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Heart Flashcards

1
Q

effects of aging on myocardium

A 
 Increased mass
 Increased subepicardial fat
 Brown atrophy
 Lipofuscin deposition
 Basophilic degeneration
 Amyloid deposits
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2
Q

Older persons develop small filiform processes _______________ on the closure lines of aortic and mitral valves resulting from the organization of small thrombi

A

(Lambl excrescences)

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3
Q

extensive lipofuscin deposition in a small, atrophied heart; often accompanies cachexia, as seen in terminal cancer

A

Brown atrophy

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4
Q

Categories of Heart Dse

A 
 Congenital Heart Abnormalities
 Ischemic Heart Diseases
 Heart diseases caused by Hypertension
 Heart diseases caused Pulmonary diseases (cor pulmonale)
 Diseases of the Cardiac valves
 Primary cardiac diseases
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5
Q

SIX PRINCIPLES OF PATHOLOGY

A 
Pump failure
Obstruction to flow
Regurgitant to flow
Shunted flow
Disorders of cardiac conduction
Rupture of the heart or a major vessel
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6
Q

Occurs when the heart is unable to pump blood at a rate sufficient to meet the metabolic demands of the tissues

A

CARDIAC HEART FAILURE

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7
Q

Physiologic mechanisms maintain arterial pressure and perfusion of vital organs in HF

A

 Frank-Starling mechanism
 Myocardial adaptations (hypertrophy)
 Activation of neurohumoral system

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8
Q

o Occurs in response to increases in pressure
o Usually due to hypertension or aortic stenosis
o Causes a concentric increase in wall thickness

A

Pressure-overload hypertrophy

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9
Q

o Characterized by ventricular dilation
o the new sarcomeres assembled are positioned in series with existing sacromeres
o As a result, the wall thickness may be increased, normal, or less than normal
o Heart weight, rather than wall thickness, is the best measure of hypertrophy in volume overloaded hearts

A

Volume-overload hypertrophy

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10
Q

3x or 4x the normal weight of the heart

A

 aortic regurgitation

 hypertrophic cardiomyopathy

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11
Q

Causes:of LEFT-SIDED HEART FAILURE

A

o Ischemic heart disease
o Hypertension
o Aortic and Mitral valvular heart disease

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12
Q

o CO is preserved at rest, but the left ventricle is
abnormally stiff or otherwise restricted in its ability to relax during diastole
o Because the left ventricle cannot expand normally, any increase in filling pressure is immediately referred back to the pulmonary circulation

A

Systolic failure

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13
Q

o There is rapid onset pulmonary edema (aka flash

pulmonary edema)

A

Systolic failure

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14
Q

o Reduction in the ability of the left ventricle to relax

and fill

A

Diastolic failure

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15
Q

o are the hemosiderein-laden macrophages
o phagocytosed RBCs store the iron recovered from
hemoglobin

A

Heart failure cells

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16
Q

o Pure right-sided heart failure
o Associated with parenchymal diseases of the lung
o Pulmonary hypertension

A

 Cor pulmonale

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17
Q

Most common congenital heart disease

A

VSD

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18
Q

Most common genetic cause of congenital heart disease is

A

trisomy 21 (Down syndrome)

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19
Q

MAJOR CATEGORIES OF CONGENITAL HEART DISEASE

A

 Malformation causing a Left to Right Shunt
 Malformation causing a Right to Left Shunt
 Malformation causing an Obstruction

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20
Q

Causes of R–>L shunt

A
  1. Tetralogy of Fallot
  2. Transposition of the great arteries
  3. Persistent truncus arteriosus
  4. Tricuspid atresia
  5. Pulmonary venous connection
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21
Q

 Most commonly encountered LRS

A
  1. ASD
  2. Patent foramen ovale
  3. VSD
  4. Patent ductus arteriosus
  5. AV septal defects
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22
Q

result from a
deficient or fenestrated oval fossa near the center of the
atrial septum

A

Secundum ASDs (90%)

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23
Q

occur adjacent to the

AV valves

A

Primum anomalies (5% of ASDs)

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24
Q

are located near the
entrance of the superior vena cava and may be
associated with anomalous pulmonary venous return to
the right atrium.

