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Cardiac System Flashcards

(104 cards)

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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
Most common type of CHD
Left to right shunt
26
Once pulmo HTN develops, structural defects of CHD are
irreversible
27
Reversal of flow shunting of unox blood back to systemic circulation
Eisenmenger Syndrome
28
Abnormal fixed opening in septum that allows unrestricted bf bet atrial chambers
ASD 90% ostium secundum
29
R atrial and ven dilation R ventricular hypertrophy Dilation of pulmonary artery Inc volume overload
ASD
30
5% of defects at lowest part of atrial septum assoc with mitral and tricuspid valve abn Close relationship with endocardial cushion
Ostium primum ASD
31
5% located high in atrial septum with anomalous drainage of pulmonary veins into R atrium and SVC
Sinus venosus ASD
32
Most common defect detected in adult
ASD
33
Site of 90% of VSDs
Basal membranous Close spont in childhood 20-30% occur in isolation most with other malf
34
High pres left to right shunt producing harsh machinery like murmur Lifesaving if with aortic or pulmonic atresia
PDA
35
``` Early cyanosis Right to Left shunt Clubbing of fingers (hypertrophic osteoarthropathy) Polycythemia Paradox embolization ```
Right to left shunt
36
Most common cause of cyanotic CHD
TOF
37
4 Cardinal features of TOF
VSD SubPulmonic stenosis (R ventricular outflow ob) Overriding of the VSD by aorta RVH
38
Cardinal features of TOF arise from
Anterosuperior displacement of infundibular septum -> abnormal septation
39
Major site of egress of blood flow from both ventricles
Overriding aorta
40
Severity of TOF depends on
pulmonary outflow obstruction
41
R to L shunt Dec pulmonary blood flow Inc aortic volume
TOF
42
Discordant connection of ventricles with vascular outflow Cyanosis
Transposition of Great Arteries
43
Narrowing or constriction of aorta | M>F twice
Coarctation of Aorta
44
CoA is assoc
Turners syndrome 2 forms 1) infantile 2) adult
45
Narrowing of aortic segment bet l subclavian and ductus arteriosus Duct is patent Pulmonary trunk is dilated RVH
Infantile CoA
46
Constriction at tissue ridge adjacent to nonpatent ligamentum arteriosum Dilated arch LVH
Adult CoA
47
Early cyanosis of lower half of body
Preductal Infant CoA
48
Asymptomatic UE HTN with weak pulses and hypotension in LE Claudication Coldness
Postductal adult CoA
49
Rib notching in CoA occurs bec
exuberant collateral circulation around coarctation develops through enlarged intercostal and internal mammary ITA
50
ACS 3 Catastrophic manifestation
1 unstable angina 2 acute MI 3 sudden cardiac death
51
<70% fixed obstruction
asymptomatic
52
>70% occlusion
critical stenosis | stable angina
53
occlusion of 90% of lumen
unstable angina
54
If chronic, compensatory mechanisms prevent MI like
collateral perfusion
55
Destabilization of plaque occurs by
Macrophage metalloproteinase secretion
56
Elements contributing to development of coronary atherosclerosis
Inflammation Thrombosis with disrupted plaque Vasoconstriction
57
Vulnerable plaques have
Large atheromatous core | Thin fibrous cap
58
Apart from lowering cholesterol, HMG COA reductase i also
Reduce inflammation and inc plaque stability
59
Sudden cardiac death post MI is causes by
Ventricular fibrillation
60
Dominance in coronary artery is dictated by
the one that gives rise to posterior descending
61
Factors contributing to reperfusion injury (5)
``` 1 mitochondrial dysfunction 2 myocyte hypercontracture 3 free radicals 4 leukocyte aggregation 5 platelet and complement activation ```
62
Histology of perfused irreversibly damaged myocytes
contraction band necrosis
