Cardiovascular Drugs Made EZ:

ACE Inhibitors
Names:
Prils Think an ACE is a Pro (kinda like a pril)
Examples: Enalapril (Vasotec), Captopril, Lisinopril
Uses:
Hypertension, Heart Failure, Protection for diabetics vs nephropathy, Decrease Mortality in post-MI patients due
to afterload reduction
Action:
blocks the enzyme that converts angio I to angio II in the lungs. Angio II leads to vasoconstriction, aldosterone
release, and sodium retention: this is blocked, which decreases blood pressure and puts less strain on heart
Common Side Effects:
Dry hacking cough; Angioedema; Hyperkalemia
Taste disturbance; Rash; Insomnia, Orthostasis
Nursing Implications:
CI: Pregnancy Category D; Bilateral Renal Stenosis
Use K supplements carefully due to hyperkalemia concerns
Stop drug if cough, angioedema
Taste of food may be diminished during first month of therapy
Angiotensin Receptor Blockers (ARBs)
Names:
Sartans
Examples: Losartan (Cozaar), Irbesartan, Valsartan (Diovan)

Uses:
Hypertension, Heart Failure
Action:
Blocks the receptor for Angiotensin II, blocking the effects of this potent vasoconstrictor
Common Side Effects:
Hyperkalemia, Angioedema, Orthostatic hypotension
Nursing Implications:
CI: Pregnancy Category D in 2nd/3rd trimesters; Bilateral Renal Stenosis
Safer side effect profile than ACE inhibitors but less studied
To understand ACE and ARB it is vital that you have an idea of what the Renin-Angiotensin-Aldosterone System
(RAAS) is. Remember the purpose of RAAS is to increase blood pressure in response to decreased renal blood
flow or pressure, and the purpose of the drugs that work here is to block this system and lower blood pressure.
Check out the pick below for a summary of the RAAS and where certain drugs work.

Beta Blockers (or beta antagonists)

Names:
OlOls: Remember Beta video tapes? They are OLdOLd
Ex: Selective B1: Metoprolol, Atenolol (I MET A TEN last night)
Ex: B1B2: Propanolol (Inderal), Labetalol, Carvedilol (Coreg) (ilol, alol-also alpha blocker)
Uses:
Hypertension, Angina, Arrhythmias, Glaucoma, MI prophy, Migraines

Action:
Block adrenergic Beta receptors (1 heart, 2 lungs), leading to lower sympathetic activity = decrease in cardiac
output, blood pressure and renin activity. Also some drugs lower aqueous humor production
Common Side Effects:
Bradycardia, fatigue, insomnia, bizzare dreams, sex dysfunction, lipid dysfunction; Respiratory distress
(wheezing), Agranulocytosis, depression
Nursing Implications:
C/I in asthma, bradycardia, severe renal/hepatic disease, hyperthyroid, CVA
Signs of hypoglycemia (DM), tachycardia (hyperthyroid) may be masked
Glucagon may reverse overdose
CALCIUM CHANNEL BLOCKERS (ANTAGONISTS)
Names:
Dihydropyridines: Pines: Amlodipine (Norvasc), Nifedipine (Procardia)
Non-Dihydropines: Diltiazem (Cardizem), Verapamil
Uses:
Angina, Arrhythmias (Non-Ds have more AV node effect)
Hypertension (Dihydros have more vasodilation effect)
HT (Pines), Dysrhythmias (Verapamil), HT/Dys (Diltiazem)
Action:
Blockade of Ca channels causes arteries to relax (vasodilate) and cardiac conduction to slow through the AV
node
Common Side Effects:
All: H/A, hypotension, dizziness, peripheral edema, Renal/Hepatic dysfunction
Dihydros: Ankle edema, flushing, tachycardia, gingival hyperplasia
Non-Ds: AV block, bradycardia, worsened systolic dysfunction
Nursing Implications:
Use very cautiously with heart failure/left ventricle inpairment, AV block
Dont abruptly stop medication; Warn patient to contact MD if irregular HR, SOB, swelling, pronounced
dizziness, constipation, nausea, hypotension
PERIPHERAL ALPHA BLOCKERS
Names:
Mixed names: Zosins for BPH, ilol for HT;
Examples: Carvedilol (Coreg), Tamulosin (Flomax), Prazosin (Minipress)
Uses:
Hypertension, Peripheral Vascular Dz (raynaulds, phlebitis, etc), BPH
Action:
Blockade of Alpha 1 relaxes smooth muscle in arteries and prostate capsule, leading to lower blood pressure,
reduction in BPH, and increased blood in tissues (warm/pink skin) as well as Renal arteries
Common Side Effects:
Orthostatic Hypotension (especially first dose), Reflex Tachycardia, Ejaculation problems, nasal congestion
Nursing Implications:
Begin with small dose and give at bedtime to avoid dizziness and syncope
Change positions slowly to decrease orthostatic hypotension
Alcohol, Excessive exercise, prolonged standing, heat make S/E worse
CENTRAL ALPHA BLOCKERS
Names:
Clonidine (Catapres); Methyldopa (Aldomet)
Uses:
Hypertension
Action:
Central acting sympatholytic stimulates pre-synaptic alpha receptors to release NE, which paradoxically reduces
peripheral NE release, inhibiting vasoconstriction = vasodilation and lower BP
Common Side Effects:
Sodium/Water retention, Dry mouth, Bradycardia, Impotence, Depression

Nursing Implications:
Advise patient not to abruptly withdrawal because significant rebound hypertension can result
C/I in impaired liver function so monitor liver function tests occasionally
Do not confuse with the benzo Klonipin (patients have done so and taken a bunch of Clonidine for a high, only to
end up with a real lowBP that is.
DIURETICS
Types:
Loop: Furosemide (Lasix), Bumetanide (Bumex), Torsemide (Demadex)
Thiazide: Hydrochlorothiazide (HCTZ)
K-sparing: Amiloride, Spironolactone
Carbonic Anhydrase Inhibitors: Acetazolamide (Diamox)
Uses: Edema associated with heart failure; Ascites with Cirrhosis; Hypertension
Action:
Loop: Inhibit Na, Cl, and H2O resorption in the loop of henle thus decreasing blood volume; Also increase the
excretion of K; Potent diuretics
Administer IV Lasix slowly because hearing loss can occur if given rapidly
Thiazide: Inhibit Na resorption and increase Cl, H2O, K, Ca, Bicarb, Mg excretion in the urine; Also cause
arterial dilatation; Moderate diuretic
While K and Na may be excreted, HyperCa is more likely to develop so never administer to patient with
hypercalcemia;
Eat foods rich in potassium, use sunscreen, and change position slowly
Caution when taking with Lithium, Digoxin, Corts, PO Diabetic meds
K-sparing: Block Na-K exchange in distal tubule causing loss of Na and water and retention of K; Weak diuretic
mostly added to preserve K
C/I in severe renal/hepatic dysfunction, hyperkalemia, Current ACE-I use
Carbonic anhydrase inhibitors:
Used to treat M.Alkalosis, Open Angle Glaucoma, Epilepsy, High altitude sickness
Inhibits the enzyme carbonic anhydrase which normally is responsible for excreting H to combine with HCO3 for
elimination of excess acidity, as well as promoting diuresis. This drug obviously leads to an increase level of H+ in
the blood (M.Acidosis) and an increased excretion of Bicarb (HCO3)
C/I with CLOSED (narrow) angle Glaucoma
S/E i/c Renal Calculi, Hypercalcemia, and Hemolytic anemia
Common Side Effects:
Loop/Thiazides: Hypokalemia, Hyperuricemia, Glucose intolerance, sexual dysfunction, increase
cholesterol/triglyceride levels
K-Sparing: Hyperkalemia especially when used with ACE inhibitors
Nursing Implications:
Caution for electrolyte disturbances; Watch for cramping, paresthesia
Administer in morning to avoid diuresis during night, Supplements (PhosL
Hemostasis
When vascular injury occurs, various mechanisms are available to stop the loss of blood
The mechanism employed depends upon the extent of injury, but the end result of all is to produce strands of
Fibrin to patch the hole; The difference in the various mechanisms is the speed and amount of Fibrin produced
1.Platelet Plug
2.Intrinsic Coagulation
3.Extrinsic Coagulation
Platelet Plug
When vascular endothelial tissue is damaged, a platelet plug can form, sealing the hole. If no deeper tissues are
exposed, this may be the extent of the healing process. If damage is more extensive, platelets, as well as tissue
exposure can initiate further coagulation. Platelet plug formation occurs in 4 steps (use pic to right of text as visual
guide):

