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M2 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

what are the three categorical causes of hypertension?

A

Blood volume - hyperaldosteronism, excessive salt intake
Cardiac output - pheochromocytoma, hyperthryoidism, early essential hypertension
PVR- renal artery stenosis

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2
Q

Primary hyperaldosteronism

A

Cause: hyperplasia or adenoma of adrenal cortex
Symtoms: none. increased sodium retention, potassium excretion, hypokalemia and metabolic alkalosis
dx: low {K}, high aldosterone w/low renin

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3
Q

Pheochromocytoma

A

Cause: tumor of neuro-ecteodermal origin usually in adrenal medulla
Patho: uncommon. paroxysms of hypertension. symptoms depend on substance secreted by tumor.
norepi: vasoconstriction, pallor, bradycardia (reflex)
epinephrine: tachycardia, orthostatic hypotension
dx: catecholamine levels, urine measurements of metanephrines and vanillymandelic acid

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4
Q

renal artery stenosis

A

cause: atherosclerosis or fibromuscular hyperplasia
patho: RAS > decreased afferent arteriolar pressure > renin release of JGA > increased angiotensin II and aldosterone
Dx: abdominal bruit, hypokalemia due to excess aldosterone
Tx: transluminal angioplasty/stenting, bypass surery or medical therapy

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5
Q

renal parenchymal disease

A

2 mechanism: inability to excrete volume&raquo_space; increased blood volume
or diseases causing increased renin secretion

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6
Q

coarctation of aorta

A

proximal aortic obstruction > decreased BP in lower body, increased renin secretion by kidneys > increased BP in upper extremities.
dx: compare BP in upper and lower extremities. Continuous murmur over coarctation, x-ray shows notching of ribs from inc. blood flow through intercostal arteries

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7
Q

cardiovascular effects of chronic hypertension

A
  1. Hypertensive heart disease: Left ventricular concentric hypertrophy leading to diastolic LV failure (dyspnea, S4 gallop, pulmonary congestion).
  2. Cerebrovascular atherosclerosis
  3. Cerebral hemorrhage and aneurysms due to microvascular damage
  4. neprhosclerosis: atherosclerosis of arterioles in kidneys > thickening basement membrane, hyalinization of glomerular capillaries > kidney failure
  5. aortic dissection: blood creates a channel in layers of aortic intima, dividing it into two channels
  6. hypertensive retinopathy
  7. malignant hypertension: renal arterioles and small arteries develop a hyperplastic arteriolar sclerosis, with fibrinoid necrosis of arterioles and glomerular capillaries, marked thickening of the intima, and narrowing of the vascular lumen (“onion-skinning”)
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8
Q

Diuretics to treat hypertension

A

a. mechanism = initial reduction in blood volume, followed by reduction of peripheral vascular resistance (probably by altering the salt and water composition of arterial smooth muscle)
b. side effects: hypovolemia, sodium and/or potassium depletion
c. drugs: thiazides (hydrochlorothiazide), loop diuretics (furosemide), potassium-sparing diuretics (spironolactone, triamterene)”

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9
Q

Beta-blockers to treat hypertension

A

a. mechanism: reduce cardiac contractility and renin activity
b. side effects: precipitation of heart failure, depression, fatigue, bronchospasm
c. drugs: propranolol, metoprolol, atenolol, etc.,

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10
Q

Agents that affect CNS to treat hypertension

A

(central alpha-agonists)

	a. mechanism = decreased sympathetic outflow from the central nervous system => decreased cardiac output &/or decreased peripheral vascular resistance
	b. side effects: dry mouth, sedation, depression
	c. drugs: methyldopa, clonidine
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11
Q

Calcium channel blockers to treat hypertension

A

a. mechanism = reduction of cardiac output and/or peripheral vascular resistance
b. side effects: peripheral edema, heart failure
c. drugs: diltiazem, verapamil, nifedipine

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12
Q

Vasodilators, alpha-blocking agents, converting enzyme inhibitors, other to treat hypertension

