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Cardiovascular > 04.21 - Ischemic HD 1 (Nichols) > Flashcards

04.21 - Ischemic HD 1 (Nichols) Flashcards

1
Q

Ischemic Cardiac myocytes die after about

A

20 minutes

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2
Q

___ often triggers the acute coronary syndromes

A

Thrombosis associated with a disrupted plaque

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3
Q

2/3 of ruptured plaques are ___ stenotic or less before rupture

A

50% (so they would be asymptomatic)

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4
Q

3 Components of Coag Necrosis

A

(1) Loss of Normal Cytoplasmic Striations; (2) Cytoplasmic Hypereosinophilia; (3) Nuclear changes

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5
Q

4 features that are “more” in Reperfusion MI

A

Contraction Band Necrosis, Macrophages, Interstitial Fibrosis, Patchy

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6
Q

90% of Transmural MI’s are associated with

A

Occlusive thrombosis superimposed on athersclerotic plaque with an acute change (disruption of plaque)

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7
Q

Acute Coronary Syndrome is applied to

A

Any of the 3 catastrophic manifestations of IHD: Unstable Angina, Acute MI, and SCD

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8
Q

Additional benefit of statins in CAD and IHD

A

Reduce plaque inflammation and increase stability

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9
Q

Are myocytes with Myocytolysis viable?

A

Yes, can be (but less effective)

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10
Q

Asystole from MI is usually preceded by

A

V Tach, then V Fib

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11
Q

By 12-24 hours, infarct can be grossly ID’d how?

A

Red-blue discoloration caused by stagnated, trapped blood

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12
Q

Cardiac Rupture is more common in

A

Females, Older patients, Hx of HTN, first MI, Anterior Wall

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13
Q

Clinically significant coronary plaques tend to occur

A

first few cm’s of LAD and LCX, and entire legnth of RCA

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14
Q

Colors of Acute, Subacute, and Old MI

A

Light brown, tain; Yellow; White

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15
Q

Critical Stenosis

A

70% of lumen

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16
Q

Cut off for gross appearance of MI (no stain)

A

12 hours

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17
Q

Dead myocytes in classic MI show what type of necrosis?

A

Coagulative

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18
Q

Death of myocytes in transmural MI starts

A

in the Subendocardial Zone, spreads to Subepicardial Zone

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19
Q

Earliest finding of Classic MI

A

Thin Wavy Myocytes (30minutes)

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20
Q

ECG evidence of Ischemia includes

A

ST-segment elevation and T-Wave Inversion

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21
Q

Explanantion for why incidence of MI is highest between 6am-12pm

A

Adrenergic stimulation with waking

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22
Q

Extensive Nuclear Dust is a feature of infarcts of what age

A

3-6 days old

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23
Q

Fissure frequently occur at

A

junction of fibrous cap and adjacent normal plaque-free arterial segment

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24
Q

Fixed obstructions that occlude less than __ of a coronary vessel lumen tend to be asymptomatic

A

70%

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25
Q

How does Myocardial Ischemia contribute to arrhythmias

A

Electrical Instability

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26
Q

How early can thin wavy myocytes appear as evidence of MI

A

30 minutes

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27
Q

How long before dead cardiac muscle shows macroscopic manifestations of death?

A

12 hours

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28
Q

How long does death of myocytes take in Transmural MI

A

3 hours

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29
Q

How long does it take for dead myocytes to show microscopic evidence of death?

A

4 hours

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30
Q

How much of ventricular thickenss has to be affected to classfiy as transmural

A

50%

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31
Q

I, aVL, V5-V6

A

Lateral: Left Circumflex

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32
Q

IHD is usually synomous with

A

CAD, unless otherwise specified

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33
Q

II, III, aVF localize MI to where?

A

Inferior: Right Coronary

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34
Q

In more than 90% of cases, IHD is a consequence of

A

Reduced Coronary Blood Flow secondary to obstructive atherosclerotic vascular disease

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35
Q

In most patients, unstable angina, infarction, and often SCD occur b/c of

A

Abrupt plaque change followed by thrombosis

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36
Q

Leading cause of mortality in US and developed nations

A

Ischemic HD

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37
Q

Most common cause of death in elderly women?