1) Adhesion: When subendothelial tissue is exposed, sticky proteins (Von

Willebrand factor) are exposed to passing blood and act as magnets to
passing platelets.
2) Aggregation: ADP, a breakdown product of ATP released from damaged
cells, stimulates the production of receptors (GPIIb) on the platelets that bind
a free floating soluble protein Fibrinogen.
Pharm Note: Plavix and Ticlid inhibit ADP, so platelets are not stimulated to
produce fibrinogen receptors and clots are more difficult to produce
Pharm Note: Abciximab (Reopro) binds to the platelet GPIIb receptor and
blocks fibrinogen from binding, and clots are more difficult to make
3) Secretion: Stimulated platelets
release chemicals like Thromboxane,
that attracts other platelets. Fibrinogen
can bind two platelets, thus platelets
begin to collect in mass.
4) Platelet Coagulation:
V, which leads to fibrinogen
incase the aggregated platelets

Stimulated platelets now produce factor

being transformed into Fibrin threads to

Pharm Note: Aspirin blocks

of the platelet, so cell
aspirin is known to make
given as prophylaxis against
allowed to bind Von Willebrand,
meaning some bleeding is
powerful an antiplatelet drug as

the release of Thromboxane for the life

aggregation is made difficult. This is why
platelets less sticky, and is so frequently
clot formation. Since platelets are still
there is still some platelet plug action,
stopped. This is why Aspirin is not as
prescription drugs like Plavix and Reopro.
(platelet aggregation)

(fibrin threads creating plug)

INTRINSIC COAGULATION
When the insult is deeper, collagen may be exposed, initiating the intrinsic coagulation cascade.
Collagen activates factor 12 then 11 then 8 + 9 then 10. 10 converts Prothrombin into Thrombin, which then
converts Fibrinogen to Fibrin. This process is faster than a platelet plug as you dont need to wait for platelets
to collect, and it forms more extensive Fibrin patches.

Pharm Note: Heparin inhibits the Intrinsic Factors,

making them slower to respond, which makes clotting
more difficult and less extensive
Lab Note: Partial Thromboplastin Time (PTT)
measures the speed of collection of these factors,
thereby measuring the effectiveness of Heparin. PTT,
usually 30-40 seconds is the amount of time it takes
all of the necessary factors to gather at site of need.
Heparin binds these factors, slowing their collection,
and lengthening PTT.
Extrinsic Coagulation
When deep injury occurs, tissue is exposed to blood,
initiating the extrinsic coagulation cascade. Tissue
factor activates factor 7 then 10. 10 then follows
same route as above. With fewer steps this cascade is faster than the intrinsic and develops more extensive
Fibrin patch. Of importance to note is just as Ca makes muscle contract stronger, its presence also makes clots
stronger.
Pharm Note: Factor 7 is made in the liver from Vitamin K. Warfarin (Coumadin) blocks Vitamin K and thereby
reduces the amount of Factor 7 made. Now it takes longer to collect enough Factor 7 to initiate this extrinsic
clotting, and you have slower clotting that is less extensive. Since the medication effects future Factor 7
production and not that currently present in the blood, it takes a few days to see its effects.
Lab Note: Prothrombin Time (PT) measures the speed of collection of Factor 7, thereby measuring the
effectiveness of Coumadin therapy. This value is converted to the INR. Think of this value as a stopwatch that
starts timing as soon as injury occurs. PT, usually 10-12 seconds is the amount of time it takes factor 7 to reach
the area of need.
(extensive fibrin patch)
Regulation of Coagulation

1) Antithrombin III (AT III): AT III

production of Thrombin by blocking
reducing the amount of Fibrin formed.
cells produce this, thereby quarantining
so clotting does not extend beyond
Pharm Note: Lovenox (Enoxaparin)
of AT III, thereby slowing clot formation.
portion of heparin is the active part
Heparin partially works here in addition
inhibition.
Lab Note: Partial Thromboplastin Time
by Low Molecular weight heparins
no Intrinsic factors are inhibited.
2) Tissue Plasminogen Activator
also release TPA, which converts free
to Plasmin. Plasmin degrades Fibrin, so
broken down, even as they are built.
system wins, depending upon how
actually needed.

To assure coagulation
does not go too far, 2
specific mechanisms
inhibit or reverse the
process:
inhibits the
Prothrombin, thereby
Healthy endothelial
off the damaged area
where it is needed.
enhances the activity
The low molecular
here, so regular
to Intrinsic factor
(PTT) is not effected
(Lovenox) because
(TPA): Injured cells
floating Plasminogen
clots are constantly
The more active
much clotting is

Pharm Note: TPA (Alteplase) can be synthetically injected to actively break down clots, such as in the case of a
Stroke or Myocardial Infarction. Great caution should be used when administering this as massive, even fatal
bleeds are possible. (Streptokinase and Urokinase are alternatives that work by same method)

BRADYARRHYTHMIAS
1.Sinus Bradycardia
HR less than 60 requires treatment with Atropine only if
symptomatic

2.AV Block
A.1st DegreeKey: PR interval above 0.2 seconds; Delay is
in AV node
Usually benign but low HR responds to Atropine

B.2nd Degree type IKey: Progressive prolongation of PR until a P wave fails to conduct and no QRS
follows a P wave; Delay is in AV node
Usually benign condition seen with normal aging not requiring treatment, but if symptomatic with bradycardia,
will respond to Atropine
C.2nd Degree type II
Key: Normal EKG with a sudden drop of a QRS;
Block usually in the His-Purkinje system usually as a
result of ischemia
Can turn into the deadly 3rd degree so temporary
transcutaneous pacer may be needed until an
implantable pacemaker can be inserted

D.3rd Degree
AV dissociation often from irreversible damage to the AV node following a MI
Key: P-P length does not equal R-R length
Ventricles do not pump fast enough to maintain CO and requires pacemaker

TACHYARRHYTHMIAS
Atrial impulse
A.Sinus TachycardiaHR 100-140, may occur with exercise or anxiety, but also may be earliest indication of
hypovolemia
Usually not symptomatic until above 140 when diastolic filling time is impaired
Count the large boxes from top of a QRS to another: 1 box = 300bpm, 2 box = 150bpm, 3 box = 100bpm, 4
box = 75bpm, 5 box = 60bpm
TX: Eliminate cause (i.e. anemia, stimulant; fluid bolus)

