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CVD > 01b: Atherosclerosis > Flashcards

01b: Atherosclerosis Flashcards

1
Q

Which vessels are favored sites of atherosclerosis/atheroma formation?

A
  1. Abdominal aorta
  2. Coronary aa
  3. Carotid aa
  4. Popliteal aa
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2
Q

Atherosclerosis: intimal lesion composed of which cell types?

A

Endothelial, smooth muscle, macrophages, inflammatory cells

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3
Q

T/F: Lipid found in atheroma is mainly cholesterol.

A

False - cholesterol esters

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4
Q

What’s a “fatty streak”?

A

Accumulation of foam cells in the intima

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5
Q

Rupture of plaque is more likely in atheromas with which main characteristics?

A
  1. Large lipid core (over 40% of atheroma volume)

2. Thin fibrous cap (with little smooth muscle)

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6
Q

Complications of atherosclerosis:

A
  1. Calcification
  2. Hemorrhage
  3. Rupture/erosion
  4. Embolization
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7
Q

Arterial stenosis: a “significant” lesion is reduction by (X)% of diameter and symptoms (present/absent) at rest.

A

X = 50-70

Absent (symptoms upon exertion)

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8
Q

Arterial stenosis: a “critical” lesion is reduction by (X)% of diameter. (Y)% stenosis will reduce resting flow.

A 
X = 75+
Y = 90+
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9
Q

Risk factors for atherosclerosis.

A
  1. Diabetes
  2. Hyperlipidemia
  3. HT
  4. Smoking
  5. Male sex
  6. Age
  7. Genetics
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10
Q

What’s a “false” aneurysm?

A

A psueudo-aneurysm; outpouching of blood vessel (not widening of the original vessel)

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11
Q

Histopathology of MI: 1-3h from infarction.

A

Wavy fiber change

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12
Q

Histopathology of MI: 4-12h from infarction.

A
  1. Coagulation necrosis
  2. Neutrophil infiltration (6-8h)
  3. Nuclear pyknosis (at 12h)
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13
Q

Histopathology of MI: when does neutrophil infiltration peak?

A

48h

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14
Q

Histopathology of MI: 3 days after infarction.

A

Vessel proliferation

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15
Q

Histopathology of MI: 4 days after infarction.

A
  1. Fibroblast proliferation

2. Macrophage infiltration

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16
Q

Histopathology of MI: 9 days after infarction.

A

Collagen deposition

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17
Q

Histopathology of MI: 2-4 weeks post-infarction.

A

Granulation tissue formation/peak

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18
Q

Histopathology of MI: when would you expect to see mature scar?

A

Over 6 weeks post-infarct

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19
Q

Infarctions can be described pathologically by the extent of (X) they produce within the myocardial wall. (Y) infarcts span its entire thickness.

A 
X = necrosis
Y = transmural
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20
Q

The (X) myocardial layers are particularly susceptible to ischemia because this zone is subjected to the highest (Y) and has few (Z) that supply it.

A 
X = subendocardium (innermost)
Y = pressure from the ventricular chamber
Z = collateral connections
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21
Q

Typical pressures in RA

A

0-6

22
Q

Typical pressures in RV

A

24/6

23
Q

Typical pressures in Pulm a

A

24-30/12

24
Q

Typical PCWP

A

6-12

25
Q

Typical pressures in LA

A

6-12

26
Q

Typical pressures in LV

A

90-140/6-12

27
Q

Typical pressures in Aorta

A

90-140/60-90

28
Q

RA wave forms and their significance.

A

v: passive filling (during systole)
y: rapid emptying
a: atrial contraction
x: atrial relaxation

29
Q

RV has one named “a” wave, which signifies (X).

A

X = atrial kick (end of diastole)

30
Q

Pulm a waveform characterized by (X) peak and (Y) trough. What wave makes it similar to aortic P waveform?

A 
X = systolic
Y = diastolic

Dicrotic notch (signifying pulmonic valve closure)

31
Q

PCWP has waveform similar in morphology to (X).

A

X = RA

32
Q

Aortic stenosis: what would you look for in the hemodynamic tracing to ID this disease state?

A

Significant systolic P drop between LV and aorta

33
Q

Aortic regurgitation: what would you look for in the hemodynamic tracing/waveform to ID this disease state?

A
  1. Continuous rise in LV diastolic filling pressure

2. Gradual decline in aortic diastolic P with absence of dicrotic notch

34
Q

Mitral stenosis: what would you look for in the hemodynamic tracing/waveform to ID this disease state?

A

High PCWP with significant P gradient between diastolic PCWP and LVEDP

35
Q

Mitral regurgitation: what would you look for in the hemodynamic tracing/waveform to ID this disease state?

A
  1. Elevated PCWP

2. Hallmark feature: pronounced V wave on PCWP (venous filling)

36
Q

Tricuspid stenosis: what would you look for in the hemodynamic tracing/waveform to ID this disease state?

A

Elevated RA P with high P gradient between diastolic Ps of RA and RV

37
Q

Pulmonic stenosis: what would you look for in the hemodynamic tracing/waveform to ID this disease state?

A

Elevated RV P with high P gradient between systolic Ps of RV and pulmonary a

38
Q

In (X) shock, all heart pressures are decreased, CO is (increased/decreased), and (SVR/PVR) is increased.

A

X = hypovolemic
Decreased
Both increased

39
Q

Why is SVR (high/low/normal) in hypovolemic shock?

A

High;

Compensatory vasoconstriction in response to hypotension (low CO)

40
Q

Cardiogenic shock: what’s the main issue?

A

Reduced tissue perfusion because heart is unable to pump adequate amount of blood (low CO)

41
Q

In (X) shock, diastolic filling pressures are increased, CO is (increased/decreased), and (SVR/PVR) is (increased/decreased).

A

X = cardiogenic
Decreased;
Both increased

42
Q

In (X) shock, all heart pressures are essentially normal. CO is (increased/decreased), and (SVR/PVR) are (increased/decreased).

A

X = septic
Increased
Decreased (systemic vasodilation via inflammatory mediators)

43
Q

In massive PE, why is PVR (high/low/normal) and SVR (high/low/normal)?

A

High because embolism causes “stenosis” of pulmonary vasculature;

High due to vasoconstriction (response to low BP)

44
Q

In massive PE, heart pressures are (high/low/normal).

A

High on R side of heart

45
Q

Hallmark feature of cardiac tamponade involves (X) of heart pressures.

A

X = diastolic equalization

46
Q

Cardiac tamponade: CO is (increased/decreased), SVR/PVR are (increased/decreased), and patient is (hyper/hypo)-tensive.

A

Decreased;
Increased;
Hypotensive

47
Q

T/F: O2 saturation in SVC, IVC, RA, RV, and PA are about the same (75%).

A

True

48
Q

A rise in O2 saturation by (X)% is considered significant and diagnostic for (R/L) to (R/L) shunt.

A

X = 7

L to R

49
Q

Patent ductus arteriosus can be detected by step (up/down) in (X).

A 
Up;
Pulm artery (inappropriate connection between PA and aorta)
50
Q

Renal a stenosis in elderly male likely caused by (X). And in young female likely caused by (Y).

A 
X = atherosclerosis
Y = fibromuscular dysplasia

CVD (8 decks)

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