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Basic Human Pathology > Ch 12: Heart > Flashcards

Ch 12: Heart Flashcards

1
Q

what is the leading cause of mortality in the world

A

cardiovascular disease (1 in 4 deaths in US)

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2
Q

what is heart type 1
-supply

A

right preponderance (dominant)
80% of people - most common
right coronary artery supplies the right ventricle, posterior half of septum, and the left posterior ventricle

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3
Q

what is heart type 2
-supply

A

balanced
8% of people - least common
each ventricle is supplied by the corresponding coronary artery

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4
Q

what is heart type 3
-supply

A

left preponderance (dominant)
12% of people - second most common
two types:
two posterior descending branches, one from each coronary artery
or
single posterior descending branch coming from the left circumflex branch

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5
Q

what are the three layers of the heart

A

epicardium (outer layer)
myocardium (muscle layer)
endocardium (inner layer)

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6
Q

what are the three layers of the pericardium

A

serious pericardium (visceral layer/epicardium)
serious pericardium (parietal layer)
fibrous pericardium (outermost layer)

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7
Q

what are the three layers of the aortic valve

A

ventricularis layer (outermost) - ventricularis because it abuts ventricle
spongiosa layer (middle)
fibrosa layer (innermost)

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8
Q

what are the three layers of the mitral valve

A

atrialis layer (outermost) - atrialis because it abuts atria
spongiosa layer (middle)
fibrosa layer (innermost)

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9
Q

what does the fibrosa layer of the aortic/mitral valves do

A

made of dense collagen
connected to the valve’s supporting structures
provides mechanical integrity

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10
Q

what does the the ventricularis/atrialis layer of the aortic/mitral valve do

A

made of elastin
provides leaflet recoil

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11
Q

what are the 6 main mechanisms that lead to heart failure

A

failure of the pump
obstruction to flow
regurgitant flow
shunted flow
disorders of cardiac conduction
rupture of the heart or major vessel

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12
Q

what is the end stage of heart failure

A

congestive heart failure

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13
Q

what are the three major conditions of heart failure

A

insufficient output to meet metabolic demands
can only meet demands when there is higher filling pressures
marked increased in tissue demand

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14
Q

what is the frank-sterling mechanism

A

compensatory mechanism
increased venous return leads to increased diastolic filling volumes
extra amount of blood causes dialation of heart
dilation is a result of cardiac myofibril stretching (more cross bridge formation)
leads to increase stroke volume and contractility

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15
Q

what is the equation for stroke volume

A

end diastolic volume (EDV) - end systolic volume (ESV)
amount of blood ventricle filled with - amount of blood left in ventricle after contraction

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16
Q

what is the activation of neurohumoral systems

A

compensatory mechanism
release of substances (norepinephrine, renin, and atrial natriuretic peptide)
affects heart function and regulates filling volumes and pressures

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17
Q

where does norepinephrine come from and how does it affect the heart

A

neurotransmitter released from ANS
elevates HR and contractility to compensate for vascular resistance

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18
Q

how does the renin-angiotensin-aldosterone system affect the heart

A

regulates blood pressure and volume
promotes water and salt retention to increases vascular tone and circulatory volume

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19
Q

how does atrial natriuretic peptide affect the heart

A

counters the renin-angiotensin-aldosterone system
causes diuresis (peeing) and vascular smooth muscle relaxation

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20
Q

what is systolic dysfunction

A

left ventricle can’t contract normally
decreases amount of blood circulating in the body

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21
Q

what are two causes of systolic dysfunction

A

hypertension
ischemic heart disease

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22
Q

what is diastolic dysfunction

A

inability of the heart to relax and fill enough

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23
Q

what are the four main causes of diastolic dysfunction

A

left ventricular hypertrophy
myocardial fibrosis
amyloid deposition
constrictive pericarditis

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24
Q

cardiac dysfunction is characterized by which three things

A

heart failure
arrhythmias
neurohumoral stimulation

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25
Q

what is the most common cause of right sided heart failure

A

left sided heart failure

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26
Q

what is the most common cause of isolated right sided heart failure

A

pulmonary disease

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27
Q

what are the four most common causes of left sided heart failure

A

ischemic heart disease
systemic hypertension
mitral or aortic valve disease
amyloidosis

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28
Q

what happens during chronic heart failure

A

RBCs leak out of capillaries, breakdown, and release their hemoglobin
alveolar macrophages engulf hemoglobin and become known as heart failure cells

