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188 Cards in this Set
- Front
- Back
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5 types of R to L shunts (early cyanosis)
Which is most common cause of early cyanosis? |
(1) Tetrology of Fallot: MCC of early cyanosis
(2) Transposition of great vessels (3) Truncus arteriosus (4) Tricuspid atresia (5) Total anomalous pulmonary venous return |
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3 types of L to R shunts (relative frequencies?)
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(1) VSD
(2) ASD (3) PDA VSD>ASD>PDA |
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Eisenmenger's Syndrome
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Uncorrected VSD, ASD, or PDA causes compensatory vascular hypertrophy, which results in progressive pulmonary HTN. As pulmonary resistance increases, the shunt reverses to R to L which causes late cyanosis (clubbing and polycythemia).
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VSD
(a) describe (b) associated w/which genetic disorders? (c)possible outcomes |
(a) defect in membranous IV septuml incr SaO2 in RV and PA
(b) cri du chat; trisomy 13; trisomy 18 (c) small defects spontaneously close; large may lead to Eisenmenger's |
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ASD
(a) describe (b) associated with what congenital disorders/diseases? (c) clinical manifestations? |
(a) patent foramen ovale is most common; incr SaO2 in RA, RV, and PA
(b) FAS and Down's (but in Down's have incomplete septum b/w ventr and atria + abnormal tricusp) (c) often delayed until later in life; PHTN and reversal of flow are late complications; can lead to paradoxical embolism. |
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PDA
(a) describe (b) assoc w/what congenital disease? (c) clinical presentation (d) associated w/what type of murmur? (e) consequence? (f) patencymaintained by? (g) closure induced by? |
(a ) failure of fetal ductus arteriosus to close; Incr SaO2 in PA; unox blood enters aorta below subclav a.
(b) congenital rubella (c) Pink upper body and cyanotic lower body . (d) Machinery murmur heard during systole and diastole. (e) If not closed eventually leads to PHTN, RVH, reversal of blood flow and late cyanosis. (f) PGE2 (g) indomethacin |
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Tetrology of Fallot
(a) describe defect (b) most important determinant for prognosis (c) clinical manifestation (d) associated w/what congenital disorder? (e) cause |
(a) pulmonary stenosis, RVH, Overriding aorta, and VSD
(b) degree of pulmonary stenosis (c) Minimal pulm sten: absence of cyanosis (more blood to lungs and less through VSD) Severe pulmonic stenosis: cyanosis (incr R to L shunting through VSD) Boot shaped heart on X ray (RVH) (d) tetrology of Fallot (e) anterosuperior displacement of infundibular septum. |
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Describe cyanotic/tet spell?
What maneuver can relieve symptoms? |
Sudden increase in hypoxemia and cyanosis. Squatting incr systemic vascular resistance causing temporary reversal of shunt.
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Transposition of great vessels
(a) describe defect (b) cause (c) result (d) associated with what maternal disorder? (e) cardioprotective shunts? |
(a) Aorta arises from RV and PA arises from LV.
(b) failure of aorticopulmonary septum to spiral. (c) Most infant die without surgical intervention (d) offspring of diabetic mother (e) ASD (delivery via aorta), VSD (delivery via PA), or PDA (shunt blood into PA for oxygenation to lungs) |
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Total anomalous pulmonary venous return
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PV empties oxygenated blood into the right atrium
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Truncus arteriosus
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Aorta and PA share common trunk and intermix blood.
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Tricuspid atresia
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Usually have an ASD w/R to L shunt
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Coarctation of Aorta (Infantile type): describe
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Aortic stenosis proximal to insertion of ductus arteriosus (preductal)
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Coarctation of aorta (adult)
(a) describe (b) manifestations (c) associated with what disease? (d) may result in what? |
(a) stenosis of aorta distant to ductus arteriosus (ligamentum arteriosum)
(b) Incr flow to collaterals (intercostal arteries) assoc w/notching of ribs, HTN in upper extremities (activate RAAS due to decr RBF), weak pulses in lower extremities/claudication. (c) Turner's syndrome (d) may result in aortic regurg; incr risk for berry aneurysms (incr CBF), and aortic dissection |
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Associated cardiac defect: 22q11 syndromes
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Truncus arteriosus
Tetrology of Fallot |
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Associated cardiac defect: Down's Syndrome
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ASD, VSD, AV septal defect (endocardial cushion defect)
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Associated cardiac defect: Congenital Rubella
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Septal defects, PDA, PA stenosis
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Turner's Syndrome
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Coarctation of aorta
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Marfan's Syndrome
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Aortic insufficiency (late complication)
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Offspring of diabetic mother
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Transposition of great vessels
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Risk factors for HTN
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Increase age
Obesity Diabetes Smoking Genetics Black>white>asian |
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Types/causes of HTN
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90% essential (related to incr CO or incr TPR); remaining secondary to renal disease.
