Path-ischemia Flashcards

1
Q

Risk factors for atherosclerosis and IHD

A
Family hx
Age
Men>women
Hypercholesterolemia 
Diet
Smoking
DM 
Lack of exercise
Obesity 
Stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Clinical syndromes of IHD

A
  1. Acute coronary syndromes:
    a. Angina pectoris (stable, prinzmetal, or unstable)
    b. MI
    c. Sudden cardiac death
  2. Chronic IHD, resulting in HF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Substernal or precordial chest pain from transient myocardial ischemia lasting from 15 seconds to 15 minutes

A

Angina pectoris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Angina pectoris is most common in ____. Pain is described as ____

A
  1. Middle aged and older males (women are usually affected after menopause)
  2. Constricting, squeezing, choking, or knife-like. May radiate, or may be diffuse. Not related to breathing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the most common variant of angina?

A

Stable angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Angina with exercise, excitement, or other sudden increase in cardiac load with subsequent in trade in demand for blood flow.

A

Stable angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

True or false:

Myocardial ischemia is usually irreversible

A

False

Only irreversible if there is myocyte necrosis. Otherwise it is reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
\_\_\_\_ angina is usually associated with >70% chronic stable stenosis of a coronary a. 
It is (usually/not usually) associated with plaque disruption. And (is/is not) relieved with rest or a vasodilator.
A

Stable
Not usually
Is

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Within a year of dx, how many people with stable angina will develop unstable angina or MI?

A

20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Episodic angina at rest due to intense coronary a. vasospasm. Unrelated to exercise, heart rate, or BP

A

Variant (Prinzmetal) Angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Variant (Prinzmetal) Angina typically responds to ___

A

Nitroglycerin (vasodilator)

Ca channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Things that can cause vasospasms

A

Primary Raynaud disease
A lot of vasoactive mediators
Elevated TSH
Autoantibodies and T cells in scleroderma
Extreme psycho stress and release of catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Occurs with progressively lower levels of physical activity or at rest
Increases in frequency over time
Often of prolonged duration

A

Unstable (Crescendo) Angina

Aka Preinfarction Angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Unstable (Crescendo) Angina is usually caused by ___

A

Disruption of plaque and superimposed partial thrombosis and possibly embolization or vasospasm or both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Sequence of events in coronary a. occlusion

A
  1. Sudden change in atheromatous plaque
  2. Collagen exposed, causing platelet adhesion and aggregation to form thrombus
  3. Vasospasm
  4. Tissue factor activates coag pathway, increasing size of thrombus
  5. Thrombus evolves to occlude lumen
  6. Occlusion causes ischemia, dysfunction, and potentially myocyte death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Vasospasm is initiated by ___

A

Mediators from platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Prolonged ischemia for greater than ___ causes damages to microvasculature

A

1 hour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Reperfusion injury probably results from ___.

A

Free radical damage to the microvascular circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Potential complications of MI

A
DARTH VADER
Death
Arrhythmia
Rupture
Tamponade
HF
Valve disease
Aneurysm of ventricle
Dressler's syndrome
Embolism
Recurrence/Regurgitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Progressive congestive heart failure as a result of long term ischemic damage to myocardium.

A

Chronic ischemic heart disease

Aka ischemic cardiomyopathy

21
Q

Chronic ischemic heart disease often results in ___

A

Cardiomegaly
LV hypertrophy
Ventricular dilation
Some degree of obstructive coronary a. atherosclerosis

22
Q

In ___ of sudden cardiac death cases you will see coronary artery atherosclerosis with critical (>___%) stenosis involving one or more of the three major coronary vessels

A

80-90%

75%

23
Q

True or false: most cases of sudden cardiac death are associated with acute MI

24
Q

Sudden cardiac death is thought to result from ___

A

Ischemia-induced myocardial irritability that initiates dangerous arrhythmias

25
___% of sudden cardiac death are of non-atherosclerotic causes
10-20
26
___ is the most common cause of death in adults in the USA
MI
27
Some causes of MI
Vasospasm Emboli from left atrium Disorders of coronary arteries
28
___ is an ST elevation infarct | ___ is a non-ST elevation infarct
Transmural infarct | Subendocardial infarct
29
True or false: most MIs are subendocardial infarcts
False. Most are transmural
30
Infarct in which ischemic necrosis involves the full thickness of the ventricular wall vs. 1/3 to 1/2 of the wall
Transmural | Subendocardial
31
A subendocardial infarct may result from ___
A thrombus lysed before necrosis that extends across the wall or from prolonged severe hypotension (global).
32
Frequencies of involvement of the three main coronary arteries?
LAD > RCA > Left circumflex
33
Corresponding sites of infarcts for LAD
Anterior wall of LV near apex Anterior portion of ventricular septum And Apex circumferentially
34
Corresponding sites of infarcts for RCA
Inferior/posterior wall of LV Posterior portion of ventricular septum Inferior/posterior RV free wall
35
Corresponding sites of infarcts for left circumflex a.
Lateral wall of LV except at the apex
36
Necrosis is usually complete within ___ after the onset of the severe ischemia
6 hours
37
Location, size; and morphologic features of an infarct depend on:
1. Location, severity, and rate of development of obstruction 2. Size of vascular bed 3. Duration 4. Metabolic/oxygen needs 5. Extent of collateral vessels 6. Vasospasm 7. Rate, rhythm, and blood oxygenation
38
Morphologic changes in infarction: | 1/2-4 hours
Gross: none Micro: none, maybe wavy fibers at border
39
Morphologic changes in infarction: | 4-12 hours
Gross: dark mottling Micro: early coag necrosis, edema, hemorrhage
40
Morphologic changes in infarction: | 12-24 hours
Gross: dark mottling Micro: coag necrosis, wavy fibers, edema fluid, neutrophils
41
Morphologic changes in infarction: | 1-3 days
Gross: dark mottling with yellow-tan infarct center Micro: coag necrosis, loss of nuclei and striations, neutrophils
42
Morphologic changes in infarction: | 3-7 days
Gross: hyperemic border, central yellow-tan softening Micro: disintegration if dead myofibers, dying neutrophils, early phagocytosis of dead cells by macrophages at infarct border
43
Morphologic changes in infarction: | 7-10 days
Gross: max yellow-tan and soft with depressed red-tan infarct margins Micro: phagocytosis of dead cells, granulation tissues at margins
44
Morphologic changes in infarction: | 10-14 days
Gross: red-gray depressed borders Micro: granulation with new vessels and collagen
45
Morphologic changes in infarction: | 2-8 weeks
Gross: gray-white scar Micro: increased collagen decreased cellularity and fewer capillaries
46
Morphologic changes in infarction: | >8 weeks
Gross: scarring complete Micro: dense collagenous scar (blue on trichrome stain)
47
Lab diagnosis of MI: | CPK/CK
- CK-MB in heart (rises within 2-4 hrs peaks at 24 hours - sensitive but not specific - elevated in other stuff too
48
Lab diagnosis of MI: | Troponin
- T and I are specific for cardiac muscle - early phase: release of free cytosolic troponin, detectable in 2-4 hours - late phase: levels peak at 48 hrs, but persist for 10-14 days