Ch 8 Pathoma Cardiac Pathology Flashcards

1
Q

Ischemic heart disease (IHD) are a group of syndromes related to ____. It is usually due to ___ of ___, which decreases ___ to the ___. Risk factors for IHD are similar to those of ____. Incidence increases with ___.

A

myocardial ischemia; atherosclerosis; coronary arteries; blood flow; myocardium; atherosclerosis (HTN, high cholesterol, smoking, diabetes, age, gender, genetics); age

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2
Q

Stable angina is ___ that arises with __ or ___. It is due to ___ of ___ arteries with greater than __% stenosis. The resultant decreased blood flow is not able to meet the ___ of the myocardium during ___.

A

chest pain; exertion; emotional stress; atherosclerosis; coronary; 70; metabolic demands; exertion

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3
Q

Stable angina represents reversible/irreversible injury to myocytes (yes/no necrosis). It presents as ___, lasting less than/more than 20 minutes, that radiates to the ___ or ___, and causes ___ and ___.

A

reversible; no; chest pain; less than; left arm; jaw; diaphoresis; SOB

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4
Q

Stable angina is relieved by these 2 things.

A

Rest or nitroglycerin (vasodilates veins - decreases preload - decreases work required by myocardium)

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5
Q

Name 3 types of angina and what they are due to

A

1) stable angina (due to atherosclerosis of coronary arteries); 2) unstable angina (due to rupture of an atherosclerotic plaque with thrombosis and incomplete occlusion); 3) prinzmetal angina (due to coronary artery vasospasm)

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6
Q

In stable angina the EKG shows ___ due to ____. In unstable angina, the EKG shows ___ due to ____. In prinzmetal angina the EKG shows ___ due to ____

A

ST segment depression; sub endocardial ischemia; ST segment depression; subendocardial ischemia; ST segment elevation; transmural ischemia

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7
Q

Nitroglycerin works by ___ arteries or veins. Describe more.

A

vasodilating; both; main function is to dilate veins, which decreases preload, which decreases work required by the myocardium

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8
Q

Unstable angina is ___ that occurs at ___. Usually due to ___ with ___ and complete/incomplete occlusion of a coronary artery.

A

chest pain; rest; rupture of an atherosclerotic plaque; thrombosis; incomplete

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9
Q

Unstable angina represents reversible/irreversible injury to myocytes (yes/no necrosis). It is relieved by ___. There is a high/low risk of progression to MI.

A

reversible; no; nitroglycerin; high

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10
Q

What is the hallmark of reversible injury to cells? What is the hallmark of irreversible injury to cells?

A

cellular swelling; membrane damage

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11
Q

Prinzmetal angina is ___ unrelated to ___. It is due to ____. It represents reversible/irreversible injury to myocytes (yes/no necrosis). It is relieved by __ or __.

A

episodic chest pain; exertion; coronary artery vasospasm (which transiently completely blocks the vessel!); reversible; no; nitroglycerin; calcium channel blockers (help to relieve calcium channel blockers

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12
Q

Of the 3 types of angina, which causes reversible injury? Which is due to exertion? Which causes ST segment depression? Elevation? Which is relieved by nitroglycerin? Calcium channel blockers? Rest?

A

all; stable angina; SA and unstable angina; prinzmetal angina; all; PA; SA

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13
Q

Myocardial infarction is ___ of ___. Usually due to ___ with __ and complete/incomplete occlusion of a coronary artery. Name 3 other potential causes.

A

necrosis; cardiac myocytes; rupture of an atherosclerotic plaque; thrombosis; complete; coronary after vasospasm (due to prinzmetal angina or cocaine use); emboli; vasculitis (e.g. kawasaki disease)

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14
Q

Name 4 clinical features of MI. Symptoms are/are not relieved by nitroglycerin.

A

1) severe, crushing chest pain (lasting more than 20 mins); 2) radiates to the left arm or jaw; 3) diaphoresis; 4) dyspnea; NOT

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15
Q

MI usually involves the ___ (part of the heart). The __ and __ are generally spared.

A

left ventricle; atria; right ventricle

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16
Q

What is the most common artery involved in MI? What is the second most common?

