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Cardiac System Flashcards

1
Q

6 principal mech of cardiovasc pathology

A 
1 Failure to pump (systolic or diastolic)
2 obstruction to flow
3 regurgitant flow
4 shunted flow
5 conduction disorder
6 rupture of heart or vessel
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2
Q

Inadequate myocardial contractile function from IHD or HTN

A

Systolic dysfunction HF

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3
Q

Inability of the heart to relax and fill (massive LVH, myocardial fibrosis, amyloid deposition, constrictive pericarditis)

A

Diastolic dysfunction HF

40-60%

Common in women, elderly, diabetics

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4
Q

CHF pathophy

A 
Dec pumping efficiency
Inc EDV
Inc EDP
Inc Venous pressure
Inadequate CO (forward failure) with 
Congestion of venous circ (backward failure)
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5
Q

Heart failure compensations (3)

A

Frank starling mechanism
Neurohormonal activation
Myocardial structural change

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6
Q

Heart failure is said to be compensated if

A

Dilated ventricle is able to maintain cardiac output

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7
Q

Inc wall tension and O2 req heart unable to propel sufficient blood to meet needs of the body

A

Decompensated

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8
Q

Neurohormonal system

A

NE

RAAS

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9
Q

Pressure overload state anatomic change (HTN valvular stenosis)

A

Parallel addition of sarcomeres - concentric hypertrophy

Inc wall thickness without inc in chamber size

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10
Q

Volume overload (valvular regurg or shunt)

A

Sarcomeres in series

Muscle fiber length inc
Dilation of ventricles

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11
Q

Best measure of hypertrophy in volume overloaded heart

A

Heart weight

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12
Q

Independent risk factor for sudden cardiac death

A

Cardiac hypertrophy

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13
Q

Severe pulmonary hypertension resulting in right sided pathology

A

Cor pulmonare

Isolated RSHF also occur in pulmonic or tricuspid valve disease, CHF, left to right shunt

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14
Q

Passive liver congestion in histology

A

Nutmeg liver

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15
Q

LSHF causes central hypoxia in liver

A

Centrilobular necrosis

Sinusoidal congestion
Severe RSHF cardiac cirrhosis

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16
Q

Hallmark of R sided HF

A

Ankle and pretibial edema

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17
Q

Chronic dilation of left atrium may lead to

A

Afib and stagnat blood formation in appendage leading to thrombi and emboli

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18
Q

MI, Systemic HTN, mitral or aortic valve disease, myocardial disease

systemic hypoperf cause renal and cerebal dysfunction

A

LVHF

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19
Q

LHF, Pulmo HTN, pulmonary valve stenosis

A

RSHF

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20
Q

Most common CHD

A

VSD
ASD
Pulmonary stenosis

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21
Q

CHD arises from faulty embryogenesis during

A

week 3-8

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22
Q

Genetic defect in ASD VSD

A

GATA4

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23
Q

Genetic defect in TOF

A

ZFPM2 or NKX2.5

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24
Q

Hemodynamic consequences in CHD

A

1 right to left shunt
2 left to right shunt
3 obstruction to flow

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25
Q

Most common type of CHD

A

Left to right shunt

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26
Q

Once pulmo HTN develops, structural defects of CHD are

A

irreversible

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27
Q

Reversal of flow shunting of unox blood back to systemic circulation

A

Eisenmenger Syndrome

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28
Q

Abnormal fixed opening in septum that allows unrestricted bf bet atrial chambers

A

ASD

90% ostium secundum

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29
Q

R atrial and ven dilation
R ventricular hypertrophy
Dilation of pulmonary artery
Inc volume overload

A

ASD

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30
Q

5% of defects at lowest part of atrial septum
assoc with mitral and tricuspid valve abn
Close relationship with endocardial cushion

A

Ostium primum ASD

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31
Q

5% located high in atrial septum with anomalous drainage of pulmonary veins into R atrium and SVC

