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222 Cards in this Set

  • Front
  • Back
in chronic stable angina, the severity of coronary artery stenosis is usually greater than ___%?
5 therapy options for chronic stable angina?
1. nitrates
2. beta blockers
3. CCBs
4. antithrombotics (ASA, clopidogrel)
5. revascularization
what is the stimulus for increased NO production by the endothelial cells?
decreased O2
two major actions of NO?
1. relaxes vascular smooth muscle
2. inhibits platelet aggregation and adhesion
how do the coronary arteries adapt to increased O2 demand?
describe the coronary artery changes upon exercise.
coronary blood flow increased 5-6x.
coronary arteries dilate to accomodate
MOA of vasodilation by NO?
1. NO binds to sulfhydryl groups
2. activates guanylate cyclase
3. increases cGMP
4. results in smooth muscle relaxation (dilation of coronary arteries as well as dilation of veins and other arteries)
how does tolerance to Nitrates occur?
sulfhydryl groups are depleted
venodilation of capacitance vessels
- venous pooling of blood
- reduced preload (LVEDP)
- decreased oxygen demand
at what dosage of nitrates does:
1. arterial dilation occur?
2. venous dilation occur?
1. arterial dilation - high dosage
2. venodilation - low dosage
why are nitrates administered sublingually?
bypass the 1st pass (hepatic) metabolism
which drug can be administered to counteract the effects of nitrates?
hepatic glutathione-organic nitrate reductase
(removes nitrate group from parent drug and inactivates organic nitrates)
what are some adverse effects caused by the excessive vasodilation seen with nitrate administration? (6)
1. orthostatic hypotension
2. tachycardia
3. throbbing headache
4. dizziness
5. flushing
6. syncope
which class of drugs are nitrates contraindicated with?
PDE type 5 inhibitors
should not be used within 24 hrs of eachother
what is the advantage of using isosorbide mononitrate vs. other isosorbide mononitrate?
- NO first pass metabolism (100% bioavailable)
- longer acting
disadvantage of transdermal TNG use?
way to overcome this?
improvement declines after 7-10 days of continuous use
(encourage 8-10 h. nitrate free period)
possible mechanisms behind nitrate tolerance? (3)
1. diminished ability to convert nitrate to NO
2. diminished release of NO b/c of depletion
3. alterations in guanylate cyclase activation
what are some factors leading to nitrate tolerance? (4)
1. Large doses
2. frequent dosing
3. sustained action formulations
4. no nitrate-free interval
two strategies to minimize nitrate tolerance?
1. nitrate free intervals of 10-12 hours/day
2. erratic dosing intervals
advice to give paitents on nitrates regarding when to come in to hospital?
if an anginal attack is not controlled by nitrates it may be an MI
* if chest pain is not relieved by nitroglycerin seek medical care*
three major effects of Beta Blockers?
1. decrease HR (at rest and exercise)
2. decrease contractility
3. reduce arterial BP
effect of beta blockers on coronary blood flow?
Little to none
(decreased HR causes an increase in diastole, therefore an increased perfusion time)
Four major MOAs of CCBs?
1. coronary vasodilation
(increase coronary blood flow, reduce coronary vasospasm)
2. arterial vasodilation (reduce afterload)
3. decreased cardiac contractility
4. decrease HR
how do beta blockers decrease O2 demand? (3)
1. HR
2. Contractility
3. systolic BP
how do CCBs decrease O2 demand? (3)
1. afterload
2. contractility
3. HR
how do CCBs increase O2 supply? (1)
decrease coronary resistance
effect of CCBs in effort induced angina syndromes?
increases exercise threshold
Strategies in Pharmacotherapy to prevent MI and Death and Reduce symptoms (5)
1. ASA
2. BBs
3. ACEIs (if diabetes & CAD)
4. LDL lowering if high LDL
what to prescribe if BBs are contraindicated?