A

LAD (left anterior descending artery) - 45% of cases; RCA (right coronary artery)

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17
Q

Occlusion of the LAD leads to infarction of the __ and ___ of the ___. Occlusion of the RCA leads to infarction of the ___, ___, and ___ of the ___. Occlusion of the left circumflex artery leads to infarction of the ___ of the ___.

A

LAD: anterior wall; anterior septum; left ventricle;
RCA: posterior wall; posterior septum; papillary muscles; left ventricle
LcircumflexA: lateral wall; left ventricle

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18
Q

Initial phase of infarction leads to ___ necrosis involving less than __% of myocardial thickness. EKG shows ___. Continued or severe ischemia leads to ___ necrosis involving most of the wall. EKG shows ___.

A

subendocardial; 50; ST-segment depression; transmural (full wall); ST-segment elevation

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19
Q

During MI, lab tests detect elevated ___. Name 2.

A

cardiac enzymes; troponin I; CK-MB

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20
Q

Which is the most sensitive and specific cardiac enzyme marker for MI (gold standard)? Which is useful for detecting reinfarction?

A

troponin I; CK-MB

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21
Q

Troponin I levels rise __ hours after infarction, peak at __ hours, and return to normal by ___. CK-MB levels rise __ hours after infarction, peak at __ hours, and return to normal by ___.

A

Troponin: 2-4 hrs; 24hrs; 7-10 days

CK-MB: 4-6 hrs; 24hrs; 72 hrs (makes it more useful for detecting reinfarction)

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22
Q

Name the 6 treatments used for MI

A

1) aspirin and/or heparin (limits thrombosis); 2) supplemental O2 (minimized ischemia); 3) nitrates (vasodilates veins and coronary arteries); 4) B-blocker (slows HR, decreasing O2 demand, and risk for arrhythmia); 5) ACE inhibitor (decreases LV dilation); 6) fibrinolysis or angioplasty (opens blocked vessel)

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23
Q

In MI, what do we give to limit thrombosis? What do we give to minimize ischemia? What do we give to vasodilate veins and coronary arteries?

A

aspirin and/or heparin; supplemental O2; nitrates;

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24
Q

In MI, what do we give to slow HR (decreased O2 demand and risk for arrhythmia)? What do we give to decrease LV dilation (decrease after load by preventing arteriole constriction and decrease blood volume by preventing release of aldosterone)?

A

Beta-blocker; ACE inhibitor

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25
Q

In MI, we do fibrinolysis or angioplasty to ___. Name to complications of them.

A

Open blocked vessel; 1) contraction band necrosis (reperfusion of irreversibly damaged cells leads to calcium influx causing hyper contraction of myofibrils); 2) reperfusion injury (return of oxygen and inflammatory cells may lead to free radical generation further damaging myocytes)

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26
Q

During the first 4 hours of MI, what are the gross and microscopic changes, and what are complications?

A

No gross or microscopic changes; cardiogenic shock (massive infarction), CHF (reduced EF), and arrhythmia

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27
Q

During the 4-24 hours after MI, what are the gross and microscopic changes, and what are complications?

A

gross: dark discoloration; micro: coagulative necrosis; complication: arrhythmia

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28
Q

During the 1-3 days after MI, what are the gross and microscopic changes, and what are complications?

A

gross: yellow pallor; micro: neutrophils; complication: fibrinous pericarditis (if there was transmural infarction) - it presents as chest pain with friction rub

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29
Q

During the 4-7 days after MI, what are the gross and microscopic changes, and what are complications?

A

gross: yellow pallor; micro: macrophages (eat up necrotic debris so wall is at its weakest); complications: rupture! (of ventricular free wall leads to cardiac tamponade; of inter ventricular septum leads to shunt; of papillary muscle leads to mitral insufficiency)

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30
Q

During the 1-3 weeks after MI, what are the gross and microscopic changes, and what are complications?

A

gross: red border emerges as granulation tissue enters from edge of infarct; micro: granulation tissue (scar) with plump fibroblasts, collagen (primarily type 1), and bv’s; no complications

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31
Q

During the month after MI, what are the gross and microscopic changes, and what are complications?

