FIRST AID * from Q&A for the

USMLE STEP 2 CK
Selected High Yield concepts
Endocrine

POOR prognostic factor**Thyroid nodule Hoarseness--< implies vocal cord impairment due to tumor
involvement of recurrent laryngeal nerve malignant tumor that has extended beyond thyroid gland and
invaded local structures
Sulfonylureasin DM type 2 Glyzipide- Glyburide >MOA: increase insulin secretion to normalize
glycemia HYPOglycemia and WT gain ADVERSE effect
***History of total thyroidectomy hypothermia, Myxedema coma and no hormonal replacement
hyponatremia-hypoglycemia- mental status changes, obesit-periorbital edema
RX: Blood thyroid function tests PRIOR to Levothyroxine T4 and T3 admon
***PT WITH HYPERTHYROIDISM, > RISK of developing60 years old GIVE Propylthiouracil. Other
risks: CARDIAC Arrythmyas- Atrial fibrillation bone density abnormalities in subclinical
hyeprthyroidism
A.C.E***HyperCALCEMIA due to sarcoidosis: ELEVATED chronic cough-constiaption-hilar adenopathy
-hypercalcemia
Sarcodosishyeprcalcemia secondary to increased 1,25 OH2 vitamin D by macs into the granulomas.
***Isolated hypercalcemia malignancy sarcoidosis granulomatous diseases bony metastasis
parathyroid adenoma..
ACEIs prevent***Nephropathy / Diabetes Mellitus convert Angiotensin I to angiotensin II //and slow
nephropathy in DM // ACE constrict ACEIs inhibit ACE, so Angiotensin II is decreased (Angiotensin II
EFFERENT arteriole in glomeruli RBF and GFR)
**Dilates So, ACEIs RBF and GFR and reduces macro-proteinuria EFFERENT arteriole
***NSAIDs prerenal failure inhibiting prostaglandings and RBF Affect kidney go chronic go to
intrarenal failureischemia, but if prolonged ischemia tubulointerstitial / acute tubular necrosis
NSAIDs inhibit prostaglandins CONSTRICT(prostaglandins dilates AFFERENT arteriole RBF GFR) So
NSAIDs AFFERENT arteriole RBF GFR
***Glycosylated Hb Measured for glycemic when Hb is exposed to much glucose; a lot of glucose bind to
Hb and control because the lifetime of an RBC is 120 days (4 months), this test is the BEST for
determining average blood glucose levels over the previous 3-4 months.
finding on 2 separated occasions of***Diabetes Mellitus type 2 a fasting blood glucose level of >126
mg/dL

-Etio: relative lack of insulin secretion, peripheral insulin resistance and impaired regulation of
gluconeogenesis in the liver.
***Diabetes Alpha glycosidase inhibitors flatulence and abdominal pain as adverse effects /reduces the
amount of carbohydrate produced from the intestine
RX with galactorrhea***Hyperprolactinemia-prolactinoma dopamine agonist that can decrease prolactin
and size of Bromocriptine adenoma
***Vitamin D defficiencyCarbamazepine therapy hypocalcemia Also: Phenytoin Theophilline
Rifampin ///Due to increase cytochrome p450 enzymes in the liver that inactivate vitamin D

Hematology
**Heparin induced thrombocytopenia
-Occur within 4-10 days of therapy with unfractionated heparin.
-Associated with thrombosis due to platelet activation
-Etio: platelet antibodies that cause limb and life threatening thrombosis at unusual sites including
arteries
-Spontaneous bleeding is rare (platelet above 20.000
-RX: immediate stop of a direct thrombin inhibitor (Argatroban lepirudin Discontinue HEPARIN)
**CTCL: Cutaneous T-Cell patch, plaque, tumor, Sezary (systemic)Lymphoma / RX by Stages:
- Early treated with topical nitrogen mustards disease- path or plaque stage outpatient basis
- Advanced disease: cpmventional radiation therapy or total skin electron beam therapy
- Sesary syndrome stage / systemic disease: systemic chemotherapy bone marrow transplant
=In Sezary: systemic form of CTCL, after the 2 first phases has persisted for years; where Sezary cells are
visible in peripheral smear and entire skin surface is affected by erythematous lesions confused with other
pathologies
**Tumor lysis syndrome.- Shortly after chemotherapy with elevations in serum uric acid
Progress to urate induced renal failure.
POTASIUM is elevated or hyperkalemia due to lysis of neoplastic cells
symptoms associated with**POEMS syndrome osteosclerotic Multiple Myeloma
P: Polyneuropathy - O: Organomegaly - E: Endocrinopathy - M: Multiple myeloma - S: Skin changes
**Sickle cell anemia RX:
1. Symptomatic pain control in acute crisis
2. Increasing oxygen tension to reduce sickling
3. Reduce occlusive crisis through Hydration
4. LONG TERM RX: Hydroxyurea (stimulates production of fetal Hb which will not sickle with low
oxygen tension)
** Waldestroms Macroglobulinemia
- Low grade malignant lymphoma of plasmacytoid lymphocytes that secrete excessive amounts of IgM.
Patient present with hyperviscosity syndrome: Raynauds phenomenon, visual disturbances (visual
floaters) and protein-protein interaction (platelet dysfunction)

- Dx: Demonstration of IgM spike on plasma Electrophoresis

- BX: Infiltration of bone marrow with plasmacytoid lymphocytes
RX:
-Plasmapheresis to control hyperviscosity initially (because chemo can take several wks)
-Chemotherapy: same as used in MM and alkilating agents and prednisone
Survival: 5 years
**Aspirin: Indicated in pts at risks for strokes or myocardial infarction 2 preventionanalgesic antiinflammatory pts at**Clopidogrel antiplatelet risk for stroke or MI pts allergic to ASA
**Warfarin: DVT Atrial Fibrillation -artificial heart valves
**Li Fraumeni syndrome: mutation in p53 tumor supressor gene. AD condition and predisposes patient
to:
--Sarcomas--CNS tumors --carcinomas.
--HIGH RISK of acquired treatment related Acute Myelogenous Leukemias (t-AML) following treatment
with cytotoxic drugs. tAML is universally refractory to known therapies.

Musculoskeletal
**Systemic sclerosis or LCSS and DCSS (Diffuse cutaneous systemic sclerosis) scleroderma
Swollen cutaneous systemic sclerosis indurated fingers and hands
***LCSS: If skin findings limited to hands (limited cutaneous systemic sclerosis) LCSS opposed to Diffuse
Systemic Sclerosis. Associated to CREST syndrome with nodules fingers pads- deposits of subcutaneous
fat, Raynauds phenomenon, episodic vasoconstriction of small arteries in the fingers causing pallor and
cyanosis; ELEVATED Anti-centromere reflux, dysphagia, esophageal dysmotility autoantibodies
**Scleroderma: pulmonary disease in 70% cases and is the leading cause of death
**DCSS: Diffuse Systemic sclerosis: ELEVATED Anti-Scl-70. Sking findings are extended proximally past
the wrists + symptoms of CREST syndrome.
-INCREASED RISK of: pulmonary fibrosis (leading cause of death)
**Patient with Wolff Parkinson White syndrome + symptoms of Drug induced lupus
Due to Procainamide class IA antiarrythmic used in WPW syndrome to prevent atrial fibrillation
**Other drugs causing Drug induced SLE: Hydralazine, isoniacid, minocycline, PTU, lithium,
carbamazepine, and phenytoin
**Duchenne muscular dystrophy DMD:
-Present at birth X-linked Rec, does not begin until age 3-5 years.
-Clues: maternal uncle..Resp failure died and normal female unaffected in the family
-Affect proximal musculature, difficulty climbing stairs
-Will roll to prone position and use their arms to climb up their legs and then thigh muscles to rise to
standing.
-Develop hyperlordosis and scoliosis because weakness of truncal muscles.
due to chest deformities and muscle-Impaired respiratory function weakness, require tracheostomy
-Cretine kinase elevated, primary muscular disorder (no neurological disorder)
-Death: 3rd decade due to Resp. failure or cardiomyopathy

history of trauma followed by an**Rhabdomyolysis extended period of inactivity or crushes injuries and
then a gross hematuria ->classic cause of rhabdomyolysis
-Urine (+) for blood by dipstick but suggest myoglobin(-) for RBCs by micro exam
-Widespread muscle cell damage leads to release of intracell components into systemic circulation. Also
elevations of K, uric acid, PO4, creatinine, BUN, structural proteins as myoglobin that accumulated in
kidney lead to hemoglobinuria and Acute Renal Failure.
**Polymyalgia rheumatica (PMR): is associated or linked to Temporal giant cell arteritis in pts > 50, with
subacute or chronic onset of symmetrical pain and morning stiffness in large proximal joints including
shoulders, hip girdle, and neck. Pt has trouble getting dressed because of stiffness.
-Pain is due to Synovitis and bursitis of joints. Wt loss and fatigue elevated ESR.
-RX: Prednisone: RAPID RESPONSE with prednisone confirm diagnosis even with low dose steroid
**Osteoarthritis pain: tend to worsen through the day with increasing activity
**Inflammatory pain: tend to worsen in the morning after a period of inactivity and improve through the
day with activity
**Rheumatoid arthritis pain: morning stiffness, similar to PMR, but involves more joints, smaller joints,
hands and feet. RX: HIGH dose steroids- difficult to manage, other anti-rheumatic drugs
**Scaphoid or navicular fracture: initial x rays not always detect the fracture, especially in any patient
with suspected scaphoid non-displaced fractures. As General Rule Splint immobilization fracture but (-)
initial x-ray should be treated with a Thumb Spica Splint and re-evaluated in 2 weeks.
In follow up visit: Repeat X ray to detect fracture of the proximal 1/3 of the scaphoid.
Open reduction: indicated in displaced fracture and nonunion fracture of scaphoid
**Soft tissues injuries not-associated with fractures: sprain-strain, contusion, tendinitis and bursitis.
RX: ice pack, rest and NSAIDs
***Reactive Arthritis:
Physiopathology: ***Nongonococcal venereal disease (most often Chlamydia) and infectious diarrhea
(Shigella, Salmonella, Yersinia) precipitate reactive arthritis. ******HLA-B27 contributes to the
pathogenesis of the disease.
**Reactive arthritis is an RF-seronegative, HLA-B27-linked spondyloarthropathy (autoimmune damage
to the cartilages of joints) often precipitated by genitourinary or gastrointestinal infections.
Reactive arthritis has symptoms similar to arthritis or rheumatism; and similar to Reiter syndrome, with
inflammatory back pain, asymmetric oligoarthritis affecting large joints
Other bacteria known to cause reactive arthritis Bacteria associated with reactive arthritis are generally
enteric or venereal***Chlamydia trachomatis***, Neisseria gonorrhoeae, Ureaplasma urealyticum,
Salmonella spp., Shigella spp., Yersinia spp., and Campylobacter
RX: Mainstays of therapy for joint symptoms are nonsteroidal anti-inflammatory drugs (NSAIDs)
**Reiter syndrome: A Spondyloarthropathy, type of Reactive Arthritis in men and woman; triad:
1. Uveitis - 2. Urethritis 3.Arthritis
Ulceration in urethral meatus due to Chlamydia trachomatis** H. yield concept
Females may have asymptomatic infection that precedes the onset
DX: Urine Polymerase Chain Reaction PCR for Chlamydia trachomatis
***Ankylosing spondylitis -late teens, early 20s with hip pain and severe lower back pain worsen in the
morning and improving through the day with activity