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HTN increases risk for:
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Ahterosclerosis
LVH Stroke CHF Renal failure Retinopathy Aortic dissection |
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Aortic dissection
(a) describe (b)assoc w/? (c) clinical manifestation (d) signs on CSR |
(a) longitudinal intraluminal tear forming a false lumen
(b)HTN, Marfan's (c) tearing chest pain radiating to back (d) mediastinal widening |
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Define atherosclerosis
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Disease of elastic arteries and large and medium sized muscular arteries; fibrous plaques and atheromas form in intima of arteries
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Risk factors for atherosclerosis
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Smoking, HTN, DM, hyperlipidemia, family hx
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Describe progression of atherosclerosis
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Endothelial cell damage causes injury; macs and platelets adhere to damaged endothelium; release cytokines cause muscle hyperplasia of medial smooth which migrate to tunica intima; cholesterol enters Sm and macs (foam cells). SM release cytokines that produce ECM. Formation of fibrous plaque around necrotic center.
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Sites for atherosclerosis in descending order
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Abdominal aorta
Coronary artery Popliteal artery Internal carotid |
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Symptoms of atherosclerosis
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Angina, claudication, but can be asymptomatic
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Possible complications of atherosclerosis
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Aneurysm (vessel wall weakness)
Thrombosis (MI, stroke, small bowel infarct) HTN (renal artery atherosclerosis may activate RAAS) Peripheral vascular disease Cerebral atrophy (if involving circle of willis or internal carotid) |
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Monckeberg's arteriolosclerosis
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Calcification in the media of the arteries esp radial or ulnar. Usually benign; "pipestem" arteries. Does not obstruct blood flow and intima not involved.
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Hyaline Arteriolosclerosis
(a) describe (b) pathogenesis (c) associated conditions |
(a) hardening of arterioles
(b) increased protein deposited in vessel wall occluding lumen (c) DM (nonenzymatic glycosylation of proteins in BM) and HTN (increased intralumenal P pushes plasma proteins into vessel wall) |
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Hyperplastic arteriolosclerosis
(a) pathogenesis (b) Histological appearance |
(a) malignant HTN (renal arteriole effect caused by acute increase in BP); causes smooth muscle cell hyperplasia and basement membrane duplication
(b) onion skinning appearance |
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Atheromas
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Plaques in blood vessel wall
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Xanthoma
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Plaque or nodule composed of lipid laden histiocytes in skin esp eyelids (xanthelasma)
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Tendinous xanthoma
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Lipid deposit in tendon esp Achilles
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Corneal arcus
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Lipid deposit in cornea, nonspecific (arcus senilis)
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At what point do you get angina?
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CAD narrowing greater than 75% of lumen
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Stable angina
(a)causes (b) pathogenesis (c) clinical finding (d) ECG findings |
(a) atherosclerotic CAD (most common)
aortic stenosis w/concentric LCH hypertrophic cardiomyopathy (b) subendocardial ischemia due to decr coronary artery blood flow (c) exercise induced substernal chest pain (30s to 30m); relieved by rest or nitroglycerin (d) Stress test show ST segment depression |
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Prinzmetal's angina
(a) pathogenesis (b) clinical findings (c) ECG findings |
(a) intermittent coronary artery vasospasm at rest; vasoconstriction due to platelet thromboxane A2 or increase in endothelin
(b) responds to nitroglycerin and CCB (vasodilator) (c) stress test shows ST segment elevation (transmural ischemia) |
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Unstable/crescendo angina
(a) pathogenesis (b) clinical findings (c) ECG findings |
(a) severe, fixed, multivessel atherosclerotic disease; disrupted plaques w/ or w/out platelet nonocclusive thrombi
(b) frequent bouts of chest pain at rest or w/minimal exertion; may progress to MI (c) ST depression on ECG |
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Sudden cardiac death
(a) define (b) pathogenesis (c) cause of death |
(a) unexpected death w/in 1hr of sx; diagnosis of exclusion after other causes ruled out
(b) severe atherosclerotic CAD, disrupted fibrous plaques, absence of occlusive vessel thrombus (>80% of the time) (c) usually ventricular fibrillation |
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Chronic ischemic heart disease
(a) define (b) clinical findings |
(a) progressive onset CHF due to chronic ischemic myocardial damage (replacement of tissue w/scar)
(b) Biventricular CHF, angina pectoris, may develop dilated cardiomyopathy |
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Causes of MI
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Acute thrombosis due to CAD (usually due to sudden disruption of plaque forming thrombus).