B.SupraVentricular Tachycardia
A conduction signal loops and reenters the
atrium causing rapid, atrial driven HR usually
above 140bpm
Atrial tachycardia results in narrow QRS
complexes
TX: Adenosine given rapid IV push

D.ATRIAL FLUTTER One foci in atrium fires rapidly, leading to sawtooth P waves and regular QRS with HR
between 75-175
Occurs most often in COPD, but may be seen with CAD and Atrial septal defects (ASD)
TX: Identical to AFib

Atrial FibrillationMultiple atrial foci cause lack of P waves and very irregular QRS waves with widely varied
HR from 75-175 bpm

Caused by CAD, MI, HT, PE, Pericarditis, Hyperthyroidism

Major risk for thrombotic events (CVA) so treat according to protocol
Treatment Protocol; Determine length/onset of AFib:
Acute: less than 48hrs
Unstable: (Hypotensive, AMS) Immediate cardioversion
Stable:
Tachycardic: Control Rate w/ Beta Blocker (Atenolol) then electrical cardioversion
NSR: Proceed directly to cardioversion (electrical preferred to pharmacologic; If electrical fails or is
unfeasible use Amiodarone to convert)
Acute: greater than 48 hrs or unknown duration
Before cardioversion: If longer than 2 days must use Warfarin to anticoagulate for 3 weeks before and 4 weeks
after
Avoid the wait: Can obtain an echo to r/o thrombus and load pt with Heparin and proceed to cardioversion;
Still require the 4 week Warfarin anticoagulation after
Chronic: Under 60 with no heart disease or risk factors require no treatment; All others get Warfarin for good
TACHYARRHYTHMIAS
Ventricular impulse
A.Ventricular Tachycardia
Ventricular foci initiate rapid HR with wide QRS complexes
Caused by prior MI (most common), active ischemia, hypotension, cardiomyopathy, Drugs, Electrolyte
abnormalitiesMay initially have a pulse, but can rapidly evolve into a deadly pulseless VTach
TX: VTach with a pulse treated with 150mg Amiodarone
TX: Pulseless VTach treated identical to VFib with Code being called: CPR, Defibrillation, Epinephrine,
Amiodarone, and Lidocaine (Alternate drugs w/ Epi being only drug you can not max out on)

B.Ventricular Fibrillation

Ventricular foci initiates rapid rhythm which causes heart to fatigue and quiver
Typically evolves from VTach
Ischemic heart disease most common cause
Always pulseless, so initiate a code as above

C.Torsades de PointeA polymorphic VTach with varying direction of QRS amplitude (points alternate down
to up)
Often caused by electrolyte problems and long QT, so give a trial of Mag and Calcium

D.Asystole
Loss of electrical signal initiation so it doesnt respond to Defibrillation (basically resets rhythm to asystole)
Epinephrine and Atropine are only hopes

Arrhythmias
Dysrhythmias
A.Premature Ventricular Contraction (PVC)Abnormal Foci causes random, wide QRS contractions
May not progress to any other rhythm and have no symptoms
Can progress to VTach and VFib, so treat more than 6/min or if symptoms present with BBs

B.ST Elevation
Usually an ominous sign of actual myocardial infarction
Treat with ACS protocol including ECG and Enzymes
If present in all 12 leads may suggest Pericarditis

C.T wave Inversion

An ominous sign of cardiac ischemia, can precede B
D.Q wave
If deeper than of QRS, suggests a prior infarction, Follows B
E.U wave
Suggestive of hypokalemia
F.ST Depression
Often a sign of ischemia, use MONA, ECG, Enzymes

G.Peaked T waveSuggestive of hyperkalemia

H.Prolonged QT
QT width is more than the width of
QRS-QRS
Often caused by low Mg or Ca, as well as
many drugs that effect these electrolytes
TX: Withdrawal medication that caused
and check/treat electrolyte abnormalities
Antibiotics made EZ
First lets take a broad look at bacteria:
Gram Positive Rods
LISTERIA

Gram Negative RodsENTERIC BUGSESCHERICHIA COLI

PROTEUS sp.

CORNYBACTERIUM DIPTHERIAEBACILLUS
ANTHRACIS (anaerobe)
CLOSTRIDIUM (anaerobes)
c. DIFFICILE
c. TETANI
c. BOTULINUM
c. PERFRINGES

Gram Positive CocciSTAPHYLOCOCCUS sp.

STAPH. AUREUS
STAPH. EPIDERMITIS
STREPTOCOCCUS sp.
STREP. PNEUMONIAE
STREP. VIRIDANS
STREP. PYOGENES (GAS)
STREP. AGALACTIAE (GBS)
ENTEROCOCCUS sp.

ENTEROBACTER sp.
HELICOBACTER sp.
SALMONELLA sp.
SHIGELLA sp.
KLEBSIELLA sp.
HAEMOPHILUS INFLUENZAE
LEGIONELLA sp.
PSEUDOMONAS AERUGINOSA
ACINETOBACTER sp.
BACTEROIDES (anaerobes)
B. FRAGILIS
Atypical Bacteria: Think Doxy!
CHLAMYDIA (intracellular)
MYCOPLASMA (no cell wall)
SPIROCHETES (curves: Syphillis)
BORRELA (Corkscrews: Lyme)
Think INH/Rifampin/Azithro
MYCOBACTER (Acid fast: TB, Leprosy, M.Avium Complex)
Gram Negative Cocci
NEISSERIA MENINGITIS
NEISSERIA GONORRHEA
MORAXELLA CATARRHALIS

Gram Positive Cocci

Staphylococcus
Staph aureus (coagulase positive)
Most pathogenic of the staphs; toxins cause Toxic Shock, Scalded Skin, Gastroenteritis
Cause skin infections, Pneumonia (nosocomial), Endocarditis, OsteomyelitisAbscess formation common; Can
initiate clotting (think DIC)
Tx: Oxacillin family; (Vancomycin if MRSA; Zyvox if VRSA; Bactrim or Doxy if Community MRSA)
Also susceptible to: 1/2/4 Gen Cephs, Carbapenems, Macrolides
MRSA: Staph resistant to Oxacillins and most other drugs; Use Vanco, Zyvox, or Synercid
Staph epidermidis (coagulase negative)
Normal flora of human skin
Causes infection in immuno-compromised or depressed patients often via Central lines
Tx: Similar to Staph Aureus (Vanco if MRSE, Zyvox if VRSE)
Streptococcus
Alpha HemolyticStrep pneumoniae (Pneumococcus): Leading cause of Pneumonia, Otitis Media, and
Meningitis
Strep viridans: Normal flora of mouth, can cause Dental abscess and Endocarditis
Beta Hemolytic
Group A (Strep pyogenes): Strep throat, Rheumatic fever, Scarlet fever, Glomulerulonephritis, Necrotizing
fasciitisGroup B (Strep agalactiae): Can colonize vagina and cause Meningitis or Pneumonia in newborn
Tx: PCN G; (Quinolone if PCN resistant; Ceftriaxone if in brain)
Also susceptible to: 1/2/4 Cephs, Macrolides, AminoPCNs, Vancomycin, Quinolones
Enterococcus
Facts
Common nosocomial infection with multi-drug resistance
Cause Sepsis, Cellulitis, Intraabdominal infx, Endocarditis, UTI
Tx: Ampicillin (or Vancomycin) + Gentamycin; (Zyvox or Synercid if VRE)
Only other effective drugs: Zosyn, Imipenem, and Quinolones
Gram Positive Rods
Listeria
Commonly reside in soil, sewage, and stream water but rarely cause disease; If the immune response is slow,
however, they move into cells and then are missed by immune cells
Cause of Listeriosis, a lethal food bourne illness with mortality rate of 25%; Can invade CNS
Tx: Ampicillin (often with Gentamicin)

