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Cardiology Exam III > Pathology: Ischemic Heart Disease > Flashcards

Pathology: Ischemic Heart Disease Flashcards

1
Q

Ischemic heart disease is also known as?

A

Coronary artery disease

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2
Q

This is an imbalance between supply (due to coronary artery stenosis or decreased PO2) of oxygenated blood to the heart and demand of oxygenated blood (increased by myocardial hypertrophy or tachycardia)

A

Ischemic heart disease

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3
Q

What does ischemic heart disease present as?

A

MI, angina pectoris, chronic IHD with heart failure, sudden cardiac death

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4
Q

What is the difference between infarction and ischemia?

A

Infarction is tissue death, while ischemia presents as pain because the heart isn’t getting the oxygen that it needs

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5
Q

What are the 2 mechanisms of insufficient coronary perfusion relative to myocardial demand? (IHD syndromes)

A
  1. Chronic progressive atherosclerotic narrowing of the epicardial coronary arteries (luminal size is narrowed)
  2. Variable degrees of superimposed acute plaque change, thrombosis, and vasospasm
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6
Q

What percentage of luminal obstruction has to be present to cause chronic stable angina (chest pain with exercise)?

A

75% or greater

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7
Q

What type of angina presents with 90% of luminal obstruction?

A

Chronic unstable angina (pain at rest)

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8
Q

What type of circulation can help combat the effects of ischemia and infarction to a certain extent?

A

Collateral

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9
Q

This type of angina is associated with pain during exercise

A

Stable angina

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10
Q

True for False: Stable angina is associated with plaque disruption

A

FALSE: Stable angina is usually not associated with plaque disruption

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11
Q

This type of angina is associated with plaque rupture complicated by a partially occlusive thrombosis and vasoconstriction causing pain at rest and of increasing frequency

A

Unstable angina

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12
Q

What is the mechanism of a MI?

A

Acute plaque change inducing total thrombotic occlusion causing ischemia and necrosis of the myocardium… death of heart muscle!

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13
Q

What is the common pathophysiologic basis for most instances of angina, MI, and sudden cardiac death?

A

Coronary atherosclerotic plaque disruption, thrombus formation, and myocardial ischemia

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14
Q

This is failure to deliver adequately oxygenated blood to tissues

A

Hypoxemia

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15
Q

This is hypoxemia along with inadequate removal of metabolites

A

Ischemia

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16
Q

Can you have hypoxemia by itself?

A

YES

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17
Q

Can you have ischemia without hypoxemia?

A

NO, ischemia includes hypoxemia

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18
Q

This type of MI involves necrosis of the full thickness of the ventricular wall

A

Transmural MI

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19
Q

This type of MI follows the distribution of a single coronary artery (often LAD, left circumflex, or RCA)

A

Transmural MI

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20
Q

In this type of MI, you have a thrombus that is superimposed on plaque resulting in complete occlusion and full thickness death

A

Transmural MI

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21
Q

A subendocardial MI is limited to what part of the ventricular wall?

A

Inner 1/3 to inner 1/2

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22
Q

Does a subendocardial MI follow the distribution pattern of a single coronary artery

A

NO, it may extend laterally beyond the distribution of the involved coronary artery

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23
Q

This type of MI is due to incomplete occlusion, with or without vasospasm

A

Subendocardial MI

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24
Q

Besides subendocardial MI, what other problems can be caused by incomplete occlusion with or without vasospasm?

A

Angina and sudden cardiac death

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25
Q

What causes a subendocardial MI?

A

This area is least well perfused (relies on diffusion of oxygenated blood from ventricular space)

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26
Q

Does the systemic BP increase or decrease with a subendocardial MI?

A

It decreases!

The thrombus is lysed before necrosis extends across the whole wall… this causes drop in systemic BP

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27
Q

Do you want a subendocardial MI or a transmural MI?

A

Neither, DUH… but if you had to choose you want a subendocardial one

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28
Q

What causes death of cardiac muscle?

A

Prolonged severe ischemia

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29
Q

If you have a MI in someone under 40, what might you be thinking caused it?

A

COCAINE

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30
Q

Are men or women at higher risk for MI?

A

MEN, but once women go through the change of life, their risk shoots up with rapid development of CAD (they loose the protective effects of estrogen)

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31
Q

Evolution of an MI

A
  1. Sudden change in atheromatous plaque exposes subendothelial collagen and necrotic plaque contents
  2. Platelets come to play (form microthrombi) and cause vasospasm stimulated by mediators released from platelets (TXA2- Vasoconstricts)
  3. Tissue factor activates the coagulation pathway
    With this, the thrombus evolves and occludes vessel lumen
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32
Q

What defines granulation tissue?

A

Edema, neovascularization, fibroblast deposition

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33
Q

What happens grossly and microscopically at 1/2-4 hours post-MI

A

Gross: Nothing (might see yellow-white area of dead tissue with a TTC stain)
Microscopic: Wavy fibers at borders

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34
Q

At this timepoint, you see gross mottling and microscopic necrosis, edema, and hemorrhage

A

4-12 hours

35
Q

What is characteristic of 12-24 hours post-MI grossly and microscopically?

A

See gross mottling that is red-blue and microscopic pyknosis, hypereosinophilia, and few neutrophils

36
Q

At this time-point, the heart has a grossly yellow-tan center with neutrophils and loss of nuclei and striations seen microscopically

A 
1-3 days
Complete necrosis (it's yellow) of the tissue, doesn't look like a heart anymore
37
Q

At 3-7 days, what do you see post-MI?