A

Sinus venosus defects (5%)

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25
Q

Complications of ASD?

A

o heart failure
o paradoxical embolization
o irreversible pulmonary vascular disease.

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26
Q

is an abnormal, fixed opening in the atrial septum caused

by incomplete tissue formation

A

ASD

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27
Q

a small hole created by an open flap of tissue in the atrial

septum at the oval fossa

A

PATENT FORAMEN OVALE

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28
Q

Incomplete closure of the ventricular septum, allowing free

communication of blood between the left to right ventricles

A

VSD

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29
Q

About 90% of VSD; involves the region of the membranous interventricular
septum

A

Membranous VSD

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30
Q

lie below the pulmonary valve () or within

the muscular septum.

A

Infundibular VSD

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31
Q

VSDs in the muscular septum may be multiple and called?

A

“Swiss-cheese” septum

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32
Q

Harsh “machinery-like” murmur

A

PATENT DUCTUS ARTERIOSUS

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33
Q

results when the ductus arteriosus remains open after birth

A

Patent (also called persistent) ductus arteriosus (PDA)

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34
Q

preservation of ductal patency is done by administering

A

prostaglandin E

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35
Q

ATRIOVENTRICULAR SEPTAL DEFECT other names

A

COMPLETE ATRIOVENTRICULAR CANAL DEFECT

ENDOCARDIAL CUSHION DEFECT

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36
Q

results from the
embryologic failure of the superior and inferior endocardial
cushions of the AV canal to fuse adequately

A

ATRIOVENTRICULAR SEPTAL DEFECT

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37
Q

consequences of ATRIOVENTRICULAR SEPTAL DEFECT

A

o incomplete closure of the AV septum

o malformation of the tricuspid and mitral valves

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38
Q

Forms of ATRIOVENTRICULAR SEPTAL DEFECT

A

Partial AVSD

Complete AVSD

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39
Q

consisting of a primum ASD and a cleft

anterior mitral leaflet,causing mitral insufficiency

A

Partial AVSD

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40
Q

consisting of a large combined AV
septal defect and a large common AV valve—
essentially a hole in the center of the heart

A

Complete AVSD

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41
Q

The diseases in this group cause cyanosis early in postnatal

life (cyanotic congenital heart disease)

A

RIGHT TO LEFT SHUNTS

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42
Q

is the most common disease in this group

A

Tetralogy of Fallot

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43
Q

RIGHT TO LEFT SHUNTS

A

Tetralogy of Fallot
persistent truncus arteriosus
tricuspid atresia
total anomalous pulmonary venous connection

44
Q

TETRALOGY OF FALLOT Four cardinal features

A

VSD
(subpulmonary stenosis)
an aorta that overrides the VSD
right ventricular hypertrophy

45
Q

“boot-shaped” heart

A

TETRALOGY OF FALLOT

46
Q

mild TOF: the abnormality resembles an isolated VSD, and the shunt may be left-to-right, without cyanosis

A

pink tetralogy

47
Q

ventriculoarterial discordance; the aorta arises from the right ventricle, and lies anterior and to the right of the pulmonary artery, which emanates from the left ventricle

A

TRANSPOSITION OF THE GREAT ARTERIES

48
Q

Right ventricular hypertrophy becomes prominent, because this chamber functions as the systemic ventricle (what dse)

49
Q

developmental failure of separation of the embryologic truncus arteriosus into the aorta and pulmonary artery

A

Persistent Truncus Arteriosus

50
Q

Complete occlusion of the tricuspid valve orifice

A

Tricuspid Atresia

51
Q

pulmonary veins fail to directly join the left atrium, results embryologically when the common pulmonary vein fails to develop or becomes atretic