Vasculitis Cocaine use Embolization of plaque material Thrombosis syndromes |
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Transmural infarction
(a) define (b) ECG findings |
(a) involves full thickness of myocardium
(b) new Q waves in ECG; ST elevation on ECG |
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Subendocardial infarction
(a) define (b) ECG findings |
(a) involves inner third of myocardium (subendocardium esp vulnerable to ischemia)
(b) Q waves absent; ST depression on ECG |
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Most common coronary arteries involved in MI
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LAD>RCA>CFX
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Gross/ microscopic findings for acute MI: 0-24hr
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Gross: none until 24hr
Microscopic: -contraction bands in first 1-2hr -early coagulative necrosis after 4h |
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Gross/ microscopic findings for acute MI: 1-3d
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Gross: pallor of infarcted myocardium
Microscopic: -myocyte nuclei and striations gone (extensive coagulative necrosis); macs begin removal of necrotic debris; dilated vessels (hyperemia) |
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Gross/microscopic findings for acute MI: 5-10d
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Gross: hyperemic border; central yellow-brown softening (max yellow and soft at 10d)
Microscopic: -granulation tissue and collagen formation well developed |
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Gross/ microscopic findings for acute MI: 2m
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Gross: gray/white area of infarction
Microscopic: scar complete (non contractile) |
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Gold standard for MI diagnosis in first 6hr
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ECG
Can include: Inverted T waves ST elevation (transmural infarct)-correlate with injured myocardial cells surrounding are of necrosis ST depression (subendocardial infarct) Pathologic Q waves (transmural infarct)-correlate w/area of necrosis |
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Cardiac markers for MI (time scale and uses in MI)
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CK-MB: rise at 4-8hr; peak at 24hr; disappears in 3d (use to test for reinfarct)
TroponinI: rise at 3-6h; peak at 24h; disappear within 10d (best for diagnosis of acute MI) LDH: rise w/in 10h; peak at 2-3 days; disapear within 7d |
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Complications of MI
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Arrythmia
LV failure and pulmonary edema Cardiogenic shock Ventricular free wall rupture Mural thrombus Aneurysm formation Fibrinous pericarditis Dressler's syndrome |
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Complications of MI: Arrhythmia
(a) importance in MI (b) timeline after MI |
(a) important cause of death (esp vfib)
(b) usually within first few days |
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Complications of MI: CHF
(a) timeline of occurrence |
(a) w/in first 24h
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Complications of MI: cardiogenic shock
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Usually due to large infarct (high risk of mortality); often assoc with arrhythmias
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Complications of MI: Ventricular free wall rupture
(a) timeline |
3-7d
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Complications of MI: anterior wall rupture
(a) assoc w/MI in assoc w/which coronary artery? (b) result |
LAD: results in cardiac tamponade
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Complications of MI: posteromedial papillary muscle rupture
(a) assoc w/MI in assoc w/which coronary artery? (b) result |
RCA: acute onset mitral regurg and LHF
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Complications of MI: interventricular septum rupture
(a) assoc w/thrombosis of which coronary artery? (b) result |
LAD: results in L to R shunt causing RHF
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Complications of MI: fibrinous pericarditis
(a) timeline after MI (b) signs/symptoms |
(a) day 3-5 after MI (b) precordial friction rub due to increased vessel permeability in pericardium; substernal chest pain relieved by leaning forward
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Complications of MI: Autoimmune pericarditis (Dressler's Syndrome)
(a) timeline after MI (b) pathogenisis (c) signs/symptoms |
(a) 6-8wks after MI
(b) autoantibodies directed against pericardial antigens (c) fever and precordial friction rub |
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Complications of MI: Ventricular aneurysm
(a) timeline after MI (b) signs/symptoms (c) complications |
(a) 4-8 wks
(b) precordial bulge during systole; blood enters aneurysm causing anterior chest wall movement (c) CHF (decr CO) due to lack of contractile tissue; risk of arrhythmia; danger of embolization of clot |
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Dilated cardiomyopathy
(a) symptoms (b) physical exam (c) pathophys (d) ultrasound/chest xray |
(a) Fatigue, weakness, dyspnea, orthopnea, PND (CHF)
(b) Pulmonary rales, S3 If RV failure: JVD, hepatomegaly, peripheral edema (c) impaired systolic contraction/fct (d) Dilated "balloon appearance" of heart on CXR. Chambers dilated on echo. |
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Dilated cardiomyopathy: etiologies
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Beriberi
Chronic alcohol abuse (thiamine def) Coxsackie B virus myocarditis Chronic cocaine use Chagas disease Doxyrubicin toxicity Peripartum cardiomyopathy |
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Hypertrophic cardiomyopathy:
(a) symptoms (b) physical exam (c) pathophys (d) echo/CXR |
(a) dyspnea, angina, syncope
(b) S4 If outflow obstruction present: systolic murmur loudest at LSB accompanied by mitral regurg (c) Hypertrophy of IV septum w/disoriented dysfctal fibers which can lead to arrythmias. Impaired diastolic relaxation; LV systolic fct vigorous often with dynamic obstruction (mitral valve leaflet drawn against septum) (d) Normal or dilated on CXR; LVH often more pronounced in septum; systolic antioer movement of MV w/mitral regurg |
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Causes of hypertrophic cardiomyopathy
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50% familial autosomal dominant (younger);betamyosin heavy chain etc
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Restrictive cardiomyopathy
(a) symptoms (b) physical exam (c) pathophys (d) echo/CXR |
(a) dyspnea, fatigue
(b) Signs of RV failure: JVD, hepatomegaly, peripheral edema (diastolic dysfct) (c) "stiff" LV w/impaired diastolic relaxation but normal systolic fct (d) usually normal size on chest x ray w/normal systolic fct on on echo |
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Major causes of restrictive/obliterative cardiomyopathy
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Sarcoidosis
Amyloidosis Postradiation fibrosis Endocardial fibroelastosis Hemachromatosis (also can cause dilated) |
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Pathophys of CHF abnormalities: dyspnea on exertion
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Failure of LV output to increase during exercise
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Pathophys of CHF abnormalities: cardiac dilation
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Greater ventricular end diastolic volume
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Pathophys of CHF abnormalities: pulmonary edema, paroxysmal nocturnal dyspnea
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LV failure leads to increased pulmonary venous pressure causing pulmonary venous distension and transudation of fluid. Presence of hemosiderin laden macrophages in lung.
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Pathophys of CHF symptoms: Orthopnea
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Increased venous return in supine opsition exacerbates pulmonary vascular congestion.