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29
Q

what are the microscopic features of acute left-sided heart failure

A

accumulation of edema/blood in alveolar macrophages

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30
Q

what are heart failure cells

A

alveolar macrophages that have engulfed hemoglobin from broken down RBCs
“hemosiderin laden macrophages”

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31
Q

alveolar macrophages that have engulfed hemoglobin from broken down RBCs
“hemosiderin laden macrophages”

A

heart failure cells

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32
Q

what are three ways to treat left sided heart failure

A

restrict salt diet
drugs
cardiac pacemakers

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33
Q

what are the top two most common congenital heart abnormalities (with percentages)

A

ventricular septal defect (42%)
atrial septal defect (10%)

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34
Q

congenital heart disease makes up what percentage (range) of all birth defects

A

20-30%

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35
Q

when is an embryo most susceptible to a congenital heart disease (week range)

A

development during weeks 3-8

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36
Q

what are the three main types of congenital heart diseases

A

septal defects
stenotic lesions
outflow tract abnormalities

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37
Q

which congenital factors can lead to congenital heart disease

A

specific loci
chromosome abnormalities (trisomies 13, 15, 18, and 21; monosomy X; turner syndrome )

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38
Q

what is a shunt

A

abnormal connection between chambers or blood vessels which allows blood to move between the two sides of the heart

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39
Q

what are the two major consequences of a right-to-left shunt

A

cyanosis + clubbed fingers/toes
deoxygenated blood is entering systemic circuit

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40
Q

what are the consequences of a left-to-right shunt

A

increased pressure and volume to pulmonary circulation
right sided heart failure

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41
Q

what is the most common congenital cardiac malformation

A

left to right shunt

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42
Q

what are the three main causes of a left to right shunt

A

atrial septal defect
ventricular septal defect
patent ductus arteriosus

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43
Q

what are the two main causes of right to left shunts

A

tetralogy of fallot
transposition of the great vessels

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44
Q

where do 90% of ventricular septal defects occur

A

membranous region of interventricular septum

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45
Q

what is the most common type of atrial septal defect

A

type 1 - secundum defect (old side of foramen ovale)

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46
Q

what is a systolic thrill and in which cardiac malformation is it mostly seen

A

a heart palpitation most commonly seen in those with a patent ductus arteriosus

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47
Q

a heart palpitation most commonly seen in those with a patent ductus arteriosus

A

systolic thrill

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48
Q

what is a common characteristic of pulmonary stenosis

A

right ventricular hypertrophy

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49
Q

what are the four components of tetralogy of fallot

A

ventricular septal defect
pulmonary stenosis
overriding aorta
right ventricular hypertrophy

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50
Q

what is coarctation of the aorta and what does it cause

A

narrowing of the aorta
causes left ventricular hypertrophy
pressure of everything above coarctation is increased and decreased below it

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51
Q

what is an atrioventricular septal defect

A

incomplete atrial and septal walls, usually with no tricuspid or mitral valves
causes mixing of arterial and venous blood

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52
Q

what congenital heart defect is most common in Down’s Syndrome

A

atrioventricular septal defect

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53
Q

what is congenital aortic stenosis and who is most at risk

A

stiffening of aortic valve that you’re born with
valve can be uni or bicuspid
maybe be asymptomatic for years
3x more common in males

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54
Q

what is transposition of the great vessels

A

reversal of the pulmonary and aortic arteries
deoxygenated blood goes to the body, oxygenated to the lungs
must be surgically repaired after birth

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55
Q

what is ischemic heart disease (IHD)

A

imbalance between perfusion and oxygen requirements of the heart

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56
Q

what causes 90% of ischemic heart disease cases

A

coronary artery disease obstruction (plaque)

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57
Q

what is the most common clinical manifestation of ischemic heart disease

A

angina due to 70% stenosis

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58
Q

what is angina pectoris

A

chest pain caused by sudden and recurrent attacks of chest pain (15 seconds to 15 minutes)
does not cause myocyte necrosis

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59
Q

what is angina pectoris (chest pain) specifically caused by

A

release of molecules that stimulate sympathetic and vagal afferent nerves

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60
Q

what is the most common form of angina

A

stable (typical)

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61
Q

what is unstable (crescendo) angina

A

prolonged (over 20 minutes) severe angina
usually caused by plaque disruption

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62
Q

how does disruption of a plaque cause a myocardial infarction

A

plaque is disrupted by some kind of force
platelets adhere and aggregate to newly exposed collagen and plaque contents
coagulation is activated
thrombus occludes the lumen