A

gross: white scar (not as strong as wall); micro: fibrosis; complications: aneurysm, mural thrombus (since scarred wall does not move well) or Dressler syndrome

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32
Q

Dressler syndrome is a complication seen ___ after an MI. It is a ___ reaction, in which the body creates ___ against ___, causing ___.

A

6-8 weeks; autoimmune; antibodies; pericardium; pericarditis

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33
Q

The papillary muscle of the heart is fed by the ___. Infarction in that artery can cause rupture of the ___, leading to ___, usually arising ___ after an MI.

A

RCA; papillary muscle; mitral insufficiency; 4-7 days

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34
Q

Fibrinous pericarditis is a post-MI complication seen ___ after an MI, and only occurs with a ___ infarction. It presents with these 2 symptoms.

A

1-3 days; transmural; chest pain; friction rub

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35
Q

Sudden cardiac death is unexpected death due to ___. It occurs with/without symptoms or less than __ after symptoms arise. Usually due to ___. Most common etiology is ___. __% of pts have pre-existing severe atherosclerosis. Name three less common causes

A

cardiac disease; without; 1 hour; fatal ventricular arrhythmia; acute ischemia; 90; mitral valve prolapse; cardiomyopathy; cocaine abuse (vasospasm related to cocaine)

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36
Q

Chronic ischemic heart disease is poor ___ due to ___ (with/without infarction). It progresses to ___.

A

myocardial function; chronic ischemic damage; with or without; CHF

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37
Q

Congestive heart failure is ___. Divided into __ and __ failure

A

pump failures; left and right sided

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38
Q

Name 5 causes of left sided heart failure

A

1) ischemia; 2) hypertension (causes LV hypertrophy, which is harder to oxygenate); 3) dilated cardiomyopathy (dilation of all chambers, leads to stretched muscle, can’t contract as well); 4) MI; 5) restrictive cardiomyopathy (can’t fill heart so it can’t pump properly)

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39
Q

Clinical features of left-sided heart failure are due to ___ and ___.

A

decreased forward perfusion; pulmonary congestion

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40
Q

Pulmonary congestion (due to left sided heart failure) leads to ___. It results in these 4 symptoms.

A

pulmonary edema; dyspnea; paroxysmal noctural dyspnea (due to increased venous return when lying flat); orthopnea; crackles (fluid in interstitia)

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41
Q

In pulmonary congestion, small congested capillaries may __, leading to ___, which is marked by ____ (aka ‘__’ cells)

A

burst; intraalveolar hemorrhage; hemosiderin-laden macrophages; heart-failure
(pulmonary congestion due to left sided heart failure

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42
Q

Left sided heart failure can also cause decreased flow to the ___, leading to activation of the ____ system. Which leads to increased ___ and ___, further exacerbating CHF. Mainstay of treatment for left sided heart failure is __.

A

kidneys; renin-angiotensin; TPR (angiotensin II); blood volume (angiotensin II - aldosterone); ACE inhibitor

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43
Q

Right sided heart failure is most commonly due to ___. Name 2 other important causes.

A

left-sided heart failure; left-to-right shunt; chronic lung disease (cor pulmonale) - failure of R side of heart due to pulmonary stenosis (pulmonary vessels constrict with hypoxia from disease)

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44
Q

Right sided heart failure clinical features are due to ___. Name 3 features.

A

congestion; 1) JVD; 2) painful hepatosplenomegaly with characteristic ‘nutmeg’ liver, may lead to cardiac cirrhosis; 3) dependent pitting edema (due to increased hydrostatic pressure)

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45
Q

In coagulative necrosis, seen ___ after an MI, myocardium loses ___, but there are still no ___.

A

4-24hrs; nuclei; neutrophils (they come 1-3 days later)

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46
Q

Congenital heart defect arise during ___ (usually ___ through __) seen in __% of live births. Most are genetic/sporadic. Often result in ___ between left (systemic) and right (pulmonary) circulations

A

embryogenesis; wks 3-8; 1; sporadic; shunting

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47
Q

Defects with left-to-right shunting may be __ at birth, but the shunt can reverse. Increased flow through the pulmonary circulation results in __ of pulmonary vessels and ___. Increased pulmonary resistance eventually leads to ___, leading to ___ (___ syndrome). Can end up with these 3 symptoms

A

asymptomatic; hypertrophy; pulmonary hypertension; reversal of shunt; cyanosis; Eisenmenger syndrome; right ventricular hypertrophy (b/c pumping against pHTN), polycythemia (deoxygenated blood - hypoxemia - inc EPO), clubbing (due to cyanosis)

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48
Q

Defects with right to left shunting usually presents as __ shortly after __.