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Pathophys of CHF symptoms: Hepatomegaly
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Nutmeg liver. Increased central venous pressure causes increased resistance to portal flow. Rarely leads to cardiac cirrhosis.
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Pathophys of CHF symptoms: Ankle, sacral edema
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RV failure leads to increased venous pressure causing fluid transudation
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Pathophys of CHF symptoms: Jugular venous distension
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Right heart failure increased venous pressure
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MCC of right heart failure
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Left heart failure
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MCC of isolated right heart failure
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Cor pulmonale
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Symptoms of a pulmonary embolus
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Chest pain
Tachypnea Dyspnea |
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What is a possible serious consequence of amniotic fluid embolism?
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DIC
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Virchow's triad: describe and what does it predispose to?
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(1) stasis
(2) hypercoagulabilty (defect in coagulative cascade proteins) (3) endothelial damage Can cause DVT (which can lead to PE) |
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Most common overall cause of infective endocarditis
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Strep viridans
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MCC of infective endocarditis in IV drug users
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Staph aureus
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MCC of infective endocarditis due to prosthetic devices
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Staph epidermidus
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MCC of infective endocarditis in ulcerative colitis or colorectal cancer
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Strep bovis
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MCC of acute bacterial endocarditis
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Staph aureus (infects normal or previously damaged valves)
Larger vegetations |
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MCC of subacute endocarditis
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Strep viridans (infects previously damaged valves)
Smaller vegetations |
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Marantic endocarditis
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Endocarditis secondary to malignancy
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Thrombotic endocarditis
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Endocarditis due to hypercoagulable state
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Libman Sacks endocarditis
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Verrucous (wartlike) sterile vegetations occur on both sides of valve (assoc w/mitral regurg and mitral stenosis). Seen in lupus
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Clinical signs of infective endocarditis
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Fever (most common)
Roth spots (white spots on retina surrounded by hemorrhage) Osler nodes (tender raised lesions on finger or toe pads) New Murmur Janeway lesions (small erythemetous lesions on palm or sole) Anemia Splinter hemorrhages on nail bed |
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Rheumatic fever
(a) cause (b) clinical manifestations (c) pathogenesis of sequelae |
(a) GAS
(b) fever, erythema marginatum, valvular damage, ESR incr, migratory polyarthritis, subcutaneous nodules (Aschoff bodies), St. Vitus dance (Sydenham's chorea) (c) Abs develop against GAS M proteins. Type II hypersensitivity rxn due to antibodies cross reacting with similar proteins in human tissue. Cell mediated immunity also involved. |
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Early sequelae of Rheumatic fever (give clinical manifestations)
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(1) Fibrinous pericarditis: precordial chest pain w/friction rub
(2) myocarditis: MCC of death in acute disease.Note aschoff bodies are present |
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Late sequelae of rheumatic fever?
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Rheumatic heart disease involving heart valves: mitral>aortic>>tricuspid (high pressure valves affected most)
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Describe histologic/serum markers in rheumatic fever
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Aschoff bodies (necrotic granuloma w/giant cells)
Anitschkow's cells (activated histiocytes) Elevated ASO titers |
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Cardiac tamponade
(a) describe (b) result (c) findings |
(a) compression of heart by fluid in pericardium
(b) decr cardiac output; equilibration of diastolic pressures in all 4 chambers (c) hypotension, increased venous pressure (JVD), incr HR, pulsus paradoxus |
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Pulsus paradoxus
(a) describe (b) seen in what pathologic states? |
(a) decr in amplitude of pulse during inspiration
(b) severe cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, croup |
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Percarditis
(a) findings (b) possible sequelae |
(a) pericardial pain, friction rub, pulsus paradoxus, distant heart sounds, ECG changes w/ST segment elevations in multiple leads
(b) can resolve without scarring or lead to chronic adhesive or constrictive pericarditis |
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Serous pericarditis caused by
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SLE, RA, viral infx, uremia
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Fibrinous pericarditis causes
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Uremia, MI (Dressler's syndrome), rheumatic fever
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Syphilitic heart disease
(a) cause (b) pathophys (c) findings (d) possible sequelae |
(a) tertiary syphilis
(b) disrupts vaso vasorum of aorta w/consequent dilation of aorta and valve ring (c) calcification of the aortic root and ascending aortic arch; leads to "tree bark" appearance of aorta (d) can result in aneurysm of ascending aorta or aortic arch and aortic valve incompetence |
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Most common primary tumor in adults
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Myxomas; benign primary mesenchymal tumor
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Myxoma
(a) most common location (b) gross appearance (c) clinical manifestations (d) complications (e) diagnosis |
(a) 90% in atria (mostly LA)
(b) sessile or pedunculated "ball-valve" obstruction (c) fever, fatigue, maliase, anemia (d) embolization, syncope (blocks mitral valve orifice) (e) transesophageal US most useful for looking at LA |
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MCC primary tumor of heart in infants and children (major association?)
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Rhambomyoma (assoc w/tuberous sclerosis)
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What are the most common tumors in the heart?