A

Grossly: Hyperemic border, central yellow-tan softening
Microscopically: Phagocytosis at borders, disintegration of myofibers and dying neutrophils

38
Q

At this time-point you have a depressed red-tan margin with a soft yellow-tan center and early granulation tissue (edema, neovascularization, fibroblast formation) with widespread phagocytosis

A

7-10 days

39
Q

What is seen at 10-14 days?

A

A depressed red-gray border with granulation tissue, neovascularization, and collagen

40
Q

When do you see a gray-white scar with collagen deposition and less ceullular?

A

2-8 weeks

41
Q

Characteristics of a healed MI?

A

Fibrotic scar with lots of collagen deposition
Myocytes still present have no structure
Lots of collagenous tissue

42
Q

What is it called when infiltrating leukocytes generate oxygen free radicals causing apoptosis and microvascular injury (hemorrhage and endothelial cell swelling)?

A

Reperfusion injury!

43
Q

What do you see with reperfusion injury

A

Contraction band necrosis

44
Q

When do half of all deaths associated with acute MI occur?

A

Within one hour of onset

45
Q

What are indicators of poor prognosis?

A

Advanced age, female, DM, previous MI

46
Q

What % of patients die within first year (mortality)?

A

30%

47
Q

What % of patients experience complications post-MI?

A

75%

48
Q

This term refers to diseases that evolve as a result of another disease process that has occurred.

A

Morbidity

49
Q

What’s mortality?

A

DEATH

50
Q

What complication of MI causes partial LV failure with hypotension, pulmonary vascular congestion, with or without pulmonary edema?

A

Contractile dysfunction

51
Q

What can contractile dysfunction lead to?

A

Cardiogenic shock or severe pump failure

52
Q

When do you see rupture in the ventricular wall post-MI?

A

3-7 days after the MI

53
Q

What can hemopericardium lead to?

A

Cardiac tamponade, which can cause rupture in ventricular wall

54
Q

A rupture in the ventricular septum causing a left to right shunt can cause?

A

Murmur and CHF

55
Q

Mitral regurgitation can result from?

A

Rupture of the papillary muscle

56
Q

When is it common to see pericarditis?

A

2-3 days after a transmural MI

-Usually resolves

57
Q

When will you see a RV infarct?

A

When you have MI of the adjacent, posterior LV and ventricular septum

58
Q

This is new necrosis adjacent to the existing infarct

A

Extension

59
Q

This is stretching, thinning, and dilation of the infarcted region of myocardium

A

Expansion

60
Q

Expansion is seen most often in what type of infarcts?

A

Anteroseptal

61
Q

What is the mechanism for mural thrombus formation?

A
  1. Focal abnormality in contractility causing stasis

2. Endocardial damage creating a thrombogenic surface

62
Q

This can result from a large anteroseptal MI that has undergone expansion.

A

Ventricular aneurysm

63
Q

Is a ventricular aneurysm at risk for rupture?

A

NO, its made of a fibrotic layer (scar tissue) with lots of fibroblasts

64
Q

So what’s the problem with ventricular aneurysm?

A

It is stiff and doesn’t move/contract how it should

This can cause mural thrombus formation, arrhythmias, and heart failure

65
Q

Dysfunction of what can cause mitral regurgitation?

A

Papillary muscle (acute rupture of this)

66
Q

This is exhaustion of the compensatory hypertrophy of viable myocardium.

A

Cardiac decompensation

67
Q

Cardiac decompensation can lead to?

A

Slow progressive onset of CHF post MI (can lead to cardiac transplant)

68
Q

What is the mechanism of sudden cardiac death most often?

A

Lethal arrhythmia

69
Q

What can help the prognosis of sudden cardiac death?

A

Implantation of an automatic defibrillator

70
Q

Congential structural abnormalities, aortic valve stenosis, mitral valve prolapse, myocarditis, dilated or hypertrophic cardiomyopathy, pulmonary HTN, hereditary or acquired abnormalities of conduction system, isolated hypertrophy due to HTN are cases you can see what complication in?

A

Sudden cardiac death

71
Q

What is an independent risk factor for sudden cardiac death due to increased demand?

A

Increased cardiac mass

72
Q

What size should the right ventricle be?

A

0.5 cm or less

73
Q

What size should the left ventricle be?

A

1.5 cm or less

74
Q

At what measurement can you say a ventricle is hypertrophied?

A

2cm

75
Q

What percentage of sudden cardiac death is due to ischemic heart disease?

A

80-90%

76
Q

What are the 4 most important treatable risk factors for atherosclerosis

A

Smoking, HTN, DM, hypercholesterolemia

77
Q

What does the presence of left ventricular hypertrophy indicate?

A

Long standing HTN

78
Q

What factors determine infarct size and risk for post-MI complications?

A
  1. Size of myocardial bed at risk and its metabolic/oxygen needs
  2. Duration of coronary artery obstruction
  3. Coronary artery anatomy, dominance/collaterals
  4. Site of coronary artery obstruction, severity of obstruction, rate at which obstruction developed
79
Q

What are common complications after MI?

A
  1. Cardiac arrhythmias (75-95%)
  2. Sudden death (20%)
  3. Cardiogenic shock (10-15%)
  4. Left ventricular aneurysm
  5. Mural thrombosis (15-40%)
80
Q

What are uncommon complications of MI?

A

Myocardial rupture, papillary muscle rupture, reinfarction, infarct extension/expansion, postinfarction pericarditis, Dressler syndrome

81
Q

How much myocardium has to be lost before signs and symptoms of cardiogenic sock are seen?

A

> 40% of the left ventricle involved

82
Q

What is the % mortality associated with cardiogenic shock?

A

70%

83
Q

What time after MI are patients at greatest risk for rupture of an acute MI?

A

During the first 3-7 days

See coagulative necrosis, neutrophilic infiltration, and lysis of myocardial connective tissue

Cardiology Exam III (12 decks)

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