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CRRAB 1 > Wk5: Witrak > Flashcards

Wk5: Witrak Flashcards

1
Q

Leading cause of M&M in developed world with 95% due to what

A

Ischemic heart disease; coronary atherosclerosis

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2
Q

What defines an unstable atherosclerotic plaque?

A

risk of rupture with partial or complete lumen occlusion by aggregated platelets/thrombosis

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3
Q

What is acute coronary syndrome?

A

Coronary blood supply is suddenly blocked - either unstable angina or MI

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4
Q

How many minutes of complete ischemia -> myocardial death

A

30 minutes +

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5
Q

EKG changes with subendocardial and transmural infarctions

A

Sub: usually non-STEMI
Transmural: more likely STEMI (older -> Q waves)

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6
Q

Subacute sequelae of MI (days to 2 weeks)

A

Mural thrombosis, LV rupture (free wall, septal, or papillary muscles), fatal hemopericardium, acute VSD, mitral regurg/flail, peri-infarct pericarditis

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7
Q

Chronic sequelae of MI

A

LV aneurysm, chronic CHF, pleural effusions, 2* RV CHF, Dressler’s pericarditis

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8
Q

What is another name for Dressler’s pericarditis, and what is it?

A

Post-cardiac injury syndrome. Believed to be an immune response to damaged tissue after MI, trauma, surgery to pericardium or heart.

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9
Q

How does stable chronic atherosclerotic disease present a risk of sudden death?

A

Sudden/fatal vent dysrhythmia from ischemic aggravation to the conduction system

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10
Q

What causes left-sided hypertensive heart disease? What happens?

A

Chronic systemic (arterial) htn -> concentric LV hypertrophy (free wall >1.5 cm) -> LV failure

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11
Q

Isolated Right Sided hypertensive heart disease (cor pulmonale) cause

A

Inc pulm artery pressure from: 1)chronic pulm parenchymal disease e.g. COPD, fibrosing 2)chronic hypoxia e.g. sleep apnea -> pulm vasoconstriction 3)pulm vasc disease e.g. 1* pulm htn and chronic recurrent thromboemboli

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12
Q

Size of RV free wall in RV hypertrophy

A

Free wall >0.5 cm.

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13
Q

Cause of most RV HF

A

LV HF

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14
Q

Possible causes of aortic valve regurg

A

Thoracic aortic aneurysm -> valves can’t close properly. Aortic dissection.

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15
Q

Causes of AV valve insufficiency

A

CHF -> valve ring dilation, papillary muscle dysfunction from LV ischemia with CAD

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16
Q

Define cardiomyopathy

A

Intrinsic myocardial disease NOT assoc w ischemic, valvular, hypertensive, or structural congen heart disease

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17
Q

What type of cardiomyopathy is essentially 100% genetic/mutational cause

A

Hypertrophic

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18
Q

What is cardiac tamponade?

A

Pericardial fluid critically compresses the heart

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19
Q

What is constrictive pericarditis?

A

progressive pericardial space fibrosis (like a growing scar) -> compression of heart

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20
Q

Causes of pericardial effusion

A

infectious and non-infectious disease, CHF, neoplastic infiltration, uremia

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21
Q

Most primary tumors of the heart are what type?

A

Atrial myxomas, very rare, usually left atrium

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22
Q

Other primary cardiac tumors

A

Rhabdomyomas - children esp tuberous sclerosis (gene defect -> growth of benign tumors). Cardiac sarcomas: very rare, usually lethal.

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23
Q

Are myocytes or the pericardium more likely to be sites of metastases?

A

Pericardium

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24
Q

What O2 sat defines cyanosis

A

<85%

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25
Q

How long does it take a troponin to become positive in AMI? When does it peak, and how long does it persist?

A

2-4 hours to be positive. Peaks ~48 hours. Persists 7-10 days.

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26
Q

How does CK-MB compare to troponin?

A

Also elevated with myocardial necrosis but less specific than trop. Does drop down sooner allowing for detection of a second event.

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27
Q

What causes release of BNP? What are significant lab values?

A

Stretch of myocardium esp LV. 400 HF more likely cause of dyspnea

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28
Q

Main cause of hypercarbia

A

(inc pCO2 @ >45 mmHg): alveolar hypoventilation, usually due to COPD

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29
Q

When can O2 saturation be normal yet the patient is hypoxemic?

A

CO poisoning

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30
Q

AMI mortality within one month

A

30%

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31
Q

How might you get a circumferential LV subendocardial infarct?

A

Global hypotension

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32
Q

What is the immune response to death of cardiac myocytes?

A

Neutrophils within a couple days, fibroblasts in 1.5-3 weeks, collagen scar formation in 4-6 weeks.

33
Q

Possible causes of CHF post infarct

A

1) Perforation of septum -> VSD -> acute CHF. 2) decreased functioning of myocardium due to necrotic regions -> CHF 3) transmural -> scarring -> loss of compliance -> akinetic -> CHF

34
Q

Define systolic and diastolic HF

A

Systolic: low EF. Diastolic: preserved EF but decreased compliance -> can’t relax -> can’t fill appropriately and backs up blood -> pulmonary sx

35
Q

How might diastolic failure lead to a-fib?

A

Associated atrial enlargement -> a-fib

36
Q

Can LVH be reversed?

A

Yes, fairly quickly with control of hypertension

37
Q

What does the LV look like in congenital LVH?

A

Thickening of septum moreso than the free wall.

