhythms
*Digoxin specific antibody
Diphenhydramine *anticholinergic sx: dry mouth,
dilated pupils, blurred vision,
reduced bowel sounds, urinary
*drowsiness, confusion
*physostigmine (cholinesterase
Ethylene glycol (antifreeze)
*degraded by alcohol
dehydrogenase oxalic acid +
glycolic acid
*oxalic acid binds calcium
*flank pain, hematuria, oliguria
*hypocalemia, calcium oxalate
crystal (rectangular
enveloped shaped) deposition
in the kidneys, anion gap
metabolic acidosis, increased
osmolar gap; kidney damage
acute renal failure
*fomepizole or ethanol
*sodium bicarbonate to alleviate
*hemodialysis for acidosis
and/or end organ damage
Lithium *diabetes insipidus
euvolemic hypernatremia
*Tremor, hyperreflexia, ataxia,
seizures, altered mental status,

N/V, hypotension
Marijuana Tachycardia, tachypnea, HTN,
euphoria, paranoia, conjunctival
injection, dry mouth, impaired
reaction time, impaired short
term memory, time distortion,
confusion, increased appetitive

Methanol (methyl alcohol) *Disinhibition, headache, N/V,
epigastric pain; vision loss
(snowfield vision), coma, acute
*optic disk hyperemia, anion gap
metabolic acidosis, very low
bicarbonate, increased osmolar

Opiod (heroin)
histamine release
Miosis, respiratory depression
(#1 predictor of mortality),
decreased bowel movement,
hypotension, bradycardia,
Dilated pupils, Piloerection,
dysphoria, myalgias, arthralgias,
abdominal pain, N/V, diarrhea,
*naloxone for acute overdose
*Methadone or buprenorphine
for long-term management of
antagonist increased Ach)
Bradycardia, miosis,
bronchorrhea, muscle
fasciculations, salivation,
lacrimation, diarrhea, urination
*atropine, pralidoxime
*immediate removal of pts
clothing & wash the body to
prevent continued absorption of
organophosphate through the
Phencyclidine (PCP, angel
Hallucinations, dissociative
feelings, agitation, confusion,
pupillary dilation, tachycardia,
vertical nystagmus (can also be
horizontal or rotary), miosis,
psychotic and violent behavior;
severe HTN, seizures,
*Benzodiazepines for
psychomotor agitation
*haloperidol (dopamine
Phenytoin Horizontal nystagmus,
cerebellar ataxia, confusion