*Spondyloarthropathy, chronic, painful, degenerative inflammatory arthritis primarily affecting spine and
sacroiliac joints, causing eventual fusion of the spine; it is a member of the group of the autoimmune
spondyloarthropathies with a probable genetic predisposition.
bamboo spine Complete fusion results in a complete rigidity of the spine seen on x-rays.
Pt has back pain and morning stiffness, systemic findings as uveitis 30% cases, cataracts, glaucoma, aortic
insufficiency and prostatitis in men
RX: NSAIDs and specifc exercises or spinal surgery later in the disease
**Psoriatic arthritis:
-Spondyloarthropathy that causes inflamatory back pain and oligoarthritis of large peripheral joints; pain
insidious onset and is worst in the morning or after a long period of inactivity. Have cutaneous signs of
psoriasis
**Exertional compartment syndrome:
--Pt has pain over anterior lower leg after exercise or activity and Relieved by REST or cessation of
exercise-As blood flow to the muscles increases with activity, muscle swells and become constricted by the
encompassing fascia, pain result from ischemia. Also, pt has numbness in the dorsum of the foot or
weakness on dorsiflexion at the ankle.
DX: measurement of the pressures on the leg at rest followed by a reading after exercise
RX: Surgical fasciotomy (release tight fascia)
**Acute compartment syndrome:
Pain occurs secondary to a traumatic injury such a fracture long bones or crush injury.
Pt has severe pain and tight compartment at the time of exam with associated apresthesias.
RX: immediate fasciotomy to prevent CELL DEATH
**Patellofemoral syndrome / anterior knee pain most common
Arises from imbalance or irregularity of patellar movement or tracking like an imbalance in quadriceps
strength, patella alta, recurrent patellar subluxation, direct trauma to patella and meniscal injuries.
RX: Strenghtening exercises of quadriceps
**Fibromyalgia:
2 criteria:
1*chronic pain for at least 3 months in all 4 quadrants of the body and along the axial skeleton
2*tenderness in 11 or 18 specific anatomic points
**Multiple associated conditions: bowel irritation, tension headaches, anxiety disorder, depression,
thyroid disorders, sleep disorders and dysmenorhea.
-C/P:
Patient has generalized musculoskeletal aching, with stiffness and fatigue that improves over the course of
the day. Has pain and tightness in the neck and upper back, along with areas of point tenderness.
Complain muscle pain and fatigue after minimal exertion, poor sleep, awakening frequently in the night
and difficulty falling back to sleep. ***It is important not to dismiss case of fibromyalgia as malingery,
because fibromyalgia is a real medical entity with viable RX.
Physical examination and x rays: do not typically demonstrate any joint abnormality
RX: amitriptiline, fluoxetine, chlorpromazine and cyclobenzaprine
**Polymyositis Dermatomyositis and - Inclusion body myositis
They are Idiopathic inflammatory myopathies. Etiology unknown, tipicaly present with progressive
bilateral muscle weakness. DX between three diseases is made on muscle biopsy and Creatine kinase

levels
CK in is normal dermatomyositis and inclusion body myositis
CK in Polymyositis is ELEVATED
Inclusion body myositis biopsy: B amyloid deposits in biopsy, pt > 50 years old, with progressive
asymmetric weakness of proximal and distal muscles and do not respond to immunosuppressive
treatment
**Frozen shoulder syndrome
Significant deficits in ROM.- Range Of Motion of the joint; adhesive capsulitis or frozen shoulder, patient
suffer progressively shoulder pain and decreased ROM w/o presence of truly intrinsic shoulder disease.
This disease follows bouts of bursitis, thickened capsule with mild inflammation changes leading to
decreased ROM and pain.
**Lumbar spinal stenosis
Narrowed spinal canal and degenerative joint changes compress nerve roots and become symptomatic.
bulging/protrusion of the intervertebral DXX: Lumbar MRI disks, osteophytes at the facet joints or
hypertrophy of the ligamentum flavum.
Patients that present with neurogenic claudication (ischemia of compressed nerves while waking) would
be a candidate for decompression injury
** Lumbar spinal stenosis linked to neurogenic claudication
Pathophysiology:
-Disk desiccation and degenerative disk disease (DDD) with resulting loss of disk height may induce
segmental instability. Such instability incites vertebral body and facet joint hypertrophy. Cephalad
vertebral body IAP hypertrophy promotes central spinal canal stenosis. Further canal volume loss results
from HNP, ligamentum flavum hypertrophy, and disk space narrowing
-Segments (L3-L4, L4-L5) are most commonly affected by degenerative stenosis
C/P: LSS classically presents as bilateral Neurogenic Claudication (NC)
Patient report insidious-onset NC manifesting as intermittent, crampy, diffuse radiating thigh or leg pain
with associated paresthesias and indeed, leg pain affects 90%
NC pain is exacerbated by standing erect and downhill ambulation and is alleviated with lying supine
more than prone, sitting, squatting, and lumbar flexion
DX: -Xrays, MRI, CT scan
This test effectively documents-Myelography central canal stenosis and remains superior in evaluating
lumbar disk herniation
- Electrodiagnosis (EDX), including needle electromyography (EMG), nerve conduction studies (NCS),
and somatosensory evoked potentials (SSEP)
Complications LSS
In Central stenosis: may provoke cauda equina syndrome with associated saddle anesthesia, bladder
and/or bowel dysfunction and altered muscle reflexes
In lateral recess stenosis-induced radiculopathy may manifest significant lower limb weakness or
numbness. Lastly, intractable axial, radicular, or NC pain may result.
RX of LSS
- Rehabilitation, physical therapy, patient education Activities of Daily Living
- Oral medication:
*First-line pharmacotherapy for LSS includes NSAIDs / Muscle relaxants may be used to potentiate
NSAID analgesia

* Membrane-stabilizing anticonvulsants, such as gabapentin and carbamazepine, may reduce neuropathic

radicular pain from lateral recess stenosis
*Tricyclic antidepressants (TCAs) are often given for neuropathic pain, but their adverse effects limit their
use in elderly persons.
*Tramadol and acetaminophen confer analgesia but do not affect inflammation.
*Oral opioids may be prescribed on a scheduled short-term basis
- Other Treatment: (injection, manipulation, etc.): Epidural steroid injection (ESI) provides aggressiveconservative treatment for LSS patients who demonstrate limited response to oral medication, physical
therapy, and other noninvasive measures. Corticosteroids may block nociceptive transmission in C fibers.
- Local anesthetic may be combined with corticosteroids to provide immediate pain relief and diagnostic
feedback on the proximity of the injectate to the putative pain generator
- Conservative versus surgical treatment for LSS remains controversial
-Surgical techniques include standard wide laminectomy and decompression, which first removes lamina
and ligamentum flavum from the lateral borders of one lateral recess to the other and then decompresses
entrapped nerve roots, foraminal enlargement -Medial facetectomy and others. In addition to
decompression and foraminal enlargement, some patients with segmental instability from facet joint
removal and pain secondary to DDD may require fusion
***Systemic onset of juvenile rheumatoid arthritis / JRA
Combination TRIAD:
1. Several weeks of high spiking fevers
2. Arthritis
3. Salmon colored macular rash (activated by heat and frequently found in warm areas of the body as the
axilla and waist and triggered by a fever spike but subsides when temperature return to normal
Physical exam: lymphadenopathy, hepatomegaly and splenomegaly.
DX: No spec. tests, DX is clinical based
Differential with Acute Rheumatic fever where Dx is based in Jones criteria requiring 2 ,ajor or one major
and 2 minor criteria in addition to evidence of strep. (Very high yield)
**ANY patient with history of malignancy and presenting with low should have further radiographic
evaluation TO RULE OUT METASTASIS back pain DISEASE (exe; prostate cancer, MM)
**Osteoarthritis pain:
-Dull aching pain worsening with activity and may resolve with REST
-Stiffness and limited mobility; multiple jopints affected, proximal and distal interphalangeal and
metacarpophalangeal is spared
distal-Heberdens and Bouchards nodes and proximal interphalangeal joints deformed
joint space narrowing -X-Rays subchondral sclerosis osteophytes subchondral cysts

Neurology
**Cerebral palsy /CP
The most prevalent non-progressive motor disorder in children, 75% cases, mental retardation in 90%
cases of pyramidal cerebral palsy.
Risk factors: IUGR, prematurity, perinatal hypoxia, asphyxia, infection, trauma, brain malformation and

hemorrhage.
-Pyramidal CP is non-progressive with spasticity, hyperreflexia, slow voluntary movements and impaired
fine motor function.
-Has delayed developmental milestones**, persistence of infantile reflexes like Babinskis, contractures
and weakness limbs. Walk in their toes and have scissor gait.
**Fragile x syndrome: MC cause of mental retardation in male, abnormal fascies, macrocephaly, elongate
face, prominent ears; macro-orchidism, stereotyped behavior.
**Herniated spinal nucleus pulposus
-RX: Initial: spontaneous resolution in 90% cases within 6 wks of pain onset.
#1-Use: conservative management:
-Bedrest 1-2 days followed by 2-3 wks of activity limitation (reduce lifting and twisting) [Reassessment or
-Follow up prior to lifting activity restriction]
- Physical therapy- moist heat-gentle exercise ROMs to promote joint motility
- Medication: NSAIDs 1 line of RX
- Imaging CT or MRI: in patients suspecting malignancy, traumas, MVA [motor vehicle accident], pt that
do not improve with conservative management
-Orthopedic spinal steroid injections and consultation in pt that do not improve with conservative
management
-Surgical decompression of nerve root reserved for intractable cases
**WEST syndrome:
- Uncommon to rare and serious form of epilepsy in infants.
-Children: infantile spasms, arrest of psychomotor development and hypsarrythmya pattern on EEG
-RX: Due to their side-effects, two drugs are currently being used as the first-line treatment.
-ACTH - Use primarily in United States and -Vigabatrin (Sabril)
**Young Woman urinary incontinence exacerbated by stress, bladder spasticity, urinary retencion.
Cystometry: Detrusor contraction to Betanechol chloride is greatly exaggerated.
Diagnosis: Multiple Sclerosis
Betanechol chloride is parasympathomimetic drug used during Cystometry to aid in diagnosis
suggest Detrussor muscle damage,-Lack of contraction inflammation
suggest Upper Motor neuron-Increased or exaggerated contraction dysfunction, Multiple Sclerosis
**First Initial Step in hemorrhagic CT imaging without contrast Strokes
**MRI is useful but is delayed and Ct is more quick to prevent complications
**A Lumbar puncture is danger!! Because to make a LP you need a prior CT scan because surrounding
edema may cause shifts in brain content and brain herniation into spinal cord!!! Leading to death!!
**Status epilepticus / SE
Any patient in ED with epilepsy for more of 5 minutes should be treated as SE! A medical emergency!
-Primary step: ABCD!
1st-NEXT Step: Admon of medication capable of ending seizure! line agents: IV-Benzodiazepine
(Diazepam-Lorazepam) + Phenytoin
-If these are Phenobarbital IV (not a 1st line agent) NEXT step ineffective
-Note- Neuromuscular blockade necessary to induction intubation to secure airway if not secure or when
pt has respiratory distress and requires paralysis and mechanical ventilation or rhabdomyolysis
-When pt is stable: EEG, complex studies, brain imaging and further workup

**Alzheimers: most common form of dementia in elderly 60-80% cases/ Criteria:

-Impairment of recent memory / inability to learn new information / long term memory is intact
-One of the following:
*Disturbance of language *inability to execute skilled motor activities in the absence of weakness
*Disturbances of visual processing*Disturbances of executive function / abstract reasoning and
concentration
*Behavioral problems *personality changes *precedes cognitive disturbance
BRAIN: extracellular deposition of amyloid B protein *intracellular neurofibrillary tangles *loss of
neurons
RX: Donezepil, Rivastigmine, Galantamine, Tacrine- cholinesterase inhibitors
**Creutzfeldt-Jakob Disease CJD
Most common of the human prion diseases
-1.- Progressive and rapidly mental deterioration and 2.- myoclonus
-DX: Gold standard DX: Brain biopsy** / EEG: triphasic discharge pattern in sporadic fashion
-Etio: iatrogenic from corneal transplant and dural grafts
-RX: no Rx and it is fatal
**Vascular dementia:
Prior strokes and focal neuro findings
-Abrupt onset of symptoms followed by deterioration and has infarcts on cerebral imaging. -Associated
with DM
**Normal Pressure Hydrocephalus dementia
Elderly, due to increased subarachnoid space volume that does not accompany increased ventricular
volume. Initial event: decreased absorption of CSF at the arachnoid villi. Symptoms result from distortion
of central portion of corona radiata by distended ventricles. Dementia result from distortion of
periventricular limbic system
1. Gait dysfunction 2. Urinary incontinence 3. Cognitive dysfunction
CT scan : dilated cerebral ventricles
**Dementia with Lewi bodies: Parkinson disease
2nd most common cause of neurodegenerative dementia after Alzheimers
1- Gradually progressive dementia 2.-fluctuations in cognitive function
3. Persistent visual hallucinations
4. Spontaneous motor features of Parkinsonism
5. Repeated falls, syncope
6. Sensitivity to neuroleptic medications
7. Delusions
8. Rapid eye movement sleep behavior disorders and depression
DX: clinical and hsitory
**Pseudomentia:
Elderly with depression that may present like cognitive impairment, occur days to wks, personality
changes, past medical history + for mood disorder
**Normal aging: decreased ability to learn new material and slowing of cognitive processes
**Delirium:
Rapid onset, fluctuating and cloudy level of consciousness, impaired orientation, disordered thinking,

reversible condition
Postoperative delirium: elderly; approach: identify and correct causes such as dehydration, electrolyte
imbalance, polypharmacy, infection
**BRAIN TUMORS: Triad
1-Headache is worse in the morning and gets better with vomiting
-Because lying down all evening while asleep causes increased ICP, which when further exacerbated by
amass lesion causes a headache in the morning relieved vomiting.
2-Seizures
3-focal neuro signs of increased ICP
**RET syndrome.- neurodevelopmental disorder- most exclussively in females, rare in males (embryonic
lethality) regress in development!-Normal until 5 months and then
-The clinical features include a deceleration of the rate of head growth (including microcephaly in some)
and small hands and feet. Stereotypic, repetitive hand movements such as mouthing or wringing are also
noted. Symptoms of the disease include cognitive impairment and problems with socialization, the latter
during the regression period. Socialization typically improves by the time they enter school. Girls with
Rett syndrome are very prone to gastrointestinal disorders and up to 80% have seizures. They typically
have no verbal skills, and about 50% of females are not ambulatory. Scoliosis, growth failure, and
constipation are very common and can be problematic
-Most affected: language and coordination
ETIO: sporadic mutations in the gene MECP2 located on the X chromosome
RX: no RX, symptomatic
**Positional vertigo / Benign paroxysmal positional vertigo
DX: is confirmed by a positive response on the Dix-Hallpike maneuver
determines whether vertigo is-Dix-Hallpike maneuver triggered by certain head movements. observe any
involuntary eye movements (nystagmus) that may occur during this test to determine if the cause of your
vertigo is central or peripheral
-Central vertigo is inside the brain, and peripheral vertigo affects the inner ear or the nerve leaving the
inner ear
A. Patient starts in sitting position on exam table
1. Facing forward with eyes open
B. Rapidly lie patient backward
1. Head turned 45 degrees to RIGHT
2. Neck extended 20 degrees hanging over end of table
3. Patient remains in this position for 30 seconds
C. Sit patient up
D. Rapidly lie patient backward
1. Head turned 45 degrees to LEFT
2. Neck extended 20 degrees hanging over end of table
3. Patient remains in this position for 30 seconds
E. Observe
1. Nystagmus
2. Vertiginous symptoms
Causes: the most probable cause of BPPV is the dislodging of otoconia (calcium particles) that are shed
from the utricular macula (which responds to linear motion) and migrate to the posterior semi-circular
canal (which responds to rotational motion). These loose otoconia stimulate the nerve endings in the
balance canals and send a message to your brain that you are moving in a direction you really are not.
Whiplash injury, falls, a severe cold or even high-impact exercises may accelerate this process and in

