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Cardiovascular > 04.22 - Ischemic HD 2 (Nichols) > Flashcards

04.22 - Ischemic HD 2 (Nichols) Flashcards

1
Q

Stunned Myocytes =

A

Myocytes injured by acute ischemia (look normal microscopically, need time to repair before they work normally again)

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2
Q

3 Different proteins that influence/ compose the mPTP

A

Voltage-dep anion Channel (VDAC), Adenine Nucleotide Translocator (ANT), Cyclophilin D (CypD)

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3
Q

5 Factors that Contribute to Reperfusion Injury:

A

(1) Mitochondrial Dysfunction; (2) Myocyte Hypercontracture; (3) ROS; (4) Leukocyte Aggregation; (5) Platelet and complement activation

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4
Q

5 Major (Jones) Criteria for Dx of Acute Rheumatic Fever

A

Fever, Polyarthritis, Sydenham’s Chorea, Subcutaneous Nodules, Erythema Marginatum

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5
Q

6 Lethal Causes of Chest pain

A

Acute Coronary Syndromes, Pulmonary Embolism, Aortic Dissection, Pneumothorax, Pericardial Tamponade, Mediastinitus

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6
Q

Angina Pectoris

A

Exertional chest pain due to inadequate perfusion, and is typically due to atherosclerotic disease causing greater than 70% fixed stenosis

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7
Q

Aschoff Bodies =

A

Foci of Fibrinoid Necrosis with Histiocytes and Anitschkow cells

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8
Q

Aschoff Body:

A

Microscopic lesion of fibrinoid necrosis w/ histiocytes and Anitschkow Cells

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9
Q

Autocoids released during ischemia that activate G proteins in preconditioning

A

Adenosine, Bradykinin, Opioids

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10
Q

Chordae in Mitral Stenosis

A

Thickened, Retracted, and Fused

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11
Q

Chronic IHD is aka

A

Ischemic Cardiomyopathy

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12
Q

Chronic Rheumatic Heart Disease is more common with

A

Recurrent Carditis, Severe Carditis, and Carditis at an early age

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13
Q

Chronically Ischemic Myocytes, which have cleared cytoplasm due to catabolism of their contractile proteins and need time to regenerate their contractile proteins before they work normally again

A

Hibernating Myocytes

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14
Q

Clinical presentation of classical MI

A

Severe, Crushing substernal chest pain that can radiate to neck, jaw, epigastrium, or left arm

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15
Q

Clinical presentation of Fibrinohemorhagic Pericarditis

A

Anterior Chest Pain and Pericardial Friction Rub

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16
Q

Clumped chromatin resembling caterpillar

A

Anitschkow Cells

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17
Q

Contraction band necrosis

A

Intense eosinophilic bands of hypercontracted sarcomeres are created by an influx of calcium across plasma membranes that enhances action-myosin interactions; In absence of ATP, sarcomeres cannot relax and get stuck in an agonal tetanic state

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18
Q

Do Ventricular Aneurysms usually rupture?

A

No

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19
Q

Epicardial manifestation of underlying myocardial inflammation

A

Fibrinohemorhagic Pericarditis

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20
Q

Fibrin + Platelet thrombi on valves and Aschoff Bodies w/ Anitschkow Cells

A

Microscopic pathology of Acute Rheumatic Heart Disease

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21
Q

Fibrinohemorhagic Pericarditis

A

Epicardial manifestation of underlying myocardial inflammation

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22
Q

Fibroblasts with multiple bodies inside them =

A

Metabolically active, not necessarily pathologic

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23
Q

Foci of Fibrinoid Necrosis with Histiocytes and Anitschkow cells

A

Aschoff Bodies

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24
Q

Gross pathology of Acute Rheumatic Heart Disease

A

Tiny (1-2mm) verrucous vegetations lined up on line of valve closure; Fibrinous pericarditis

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25
Q

Hibernating Myocytes

A

Chronically Ischemic Myocytes; Cleared cytoplasm due to catabolism of contractile proteins; Need time to regenerate those proteins

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26
Q

How common is Myocardial rupture as a complication of MI

A

1-5%, but frequently fatal if occurs

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27
Q

How do leukocytes contribute to ischemia reperfusion injury

A

May occlude microvasculature; Elaborate proteases and elastases

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28
Q

How does complement activation contribute to ischemia reperfusion injury

A

No-reflow phenomenon

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29
Q

How does mitochondrial dysfunction contribute to ischemic injury

A

Alters permeability, apoptotic mediators released from mito

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30
Q

How long before Stunned Myocytes work normally again

A

Several days at least

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31
Q

How often do isolated Right Ventricular Infarcts occur relative to all

A

1-3%

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32
Q

In the vast majority of cases, cardiac ischemia is due to

A

Coronary Artery Atherosclerosis

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33
Q

In whom are silent infarcts more likely

A

DM, Elderly

34
Q

Is classic MI chest pain relieved by Nitroglycerin

A

No

35
Q

Ischemic Preconditioning

A

Resistance to mild-moderate ischemia due to induction of protective proteins by brief episodes of ischemia