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Metastasis (MCC place is the pericardium)
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Telangiesctasia
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AV malformation in small vessels (dilated vessels on skin in mucous membranes)
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Osler Weber Rendu Syndrome
(a) description (b) inheritance (c) clinical presentation |
(a) hereditary hemorrhagic telangiectasia
(b) AD (c) nosebleeds and skin discolorations |
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Raynaud's disease vs Raynaud's phenomenon
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Decr blood flow in skin due to arteriolar vasospasm in response to cold temp or emotional stress. Most often in fingers and toes. Called Raynaud's phenomenon when secondary to a mixed connective tissue disease
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Sturge Weber disease
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Congenital vascular disorder. Affects capillaries. Port wine stain on face and leptomeningeal angiomatosis (intracerebral AVM)
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Takayasu's arteritis
(a) description/location (b) epidemiology/etiology (c) lab (d) clinical manifestations (e) treatment |
(a) "pulseless disease"; granulomatous large vessel arteritis (aortic arch + proximal great vessels)
(b) asian female <40YO (c) elevated ESR (d) absent upper extremity pulses; skin nodules; ocular disturbances Also: fever, arthritis, myalgia, night sweats; can result in stroke (e) n/a |
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Giant cell arteritis
(a) description/location (b) epidemiology/etiology (c) lab (d) clinical manifestations (e) treatment |
(a) "temporal" arteritis; granulomatous large vessel arteritis; (superficial temporal and opthalmic arteries)
(b) elderly females (c) elevated ESR (d) unilateral HA; jaw claudication; impaired vision (may lead to blindness); polymyalgia rheumatica (e) high dose steroids |
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Polyarteritis nodosa
(a) description/location (b) epidemiology/etiology (c) lab (d) clinical manifestations (e) treatment |
(a) necrotizing medium vessel arteritis (renal, coronary, and mesenteric arteries)
(b) middle aged men; assoc w/hepB (30%); immune complex inflammation (c) lesions @ different ages (d) HTN; neuro dysfct; cutaneous eruptions; abd pain; melana Also: myalgia, fever, wt loss, malaise Infarction: kidney (RF), heart (acute MI), bowels (bloody diarrhea), skin (ischemic ulcer) |
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Kawasaki's
(a) description/location (b) epidemiology/etiology (c) lab (d) clinical manifestations (e) treatment |
(a) necrotizing medium vessel vasculitis (coronary)
(b) children <4YO; strong assoc w/asians (c) abnormal EEG if acute MI (d) may have coronary aneurysms; strawberry tongue; congested conjunctiva; lymphadenitis; fever (e) NO corticosteroids!!! Danger of vessel rupture |
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Thromboangitis obliterans (Buerger's)
(a) description/location (b) epidemiology/etiology (c) lab (d) clinical manifestations (e) treatment |
(a) "digital vessel thrombosis"; small and med peripheral artery and vein vasculitis; idiopathic thrombosis
(b) heavy smokers (c) n/a (d) claudication; superior nodular phlebitus; Raynaud's; may lead to gangrene and autoamputation (e) smoking cessation |
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Wegener's granulomatosus
(a) description/location (b) epidemiology/etiology (c) lab (d) clinical manifestations (e) treatment |
(a) granulomatous small vessel vasculitis (upper resp tract, lung, kidney)
(b) childhood to middle aged (c) c-ANCA (d) perforation of nasal septum; sinusitis; otitis media; mastoiditis; cough; hemoptysis; hematuria (e) cyclophosphamide/corticosteroids |
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Microscopic polyangitis
(a) description/location (b) epidemiology/etiology (c) lab (d) clinical manifestations (e) treatment |
(a) small vessel vasculitis (lung, GI, kidney)
(b) children and adults; precipitated by drugs, infx, immune disorder (c) p-ANCA; vessels all at same stage of infl (d) palpable purpura (e) |
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Churg strauss
(a) description/location (b) epidemiology/etiology (c) lab (d) clinical manifestations (e) treatment |
(a) small vessel vasculitis (skin, lung, heart)
(b) children and adults esp atopic (c) p-ANCA; eosinophilia (d) allergic rhinitis, asthma (e) |
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Henoch Schonlein Purpura
(a) description/location (b) epidemiology/etiology (c) lab (d) clinical manifestations (e) treatment |
(a) small vessel vasculitis (skin, kidney, GI, joints)
(b) children and young adults; assoc w/IgA nephropathy (c) IgA complexes; lesions at same stage (d) palpable purpura; intestinal hemorrhage/pain; arthralgia (e) |
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Cryoglobulinemia
(a) description/location (b) epidemiology/etiology (c) lab (d) clinical manifestations (e) treatment |
(a) small vessel vasculitis (skin, GI, renal)
(b) adults; assoc w/HCV (type I MPGN) (c) cryoglobulins (d) palpable purpura; acral cyanosis of nose/ears; Raynaud's (e) |
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Primary Pauci Immune crescenteric GN
(a) description/location |
(a) small vessels vasculitis (just kidney)
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Serum sickness
(a) description/location (b) epidemiology/etiology (c) clinical features |
(a) small vessel vasculitis of skin
(b) children and adults; due to venom treatment with horse or sheep antivenom (c) fever, urticaria, arthralgia, GI pain; melana |
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Infectious vasculitis
(a) description/location (b) epidemiology/etiology |
(a) small vessel vasculitis (skin)
(b) children and adults; can be caused by all microbial pathogens; Key examples include: Rocky mountain spotted fever, N meningitidis (disseminated) |
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Mitral stenosis murmur (quality and location)
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Delayed rumbling late diastolic murmur following an opening snap. Heard at apex (mitral area)
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Mitral regurgitation (quality and location)
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Holosystolic high pitched "blowing murmur"