Theophylline Seizures, hyperthermia, cardia
arrhythmias, hypotension

Tricyclic antidepressant (TCA) *CNS depression (seizures),
cardiac arrhythmias (decreased
conduction velocity QRS
prolongation), hypotension
*anticholinergic signs:
hyperthermia, flushing, dilated
pupils, decreased bowel sounds,
intestinal ileus, urinary
*duration of QRS complex is
best indicator of severity
*IF QRS >0.1 secsodium
bicarbonate (narrows QRS
complex by alleviating
depressive action on sodium
warfarin Vitamin K, fresh-frozen plasma
Neuroleptic malignant syndrome
o Drug induced idiosyncratic reaction
Drugs: dopaminergic antagonists (haloperidol and other typical neuroleptic agents, atypical neuroleptics)
Sx start w/in 2 weeks of starting the precipitating drug
o Sx: fever (hyperthermia), muscle rigidity, autonomic instability (diaphoresis), altered mental status (confusion)
o Dx: elevated creatine kinase, leukocytosis, electrolyte abnormalities
o Tx: immediate cessation of the causative drug, dantrolene (muscle relaxant), bromocriptine (dopamine agonist), amantadine (antiviral with
dopaminergic properties)
Chemical damage to eye #1 step is to wash the eye with copious amounts of water >15 min
o Acid exposure has higher chance of recovery; alkaline exposure causes permanent corneal damage
Alcohol: 12 Oz beer, 8 Oz wine, 5 oz liquor are all equivalent to 14 g alcohol; recommended weekly limit is 40 g
Side effect overview
o Ototoxic: cisplatin, carboplatin, aminoglycosides
o Optic neuritis: ethambutol, hydroxychloroquine
o Peripheral neuropathy: phenytoin, isoniazid, vincristine, heavy metals, chronic alcoholism
o Thyroid dysfunction: amiodarone, lithium
ACE inhibitors (-pril)
o Inhibit conversion of angiotensin I angiotensin II (vasoconstrictor)
o Action in heart: reduces preload & afterload, prevents remodeling
Drug of choice for CHF d/t survival advantage
o SE: cough, hyperkalemia, angioedema, acute renal failure, dry cough, urticarial skin rash, altered sense of taste, leukopenia, pancytopenia,
Contraindicated: pregnancy, renal failure, bilateral renal artery stenosis
o Carbonic anhydrase inhibitor decreases serum bicarbonate production, hypokalemia
o SE: crystalline nephropathy (prevent/treat with aggressive IV hydration)
Angiotensin receptor antagonist (ARBs; -sartan)
o MOA: Competitive inhibition of angiotensin II receptor
o SE: leukopenia, pancytopenia, hypotension, hyperkalemia, acute renal failure
Contraindications: pregnancy, bilateral renal artery stenosis
o Se: tinnitus, sensorineural hearing loss (high dose 6-8 g/day)
o Purine analog; converted to 6-mercaptopurine; inhibits purine synthesis
o SE: diarrhea, leukopenia, hepatotoxicity
o Lorazepam (atovan) has no decreased respiratory drive (so can be given continuously or at higher doses)
Uses: alcohol withdrawal
o Avoid in elderly patients (exacerbates mental status changes and increases fall risk)
Beta-blocker (atenolol, metoprolol)
o Action in heart: prevent and reverse adrenergically mediated intrinsic myocardial dysfunction and remodeling
o Kidney: decreases renin synthesis/release
o SE: bronchospasm, bradycardia, depression, sleep disturbances (insomnia), fatigue, may increase TGs and decrease HDL (hyperlipidemia),
sedation, erectile dysfunction
May mask hypoglycemia sx in diabetic pts on insulin
Contraindications: asthma, 2
or 3
degree heart block
o Use: smoking cessation
Calcium channel blockers (amlodipine, nifedipine, diltiazem, verapamil)
o Blockade of L-channels, reducing intracellular calcium vasodilation
Contraindications: heart failure, significant heart block
o Dihydropyridines (amlodipine, nifedipine)
SE: tachycardia, flushing, hyperkalemia, edema
o Non-dihydropyridines (diltiazem, verapamil)
SE: heart block, constipation
o Alpha & beta blocker
o SE: diarrhea, bone marrow suppression neutropenia; contraindicated in renal insufficiency
o Alpha-2 agonist
o SE: postural hypotension, drowsiness, dry mouth, rebound hypertension with abrupt withdrawal
o SE: agranulocytosis (monitor CBC q 1-2 wks)
o SE: acute hemorrhagic cystitis, bladder cancer, sterility, myelosuppression
MESNA and increased fluid intake help to avoid bladder SE (d/t acrolein)
o MOA: calcineurin-inhibitor; inhibits transcription of IL-2 and other cytokines (mainly inhibits T-helper lymphocytes)
o SE: nephrotoxicity (azotemia, hyperuricemia, hyperkalemia, hypophosphatemia, hypomagnesemia; HUS rare), HTN (renal
vasoconstriction and sodium retention; tx calcium channel blocker), neurotoxic (headache, visual changes, seizures, mild tremor, akinetic
mutism), glucose intolerance, infection, malignancy (increased risk of squamous cell carcinoma of the skin and lymphoproliferative
disorders), gingival hypertrophy, hirsutism, GI (anorexia, N/V, diarrhea)
o Verapamil decreases the renal clearance of digoxin
o SE: anorexia, N/V, bidirectional ventricular tachycardia, accelerated junctional rhythms
o Typical antipsychotic; injected every 2-3 wks in schizophrenics with poor copmlicant
More potent than haloperidol
o SE: hypothermia (inhibits shivering mechanism and/or autonomic thermoregulation)
o MOA: arterial vasodilation
o SE: reflex tachycardia, headache, angina, SLE-like syndrome