A

Sinus venosus ASD

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32
Q

Most common defect detected in adult

A

ASD

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33
Q

Site of 90% of VSDs

A

Basal membranous

Close spont in childhood

20-30% occur in isolation most with other malf

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34
Q

High pres left to right shunt producing harsh machinery like murmur

Lifesaving if with aortic or pulmonic atresia

A

PDA

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35
Q 
Early cyanosis
Right to Left shunt
Clubbing of fingers (hypertrophic osteoarthropathy)
Polycythemia
Paradox embolization
A

Right to left shunt

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36
Q

Most common cause of cyanotic CHD

A

TOF

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37
Q

4 Cardinal features of TOF

A

VSD
SubPulmonic stenosis (R ventricular outflow ob)
Overriding of the VSD by aorta
RVH

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38
Q

Cardinal features of TOF arise from

A

Anterosuperior displacement of infundibular septum -> abnormal septation

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39
Q

Major site of egress of blood flow from both ventricles

A

Overriding aorta

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40
Q

Severity of TOF depends on

A

pulmonary outflow obstruction

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41
Q

R to L shunt
Dec pulmonary blood flow
Inc aortic volume

A

TOF

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42
Q

Discordant connection of ventricles with vascular outflow

Cyanosis

A

Transposition of Great Arteries

43
Q

Narrowing or constriction of aorta

M>F twice

A

Coarctation of Aorta

44
Q

CoA is assoc

A

Turners syndrome

2 forms

1) infantile
2) adult

45
Q

Narrowing of aortic segment bet l subclavian and ductus arteriosus
Duct is patent
Pulmonary trunk is dilated
RVH

A

Infantile CoA

46
Q

Constriction at tissue ridge adjacent to nonpatent ligamentum arteriosum
Dilated arch
LVH

47
Q

Early cyanosis of lower half of body

A

Preductal Infant CoA

48
Q

Asymptomatic
UE HTN with weak pulses and hypotension in LE
Claudication
Coldness

A

Postductal adult CoA

49
Q

Rib notching in CoA occurs bec

A

exuberant collateral circulation around coarctation develops through enlarged intercostal and internal mammary ITA

50
Q

ACS 3 Catastrophic manifestation

A

1 unstable angina
2 acute MI
3 sudden cardiac death

51
Q

<70% fixed obstruction

A

asymptomatic

52
Q

> 70% occlusion

A

critical stenosis

stable angina

53
Q

occlusion of 90% of lumen

A

unstable angina

54
Q

If chronic, compensatory mechanisms prevent MI like

A

collateral perfusion

55
Q

Destabilization of plaque occurs by

A

Macrophage metalloproteinase secretion

56
Q

Elements contributing to development of coronary atherosclerosis

A

Inflammation
Thrombosis with disrupted plaque
Vasoconstriction

57
Q

Vulnerable plaques have

A

Large atheromatous core

Thin fibrous cap

58
Q

Apart from lowering cholesterol, HMG COA reductase i also

A

Reduce inflammation and inc plaque stability

59
Q

Sudden cardiac death post MI is causes by

A

Ventricular fibrillation

60
Q

Dominance in coronary artery is dictated by

A

the one that gives rise to posterior descending

61
Q

Factors contributing to reperfusion injury (5)

A 
1 mitochondrial dysfunction
2 myocyte hypercontracture
3 free radicals
4 leukocyte aggregation
5 platelet and complement activation
62
Q

Histology of perfused irreversibly damaged myocytes

A

contraction band necrosis

63
Q

Happens 3-7 days post MI most common rupture in

A

Left ventricular free wall

64
Q

90% of MI patients develop

A

Arrhythmia conduction disturbance

65
Q

Most common cause of arrhythmia

66
Q

Ultimate mech of SCD

A

Lethal arrhythmia

67
Q

Criteria for diagnosis of systemic hypertensive heart disease (2)