A

cyanosis; birth

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49
Q

What is the most common congenital heart defect?

A

ventricular septal defect

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50
Q

Ventricular septal defect is a defect in the __ that divides the ___. It is associated with ___. Results in a ___ shunt. Size of defect determines ___ and ___. Small defects are often ___. Large can lead to ___.

A

septum; right and left ventricles; fetal alcohol syndrome; left-to-right shunt; extent of shunting; age at presentation; asymptomatic; Eisenmenger syndrome

51
Q

Tx of ventricular septal defect involves ___; small defects may close spontaneously

A

surgical closure

52
Q

Atrial septal defect is a defect in the ___ that divides ___. Most common type is ___ (__%) of cases. The less common type is ___, that is associated with ___.

A

septum; left and right atria; ostium secundum; 90; ostium primum; Down syndrome

53
Q

ASD results in ___ shunt and __ on auscultation, due to delayed closure of __ b/c of increased blood in right heart). ___ are an important complication.

A

left-to-right; split S2; pulmonary valve (relative to aortic valve); paradoxical emboli

54
Q

Patent ductus arteriosus is the failure of ___. It is associated with ___. Results in a ___ shunt btwn the ___. As a fetus the DA normally shunts blood from the ___ to the __, in order to ___.

A

ductus arteriosus to close; congenital rubella; left-to-right shunt; aorta and pulmonary artery; pulmonary artery; aorta; bypass the lungs

55
Q

Patent ductus arteriosus is __ at birth with continuous ___ murmur. May lead to ___, resolution in ___ cyanosis. Treatment of PDA involves ___, which decreases __, resulting in PDA closure.

A

asymptomatic; machine-like; Eisenmenger syndrome; lower extremity (since DA arises after the major branches of the aorta); indomethacin (NSAID); PGE (PGE maintains potency of the ductus arteriosus)

56
Q

Name the 4 problems in tetralogy of fallot. What is the X-ray appearance?

A

1) stenosis of the RV outflow tract; 2) right ventricular hypertrophy; 3) VSD; 4) aorta that overrides the VSD; boot shaped heart

57
Q

In tetralogy of fallot, ___ shunt leads to early ___. The degree of ___ determines the extent of __ and __. Patients learn to __ in response to a cyanotic spell. This increases __, which decreases ___ allowing more blood to reach the lungs

A

right-to-left; cyanosis; stenosis (RV outflow tract stenosis); shunting; cyanosis; arterial resistance; shunting

58
Q

In transposition of the great vessels, the __ and __ arteries arise from the left ventricle and right ventricle respectively. It is associated with ___. Presents with ___, since the pulmonary and systemic circuits ___. Results in ___ of the right ventricle and __ of the left ventricle.

A

pulmonary; aorta; maternal diabetes; early cyanosis; do not mix; hypertrophy (since blood stays in systemic circulation); atrophy (since little blood will be in pulmonary circulation)

59
Q

To treat pts with transposition of the great vessels, you create a ___. Usually __ is administered in order to ___ until surgical repair can be performed.

A

shunt (allowing blood to mix); PGE; maintain a PDA

60
Q

Truncus arteriosus is characterized by ___. The truncus fails to ___. It presents with ___. Deoxygenated blood from right ventricle ___ with oxygenated blood from left ventricle before pulmonary and aortic circulations ___.

A

single large vessel arising from both ventricles; divide; early cyanosis; mixes; separate

61
Q

Tricuspid atresia is when the ___ fails to develop. The ___ is hypoplastic. It is often associated with ___, resulting in a __ shunt. Presents with __.

A

tricuspid valve orifice; right ventricle (no blood going to it); ASD; right-to-left; early cyanosis

62
Q

Coarcation of the aorta is the ___ of the aorta. It is classically divided into ___ and __ forms.