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63
Q

how long does it take for a myocardial infarction to achieve its full extent

A

3 to 6 hours

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64
Q

what are the three factors that impact a myocardial infarction

A

rate of development and duration of occlusion
metabolic demands of myocardium
extent of collateral supply

65
Q

when do myocytes lose their contractility during an MI

A

before two mintues after the event began

66
Q

what is the timeframe of irreversible cell injury during a myocardial infarction

A

20-40 mins
myocytes are damaged beyond repair

67
Q

what is a transmural infarct

A

death of myocytes due to prolonged total occlusion of an artery (MI)
includes the entire thickness of wall

68
Q

what are multiple diffuse infarcts

A

small, intramural vessel occlusions that cause myocyte death
do not include entire thickness of wall

69
Q

what is the most common occluded artery to cause an MI (40-50% of cases)

A

left anterior descending (interventricular)

70
Q

which parts of the heart are most affected by an MI involving the left anterior descending (interventricular) artery

A

anterior wall of ventricle
2/3rds interventricular septum
apex

71
Q

which parts of the heart are most affect by an MI involving the left circumflex artery

A

lateral left ventricle

72
Q

which parts of the heart are most affected by an MI involving the right coronary artery

A

most of the right ventricle

73
Q

which parts of the heart are most affected by an MI involving the posterior descending artery

A

posterior 1/3rd of septum and posterior left ventricle

74
Q

what is the second most common occluded artery to cause an MI (30-40% of cases)

A

right coronary artery

75
Q

global hypotension leads to a non-transmural infarct that can be seen where on the heart

A

causes a circumfrential subendocardial infarct

76
Q

what are the three results of reperfusion during an MI

A

vascular injury (leakiness)
no ATP - sarcomeres get stuck in tetanic state
saves injured cells but changes morphology

77
Q

when is troponin at its highest after an MI

A

3 to 12 hours after MI
stays elevated for 14 days

78
Q

when is creatine kinase myocardial band fraction highest after an MI

A

increases within 3 to 4 hours
peaks at 24 hours
returns to normal within 36 hours

79
Q

what are the three treatments for an MI

A

thrombolytic drugs
angioplasty with stent
bypass surgery

80
Q

what are the three criteria used to diagnose an MI

A

clinical history of chest pain
elevation of cardiac markers (troponin-1, CK-MB, myoglobin)
changes on an electrocardiographic
must have 2/3 to consider it an MI

81
Q

what is the weight of a male heart

A

270-360g (300 g)

82
Q

what is the average weight of a female heart

A

200-280g (250 g)

83
Q

what is the thickness of the left ventricle

A

1.0-1.5 cm

84
Q

what is the thickness of the right ventricle

A

0.2-0.4 cm

85
Q

what is the average circumference of the aortic valve (males and females)

A

males: 6.7 cm
females: 6.3 cm

86
Q

what is the average circumference of the pulmonary valve (males and females)

A

males: 6.6 cm
females: 6.2 cm

87
Q

what is the average circumference of the mitral valve (males and females)

A

males: 9.6 cm
females: 8.6 cm

88
Q

what is the average circumference of the tricuspid valve (males and females)

A

males: 11.4
females: 10.6

89
Q

what are the three predictors of how damaging a MI will be

A

size, site, and type of infarct

90
Q

what are three things that large transmural infarcts increase your risk for

A

cardiogenic shock
arrhythmias
late congestive heart failure

91
Q

what are three things that anterior transmural infarcts increase your risk for

A

free wall rupture or expansion
aneurysm formation
mural thrombi formation

92
Q

what are two things posterior transmural infarcts are more complicated by

A

conduction blocks
right ventricular involvement

93
Q

what is the main thing that a subendocardial infarct increases your risk for

A

thrombi
rarely pericarditis, rupture, or aneurysms

94
Q

what is the first piece of macro/microscopic evidence of an MI and when is it first seen

A

variable waviness of fibers at border
seen 30 mins to 4 hours after

95
Q

what macroscopic/microscopic changes from an MI do you see 4-12 hours in

A

macroscopic changes: dark mottling
microscopic changes: early coagulative necrosis, edema, hemorrhage

