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Boards > Cardio > Flashcards

Cardio Flashcards

1
Q

Murmur associated with Rheumatic Fever:

A

Mitral stenosis

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2
Q

Murmur associated with Infective endocarditis:

A

Mitral and/or tricuspid regurgitation

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3
Q

Mutation on HCM:

A

AD mutation in the beta-myosin heavy chain

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4
Q

Histo of HCM:

A

Inappropriate hypertrophy of LV myocardium and disordered arrangement of cardiac myofibrils (myofibril disarray)

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5
Q

Physiological changes in HC:

A 
Diastolic dysfunction
LV outflow obstruction (increase afterload)
Myocardial ischemia (d/t increased work of LV)
Normal coronary arteries
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6
Q

Murmur associated with HCM:

A

Systolic crescendo-decrescendo murmur b/w apex and left sternal border, radiating to the suprasternal notch

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7
Q

Murmur changes in HCM:

A

Decrease with increased preload and afterload (to relieve obstruction)
Increase with decrease preload and afterload

Decrease with squatting
Increase with standing after squatting

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8
Q

A split S2 indicates:

A

Lengthening of the RV ejection time with delayed closure of the pulmonary valve

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9
Q

When can you hear an S2:

A

Complete RBBB, pulmonary stenosis, and pulmonary HTN

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10
Q

What structure lies behind the LA and esophagus on TEE?

A

descending aorta

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11
Q

fever, pericardial friction rub, ST elevations in all leads

A

pericarditis

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12
Q

tx of pericarditis

A

NSAIDs

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13
Q

distended neck veins, distant heart sounds, hypotension, pulsus paradoxus

A

cardiac tamponade

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14
Q

electrical alternans

A

cardiac tamponade

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15
Q

prevents intestinal reabsorption of bile acid and forces liver to use cholesterol to make more bile acids

A

bile acid resins

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16
Q

prevents cholesterol absorption at the intestinal brush border

A

ezetimbe

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17
Q

upreulates LPL to increase TG clearance and activates PPAR-a to induce HDL synthesis

A

fibrates

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18
Q

inhibits lipolysis (HSL) in adipose tissue and reduces hepatic VLDL synthesis

A

niacin

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19
Q

inactivates LDL-R degradation, increasing the amount of LDL removed from bloodstream

A

PCSK9 inhibitors

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20
Q

hepatotoxicity and myopathy

A

AEs of statins

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21
Q

upset GI, decreased absorption of fat soluble vitamins and drugs, increased risk of chol. gallstones

A

AEs of bile acid resins

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22
Q

increased LFTs and diarrhea

A

AEs of ezetimbe

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23
Q

myopathy, cholesterol gallstones

A

AEs of fibrates

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24
Q

red flushed face decreased by NSAIDs, hyperglycemia, hyperuricmia, rash

A

AE of niacin

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25
Q

myalgias, delirium, dementia, neurocognitive effects

A

AEs of PCSK9 inhibitors

26
Q

renal impairment is a CI for use of…

A

fibrates

27
Q

why you shouldn’t use fibrates in patients with severe renal impairment….

A

fibrates can increase serum creatinine

28
Q

treatment for chronic atrial fibrillation

A

Calcium channel blockers and beta blockers

29
Q

bioprosthetic heart valves are subject to….

A

wear and tear, calcification leading to stenosis, perforation or tearing, leading to insufficiency

30
Q

acute rheumatic fever presents with

A

pancarditis and acute LV failure

31
Q

most common cause of hemorrhagic pericarditis

A

TB and metastatic carcinoma

32
Q

LA dilation, systemic abscess, arterial aneurysm

A

complications of staphylococcal septicemia followed by mitral endocarditis

33
Q

what medications should patients who undergo mechanical prosthesis be put on to avoid thrombotic complications?

A

anticoagulants (warfarin)

34
Q

the most common toxin producing dilated cardiomyopathy

A

alcohol

35
Q

most important cause of LVH and failure

A

systemic HTN

36
Q

how long does troponin I levels stay elevated?

A

7-10 d

37
Q

sensitive marker for myocardial injury w/in the first 24-48 hrs

A

CK-MB

38
Q

How long does it take CKMB to return to normal

A

72 hrs

39
Q

gross findings 0-24 hr post MI

A

none

40
Q

light microscopy findings 0-24 hrs post-MI:

A

early coagulative necrosis, release of necrotic cell contents into blood stream (troponin), edema, hemorrhage, wavy fibers, neutrophils appear, reperfusion injury, hypercontraction of myofibrils via increased free calcium influx

41
Q

complications 0-24 hrs post MI

A

ventricular arrhythmia, HF, cardiogenic shock

42
Q

gross findings 1-3 days post MI:

A

hyperemia

43
Q

light microscopy findings 1-3 days post MI

A

extensive coagulative necrosis, acute inflammation with neutrophils

44
Q

complications 1-3 days post MI:

A

postinfarction fibrinous pericarditis, arrhythmia

45
Q

gross findings 3-14 days post MI:

A

hyperemic border; central brown-yellow softening

46
Q

light microscopy findings 3-14 days post-MI:

A

macrophages and granulation tissue at borders

47
Q

what comprises granulation tissue?

A

type III collagen (fibroblasts), capillaries, and myofibroblasts

48
Q

complications 3-14 days post-MI:

A

free wall rupture leading to cardiac tamponade; papillary muscle rupture leading to mitral regurgitation; interventricular rupture d/t macrophage mediated structural damage; LV pseudoaneurysm

49
Q

gross findings 2 wks-months post-MI:

A

recanalized artery, gray-white scar

50
Q

light microscopy findings 2 weeks-months post-MI:

A

contracted scar complete, increased collagen deposition and decreased cellularity

51
Q

complications 2 weeks-months post-MI:

A

Dressler syndrome, HF, arrhythmia, true ventricular aneurysm (w/ a risk of mural thrombus)

52
Q

plaque disruption with superimposed mural thrombosis gives rise to…

A

unstable angina

53
Q

MC of fibrinous pericarditis…

A

uremia following renal failure

54
Q

top 3 causes of fibrinous pericarditis:

A

uremia, RA and Dressler syndrome

55
Q

top 2 causes of serous pericarditis:

A

Lupus and rheumatic fever

56
Q

MC cause of suppurative pericarditis:

A

infection of the pericardium

57
Q

nonbacterial (marantic/thrombotic) vegetations can occur on any valve and is associated with…

A

malignancy (especially mucin-secreting adenocarcinomas)and a hypercoaguable state

58
Q

along with mitral stenosis, what is an additional late complication of rheumatic fever?

A

aortic stenosis

59
Q

mutation associated with TOF:

A

NOTCH pathway

60
Q

pathway that plays a major role in in modulations of vascular development, including cardiac outflow tracts

A

NOTCH

61
Q

mutation seen in long QT syndrome:

A

KCNQ1 mutations

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