Individuals with prolonged inactivity

RX: The Canalith Repositioning Procedure (CRP) is the treatment of choice for patients with the classic
signs of BPPV. Also known as the Epley maneuver, the patient is moved through several positions to
slowly move the otoconia particles from the posterior semicircular canal back into the utricle. The entire
CRP maneuver takes approximately 5 minutes.
-The patient is instructed to wear a neck brace for 48 hours and to not bend down or lay flat for 48 hours
after the procedure
- The First 48 Hours: Sleeping: Do Not Lie Flat in Bed, sleep in a in a recliner no further than 30-45
degrees
- The Following Week: Sleeping -Do Not Sleep on yourRight Side/ Left Side Whichever side was treated
- After 1 week you can resume your daily activities without any restrictions
- For patients who fail to improve with CRP, the possibility of positional vertigo has been eliminated and
the diagnosis of a concomitant vestibular problem must be considered.
**After rupture of Occur vasospasm in 70-90% cases and in the of aneurysm strokes

**Strokes: caused by thrombosis or embolism, or due to a hemorrhage

20-30 % from cardiogenic thromboembolism and caused by several pathogenic factors.
--Most common: Atrial fibrillation and MI and endothelial abnormalities due to valvular disease
REST: 80% of strokes are due to ischemia; carotid occlusion, atherosclerosis the remainders are due to
hemorrhage due to rupture of a blood vessel or an abnormal vascular structure
blood supply to part of the brain is decreased,1-Ischemic stroke leading to dysfunction-necrosis of the
brain tissue area
*thrombosis (obstruction of a blood vessel by a blood clot forming locally), embolism (idem due to a blood
clot from elsewhere in the body), systemic hypoperfusion (general decrease in blood supply, e.g. in shock)
and venous thrombosis
2-Thrombotic a thrombus (blood clot) usually forms around atherosclerotic plaques stroke. Since
blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slower
--Large vessel disease involves the common and internal carotids, vertebral, and the Circle of Willis
--Small vessel disease involves the smaller arteries inside the brain: branches of the circle of Willis,
middle cerebral artery, stem, and arteries arising from the distal vertebral and basilar artery
blockage of an artery by an embolus (fat3-Embolic stroke (e.g. from bone marrow in a broken bone),
air, cancer cells or clumps of bacteria), arising from elsewhere and traveling particle or debris in the
arterial bloodstream. Most commonly arise from the heart (especially in atrial fibrillation
4-By Systemic hypoperfusion
Reduction of blood flow to all parts of the body. It is most commonly due to cardiac pump failure from
cardiac arrest or arrhythmias, or from reduced cardiac output as a result of myocardial infarction,
pulmonary embolism, pericardial effusion, or bleeding. Because the reduction in blood flow is global, all
parts of the brain may be affected, especially "watershed" areas - border zone regions supplied by the
major cerebral arteries
Cerebral venous sinus thrombosis5- Venous thrombosis leads to stroke due to locally increased venous
pressure, which exceeds the pressure generated by the arteries. Infarcts are more likely to undergo
hemorrhagic transformation (leaking of blood into the damaged area) than other types of ischemic stroke
6-Hemorrhagic stroke
Accumulation of blood anywhere within the skull vault. Intracerebral, epidural hematoma, subdural
hematoma
DX stroke:

* The diagnosis of stroke itself is clinical, with assistance from the imaging techniques * Neurological
examination, CT scans (most often without contrast enhancements) or MRI scans, Doppler ultrasound,
and arteriographyan angiogram of the cerebral vasculature (if a bleed is thought to have originated from
an aneurysm or arteriovenous malformation) **blood tests to determine hypercholesterolemia, bleeding
diathesis and some rarer causes such as homocysteinuria
**For diagnosing ischemic stroke in the emergency setting
-CT scans (without contrast enhancements)
sensitivity= 16%
specificity= 96%
-MRI scan
sensitivity= 83%
specificity= 98%
**For diagnosing hemorrhagic stroke in the emergency setting: **For detecting hemorrhages, MRI scan is
more sensitive***
-CT scans (without contrast enhancements)
sensitivity= 89%
specificity= 100%
-MRI scan ***
sensitivity= 81%
specificity= 100%
***Stroke treatment
Hemorrhagic stroke must be1-Ischemic stroke 1st step: Imaging ruled out with medical imaging
-ABCD if needed
-Medication (aspirin, clopidogrel, dipyridamole)
-Anticoagulant medication (warfarin-heparin)
Thrombolysis within three hours of onset of symptoms and tPA Contraindications (such as abnormal lab
values, high blood pressure, or recent surgery).
-Workup: Blood tests, such as a full blood count, coagulation studies (PT/INR and APTT), and tests of
electrolytes, renal function, liver function tests and glucose levels are carried out
-Protect brain:
-Ensuring that blood sugar is as normal as possible
-Stroke patient is receiving adequate oxygen and intravenous fluids
-Pt Positioned so that his or her head is flat on the stretcher, rather than sitting up, since studies have
shown that this increases blood flow to the brain
-Additional therapies for ischemic stroke include aspirin (50 to 325 mg daily), clopidogrel (75 mg daily),
and combined aspirin and dipyridamole
**If studies show carotid stenosis >70% symptomatic, and the patient has residual function in the affected
side, carotid endarterectomy removal**Thrombectomy // In acute ischemic stroke of the offending
thrombus directly by catheter into the femoral artery
2-Embolic stroke Anticoagulation can prevent recurrent stroke
require neurosurgical evaluation to detect and3-Hemorrhagic stroke treat the cause of the bleeding
Careful: Anticoagulants and antithrombotics, key in treating ischemic stroke, can make bleeding worse
and cannot be used in intracerebral hemorrhage **Important: Care and rehabilitation and prevention!!!
**Thiamine deficiency.- from Korsakoff syndrome evidenced by Be aware with Glucose admon (AVOID)
because high dose glucose can amnesia precipitate symptoms
**The basal ganglia and thalamus are the classic sites of a acute hypertensive bleed
due to***Bleeding in the brain stem hemorrhagic stroke, poor prognosis from***Bleeding in the
ventricles subarachnoid hemorrhage in adults

**Bleeding in epidural space: epidural hematoma

**Bleeding bridging veins: subdural hematoma
**Absence seizures Rx: 1st line: Ethosuximide and 2nd line: Valproate, lamotrigine, topiramate
CONSIDER Carbon **Any case of headache with altered mental status monoxide poisoning. Children is
at high risk due to increased RR and minute volume** Mild exposure: headache, somnolence, dizziness,
nausea // Moderate to severe exposure: chest pain-dyspnea-ataxia-confusion-seizures-coma // Severe
exposure: increase anion gap metabolic acidosis, 2nd to lactic acid production loss of consciusness and
difficulty walking
-CT scan suspecting stroke: without contrast
-Cerebral Angiography aneurisms,: for vascular pathology occlusion
-X Rays: in acute neuro injuries unless cervical injury is suspected (odontoid view and lateral)
-Carotid stenosis: Doppler ultrasound
-MRI is more sensitive for detecting early ischemia, imaging brain stem, date of injurybut CT scan has
the result more quickly. Reserve MRI for subacute settings and for Follow up
**Open angle glaucoma
C/P: Increased intraocualr pressure -abnormal disk findings and typical visual field loss. Eye no red no
painful, pupil and cornea normal. Affect both eyes
RX: Medication that open trabecular meshwork arounf Schlemms canal, increasing drainage of aqueous
humor and decreasing intraocular pressure.
-Pilocarpine- muscarinic agonist, rapid miosis and contriction of ciliary muscle (in open and closed
glaucoma)
-Prostaglandins-- latanoprost and epinephrine
-Agents that decrease secretion: B-blockers timolol, carbonic anhydrase inhibitors-and alpha agonistbrimonidine
-No steroids!
**In case of pupil dilation and open-angle glaucoma or narrow angle:
Dilation of pupil precipitates the condition.
RX: 1- Pilocarpine (miosis)
-topical B blockers, Carbonic Anhydrase inhibitors and alpha2 agonists
-IV mannitol (draws water out the eye and decrease pressure) Contraindicated in chronic glaucoma!!
Age related, degenerative loss of***Macular degeneration central vision, WET (neoascular or exudative)
or Dry (atrophic). Risk factor: smoking. RX: laser photocoagulation ohotodynamic therapy- Avastin***In emergencies, lifethreatening conditions: not consent required; If neuro emergency with hematoma
for example: go for surgery and evacuate hematoma and stabilize patient.
When all relevant parties are present: Next of sin rules
1. - Spouse
2.-Adult Children acting as the sole decision maker (who has waiver and consent of all other qualified
adult children of the patient)
3. A majority of the pts reasonably available adult children
4. Patients parents
5. Individual identify to act for the pt before became incapacitated, nearest relative or member of the
clergy
**Contraindications Thrombolytic therapy in strokes:
-Stroke or head trauma in the past 3 months -Recent MI
-Prior intracranial hemorrhage -Major surgery in the past 14 days
-GI or urinary bleeding in the past 21 days -Seizures at onset of stroke
***A diagnosis of brain death requires a body temperature of 32.2C or 90 F, lower temperature exhibit

a neuroprotective effect via enzyme inhibition.

Other requirements: absence of poisoning, intoxication, metabolic-endocrine disorders, cerebal events,
absence of brain stem reflexes and vestibulocochlear reflex
Obstetrics
***Eclampsy: Immediate delivery!! Once the patient is stabilized to prevent maternal and fetal mortality
**Deceleration: slowing of fetal heart rate lasting 10-15 minutes
symmetric***Early decelerations decelerations in which the nadir is coincident with the peak of uterine
contraction. -Are mediated by vagal stimulation due to fetal head compression from contracting uterus
-Indicate a normal functioning fetal autonomic nervous system. NOT associated to hypoxia-acidosis RX:
No further management is needed, only Reassuring
**Variable decelerations: Sign of cord compression that can compromise fetal blood flow and
oxygenation.
Tracing- sharp falls in fetal HR followed by a variable recovery time, not association with contractions.
-NON-reassuring tracing! -RX: change patient position from back to side or side to back to relive cord
compression. Also, amnioinfusion used to prevent or relieve umbilical cord compression
**Fetal hypoxia: from fetal anemia, regular and smooth appearing sinusoidal wave pattern. Associated
with HIGH fetal morbidity and mortality!
**Fetal scalp probe: invasive procedure, transvaginal, indicated when external fetal heart rate minitoring
is inadequate. Internal monitoring provides an accurate beat-to-beat and baseline of the fetal heart rate
variability
***Pregnant patients with mild Usually, drugs such as #1- propylthiouracil medical management
hyperthyroidism (PTU)& methimazole 2nd line. Surgery indicated for intolerance to thioamides or in
severe disease.
**The most important factors that affect thyroid physiology in the pregnant patient are Estrogen and Bhuman chorionic gonadotropin.
pt can have**1-12 weeks of gestation: Peak levels of B-hCG subclinical hyperthyroidism because hCG is a
weak stimulator of TSH-recptors and cause excess of production of thyroid hormones and decrease in
TSH due to negative feedback on the pituitary -Occur in 10-20% cases and do not require treatment
hydatiform mole and-Severe hyperthyroidism in choriocarcinoma
***B-hCG can cause hyperemesis gravidarum with severe nausea, vomiting and WT loss
**Pregnant woman, preterm labor, unsure of serial assessment of the cervix for changes next step the
status of membranes in dilation and effacement (speculum examination). Contraindicated digital
examination if membranes are broken, danger of chorioamnionitis!!
**Postpartum endometritis: polymicrobial infection by anaerobes & aerobes from genital tract (exe-Group
B strep) and organism introduced via instrumentation* Risks: nonspontaneous rupture of membranes,
internal fetal monitoring, cesarean section * Management: Blood cultures sending to lab and parenteral
broad-spectrum antibiotics, coverage B-lactamase producing microbes. Gold standard: IV Clindamycin
and Gentamicin--Endometrial cultures --not helpful!
**Polyhydramnios: Associated with Duodenal atresia, tracheoesophageal fistula, or anencephaly

