HEART 1 Flashcards

1
Q

The human heart is an efficient organ that can pump around

A

7500l/day

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2
Q

female heart weight

A

250-320g

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3
Q

male heart weight

A

300-360g

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4
Q

right ventricle thickness

A

0.3-0.5cm

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5
Q

left ventricle thickness

A

1.3-1.5cm

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6
Q

increased in weight/thockness

A

hypertrophy

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7
Q

enlarged ventricular chamber size

A

dilation

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8
Q

increased cardiac weight/size resulting from hypertrophy and/or dilatation

A

cardiomegaly

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9
Q

additional fxn of cardiomyocytes

A

endocrine (anp and bnp)

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10
Q

pumping fxn

A

myocardium

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11
Q

coordinated contraction: systole; coordinated relaxation:_____

A

diastole

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12
Q

left ventricular myocytes are arranged in a_________

A

spiral circumferential orientation

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13
Q

endocrine fxn:

B-type natriuretic peptide

A

Ventricle

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14
Q

generates overall less robust contractile force

A

right ventricular myocytes

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15
Q

shortening of serial contractile elements aka sarcomeres within parallel myofibrils

A

contraction

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16
Q

atrioventricular valves

A

tricuspid and mitral valve

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17
Q

semilunar valves

A

aortic and pulmonary

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18
Q

dilatation of the aortic root can result in

A

valvular regurgitation

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19
Q

atrioventricular valves depends on the proper function not only of the leaflets but also

A

the tendinous cords and the attached papillary muscles of the ventricular wall.

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20
Q

Left ventricular dilation, a ruptured cord, or papillary muscle dysfunction can all interfere with mitral valve closure, causing

A

valvular insufficiency

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21
Q

A dense collagenous layer at the outflow surface, connected to the valvular supporting structures and providing mechanical integrity

A

fibrosa layer

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22
Q

A central core of loose connective tissue

A

spongiosa layer

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23
Q

A layer rich in elastin on the inflow surface, providing leaflet recoil

A

ventricularis or atrialis layer

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24
Q

pacemaker

at the junction of the right atrial appendage and SVC

A

SA node

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25
Q

located in the RA along the interatrial septum

A

AV node

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26
Q

connecting the RA to the ventricular septum

A

bundle of his

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27
Q

stimulates ventricles via
arborization into the Purkinje
network

A

R and L bundle branch divisions

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28
Q

Nutrients and oxygen are delivered via

the

A

coronary arteries

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29
Q

external surface of the heart

A

epicardial coronary arteries

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30
Q

myocardium

A

intramural arteries

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31
Q

Blood flow to the myocardium occurs during

A

ventricular diastole

32
Q

changes in aging heart (chambers)

A

increased left atrial cavity size
decreased left ventricular cavity size
sigmoid-shaped ventricular septum

33
Q

changes in the aging heart (valves)

A
aortic valve calcific deposits
mitral valve annular calcific deposits
fibrous thickening of leaflets
buckling of mitral leaflets toward the left atrium
lambl excrescences
34
Q

Epicardial Coronary arteries

A

Tortuosity
Diminished compliance
Calcific deposits
Atherosclerotic plaques

35
Q

Changes in the aging heart (myocardium)

A
Decreased mass
Increased subepicardial fat
brown atrophy
Lipofuscin deposition
Basophilic Degeneration
Amyloid deposits
36
Q

Changes in the aging heart (aorta)

A

Dilated ascending aorta with rightward shift
elongated thoracic aorta
Sinotubular junction calcific deposits
Elastic fragmentation and collagen accumulation
Atherosclerotic plaque

37
Q

increased filling volumes of the hearts, thereby increasing actin-myosin cross-bridge formation, and enhancing contractility and stroke volume

A

Frank-starling mechanism

38
Q

These augment heart function and/or regulate filling volumes and pressures (and many of the therapies for CHF affect
these systems when they become maladaptive).

A

activation of neurohumoral systems

39
Q

counterbalance for RAAS, because it stimulates diuresis

A

ANP

40
Q

is the general term applied to the collective molecular, cellular, and structural changes that
occur in response to injury or altered ventricular loading.

