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Cardio II > Path-ischemia > Flashcards

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
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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
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3
Q

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

A

Angina pectoris

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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
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5
Q

What is the most common variant of angina?

A

Stable angina

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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

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7
Q

True or false:

Myocardial ischemia is usually irreversible

A

False

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

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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

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9
Q

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

A

20%

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10
Q

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

A

Variant (Prinzmetal) Angina

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11
Q

Variant (Prinzmetal) Angina typically responds to ___

A

Nitroglycerin (vasodilator)

Ca channel blockers

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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

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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

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14
Q

Unstable (Crescendo) Angina is usually caused by ___

A

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

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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
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16
Q

Vasospasm is initiated by ___

A

Mediators from platelets

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17
Q

Prolonged ischemia for greater than ___ causes damages to microvasculature

A

1 hour

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18
Q

Reperfusion injury probably results from ___.

A

Free radical damage to the microvascular circulation

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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
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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

A

False

24
Q

Sudden cardiac death is thought to result from ___

A

Ischemia-induced myocardial irritability that initiates dangerous arrhythmias

25
Q

___% of sudden cardiac death are of non-atherosclerotic causes

A

10-20

26
Q

___ is the most common cause of death in adults in the USA

A

MI

27
Q

Some causes of MI

A

Vasospasm
Emboli from left atrium
Disorders of coronary arteries

28
Q

___ is an ST elevation infarct

___ is a non-ST elevation infarct

A

Transmural infarct

Subendocardial infarct

29
Q

True or false: most MIs are subendocardial infarcts

A

False. Most are transmural

30
Q

Infarct in which ischemic necrosis involves the full thickness of the ventricular wall vs. 1/3 to 1/2 of the wall

A

Transmural

Subendocardial

31
Q

A subendocardial infarct may result from ___

A

A thrombus lysed before necrosis that extends across the wall or from prolonged severe hypotension (global).

32
Q

Frequencies of involvement of the three main coronary arteries?

A

LAD > RCA > Left circumflex

33
Q

Corresponding sites of infarcts for LAD

A

Anterior wall of LV near apex
Anterior portion of ventricular septum
And Apex circumferentially

34
Q

Corresponding sites of infarcts for RCA

A

Inferior/posterior wall of LV
Posterior portion of ventricular septum
Inferior/posterior RV free wall

35
Q

Corresponding sites of infarcts for left circumflex a.

A

Lateral wall of LV except at the apex

36
Q

Necrosis is usually complete within ___ after the onset of the severe ischemia

A

6 hours

37
Q

Location, size; and morphologic features of an infarct depend on:

A
  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
Q

Morphologic changes in infarction:

1/2-4 hours

A

Gross: none
Micro: none, maybe wavy fibers at border

39
Q

Morphologic changes in infarction:

4-12 hours

A

Gross: dark mottling
Micro: early coag necrosis, edema, hemorrhage

40
Q

Morphologic changes in infarction:

12-24 hours

A

Gross: dark mottling
Micro: coag necrosis, wavy fibers, edema fluid, neutrophils

41
Q

Morphologic changes in infarction:

1-3 days

A

Gross: dark mottling with yellow-tan infarct center
Micro: coag necrosis, loss of nuclei and striations, neutrophils

42
Q

Morphologic changes in infarction:

3-7 days

A

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
Q

Morphologic changes in infarction:

7-10 days

A

Gross: max yellow-tan and soft with depressed red-tan infarct margins
Micro: phagocytosis of dead cells, granulation tissues at margins

44
Q

Morphologic changes in infarction:

10-14 days

A

Gross: red-gray depressed borders
Micro: granulation with new vessels and collagen

45
Q

Morphologic changes in infarction:

2-8 weeks

A

Gross: gray-white scar
Micro: increased collagen decreased cellularity and fewer capillaries

46
Q

Morphologic changes in infarction:

>8 weeks

A

Gross: scarring complete
Micro: dense collagenous scar (blue on trichrome stain)

47
Q

Lab diagnosis of MI:

CPK/CK

A
  • CK-MB in heart (rises within 2-4 hrs peaks at 24 hours
  • sensitive but not specific
  • elevated in other stuff too
48
Q

Lab diagnosis of MI:

Troponin

A
  • 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

Cardio II (16 decks)

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