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1 STEP Cardio pathology > Ischemic diseases and MI pathology 12/02 > Flashcards

Ischemic diseases and MI pathology 12/02 Flashcards

1
Q

In what states there are no cells necrosis?

A

Stable angina, unstable angina, prinzmetal angina.

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2
Q

Which states ar primary to chest pain, which secondary? What mechanisms?

A

Primary - ischemic myocardium, e.i. unstable angina.
Secondary - due to coronary narrowing or spasm, e.i. stable angina (secondary to atherosclerosis) and prinzmetal/vasospastic angina.

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3
Q

Which state is in 70proc. occlusion?

A

Stable angina.

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4
Q

Which state is in incomplete occlusion?

A

Unstable angina.

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5
Q

Which state is in complete occlusion?

A

MI.

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6
Q

Which state is caused by exertion?

A

Stable angina.

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7
Q

Which state is caused by emotional stress?

A

Stable angina.

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8
Q

Which state is caused at rest?

A

Unstable angina.

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9
Q

Which state is episodic and not related to exertion?

A

Prinzmetal angina.

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10
Q

Subendocardial ischemia causes ST…………….

A

Depression.

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11
Q

Transmural ischemia causes ST …………….

A

Elevation.

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12
Q

Which angina has ST depression and which elevation?

A

Depression - stable and unstable.

Elevation - prinzmetal.

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13
Q

Which angina has subendocardial ischemia?

A

Stable and unstable angina.

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14
Q

Which angina has transmural ischemia?

A

Prinzmetal.

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15
Q

Which angina has high risk of progression to MI?

A

Unstable.

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16
Q

Which angina is relieved by nitroglyrecin?

A

Stable, unstable and prinzmetal.

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17
Q

Which angina is relieved by CCB?

A

Prinzmetal angina. (because of smooth muscle relaxation).

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18
Q

Which angina is relieved by rest?

A

Stable angina.

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19
Q

Smoking is a risk factor, hypertension and hypercholesterolemia are not. What type of angina?

A

Prinzmetal.

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20
Q

What are 4 risk factors for prinzmetal angina?

A

Smoking, cocaine, alcohol, triptans.

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21
Q

Treatment of stable angina?

A

Rest, Nitroglycerine.

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22
Q

Treatment of unstable angina?

A

Nitroglycerine.

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23
Q

Treatment of prinzmetal angina?

A

Nitroglycerine, CCB, smoking cessation.

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24
Q

What type ischemia and ECG changes are at stable angina?

A

Subendocardial. ST depression.

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25
Q

What type ischemia and ECG changes are at unstable angina?

A

Subendocardial. ST depression and/or T wave inversion.

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26
Q

What type ischemia and ECG changes are at vasospastic angina?

A

Intramural. ST elevation.

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27
Q

How long last ST elevation and prinzmetal angina?

A

Transient.

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28
Q

Is there increase of biomarkers in angina?

A

No.

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29
Q

What other part of ECG is affected in unstable angina?

A

T wave. It can be conversed with ST depression or only its conversion.

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30
Q

Clinical symptoms of stable angina.

A

Pain <20 min, radiates to left jaw, arm, diaphoresis, shortness of breath.

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31
Q

What is principle of Coronary steal syndrome?

A

Shunted artery –> bellow it decreases pressure, artery dilates –> from good perfused arteries via collaterales blood goes down to pressure gradient –> dilated artery with decreased perfusion gets blood.

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32
Q

What drugs dilate normal vessels in coronary steal syndrome? How affect vessels?

A

Dipyridamole, regadenoson.

Vasodilation.

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33
Q

How act drugs used in coronary steal syndrome?

A

Dilate normal (not shunted) vessels –> blood goes to good perfused areas, not below shunted artery –> Ischemia in myocardium perfused by stenosed/shunted artery.

34
Q

How is diagnosed coronary steal syndrome?

A

Pharmacologic STRESS TEST with coronary vasodilator, e.i. dipyridamole, regadenoson.

35
Q

What changes in ECG are seen in coronary steal syndrome stress test?

A

ST segment depression.

36
Q

What is the main reason of sudden cardiac death?

A

Ventricular artthythmia (VF).

37
Q

What disease cause 70-90proc. of sudden cardiac death?

A

CAD/atheroslerosis.

38
Q

What are 5 causes of sudden cardiac death?

A

CAD, cardiomyopathy (dilated, hypertrophic), cocaine abuse, MV prolapse, hereditary ion channelopathies (long QT syndrome, Brugada syndrome).

39
Q

What prevents sudden cardiac death?

A

ICD - implantable cardioverter defibrillator.

40
Q

What is chronic ischemic heart disease? What is the outcome?

A

Poor myocardial function due to chronic ischemic damage. Progress to CHF.

41
Q

NSTEMI. How many wall is affected, what is ECG change?

A

Subedocardial (inner 1/3 wall). ST depression.

42
Q

STEMI. How many wall is affected, what is ECG change?

A

Transmural (full thickness). ST elevation, Q waves.

43
Q

When are indicated cardial biomarkers?

A

in MI. Not in Angina.

44
Q

Common occluded coronary arteries.&raquo_space;>

A

LAD>RCA>circumflex.