96
Q

what macroscopic/microscopic changes from an MI do you see 12-24 hours in

A

macroscopic: dark mottling
microscopic: pyknosis (shrinking of nucleus), early neutrophilic infiltrate, contraction band necrosis

97
Q

what macroscopic/microscopic changes from an MI do you see 1-3 days in

A

macroscopic: mottling with yellow-tan infarct center
microscopic: loss of nuclei and striations more infiltrate of neutrophils

98
Q

what macroscopic/microscopic changes from an MI do you see 3-7 days in

A

macroscopic: blood boarder with central yellow-tan softening
microscopic: dead myofibers start to break down, dying neutrophils, phagocytosis by macrophages at boarder

99
Q

what macroscopic/microscopic changes from an MI do you see 7-10 days in

A

macroscopic: yellow-tan with depressed red-tan margins
microscopic: phagocytosis and granulation at margins

100
Q

what macroscopic/microscopic changes from an MI do you see 10-14 days in

A

macroscopic: red-grey depressed borders
microscopic: new blood vessels and collagen deposition

101
Q

what macroscopic/microscopic changes from an MI do you see 2-8 weeks in

A

macroscopic: grey-white scar staring at infarct border; gelatenous appearance
microscopic: more collagen, less cells

102
Q

what macroscopic/microscopic changes from an MI do you see after 2 months in

A

macroscopic: fully formed scar
microscopic: dense collagenous scar

103
Q

where is the most common spot to get a myocardial rupture

A

free ventricular wall

104
Q

what is a cardiac tamponade and when is it most commonly seen after an MI

A

collection of blood in the pericardial sac due to a myocardial rupture
usually seen around 7 days after an MI

105
Q

what are the two most common consequences of myocardial ischemia

A

arrhythmia and conduction defects which can cause sudden death

106
Q

what percentage of patients experience one or more complications of myocardial ischemia

A

75%

107
Q

what is ventricular remodeling

A

consequence after an MI
scarring and thinning of the infarcted zones
hypertrophy
dilation

108
Q

what is the mortality rate (%) of an MI in the first year

A

90% mortality rate

109
Q

what does the Bundle of His (AV) bundle do

A

part of the heart’s conduction system that connects the right atrium to the ventricular septum

110
Q

what is atrial fibrillation

A

atria become irritable and depolarize independently and sporatically
leads to upper and lower chambers being uncoordinating
cause all different types of rythyms (tachy, brady, sytole, etc)

111
Q

what are the two duration types of arrhythmias

A

sustained
sporadic (paroxysmal)

112
Q

what are the three treatments of atrial fibrillation

A

anticoagulants
electrical conversion
ablation

113
Q

what is atrial fibrillation a major risk factor for

A

stroke (15%)

114
Q

what are the four contributing factors to atrial fibrillation

A

alcohol
smoking tobacco
diabetes mellitus
thyrotoxicosis (high levels of T3/T4)

115
Q

what is the most common location of a heart block

A

interventricular septum

116
Q

what is a bundle branch block

A

complete or partial interruption of the electrical pathways inside the wall of the heart

117
Q

what are primary electrical disorders

A

inherited disorders that cause sudden death in the absence of structural caridac pathology
diagnosed through genetic testing
most are channelopathies
ex. long QT syndrome

118
Q

what is the most common cause of sudden cardiac death

A

coronary artery disease leading to ischemia

119
Q

what is the drug used to help more easily identify an early MI

A

nitro blue tetrazolium - regular tissue appears dark maroon, MI is much paler in color

120
Q

what does pulmonary hypertensive heart disease (cor pulmonale) cause

A

right ventricular hypertrophy and dilation

121
Q

what is valvular insufficiency

A

valve is unable to open or close all the way which leads to regurgitation of blood

122
Q

what is a mitral valve prolapse and what does it cause

A

mitral valve bulges into the atrium and may not close properly, leading to a leak or regurgitation

123
Q

what is a thrill

A

palpation of a severe lesion that can be felt on the skin over area of turbulence

124
Q

what are heart murmurs caused by

A

turbulent flow through diseased valves

125
Q

what is a prolapsed ventricle

A

leaflets of valve balloon upwards as the ventricle contracts

126
Q

what is regurgitation

A

valve leaflets do not properly close, forcing blood back into the atrium

127
Q

what is the most common congenital valvular lesion

A

bicuspid aortic valve

128
Q

what is myxomatous degeneration

A

ballooning of the mitral valve leaflets
due to deposition of myxomatous mucoid material in the spongiosa layer of the valve