A

IHD (menopause, and decline in estrogen, exacerbates CAD)

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38
Q

Myocyte death leads to what type of necrosis

A

Coagulative

39
Q

Myocytolysis

A

Cytoplasmic clearing of contractile proteins; Seen in Thin Subendocardial layer of cardiac myocytes after infarct

40
Q

Occlusion of what coronary artery is most often responsible for MI

A

LAD (40-50%)

41
Q

Organizing thrombi produce potent activators of

A

SM proliferation

42
Q

Pain of Stable Angina

A

Crushing or squeezing, often radiating down left arm

43
Q

SCD in setting of myocardial ischemia is most often due to

A

V Fib caused by Myocardial Irritability (80-90% of cases)

44
Q

Severe ischemia lasting at least ___ causes irreversible damage

A

20-40 mintues

45
Q

Subendocardial Infarction vs Transmural

A

More likely to be patchy, have episodic extension, becoming more common

46
Q

Sudden Cardiac Death most commonly results from

A

a lethal arrhythmia without myocyte necrosis

47
Q

T/F: HF from MI is often sudden

A

False, rarely sudden

48
Q

T/F: Left and Right ventricular infarcts occur at comparable frequency

A

False, isolated right 1-3%

49
Q

T/F: Once an MI is healed, it is impossible to distinguish its age

A

True can be 8 weeks or 10 years old

50
Q

T/F: Plaque ruptures are often predicatble

A

FALSE

51
Q

T/F: Prinzmetal angina always occurs at atherosclerotic plaques

A

FALSE

52
Q

T/F: significant atherosclerosis and thrombosis of penetrating coronaries is also relatively common

A

FALSE

53
Q

T/F: Women have higher risk of MI during reproductive years?

A

False, protective effect

54
Q

The PDA usually arises from which other artery

A

RCA (90%), or LCX

55
Q

The vast majority of MI’s are caused by

A

Acute Coronary Thrombosis

56
Q

Typcial ECG findings in Subendocardial Infarctions

A

Typically do not have ST elevation or Q waves

57
Q

Typical ECG findings in Transmural Infarctions

A

STEMI, negative Q wave, loss of R wave amplitude

58
Q

V1-V4 localize MI to where?

A

Anterior: LAD

59
Q

Vacuolated (cleared) cytoplasm =

A

Myocytolysis

60
Q

What causes destabilization of atherosclerotic plaque

A

Macrophage Metalloproteinase Secretion

61
Q

What causes Myocyte Vacuolization

A

Sublethal ischemia

62
Q

What color is a Subacute MI

A

Yellow

63
Q

What color is an Acute MI

A

Light brown to tan

64
Q

What color is an old MI

A

White

65
Q

What determines dominant vessel of heart

A

The one, either RCA or LCX, that gives of the PDA

66
Q

What does Coagulation necrosis look like histologically

A

Hypereosinophilia, Loss of Striations, Nuclear Chanes

67
Q

What is becoming more common than Transmural MI

A

Subendocardial Infarction

68
Q

What is Prinzmetal Angina

A

Caused by vessel spasm

69
Q

What is stable angina

A

Occuring predictably at certain levels of exertion

70
Q

What is the widow maker lesion

A

Occlusions in Left Main

71
Q

What is unstable angina

A

Occurs with progressively less exertion or even at rest

72
Q

What leads localize to LAD MI

A

V1-V4

73
Q

What leads localize to Left Circumflex (Lateral) MI?

A

I, AVL, V5-V6

74
Q

What leads localize to Right Coronary (Inferior) MI?

A

II, III, aVF

75
Q

What percent stenosis causes Unstable Angina

A

90%

76
Q

What serves as nidus for thrombus generation in most instances of MI

A

Disruption of pre-existing athersclerotic plaque

77
Q

What type of myocytes may be visible as early as half hour after infarct?

A

Dead thin wavy

78
Q

What types of plaques are more likely to rupture

A

Large atheromatous cores, or have thin overlying fibrous caps

79
Q

When are features of Coag Necrosis visible microscopicaly

A

4-12 hours

80
Q

When are infarcts ringed by hyperemic granulation tissue

A

10-14 days

81
Q

When can MI’s be visualized grossly with vital stain

A

3 hours (LDH stain)

82
Q

When do Fibroblasts first enter in Classic MI

A

Day 4

83
Q

When do Lymphocytes first enter in Classic MI

A

day 2

84
Q

When do Macrophages first enter in classic MI

A

day 3

85
Q

When do neutrophils in acute MI begin contributing their breakdown debris

A

After a few days

86
Q

When does Acute Neutrophilic Response to Acute MI reach maximum

A

Around 2 days

87
Q

When does neovascularization occur in Classic MI?

A

Day 4, same as fibroblasts

88
Q

When is acute inflammation most prominent following MI

A

1-3 days after

89
Q

When is Cardiac Rupture most common following MI

A

5th day

90
Q

When is granulation tissue replacement most prominent

A

1-2 weeks after

91
Q

When is Neutrophilic Infilatration visible following Classic MI

A

6-12 hours

92
Q

When is wave of macrophages most prominent following MI

A

5-10 days after

93
Q

Where is the fibrous cap the thinnest

A

Junction of fibrous cap and adjacent normal plaque-free arterial segment

94
Q

Which are more affect by MI: blacks or whites?

A

Equal

Cardiovascular (18 decks)

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