Loudest at apex and radiates towards axilla |
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Mitral valve prolapse (quality and location)
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Late systolic murmur w/midsystolic click
Loudest during S2 Decr preload causes click/murmur to move closer to S1 (anxiety, Valsalva-holding breath w/epiglottis closed, standing) Incr preload causes click/murmur to move closer to S2 (reclining, squatting or sustained hand grip). |
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Aortic stenosis (quality and location)
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Systolic ejection murmur following an ejection click-crescendo decrescendo
Radiates towards apex and carotids |
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Aortic regurgitation (quality )
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Early high pitched "blowing" diastolic murmur
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Tricuspid regurgitation (quality)
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Pansystolic murmur that increases with intensity with inspiration
Loudest at tricuspid area |
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Mitral stenosis
(a) etiology (b) pathophys (c) clinical manifstations |
(a) usually rheumatic fever
(b) narrowed mitral valve orifice; left atrium dilates and hypertrophies (c) dyspnea and hemoptysis w/rust colored sputum due to pulmonary congestion and hemorrhage into alveoli; afib (LA dilation and LAH); pulmonary venous HTN (RVH eventually develops); dysphagia for solid foods (dilated LA compresses esophagus) |
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Mitral regurgitation
(a) etiology (b) pathophys (c) clinical manifestations |
(a) mitral valve prolapse most common cause
Left sided heart failure IE Rupture or dysfct of papillary muscle (b) Incompetent valve or dilated ring; volume overload intoLV and LA leads to left heart failure (c) dyspnea and cough from LHF |
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Mitral valve prolapse
(a) epidemiology/etiology (b) pathophys (c) clinical manifestations |
(a) AD inheritence in some cases; F>M; assoc w/Marfan and Ehler's Danlos
(b) Posterior bulge of ant/pos leaflets into LA during systole (c) Most asymptomatic. Palpitations, chest pain, rupture of cordae may occur. |
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Aortic stenosis
(a) Etiology (b) pathophys (c) clinical manifestations |
(a) Dystrophic calcification
Congenital bicuspid aortic valve Rheumatic fever (b) obstruction of LV during systole producing concentric LVH (c) angina w/exercise (less filling of coronaries); syncope w/exercise (decr coronary flow); hemolytic anemia w/schistocytes |
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Aortic regurgitation
(a) etiology (b) pathophys (c) clinical manifestations |
(a) isolated aortic root dilation
Rheumatic fever Chronic essential HTN Aortic dissection Coarctation (b) retrograde flow into LV from invompetent valve or dilated ring; decrease diastolic pressure; volume overload on LV; increased pulse pressure (c) bounding pulses (incr pulse pressure) |
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Tricuspid regurgitation
(a) etiology (b) pathophys (c) clinical manifestations |
(a) RHF
IE in IV drug abuse Carcinoid disease (b) retrograde flow into right atrium during systole; volume overload in RA and RV (c) pulsating liver (blood regurgitates into venous system w/systole) |
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Carcinoid heart disease
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Due to liver mets from carcinoid tumor of small intestine; serotonin causes fibrosis of tricuspid valve and pulmonary valve; produces tricuspid and regurg and pulmonary valve stenosis
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Major classes of antihypertensive drugs
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Diuretics
Sympathoplegics Vasodilators ACE inhibitors Angiotensin II receptor inhibitors |
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Major examples of antihypertensive diuretics
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Hydrachlorothiazide
Loop diuretics |
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Major examples of antihypertensive sympathoplegics (mech)
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Clonidine (alpha 2 agonist)
Methyldopa (alpha 2 agonist) Reserpine (prevent transport into vesicles leading to MAO metabolism) Guanethidine (reduces release of catecholamines by inhibiting Na/ATPase dependent pump) Prazosin (alpha 1 blocker veins and arteries) Beta blockers |
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Major examples of antiHTN vasodilators (mech)
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Hydralazine (incr influx of K, leading to membrane hyperpolarization of smooth muscle cells)
Minoxidil (open K+ATPase, hyperpolarization of SM cells) Nifedipine (CCB selective for SM) Verapamil (non selective CCB) Nitroprusside (cause release of NO from RBC's-direct vasodilator) Diazoxide (open K+ channels in SM and beta islet cells-decr insulin secretion) |
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Major examples of antiHTN ACEI's
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Captopril
Enalapril Fosinopril |
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Major examples of angiotensin II receptor inhibitors
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Losartan
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Antihypertensive drug side effects: HCTZ
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Hypokalemia, mild hyperlipidemia, hyperuricemia, lassitude (weariness), hypercalcemia, hyperglycemia
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Antihypertensive drug side effects: loop diuretics
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Potassium wasting, metabolic alkalosis, hypotension, ototoxicity
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Antihypertensive drug side effects: clonidine
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Dry mouth, sedation, severe rebound hypertension
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Antihypertensive drug side effects: methyldopa
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Sedation, positive Coomb's
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Antihypertensive drug side effects: reserpine
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Sedation, depression, nasal stuffiness, diarrhea