129
Q

what is rheumatic valvular disease

A

caused by A B-hemolytic strep infections
clinical manifestation of rhematic fever
can cause vegetations and stenosis of mitral or aortic valves

130
Q

who is most affected by acute rhematoid fever

A

80% of cases affect children

131
Q

what are aschoff bodies

A

myocardial inflammatory lesions that are only seen in rheumatic fever
made of T lymphocytes, plasma cells, and macrophages

132
Q

what is infective endocarditis and what does it look like

A

microbial infection of the heart valves or endocarium
causes formation of bright red, friable vegetations mostly on valves
can be acute or subacute

133
Q

which organism causes 50-60% of infective endocarditis cases with exsisting damaged valves

A

streptococcus viridans
95% cure rate

134
Q

which organism causes 10-20% of infective endocarditis cases seen in damaged or non-damaged valves

A

staph. auerus
seen mostly in acute cases and has a 60-90% cure rate

135
Q

what are the three characteristic signs of endocarditis

A

roth spots
osler nodes
janeway lesions

136
Q

what are roth spots

A

white centered retinal hemorrhages in acute endocarditis

137
Q

what are janeway lesions

A

irregular, nontender hemorrhagic macules located on palms and soles seen in acute endocarditis cases

138
Q

what are osler nodes

A

tender, purple pink nodules with a place center found on fingers and toes in cases of subacute endocarditis

139
Q

what are four adverse reactions of endocarditis

A

glomerulonephritis
septicemia
arrhythmias
systemic embolization

140
Q

what is the treatment of endocarditis

A

6+ weeks of antibiotic therapy or valve replacement

141
Q

what is nonbacterial thrombotic endocarditis

A

deposition of sterile thrombi on cardiac valves
ususally nondestructive and can occur in healthy individuals

142
Q

what are three precursor conditions of nonbacterial thrombotic endocarditis

A

malignancy
DIC
endocardial trauma

143
Q

what is libman-sacks endocarditis

A

sterile vegetations on valves associated with SLE (10%)
vegetations on both sides of valve surrounded by fibrinoid necrosis

144
Q

what are the two most common valves affected by libman-sacs endocarditis

A

aortic and mitral valves

145
Q

what is the most common type of cardiomyopathy

A

dilated cardiomyopathy (dilation of atria/ventricles) which has a high mortality rate

146
Q

what is hypertrophic cardiomyopathy and what causes it

A

myocardial hypertrophy
genetic causes manifesting during a post puberty growth spurt

147
Q

what is restrictive cardiomyopathy and which special stain helps to diagnose it

A

extracellular deposition of amyloid leading to loss of normal tissue architecture
diagnosed through congo red stain
caused by: fibrosis, amyloidosis, or sarcosis

148
Q

what is dilated cardiomyopathy

A

hypertrophy of myocytes with enlarged nucleis and fibrosis
most commonly caused by myocarditis or it’s hereditary

149
Q

what is arrhythmogenic right ventricular cardiomyopathy and how does it present under the microscope

A

type of dilated cardiomyopathy
usually caused by right-sided heart failure and rhythm disturbances
fat replacement seen microscopically
causes 10% of sudden death in atheletes

149
Q

what are the two most common viral infections to cause myocarditis

A

enteroviruses
coxsackieviruses A and B

150
Q

what percentage of cardiac tumors are benign

A

80-90%

151
Q

what are the four types of cardiac tumors

A

myxomas (most common)
fibromas
papillary fibroelastomas
rhabdomyosarcomas

152
Q

what do myxomas of the heart look like

A

lobulated and polypoid with soft gelatinous appearence (look like a brocolli floret made of jelly)
usually found in left atrium

153
Q

what is a papillary fibroelastoma

A

benign tumor on aortic or mitra valves
surfaces have fronds
can have a stalk

154
Q

what is the most frequent primary tumor of pediatric heart

A

rhabdomyoma

155
Q

what are the four most frequent tumors that metastasize to the heart

A

lung and breast carcinomas
melanomas
leukemias
lymphomas

156
Q

what is carcinoid heart disease

A

carcinoid tumors release bioreactive components and cause valvular plaque thickening

157
Q

what is allograft arteriopathy

A

most important long term limitation for cardiac transplantation
intimal proliferation of coronary arteries leads to stenosing and ischemia

Basic Human Pathology (18 decks)

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