Cornybacterium diptheriae
Toxin producing (2nd most lethal toxin to humans) causes Pharyngitis w/heart/CNS damage
Tx: Antitoxin + PCN (Erythromycin if PCN allergic)
Bacillus anthracis
This anaerobic bacteria is the cause of Anthrax (meaning Coal = large black lesions)
Lives in soil, and can be ingested by grazing animals where it causes rapid death (is then possible to inhale or
ingest the bacteria from dead animals)
Tx: PCN; (Cipro or Doxycycline if PCN allergic)
Clostridium (anaerobic species)
C. difficile
Overgrowth in gut after Antibiotic treatment (Clindamycin, 3/4 Gen Cephs, Amp/Amox), causes
Pseudomembranous ColitisTx: PO Metronidazole (or PO Vancomycin if relapse after taking Metro)
C. tetani
Toxin producing (3rd most lethal toxin to humans) causes PNS blockade (Tetany, Seizure, Death)
Tx: Toxin irreversible once bound, so rapid treatment with PCN or Metronidazole imperative
C. botulinum
Toxin producing (Most lethal toxin to humans; 500 g could kill the entire world) that causes Botulism (a nerve
blockade disease that leads to rapid paralysis and death)
Bacteria can not survive in high oxygen or acidic environment, so usually ingesting bacteria not fatal as they are
killed rapidly in GI tract; Must ingest toxins to have effects
Infants (pre solid food) have a less acidic GI tract, so things harboring this bacteria (honey) can deliver the
organism, which is then allowed to grow in more basic pH GI tract
Tx: Hardy bacteria are not killed by antibiotics; Antitoxin very hard to find so Mechanical Ventilation and removal
of cause (i.e. vomiting or debridement of wound) usually only thing possible
Gram Negative Cocci
Neisseria meningitidis (aka Meningococcus)
Common cause of meningitis; Also Meningococcemia (a rapidly fatal sepsis that kills over 50% of effected
infants) and DIC
Tx: PCN G (Ceftriaxone if PCN allergic) ; Best treatment is prevention with vaccine
Neisseria gonorrheaCause of the STD Gonorrhea, as well as Conjunctivitis in newborn of infected mom
Tx: Ceftriaxone (or Ciprofloxacin) and Azithromycin for possible concurrent Chlamydia
Moraxella catarrhalis
Causes URI and Otitis Media, as well as Pneumonia in smokers; Also COPD exacerbations
Tx: Augmentin and Erythromycin
Also susceptible to 2/3 Gen Cephs, Quinolones, Bactrim
Gram Negative Rods
Urinary pathogens
E. coliNormal intestinal flora cause 90% of UTI; Also Pyelonephritis
Pathogenic varieties are not normal flora and can cause Infectious diarrhea, Hemolytic Anemia
Tx: Ciprofloxacin or Bactrim (Zosyn also effective)
Proteus
Causes UTI, in addition to renal calculi (struvite, CaCO3)
Tx: Levaquin or Bactrim (Often treated without knowing you are treating Proteus)
Respiratory pathogens
Haemophilus influenzae
Cause: Pneumonia, AOM; Also Sepsis, Meningitis, Cellulitis
Tx: Azithromycin
Also susceptible to po 3/4 Gen Cephs, Augmentin, Doxycycline, Quinolones, Carbapenems

Klebsiella pneumoniae
Usually only pathogenic in hospitalized immunocompromised causing Pneumonia and/or Sepsis
Rapid resitance develops, especially against Cephalosporins and Quinolones
S/S: Profuse, Jelly-like, Bloody sputum and high mortality rate
Tx: Carbapenems or Zosyn
LegionellaPneumonia, derived airborn from water ducts, air conditioning units, water towers
Tx: Macrolide (or Quinolone or Doxycycline)
Pseudomonas aeruginosa
Opportunistic infection causes Pneumonia, Sepsis, UTI, Right side Endocarditis, Osteomyelitis in Diabetic foot
ulcersFirst s/s often overwhelming Gram negative sepsis; 2nd most common cause of infection in ICU
Extremely resistant to many drugs; All effective drugs IV, except Cipro and Levaquin so their use is severely
restricted to avoid development of resistant strains
Tx: Ceftazidime and Gentamycin (or Imipenem or Zosyn- varies widely between hospitals)
Also susceptible to the following: Tobramycin, Cefipime, Colistin, Aztreonam
Acinetobacter
Pneumonia, Sepsis, Shock common, Up to 70% mortality; Can live 3 weeks on dry surface
Tx: Imipenem
Colistin or Doxycycline is alternative
Gastrointestinal pathogens
Helicobacter Pylori
Common cause of Peptic Ulcer Disease
Tx: (CAP) Clarithromycin, Amoxicillin, PPI (proton pump inhibitor)
Salmonella
Common cause of Diarrhea; Some forms also cause Typhoid or Sepsis
Ciprofloxacin (rule out C.Dif with any infectious diarrhea)
Shigella
Causes bloody, purulent diarrhea in nursing homes and preschools
Tx: Ciprofloxacin
Vibrio Cholera
Causes rice water diarrhea, with death from dehydration
Tx: Doxycycline, fluids and electrolytes
YerseniaOne form causes diarrhea; Another form causes Bubonic Plague
Tx: Gentamicin
GNR and Sepsis: Notes of Interest
Many GNR have endotoxins, which are actually components of their cell wall
When antibiotics begin their destruction, these toxins are released into the bloodstream in massive quantities,
leading to Sepsis (Massive immune response) and eventually Septic Shock (Low BP and organ dysfunction)
For this reason, Bacteremia (bugs in blood) with GNR is among the most serious of diseases, and should be
treated aggresively in an ICU
With Shock and 2 organs dysfunctioning the mortality rate is over 40%; With each additional organ dysfunction
add 15%
Sepsis is the #1 killer in the ICU, but is more preventable than you would think; The dirty source, is more often
than not, indwelling catheters, so take extreme care with hygiene if you are ICU bound!!!
Beta Lactams: the Penicillins
Penicillins (PCNs)
MOA: All Beta Lactams are Bactericidal, inhibiting cell wall synthesis; Preg Cat B
Natural Penicillins