CCBs or LA nitrates
what to prescribe if initial BB treatment is not successful?
CCBs or LA nitrates
What is the drug of first choice in angina due to coronary spasms?
when would Clopidogrel be indicated along with ASA?
indicated for patients with stable chronic CAD with a risk profile INDICATING A HIGH LIKELIHOOD OF DEVELOPING AN AMI
three revascularization therapies?
1. PTCA (Percutaneous Transluminal Coronary Angioplasty)
2. PCI (Percutaneous Coronary Intervention)
3. CABG (Coronary Artery Bypass Grafting)
which BP (by convention) is classified as a hypertensive crisis even if the patient is asymptomatic?
We often rank hypertensive patients according to clinical presentation. What are those three rankings?
1. Hypertensive emergencies
2. Hypertensive urgencies
3. Uncontrolled severe hypertension
what is the difference between a hypertensive emergency and a hypertensive urgency?
hypertensive emergency - severe BP elevation WITH rapid and progressive damage of target organs

hypertensive urgency - severe BP elevation w/o progressive organ damage or dysfunction
symptoms of hypertensive urgency? (4)
severe headache
severe anxiety
How does the treatment of hypertensive emergency differ from the treatment of hypertensive urgency?
emergency: immediate BP lowering required (must prevent target organ damage)

urgency: can lower over a few hours
ptwo classes of drugs available for hypertensive emergencies?
1. Vasodilators

2. Adrinergic Inhibitors
vasodilators indicated for treatment of a hypertensive emergency? (6)
1. Nitroprusside
2. Nicardipine
3. Fendolopam
4. Nitroglycerine
5. Enalaprat
6. Hydralazine
adrinergic inhibitors indicated for treatment of a hypertensive emergency? (3)
1. Labetalol
2. Esmolol
3. Phentolamine
MOA of nitroprusside?
decreases afterload and preload by arterial and venous vasodilation (POTENT)
Adverse Effects of nitroprusside? (3)
1. may increase intracranial pressure
2. "coronary steal" - reduction in coronary blood flow increases chance of mortality by infarct
3. cyanide toxicity (contains 44% cyanide)
strategies to prevent cyanide toxicity in nitroprusside treatment? (5)
1. use only when other IV agents not available
2. use only with normal renal and hepatic function
3. short as possible treatment
4. slow infusion rate
5. add other ingredients to infusion (hydroxycobalamin, thiosulfate)
nicardipine is an IV CCB used to treat hypertensive emergencies. Unlike nitroprusside, it is effective against which types of ischemia?
reduces both cardiac and cerebral ischemia
*as effective as nitroprusside*
MOA of Fendolopam?
(FDA approved for acute HTN)
Dopamine (DA)1 agonist
- increases renal blood flow and Na+ excretion
- diuretic
What is fendolopam the drug of choice for?
severely hypertensive patients with impaired renal function
MOA of nitroglycerin?
(high doses - arterial tone affected as well)
- reduces BP by decreasing preload and CO
(at high doses decreases afterload too)
nitroglycerin may compromise perfusion where?
may compromise renal and cerebral perfusion
three indications for nitroglycerin?
1. hypertensive emergencies
2. acute coronary syndromes
3. cardiogenic shock pts. with adequate to high B/P
nitroglycerin may increase pressure where?
may increase intracranial pressure
MOA of hydralazine?
Direct ARTERIAL vasodilator
why is hydralazine not usually used?
-unpredicatable antihypertensive effects
-unpredictable but LONG half life (antihypertensive effects are prolonged)
Besides hydralazine, what is another drug that is not 1st line in controlling BP because of it's variable hemodynamic response?
*sometimes too much BP lowering*
which short acting beta blocker is safe to use in an acute MI, supraventricular dysrythmias and post-op hypertension?
MOA of Labetolol?
combined alpha and beta blocker activity. results in:
- decreased PVR without reducing peripheral blood flow (cerebral, renal, coronary blood flow maintained)
what are the four classes of inotropic agents?