**Vaccination and pregnancy:

-Varicella: live attenuated/women who have not contracted varicella as children should be vaccinated
BEFORE considering pregnancy
-Hepatitis B: in pregnant woman who are completing an immunization series that has begun prior to
conception and to non-immunized women who are at high risk
-Influenza: safe in all pregnant women prior to influenza season.
-Thyphoid vaccine- capsualr polysaccharide parentheral, can be given to pt traveling to endemic area
-Tetanus vaccine- modified bacterial toxoid, inactive, safe in pregnancy, indicate din any woman who has
not completed her 3 dose primary immunization or has not has a booster dose in 10 years.
***Amnioinfusion: Indications:
-Severe variable decelerations by cord compression during labor
-As dilutional method in labors that are complicated by thick meconium stained amniotic fluid.
***Oligohydramnios in 3rd trimester:
Sign of uteroplacental insufficiency, placental abruption, infarction, congenital abnormalities (kidney
agenesis), growth restriction, fetal demise or ruptured membranes. This poses risks to fetus through an
increase incidence of cord compression and pulmonary hypoplasia & Potter syndrome when baby is born.
-Do not require immediate delivery if there is no fetal or maternal distress
RX: prudent course of action with regular monitoring with BPP- Biophysical Profile testing to ensure fetal
well-being and induction of labor when fetal maturity has been achieved.
**During 3rd monitor the fetus to regular intervals for signs of distress. BPP trimester bi-weekly!
**Apgar score summarizes infants overall condition at birth and predicts which aby are going to require
resuscitation.
Apgar 0-3 indicate IMMEDIATE resuscitation, bag-mask ventilation or intubation
Apgar 4-7 indicate possible resuscitation
Apgar 8-10 indicate good cardiopulmonary adaptation
***Causes of IUGR:
-Symmetric IUGR: In utero infection -Multiple pregnancies -maternal disease
-Asymmetric IUGR is due to uteroplacental insufficiency from maternal HTN, smoking, alcohol, poor
nutrition, inadequate WT gain
**Any patient in childbearing age with abnormal bleeding and abdominal/ should be evaluated to rule out
pelvic pain ECTOPIC pregnancy (due to high risk of mortality after tubal rupture, hemodinamic
instability, shock)
**Progesterone challenge test: determine etiology of a anovulatory bleeding:
(+) bleeding: indicates adequate endogenous Estrogen production
(-) no bleeding: indicates insufficient endogenous Estrogen production
**Infertility:
1/3 female factor / 20% male factor / 20% combination male-female factors
Most common male factors: semen volume abnormalities, low sperm concentartion, decreased sperm
motility and atypical morphology
Most common female factors: hormonal problems: ovulation problems- luteal phase insufficiency; tubal
occlusion factor with antecedents of pelvic surgery, PID, endometriosis
***Abruptio Placentae:

-Premature separation of an implanted placenta from myometrium

-Etio: trauma, rapid acceleration-deceleration can lead to shear stress b/w placenta and uterus, disruption
of maternal vessels at the decidua causes discection basalis that leads accumulation of blood. Expanding
hematoma b/w placenta and uterus.
-C/P: PAINFUL bleeding dark vaginal discharge uterine contractions non-reassuring fetal heart
tracing.
***Placenta previa:
Abnormal location of placenta directly or adjacent to cervical os
Etio: multiparity-multiple previous cesarean sections..
C/P: PAINLESS vaginal bleeding beyond 24 wks of gestation no uterine contractions
***Preterm labor
-Onset of labor b/w 20-37 wks of gestation with regular contractions > = 3 contractions every 30 minutes
lasting 30s each and cervical changes assesed by sterile speculum exam. C/P: abdominal, pelvic, back
discomfort, menstrual-like cramps, vaginal D/C or bleeding

Gynecology
performed in all women older***Endometrial biopsy than 35 years who have abnormal uterine bleeding
***Pelvic Ultrasound & in all women in postmenopausal age with adnexal masses further evaluation to
rule out neoplasm (because ovarian should be atrophic at this age)
***Adnexal mass examples (pre-pubertal / reproductive age and post-menopausal women)
Exe#1: pre-pubertal girl with adnexal mass
First: Confirm presence of mass with ultrasound
Completely abnormal - consider neoplasm (because ovaries in pre-pubertal age are not functioning)
Exe#2: Reproductive age with adnexal mass:
#1-Ultrasound: And rule out Pregnancy cause#1
Simple mass - physiologic cyst /most common, ovaries continually functioning at this age #1: Leave
alone; follow up in 2 months or Birth control pills
Complex mass - dermoid cyst - surgical excision
Exe#3: postmenopausal women presents with enlarged ovary (6-7 cm)
First: Confirm presence of mass with ultrasound
Second: Surgical excision r/o carcinoma / consider neoplasm
** General: Premenarchal or postmenopausal adnexal masses consider neoplasms
***Reproductive age woman presents with adnexal mass, Endometriosis // Exam: dysmenorrhea,
dyspareunia, dysquezia and infertility nodularity in uterus and sacral ligament // Endometrioma in
ovary: chocolate cyst / Definitive Diagnosis by laparoscopy
in all**Vulvar lesion Biopsy woman with vulvar lesion itching. More seen in woman > 50s > 60s
*** Nitrazine and Fern tests, for the determination of ruptured membranes during a sterile speculum
examination.
***OCPs: Indicated in PCOS- First line: OCPs due to androgen excess and useful in control and hirsutism
mentrual cycles
***Danazol: Synthetic androgen / First line drug for Endometriosis
***Pergolide- Dopamine agonist -inhibit prolactin / In Hyperprolactinemia
***PCOS: Risk for Endometrial cancer [chronic anovulatory Regular cycles] and breast cancer. Due to

unopposed estrogen secretion Screenings: annual mammogram for detect breast cancer due to high risk
***PCOS: precocious puberty, early menarche, menstrual irregularity, hirsutism, acanthosis nigricans and
obesity
***Risk of endometrial cancer OBESITY 3-10% risk due to high levels of strone and endometrial
hyeperplasia from aromatization of androstenedione in peripheral fat leading to unopposed circulating
estrogen.
***Risks for Endometrial cancer: high estrogens time of exposure during lifetime***
Body habits- Obesity -- particularly being more than 50 pounds overweight
early menarche (periods starting before age 12) more cycles-more estrogen
late menopause (after age 52) more cycles-more estrogens
nulliparity or a history of infertility
HRT with estrogens without progesterone
PCOS / chronic anovulatory state
tamoxifen use
***Unopossed estrogen exposure: Risk endometrial and breast cancer
***Asherman syndrome/ amenorrhea-hypomenorrhea after instrumentation, abortion, D& Confirmatory
Diagnosis: Cause intrauterine synequiae C.. Hysteroscopy
complete or***Cervical stenosis: Amenorrhea or hypomenorrhea partial obstruction of menstrual flow
due to: congenital cause, inflammatory, neoplastic, electrosurgery, conization, laser, cervical
amputation
***Prior Cesarean section- midline incision: (generally in emergency cesarean) Indication for cesarean
section next delivery (high risk uterine rupture)
*** Prior Cesarean section / LOW transverse incision: NOT indication of cesarean in next deliveries
***TOCOLYSIS: Indicated in preterm labor allowing corticoid therapy to promote fetal lung maturity
***To properly stage OVARIAN cancer: Only by Surgical exploration and debulking-nodal sampling
***Chorioamionitis: maternal fever, fetal/maternal tachycardia, uterine tenderness, malodorous Group BStrep*** or E.coli.vagial D/C. Microorganisms: from vagina generally RX: Antibiotic intrapartum/
penicillin
***Vaginal SCC: RX depends of lesion location:
surgery-radical hysterectomy+upper*Upper vagina vaginectomy+bilateral LNs dissection
*Lower vagina: difficult, RADIATION primary RX
follow up with Colposcopy every 3-4***CIN-stage I months time of malignant transformation: 4 years or
quicker***CIN-stage II for CIN II or III: Local excision by LEEP at office setting generally
***Perimenopause: 2 years prior to cessation of menses w. hot flashes, menstrual irregualrity or
amenorrhea.
*If the patient had not had amenorrhea for a FULL year, she is considered peri-menopausal and the
management is REASSURANCE or follow up in 6 months if she has a sporadic bleeding
***Menopause: amenorrhea > 1 year duration + Elevated Gonadotropins (FSH, LH)
indicated in CIN II and III***Cold knife cone excision and LEEP (cervical precancer) and in young
women with malignant invasion<3mm and wishing fertility
***Uterine artery embolization: used in uterine fibroids treatment, because they fed by uterine artery and
embolization of their vascular supply reduces bulk symptoms and menorrhagia

***In PID: risk for due to bowel adhesions, intraabdominal scars, adhesions, bowel obstruction
abdominal processes, laparoscopy, antecedents of ectopics, surgeries
***Etiology Uterine fibroids: unknown or from benign neoplasms growths of abnormal myocytes in
uterus
***Adenomyosis: invasion of undergo hypertrophy and hyperplasia, endometrial glands into the
myometrium associated with incidence of uterine fibroids
***Chlamydia trachomatis often asymptomatic or STD, urethritis, cervicitis, late postpartum
endometritis, and UTIs. In UTIs by chlamydia: disuria piuria but not visible organism on Gram stain of
sterile urine sample.
**Further exams: Direct fluorescent antibody tests and DNA detection tests-PCR
**RX: oral macrolides: Erythromycin-Azithromycin or amoxicillin + prophylactic for gonococcus: IM
ceftriaxone
VALACYCLOVIR for primary and recurrent***Genital Herpes episodes of herpes and for supression
therapy
***Mifeprisotne: antiprogestin used for preventing pregnancy when given 72 hrs of unsafe intercourse: at
one time 600mg or with only 10 mg w. equal efficacy
***Overflow incontinence: 1- by outflow obstruction-urethral stricture or 2- neurologic (sphinteric
spasticity)
Stricture formation: from recent surgery and pelvic radiations
***Stress incontinence: urine leakage when intraabdominal pressure is increased during couging,
sneezing. MC: multiparous woman by sphinteric insufficiency and pelvic floor relaxation
GYN cancers and risks
Cancer RISK factors Protective
Cervix

HPV**
STD *Human papillomavirus infection high-risk" types of HPV:
HPV 16, HPV 18,*** HPV 31, HPV 33, and HPV 45
*Sexual habits:
having sex at an early age
having many sexual partners
having a partner who has had many sex partners
having sex with uncircumcised males
*Smoking * Family history
*Human immunodeficiency virus (HIV)
*Immunosupression
*STD, chlamydia
* Diet: Women with diets low in fruits and vegetables
* Oral contraceptives (long term)
* Multiple pregnancies
* Low socioeconomic status/no screening *Adolescent Sex Abstinence or preventive with safe sex,
condom

*Avoid self and partner promiscuity

*Avoid STDs and HPV
*HPV new vaccine in teens
*No smoking
*Good diet
*Proper Screenings
Beginning: >21 or after 3 years onset sexual relations in low risk pts
Etc
Endometrial
High
Estrogen exposure** Body habits- Obesity -- particularly being more than 50 pounds
HTN and DM
Early menarche (periods starting before age 12)
Late menopause (after age 52)
Nulliparity or a history of infertility
Chronic anovulatory PCOS, *higher-than-normal estrogen levels and lower progesterone conditions
levels
tamoxifen use
HRT- Hormone replacement therapy with exogenous estrogen (i.e., without progesterone) ***
Presence of an Estrogen-secreting tumor *Avoid obesity
*Prevention HTN, DM
*Late menarche (less ovulatory cycles, less estrogen exposure)
*Early menopause- less cycles under estrogen exposure
*Avoid HRT w/o add progesterone in women with a uterus

Ovarian
ovaries are Prepubertal and postmenopausal ages so high suspicion of cancer *+ Family history, BRCA-1
gene *Age no functioning >50
*Past medical history or other cancers: breast-uterus-colon cancer
*African American women/ Jewish descent
** Conditions that increase the number of lifetime # of ovulations:
*Nulliparity (more ovulations) OR Infertility
*Early menarche and late menopause or long reproductive age
*HRT- Hormone replacement therapy in post-menopausal women >estrogen w/o progesterone
* Infertility drugs, use talcum powder, or being obese are risk factors
* High fat diet -Conditions that decrease the number of lifetime # of ovulations
*OCPs
*Chronic anovulation
(PCOS)
*Long breast feeding
*Late menarche and early menopause
*Short reproductive life
*Prophylactic BSO in strong family history