A

Total Anomalous Pulmonary Venous Connection

52
Q

OBSTRUCTIVE CONGENITAL ANOMALIES

A

 COARCTATION OF AORTA
 PULMONARY STENOSIS AND ATRESIA
 AORTIC STENOSIS AND ATRESIA

53
Q

form with tubular hypoplasia of the aortic arch
proximal to a patent ductus arteriosus that is often
symptomatic in early childhood

54
Q

form in which there is a discrete ridgelike infolding

of the aorta, just opposite the closed ductus arteriosus (ligamentum arteriosum)distal to the arch vessels

A

“adult”

55
Q

(“notching”) of the undersurfaces of the ribs –collateral circulation of the intercostal & mammary arteries assoc with what dse?

A

Coarctation of Aorta

56
Q

Coarctation of aorta is associated commonly with what syndrome?

A

Turner syndrome

57
Q

Congenital narrowing and obstruction of the aortic valve can

occur at three locations

A

Valvular
Subvalvular
Supravalvular

58
Q

Syndrome of Ischemic Heart Disease/CAD: Presents as one or more of the ff:

A

 Myocardial infarction (MI)
 Angina pectoris
 Chronic IHD with heart failure
 Sudden cardiac death

59
Q

Leading cause of death worldwide for both men and women

A

Ischemic Heart Disease/CAD

60
Q

The coronary artery that perfuses the

posterior third of the septum (called “dominant” coronary arteries)

A

Right coronary artery

Left circumflex

61
Q

Paroxysmal and usually recurrent attacks of substernal or precordial chest discomfort

A

ANGINA PECTORIS

62
Q

Three Types of Angina pectoris

A

Stable (Typical) Angina
Prinzmetal Variant
Unstable (Crescendo) Angina

63
Q

Increase in myocardial oxygen demand that outstrip the ability of stenosed coronary arteries to increase oxygen delivery

A

Stable (Typical) Angina

64
Q

Complicated by partially occlusive thrombosis and vasoconstriction  severe but transient reductions in coronary blood flow

A

Prinzmetal Variant

65
Q

Cause: disruption of an atherosclerotic plaque with superimposed partial (mural) thrombosis and possibly embolization or vasospasm (or both)

A

Unstable (Crescendo) Angina

66
Q

 “Heart attack”

 Death of cardiac muscle due to prolonged severe ischemia

A

MYOCARDIAL INFARCTION

67
Q

initial event: sudden change in an atheromatous plaque

A

Coronary arterial occlusion

68
Q

Progression of myocardial necrosis after coronary artery occlusion

A

MYOCARDIAL RESPONSE

69
Q 
Onset of:
ATP depletion \_\_\_\_\_\_\_\_
Loss of contractility \_\_\_\_\_\_\_
ATP reduced:
to 50% of normal \_\_\_\_\_\_
to 10% of normal \_\_\_\_\_\_
Irreversible cell injury \_\_\_\_\_\_\_
Microvascular injury \_\_\_\_\_\_\_
A

Seconds

1 hr

70
Q

Ischemia is most pronounced in the (what zone in the heart)

A

subendocardium:

71
Q

Most common infarction; Near full thickness (>60%) of the ventricular wall in the distribution of a single coronary artery

o “ST elevation infarcts

A

Transmural – (“Q” wave infarct)

72
Q

Inner third to half of wall type of infarct; Normally the least perfused region: most vulnerable to
any reduction in coronary flow

A

Subendocardial (nontransmural)

73
Q

o “Non-ST elevation infarcts”

A

Subendocardial (nontransmural)

74
Q

o “ST elevation infarcts

A

Transmural – (“Q” wave infarct)

75
Q

 Most effective way to “rescue” ischemic myocardium

threatened by infarction

A

INFARCT MODIFICATION BY REPERFUSION

76
Q

Severe ischemia lasting _______minutes or longer leads to irreversible damage

77
Q

The typical changes of coagulative necrosis become

detectable in the first _____ hours.

