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Pathology > Chapter 12 - The Heart > Flashcards

Chapter 12 - The Heart Flashcards

0
Q

How are sarcomeres arranged in volume overload hypertrophy? What happens to the ventricles

A

Sarcomeres are arranged in series with existing sarcomeres. There is ventricular dilation

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1
Q

What happens to the sarcomeres in pressure overload hypertrophy and what happens to the ventricles?

A

Sarcomeres are assembled in parallel and there is a concentric increase in wall thickness

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2
Q

What happens to gene expression with hemodynamic overload in the heart

A

Gene expression pattern begins to resemble that seen during fetal cardiac development

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3
Q

Left sided heart failure is most likely caused by (4)

A

Ischemic heart disease, hypertension, valvular disease, myocardial diseases

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4
Q

Microscopic change in myocytes in left-sided heart failure

A

Hypertrophy and variable degrees of interstitial fibrosis

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5
Q

What do the lungs look like in left-sided heart failure? What causes them to be like this?

A

Heavy, wet lungs caused by pulmonary congestion and edema

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6
Q

What is seen on chest radiograph that is characteristic of left-sided heart failure

A

Kerley B lines from septal edema

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7
Q

What is a sign of previous episodes of pulmonary edema and what makes these signs

A

Heart failure cells, which are hemosiderin laden macrophages that store iron recovered from RBCs that have escaped into edema fluid

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8
Q

Symptoms of left sided heart failure

A

Cough, dyspnea, orthopnea, paroxysmal nocturnal dyspnea (choking sensation at night when patient is supine)

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9
Q

Pathophysiology of Left-sided heart failure, renal system, and coma

A

Decrease in cardiac output –> decrease in renal perfusion –> renin-angiotensin-aldosterone system –> retains water and sodium –> increased interstitial volume –> pulmonary edema –> decrease secretin of nitrogenous wastes –> hypoxic encephalopathy –> stupor/coma

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10
Q

What is diastolic left-sided heart failure

A

Cardiac output is preserved at rest but the left ventricle is abnormally stiff and unable to relax during diastole

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11
Q

What are risk factors for diastolic heart failure

A

Patients women over 65, hypertension, diabetes mellitus, obesity, bilateral renal artery stenosis

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12
Q

What is commonly a cause of right sided heart failure

A

Left sided heart failure

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13
Q

What is pure right sided heart failure called

A

Cor pulmonale

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14
Q

What does the heart look like with right sided heart failure

A

It is hypertrophic and the right atrium and ventricle is dilated

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15
Q

What other organs are involved in right sided heart failure and what happens to them?

A

Systemic/portal venous congestion (like JVD) –> hepatoplenomegaly (nutmeg liver, cardiac sclerosis/cirrhosis), ankle and pretibial edema, pleural effusions, ascites

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16
Q

What does the first heart field form

A

Left ventricle

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17
Q

What does the second heart field form

A

The outflow tract, right ventricle and most of the atria

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18
Q

When does the second heart field migrate?

A

Day 15

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19
Q

What causes the septa tigon of outflow aortic arches III, IV, VI

A

Neural crest cells

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20
Q

What does the extra cellular matrix produce in heart development

A

Forms endocardium cushions that participate in valve development

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21
Q

What are the main known causes of congenital heart disease

A

Sporadic genetic abnormalities

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22
Q

What is the most common genetic cause of congenital heart disease?

A

Down syndrome

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23
Q

What are some clinical signs of right to left shunts

A

Hypoxemia, cyanosis result from the mixture of poorly oxygenated blood with systemic arterial blood

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24
Q

Consequences of right to left shunts

A

Paradoxical embolism, clubbing of tips of fingers and polycythemia

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25
Q

Some diseases that have right to left shunts

A

Tetralogy of Fallot, transposition of the great arteries, persistent truncus arteriosus, tricuspid atresia, and total anomalous pulmonary venous connection

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26
Q

What are some clinical signs that left to right shunts are associated with

A

Pulmonary HTN, Hypertrophy, reversal of the shunt (eisenmenger syndrome)

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27
Q

Obstructive congenital heart disease examples

A

Coarctation of the aorta, aortic valvular stenosis, and pulmonary valvular stenosis

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28
Q

What type of ASD is most common and where is it located, what kind of shunt is an ASD

A

Secundum ASD, oval fossa near center of atrial septum, left to right shunt

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29
Q

What other less common types of ASDs are there? And where are they located?

A

Primum (adjacent of AV valves) and sinus venosus (by the entrance of the superior vena cava-associated with anomalous pulmonary venous return to the right atrium)

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30
Q

When do ASDs become symptomatic?

A

Age 30

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31
Q

What kind of sound is heard with an ASD, why is this kind of sound heard

A

Murmur due to excessive flow through the pulmonary valve

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32
Q

Where is a patent foramen ovale located? What kind of shunt is it?

A

In atrial septum at the oval fossa, right to left shunt with fetus

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33
Q

What does a patent foramen ovale do in the fetus?

A

Allows oxygen rich blood from the placenta to bypass the not yet inflated lungs by traveling directly from the right to left atrium

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34
Q

What is the most common type of congenital cardiac anomaly, and what kind of shunt is it?