Vulva
precancer HPV
cancer *Age: Almost 85% of women with vulvar cancer are over age 50
*Human papillomavirus (HPV) and immunosupression
*Smoking *Other genital cancers assoiated with HPV
*Liquen sclerosus et atrophicus
* Melanoma or atypical moles on nonvulvar skin
* Precancer: Vulvar intraepithelial neoplasia, need follow ups *none or:
*Prevention w good Sexual habits, condom..
*Avoid STDs and HPV
Vagina
precancer HPV
cancer *Age: Squamous cell cancer of the vagina occurs mainly in older women
* Diethylstilbestrol (DES) exposure Vaginal adenosis during fetal development
* Human papillomavirus and immunosupression
* Cervical precancer and cancer
* Long term Vaginal irritation, prolapse, pesaries use
*Smoking *HIV -Avoid DES exposure during pregnancy
safe sex-prevention sexual-Avoid HPV and STDs untreated habits
-Avoid long term pesaries use, vaginal irriattions..
Tubes
unknown *A family history of ovarian or breast cancer *Chronic infection
Pulmonary
*** Sleep apnea is defined as the cessation of airflow (greater than 10 seconds) that occurs at least 10-15
times per hour during sleep. Oxygen saturation decreases during these apneic episodes, and pulmonary
pressures increase. Can be Central or Obstructive
***Complications: Systemic hypertension and when severe, sleep apnea will cause pulmonary
hypertension and cor pulmonale.
***Central sleep apnea occurs in less than 5% of patients with sleep apnea and is caused by inadequate
ventilatory drive. Treatment is acetazolamide, progesterone, and supplemental oxygen
*** The diagnosis of the sleep apnea syndromes is made by polysomnography (sleep studies) included in
medical workup for sleep apnea. Daytime somnolence is mandatory for the diagnosis of sleep apnea.
*** lung disease of INTERSTITIAL LUNG DISEASE: Idiopathic Pulmonary Fibrosis unknown origin
occuring in the 5th decade of life that causes lung fibrosis and restrictive lung disease. Involves only the
lung and has no extrapulmonary manifestations except clubbing.
*The chest x-ray reveals reticular or reticulonodular disease. CT scan will show ground-glass appearance.
A restrictive intrapulmonary process is evident on PFTs. Bronchoalveolar lavage will show nonspecific
findings, specifically increased macrophages.
RX: Treatment with steroids with or without azathioprine. Complications: Lung fibrosis
*** Sarcoidosis is a systemic disease of unknown cause, characterized by noncaseating granulomas in the
lung and other organs, in blacks, patients 20-40 years of age. Uveitis and conjunctivitis are found in
greater than 25% of the cases and skin lesions.
Chest X-Ray: Chest x-ray findings can show four stages of disease (the stages are not progressive), which
include bilateral hilar adenopathy, hilar adenopathy with reticulonodular parenchyma, reticulonodular
parenchyma alone, or honeycombing of bilateral lung fields with fibrosis.

Laboratory Findings:
*Hypercalcemia or hypercalcuria, caused by increased circulation of vitamin D produced by macrophages.
*Elevation in angiotensin-converting enzyme (ACE).
*Abnormalities in liver functions tests
*Pulmonary function tests may be normal or show a restrictive pattern
*Kveim-Siltzbach skin test (injection of sarcoid) + in 70-80%, is now less used
**The definitive diagnosis of sarcoidosis rests on biopsy of suspected tissues, which show noncaseating
granulomas.**/ Transbronchial biopsy of lung parenchyma
HY: Similar patterns to SARCOIDOSIS: in Berylliosis, Lymphoma, TB, fungal infection and brucellosis)
***Berylliosis: Similar to Sarcoidosis!!! X rays: has bilateral hilar lymphadenopathy, interstitial infiltrates
and biopsy has non-caseating granulomas but tissue levels of Beryllium are ELEVATED! And lood for
antecedent of working in electronic plant, etc. (pneumoconiosis)
***Known Functional pulmonary test parameters to differentiate Restrictive pattern of Obstructive
patterns
Restrictive: volumes decreased
Obstructive: volumes increased
Both: FEV1 and FVC reduced (FEV1 more reduced in obstructive) Decreased FEV1 ratio
FEV1**In hyperresponsive airway obstruction (asthma) ratio can improve with bronchodilators
***Epiglotitis: staph aureus, group Asterp, strep. Pneumoniae, H. Influenzae types A, and less common H.
Influenzae type B due to vaccination.
DX: Laryngoscopy: visualization of a cherry-red swollen epiglottis Lateral X rays show thumb sign
RX: Is an ABCD; A: nasotracheal intubation. If severe edema preventing emergency intubation:
Tracheostomy
***In pregnant woman suspecting a venous thromboembolism: Definitive diagnosis of choice: V/Q lung
scan
***Pulmonary angiography: the most specific test for PE, but indicated if: following test has been treated
and:
1-Has a low or intermediate-probability lower V/Q scan
2-Has a Negative lower extremity Doppler ultrasound
***MRI: not used in pregnant women for PE/risk to harm fetus
combination of:***COPD: Acute RX
-Anticholinergic agents are 1st line of RX: ipratropium bromide +
-B-agonist (Short acting: Albuterol or long acting: Salmeterol) +
-Supplemental Oxygen
***Asthma exacerbations: IV steroids are 1st line of therapy
***Asthma- lifethreatening cases, very refractory to RX: Magnesium sulfate (bronchodilating effect)
***RDS in risk of premature newborn and treatment with oxygen and mechanical ventilation
Retinopathy of prematurity and risk of Bronchopulmonary dysplasia, persistent truncus arteriosus and
necrotizing enterocolitis.
***Standard first line therapy for TB: R I P E
*Combination of: Rifampin Isoniazid Pyrazinamide in single daily ORAL doses Ethambutol
*Side effects:

R- Rifampin: hepatotoxicity (induce hepatic p-450, so reduce efficacy of other drugs) - orange body fluids
I Isoniazid: hepatotoxicity
P- Pyrazinamide: hepatotoxicity- GI intolerance
E- Ethambutol: optic neuritis
***Reactivation of TB: immigrant, non-productive cough, fevers, night sweats, anorexia
Definitive Diagnosis: Acid fast bacilli on sputum smear or culture of Mycobacterium TB from sputum
RX: multidrug Resistance R I Q problem (to isoniazid +Rifampin) use: 4th drug regimen in endemic area
A
Rifampin +Isoniazid + Quinolone (Levo-moxifloxacin) +Aminoglycoside (Streptomycin or Amikacin)
***Purified Protein Derivative (PPD) is useful to diagnose TB infection only among HIV infected
Reactivity: individuals with CD4 >500.
lowering cut Individuals with LOW CD4 counts off levels or using an anergy panel does not permit
comparable reactivity with unininfected HIV
*** Solitary pulmonary nodule: lung nodule <3cm discovered in x rays or CT of the chest, has 40% risk of
malignancy and review old x ray or film is crucial because they can give an indication of the Nodule the
most important factor conncerning malignancydoubling time
Malignant (doubling b/w 20-400 days) and border are irregular nodule
**SCC (poorest doubles every 30 days! prognosis)
**Adenocarcinoma (2nd poor prognosis doubles every 180 days [25%])
Benign nodules: Doubles < 20 days in infections or >450 days in old granulomas and tend to have a
smooth discrete border and the presence of certain calcification patterns, (but an eccentric lesion having
an asymmetric area of calcification should be malignancy)
diffuse ground***Pneumocystic jiroveci (carinii) pneumonia glass infiltrates (most common in HIV with
CD4 <200, intravenous abuser, etc)
***Complication: associated with necrosis and pneumothorax
***Baclofen: muscle relaxant that reduces the involuntary, abnormal movements and posturing affecting
children patients with cerebral palsy by inhibiting reflex pathways in the spinal cord.
***Large pulmonary embolus:
History of stasis, tachypnea, dyspnea, venous jugular distension, accentuated pulmonic component of the
2nd heart sound, elevated D-dimer on ELISA, CT scan +Pulmonary physiology changes with PE:
**DECREASES: Lung compliance (due to edema, lung hemorrhage and loss surfactant)
**INCREASES: Airway resistance (bronchoconstriction of underperfused portions), Alveolar dad space,
Alveolar Ventilation and Pulmonary Vascular Resistance.
type of inhalation of cotton dust ***Byssinosis Hypersenitivity pneumonitis. May recur with reexposure, and after 10 years have an obstructive pattern on PFTs.
***50% pts with ASBESTOSIS has multiple pleural plaques
***Bacterial pneumonia: Consolidation of lung tissue, acute onset of Fever, Productive cough and
decreased sounds over the consolidation
***ARDS: pulmonary edema in the absence of volume overload or depressed left ventricular function.

ETIO: more common occur by INFECTION or sepsis principally with history of alcoholism
To asses Respiratory status: PaO2/FiO2 ratio:
-Values <Bilateral infiltrates and PCWP300 <18 Acute Lung Injury ALI (noncardiogenic pulmonary
edema)
-Values < ARDS 200 / is a more sevre form of ALI
***Primary spontaneous pneumothorax: principally due to rupture of subpleural blebs in tall, thin, young
men/ associated with Marfan
Pneumothorax <15% of hemithorax: management: Observation with supplemental OXYGEN is the best
approach because they resolve spontaneously
***Recurrent bronchitis is a frequent pulmonary symptom of Mitral Stenosis due to congestion
C/P: Low pitched Diastolic rumble audible at the apex and an opening snap.
Mitral stenosis causes pulmonary edema and dyspnea precipitated by tachycardia during exercise, volume
overload and atrial fibrillation
Cardiogenic pulmonary edema:
***Aortic stenosis causing Pulmonary Edema Cardiogenic Pulmonary edema, failure of left ventricle to
move blood forward resulting in INCREASED filling pressures in pulmonary capillaries.
*IINCREASE in capillary fluid Hydraulic Pressure due to Left Ventricular systolic or Diastolic
Dysfunction****
C/P: Dyspnea- orthopnea-paroxysmal nocturnal dyspnea-and rales to auscultation and cardiomegaly and
pulmonary vascular congestion on x rays.
TRIAD: 1-CHF 2-Syncope 3-Angina
Neurogenic pulmonary edema:
From Subarachnoid Hemorrhage due to massive sympathetic discharge
Other causes: Epilectic seizure head injury
***Exercise Tolerance Tests: to diagnose CAD, localize inchemia and risk-stratify pts after acute coronary
syndromes
***Cystic fibrosis and lung disease: Bacteria tipically results in Pseudomona or Burkholderia cepacia
bronchiectasis
***Aspergillus: pulmonary disease or Allergic pulmonary aspergillosis or aspergilloma. Occur in CF pts
and asthma with bronchial obstruction, fever, malaise, expectoration brownish mucus plugs.-upper lobe
infiltration on x rays and atelectasis from mucoid impaction. Ussually arises from cavities from TB
Diagnosis: Skin tests reactivity or serum IgG and IgE to Aspergillus
RX: surgery of aspergilloma ball or lobectomy
***Pulmonary lipoma: in pulmonary parenchyma, peripheral located, asymptomatic, casual finding on x
rays or CT, uniform fatty density with soft tissue strands due to fibrous stroma.
***Infectious granulomas presenting as solitary pulmonary nodules: TB, fungi, histoplasmosis and
coccidioidomycosis
***Neurilemmoma is a neurogenic tumor arising from cells of the nerve sheath and paraganglionic and
autonomic ganglia, Scwann cell derived-mediastial 21%, well encapsulated and have a unique histologic

pattern. Can cause cosmetic deformity, palpable mass and compressive neuropathy late in the course.
***VERY HY concept for usmle step2 CK: lung cancer!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

Lung cancer Review

1. SCLC: non considerable to surgery (chemo and radiations)
2. surgical resection in early NSCLC: (Squamous cell, Adenocarcinoma, large cell) stages, radiation,
chemotherapy
=CENTRAL: Originating from bronchioles greater than 1mm in diameter, and assoc. with
smoking.DX:Bronchoscopy
=PERIPHERAL: from lung parenchyma, airspaces < 1mm, and not associated w smoking. DX:needle
aspiration Bx
-Sites of metastasis: 1. adrenal gland*, 2. liver, 3. bone 4.brain 5. bone marrow
Cancer Loc. Charac. C/P DX & RX
Small cell
Lung
carcinoma
ACTH
ADH
COIN lesion
Bronchogenic Central
Types:
Oat Cell: Smallest
cells. Interme-diate:
Large Smoking cells. Combined: with adeno-carcinoma or squamous carcinoma. Men
-Rapidly growing and metastasis /brain-liver-bone
-DO NOT Tend to cavitate
-Recurrence after treatment
-Associated with paraneoplastic syndromes:
**Ectopic hormone production:***
-ACTH, ADH
Cushing syndrome, SIADH
-Rapidly growing with early distant metastasis to extrathoracic sites such as liver, adrenal glands, brain,
and bone
**Histology:
Epithelial cells, small, round (oat cells)
- Kulchitsky cells -Neuroendocrine cells origin or granules Anapalstic cells with basophilic nuclear
material -Wheezing, cough, marker Bombesin dyspnea
-weight loss
Peripheral neuropathy
-Subacute cerebellar degeneration
-Lambert Eaton syndrome
*X rays: COIN lesion !!!!