1. stimulators of Adenylyl Cyclase
2. blockers of cAMP Degradation
3. Blockers of Na+/K+/ATPases
4. Adrinergic Agonists
two naturally occuring sympathomimetics?
1. Dopamine
2. Epinephrine, NE
of the beta agonists:
1. list one non-specific
2. list one B1 selective
1. Isoproterenol
2. Dobutamine
list two stimulators of adenylyl cyclase that are independant of the B receptor
1. histamine
2. glucagon
MOA of milnirone?
Phosphodiesterase inhibitor
(Blocks cAMP degradation)
Name a class of drugs that block the Na+/K+/ATPase
digitalis glycosides
(Digoxin, Digitoxin)
Describe the onset and duration of action of catecholamines. (Epi, NE, Isoproteronol, Dopamine, Dobutamine)
Rapid onset
Rapid duration of action
(metabolized by COMT and MAO)
Non-catecholamines have a longer duration of action of action than catecholamines. List three
MOA of direct acting adrinergic antagonists?
direct action on alpha and/or beta receptors
list some direct acting adrinergic agonists (6)
MOA of indirect acting adrinergic agonists?
list two
cause release of stored NE
(Amphetamine, tyramine)
give an example of a mixed action adrinergic agonist (both direct and indirect action)
location and action of alpha-1 receptors?
cause vasoconstriction
location and action of beta-1 receptors?
increase HR, conractility, AV conduction
location and action of beta-2 receptors?
arterioles, veins
location and action of DA1 receptors?
renal, mesenteric, coronary vasculature
effects of epinephrine (receptors, actions)
alpha-1, beta-1 and 2 effects
beta-1: inotropic, inreased HR, CO
alpha-1: increased systolic BP
beta-2: slight decrease diastolic BP (vasodilation of skeletal muscle vasculature)
indications for epinephrine?
1. cardiac arrest
2. alaphylactic shock
3. hemodynamic support after CABG
adverse effects of epinephrine? (5)
1. arrythmias, palpitations
2. HTN (peripheral vasoconstriction)
3. angina (increases myocardial O2 demand)
4. transient increase in lactate levels
5. tissue necrosis
norepinephrine is an agonist of which receptors?
mostly alpha-1 (some beta-1)
effects of NE?
alpha-1 effects: vasoconstriction, increased SVR
-mild increase in inotropy and CO
indications for NE? (2)
1. septic shock
2. cardiogenic shock
potential adverse effect of NE?
intense vasoconstriction
phenylephrine is a potent agonist of which receptors?
results in vasoconstriction
why does phenylephrine have no direct effect on contractility or HR?
no beta receptor activity
two indications for phenylephrine?
1. shock
2. decongestant
adverse effects of phenylephrine?
peripheral vasoconstriction (can result in tissue necrosis and reduction of SV)
vasopressin is an antidiuretic hormone. Where is it synthesized and stored?
synthesized in hypothalamus
stored in pituitary
what stimulates the release of vasopressin from the pituitary?
increased serum osmolality
pharmacologic effects of vasopressin? (4)
1. vasoconstriction
2. increases vascular responsiveness to NE and EPI
3. increases BP by inhibiting endotheilal NO production
4. antidiuretic effect (incr. water resorption in collecting tubules)
advantage of vasopressin over EPI or NE?
longer duration of action
indications for vasopressin? (2)
1. septic shock not responding to other vasopressors (EPI, NE etc)
2. alternative to EPI for shock refractory v-fib or v-tach
adverse effects of vasopressin? (3)
1. reduce CO in pts. with ventricular dysfunction
2. dilutional hyponatremia
3. local tissue necrosis
what is the natural precursor of EPI and NE?
which receptors does dopamine have an effect on?
agonist of:
alpha receptors
beta receptors
DA1 and DA2 receptors
(dose dependent effects)
action of low dose dopamine?
