01b: Atherosclerosis Flashcards
Which vessels are favored sites of atherosclerosis/atheroma formation?
- Abdominal aorta
- Coronary aa
- Carotid aa
- Popliteal aa
Atherosclerosis: intimal lesion composed of which cell types?
Endothelial, smooth muscle, macrophages, inflammatory cells
T/F: Lipid found in atheroma is mainly cholesterol.
False - cholesterol esters
What’s a “fatty streak”?
Accumulation of foam cells in the intima
Rupture of plaque is more likely in atheromas with which main characteristics?
- Large lipid core (over 40% of atheroma volume)
2. Thin fibrous cap (with little smooth muscle)
Complications of atherosclerosis:
- Calcification
- Hemorrhage
- Rupture/erosion
- Embolization
Arterial stenosis: a “significant” lesion is reduction by (X)% of diameter and symptoms (present/absent) at rest.
X = 50-70
Absent (symptoms upon exertion)
Arterial stenosis: a “critical” lesion is reduction by (X)% of diameter. (Y)% stenosis will reduce resting flow.
X = 75+ Y = 90+
Risk factors for atherosclerosis.
- Diabetes
- Hyperlipidemia
- HT
- Smoking
- Male sex
- Age
- Genetics
What’s a “false” aneurysm?
A psueudo-aneurysm; outpouching of blood vessel (not widening of the original vessel)
Histopathology of MI: 1-3h from infarction.
Wavy fiber change
Histopathology of MI: 4-12h from infarction.
- Coagulation necrosis
- Neutrophil infiltration (6-8h)
- Nuclear pyknosis (at 12h)
Histopathology of MI: when does neutrophil infiltration peak?
48h
Histopathology of MI: 3 days after infarction.
Vessel proliferation
Histopathology of MI: 4 days after infarction.
- Fibroblast proliferation
2. Macrophage infiltration
Histopathology of MI: 9 days after infarction.
Collagen deposition
Histopathology of MI: 2-4 weeks post-infarction.
Granulation tissue formation/peak
Histopathology of MI: when would you expect to see mature scar?
Over 6 weeks post-infarct
Infarctions can be described pathologically by the extent of (X) they produce within the myocardial wall. (Y) infarcts span its entire thickness.
X = necrosis Y = transmural
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.
X = subendocardium (innermost) Y = pressure from the ventricular chamber Z = collateral connections
Typical pressures in RA
0-6
Typical pressures in RV
24/6
Typical pressures in Pulm a
24-30/12
Typical PCWP
6-12
Typical pressures in LA
6-12
Typical pressures in LV
90-140/6-12
Typical pressures in Aorta
90-140/60-90
RA wave forms and their significance.
v: passive filling (during systole)
y: rapid emptying
a: atrial contraction
x: atrial relaxation
RV has one named “a” wave, which signifies (X).
X = atrial kick (end of diastole)
Pulm a waveform characterized by (X) peak and (Y) trough. What wave makes it similar to aortic P waveform?
X = systolic Y = diastolic
Dicrotic notch (signifying pulmonic valve closure)
PCWP has waveform similar in morphology to (X).
X = RA
Aortic stenosis: what would you look for in the hemodynamic tracing to ID this disease state?
Significant systolic P drop between LV and aorta
Aortic regurgitation: what would you look for in the hemodynamic tracing/waveform to ID this disease state?
- Continuous rise in LV diastolic filling pressure
2. Gradual decline in aortic diastolic P with absence of dicrotic notch
Mitral stenosis: what would you look for in the hemodynamic tracing/waveform to ID this disease state?
High PCWP with significant P gradient between diastolic PCWP and LVEDP
Mitral regurgitation: what would you look for in the hemodynamic tracing/waveform to ID this disease state?
- Elevated PCWP
2. Hallmark feature: pronounced V wave on PCWP (venous filling)
Tricuspid stenosis: what would you look for in the hemodynamic tracing/waveform to ID this disease state?
Elevated RA P with high P gradient between diastolic Ps of RA and RV
Pulmonic stenosis: what would you look for in the hemodynamic tracing/waveform to ID this disease state?
Elevated RV P with high P gradient between systolic Ps of RV and pulmonary a
In (X) shock, all heart pressures are decreased, CO is (increased/decreased), and (SVR/PVR) is increased.
X = hypovolemic
Decreased
Both increased
Why is SVR (high/low/normal) in hypovolemic shock?
High;
Compensatory vasoconstriction in response to hypotension (low CO)
Cardiogenic shock: what’s the main issue?
Reduced tissue perfusion because heart is unable to pump adequate amount of blood (low CO)
In (X) shock, diastolic filling pressures are increased, CO is (increased/decreased), and (SVR/PVR) is (increased/decreased).
X = cardiogenic
Decreased;
Both increased
In (X) shock, all heart pressures are essentially normal. CO is (increased/decreased), and (SVR/PVR) are (increased/decreased).
X = septic
Increased
Decreased (systemic vasodilation via inflammatory mediators)
In massive PE, why is PVR (high/low/normal) and SVR (high/low/normal)?
High because embolism causes “stenosis” of pulmonary vasculature;
High due to vasoconstriction (response to low BP)
In massive PE, heart pressures are (high/low/normal).
High on R side of heart
Hallmark feature of cardiac tamponade involves (X) of heart pressures.
X = diastolic equalization
Cardiac tamponade: CO is (increased/decreased), SVR/PVR are (increased/decreased), and patient is (hyper/hypo)-tensive.
Decreased;
Increased;
Hypotensive
T/F: O2 saturation in SVC, IVC, RA, RV, and PA are about the same (75%).
True
A rise in O2 saturation by (X)% is considered significant and diagnostic for (R/L) to (R/L) shunt.
X = 7
L to R
Patent ductus arteriosus can be detected by step (up/down) in (X).
Up; Pulm artery (inappropriate connection between PA and aorta)
Renal a stenosis in elderly male likely caused by (X). And in young female likely caused by (Y).
X = atherosclerosis Y = fibromuscular dysplasia