A

narrowing; infantile; adult

63
Q

Infantine coarcation of the aorta is associated with a ___. The coarcation lies distal to the ___ and proximal to the ___. It presents with ___ in infnats, often at birth. It is associated with ___ syndrome.

A

PDA; aortic arch; PDA; lower extremity cyanosis; Turner

64
Q

Adult coarctation of the aorta is not associated with a ___ like the infantile one is. Coarctation lies proximal/distal to the aortic arch. It presents as ___ in the upper extremities and __ with strong/weak pulses in the lower extremities. Classically discovered in ___.

A

PDA; distal; HTN; hypotension; weak; adulthood

65
Q

In adult coarctation of the aorta, ___ develops across the ___ arteries. Engorged arteies cause ___ of the __ on xray. Adult CotA is associated with ___.

A

collateral circulation; intercostal; notching; ribs; bicuspid aortic valve

66
Q

Name 8 congenital heart defects

A

1) ventricular septal defect (VSD); 2) atrial septal defect (ASD); 3) patent ductus arteriosus (PDA); 4) tetralogy of fallot; 5) transposition of the great vessels; 6) truncus arteriosus; 7) tricuspid atresia; 8) coarctation of the aorta

67
Q

Which congenital heart defect is associated with Turner syndrome? Which is associated with maternal diabetes? Fetal alcohol syndrome? Down syndrome? Bicuspid aortic valve? Which is associated with congenital rubella?

A

Infantile coarctation of the aorta; transposition of the great vessels; VSD; ASD (specifcally ostium primum); adult coarctation of the aorta; PDA

68
Q

Which congenital heart defect causes a boot shaped heart on xray? Which causes notching of ribs on xray? Which casues a machine like murmur? Which causes a split S2?

A

tetralogy of fallot; adult coarctation of the aorta; PDA; ASD

69
Q

Which congenital heart defects cause cyanosis of the lower extremities?

A

PDA (when shunt becomes right-to-left, it arises since DA arises after aortic arch); coarctation of the aorta (since the narrowing occurs after the aortic arch)

70
Q

Paradoxical emboli is an important complication of which congenital heart defect

A

ASD (patent foramen ovale)

71
Q

Which congenital heart defects present with early cyanosis? (4)

A

1) tetralogy of fallot (right-to-left shunt); 2) transposition of the great vessels; 3) truncus arteriosus; 4) tricuspid atresia (right-to-left shunt)

72
Q

The heart has ___ valves that prevent back flow. Name them. Valvular lesions generally result in __ or __.

A

4; tricuspid; pulmonary; mitral; aortic; stenosis (decreased caliber of valve orifice; regurgitation (backflow)

73
Q

Acute rheumatic fever is a systemic complication of ___ due to ___. It affects adults/children ___ after an episode of ___. It is caused by ___, since ___ resembles proteins in human tissue.

A

pharyngitis; group A B-hemolytic streptococci; children; 2-3 wks; streptococcal pharyngitis (strep throat); molecular mimicry; bacterial M protein

74
Q

Diagnosis of acute rheumatic fever is based on ___ criteria. You must have evidence of prior ___ with the presence of major and minor criteria. Minor criteria are ___ and include __ and ___.

A

Jones; group A strep infxn (elevated ASO or anti-DNase B titers); nonspecific; fever; elevated ESR

75
Q

What is the Jones criteria for diagnosis acute rheumatic fever?

A

Joint (migratory polyarthritis); O (heart = pancarditis); Nodules (subcutaneous nodules); Erythema marginatum; Sydenham chorea (rapid involuntary muscle mvmts)

76
Q

In the Jones criteria for acute rheumatic fever, the joint problem is ___. It causes swelling and pain in a ___ that resolves within hours/days/weeks/months and ___ to involve another ___.

A

migratory polyarthritis; large joint (wrist, knees, ankle); days; migrates; large joint

77
Q

Pancarditis that ensues from acute rheumatic fever can affect the endocarditis, specifically the ___, which is more commonly involves than the ___. It is characterized by __ along lines of closure that lead to ___.

A

mitral valve; aortic valve; small vegetations; regurgitation

78
Q

Pancarditis that ensues from acute rheumatic fever can affect the myocarditis, with ___ forming that are characterized by these 4 things.