A
  1. Direct vasodilators
    a. mechanism = reduction in peripheral vascular resistance
    b. side effects: reflex tachycardia (can precipitate angina), headache
    c. drugs: hydralazine, minoxidil
  2. Alpha blocking agents
    a. mechanism = reduction in peripheral vascular resistance
    b. side effects: orthostatic hypotension
    c. drugs: prazosin, etc.
  3. Converting enzyme inhibitors
    a. mechanism = inhibit conversion of angiotensin I to angiotensin II => decreased peripheral vascular resistance, decreased secretion of aldosterone
    b. side effects: cough (blocked conversion of bradykinin), renal failure
    c. drugs: captopril, lisinopril, variety of other “-prils”)
  4. Angiotensin II blockers
    a. mechanism = block angiotensin II receptors
    b. side effects: (no cough)
    c. drugs: losartan
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13
Q

Etiology of dilated cardiomyopathy:

A
  1. genetic - most common
  2. viral - coxsackie B
  3. infectious: trypanosomiasis (Chagas’ disease), Rickettsia (Rocky Mountain spotted fever, typhus, Q fever), trichinosis
  4. toxic, including alcohol, cocaine, etc
  5. postpartum CM
  6. 2º to neuromuscular disorders (duchenne’s, muscular dystrophy, etc)
  7. rheumatic fever, lupus
  8. metabolic disorders (hyperthyroid, kwashiorker, etc)
  9. ischemic cardiomyopathy
  10. tachymyopathy: heart in Afib for weeks
  11. infiltrative: amyloidosis, sarcoidosis
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14
Q

cardiac volume overload

A

compensating for fraction of blood not going out by increasing volume. NOT increase blood volume. = to flow load, cardiac output load, stroke volume load. The heart has to generate an increased cardiac output (increased stroke volume) acutely by cardiac dilatation, chronically by eccentric hypertrophy.

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15
Q

Pressure overloads

A

pressure increased DOWNSTREAM to ventricle. LV: systemic hypertension, aortic stenosis. RV: pulmonic hypertension, cor pulmonale

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16
Q

Ventricular underloading

A

ventricles not stretched to ideal tension due to mitral stenosis, hypovolemia, or pericardial restriction.

17
Q

Primary myocardial failure

A

dilated cardiomyopathy, ischemic cardiomyopathy, and hypertrophic cardiomyopathy.

18
Q

Primary distinction between non-ischemic dilated cardiomyopathy and ischemic cardiomyopathy

A

Ischemic: segmental wall motion abnormality (aneurysm) vs diffuse hypokinesis.

19
Q

hyptrophic cadriomyopathy

A

pathological features: myocardial fiber disarray&raquo_space; inefficent contraction&raquo_space; asymmetric concentric hypertrophy. thickening most pronounced in septum.
dx: listen to murmur. louder w/interventions that make ventricle smaller or increase velocity of contraction: valsalva standing, positive inotropic agent. quieter w/: supine position legs up, squatting (increase SVR), negate inotropic agents
heart failure: dyspnea, orthopnea, S4 gallop, angina, syncope,

20
Q

Pericarditis

A

Signs: pericardial rub, respirophasic pain, ST segment elevation, pericardial effusion (big left ventricle on CXR)

tx: antibiotics
complications: pericardial tamponade: restriction of RV filling –> decreased LV volume –> dec BP (paradoxical pulse) increased JVP on inspiration (Kussmaul)

21
Q

Acute Coronary Syndrome

A

Definition: clinical condition caused by rapid-onset reduction in myocardial blood flow resulting in acute myocardial ischemia.
Symptoms: angina, dyspnea, abdominal pain
Three subcategories: 1. STEMI w/persistent ST-elevation 2. NSTEMI troponin abnormal, ST/T abnormalities 3. Unstable angina w/normal troponin and normal or undet. EKG
epi: leading cause of morbidity and mortality
patho: myocardial plaques - fatty streaks > pooling of lipid-rich material > infiltration by monocytes/macrophages > soft plaque > plaque instability > calcification of plaque. Suddenly - plaque rupture > clot