DA effects predominate
- increase in GFR, renal blood flow
- decrease proximal tubular resorption of Na+
(some B1 activity)
action of moderate dose dopamine?
B1 effects predominate
-increase in contractility
-increase in HR
(still have DA activity, also minor a1 effects)
effects of high dose dopamine?
a1 effects predominate
- arterial vasoconstriction
- increase in BP
dopamine is sometimes used in a low dose for?
renal effects
-prevent renal failure by maintaining urine output and increasing renal blood flow
three indications for Dopamine use?
1. maintain urine output?
2. decompensated HF
3. Hypotension and shock
adverse effects of DA? (5)
1. tachycardia
2. arrythmias
3. excessive vasoconstriction
4. hypertension
5. tissue necrosis
treatment for tissue necrosis with extravasation as a result of dopamine treament?
infiltrate area with phentolamine
dobutamine is a synthetic catecholamine. which receptors does it act on?
B1 > B2
(little effect on a1)
effect of dobutamine on renal blood flow?
NO direct effects
(does not act on DA receptors)
however, does increase CO which increases renal blood flow
cardiovascular effects of dobutamine?
increased contractility
increased CO
contraindication for dobutamine Tx?
hypotension not due to HF
indications for dobutamine? (2)
1. decompensated HF
2. cardiogenic shock
major problem with isoproteronol treatment?
(rarely used)
effects of isoproteronol treatment?
nonselective beta agonist
- increase HR
- increase contractility
- increase AV conduction
two indications for isoproteronol use?
1. AV block (cardiac stimulant)
2. asthma
milnirone is a phosphodiesterase inhibitor and reduces cAMP breakdown. what are the physiological results of increased cAMP?
cAMP activates protein kinase
protein kinase phosphorylates the Ca++ channel

increased [Ca++] = increased contractility
actions of PDE inhibitors:
1. on myocardial muscle
2. on vascular smooth muscle
3. compared to dobutamine
1. increased contractility and SV
2. vasodilator = decreased afterload (resistance)
3. less potent inotrope and more potent vasodilator, less increase in HR
indication for milnirone?
Severe heart failure
three adverse effects of milnirone?
1. tachyarrythmias
2. hypotension
3. thrombocytopenia
what is nesiritide?
recombinant BNP (Brain Natriuretic Peptide)
when and where is normal BNP released?
released by atria and ventricles during pressure/volume overload
effects of BNP (3)
1. natriuretic
2. diuretic
3. vasodilator
MOA of nesiritide?
-reduces volume and vasodilates
-dilates renal afferent and constricts renal efferent arterioles (increased GFR and causes natriuresis and diuresis)
-lowers pulmonary wedge pressure
indications for nesiritide?
1. acutely decompensated HF with dyspnea at rest or with minimal activity
2. pt. awaiting cardiac transplant
significance of nestiritide lowering pumonary capillary wedge pressure?
lowers systolic BP and dyspnea in decompensated HF
what was the recent FDA warning on nesiritide?
may have adverse effects on survival and kidney function
which cardac disorder is the #1 cause of hospitalizations in the elderly?
Heart Failure
what are the two cardinal signs of HF?
1. dyspnea and fatigue
2. Fluid retention (pulmonary congestion/peripheral edema)
what are the three determinants of SV?
what is the primary determinant of the Starling curve mechanism?
vasodilation will effect which determinant of the SV?
describe the pathophysiology behind HF.
1. cardiac damage
2. LV performance decreases
3. results in decreased CO
4. body compensates by increasing RAAS and sympathetic activity
5. Na+ and H20 retention results in an increase in vascular resistance
6. results in increase in LV afterload
7. LV remodels to accomodate
*circle begins again*(decrease in LV performance)
in HF, which drug will:
1. inhibit angiotensin II production?
2. block physiologic actions of ATII?
3. block Beta receptors?
4. inhibit Na+ and K+ transport across membranes?