A

Aschoff bodies; 1) foci of chronic inflammation; 2) giant cells; 3) fibrinoid material; 4) Anitschkow cells (reactive histiocytes with slender, wavy nuclei)

79
Q

____ are reactive histiocytes with slender, wavy nuclei found in aschoff bodies in myocarditis from acute rheumatic fever.

A

Anitschkow cells

80
Q

Pancarditis that ensues from acute rheumatic fever can affect the pericarditis, leading to ___ and ____.

A

friction rub; chest pain

81
Q

What is the most common cause of death during the acute phase of rheumatic fever?

A

myocarditis

82
Q

Erythema marginatum, seen in ___, is an annular, pruritic/nonpruritic rash with ___ borders, commonly involving these 2 areas.

A

rheumatic fever; nonpruritic; erythematous; trunk and limbs

83
Q

Acute rheumatic fever usually resolves/worsens. It can progress to ___. Repeat exposure to ___ results in relapse of acute phase and increases risk for ___.

A

resolves; chronic rheumatic heart disease; group A strep; chronic disease

84
Q

Chronic rheumatic heart disease involves __ that arises as a consequence of rheumatic fever. It results in ___, with a classic ‘__’ appearance. It almost always affects the __ valve, leading to thickening of __ and __. Occasionally involves the __ valve leading to ___.

A

valve scarring; stenosis; fish-mouth; mitral; chordae tendineae; cusps; aortic; fusion of the commissures

(other valves less commonly involved)

85
Q

Complications of chronic rheumatic heart disease include ____.

A

infectious endocarditis

86
Q

Aortic stenosis is ___. It is usually due to __ and __ from ___. It presents in early/late adulthood (age __). ___ increases risk and hastens disease onset. Treatment is ___ after ___.

A

narrowing of the aortic valve orifice; fibrosis; calcification; wear and tear; late; greater than 60; bicuspid aortic valve; valve replacement; onset of symptoms

87
Q

A normal aortic valve has ___ cusps. Fewer cusps results in increased ___ on each cusp and can increase the risk of ___.

A

3; wear and tear; aortic stenosis

88
Q

In addition to wear and tear, aortic stenosis may also arise from ___. Name two ways to distinguish it from the wear and tear.

A

chronic rheumatic valve disease; 1) coexisting mitral stenosis (the mitral valve is affected first in rheumatic); 2) fusion of the aortic valve commissaries (they are not fused in wear and tear)

89
Q

In aortic stenosis, cardiac compensation leads to a prolonged ___ stage during which a ____ followed by a ___ is heard.

A

asymptomatic; systolic ejection click; crescendo-decrescendo murmur

90
Q

Name 3 complications of aortic stenosis

A

1) concentric left ventricular hypertrophy (may progress to HF); 2) angina and syncope with exercise (limited ability to increase blood flow across the valve leads to decreased perfusion of myocardium and brain); 3) microangiopathic hemolytic anemia (RBCs are damaged forming schistocytes while crossing calcified valve)

91
Q

Aortic regurgitation is the ___ of blood from the ___ into the ___ during ___. Most common cause is ___. Name two other causes and examples. Treatment is ___ once ___ develops

A

regurgitation; aorta; left ventricle; diastole; isolated root dilation; aortic root dilation (syphilitic aneurysm and aortic dissection); valve damage (infectious endocarditis); valve replacement; LV dysfunction

92
Q

Name 3 clinical features of aortic regurgitation

A

1) early, blowing diastolic murmur; 2) Hyperdynamic circulation due to increased pulse pressure; 3) LV dilation and eccentric hypertrophy (due to volume overload)

93
Q

Pulse pressure is the ___. In aortic regurgitation, __ pressure decreases due to regurgitation, while __ pressure increases due to increased stroke volume. This increase/decrease in pulse pressure leads to these 3 symptoms

A

difference btwn systolic and diastolic pressures; diastolic; systolic; increase; 1) bounding pulse (water-hammer pulse); 2) pulsating nail bed (quincke pulse); 3) head bobbing

94
Q

Mitral valve prolapse is ___ of the mitral valve into the ___ during ___. It is seen in __% of US adults. Due to ___ (accumulation of __) of the valve, making it floppy. Etiology is ___. May be seen in these two syndromes.