Spectrum: G(+): Strep, Bacillus, Clostridium; G(-): Neisseria

Facts: Relatively few side effects; Allergic reactions relatively common; 98% of Staph are resistant to PCN
due to enzyme able to destroy medication (PCNase)
PCN G: IV, IM (often only 1 injection need, i.e. Syphillis)
PCN V: PO, poorly absorbed so only for minor infections
Penicillinase (PCNase) Resistant PCNs
Spectrum: G(+): Staph (only indication though spectrum similar to PCN)
Facts: Original Drug was Methicillin but caused too much Interstitial Nephritis and was withdrawn; Despite this,
Staph resistant to this class was termed Methicillin resistant (MRSA or MRSE)Oxacillin (PO, IV); Cloxacillin &
Dicloxacillin (PO); Nafcillin (IV)
Aminopenicillins
Spectrum: G(+): Same as PCN plus Enterococcus plus G(-): Moraxella, E.Coli, Salmonella, H.influenzae,
H.Pylori;Facts: NH3 group makes enhanced activity against G(-); 2nd most common cause of C.Dif Colitis
Amoxicillin: PO; ENT infections, Cellulitis, Gonorrhea, C.A.Pneumonia (Strep)
Ampicillin: IV; Listeria, Enterococcus
Extended Spectrum PCNs
Spectrum: Same as AminoPCNs plus G(-): Pseudomonas, Proteus, Bacteroides
Facts: Broad Spectrum, usually reserved for serious infections with susceptible bacteria; No PCNase resistance
when given alone; Often combo w/Aminoglycoside for Pseudomonas
Ticarcillin (IV); Piperacillin alone withdrawn (Combination drug Zosyn still available)
PCN/Beta Lactamase Inhibitor Combinations
Facts: PCNase inhibitor added to a Beta Lactam to extend coverage, mainly against S.aureus
Unasyn: Ampicillin + PCNase inhibitor
Augmentin: Amoxicillin + PCNase inhibitor
Zosyn: Piperacillin + PCNase inhibitor (Very Broad Spectrum)
Beta Lactams: the Cephalosporins
Class Facts:
Similar to PCN in most ways, but only 5-10% of PCN allergic will be allergic to Cephs
Generally avoided only if history of Anaphylaxis with PCN
Generally do not cover Anaerobes, Pseudomonas or cross BBB unless indicated
Do not cover MRSA (except Ceftaroline) or Enterococcus
Preg Cat B; Do not take with Alcohol; Consume at least 3 L water daily; Take w/food (avoid GI probs)
All Cephs can cause PT/INR (give Vit K) and C.Dif Colitis
1st GenerationSpectrum: Broad G (+) i/c PCNases; limited G (-): E.Coli, Proteus, Klebsiella
Cephalexin (Keflex): PO; Cellulitis, Cystitis
Cefazolin (Ancef, Kefzol): IV; Surgical prophylaxis (protect against skin bugs)
2nd GenerationSpectrum: G (+): Same as 1st Gen plus G (-): H.Influenzae, Neisseria
Cefuroxime (Zinacef): PO, IV; Limited anaerobes; Cross BBB
Cefoxitin (Mefoxin): IV; Abdominal surgery prophylaxis; Excellent against Anaerobes (i.e. DM foot infections,
Peritonitis, etc)
3rd GenerationSpectrum: Excellent G (-) coverage; limited G (+)
Ceftriaxone (Rocephin): IV; qd dosing; Crosses BBB; Meningitis, Encephalitis, Gonorrhea
Ceftazidime (Fortaz): IV; Pseudomonas, Neutropenic Sepsis, Serious infx only; Cross BBB
4th GenerationSpectrum: Excellent G (+), Excellent G (-) coverage i/c Pseudomonas; Cross BBBSE:
Psuedomembranous Colitis (C.Dif) most frequent in class
Cefipime: IV; Cross BBB; Complicated UTI, Severe Sepsis
Cefdinir: PO
5th Generation
Spectrum: Excellent G (+), Excellent G (-) coverage i/c MRSA
Ceftaroline: IV/IM; Pneumonia and Skin infections including MRSA

Ceftobiprole (proposed): Not yet available, but on FDA Fast-track; Claims more extensive coverage with less
susceptibility though FDA states studies not conclusive

Beta Lactams: The Carbapenems

Carbapenems
Spectrum: Broadest Spectrum of any Antibiotic; Indicated for severe bone, skin, tissue infections, as well as
Endocarditis, Abdominal infx, Pneumonia, UTIs, Sepsis, Acinetobacter
Used as last resort in hospitalized patientOnly obvious omission is lack of coverage against C.Difficile, Atypicals,
and MRSA
Restricted use by ICU IV infusion for significant infections, to keep resistance low
SE: Nephrotoxicity and Seizures (usually with preexisting Renal or CNS disease) Preg Cat C
Imipenem (Primaxin): IV; Combined with Cilastatin to block enzyme that breaks down drug
SE: Sz in 1.5% of pts on typical dose, 10% if above 500 mg q6h (So not for Meningitis)
Meropenem: IV; May kill G (+) a bit slower than Imipenem, but less Sz, no need for Cilastatin
Beta Lactams: The Monobactams
Monobactams
Spectrum: Limited to aerobic G (-) i/c Pseudomonas; Severe systemic infections and UTIsThis powerful GNR
drug is usually combo with Vanco or Clinda for Powerful Broad spectrum
Preg Cat B
Safe to administer to pt w/PCN allergy
Crosses BBB
SE: Severe nephrotoxicity if given with aminoglycosides; Monitor renal function even if given alone; Eosinophilia
rarely
Aztreonam: IV, Advantage of preserving all normal G (+) and anaerobic flora
Macrolides
Class Facts:
Broad Spectrum: Similar coverage to PCN plus Atypicals (Chlamydia and Mycloplasma), plus Spirochetes
(Syphillis and Lyme) plus additional G (-) i/c H.influenzae
As a rule, Clarithromycin has most and Azithromycin the least G (+) coverage
Bacteriostatic, inhibiting protein synthesis
Do NOT cross BBB, so not for meningitis
Except Azithromycin, CP450 inhibited, increasing drug levels of Theophylline, Digoxin, Coumadin, etcFood
decreases absorption of Macrolides
Often used as alternative when pt is PCN allergic
Can cause QT prolongation and Rhabdomyolysis (especially with Statins)
Exhibits Enterohepatic recycling (excreted in bile, then reaborbed; cx for buildup to toxic levels)
Since excreted in bile, not kidneys, no need for adjustment in renal failure
Azithromycin: IV, PO; qd dosing; No effect on CP450 so fewer drug interactions, and no enterohepatic recycling;
Atypical Pneumonia, Chlamydia
Clarithromycin: PO; H.Pylori, Pneumonia, M.Avium Complex
Erythromycin: PO, IV, Topical, Opthalmic; Acne, Skin Infx, Eye infx, Diabetic Gastroparesis
SE: Cholestatic jaundice, GI distress (overall a very safe drug)
Fluoroquinolones
Class Facts:
Spectrum: Broad coverage of G (-), variable G (+), broad coverage of Atypicals
As a rule, increasing Generations have better G (+) and anaerobic coverage, but less Pseudomonas
Bactericidal, inhibiting bacterial DNA production
Precautions
Cx w/arrhythmias, CI if pt on antiarrhythmic meds
As a rule, any abx that targets bacterial flora (G -), effects coagulation by inhibiting Vitamin K
Preg Cat C
Binds Ca, Al, Zn, Mg so do not administer with Milk, Vitamins, or Antacids
Electrolyte interference may cause arrhythmias (QT prolongation), Seizures, Neuropathy, and this is increased

when taking with NSAIDs

May cause weakness in M.Gravis
May cause Pseudomembranous colitis, Rhabdomyolysis
Spontaneous tendon rupture can occur when taken with Corticosteroids
Do not administer with Milk, Vitamins, or AntacidsHigh % of unmetabolized drug is excreted in urine, making it
excellent for UTI
1st Gen: Did not contain Fl, and were just Quinolones; Much less effective, not used today
2nd Gen: Best antipseudomonal and G (-) in class; weakest G (+) and anaerobe
Ciprofloxacin: PO, IV, Opthalmic; Nosocomial Pneumonia, UTI, Infx Diarrhea (not C.Dif); Not for children below
18
3rd Gen: Levofloxacin (Levaquin): IV, PO; qd dosing; UTI, Community (CAP) or Legionella Pneumonia
4th Gen: Best G (+) and anaerobe in class; weakest G (-) and antipseudomonal in class Moxifloxacin:
Pneumonia (CAP); Only Quinolone not renally excreted