Complications: SPHERE
Superior vena cava syndrome
Pancoast tumor
Horner syndrome ( miosis, ptosis, anhidroses)
Endocrine paraneoplastic (hormone prod.)
Recurrent laryngeal symptoms (hoarseness)
Effusions (pleural or pericardial) *Sputum cytology
*Bronchoscopy is best for central lesions
*X rays..
*CT scan
*Mediastinos-copy
*Prognosis is the poorest
Treatment:
No surgery, Radiation, chemotherapy
Squamous
cell carcinoma
- PTH
-Ca
-TNF alpha
-IL-1
Smoking Bronchogenic Central Men
-Hilar mass, circular, sesile arising from bronchus (bronchial epithelium (Central)
-Tend to cavitate!!!
-Endocrine syndromes:
1- PTH-ectopically Hyperparathyroidism 2:PTH, Ca, secreted PO4
-Hypercalcemia
-Pathologic fractures Kidney stones
**Histology: Well differentiated cells
Keratin production (keratin pearls) bronchial epithelium- Intercellular bridges -Wheezing, cough
-Hemoptysis, dyspnea
-weight loss
-Pathologic fractures Kidney stones-from hypercalcemia
-no breath sounds- affected lobe, decreased tactile fremitus
*X rays: circular lesion-inters-titium of lung-Centrally located
-Cavitary!!!
*Complications: Horner synd. -Sputum cytology
-Bronchoscopy is best for central lesions
Treatment: *Surgical if good FPTs and no metastasis
Pneumonectomy
*chemo + radiation
Carcinoid
tumor -Central 90%
-Peripheral -Not associated with smoking
-Low grade cancer of neuroendocrine origin -Secrete: Serotonin, peptides, hormones or inactive. Growth
slowly -Wheezing, cough
-Flushing diarrhea -salivation -low malignant
-Can cause carcinoid syndrome -x rays
-CT scan -MRI

-Bronchoscopy
-Biopsy
Bronchial hamartoma
Coin lesion Central Non-neoplastic or BENIGN lesion of cartilage and adipose tissue
Solitary coin lesion on chest radiograph -Asymptomatic, incidental finding
*x rays: solitary coin lesion
with popcorn calcification -Sputum cytology
-*Bronchoscopy
AdenoCarcinoma
Solitary pulm. nodule Peri-pheral
non-Smoking Most Common: Women
*ACINAR: Well differentiated "back-to-back" acinar glands. SOLID: Poorly differentiated. *PAPILLARY:
Rare, finger-like projections.
it is a low-grade*BRONCHO-ALVEOLAR carcinoma carcinoma that can occur in single or multiple
nodules in bronchioles with high sputum production & interstitial infiltration
- Asbestos exposure can be underlying causative agent, usually after a latent period of 30 years.
**Histology: clara cells. Mucin producing cells -Pleural effusions !!
-Wheezing, cough, dyspnea
*Digital clubbing!!! Hypertrophic Pulmonary Osteoarthropathy]
1-Bronchial: develops in site prior injury -lobar neumonia
2-Bronchoalveolar: not linked to smoking -hemoptysis, chest wall pain, and repeated pneumonia
X rays: Multiple densities or Solitary pulm. nodule-Coin lesions in periphery or scars -Needle aspiration
biopsy
-Thoracotomy with pleural biopsy often needed
-If surgery:
lobectomy
Large cell carcinoma
Lung cancer
Solitary pulm. nodule Peri-pheral -Undifferentiated, metastasizes early and late to distant locations late in
the course of disease.
-In early stages is associated with cavitation
*Histology: Pleomorphic giant cells with leukocyte fragments in cytoplasm -Wheezing, cough, dyspnea
-weight loss unintentional
- Solitary pulm. nodule
-Increased Gynecomastia, milky breast discharge. -Needle aspiration Bx B-hCG
-Surgery: lobectomy
*poor prognosis 25%
Metastasis
Multi-focal -More common than primary cancer!
-Dyspnea. Often there is also lymphangiitis, or metastases that reached the lung through lymphatic
system. -Wheezing, cough, weight loss
-Metastases: - Brain, bone (fractures), liver (jaundice-hepatomegaly). Tumor sharp -Metastasis workup
-Palliative RX

Renal / Genitourinary
Fluid and electrolyte disorders High Yield
Disorder DX RX
Hyponatremia Clinical: Entirely neurologic in nature. Headache, lethargy, obtundation, and eventually
coma and seizures are most common. Serious at less than 120.
Urine osmolality greater than serum osmolality in the presence of hyponatremia is generally diagnostic.
Serum antidiuretic hormone/vasopressin levels are not used.
Serum sodium decreased <136-140
Urine sodium >than 40 (Increased) Corrections should not be faster than 12 milliequivalents per day.
Overly rapid correction results in central pontine myelinolysis. This is destruction of the brainstem, giving
paraparesis, dysarthria, or dysphagia.
1. Mild (approximately 120 to 130) fluid restriction to less than 1,000 ml.
2. Moderate (approximately 110 to 120) loop diuretic and normal saline to give a net free-water loss.
3. Severe (approximately less than 110 with symptoms), hypertonic saline.
4. Chronic: Lithium and demeclocycline cause a nephrogenic diabetes insipidus. This makes the kidney
insensitive to antidiuretic hormone/vasopressin.
Hypernatremia
Clinical: Primarily neurologic: Lethargy, weakness, irritability, seizures, and coma are present with severe
hypernatremia of any cause.
Diabetes insipidus gives a dilute diuresis of 3-20 liters per day.
Serum Sodium increased
Urine sodium decreased
Acute hypernatremia is treated with isotonic fluids intravenously. Correction of sodium should not be
greater than 1 mEq every 2 hours or 12 mEq per liter per day. Complications of overly rapid correction
include cerebral edema, permanent neurologic damage, or seizures.
1. Central Diabetes Insipidus: Correct the underlying cause, if possible. Give vasopressin (antidiuretic
hormone). It can be given subcutaneously, intravenously, intramuscularly, or by nasal spray (all routes
except oral).
2. Nephrogenic Diabetes Insipidus: Correct underlying cause, if possible.
Diuretic or NSAIDS. NSAIDS work by inhibiting prostaglandins, which impair concentrating ability.
NSAIDS will increase the action of antidiuretic hormone at the kidney.
Hypokalemia Symptoms usually start when potassium falls to less than 2.5 to 3.0 milliequivalents per
liter.
Muscle weakness, paralysis, cardiac arrhythmias
U-wave on electrocardiogram, T-wave flattening, rhabdomyolysis, nephrogenic diabetes insipidis.
Correction of underlying cause when possible.
Repletion. Intravenous maximum 10-20 milliequivalents potassium per hour.
Oral: need 200-400 mg. of potassium.
GI tract slows absorption; dextrose brings increased potassium into cells;
use half normal saline or normal saline.
Hyperkalemia Diagnosis: Increased K above 5.0
Electrocardiogram findings:
1. Peaked T waves
2. Widened QRS
3. short QT

4. Prolonged PR. 1. Calcium chloride: Membrane stabilization (most emergent treatment in presence of
electrocardiogram abnormalities). Effect is immediate and short lived.
2. Sodium bicarbonate: Alkalosis drives potassium into cells. Do not give in the same intravenous line as
calcium, otherwise it forms calcium carbonate precipitate.
3. Glucose and insulin: Drives potassium intracellularly, takes 30-60 minutes to work.
4. Diuretics.
5. Beta agonists.
6. Cation exchange resins (Kayexalate): orally.
7. Dialysis.
***
RENAL TUBULAR ACIDOSIS:
Distal Renal Tubular Acidosis Type I
Etiology:
Usually sporadic.
- Secondary to autoimmune disease (e.g., Sjogren syndrome).
Drugs: Amphotericin, lithium, analgesics. Nephrocalcinosis, sickle cell, chronic infection.
Presentation:
Inability to develop a high hydrogen concentration in urine.
Urine pH is greater than 5.4. Secondary hyperaldosteronism and hypokalemia.
Nephrocalcinosis and nephrolithiasis.
Diagnosis: K
1. Acid load test; give ammonium chloride, which should lower urine pH secondary to increased hydrogen
formation. With type 1 renal tubular acidosis, the urine pH remains elevated.
2. Serum bicarbonate equals 10.
Treatment: HCO3
Oral bicarbonate because bicarbonate reabsorption in the proximal tubule still works; potassium
replacement.
Proximal Renal Tubular Acidosis Type II
Etiology:
Fanconi syndrome, Wilson disease, amyloidosis myeloma, vitamin D deficiency, chronic hypocalcemia,
heavy metals, chronic hepatitis, autoimmune diseases such as systemic lupus erythematosus and Sjogren
syndrome.
Presentation:
Inability to absorb bicarbonate.
The initial urine pH is basic (until the body loses enough bicarbonate that it is within the range of
absorption of the distal tubule), then the urine will become acidic (pH less than 5.4).
Also with hypokalemia and a serum bicarbonate of 18-20.
Patients with type 2 get bone lesions (osteomalacia and rickets), whereas type 1 get kidney stones. Both
get hypokalemia.
Diagnosis: K
Patients are unable to absorb bicarbonate loading (sodium bicarb intravenous) and have a basic urine in
the presence of acidemia.
Normal individuals do not excrete bicarbonate in their urine until serum bicarbonate is greater than 24.

Treatment: K
Give potassium; mild volume depletion will enhance proximal bicarbonate reabsorption (a type of
contraction alkalosis). Thiazide diuretics: very large amounts of bicarbonates.
Renal tubular Acidosis TYPE IV
Hyporeninemic Hypoaldosteronism NON-GAP Metabolic Acidosis Hyperkalemic Hyperchloremic
Etiology:
An aldosterone deficiency of any cause or adrenal insensitivity to angiotensin 2, which normally
stimulates aldosterone release.
Diabetes (50%). Addison disease.
Sickle cell disease.
Renal insufficiency.
Presentation:
Usually asymptomatic hyperkalemia. K
Mild to moderate renal insufficiency.
Hyperchloremic metabolic acidosis (non-anion gap). Cl
Hypophosphatemia PO4 and Glycosuria with normal glucose in serum
Diagnosis: . K
Continue high urine sodium with oral salt restriction.
Treatment: Fludrocortisone
***Nephrotic syndrome, nonspecific, focal segmental glomerulosclerosis FSG: Secondary to heroin abuse
IV or drugs as Lithium or to malignancy like lymphoma -----Hypoalbuminemia and marked proteinuria
***Goodpasture syndrome: Abs deposition in glomerular basement membrane/ nephritic syndrome,
hemoptysis and respiratory symptoms+ renal symptoms
***Most bladder cancers:
Transitional cell carcinoma: Most common**
Risk factor**MC: smoking and industrial solvents and dyes as aniline, male, 65 years and up. Painless
hematuria and irritative voiding symptoms
Adenocarcinoma of bladder less common, 2% only
***Acute bacterial prostatitis: perineal suprapubic or sacral pain, irritative voiding symptoms, pain, fever
or urinary obstruction; contraindicated prostate examination (risk of sepsis)
DX: Urine culture after massage if possible and analyzed microscopically.
--Only do gentle massage with extreme care (risk of sepsis and bacteremia and very painful)
--If obstruction: suprapubic tube is safer than Foley catheter
***Prostatic abscess and not respond to antibiotic therapy: Transrectal ultrasound and CT scan
***Transrectal ultrasound and transrectal biopsy: in prostatic cancer suspected
***Prostate cancer examination: Digital rectal exam: focal nodule within the prostate or detected by
biopsy
***Prostate Biopsy when PSA >4.0 or digital exam is abnormal. Only way to confirm cancer (not a

screening testing)
***The most sensitive method for screening men for prostate cancer:
1- PSA
2- Digital rectal exam (when not elevation of PSA)
***Hematuria workup: Cystoscopy***
***Benign prostatic hypertrophy of the prostate: obstructive symptoms, enlarged prostate on digital exam
* Can be managed expectantly with medication (alpha blockers, and inhibitors of 5-alpha reductase)
* Or with surgery (transurethral resection of the prostate) in severe cases or with renal disease associated
to prevent further renal damage
*Prostate carcinoma biopsy: Surgery is Radical retropubic prostatectomy
***Interstitial cystitis: pain during periods of bladder distention relieved by voiding. Has frequency,
urgency, nocturia and diagnosis by exclusion or cystoscopy
***For each 1g/dL reduction in albumin levels in the body = Lowered Total calcium by 0.8 mg/dL
In states of undernourished in elderly, hypoalbuminemia, hypoproteinemia
-BUN correlates to dietary intake and hydration status. If protein intake is decreased = BUN is decreased,
but not role in measurement of total or ionized calcium. Because active, ionized calcium is only a fraction
of total calcium (45%).
When the 40% of total calcium that is normally bound to albumin is Albumin is low also LOW, so
calcium total is low. This reduction does not represent a reduction in ionized calcium and will not cause
clinical hypocalcemia
-Elderly low calcium undernourished with BUN low
***BUT this hypocalcemia does not so the patient does NOT need calcium represent a decrease in
ACTIVE calcium therapy or repletion***
***Uremic pericarditis/ HEMODIALYSIS
Azotemia, friction rub, ECG with ST segment elevations (early pericarditis)
Determine absence of pulsus paradoxus, gral if not associated with Tamponade appearanceImportant
for initial management!
If Tamponade associated: Drainage of the effusion is crucial before other management
If NOT Tamponated associated: Initial: Emergent HEMODIALYSIS and avoid heparin (pt is
coagulopathic)
*** Peyronie's disease is a connective tissue disorder involving the growth of fibrous plaques in the soft
tissue of the penis, is also formally known as "penile induration" The disease may cause pain, hardened,
cord-like lesions ("plaques"), or abnormal curvature of the penis when erect. In 50% the induration can
resolve spontaneously. RX: No medical treatment needed and observation and emotional support is
advised as 1st line of therapy
Medical RX: Vitamin E, Ca channel blockers and local injected steroids or surgical if severe
in children***Vesicoureteral reflux grally, from abnormal connection of the ureters and bladder and is
associated with urinary UTIs and renal damage. DX: VOIDING Cystourethrogram
***Pt RX: Urine alkalinization with Potassium bicarbonate (prevention with cystinuria of cysteine stones
by increasing urine PH with low urine volume // But associated with new stones of calcium phosphate