22
Q

Myocardial infarction

A

detection of rise and /or fall of cardiac biomarkers and at least 1 of the following:
ECG changes indicative of new ischemia, development of Path. q waves, imaging evidence of new loss of heart viability

23
Q

Clotting cascade (secondary hemostasis)

A

Last steps: Prothrombin&raquo_space; thrombin which converts fibrinogen > fibrin > cross-linked fibrin clot

24
Q

subendocardial vs. transmural infarction

A

sub: incomplete coronary obstruction, subendocardium most susceptible
trans: total obstruction. all layers affected

25
Q

Complications of STEMI

A
  1. LV failure - treat w/ ACE inhibitors, diuretics, B-blockers
  2. cardiogenic shock - low CO & BP > intensified ischemia > more severe hypotension. treat w/afterload reducers, catecholamine infusions, or intra-aortic balloon pump, or CABG or PCI
  3. Pericarditis - acute within 1-2 days of infarction
    Dressler syndrome - autoimmune w/in 1-2 weeks
  4. RV infarction due to inferior infarction. dec RV output, elevated JCP. ST elevation over right chest leads
  5. arrhythmias
  6. rupture of myocardium
26
Q

Morphologic changes in myocardial infarction

A

<4 hours: none
4-24: dark discoloration/coagulative necrosis
1-3 days: yellow pallor/neutrophils
4-7 days: yellow pallor/macrophages
1-3 weeks: red border/grandulation tissue
months: white scar/fibrosis

27
Q

2 types of cardiac fibers

A
  1. Slow
    a. calcium current b. Sinus node & A-V node
    c. AV corresponds to PR interval. d. digitalis stimulates vagus to slow AV velocity.
  2. Fast
    a. sodium. not automatic unless failure of normal pacemakers or hypokalemia, hypoxia, ischemia, digitalis toxicity
    b. not affected by sympathetic stimulation, vagal stimulation or Ca channel blockers. ARE blocked by local anesthetic drugs
    c. His Purkinje
    d. Phase 0 - Na influx - QRS complex
    e. Phase 2 - Ca influx
    f. Phase 3 - K efflux
28
Q

Marfan Syndrome

A

Cause: Autosomal dominant disorder caused by FBN1 > fibrillin 1 disfunction. 1/4 have new mutation, 3/4 have affected parents. 1:5,000-10,000 prevalence.
Presentation: long lanky tall, back joint & chest pain, often athletic, rarely: sudden death from aortic aneurysm dissection
Phenotypic: ectopia lentis - lens dislocated; pectus excavatum or carinatum; dolichostenomelia, joint hypermobility, scoliosis; dural ectasia; downslanting palpebral fissures, malar hypoplasia; flat feet; dilatation of ascending aorta
Medical therapy: B-blockers to reduce afterload, Losartan in mice models

29
Q

Genetic pleiotropy

A

one single gene causes multiple phenotypes

30
Q

Chronic constrictive pericarditis

A
  1. patho: usually occurs long after acute pericarditis. fibrotic pericardium restricts diastolic ventricular filling > ventricular under loading. increased diastolic pressures disproportionately affect right side > right-sided HF.
  2. signs: right sided failure w/small heart. Kussmaul sign. pericardial knock (similar to S3 gallop)
  3. therapy - pericardiectomy
31
Q

acute pericardial tamponade

A
  1. patho: occurs w/rapid accumulation of pericardial fluid due to acute hemorrhage (usually). restriction of diastolic filling > under loading of ventricles > dec. CO > sympathetic stimulation and high venous pressures. All vessels leading to and away from heart are compressed.
  2. signs: rapid onset. acute circulatory failure. tachycardia and diaphoresis. Beck’s triad (dec arterial pressure, increased venous pressure, quiet heart)
  3. therapy: pericardiocentesis

M2 (5 decks)

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