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Antihypertensive drug side effects: guanethidine
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Orthostatic hypotension, dizziness, headache
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Antihypertensive drug side effects: prazosin
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1st dose orthostatic hypotension, sexual dysfct, diarrhea
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Antihypertensive drug side effects: beta blockers
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Impotence, asthma, CV effects (bradycardia, CHF, AV block) CNS effects (sedation, sleep alterations)
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Antihypertensive drug side effects: hydralazine
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Nausea, HA, lupus like syndrome, reflex tachy, angina, salt retention
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Antihypertensive drug side effects: minoxidil
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Hypertrichosis, percardial effusion, reflex tacycardia, angina, salt retention
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Antihypertensive drug side effects: nifedipine, verapamil
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Dizziness, flushing constipation (verapamil), AV block (verapamil), nausea, edema
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Antihypertensive drug side effects: nitroprusside
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Cyanide toxicity (release CN)
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Antihypertensive drug side effects: diazoxide
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Hyperglycemia (reduce insulin release, hypotension)
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Antihypertensive drug side effects: ACEI
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Hyperkalemia, cough, angioedema, taste change, hypotension, pregnancy problems (fetal renal damage), rash, incr renin
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Antihypertensive drug side effects: ARBs
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Fetal renal toxicity, hyperkalemia
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Hydralazine
(a) mechanism (b) clinical use (c) toxicity |
(a) increase cAMP which causes SM relaxation. Vasodilates arterioles>veins; afterload reduction
(b) severe HTN; CHF. First line therapy for HTN in pregnancy w/methyldopa (c) compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, HA, angina. Lupus like syndrome |
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Minoxidil
(a) mechanism (b) clinical use (c) toxicity |
(a) K+ chanel opener-hyperpolarizes and relaxes smooth muscle
(b) severe HTN (c) hypertrichosis; pericardial effusion; reflex tachycardia; angina; salt retention |
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CCB's
(a) major examples (b) mechanism (c) clinical use (d) toxicity |
(a) nifedipine, cerapamil, dilitiazem
(b) block voltage dependent L type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility. (c) HTN, angina, arrhythmias (not nif), Pirnzmetal's angina, Raynaud's (d) cardiac depression, peripheral edema, flushing, dizziness, and constipation |
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Nitroglycerin, isosorbide dinitrate
(a) mechanism (b) clinical use (c) toxicity |
(a) vasodilate by releasing NO in smooth muscle causing incr cGMP and smooth muscle relaxation. Dilate veins>>arteries. Decr preload.
(b) angina, pulmonary edema. Also used as aphrodisiac and erection enhancer (c) tachycardia, hypotension, flushing, HA, "Monday disease" in industrial exposure; tolerance during work week and loss of tolerance over weekend resulting in tachycardia, dizziness, and HA on reexposure |
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Malignant HTN treatment (and mechs)
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Nitroprusside (short acting; increase cGMP via direct release of NO)
Fenoldopam (dopamine D1 receptor antagonist-relax renal vascular smooth muscle) Diazoxide (K+ channel opener-hyperpolarizes and relaxes vascular smooth muscle) |
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Antianginal therapy: Nitrates
Affect on: (a) preload or afterload (b) end diastolic volume (c) contractility (d) HR (e) ejection time (f) mycoardial O2 consumption (g) BP |
(a) preload
(b) decrease EDV (c) increase contractility (reflex resp) (d) increase HR (reflex resp) (e) decr ejection time (f) decrease MVO2 (g) decr |
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Antianginal therapy: beta blockers
(a) preload or afterload (b) end diastolic volume (c) contractility (d) HR (e) ejection time (f) mycoardial O2 consumption (g) BP |
(a) afterload
(b) EDV incr (c) contractility decr (d) HR decr (e) Ejection time incr (f) MVO2 decr (g) BP |
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Antianginal therapy: beta blockers + nitrates
(a) end diastolic volume (b) BP (c) contractility (d) HR (e) ejection time (f) MVO2 |
(a) no effect or decr EDV
(b) decr BP (c) little/no effect on contractility (d) decr HR (e) ejection time little or no effect (f) MVO2 drastically decreased |
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Calcium channel blockers in angina: nifedpine vs verapamil
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Nifedipine has similar effects to nitrates
Verapamil has similar effects to beta blockers |
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Major types of lipid lowering agents
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HMG CoA reductase inhibitors
Niacin Bile acid resins Cholesterol absorption blockers "fibrates" |
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HMGCoA Reductase inhibitors
(a) effect on LDL (b) effect on HDL (c) effect on TG's (d) mechanism (e) side effects/problems |
(a) effect on LDL:
(b) effect on HDL: + (c) effect on TG's: decr (d) mechanism: inhibit cholesterol precursor mevalonate (e) side effects/problems: reversible incr in LFT's |
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Niacin
(a) effect on LDL (b) effect on HDL (c) effect on TG's (d) mechanism (e) side effects/problems |
(a) effect on LDL: decrease
(b) effect on HDL: ++ (c) effect on TG's: decrease (d) mechanism: inhibit lipolysis in adipose tissue; reduce hepatic VLDL secretion into circulation (e) side effects/problems: red, flushed face which is decr by aspirin or LT use |