2. ARBs
3. beta blockers
4.Digitalis toxin
which two aspects of Heart failure, if treated, give a better prognosis for the HF patient?
1. inhibition of RAAS
2. inhibition of Adrinergic system
what are the 5 drug classes a HF paitent is indicated for that will decrease morbidity/mortality?
1. Hydralazine/Isosorbide
2. ACEIs
3. BBs
4. Aldosterone antagonists
5. ARBs
indications for a diuretic in HF?
symptomatic HF with fluid retention
(asymptomatic HF -> no diuretic)
what must be taken into consideration when monitoring K+ levels in a HF patient?
1. diuretic could be K+ wasting
2. ACEIs and ARBs increase K+ levels
diuretic class of choice in treatment of HF?
Loop diuretics
(thiazides are 2nd)
what is the prototype vasodilator of the veins?
what is the prototype arterial dilator?
when is hydralazine indicated?
as a second line drug if ACEIs are not tolerated or ineffective
-also in African Americans as Hydralazine/Isosorbide Dinitrate
compare HF in black vs. white pts.
black HF pts have:
1. less active RAAS
2. endothelial function and bioavailability of NO may be less (NO can prevent myocardial and vascular remodeling)
MOA of isosorbide dinitrate and Hydralazine in the African American HF pt.
isosorbide dinitrate: NO donor
hydralazine: antioxidant, prevents against degradation of NO
MOA of digitalis?
1. inhibits Na+/K+/ATPase
- results in increase in intracellular Ca++ via a Na+/Ca++ exchanger
- results in increased myocardial uptake of Ca++ = increased inotropic response
digitalis acts during which phase of the cardiac cycle?
phase 3 (repolarization phase)
compare the actions of digitoxin and beta blockers on cardiac activity
digitoxin only increases contractility, not HR
BBs increase both HR and contractility: less energy efficient
effects of K+ on digitoxin binding?
-high extracellular K+ INHIBITS digoxin binding to NA+/K+/ATPase (competitive inhibition)
-low extracellular K+ increases binding
what is the dominant indirect effect of digitalis in therapeutic doses?
parasympathomimetic (increases vagal tone)
-lowers HR
-increases refractory period
effects of digoxin on AV conduction velocity?
decreases AV cond. velocity
(direct and indirect (Vagal)effects)
what is the "digoxin effect" as seen on an ECG?
1. P wave changes
2. Lengthened PR interval
3. ST depression
4. T wave inversion
effects of digitalis on longevity?
what are 5 relative digitoxin contraindications?
1. advanced AV block w/o pacemaker
2. bradycardia or sick sinus w/o pacemaker
3. frequent PVCs
4. marked hypokalemia
5. W-P-W with A-fib
s/s of chronic digitalis toxicity? (7)
1. exacerbation of HF
2. weight loss
3. cachexia
4. neuralgias
5. gynecomastia
6. yellow vision
7. delirium
which arrythmia is almost always due to digitalis toxicity?
(Paoxysmal Atrial Tachycardia)
treatment for severe cases of digitalis toxicity?
(digitoxin specific antibody)
management of digitalis toxicity?
1. assess severity and risk of arrythmias
2. if hypokalemia - give K+
3. lidocaine or phenytoin for arrythmias
effect of ACEIs on arteries and veins?
arteriovenous dilation
(decreases preload, SV, BP)
(increases CO and exercise tolerance)
effects of ACEIs on HR/contractility?
(ACEIs are not + inotropes)
effects of ACEIs on renal blood flow and function?
increase renal blood flow
clinically relevant effect of ACEIs post-MI
inhibits LV remodeling post-MI (this increases survival and improves quality of life)
adverse effects of ACEIs? (6)
1. hypotension
2. worsening renal function
3. hyperkalemia
4. Cough
5. angioedema
6. rash, neutropenia
contraindications of ACEIs? (2)
1. angioedema or anuric renal failure from ACEIs
2. Pregnancy
caution of ACEIs?