38
Q

Define cor pulmonarle

A

Right-sided hypertensive heart disease due to chronic hypoxemic pulm disease (e.g. COPD) or pulm htn

39
Q

Causes of valvular stenosis

A

Valvulitis (RF, SLE, RA), congen deform, CALCIFIC degen change, carcinoid syndrome, radiation

40
Q

Commonest cause of mitral stenosis

A

Rheumatic fever

41
Q

2/3 of clinically significant valve disease = acquired aortic or mitral stenosis. Causes?

A

1) gradual obstruction due to post inflam fibrosis/deform (RF, SLE, RA) 2)atherosclerotic or calcific degen (esp AS)

42
Q

What is ankylosing spondylitis?

A

Inflammatory disease -> fusing of vertebrae

43
Q

How are valvular diseases diagnosed?

A

echo

44
Q

What is myxomatous degeneration?

A

Pathological weakening of connective tissues

45
Q

Most common cause of isolated mitral regurg in N Amer requiring surgery

A

Myxomatous degeneration -> ballooning of valve leaflets and elongation of chordae tendinae

46
Q

What is “fish mouth” associated with?

A

A valve with typical rheumatic fever damage

47
Q

Other than IE, what may result in vegetations on heart valves?

A

hypercoagulable state due to malignancy

48
Q

What is systolic click murmur syndrome?

A

Mitral valve prolapse

49
Q

What is dilated CM?

A

Dilated ventricles -> systolic LV dysfunction with decreased LVEF

50
Q

What is hypertrophic CM?

A

Thickened LV wall esp septum with normal to reduced LV chamber size -> diastolic LV dysfunction

51
Q

What is restrictive CM? What causes it?

A

Diastolic LV dysfunction assoc with usually non-dilated, usually non-hypertrophic ventricles due to primary dec in vent compliance.

52
Q

Dilation of atrium = risk for ?

A

Clot formation

53
Q

Dilated CM associated with what

A

Increased cardiac mass, HF symptoms e.g. dyspnea and fatigue, atrial of ventricular arrhythmias, possible sudden death

54
Q

Causes of dilated CM (6)

A

Genetic 20-50%, myocarditis, alc abuse, chemo e.g. doxorubicin, hemochromatosis, peripartum, idiopathic

55
Q

Dilated CM age of onset and mortality

A

Commonly 20-50 y.o. and leading to 50% mortality within 2 years.

56
Q

Treatment for dilated CM

A

Supportive HF measures, possibly a LVAD (for myocardial recovery or bridge to transplant)

57
Q

Commonest cause of hypertrophic CM (specific)

A

Autosomal dominant defect in sarcomeric contractile proteins (60–70%)

58
Q

How does the ventricle appear in hypertrophic CM (specifically)

A

Asymmetrically thickened septum, especially in subaortic/basal region

59
Q

What component of functioning is impaired in hypertrophic CM?

A

Diastolic relaxation/ filling -> limited CO -> inc LVEDP. May have syst murmur due to blood trying to pass by fat septum

60
Q

Top 3 causes of sudden death in young athletes

A
  1. hypertrophic CM 2. anomalous coronary artery origin 3. myocarditis
61
Q

Symptoms of HCM

A

DOE, myocardial ischemia without CAD, risk of a-fib, eventual vent. failure/dilation, vent arrhythmias, sudden death

62
Q

How does LVH appear when due to inc BP or aortic stenosis

A

Usually concentric thickening

63
Q

Treatment for hypertrophic CM

A

Beta blockers, occasionally partial septal ablation

64
Q

How does restrictive CM present?

A

Manifests as right HF. Systolic fx usually normal early.

65
Q

A few causes of RCM

A

Familial, amyoidosis, diabetic CM, sarcoidosis, chemo (esp anthracyclines), metabolite deposition from inborn errors of metab, radiation fibrosis

66
Q

What is arrhythmogenic RV CM? What causes it?

A

Autosomal dominant. Markedly thinned RV wall with fibroadipose tissue -> conduction disturb -> RV failure

67
Q

What disease is arrhythmogenic RV CM associated with?

A

palmar/plantar hyperkeratosis. The combo = Naxos syndrome

68
Q

Mechanism of stress-induced CM

A

Catecholamine surge -> “myocardial stunning” with transient systolic dys

69
Q

How does stress-induced CM present

A

ischemic heart sx, foci of myocardial necrosis

70
Q

Other causes of CM

A

Pheochromocytoma (adrenal tumor), cocaine use

71
Q

Clinical sequelae of hemochromatosis

A

CM/HF (usually dilated type), conduction disturbance, cirrhosis/hepatoma, endocrine dys, arthritis

72
Q

What effect does excess hemosiderin have on myocytes?

A

Toxicity -> secondary fibrosis

73
Q

How is hemochromatosis diagnosed

A

> 45% transferrin saturation, HFE gene mut, hepatic iron index noted on liver biopsy

74
Q

What occurs in amyloidosis?

A

deposition of amorphous proteinaceous substance that is congo red positive

75
Q

Sequelae of cardiac amyloidosis

A

usually restrictive CM -> HF, low EKG voltage, increased vent thickness, non-dilated LV cavity

76
Q

Most common causes of myocarditis in US

A

Viral: entero, coxsackie B, adenovirus, parvo B19, hep C, HHV-6, CMV, HIV

77
Q

Cause of myocarditis in developing/ endemic latin American countries

A

Chagas: attacks heart and esophagus -> HF + dysphagia

78
Q

Acute HF within weeks of viral prodrome, possibly with CP, arrhythmia, sudden death = classic presentation of ?

A

Myocarditis

79
Q

Most common cause of HF in children

A

myocarditis

CRRAB 1 (12 decks)

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