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Bile acid resins
(a) major examples (b) effect on LDL (c) effect on HDL (d) effect on TG"s (e) mechanism (f) side effects/problems |
(a) major examples: cholestyramine, colestipol, colesevelam
(b) effect on LDL: decrease (c) effect on HDL: slightly incr (d) effect on TG's: slightly incr (e) mechanism: prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more (f) side effects/problems: Tastes bad and causes GI discomfort; decr absorption of fat soluble vits; contraindicated in pts w/gallstones |
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Cholesterol absorption blockers
(a) major examples (b) effect on LDL (c) effect on HDL (d) effect on TG"s (e) mechanism (f) side effects/problems |
(a) major examples: ezetimibe
(b) effect on LDL: decrease (c) effect on HDL: none (d) effect on TG"s: none (e) mechanism: prevent cholesterol reabsorption at small intestine brush border (f) side effects/problems: rare incr LFT's |
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"Fibrates"
(a) major examples (b) effect on LDL (c) effect on HDL (d) effect on TG"s (e) mechanism (f) side effects/problems |
(a) major examples: gemfibrozil, clofibrate, bezafibrate, fenofibrate
(b) effect on LDL: decr (c) effect on HDL:+ (d) effect on TG"s: majorly decr (e) mechanism: upregulate LPL which increases TG clearance (f) side effects/problems: myositis; incr LFTs |
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Cardiac glycosides
(a) major example (b) mechanism (c) clinical use |
(a) digoxin (protein bound; urinary secretion)
(b) direct inhibition of NaK pump leads to indirect inhibition of Na/Ca antiporter. Increase intracellular Ca2+ positive inotropy. Also stimulates vagus. (c) CHF to incr contractility; afib (decr conduction to AV node and depress SA node) |
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(a) ECG changes seen in digoxin toxicity
(b) side effects of digoxin toxicity (c) enhancers for digoxin toxicity (c) antidote |
(a) may cause incr PR, decr QT, scooping of ST, T wave inversion
(b) Incr parasymp; n/v/d. blurry yellow vision; arrhythmia (c) renal failure (decr exretion), hypokalemia (digoxing competes with K+ binding at Na/K pump) and quinidine (decr dig clearance; displaces dig from tissue binding sites) (d) slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab frags, Mg2+ |
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Class I antiarrhythmics
General effects |
Slow or block conduction esp in depolarized cells. Decr slope of phase 4 depol, incr threshold for firing in abnormal pacemaker. Are state dependent (selectively depress tissue that is frequently depolarized).
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Class IA
(a) examples (b) effect (c) clinical use (d) toxicity |
(a) Quinidine, Procainamide, Disopyramide
(b) incr AP duration, incr effective refractory period, incr QT interval (c) atrial and ventricular arrhythmias esp reentrant and ectopic supraventricular and ventricular tachycardia (d) quinidine (HA, tinnitus, thombocytopenia, torsades de pointes due to prolonged QT); procainamide (reversible SLE like syndrome) |
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Class IB
(a) examples (b) effect (c) clinical use (d) toxicity |
(a) Lidocaine, Mexiletine, Tocainide
(b) decr AP duration; affect depolarized Purkinje and ventricular tissue (c) useful in acute ventricular arrhythmias (d) toxicities: local anesthetic. CNS stimulation/depression, cardiovascular depression |
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Class I C
(a) examples (b) effect (c) clinical use (d) toxicity |
(a) Flecainide, envainide, propafenone
(b) NO effect on AP duration (c) useful in V tachs that progress to VF and intractable SVT; usually used as last resort in tachyarrhythmias; for patients without structural abn (d) proarrhythmic esp post MI (CI); significantly prolongs refractory period in AV node |
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Class II antiarrhythmics
(a) examples (b) mechanism (c) clinical use (d) toxicity |
(a) beta blockers (-alolols)
(b) decr cAMP, decr Ca2+ currents, suppress abnormal pacemakers by decr slope of phase 4; AV node part sensitive (incr PR) (c) Vtach, SVT, slow ventr rate during afib and aflut (d) impotence, exacerbation of asthma, CV effects (bradycardia, AV block, CHF), CNS (sedation, sleep alterations). May mask hypoglycemia signs. Metoprolol can cause dyslipidemia. |
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Class III antiarryhthmics
(a) examples (b) mechanism (c) clinical use |
(a) Sotalol, ibutilide, amiodarone
(b) increase AP duration, incr ERP (c) used when other antiarrythmics fail; incr QT |
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Side effect: ibutilide
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Torsades
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Side effect sotalol
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Torsades, excessive beta block
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Side effect: bretylium
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New arrythmias hypotension
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Side effect amiodarone
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Pulmonary fibrosis
Corneal and skin deposits Neuro effects Constipation CV effects (bradycardia, heart block, CHF) Hypothyroidism, hyperthyroidism |
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Class IV antiarrythmics
(a) examples (b) mechanism (c) toxicity |
(a) verapamil, diltiazem
(b) CCB' s that primarily affect AV node cells. Decr conduction velocity, incr ERP and PR interval. Used in prevention of nodal arrythmias (SVT) (c) constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression) |
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Adenosine
(a) mechanism of antiarrhythmic action (b) clinical use (c) toxicity |
(a) incr K+ out of cells hyperpolarizing cell and decreasing incracellular Ca+.
(b) drug of choice indiagnosing/abolishing AV nodal arrythmias (c) flushing, hypotension, chest pain |
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K+ use as an arrhythmias
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Depresses ectopic pacemakers in hypokalemia (e.g. digoxin toxicity)
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Mg2+ use in arrhythmias
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Effective in torsades de pointes and digoxin toxicity
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