45
Q

Symptoms of MI.

A

Severe, crushing retrosternal pain. Pain in left arm, jaw, shoulder, back. Pain longer than 20 min. Nausea, vomiting, fatigue. Diaphoresis, shortness of breath. Nitroglycerin doesn’t relieve symptoms.

46
Q

In what disease there is cell necrosis?

A

MI.

47
Q

What is the main cause/mechanism of MI?

A

Rupture of atherosclerotic plaque –> COMPLETE obstruction of a coronary artery.

48
Q

What 4 causes of MI?

A

Rupture of atherosclerotic plaque, vasospasm (Prinzmetal, cocaine abuse), emboli, vasculitis (Kawasaki disease).

49
Q

What part of the heart is usually involved in MI?

A

Left ventricle.

50
Q

What parts are affected by LAD occlusion?

A

Anterior wall and anterior septum of LV.

51
Q

What parts are affected by RCA occlusion?

A

Posterior wall and posterior septum. PAPILLARY MUSCLES of LV.

52
Q

What artery occlusion cause rupture of LV papillary muscles?

A

RCA.

53
Q

What parts are affected by LCX occlusion?

A

Lateral wall of LV.

54
Q

What changes of myocardium are in initial phase of MI?

A

Subendocardial necrosis. ST depression.

55
Q

What changes of myocardium are in continued or severe phase of MI?

A

Transmural necrosis. ST elevation.

56
Q

What necrosis (myocardial wall) is in severe MI?

A

Transmural.

57
Q

What is gold standart cardiac enzyme for MI?

A

Troponin I.

58
Q

What are 2 main cardiac enzymes in MI?

A

Troponin I and CK-MB.

59
Q

When is Troponin I rise?

A

Rise after 2-4h after MI, peak after 24. Return to normal after 7-10 days.

60
Q

When is CK-MB rise?

A

After 4-6h (6-12h FA). Peak after 24h, returns to normal by 72h (48 FA).

61
Q

Why is CK-MB important?

A

Useful in diagnosing reinfarction following acute MI, because levels return normal after 48 h FA (by 72h in Pathoma).

62
Q

What are changes <4h from MI?

A

No gross or micro.

63
Q

What are complications 0-24 hours from MI?

A

Cardiogenic shock (massive MI), CHF, ventricular arrhythmia.

64
Q

What are changes 4-24h from MI?

A

Gross - dark discoloration/mottling. Micro - coagulative necrosis. Necrotic cell contents in blood. Edema, hemorrhage, wavy fibers. Appear neutrophils.

65
Q

What are complications 4-24h from MI? ISTRTINTI, Palikti 0-24, kur kardiogeninis sokas etc

A

Arrhythmia.

66
Q

What are changes 1-3 days from MI?

A

Gross - yellow pallor; hyperemia. Micro - Extensive coagulative necrosis. Acute infl. with Neutrophils.

67
Q

What are complications 1-3 days from MI?

A

Fibrinous pericarditis (chest pain with friction rub).

68
Q

What are changes 3-7 days from MI? ISTRINTI SITA

A

Gross - yellow pallor. Micro - Macrophages.

69
Q

What are complications 3-14 days from MI?

A

Ventricular wall rupture –> tamponade.
Papillary muscule rupture –> mitral regurgitation/mitral insufficienty.
Intraventricular septum rupture –> shunt.
LV pseudoaneurysm –> risk of rupture.

70
Q

What causes interventriculat septum rupture in MI?

A

It’s macophage mediated structural degradation.

71
Q

What are complications 3-14 days from MI?

A

Ventricular wall rupture –> tamponade.
Papillary muscule rupture –> mitral regurgitation/mitral insufficienty.
Intraventricular septum rupture –> shunt.
LV pseudoaneurysm –> risk of rupture.

72
Q

What are changes 3-14 days from MI?

A

Gross - hyperemic border; central yellow-brown softening. Micro - granulation tissue at margins with: fibroblasts, collagen and blood vessels.

73
Q

What are changes 2 weeks to several months from MI?

A

Gross - white scar. (+recanalized arteries).

Micro - fibrosis (completed scar).

74
Q

What are complications 2 weeks to several months from MI?

A

Dressler syndromes, HF, arrhythmis, true ventricular aneurysm (risk of mural thrombus).

75
Q

What leads change in Anteroseptal STEMI?

A

V1-V2

76
Q

What leads change in Anteroapical STEMI?

A

V3-V4

77
Q

What leads change in Anterolateral STEMI?

A

V5-V6

78
Q

What leads change in Lateral STEMI?

A

I, aVL.V5-V6

79
Q

What leads change in Inferior STEMI?

A

II, III, aVF.

80
Q

What leads change in Posterior STEMI?

A

V7-V9, ST depression in V1-V3 with tall R waves.

81
Q

Treatment of acute coronary syndromes.

A

Unstable angina/NSTEMI - anticoagulants (heparin), antipltelets (aspirin), ADP inhibitoriai (clopidogrelis), Beta blockers, ACE inhibitors, Statins. Symptoms controled with nitroglycerine and morphine.

STEMI - same as above, but reperfusion therapy is most important.

1 STEP Cardio pathology (8 decks)

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