A

ballooning; left atrium; systole; 2-3; myxoid degeneration; ground substance; unknown; Marfan or Ehlers Danlos syndrome

95
Q

Mitral valve prolapse presents with an incidental __ followed by a ___. It is usually symptomatic/asymptomatic. Complications are common/rare. They include these 3. Treatment is ___.

A

mid-systolic click; regurgitation murmur; asymptomatic; rare; infectious endocarditis; arrhythmia; severe mitral regurgitation; valve replacement

96
Q

Mitral regurgitation is __ of blood from the __ into the __ during ___. Usually arises as a complication of ___. Name 4 other causes.

A

reflux; left ventricle; left atrium; systole; mitral valve prolapse; 1) LV dilatation (e.g. left sided HF); 2) infective endocarditis; 3) acute rheumatic heart disease; 4) papillary muscle rupture after a MI

97
Q

Name 2 clinical features of mitral regurgitation

A

1) holosystolic “blowing” murmur, that is louder with squatting (increased systemic resistance decreases LV emptying) and expiration (increased return to LA); 2) results in volume overload and left-sided heart failure

98
Q

Mitral stenosis is ____. Usually due to ___. On auscultation, there is a ___ followed by ___.

A

narrowing of the mitral valve orifice; chronic rheumatic valve disease; opening snap (valve is blown open); diastolic rumble (blood flows through stenosed valve)

99
Q

In mitral stenosis, there is volume overload leading to dilatation of the ___, resulting n these 3 things.

A

left atrium; 1) pulmonary congestion (with edema and alveolar hemorrhage); 2) pulmonary hypertension and eventual right sided heart failure; 3) atrial fibrillation and associated risk for mural thrombi (stretched LA messes with conducting system)

100
Q

Endocarditis is inflammation of endocardium that lines the ____; usually due to ___. ___ is the most common overall cause.

A

surface of cardiac valves; bacterial infection; streptococcus viridans

101
Q

Streptococcus viridans is a high/low virulence organism that infects previously damaged ___ (e.g. chronic rheumatic heart disease and mitral valve prolapse). Results in ___ that do/do not destroy the valve (aka ___). Damaged endocardial surfaces develops ___. Transient bacteremia leads to trapping of __ in the ___. ___ decrease the risk of endocarditis

A

low; valves; small vegetations; do not; subacute endocarditis; thrombotic vegetations (platelets and fibrin); bacteria; vegetations; prophylactic antibiotics

(see this with dental procedures)

102
Q

Staph aureus is the most common cause of endocarditis in ___. High/low virulence organisms that infect __ valves, most commonly the ___. Results in small/large vegetations that do/do not destroy the valve (aka ___)

A

IV drug abusers; high; normal; tricuspid (first valve exposed to returning circulation); large; do; acute endocarditis

103
Q

Which bacteria is associated with endocarditis of prosthetic valves. Endocarditis of __ is seen in patients with underlying colorectal carcinoma.

A

Staph epidermidis; strep bovis

104
Q

HACEK organisms are associated with endocarditis with ___. Name them.

A

negative blood cultures; Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella

105
Q

Name 4 clinical features of bacterial endocarditis

A

1) fever (due to bacteremia); 2) murmur (due to vegetations on heart valve); 3) Features due to embolization of septic vegetations (Janeway lesions, osler nodes, splinter hemorrhages in nail beds, Roth spots); 4) anemia of chronic disease (due to inflamm)

106
Q

Name the 4 clinical presentations of embolization due to septic vegetations (infectious endocarditis)

A

1) Janeway lesions (erythematous contender lesions on palms and soles); 2) Osler nodes (tender/ouch lesions on fingers or toes); 3) splinter hemorrhages in nail bed; 4) Roth spots (retinal hemorrhages)

107
Q

___ is useful for detecting lesions on valves (endocarditis). Might also have positive ___, and cbc might show ___.

A

Transesophageal echocardiogram; blood cultures; anemia of chronic disease (low Hb, inc ferritin, low TIBC, low serum iron, low % sat)

108
Q

Nonbacterial thrombotic endocarditis is due to ___ that arise in association with ___ or ___. Vegetations arise on the ___ valve along the lines of closure and result in ___.