36
Q

Light Microscopic appearance of Hibernating Myocytes

A

Myocytolysis

37
Q

Marantic Endocarditis =

A

Nonbacterial Thrombotic Endocarditis

38
Q

Marantic Endocarditis is common with

A

Cancer, DIC, Hypercoagulable states, Long-term venous catheterization

39
Q

Microscopic findings in Chronic IHD

A

Myocardial hypertrophy, Diffuse Subendocardial Myocyte Vacuolization, and Fibrosis from previous infarction

40
Q

Microscopic lesion of fibrinoid necrosis w/ histiocytes and Anitschkow Cells

A

Aschoff Body:

41
Q

Microscopic pathology of Acute Rheumatic Heart Disease

A

Fibrin + Platelet thrombi on valves and Aschoff Bodies w/ Anitschkow Cells

42
Q

Microscopically, irreversibly damaged myocytes subject to reperfusion show

A

Contraction band necrosis

43
Q

Mitral stenosis is almost all

A

Rheumatic, Marked femal predominance

44
Q

Myocardial ischemia leads to loss of myocyte function within

A

1-2 minutes, but causes necrosis only after 20-40 minutes

45
Q

Nonbacterial Thrombotic Endocarditis

A

Marantic Endocarditis =

46
Q

Opening of what is prevented in Ischemic Preconditioning

A

mPTP

47
Q

Overall death rate in first year after MI

A

30%, then 3-4% annually

48
Q

Pathology of Marantic Endocarditis

A

Small (1-5mm) fibrin + platelet thrombi

49
Q

Pathology of Mitral Stenosis

A

Slitlike fishmouth; or Round Buttonhole Stenosis w/ fibrous thickening and rigidity of valve

50
Q

Patients with Anterior Transmural MI’s are at greatest risk for

A

Free Wall Rupture, Expansion, Formation of Mural Thrombi, and Aneurysm Formation

51
Q

Patients with Chronic IHD typically exhibit

A

LV dilation and hypertrophy

52
Q

Patients with Posterior Transmural MI’s are at greatest risk for

A

Serious conduction blocks, RV involvement

53
Q

Presence of Fibroblasts indicates about what age

A

6 days old

54
Q

Primary mechanism of Ischemic Preconditioning

A

Preservation of Mitochondrial function and ATP production

55
Q

Prime target of excess oxygen radicals and calcium is

A

Mitochondrial Permeability Transition Pore (mPTP)

56
Q

Slitlike fishmouth; or Round Buttonhole Stenosis w/ fibrous thickening and rigidity of valve

A

Pathology of Mitral Stenosis

57
Q

Sudden cardiac death usually results from

A

A fatal arrhythmia, typically without significant acute myocardial damage

58
Q

Time course of CK-MB in MI

A

Begins 2-4 hours; Peaks 24-48 hours; normal within 72 hours

59
Q

Time course of Troponin

A

Begins 2-4 hours; Elevated for 7-10 days

60
Q

Tiny (1-2mm) verrucous vegetations lined up on line of valve closure; Fibrinous pericarditis

A

Gross pathology of Acute Rheumatic Heart Disease

61
Q

Unstable Angina Results from

A

Small fissure or rupture of atherosclerotic plaque triggering platelet agg, vasoconstriction, and formation of mural thrombus

62
Q

What accounts for the vast majority of MI-related deaths before hospitalization

A

Lethal Arrhythmias

63
Q

What causes mycocyte hypercontracture in ischemia

A

Ca increased; After reperfusion, contraction is uncontrolled and causes damage

64
Q

What is result of ROS and Ca binding mPTP

A

Opening –> Collapsing mitochondrial function

65
Q

What is the mPTP

A

Mitochondrial Permeability Transition Pore: V-dependent channel regulated by Ca and Oxidative stress

66
Q

What is the precursor for infective endocarditis

A

Marantic Endocarditis

67
Q

What large influx occurs in Reperfusion injury

A

Calcium

68
Q

What layers are inflamed in Acute Rheumatic Heart Disease

A

All

69
Q

What percent of MI’s result in rhythm disturbance

A

90% (higher in stemis vs non-stemis)

70
Q

What percent of ventricle must be affected in MI to cause cardiogenic shock

A

40%

71
Q

When does myocardial rupture occur?

A

3-7 days after infarction

72
Q

When does pericarditis occur in timeline after MI

A

2-3 days, then usually gradually resolves

73
Q

When does Ventricular Aneurysm occur in timline after MI

A

Late

74
Q

When is serious arrhythmia risk highest in timeline of MI

A

In first hour then declines

75
Q

Where is Marantic Endocarditis most common:

A

First: Atrial Side of Mitral Valve; Ventricular side of Aortic Vavle

76
Q

Which has worse prognosis: anterior or posterior infarct

A

Anterior

77
Q

Which is more sensitive in early stages of MI: CK-MB or Troponin?

A

Equal

78
Q

Why are Anitschkow Cells also called caterpillar cells

A

Clumped chromatin resembling a caterpillar

79
Q

Why can large infarct cause hemiparalysis and when does it usually occur

A

Embolus from Mural Thrombus, day 7

80
Q

Why do myocardial ruptures occur 3-7 days after infraction

A

Time in healing process when lysis of myocardial CT is maximal, and when much of infarct has been converted to soft, friable granulation tissue

Cardiovascular (18 decks)

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