A

Ventricular remodeling

41
Q

new sarcomeres are predominantly assembled parallel to the long axes of cells, expanding cross-sectional area of myocytes in ventricles and causing a concentric increase in wall thickness

A

Pressure-overload hypertrophy (due to hypertension or aortic stenosis)

42
Q

new sarcomeres being assembled in series, elongating the myocyte. (eccentric hypertrophy)

A

Volume-overload hypertrophy (due to valvular regurgitation, valvular insufficiency

43
Q

hypertrophy is also typically accompanies by

A

fibrous tissue deposition

44
Q

promote cellular growth and alters protein expression

A

FOS
JUN
MYC
EGR1

45
Q

there is generally heavy and

dilated heart with variable degrees of myocardial hypertrophy

A

CHF

46
Q

loss of myocardial mass

because of the death of myocardium leads to the hypertrophy of surrounding myocardium

A

acute MI

47
Q

overload due to problems on cusps

A

valvular heart diseases

48
Q

associated with volume load

hypertrophy with increases in capillary density

A

aerobic exercise

49
Q

regular aerobic activity

A

decreases the resting heart rate and blood pressure

50
Q

induces mild pressure hypertrophy

A

purely static exercise

51
Q

end point if most forms of cardiac diseases

A

heart failure

52
Q

abrupt onset of CHF

A

Large MI

Acute valve dysfunction

53
Q

deposition of fibrous tissue limiting its pumping relaxation movements can cause ______.

Passive congestion of the pulmonary circulation

A

lett sided heart failure

54
Q

causes of Left sided heart failure

A

Ischemic heart dse
Systemic HTN
aortic and mitral valvular dse
primary myocardial dse

55
Q

in microscopic findings, if caused by ischemia, tthere is _________

A

coagulative necrosis and significant numbers of acute inflammatory cells

56
Q

pulmonary congestion and edema

A

heavy, wet lungs

57
Q

telltale signs of previous episodes of pulmonary edema

A

hemosiderin-laden macrophages

58
Q

arise from
elevated pleural capillary and lymphatic pressure and the resultant transudation of fluid into the pleural cavities.

A

pleural effusions

59
Q

Early left-sided heart failure symptoms are related to

A

pulmonary congestion and edema

60
Q

3rd heart sound due to

A

volume overload

61
Q

4th heart sound

A

due to increase myocardial stiffness

62
Q

If heart failure is associated with progressive ventricular dilation, the papillary muscles are displaced outward, causing

A

mitral regurgitation

63
Q

Subsequent chronic dilation of the left atrium can cause

A

atrial fibrillation

64
Q

In moderate CHF, a reduced ejection fraction

leads to diminished renal perfusion, causing

A

activation of RAAS

65
Q

if the hypoperfusion of the kidney becomes sufficiently severe,

A

impaired excretion of nitrogenous products may cause azotemia

66
Q

insufficient ejection fraction

A

systolic failure

67
Q

caused by any disorder that
damages the contractile function of the left ventricle. So, you can have ischemia there, fibrosis, tumor in the left ventricle

A

pump failure

68
Q

is secondary to abnormally stiff left ventricle during diastole

A

diastolic failure

69
Q

can also limit myocardial
relaxation and therefore mimics primary diastolic
dysfunction.

A

constrictive pericarditis

70
Q

Consequence of left-sided heart failure.

A

right sided heart failure

71
Q

Isolated right- sided heart failure is infrequent
and typically occurs in patients with one of a
variety of disorders affecting the lungs; hence it
is often referred to as

A

cor pulmonale

72
Q

In some instances, especially when left-sided

heart failure with hypoperfusion is also present, severe centrilobular hypoxia

A

centrilobular necrosis

73
Q

hallmark of right-sided heart failure.

A

Edema of the peripheral

and dependent portions of the body, especially foot/ankle (pedal) and pretibial edema

74
Q

tool to quantitatively assess the extent of CHF.

A

serum levels of B-type Natriuretic Factor

75
Q

is also an extremely valuable
tool in following patients with CHF, providing a measure of ejection fraction, wall motion, valvular function, and possible mural thrombosis.

A

echocardiograophy