1. SBP<80
2. SCr>3
3. Renal Artery Stenosis
4. hyperkalemia
major indication for ACEIs?
every patient with HF unless contraindicated!
(ACEIs are the "workhorses")
what is important about the dosage of ACEIs in a HF patient?
dose is not determined by the symptoms
(must increase dose as tolerated to the recommended HF dose)
what is the #1 reason patients can't tolerate ACEIs?
(Then prescribe ARBs)
MOA of ARBs?
block the effects of Angiotensin of AT1 receptor
results in:
- reduced BP
- decreased afterload
- may block growth promoting actions of angiotensin
what is seen when ARBs block the growth promoting actions of angiotensin?
- vascular hypertrophy and atherosclerosis reduced
- LV hypertrophy regresses
what are the only 3 BBs shown to have benefit in HF?
MOA of BBs in relation to HF?
inhibit negative actions of increased sympathetic stimulation on the failing heart
why were BBs historically contraindicated in HF?
negative inotropes
slow HR
which BB is a nonselective Beta blockade with a1 blockade used in the treatment of HF?
which BBs are a selective B1 blockade used in the treatment of HF?
clinical effects of Beta blockers? (5)
1. improve symptoms w/long term use
2. reduce remodeling and progression of LV dysfunction
3. reduce hospitalizations
4. reduce sudden death
5. improve survival
indications for BBs in HF?
ALL patients with HF should be on BBs if no contraindications
effects of aldosterone on Na+ and H20 Retention?
increases retention
(results in edema)
aldosterone increases K+ and Mg++ excretion - what is the result of this?
other CV effects of aldosterone? (6)
1. endothelial fibrosis, dysfunction
2. increased blood clotting and plt. activation
3. cytokine activation (vascular inflammation)
4. autonomic dysfunction
5. LV dysfunction
6. arrythmogenic
name of nonselective aldosterone receptor antagonist used to treat HF?
effect of spironolactone on CHF?
30% reduction in risk of death
35% < hospitalizations
contraindications to spironolactone use? (2)
1. hyperkalemia
2. renal failure
prescribe spironolactone along with which 3 other CHF drugs?
2. loop diuretic
3. digoxin
effect of spironolactone on [K+]?
increases [K+]
-if K+ is high, reduce dose
- if K+ is low, maximum dose
MOA of Eplernone?
selective aldosterone blocker (SAB)
-may have cardioprotective and renoprotective effects
-less adverse effects than spironolactone
indications for spironolactone?
1. moderately severe or severe HF symptoms & recent decompensation
2. with LV dysfunction early after MI
how does the body compensate in Stenotic valvular heart disease?
increases pressure to overcome resistance caused by insufficient opening of valve.
how does the heart compensate in regurgitation?
increases stroke volume
Rheumatic Heart Disease is diagnosed by the Jones criteria. What of each is needed for diagnosis?
2 major
1 major and two minor
what are the major Jones criteria? (5)
1. carditis
2. polyarthritis
3. subcutaneous nodules
4. erythema marginatum
5. sydenham's chorea
what are the minor Jones criteria? (4)
1. arthralgias
2. elevated ESR
3. elevated CRP
4. prolonged PR interval
what do we mean when we day that acute rheumatic heart disease is a PANCARDITIS?
affects all layers:
what are the microscopic lesions seen in the myocardium of a patient with acute rheumatic disease called?
Aschoff bodies
which valve is most commonly affected in chronic RHD?
(aortic valve #2, but always seen eith mitral)
describe the murmur heard in aortic stenosis
systolic murmur
crescendo-decrescendo type
starts slightly after S1
how does the heart compensate in aortic stenosis?
compensatory LV hypertrophy
symptoms of aortic stenosis?
3 causes of aortic stenosis?