Aminoglycosides
Class Facts:
Spectrum: Primarily aerobic G (-) coverage i/c Pseudomonas, some G (+) staph
Often used in combination with G (+) drugs for Broad Spectrum coverage; Rarely used alone
Quinolones are often used initially instead, due to high resistance to this class, unless high suspicion of
Pseudomonas
Bactericidal, blocking protein synthesis
Allergies are very uncommon with this class
Precautions:Nephrotoxicity (renal failure) and Ototoxicity (hearing loss) fairly common, so not for long
term Nephrotoxicity risk increased when taking with Vanco, Cyclosporine, or IV contrastOtotoxicity risk
increased when taking with Loop Diuretics
Measure Trough concentrations to assure efficacy, at least every 5d (30m before next dose)
Most Preg Cat D (exception is Streptomycin which is a B)
Decrease intestinal Vitamin K synthesis (anticoagulant quality)
Can bind Ca, causing neuromuscular weakness and neuropathy
Not absorbed well, so no PO
Streptomycin: Eye infx, Tuberculosis; Limited use due to high resistance
Tobramycin: Best antipseudomonal in class; MRSA (w/Ampicillin)
Gentamicin: Excellent antipseudomonal; Endocarditis (w/PCN)
Neomycin: Hepatic Encephalopathy (kills Ammonia producing GI flora); Only drug in class given PO as it is
used to clean GI tract and is not absorbed; Very toxic if given IV
Amikacin: Synthetic derivative of Neomycin; Often still effective when bugs are resistant to all other
Aminoglycosides
Tetracyclines
Class Facts:
Spectrum: Very broad coverage of G (-), G (+), Atypicals, Protozoa; i/c Chlamydia, Mycoplasma, and
AcinetobacterBroad spectrum limited only by significant resistance, and indications now i/c: Acne, Rosacea,
Anthrax, Bubonic Plague, Elephantitis, Malaria, Cholera, Syphillis, Rickettsia (Q fever)Also inhibits ADH,
and is used for SIADHBacteriostatic, inhibiting protein synthesis
Precautions
With odd strength comes odd SE; These i/c: Candida superinfections, Pseudomembranous Colitis (C.Dif),
Thrombocytopenia, Coagulation irregularities, Hemolytic anemia, Lupus exacerbations, NephrotoxicityBind Ca,
Mg, Al, so do not give with milk, antacids, or iron salts; Also cause tooth discoloration in growing teeth (young
pts); Cause weakness in M.Gravis
Preg Cat DCause fibrosis in pleura, so used for direct administration to resolve pleural effusions
Doxycycline (Vibramycin): PO, IV; You name it this will treat it, but use less harmful drugs, if effective, first
Demeclocycline (Declomycin): PO; Reserved for the treatment of SIADH

Miscellaneous

Bactrim
PO, IV; Sulfonamide, primarily used for UTI and Pneumocystis Carinii Pneumonia (in HIV pt)
SE: Renal stones, Stevens Johnson syndrome, Allergic reaction common; Many drug interactions; Blood
Dyscrasias (report any s/s of new infx)
VancomycinPO, IV; Spectrum i/c all G (+); Used for MRSA and MRSE; PO is useful for C.Dificile Colitis
SE: Nephro/Ototoxic (Measure Peak/Trough levels); Red Man Syndrome (from rapid infusion; 60m min)
Metronidazole
PO, IV; Excellent GPR/GNR Anaerobic coverage, used for intrabdominal; C.Dificile Colitis
SE: Serious reaction if taken within days of Alcohol
Clindamycin
PO, IV; Excellent Anaerobic coverage (rule is Clinda above diaphragm, Metro for below) as well as G (+)
Often used for serious G (+) sepsis w/possible anaerobic component (i.e. postop abdomen surgery)
Does not cross BBB; Esophagitis common if not administered with water
SE: Pseudomembranous Colitis (C.Dif) common post treatment (10%)
Linezolid (Zyvox)
PO, IV; Spectrum similar to Vanco plus most anaerobes; Used for VRSA, VRE
SE: May decrease platelet count (3%); MAOI w/high risk of Serotonin Syndrome with SSRIs
Synercid
IV; Alternative to Zyvox for VRSA, VRE
SE: Serious arthralgia, myalgias; Central line only as thrombophlebitis in up to 75% of pts via Peripheral
Colistin
IV; Mainly used for treatment of Acinetobacter and severe Pseudomonal infx; Spectrum i/c GNR
Was actually first G (-) drug on market, gradually replaced by Aminoglycosides, then brought back into use by
developing resistance to those drugs
Developed so long ago, no actual recommended dosages have been studied (nightmare to prescribe)
SE: Nephrotoxicity, Neurotoxicity (less common than with Aminoglycosides)
Asthma drugs made EZ
Pharmacology is often considered a dirty word in nursing and medical school, and unfortunately the NCLEX and
the USMLE loves to test you on this. One subject we recently tackled in our NCLEX review course was the
treatment of Asthma. Here is a summary of what we talked about...
Obstructive Pulmonary Disease (Asthma, COPD)Medications: Site of Action
1.Adrenergic Agonists (Albuterol, etc)
2.Anticholinergics (Ipratroprium Bromide)
3.Xanthines (Theophylline)
4.Corticosteroids (Beclomethasone, etc)
5.Mast Cell Stabilizers (Cromolyn)
6.Leukotriene Antagonists (Montelukast-Singulair)
key to above figure: Allergen+IGE causes Mast cell to release histamine and leukotrienes which then seep out of
blood stream and cause immune cells to inflame bronchioles. Various drugs work at different steps of this
process. Some stop mast cells from releasing their products, some stop the products from leaving the blood
stream, and some stop the products from causing the inflammation in the bronchioles. All three of these work
directly on the immune system. On the other side of that, some drugs directly open the airway, not effecting the
immunity at all. See below for the most critical details on these drugs and when we use them...

Obstructive Pulmonary Disease:

Bronchodilators
1.Adrenergic Agonists (Albuterol, etc)
Selective B2 agonists directly dilate
airway; DOC for acute attack
Albuterol: PO, inhaled via MDI; NOT for
maintenance therapy
Levalbuterol (Xopenex): Possibly less
cardiac SE
Salmeterol: Long acting (12hrs) for night
s/s
Terbutaline: Also relaxes uterus, tocolytic
for premature labor
2.Anticholinergics (Ipratroprium Bromide)
*technically not a dilator
Atrovent is often combined with Adrenergics to tx COPD, as scarred airways need extra help dilating
Slow onset, long acting best used for prevention, not acutely
SE: Dry mouth, GI distress
3.Xanthines (Theophylline)
Similar to Caffeine, causes bronchodilation, CNS stimulation of the respiratory center, Inotropy/chronotropy
renal perfusion urine
Used in cases where overuse of other bronchodilators has caused decreased effectiveness, especially used with
COPD
Slow onset, long acting best used for prevention, not acutely
Stimulant C/I with arrhythmias, SZ, hyperthyroid, PUD
Monitor therapeutic levels (10-20)
Aminophylline is IV form of Theophylline
Obstructive Pulmonary Disease: Inflammation Modulators
1.Corticosteroids (Beclomethasone, etc)
Steroids prevent further inflammation of constricted airways
Available IV, PO or inhaled; Inhaled have benefit of being used at site of constriction without systemic effects
(Rinse after!)
DOC for asthma preventionBeclomethasone excellent antiinflammatory with few SE
Patients have died from not being tapered off of systemic steroids when switching to inhaled forms
Can be used WITH albuterol for acute attacks and is given IV (Solu-Medrol)
2.Mast Cell Stabilizers (Cromolyn)
Used to prevent the release of inflammatory mediators
Most effective for exercise or allergen induced bronchospasm
Also useful to control perennial allergic rhinitis
Available PO, inhaled, and opthalmic
3.Leukotriene Antagonists (Montelukast-Singulair)
Leukotriene receptor blockade prevents inflammatory migration into bronchiole tissue
Used for maintenance, with effects taking up to a week
SE: Dyspepsia, insomnia, diarrhea, and liver dysfunction
Other ex. Zafirlukast (Accolate), Zileuton (Zyflo)