63
Happens 3-7 days post MI most common rupture in
Left ventricular free wall
64
90% of MI patients develop
Arrhythmia conduction disturbance
65
Most common cause of arrhythmia
Ischemia
66
Ultimate mech of SCD
Lethal arrhythmia
67
Criteria for diagnosis of systemic hypertensive heart disease (2)
1 LVH in absence of other valvular pathology | 2 history or evidence of HTN
68
Pathognomomic of LSHHD
LVH with dilation in the long run | Nuclear enlargement and hyperchromasia or boxcar nuclei and intercellular fibrosis
69
Acute cor pulmonale
R ventricle dilation
70
Chronic cor pulmonale
R ventricle hypertrophy
71
Most common congenital valvular lesion
bicuspid aortic valve
72
Bicuspid aortic valves are neither stenotic nor incompetent but prone to
calfication
73
Floppy and prolapsing mitr valve
Myxomatous mitral valve
74
Myxomatous MV is a feature of
Marfans due to fibrillin 1 mutation CT disorder
75
Essential change in myxomatous MV
thinning of fibrosa of valve | expansion of middle spongiosa due to inc deposition of mucus myxomatous material
76
Inflammation of heart with valvular inflamm and scarring as most impt
RVD
77
Pathognomonic for acute rheumatic fever
Aschoff bodies | inflammatory foci of lymphocytes
78
Activated mac punctuating zones of fibrinoid necrosis
Anitschkow cell
79
Most important fxl consequence of RHD
Valvular stenosis | regurgitation
80
60% of endocarditis occur due to
Streptococcus viridans
81
Small warty inflammatory vegetation in lines of valve closure
RHD
82
large irregular destructive masses from leaflets to adjacent structures
Infective endocarditis
83
Small to medium sized bland non destructive vegetation due to hypercoag state, estrogen or mucinous adenoCA procoagulant
Nonbacterial thrombotic Endocarditis
84
Small to medium sized inflammatory veg at leaflets | Occur in SLE and APAS
Liebmann sacks
85
Cardiac manif of mediators (5HT and 5hydroxyindoleacetic acid) causing glistening white intimal plaquelike thickening on cardiac chamber and valve leaflets
Carcinoid heart disease
86
Progressive cardiac dilation and contractile dysfunction with concurrent hypertrophy
Dilated cardiomyopathy
87
DCM is related to mutation of
dystrophin gene
88
Fundamental defect in dilated cardiomyopathy is
Ineffective contraction
89
Severe thinning of the right ventricular wall due to myocyte replacement by fatty infiltration and fibrosis
Arrhythmogenic Right Ventricular Cardiomyopathy
90
Myocardial hypertrophy Defective diastole Ventricular outflow obstruction 100% genetic in origin
Hypertrophic cardiomyopathy
91
HCM is a disorder of
sarcomeric protein Beta myosin most affected
92
Problem with compliance resulting in impaired filling during diastole Stiff wall
Restrictive cardiomyopathy
93
Biatrial dilation
Restrictive cardiomyopathy
94
3 forms of restrictive cardiomyopathy
1 Amyloidosis 2 Endomyocardial fibrosis 3 Loeffler endomyocarditis
95
Amyloidosis is due to
Beta pleated sheet deposition | Senile - transthyretin (protein transporting thyroxine and retinol)
96
Most common form of restrictive cardiomyopathy
Endomyocardial fibrosis
97
Most common systemic condition assoc with pericarditis
Uremia
98
Irregular shaggy appearance Bread butter pericarditis In acute viral or uremic pericarditis
fibrinous
99
Acute bacterial pericarditis
Fibrinopurulent
100
Most common malignancy of the heart
Tumor mets Lung lymphoma breast
101
Most common primary tumor of the heart
Myxomas 90%
102
90% of myxomas occur in
left atrium
103
Most frequent primary tumors of the heart in infants and children
Rhabdomyoma
104
Rhabdomyomas occur in frequently
Tuberous sclerosis

Pathology (24 decks)

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