***Renal insufficiency
Renal dysfunction: Present with a wide range of symptoms because of the crucial role pt of kidneys is
filtering toxins from the plasma. As Uremic tosins increase present with pruritus, nausea, vomiting,
hiccups, metallic taste, altered sensorium, malaise, asterixis and pericardial friction rub in cases of uremic
pericarditis.
Real failure can be caused by: hypovolemia (PRERENAL failure) or can cause hypervolemia (oliguria or
anuria)
***After a crush intrarenal Myoglobinuria (blood in urine w/o RBCs) Rhabdomyolysis injury failure
Increased: LDH, CK, uric acid, PO4 and K. Monitor for arrhythmias, muscle weakness due to
hyperkalemia
RX:
-Rhabdomyolysis: follow CK levels, Alkalinization of urine and aggressive hydration
-Maybe pt would be need dialysis in severe hyperkalemia
***Klinefelters syndrome: associated with increased incidence of Germ cell tumors in extragonadal sites
***Common complication of polycystic kidney disease RX: Gentamicin+Ampicillin pyelonephritis
If pt has an infected cyst percutaneous cyst drainage would be useful, but it is an invasive procedure and
carries risk of iatrogenic injuries: infection and bleeding. AVOID if pyelonephritis
***ACEIs: minimize and slow glomerular injury. Indicated in diabetic nephropathy with HTN and in
polycystic kidney + HTN
***Diet low in protein: slow progression of kidney disease: reduce intraglomerular pressure and may slow
the decrease in GFR
***Blood in urethral meatus suggest urethral injury
a rectal examination to evaluate DX: First step prostate position (a high-riding balotable prostate, which
further suggests a urethrogram urethral injury) or presence of gross blood. 2nd step:
-Avoid Foley catheter!
***Jackson-Pratt creatinine test:
Is a test for confirm possible injury to ureter, kidney, bladder caused by iatrogenic in OB/GYN or in
urologic surgeries). The fluid in the JP drain light pink would be urine leaking; and this fluid is sending to
lab to confirm high creatinine levels.
***Aminoglycosides affect tubular renal function and have a high associated with Acute Tubular risk of
nephrotoxicity necrosis
***Enalapril, ACEI: causing pre-renal failure, decreasing GFR and dilating afferent arteriole.
ACEIs are**In Renal artery stenosis relatively contraindicated
if has***Patient in postoperatory setting lab results for hyponatremia with no apparent symptoms
(confusion, stupor, next step: draw blood for laboratory tests from the other arm to seizures) confirm
REAL Hyponatremia; because is a common occurrence in pts who are phlebotomized in the same arm as
the IV infusion proximal to the catheter site.
**If REAL mild asymptomatic hyponatremia (Na<120): fluid restriction

correction of Na and do not**If severe hyponatremia + neuro symptoms exceed 1.5 to 2 mEq/hr (avoid
central pontine myelinolysis)
**CREST syndrome: produce hypercalcemia and the initial treatment is HYDRATION which can
normalize Ca level w/o further RX. Empiric use of acid-reducing agents, PPIs** to prevent esophageal
stricture. Raynauds: Ca channel blockers. Telangiectasias: laser therapy.
***Renal stones, hyeprcalciuria: can be caused by reduced calcium intake in diet. Recommended: a lot of
fluids
***Drugs: antibiotics like penicillin, cephalosporins and sulfas cause intrarenal failure by Acute
Interstitial Nephritis, acute inflammatory process of renal tubules similar to an allergic reaction. RASHFEVER & EOSINOPHILIA and WBS-RBC casts in urine
Renal Failure summary
Pre-renal Failure Intra-Renal Failure Post-renal Failure
General RPF Renal Plasma Flow or renal perfusion From injury within the nephron unit or renal
parenchyma From urinary out flow obstruction
Urine-Osmo > 500 < 350 < 350
Urine Na < 20 - 40 > 20- 40 > 40
Fe/Na excre < 1% > 1 % > 1%
BUN/Cr ratio >> 15/1 or >>20 < 15/1 or < 10-15 > 15/1 or > 15
If tubular damage: become < 15/1
Urinalysis
Scant; few hyaline casts Acute tubular necrosis Epithelial cells, muddy-brown, granular casts, WBCs,
proteinuria
Allergic interstitial nephritis WBC, RBC, epithelial cells, eosinophils, WBC cast, low to moderate
proteinuria
Glomerulonephritis RBC casts, dysmorphic red cells, proteinuria
Scant; no casts, few WBCs, possible red cells

Causes -Hypovolemia -volume deficits..-Ischemia-hypoxia

Hemodynamic effects
RBF GFR CO
1. True intravascular depletion
Hypovolemia
-Sepsis, hemorrhage, over- diuresis -Sweating
-poor fluid intake
-vomiting, diarrhea burns
-Shock, sepsis, anaphylaxis
2- Decreased effective circulating volume to the kidneys / hypoxia
-CHF: Congestive heart failure
-CVS: Pericarditis, tamponade
*-Hepatorenal syndrome -Cystic fibrosis
-Nephrotic syndrome and catabolic states ( oncotic pressure)
-Renal Artery Stenosis
3. Impaired renal blood flow because and GFR by drugs- exogenous agents
-ACEIs- --- -NSAIDs-**

go to intarrenal azotemia or failure If ischemia is prolonged 1-Tubular disease 2-Glomerular disease

3-Vascular disease 4-Interstitial disease
1*Tubular Disease*Acute tubular necrosis is the most common cause of intrinsic acute renal failure in
hospitalized patients
- Usually induced by Ischemia or Toxins (Nephrotoxic tubular necrosis)
a) Ischemic tubular necrosis
GFR does not improve with the restoration of RPF. Ischemic acute tubular necrosis is reversible, but if the
ischemia is severe w. cortical Irreversible renal failure necrosis
-#1 cause: from prerenal azotemia
-Basement membrane disrupted
-TAL medulla most sensitive zone
b) Nephrotoxic Tubular Necrosis:
-Basement membrane intact -Damage PT
-By Contrast agents and aminoglycosides
-By pigment from myoglobinuria (rhabdomyolysis) or hemoglobinuria (hemolysis)
**Acute tubular necrosis phases**
1-Initiation 2-Maintenance 3-Recovery
4. *Interstitial disease
Acute interstitial nephritis usually:
TRIAD: Fever, Rash and Eosinophilia
-By drugs NSAIDs, peni, sulfas, TB drugs, Allopurinol, infections Urinary tract flow obstruction
-Benign prostatic hypertrophy or prostate cancer
-Cervical cancer
-Retroperitoneal disorders
-intratubular obstruction (crystals or myeloma light chains)
-Pelvic mass or invasive pelvic malignancy, intraluminal bladder mass (clot, tumor or fungus ball)
-Neurogenic bladder
-Urethral strictures
Diagnosis -Function tests: urine osmolality urine sodium urine urea:-plasma urea ratio -fractional
excretion of sodiumUrinalysis #1- Urinalysis Best initial test
#2- Renal function tests
** Renal Biopsy more definitive test -By clinical and exam
-Urinalysis
-Bladder Catheter
-Ultrasound- Gold standard test
Treatment **If volume depleted: Normal saline/ isotonic saline- Rehydration
**Stop offending agents
**Gral treatment **Ischemic
**If nephrotoxic: Stop offending agents -Treat underlying cause
-Lithotripsy (stones)
-Ureteral stenting
-Percutaneous nephrostomy

Gral treatment 1- Correct Fluids (M.C: hyperkalemia and acidosis) and Uremia and electrolytes
*If Hyperkalemia: Intravenously administered calcium, K excretion is achieved with (Kayexalate) or
diuretics
*Acidosis is treated with intravenously or orally administered sodium bicarbonate
2- If volume depleted: Normal saline/ isotonic saline
3- If volume overload: loop diuretic: Furosemide
4- Because acute renal failure is a catabolic state, patients can become nutritionally deficient.
Combination of carbohydrate and lipids, and protein intake should be restricted to 0.6 g/kg/day (dialysis:
1-1.5 g/kg/day)
5- Last resort: Dialysis Indications: Severe irreversible Renal Failure: acidosis or electrolyte disturbances
that do not respond to pharmacologic therapy, fluid overload that does not respond to diuretics, and
uremia.
Full examinations / MIX
***Progression Skin cancers:
1- BCC: MC skin cancer*
***Slow growing with destruction of local tissue that may extend along nerves to penetrate into the
Central Nervous system if untreated, but has very LOW % of metastasis
-Pearly, telangiectatic nodular lesion with rolled borders, central crusting or ulceration
Referred to as an epithelioma due to the low metastatic potential
Risk factors: childhood sunburns, xeroderma pigmentosum, chronic dermatitis, fair skin
2- SCC:
***Prognosis is GOOG if removed or excised early but has 3% propensity to LNs metastasis demanding
frequent F/Ups after excision
Scaly, erythematous that may ulcerate, 3% metastasize to adjacent LNs
Risk factors: immunodeficiency, exposure to x rays and sun exposure, location head and neck
3- Malignant melanoma
***Undergoes an initial radial growth phase but then is followed by a vertical growth phase, HIGH
metastatic potential
Risk factors: male >50 years old, excessive sun exposure, childhood sunburns, ultraviolet radiation used
in indoor tanning equipment fair-skinned sun-sensitive people, persons with>50 or 100 moles, irregular
borders, atypical or dyspalstic moles, family history- xeroderma pigmentosum or familial atypical mole
melanoma syndrome
ABCDs of Melanoma-Asymmetry, Borders [irregular], Color [variated] and Diameter [>6cm]
***Pt depressed with suicidal thoughts in great danger to NEXT step: Always ask a nonjudgmental Qs,
yet direct have you thought himself of any plan or a way to commit suicide? Elucide details of the plan
***Pt stimulant drugs or dopamine agonists with MOTOR tic (blinking for example) contraindicated (risk
of worsen tics and anxiety) Correct RX: Haloperidol, pimozide or clonidine
Peritoneal***MC cause of bowel obstructions: ADHESIONS (from previous abdominal or pelvic surgery,
laparo, procedures, PIDs, etc)
***Hodking disease: pt with night sweats, awake with panic attack like symptoms, Pel-Ebstein or cyclic
fevers, shortness of breath due to mediastinal mass or adenopathy. NEXT STEP: X Rays chest (rule out
other pathologies like TB, asthma, cardiomyopathy)

***Pseudomona aeruginosa septicemia or peritonitis= in pts with recent kidney transplant, cystic
Fibrosis, HIV
***Enterococci = Recent liver transplant
***Pneumocystic jiroveci pneumonia= HIV, CD4 low <200, and infants 2-8 months old
***Strep. Pneumoniae & encapsulated= pts with bone marrow transplant, asplenia
***Trivalent influenza A vaccine or inactivated flu vaccine children > 6 months with asthma, CF, DM,
HIV, bronchopulmonary dysplasia, sickle cell anemia, chronic heart disease
***Also for: >65 years old, adult chronic pulmonary disease, asthma, DM, hemoglobinopathies
***Metformin = GI symptoms and Metabolic Acidosis anion gap elevated, lactic acidosis
***Pt with Hemophilia A (factor VIII deficiency)
Prophylactic RX before a surgery: Desmopressin (vasopressin analog) promotes release of factor VIII or
von-Villebrand.
RX in severe Hemphilia A or active bleeding: Factor VIII replacement therapy, Cryoprecipitate (has all
factors) but is avoided if viral antecedents
***Hemophilia B: RX: Factor IX Concentrate, or FFP / No desmopressin
**Know hereditary hypercoagulable states:

Hypercoagulable states Hereditary syndromes

Antithrombin III Deficiency A. Anticoagulation with either heparin or warfarin is the mainstay of
treatment.
B. AT concentrates are available.
C. In patients with recurrent thrombotic episodes, anticoagulation is required indefinitely.
D. In pregnancy, maintain the mother on subcutaneous heparin throughout the pregnancy. If used, AT
concentrates are most useful during labor, delivery, or obstetric complications.
E. DIC - may use AT concentrates
F. In acquired AT deficiency, treatment of the underlying disease

Protein C Deficiency **Congenital

-Increased risk of thromboembolism, primarily DVT and PE -Begin in mid-late teenage years.
Homozygous patients often die early
-can also occur in the cerebral veins, retinal veins, mesenteric veins, renal veins, and IVC
-Clotting precipitated by surgery, trauma, pregnancy, or oral contraceptive use.
-Arterial thrombotic events are rare.
-Neonatal purpura fulminans: neonate w. ecchymoses
-Coumadin Skin Necrosis
**Acquired Protein C Deficiency: DVT, PE, cancer - Acute thrombosis should be treated with Heparin.
-Long term prophylaxis can be undertaken with Warfarin.

