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STEP > Cardiology Part II > Flashcards

Cardiology Part II Flashcards

1
Q

Common presentation of ischemic heart disease in women

A

jaw paint + epigastric pain

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2
Q

AST elevation without accompanying ALT elevation..

A

ischemic heart disease

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3
Q

Where is AST found?

A

Spartan sitting on a heart + giraffes on either side of him + hippo eating heart + RBC pucks all around him/AST is found in cardiac tissue + kidneys + heart muscle + liver parenchyma + RBCs.

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4
Q

Where is ALT found?

A

Alan riding a hippo on left side/ALT is exclusively found in liver parenchyma and is thus far more specific for liver damage. Biliary tree on top of Alan’s head/ALT is primarily found in cells of bile ducts and biliary tree. Thus, an elevation of ALT usually indicates pathology within the biliary tree.

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5
Q

Histology of repeated episodes of angina?

A

gradual loss of myocytes, which is seen pathologically as small patches of fibrosis + vacuolization of damaged myocytes.

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6
Q

What can you use to test for variant angina?

A

ergonovine best. Can also use acetylcholine.

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7
Q

Most common location of MI?

A

LV following occlusion of LAD

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8
Q

cardiopulmonary arrest manifestation as acid-base disorder

A

♣ Code: Justin coding on the floor/cardiopulmonary arrest. Green gue dripping from ceiling + wings dripping green gue/classic condition for metabolic + respiratory acidosis (absent blood circulation causes tissue hypoxia anaerobic glycolysis lactic acidosis. Simultaneous respiratory acidosis due to abnormal or absent breathing).

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9
Q

HOCM genetics

A

almost all due to point missense mutations in the genes for beta-myosin heavy chain, myosin-binding protein C, troponin T, or tropomyosin. These mutations cause myofibril and myocyte structural abnormalities and possible deficiencies in force generation

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10
Q

HOCM pathophys

A

Anything that reduces preload will worsen the murmur. Dynamic left ventricular outflow tract obstruction is worsened with decreased LV volume. Vasodilators are contraindicated because they decrease SVR, leading to decreased afterload and lower LV volumes (By pushing against higher pressure, heart can maintain preload).

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11
Q

ejection fraction in HOCM?

A

compliance is reduced but systolic performance is not depressed and heart is hypercontractile. Thus, ejection fraction is often increased.

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12
Q

pathophys of sudden cardiac death in HOCM?

A

VFib or Vtach

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13
Q

when does culture negative endocarditis usually occur?

A

Immunocompromised + people with previously damaged valves.

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14
Q

acute endocarditis presentation

A

spiking fevers + rapid deterioration.

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15
Q

Common complications of acute endocarditis?

A

Brain + lung abscesses

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16
Q

pathophys of roth spots in subacute bacterial endocarditis?

A

septic emboli occlude the central retinal artery.

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17
Q

eye presentation in subacute bacterial endocarditis?

A

Acute onset of painless monocular visual loss.

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18
Q

hypersensitivity type associated with subacute bacterial endocarditis?

A

Type III

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19
Q

pathophys of subacute bacterial endocarditis

A

abnormal valve turbulent blood flow damaged endothelium platelet and fibrin deposition

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20
Q

osler vs laneway lesions

A

Oystein near fridge screaming in pain/osler nodes = *painful + *raised + purplish lesions on pads of *fingers/toes. /Janeway lesions = *painless + erythematous + *flat + macular + lesions on *palms and soles.

21
Q

prophylaxis for fro patients at high risk of endocarditis?

A

Mike on phils shoulder ouring amoxi all over Vincenzo/for patients at high risk of endocarditis and undergoing surgical or dental procedures, use amoxicillin for prophylaxis.

22
Q

primary cause of acute morbidity in ARF?

A

pancarditis (inflammation of pericardium, myocardium, and epicardium).

23
Q

What are aschoff bodies

A

granulomatous heart nodules

24
Q

Timeframe of ARF

A

Shark with long hair + in a chicken suit near entrance/ARF happens 2-4 weeks after untreated group A streptococcal pharyngitis.

25
Q

cause of aortic dissection?