Asthma Treatment Protocol (med first introduced)

Step 1, Mild Intermittent S/S: Short acting B2 agonists prn
Step 2, Mild Persistent: Inh steroid + short B2 ag prn; Cromolyn + B2 ag prn for children; Theophylline or
Montelukast alternative agents if above protocol ineffective
Step 3, Moderate Persistent: Med dose inh steroid + Salmeterol (long acting B2) + short B2ag prn
Step 4, Severe Persistent: High dose inh steroid + Salmeterol + Systemic steroid + short B2 ag prn
Thyroid Disorders

Hypothyroidism
1o: Surgical resection, Amiodarone, Low Iodine, Hashimotos
Hashimotos: Autoimmune destruction, usually in women 20-60 y.o.
2o: Hypothalamus or Pituitary disorders
S/S:
Early: Fatigue, cold intolerance, wt gain, dry skin, brittle hair/nails, hi DBP
Late: Slow speech, hoarse, loss of outer 1/3 eyebrow, myxedema (thickened skin), periorbital puffiness, low HR,
effusions
Critical (Myxedema Coma): Low Temp, Low BP, Low R, AMS
TX: Levothyroxine (Synthroid)
Myxedema Coma: T4 IV (can use T3 if T4 ineffective but CX for arrhythmias); Adrenal replacement meds
(steroids) usually necessary

Hyperthyroidism
1o: 3/4 of all hyperthyroidism is Graves; Goiter, Adenoma, and Amiodarone also cause
Graves: Autoimmune induced, usually in women 20-40 y.o.
2o: Pituitary adenoma
S/S:
All: Insomnia, heat intolerance, wt loss, sweaty, fine hair, hi HR, AFib, incr. bowel movements
Graves: Above + non-tender goiter, pretibial myxedema, exopthalmos
Storm: Fever, hi HR, hi SBP/Wide pulse pressure/ low MAP (i.e. 150/40) CX: 50% MORTALITY!
TX:
1o: Propranolol ( lowers HR and lowers T4/T3 conversion)
2o: PTU or Methimazole (antithyroid medications used as 1st line tx attempt prior to ablation of thyroid)
3o: Radioactive Iodine (Cat X drug used to diagnose nodules and destroy thyroid tissue; Highly radioactive so
strict precautions are necessary, i.e. keep distance from pt when possible, tell pt to avoid close contact for 3 d
after
Storm: BB then PTU wait 1hr then Iodide then Steroids
Amiodarone: The Thyroid Killer
Over 10% of those treated with Amiodarone will develop hypothyroidism
Amio looks like Iodine = Thyroid takes it up instead of Iodine = cant make T3/T4 = Hypothyroid (often resolves
in 1-3 months)
Some have antibodies that attack and destroy thyroid when combined with amio = Hypothyroid (nonreversible)
Up to 20% of those treated with Amiodarone will develop hyperthyroidism
Amiodarone has a special affinity for the thyroid and when it accumulates there, tissue becomes hyperemic,
allowing pre-formed T3/T4 to dump into bloodstream = Hyperthyroid (often becomes hypothyroid when supply is

used up, then can normalize)

Adrenal disorders
Cushings
Cushings Syndrome: Hi Cortisol from any cause
Cushings Disease: Hi Cortisol from a Pituitary cause (2o)
Iatrogenic Cushings: Prescribed steroids (most common cause)
Ectopic Cushings: Lung CA can release an ACTH like hormone that causes Cushings
Patho:
Cortisol (Glucocorticoid) has the following effects on the body: Impaired collagen production,
Enhanced protein catabolism, Anti-insulin effect (hyperglycemia), Inhibitory effect on T-cells (Impaired immunity),
Enhanced catecholamine activity (HT)
S/S:
Syndrome: Central obesity, moon facies, buffalo hump, purple striae on abdomen, acne, easy bruising, HT, Hi
Glucose, Hi Na, Low K, Psychiatric issues
Disease only (symptoms caused by faulty release of Melanocyte stim hormone during release of increased
ACTH): Hyperpigmentation, Masculinization in females
Diagnosis: Dexamethasone suppression test

 TX: If Iatrogenic, taper steroids

Disease: Transphenoid resection of tumor
Adrenal: Adrenalectomy
Adrenal Insufficiency
1o: Addisons (autoimmune most common in 1st world, infection most common in rest); Only
type of insufficiency where aldosterone is also low
2o: Iatrogenic (Pts on long term steroids can not produce their own steroids when stressed or
upon abrupt withdrawal)
S/S:
All: Wt loss, anorexia, nausea, abdomen pain
1o: Low Aldosterone (Low Na, Hi K), Glucose, Orthostasis, Pigment (from Hi ACTH)
Addisonian Crisis: Severe Low BP, Cardiac collapse, Ab pain, ARF; Crisis brought on by stress, trauma, or
infection
Fatal if untreated
TX: IV fluids (min 2 L D5 NS) + Hydrocortisone
DX: 1) Measure plasma Cortisol; If Low, check Plasma ACTH, Aldosterone, and Renin
Primary (addisons): Hi ACTH, Hi Renin, Low Aldosterone
Secondary: Low ACTH, Normal Renin/Aldo
TX:
1o: PO Hydrocortisone or Prednisone QD + Fludrocortisone QD
2o: Same as above but no need for Fludrocortisone since no low mineralcorticoids in 2o

Pheochromocytoma
Hi Catecholamines from Adrenal Medulla mass
S/S: Very hi BP, pounding headache, severe sweating, anxiety, impending doom, hi glucose, hi K, Hi Lipids
DX: Urine screen for metanephrine (an epi breakdown product), will be elevated; May also

check urine/serum epi/norepi levels; CT/MRI to detect location of mass

TX: Alpha blockers, followed by surgical resection
Hyperaldosteronism
Usually from Adrenal Cortex adenoma (Conns syndrome) or hyperplasia
Patho: Aldosterone is the primary mineralcorticoid in the body that is responsible for saving
Na in the DCT/CD of the kidneys, thus preserving water and increasing volume; K is wasted
in exchange for Na; Responds to Renin; Fludricortisone is pharm version of this hormone
S/S: hi Na, Low K, HT, Polydipsia, Polyuria, no peripheral edema, M.Alkalosis
DX: Aldosterone/Renin ratio (Hi/Lo which shows Renin is not the cause of hi Aldo)
TX:
Hyperplasia: Spironalctone
Adenoma: Resection
Steroids: Just so you don't get confused, here is a chart that shows which of the steroids we use in the hospital
have solely Glucocorticoid effects, which have Mineralcorticoid effects, and their strength compared with the
natural steroid Cortisol.