78
Q

result from the forceful systolic tugs of the viable fibers on immediately adjacent, noncontractile dead fibers

A

Wavy fibers

79
Q

areas of necrosis are stained by (MI)

A

triphenyltetrazolium chloride

80
Q

most common cause of death (90% of

cases)

A

Post infarct arrhythmia

81
Q

complication of MI that is due to myocardial

inflammation

A

Fibrinohemorrhagic pericarditis

Also called DRESSLER SYNDROME

82
Q

COMPLICATIONS OF MI

A

Post infarct arrhythmia
CHF – 60%
Hypotension and cardiogenic shock – 10%
Myocardial rupture – 1-5%

83
Q

CHRONIC ISCHEMIC HEART DISEASE

A

Progressive heart failure as a result of ischemic myocardial damage

84
Q

Unexpected death from cardiac causes early after symptom

onset (within 1hr) or without the onset of symptoms

A

SUDDEN CARDIAC DEATH

85
Q

Causes pressure overload and ventricular hypertrophy; Most commonly seen in the left side of the heart

A

HYPERTENSIVE HEART DISEASES

86
Q

Pulmonary HPN may cause:

A

o Right-sided HHD

o Aka COR PULMONALE

87
Q

Cross section: Normal crescent shape of the RV is transformed to a dilated ovoid

A

Acute Cor Pulmonale

88
Q

Due to stenosis, insufficiency (regurgitation or incompetence), or both

A

VALVULAR HEART DISEASE

89
Q

 failure of a valve to open completely

 impediment of forward flow

A

o stenosis

90
Q

 failure of a valve to close completely

 allowing reversed flow

A

o insufficiency

91
Q

 incompetence of valve stemming from an abnormality in one of its support structures
 allowing reversed flow

A

o functional regurgitation

92
Q

Most common of all valvular abnormalities

A

CALCIFIC AORTIC STENOSIS

93
Q

most frequent congenital CV malformation in humans

A

CALCIFIC STENOSIS OF CONGENTITALLY BICUSPID AORTIC VALVE

94
Q

degenerative calcific deposits develop in the peripheral fibrous
ring (annulus) of the mitral valve

A

MITRAL ANNULAR CALCIFICATION

95
Q

“floppy” mitral valve

A

MITRAL VALVE PROLAPSE (MYXOMATOUS

DEGENERATION OF THE MITRAL VALVE)

96
Q

Key histologic feature of MITRAL VALVE PROLAPSE

A

o Myxomatous degeneration

97
Q

disease associated with mitral valve prolapse

A

Marfan’s Syndrome

98
Q

Major Manifestations of Rheumatic Fever

A 
o Migratory polyarthritis
o Pancarditis
o Subcutaneous nodule
o Erythema marginatum of the skin
o Sydenham Chorea
99
Q

Minor Manifestations of Rheumatic Fever

A

o Fever
o Arthralgia
o ↑ blood levels of acute phase reactants

100
Q

 Aschoff bodies
o distinctive lesions in the heart
o consist of:

A

 foci of lymphocytes (primarily T cells)
 occasional plasma cells
 Anitschkow cells: plump activated macrophages

101
Q

o pathognomonic for RF

A

 Anitschkow cells

102
Q

o leaflet thickening
o commisural fusion and shortening
o thickening and fusion of the tendinous cords

A

Cardinal anatomic changes of the mitral valve in chronic RHD

103
Q

o maplike thickening of endocardiumover lesions, usually in

left atrium

A

MacCallum’s plaques

104
Q

more commonly:

o following recurrent ARF

A

Chronic Rheumatic Heart Disease

105
Q

Heart disease resulting from a primary abnormality in the

myocardium

A

CARDIOMYOPATHY

106
Q

o diseases predominantly confined to the heart muscle

A

 Primary cardiomyopathies

107
Q

o myocardial involvement as a component of a systemic or

multiorgan disorder

A

 Secondary cardiomyopathies

PATHOLOGY (9 decks)

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