Glossary of BVI, WII
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- 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
4. antithrombotics (ASA, clopidogrel)
- 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
- what do many consider the PRIMARY THERAPEUTIC ACTION OF NITRATES?
- 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
3. throbbing headache
- 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)
3. systolic BP
- how do CCBs decrease O2 demand? (3)
- 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
3. ACEIs (if diabetes & CAD)
4. LDL lowering if high LDL
5. SL TNG
- 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
- 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
- adrinergic inhibitors indicated for treatment of a hypertensive emergency? (3)
- 1. Labetalol
- 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
- What is fendolopam the drug of choice for?
- severely hypertensive patients with impaired renal function
- MOA of nitroglycerin?
- POTENT VENODILATOR
(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
- list two stimulators of adenylyl cyclase that are independant of the B receptor
- 1. histamine
- MOA of milnirone?
- Phosphodiesterase inhibitor
(Blocks cAMP degradation)
- Name a class of drugs that block the Na+/K+/ATPase
- digitalis glycosides
- 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?
- cause release of stored NE
- give an example of a mixed action adrinergic agonist (both direct and indirect action)
- location and action of alpha-1 receptors?
- 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
- 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:
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
3. excessive vasoconstriction
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
- contraindication for dobutamine Tx?
- hypotension not due to HF
- indications for dobutamine? (2)
- 1. decompensated HF
2. cardiogenic shock
- major problem with isoproteronol treatment?
- effects of isoproteronol treatment?
- nonselective beta agonist
- increase HR
- increase contractility
- increase AV conduction
- two indications for isoproteronol use?
- 1. AV block (cardiac stimulant)
- 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
- 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
- MOA of nesiritide?
- REDUCES PRELOAD
-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)
- CO=SV x HR
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?
- 1. ACEI
3. beta blockers
- 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
4. Aldosterone antagonists
- 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)
-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
6. yellow vision
- 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
6. rash, neutropenia
- contraindications of ACEIs? (2)
- 1. angioedema or anuric renal failure from ACEIs
- caution of ACEIs?
- 1. SBP<80
3. Renal Artery Stenosis
- 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
- 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
- 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
- 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?
- 1. ACEI
2. loop diuretic
- 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
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
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
starts at S2
- symptoms of aortic regurgitation? (3)
- 1. exertional dyspnea
- 6 causes of aortic insufficiency?
- 1. RHD
2. bacterial IE
4. dissecting hematoma/steering wheel injury
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?
- 1. USUALLY ASYMPTOMATIC
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?
- RIGHT HEART VALVES
- 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
- 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
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