A

1 LVH in absence of other valvular pathology

2 history or evidence of HTN

68
Q

Pathognomomic of LSHHD

A

LVH with dilation in the long run

Nuclear enlargement and hyperchromasia or boxcar nuclei and intercellular fibrosis

69
Q

Acute cor pulmonale

A

R ventricle dilation

70
Q

Chronic cor pulmonale

A

R ventricle hypertrophy

71
Q

Most common congenital valvular lesion

A

bicuspid aortic valve

72
Q

Bicuspid aortic valves are neither stenotic nor incompetent but prone to

A

calfication

73
Q

Floppy and prolapsing mitr valve

A

Myxomatous mitral valve

74
Q

Myxomatous MV is a feature of

A

Marfans due to fibrillin 1 mutation CT disorder

75
Q

Essential change in myxomatous MV

A

thinning of fibrosa of valve

expansion of middle spongiosa due to inc deposition of mucus myxomatous material

76
Q

Inflammation of heart with valvular inflamm and scarring as most impt

77
Q

Pathognomonic for acute rheumatic fever

A

Aschoff bodies

inflammatory foci of lymphocytes

78
Q

Activated mac punctuating zones of fibrinoid necrosis

A

Anitschkow cell

79
Q

Most important fxl consequence of RHD

A

Valvular stenosis

regurgitation

80
Q

60% of endocarditis occur due to

A

Streptococcus viridans

81
Q

Small warty inflammatory vegetation in lines of valve closure

82
Q

large irregular destructive masses from leaflets to adjacent structures

A

Infective endocarditis

83
Q

Small to medium sized bland non destructive vegetation due to hypercoag state, estrogen or mucinous adenoCA procoagulant

A

Nonbacterial thrombotic Endocarditis

84
Q

Small to medium sized inflammatory veg at leaflets

Occur in SLE and APAS

A

Liebmann sacks

85
Q

Cardiac manif of mediators (5HT and 5hydroxyindoleacetic acid) causing glistening white intimal plaquelike thickening on cardiac chamber and valve leaflets

A

Carcinoid heart disease

86
Q

Progressive cardiac dilation and contractile dysfunction with concurrent hypertrophy

A

Dilated cardiomyopathy

87
Q

DCM is related to mutation of

A

dystrophin gene

88
Q

Fundamental defect in dilated cardiomyopathy is

A

Ineffective contraction

89
Q

Severe thinning of the right ventricular wall due to myocyte replacement by fatty infiltration and fibrosis

A

Arrhythmogenic Right Ventricular Cardiomyopathy

90
Q

Myocardial hypertrophy
Defective diastole
Ventricular outflow obstruction
100% genetic in origin

A

Hypertrophic cardiomyopathy

91
Q

HCM is a disorder of

A

sarcomeric protein Beta myosin most affected

92
Q

Problem with compliance resulting in impaired filling during diastole
Stiff wall

A

Restrictive cardiomyopathy

93
Q

Biatrial dilation

A

Restrictive cardiomyopathy

94
Q

3 forms of restrictive cardiomyopathy

A

1 Amyloidosis
2 Endomyocardial fibrosis
3 Loeffler endomyocarditis

95
Q

Amyloidosis is due to

A

Beta pleated sheet deposition

Senile - transthyretin (protein transporting thyroxine and retinol)

96
Q

Most common form of restrictive cardiomyopathy

A

Endomyocardial fibrosis

97
Q

Most common systemic condition assoc with pericarditis

98
Q

Irregular shaggy appearance
Bread butter pericarditis
In acute viral or uremic pericarditis

99
Q

Acute bacterial pericarditis

A

Fibrinopurulent

100
Q

Most common malignancy of the heart

A

Tumor mets

Lung lymphoma breast

101
Q

Most common primary tumor of the heart

A

Myxomas

90%

102
Q

90% of myxomas occur in

A

left atrium

103
Q

Most frequent primary tumors of the heart in infants and children

A

Rhabdomyoma

104
Q

Rhabdomyomas occur in frequently

A

Tuberous sclerosis

Pathology (24 decks)

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