-When starting warfarin, very low doses must be used initially to prevent skin and fat necrosis. -Longterm low dose subcutaneous heparin can be used as an alternative to warfarin.
- Protein C concentrates are also available. Factor IX concentrates also contain Protein
Protein S Deficiency -Congenital-similar to C def.
-Adquired -in DIC or extensive DVT/PE, warfarin RX - Heparin for acute thrombosis.
- Maintenance anticoagulation with warfarin or low dose subcutaneous heparin.
- Prophylactic heparin during pregnancy & partum
- Perioperative prophylaxis with heparin.
Activated Protein C Resistance (Factor V Leiden) MC* -Congenital, AD
-C/P similar to Antithrombin III, Protein C, and Protein deficiencies.-Increased risk venous thrombosis, PE
-Deep veins of the lower extremities.
-Events in mid-late teenage years.
- Mesenteric veins, IVC, renal veins -Cerebral vein
- Thrombosis may be precipitated by surgery, trauma, pregnancy, OCP use, sepsis -Acute thrombosis
should be treated with intravenous Heparin.
- Long term prophylaxis should be undertaken with warfarin.
-. Long term low dose subcutaneous heparin can be used as an alternative to warfarin.
Perioperative prophylaxis with intravenous heparin.
Antiphospholipid Syndrome
*Anticardiolipin Abs
*Lupus
Anticoagulant -Autoimmune or 2nd to autoimmune disease (SLE)
1 -Anticardiolipin Abs
-Thrombosis and Thromboembolus
-Recurrent DVT (intracranial veins, retinal veins, upper extremities, hepatic veins, portal veins, renal
veins, inferior vena cava, lower extremities) & PE
-Arterial thrombosis (coronary arteries, retinal arteries, brachial arteries, mesenteric arteries, peripheral
arteries, aorta).
-First event in early-mid teenage years. Women may experience recurrent fetal loss, 2nd, 3rd trimester
- Migraine headaches, transient ischemic attacks, or Guillain-Barre syndrome is often seen.
-Mild thrombocytopenia is often seen.
-There is often a dermatologic condition known as livido reticularis in which the skin appears mottled.
This is usually most notable in the lower extremities.
-Postpartum syndrome, which occurs 2-10 weeks after delivery and consists of fevers, dyspnea, and
pleuritic chest pain, pulmonary infiltrates- pleural effusions, cardiomyopathy, and arrhythmias.
2- Lupus Anticoagulant
-In 10% pts with SLE, or by drugs chlorpromazine, fansidar, assoc. w. HIV, scleroderma. Prolonged PT
and PTT. Abnormal dilute Russell Viper Venom test -short term anticoagulation with heparin
-long term anticoagulation with warfarin
C/P Similar to *Anticardiolipin Abs
1. Thrombosis and thromboembolism
2. False positive VDRL
3. Thrombocytopenia
4. Recurrent fetal loss

5. Prothrombin deficiency
6. Livido reticularis
***RX for abort a Acetaminophen/caffeine next step if NSAIDs not effective Migraine attack (Excedrin)
Triptans, Valproate, B***Prophylaxis Migraine blockers
MI inferior wall***ST elevation in leads II, III and aVF [Posterior Descending Artery)
MI*** ST elevation in leads V1, V2, V3, V4 anterior wall [Left Ant Desc Artery]
MI***ST elevation in leads V5, V6 lateral wall [LT circumphex artery]
***ALL HIV-infected individual SHOULD BE SCREENED FOR LATENT TB INFECTION BY A PPD
TEST!!
-If PPD > 5mm Give prophylactic RX for TB!!!or having a household contact
***Know MEN I, II and III
***Pt with Mitral stenosis and Atrial fibrillation (give warfarin) and pulmonary congestion (give
Diuretics)
***Antipsychotic Acute dystonic medication high potency typical [haloperidol] and Torticollis reaction.
Management or RX: Anticholinergic like Benztropine or with Diphenhydramine / Prophylaxis:
Benztropine
***Vesicoureteral reflux- high grade untreated and persistent past puberty in Females, with recurrent
UTIs & uri Managed Surgically: Bilateral ureteral NEXT step nary incontinence reimplant
To prevent UTIs and complications, especially during pregnancy (morbidity/mortality fetal/maternal)
and to prevent urinary incontinence and renal failure
***Impetigo: strep aureus or Group A strep / RX: mild infection: topical antibiotic mupirocin // severe
infection: oral antibiotics Erythromycin, cephalexin, dicloxacillin
***Topical steroid creams: in contact dermatitis, seborrhea dermatitis, atopic dermatitis (eczema)
***Carpal tunnel syndrome= clinical diagnosis or by NCV {nerve conduction studies, Electromyography}
**Pt with Allergen induced Contraindication: Latetalol /B blockers, worsen Anaphylaxis, type 1 HS
hypotension and bronchospasm
***Allergen induced Anaphylaxis, type 1 HS, and may be refractory to treatmentusing chronically Bblockers (exe Labetalol) use Glucagon {inotropic and chronotropic with epinephrine and in these patients
effects not mediated by B-receptors
***Cerebellar lesions cause motor movement disorders (not paralysis) and deficits in equillibrium,
posture and motor learning. Gait ataxia=typical vermis lesion
***Normal Pressure Hydrocephalus TRIAD: 1-Gait disturbance 2-Urinary incontinence 3-Cognitive
disturbance
***Torn, tear meniscus: knee pain, catching, locking, giving away, tenderness and efusion

***Chondromalacia patella: chronic overuse injury insidious onset and anterior knee pain, problems w.
patella tracking
***Pes anserine bursitis.- pain medial aspect of proximal tibia, insidious
Contraindicated***Positive-pressure mechanical ventilation or avoided in injured or trauma pt with
cardiac tamponade from hemopericardium because increases intrathoracic pressure and leads to further
decrease in C.O
***Screening colon cancer!! HY
Pt w. family history, polyps in ONE 1st degree relative diagnosed <60 y/old or TWO 1st degree relative
diagnosed Screen for colorectal cancer beginning 10 years prior to the age atat any age which the
youngest family member with colon cancer was diagnosed or beginning at 40 years old if earlier
first step medical***Pheochromocytoma management before surgery!!: alpha blockers as
phenoxybenzamine are started. After aproximately 2 weeks pt is ready for Surgey
***If a stone is produce pancreatic inflammation obstructing Ampulla of Vater [hepatoduodenal) or 2nd
pancreatitis from concomitant obstruction of common bile duct and RX: Cholecystectomy with
pancreatic duct and AMYLASE-LIPASE are increased cholangiography
***Choledocolithiasis: Stone obstructing common bile elevated bilirubin and hepatic enzymes from
hepatocellular damage from duct backup of bile into the liver, and ***Elevated AP indicates biliary
obstruction.
extraction of stones endoscopically by ERPG and*RX of choledocholithiasis sphincterotomy or
SURGERY
RX biliary colic***Stone obstructing cystic duct surgery
***Cholecystectomy: for pts symptomatic or active disease
***Genital tract infections and pregnancy= preterm labor // Chlamydia=premature labor and
chorioamionitis
***QT prolongation drug: Ziprasidone/antipsychotic
from maternal***Neurologic endemic cretinism iodine deficiency during early pregnancy {India, China,
Indonesia, Peru, Ecuador, Bolivia
***Myxedematous endemic cretinism ***Maternal iodine cause myxedematous endemic cretinism in
Congo, deficiency LATE in pregnancy Africa, endemic hypothyroidism
***Breast feeding jaundice is the most common cause of: non-physiologic jaundice, in neonates on day 3
of life, with exclusively breast fed usually because poor intake (increased enterohepatic circulation and
abnormal reabsorption of bilirubin excreted in feces
Cardiovascular system
*** Cardiac Enzymes MI
Begins to Elevate Lasts
CPK-MB 4-6 hr 2 days
Troponin 4-6 hr 1-2 wk

Myoglobin 1-4 hr s
LDH 12-24 hr s
LDH currently is not useful. Never answer it.
**Which has the best sensitivity, but poor specificity?
Myoglobin
**Which has the best specificity?
Troponin
**CPK-MB is sensitive and specific, but not as sensitive as myoglobin or as specific as troponin.
***Treatment of Acute MI in ALL Patients
Decrease Mortality Time Dependant
Aspirin YES (25%) YES
Nitrates ?? ?
Morphine (Analgesics) ?? ?
Thrombolytic YES (25%) YES
-Blockers YES (10-20%) NO
Angioplasty
o Patients with major bleeding or risk of bleeding
o Patients who cant receive thrombolytics for any reason
o Patients failing thrombolytics and progressing to hemodynamic instability
ACE Inhibitor
o Patients with decreased left ventricle function or CHF
Lidocaine
o Never as prophylaxis
o All patients who develop major vertricular arrhythmias (ventricular tachycardia or fibrillation)
Pacemakers
Anything slow or that could become slow *Third-degree AV block *Mobitz II second degree block
Left bundle branch block
*** Treatment of Pulmonary Edema
First Step: Preload reduction
Diuretics any loop diuretic intravenously
Morphine
Nitrates
Second Step: Only if preload reduction is ineffective
Positive inotropes
Dobutamine
Amrinone
Third Step: Afterload reduction
Ace inhibitors - IV
Nitroprusside
*** Congestive Heart Failure
Treatment when the patient has been stabilized
Ace inhibitors
Diuretics
Digoxin
Blockers (carvedilol-b or metoprolol)
Blockers-b
Reduce mortality
Increase ejection fraction

 Improve symptoms
***Heart failure / Diastolic dysfunction: normal EF in the setting of a clear heart failure!
Main etiology
1- Systemic HTN
2- Left ventricular hypertrophy
RX: aggressive B-blockers lowering HR for more ventricular filling time.
***AAA; Abdominal Aortic Aneurism:
flank pain, Asymptomatic before rupture, but if next of leaking dull lower back pain; findings of pulsatile
abdominal mass; 90% ocurring below renal arteries
GOLD STANDARD TEST: Real time ultrasound 100% sensitivity
RX: Surgery if diameter is >4.5cm!
MIX
***Meconium aspiration pneumonia prophylaxis: suction oropharynx/trachea as the head is delivered
and then again after delivery
***Patien with Pain disorder, psychological syndrome, somatoform realizes a secondary gain from their
symptoms, time off from work, disorder sympathy from others
***Postpartum hemorrhage2nd to uterine atony (MC) risk factors: uterine overdistention 2nd to DM,
macrosomia, myometrial exhaustion by prolonged labor.
Bimanual uterine First step: #1 massage
#2: oxytocin to promote continued contraction and homeostasis
#3: Methylergonovine (IM) 2nd or 3rd line of therapy (avoid in HTN)
***Partial Arterial CO2 pressure> SEVERE50 mmHg indicates hypercarbia in the setting of respiratory
distress
***Partial Arterial O2 pressure<SEVERE hypoxemia in the setting of resp50 mmHg indicates distress
BOTH ARE crucial reasons for INTUBATION
***Direct coombs measures presence of Abs attached to RBCs test
***Indirect coombs measures presence of Abs vs. the RBCs in the blood test
***A Coombs (+) mother has Abs vs. fetal Hb & the MC causes: Rh and AB incompatibility from prior
exposure to promote antibody formation
**Reticulocyte count: increased if HEMOLYSIS (hemolytic anemias)
***Stroke lenticulostriate arteries: MCA affecting subcortical brain areas: INTERNAL CAPSULE**, pons,
and basal ganglia. Motor and sensory symptoms instead of aphasia (that is a manifestation of cortical
damage of brain)
***Repeated spontaneous 20% pregnancy loss due to uterine and internal genital tract abortium next
step in study: Hysterosalpingogram. Then though in hormonal abnormalities causes, luteal insufficiency,
etc
**Body dysmorphic disorder pt demanding Drs advise next step: referral for3rd cosmetic surgery

psychotherapy
***Adenocarcinoma of lung (most common of peripheral lung cancer) == associated with HPOA
[Hypertrophic Pulmonary Osteoarthropathy] DIGITAL CLUBBING, periostosis of long bones and
synovial effusions of larger joints
Chest X NEXT step**Pt with Hypertrophic Pulmonary Osteoarthropathy Ray, rule out Adenocarcinoma
of lung!!
***A presentation suspicious for ULTRASOUND initial/next step ACUTE cholecystitis