1. RHD
2. congenital bicuspid valve that calcified
3. calcified normal valve
describe the murmur heard in aortic regurgitation
diastolic murmur
decrescendo type
starts at S2
symptoms of aortic regurgitation? (3)
1. exertional dyspnea
2. syncope
3. angina
6 causes of aortic insufficiency?
1. RHD
2. bacterial IE
3. Syphilis
4. dissecting hematoma/steering wheel injury
5. Marfan's
6. dilated ring (RA, syphilis)
how does valsalva maneuver help us when listening for a murmur?
valsalva = decreased venous return
- get decreased TPR
- get decreased LV volume
- get decreased arterial BP
which murmur is decreased in intensity with valsalva?
aortic stenosis
which murmur is increased with the valsalva?
mitral prolapse
describe the murmur heard in mitral stenosis
soft rumbling quality
cause of mitral stenosis?
Rheumatic heart disease
(L atrial myxoma may be present)
possible complications of mitral stenosis?
1. L atrial dilation
2. atrial fibrillation
3. L atrial thrombus formation with potential embolization
4. pulmonary venous HTN
5. pulmonary edema
describe the murmur heard in mitral regurgitation
holosystolic murmur
starts at S1
symptom of mitral regurgitation?
exertional dyspnea
primary causes of mitral regurgitation?
1. RHD
2. mitral valve prolapse
3. rupture/dysfunction of chordae/papillary muscles
4. calcification of mitral annulus
describe the heart sounds heard in mitral valve prolapse
mid systolic click (snapping of chordae with prolapse)
symptoms of mitral valve prolapse?
2. may see fatigue, anxiety, syncope, endocarditis
what causes carcinoid heart disease?
seen in pts with gastrointestinal carcinoid tumors which have metastasized to the liver - causes endocardial disease
describe the endocardial disease seen in carcinoid heart disease
uniform pearly grey fibrous tissue on endocardial surface of right heart (esp. pulmonary, tricuspid valves)
carcinoid heart disease usually effects which valves?
tricuspid (regurg/stenosis)
pulmonary (stenosis)
which heart disease usually resembles carcinoid heart disease?
Fen-Phen heart disease
MOA of Fen-Phen?
affects systemic seratonin metabolism
in Fen-Phen heart disease, what symptom usually accompanies those that resemble carcinoid HD?
pulmonary hypertension
which bacteria are most likely to cause:
1. acute IE
2. subacute IE
1. Staph aureus, Beta hemolyic strep
2. alpha hemolytic strep
prognosis of acute IE?
leads to death within days to weeks, mortality rate up to 50% in spite of abx therapy or surgery
prognosis of subacute IE?
insidious course, over weeks to months
most respond to abx therapy
classic signs of IE? (5)
1. petechiae
2. splinter hemorrhages (nails)
3. Osler's nodes
4. Janeway lesions (tender)(nontender, palms and soles)
5. Roth spots (retinal hemorrhages with clear centers)
which three types of congenital heart disease often have complications of IE?
1. PDA
2. Tetrology of Fallot
3. VSD
which valve is most commonly infected in IF caused by IV drug use?
which bacteria most often causes IE in an IV drug user?
Staph aureus
what is IE caused by Strep bovis associated with?
villous adenoma of the colon
complications of IE? (4)
1. valvular insufficiency (CHF)
2. emboli (can cause infarcts and abcesses)
3. glomerulonephritis (could be due to immune complex deposition)
4. myocardial ring abcesses
what is marantic endocarditis?
non-bacterial thrombotic endocarditis (often associated with a malignancy and/or debilitating disease)
which two valves are most commonly involved in marantic endocarditis?
mitral and aortic
hypothesis behind formation of marantic endocarditis?
1. hypercoagulability
2. disseminated intravascular coagulation
possible complication of marantic endocarditis?
four causes of endocarditis of autoimmune disease?
1. SLE (aka. Libmann-Sacks endocarditis)
2. anti-phospholipid syndrome
3. RA
4. RHD