Contraindications: severe coronary artery disease
o SE: liver damage
o Folinic acid (derivative of tetrahydrofolic acid); antidote to methotrexate; folate rescue for bone marrow and GI mucosa cells
Loop diuretics (furosemide)
o MOA: inhibit Na-K-2Cl carrier in thick ascending limb or loop of henle
o Se: sensorineural hearing loss, hypokalemia, metabolic alkalosis (d/t excretion of H+), prerenal renal failure (d/t decreased circulating
blood volume), rash, hyperuricemia, hyperglycemia, hypocalcemia
Contraindications: gout, hypokalemia
o Azithromycin
SE: prolonged QT interval
o SE: severe lactic acidosis
Stop metformin if Cr>1.3-1.4
o Dopamine receptor antagonist; prokinetic (increased peristalsis, increased strength of gastric contractions, relaxation of the pyloric
o Tx: nausea, gastroparesis
o SE: agitation, loose stools, extrapyramidal sx (tardive dyskinesia, dystonic reactions, parkinsonism)
o MOA: reversible inhibitor of inosine monophosphate dehydrogenase (rate-limiting enzyme in de novo purine synthesis)
o SE: bone marrow suppression
o Vasodilator; direct arterial & venous dilator
o SE: weakness, fatigue, nausea, muscle twitching, cyanide toxicity
Neuromuscular blocking agents
o Succinylcholine
Depolarizing neuromuscular blocker; rapid onset (45-60 sec), rapid offset (6-10 min)
SE: hyperkalemia arrhythmias
Contraindications: hyperkalemia, crush/burn injuries >8hrs old (d/t risk of rhabdomyolysis), pts with demyelinating
syndrome (Guillain-barre), pts with tumor lysis syndrome
o Atracurium
Metabolized in plasma and hydrolyzed by serum esterases
Safe to use in pt with renal and liver disease
o Pancuronium
Excreted mostly unchanged in the urine
o Mivacurium
Excreted mostly unchanged in the urine
o Rocuronium
Clearly mostly by the liver
Potassium sparing diuretics (spironolactone)
o MOA: competitive inhibition of aldosteronerenal sodium loss
o SE: hyperkalemia, gynecomastia, diarrhea
Contraindication: renal failure
Proton pump inhibitors (omeprazole)
o SE: increased gastrin levels
o Calcineurin-inhibitor (similar to cyclosporine); inhibits IL-2 transcription; macrolide antibiotic produced by fungi
o SE: nephrotoxicity (azotemia, hyperuricemia, hyperkalemia, hypophosphatemia, hypomagnesemia; HUS rare), HTN (renal vasoconstriction
and sodium retention; tx calcium channel blocker), neurotoxic (headache, visual changes, seizures, mild tremor, akinetic mutism), glucose
intolerance, infection, malignancy (increased risk of squamous cell carcinoma of the skin and lymphoproliferative disorders), GI (anorexia,
N/V, diarrhea)
Most common: neurotoxic, diarrhea, glucose intolerance
Unlike cyclosporine, it does not cause gum hypertrophy or hirsutism
o Doxycycline
SE: phototoxicity (exaggerated sunburn reaction with less sun exposure time)
Thiazide diuretics (hydrochlorothiazide, chlorthalidone)
o MOA: inhibit Na-Cl transporter in the early distal tubule
sodium diuresis, volume depletion, possibly lower peripheral vascular resistance
o SE: hypokalemia, hyponatremia, hypercalcemia, hyperuricemia, hyperglycemia (carbohydrate intolerance), elevation of cholesterol &
triglyceride levels (hyperlipidemia), metabolic alkalosis, hypomagnesemia, orthostatic hypotension, photosensitivity
Contraindications: DM, gout, hypokalemia
Toradol (ketorolac)
o NSAID that can only be given <5 days for severe pain management
TMP-SMX (trimethoprim + sulfamethoxazole)
o Used to tx: UTIs (gram (-) rods), PCP pneumonia, community acquires MRSA skin infections, nocardiosis
o Sx: hyperkalemia
o Vanco trough goal 15-20
o Se: nephrotoxicity, ototoxicity, red man syndrome
Fibrinolytic (thrombolytic) therapy in acute pulmonary embolism and lower extremity DVT
o MOA: activation of plasminogen plasmin
Recombinant tissue type plasminogen activator (tPA, alteplase), Streptokinase, Recombinant human urokinase
o PE
Pros: accelerates clot lysis. Improves pulmonary arterial BP, RV function, and pulmonary perfusion in the short-term
Indications (only after confirmed acute PE)
Persistent hypotension d/t PE (systolic <90 or a drop >40 mmHg from baseline)
Severe hypoxemia, large perfusion defect on VQ scans, extensive embolic burden on CT scan, RV dysfunction, free-
floating right atrial or ventricular thrombus, patent foramen ovale, cardiopulmonary resuscitation (when cardiac arrest
d/t PE)
Cons: No trial has show that thrombolytics decrease recurrent thromboembolism or mortality more than anticoagulation alone;
increased risk of bleeding, intracranial hemorrhage
Streptokinase: allergic reactions, hypotension
Contraindications for use: intracranial neoplasm, recent (<2mo) intracranial surgery or trauma, active or recent internal bleeding
in last 6mo, hx of hemorrhagic stroke, bleeding diathesis, severe uncontrolled HTN (systolic >200 or diastolic >110),
nonhemorrhagic stroke w/in 2 mo, surgery w/in past 10 days, thrombocytopenia (<100,000 platelets)
For most patients it is NOT indicated
Indications: massive iliofemoral or proximal femoral DVT with a high risk of limb gangrene w/ sx for >14 days and do not have an
increase risk of bleeding
other options for tx= catheter extraction, catheter fragmentation, surgical thrombectomy