Pituitary disorders
SIADH
Often hi ADH is seen after stroke, trauma or pain due to hi blood flow and release of hormone
Iatrogenic: Meds (SSRIs, Morphine, Oxytocin) can also cause
Lung: CA, pneumonia or TB can release an ADH-like hormone
S/S: Low Na (free water retention) w/CNS changes (lethargy, falls, Sz, coma), low Renin,
hypervolemia, low BUN/Creatinine
TX:
1o: Water restriction (usually sufficient)
2o: NS + Lasix if faster results desired
3o: Lithium or Demeclocycline inhibit ADH if severe; May also add Hypertonic saline if neuro s/s
CX: NEVER raise Na more than 0.5 meq/L/hr (12/d) or will develop pontine myelinolysis
Diabetes Insipidus
Central: Most common form, low ADH from surgery or head trauma
Nephrogenic: poor response to ADH due to low K, hi Ca or Lithium
S/S: Polyuria (5-15 L/d), clear urine, polydipsia, hi Na, low Urine osmolality , hi plasma osmol
DX: DDAVP-if response you have both diagnosed and treated central DI

 TX:
Central: DDAVP (Desmopressin-synthetic ADH/Vasopressin that is much stronger and longer acting), nasally,
PO or injection; Chlorpropramide increases response to ADH
Nephrogenic: Thiazide diuretics (block DCT Na uptake forces PCT to reabsorb Na and water, so less water
reaches the faulty ADH channels)

Parathyroid disorders

Hypoparathyroidism
Facts: Hyposecretion of parathyroid hormone, often following thyroidectomy
S/S:
Subjective: Numbness/Tingling in face, depression, Muscle cramps
Objective:
Hypocalcemia, hyperphosphatemia, Hypotension
+ Trousseau (BP cuff causes carpal spasms)
+ Chvostek (Tap facial nerve contracts face muscle)
Hyper DTRs, Seizures
Cardiac arrhythmias, Prolonged QT interval (Primary r/o with long QT)
TX: Calcium gluconate (Serious: IV; Mod: PO); Vitamin D
NX:
Calcium and Vitamin D can increase Ca excretion = stones
Initiate Seizure precautions
Place Tracheotomy set, Oxygen, Suction at bedside
Monitor for Tetany: s/s include arrhythmias, carpopedal spasm, dysphagia, cramping,
numbness/tingling in face/extremeties, + Chvostek/Trousseau, Seizures, Photophobia,
Wheezing/Dyspnea (Broncho/laryngospasm)

Hyperparathyroidism
Facts: Hypersecretion of Parathyroid hormone
S/S:
Stones: Nephrolithiasis (Renal calculi/stones)
Bones: Bone pain, Bone deformities, Pathological fractures
Groans: Muscle pains/weakness, PUD, Pancreatitis, Gout, Constipation
Psychiatric overtones: Depression, Anorexia/weight loss, lethargy
Others: Hypercalcemia, Hypercalciuria, Hypophosphatemia, HT, Polyuria, Polydipisia, Shortened QT Interval
TX:
Furosemide (Lasix) to lower calcium levels by up excretion
IV fluids of NS
Calcitonin (Calcimar) to lower skeletal calcium release
NX:
Notify MD if rapid drop in Ca occurs and assess for s/s of tetany
Pancreas disorder

Diabetes Mellitus
Facts: Inability to control blood glucose
Type 1: Autoimmune beta islet cell destruction, usually presents as a kid, less than 10% of all DM
Type 2: Insulin resistance = hi glucose = hi Insulin = pancreas fails = overt DM, more than 90% of DM
S/S:
Type 1: Develop hyperglycemia rapidly, often after illness, usually presents in DKA
Type 2: Polyuria, polyphagia, polydipsia, frequent infections; May present w/comorbidities such as MI, stroke,
claudication, neuropathy, proteinuria; often discovered on routine UA or sugar check
DX: Diabetes; 4 independent methods
more than126 after 8 hour fast (preferred method) (less than 110 norm)
more than 200 at anytime w/DM s/s
more than 200 2 hr after 75g oral glucose load (less than 140 norm)
more than 6.5 hbA1C at anytime

DX: Impaired glucose tolerance (not quite DM but hi risk of future development)
110 -126 after 8 hour fast
140 - 200 2 hr after 75g oral glucose load
5.8-6.5 hbA1C
TX considerations:
HbA1C: Gives an estimate of glucose control over previous 3 mos as it measures how many
hemoglobin are coated in glucose
less than 5.8 (perfect); below 7% (ok); 7-8.5% (good); 8.5-10% (fair); above 10% (poor)
Check sugar/Administer Insulin 4x/d: qmeals and qhs
Annual urine check for albumin: Microalbuminuria (30-300) gets ACEI and Statins right away
ASA for macrovascular complications, NSAIDs for neuropathy
Other goals: BP less than130/80, LDL less than 100, TG less than 150, HDL more than 40
Dawn Phenomenon: Morning Hyperglycemia (8am glucose hi + 3 am glucose hi = incr evening dose)
Somogyi Effect: Morning Hyperglycemia (8am glucose hi + 3 am glucose low = decr evening dose)
Type 1: Insulin required to live, SQ in ab/butt/arm/leg; Regular insulin IV for emergency or
hospital maintenance; Can also add to TPN for maint

Type 2: PO meds after diet and exercise have failed to increase sensitivity; Add insulin after PO meds have
failed
PO Hypoglycemics:

 Ex: Metformin (Glucophage)

Lowers glucose absorption and production; hold prior to using IV contrast
S/E: Hypoglycemia, Bloating, N/V/D
Rosiglitazone (Avandia)
Improves insulin sensitivity
S/E: CHF/Edema, Hives, Anemia, Increased Cholesterol, Wt gain

Acute TX of poor glucose control

DKA: (5-10% mortality)
Almost exclusively in Type 1 diabetics
S/S: Polyuria, dehydration, ab pain, fruity breath, AMS, low Na/Mg/Phos, hi K (but low total body), + following:
Hyperglycemia (more than 250)
Metabolic acidosis (pH below 7.3, HCO3 below 15, AG above 20)
Ketonuria/Ketonemia
TX:
1o: IV insulin bolus (0.1 unit/kg) then IV infusion with same amount per hr AFTER making sure pt is not low K
Continue until acidosis corrects then taper
1oa: NS immediately upon diagnosis
Switch to D5NS when glucose less than 250
2o: Add KCl to IV fluids once K less than 5; replenish other electrolytes as necessary
Hyperosmolar Hyperglycemic nonketotic syndrome:
Severe hi Glucose, almost exclusively in Type 2 diabetics
Similar to DKA but usually have much higher glucose (above 600) and NO acidosis or ketonuria/emia
Treat with fluids and low dose Insulin infusion
Hypoglycemia:
Patho: When glucose drops to 80 = insulin levels decr ; 70 = Glucagon incr; 50 = epinephrine incr along with
signs such as sweat, hi BP, hi HR, tremors; Also around 50 CNS s/s (drowsy, h/a, confused) begin
Note: S/S from epinephrine release are absent if pt is on a BB
TX: If pt is alcoholic give Thiamine before any other treatment to prevent encephalopathy
1o: Can eat = hi sugar food; Can Not eat = 1/2 - 2 amps D50 IV push; (Glucagon alternative option if no IV
access is available, however is of no use in prolonged hypoglycemia because stores of glycogen are depleted)