A

weakness of the *media

26
Q

caveat about auscultation with aortic dissection related regurg

A

while primary aortic regurg presents at LSB, aortic dissection associated regurg occurs at Right sternal border

27
Q

renal presentation of aortic dissection?

A

bilateral renal hypoperfusion can develop (due to occlusion of the renal arteries), presenting with bilateral infraction with flank pain and hematuria.

28
Q

Dont confuse constrictive pericarditis with acute pericarditis.

A

Constrictive is a chronic process taking a long time to develop.

29
Q

other name for Loeffler’s

A

endomyocardial fibrosis with hypereosinophilia syndrome

30
Q

etiology of Loeffler’s

A

Parasites crawling around on the floor/results from direct toxicity to the heart by proteins in eosinophil granules designed to kill large parasites (can be caused by Chagas)

31
Q

CXR of cardiac tamponade

A

enlarged cardiac silhouette

32
Q

Hypotension that doesn’t respond to fluid resuscitation?

A

Cardiac tamponade

33
Q

Description of macrophages and alvolar hemorrhaging with pulmonary edema?

A

Golden cytoplasmic granules in macrophages that turn blue with Prussian blue staining

34
Q

Pressure volume loop problem approach

A

1) Think about how condition is going to affect preload, after load, contractility, and *stroke volume.

35
Q

Milrinone

A

positive inotrope like dobutamine.

36
Q

inotropes you can use for cariogenic shock

A

dobutamine, milrinone.

37
Q

structure of left bundle branch

A

Divides into anterior and posterior bundles.

38
Q

Effect of beta-blockers and nitrates and combined effect on ejection time

A

Beta-blockers will increase ejection time by slowing heart rate and contractility.
Nitrates will decrease ejection time by reducing preload so there’s less volume to be ejected.

39
Q

Combined effect of nitrates and beta-blockers on EDV?

A

no effect or decreased

40
Q

Combined effect of nitrates and beta-blockers on contractility?

A

no effect

41
Q

dipyridamole vs disopyramide

A 
disopyramide = Class 1A anti arrhythmic (dice pyramid)
dipyridamole = phosphodiesterase inhibitor (2 pyramids stacked on top of each other)
42
Q

Class IA antiarrhythmics

A

QUINIDINE
procainamide
disopyramide

43
Q

2 types of ASD and what they’re accompanied by

A

1) ostium secundum defects more common and usually occur as isolated findings.
2) ostium primum defects rarer yet usually occur with other cardiac anomalies

44
Q

When is wide splitting seen?

A

1) Right bundle branch block

2) Pulmonic stenosis

45
Q

Atheroma formation from codebook

A

Code: David Mack’s pouring through the door/endothelial cell injury increased endothelial permeability enhanced leukocyte adhesion (macrophage) + altered gene expression. Windows outside lined with platelets + platelets secreting substance that attracts smooth muscl cells + smooth muscle worms crawling through platelets /endothelial dysfunction also promotes platelet adhesion + aggregation + release of growth factors (PDGF) and cytokines. PDGF promotes migration of smooth muscle cells from the media into the intima + increases SMC proliferation. White collagenous substance pouring out of the VSMCs + neo from matrix crawling out of them + cap forming/VSMCs are stimulated to synthesize extracellular matrix proteins (eg collagen + elastin + proteoglycans) that form the fibrous cap typical of mature atheromas. Clusters of big milk glass balls hanging from ceiling/foci of calcification are characteristic of atherosclerotic plaques. Presence of calcification signifies the development of a complicated atheromatous plaque (dystrophically calcified fibrous plaque).
Location: Diner I went to with Anna across from the hotel.

46
Q

BNP characteristic as a test for heart failure

A

Good negative predictive value

47
Q

APO E defects associated with

A

1) type III hyperlipoproteinemia

2) dysbetalipoproteinemia

48
Q

VLDL vs chylomicron function

A
  • VLDL transports endogenous products (assembled in liver from TGs, cholesterol, and apoliproteins) –> transported to tissue where LPL breaks it down to FFAs.
  • chylomicrons transport exogenous (dietary) products.
49
Q

Relation of VLDL to LDL

A

LDL particles are formed as VLDL lipoproteins lose TGs through the action of lipoprotein lipase and they become smaller and denser.

STEP (85 decks)

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