A

sterile vegetations; hypercoagulable state; underlying adenocarcinoma; mitral valve; mitral regurgitation

109
Q

Libman-Sacks endocarditis is due to __ vegetations that arise in association with ___. Vegetations are present on the __ and __ of the __ valve and result in ___.

A

sterile vegetations; SLE; surface; undersurface; mitral; mitral regurgitation (vegetations on both sides of valve is strongly suggestive of lupus!)

110
Q

Cardiomyopathy is a group of __ that result in __. What is the most common form of cardiomyopathy?

A

myocardial disease; cardiac dysfunction; dilated cardiomyopathy

111
Q

Dilated cardiomyopathy is dilation of ____. Results in ___ dysfunction (ventricles cannot ___), leading to biventricular ___. Complications include ___ and ___. Treatment is ___.

A

all four chambers of the heart; systolic; pump; CHF; mitral and tricuspid regurgitation (dilation of heart stretches valves); arrhythmia (stretching of heart messes with conduction system); heart transplant

112
Q

Dilated cardiomyopathy is most commonly due to ___. Name 6 other causes.

A

idiopathic (unknown); 1) genetic mutation (usually AD); 2) myocarditis; 3) alcohol abuse; 4) drugs; 5) pregnancy (late or soon after childbirth); 6) hemochromatosis

113
Q

Myocarditis that eventually leads to dilated cardiomyopathy is usually due to ___. It is characterized by a ___ infiltrate in the myocardium. Results in these 3 clinical findings. Dilated cardiomyopathy is a early/late complication

A

coxsackie A or B; lymphocytic (virus!); chest pain; arrhythmia with sudden death; heart failure; late

114
Q

Name two drugs that can cause dilated cardiomyopathy

A

1) doxorubicin; 2) cocaine

115
Q

Hypertrophic cardiomyopathy is massive hypertrophy of the ___. Usually due to __ in __. Biopsy shows __ with __.

A

left ventricle; genetic mutations (most common form is AD); sarcomere proteins; myofiber hypertrophy; disarray

116
Q

Name 3 clinical features of hypertrophic cardiomyopathy

A

1) decreased cardiac output (LV hypertrophy leads to diastolic dysfunction since ventricles cannot fill); 2) sudden death due to ventricular arrhythmia (common cause of sudden death in young athletes); 3) syncope with exercise (subaortic hypertrophy of the ventricular septum results in functional aortic stenosis)

117
Q

What is the most common cause of sudden death in young athletes?

A

Hypertrophic cardiomyopathy

118
Q

Restrictive cardiomyopathy is increased/decreased compliance of the ___ that restricts ___ during ___. Presents as __. Classic finding is __ with diminished __.

A

decreased; ventricular endomyocardium; filling; diastole; congestive heart failure; low voltage EKG (stuff in the way); QRS amplitude

119
Q

Name 4 causes of restrictive cardiomyopathy and which one is seen in children

A

1) amyloidosis; 2) sarcoidosis; 3) endocardial fibroelastosis (fibrosis of endocardium - children); 4) Loeffler syndrome (endomyocardial fibrosis with an eosinophilic infiltrate and eosinophilia)

120
Q

Name 3 types of tumors found in the heart

A

1) myxoma; 2) rhabdomyoma; 3) metastasis

121
Q

Myxoma is a benign/malignant ___ tumor with a __ appearance and abundant __ on histology. It is the most common primary cardiac tumor in ___. Usually forms a __ mass in the __ that causes syncope due to obstruction of the ___.

A

benign; mesenchymal; gelatinous; ground substance; adults; pedunculated (grows off a stalk); left atrium; mitral valve

122
Q

Rhabdomyoma is a benign/malignant ___ of cardiac muscle. Most common primary cardiac tumor in ___. Associated with ___. Usually arises in the ___.

A

benign; hamartoma; children; tuberous sclerosis; ventricle

123
Q

Metastatic tumors are more/less common in the heart than primary tumors. Common mets to the heart include these 4 cancers. Most commonly involve the __, resulting in ___

A

more; breast and lung carcinoma, melanoma, lymphoma; pericardium; pericardial effusion

124
Q

What is the most common primary cardiac tumor in adults? Children?

A

Myxoma; rhabdomyoma