A

Ventricular septal defect, left to right shunt

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35
Q

What types of ventricular septal defect are there? And where are these located? Which is the most common VSD

A

90% membranous VSD (region of membranous inter ventricular septum), and infundibular VSD (below the pulmonary valve), and in the muscular septum (muscular VSD)

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36
Q

What do most VSDs occur with?

A

Other heart defects

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37
Q

Is surgical treatment immediately necessary for a VSD?

A

No, if the defect is small enough, surgery is delayed in hope of spontaneous closure (30-50% of cases)

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38
Q

What is the role of the ductus arteriosus in fetal circulation, and what kind of shunt is it

A

Shunts blood from the pulmonary artery to the aorta in order to bypass the lungs, left to right

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39
Q

What sound is heard on physical exam with a PDA

A

Machinery like murmur

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40
Q

If there is aortic valve atresia, what is required for patient survival

A

PDA

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41
Q

What embryological defect causes an AVSD and what type of shunt is it

A

Failure of the superior and inferior endocardium cushions of the AV canal to fuse adequately, left to right

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42
Q

What are the two most common forms of AVSD

A

Partial (primum ASD with a cleft anterior mitral leaflet) and a complete (large AV septal defect and a large common AV valve)

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43
Q

1/3 of patients with a complete AVSD have what…

A

Down syndrome

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44
Q

What type of shunt is tetralogy of Fallot and what are the features of this disease

A

Right to left shunt

  1. VSD
  2. Obstruction of right ventricular outflow tract
  3. Aorta overriding the VSD
  4. Right ventricular hypertrophy
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45
Q

What is the appearance of the heart in tetralogy of Fallot

A

Boot shaped

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46
Q

If the pulmonary valve becomes atretic instead of stenosed, what will you need to survive in tetralogy of Fallot

A

PDA or dilated bronchial arteries

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47
Q

What is pink tetralogy

A

If the pulmonary stenosis is mild, the tetralogy may resemble an isolated VSD, the shunt may be left to right without cyanosis. If it’s severe or enough time develops, the classic tetralogy develops

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48
Q

What are the vessel defects in the transposition of the great vessels? What kind of shunt is this

A

Aorta arises from the right ventricle, pulmonary artery arises from the left ventricle. Right to left shunt

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49
Q

What do patients with transposition of the great arteries need in order to survive

A

A shunt, ASD, VSD, PDA

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50
Q

What kind of shunt is a persist ant truncus arteriosus, and what is the anomaly in this disease?

A

Aorta and pulmonary artery share a common trunk and intermix blood

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51
Q

What kind of shunt is tricuspid atresia, and what is usually associated with this disorder?

A

Usually has an ASD to maintain circulation and it is a right to left shunt

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52
Q

What are some obstructive congenital heart anomalies?

A

Coarctation of hype aorta, pulmonary stenosis and atresia, aortic stenosis and atresia

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53
Q

What are the anatomical differences between the 2 types of coarctations

A

Infantile (aorta constricted between subclavian artery and ductus arteriosus) and adult form (consriction is distal to the ligamentum arteriosum and arch vessels)

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54
Q

What symptoms would be noted with the infantile form of coarctation of the aorta

A

Cyanosis in lower half of the body

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55
Q

What disease is associated with coarctation of the aorta

A

Turners syndrome

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56
Q

What symptoms are associated with the adult form of coarctation of the aorta

A

Hypertension in the upper extremities, weak pulses and hypotension in the lower extremities, claudication and coldness in lower extremities, rib notching (collateral circulation develops pre and post coarctation branches

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57
Q

What are som ischemic heart disease syndromes (4)

A

MI, angina pectoris, chronic ischemic heart disease with heart failure, sudden cardiac death

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58
Q

What is the leading cause of death for males and females in the US

A

Ischemic <3 disease !

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59
Q

Symptomatic cardiac ischemia needs to have what percent of the vessel occluded during exercise

A

75%

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60
Q

What percent of the vessel must be occluded in symptomatic ischemia even during rest

A

90%

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61
Q

What are the common coronary arteries involved in atherosclerosis

A

Left anterior descending (LAD), left circumflex (LCX), right coronary (RCA)

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62
Q

What are the differences between the 3 types of angina

A

Stable: physical/emotional excitement increases cardiac workload, relieved by rest, responds to vasodilators
Unstable: increasingly frequent pain that begins with progressively lower levels of physical activity (pre-infarction)
Prinzmetal: coronary artery spasm, responds to vasodilators, unrelated to physical activity

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63
Q

Which is the most common form of angina

A

Stable angina

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64
Q

Population and age group of MIs

A

Older men (40-65) women protected till menopause

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65
Q

What is the time frame for reversible cardiac myocyte damage

A

Severe ischemia lasting greater than 20-30 minutes

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66
Q

In an acute MI at what time after onset does permanent damage occur to the myocardium

A

2-4 hours

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67
Q

What are the types of myocardial infarctions? And what is the difference between them

A

Transmural (full thickness of the ventricular wall, ST elevation) and sub-endocardial (involves the inner third of the myocardium, non ST elevation), also circumferential subendocardial infarct (from global hypotension) and microinfarcts (from small intramural vessels)

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68
Q

Which is the most common type of myocardial infarct

A

Transmural

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69
Q

What areas does the left anterior descending coronary artery cover?

A

Anterior left ventricle, anterior 2/3 of interventricular septum

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70
Q

What areas does the right coronary artery cover?

A

Right ventricle, posterior part of the interventricular septum, posteroinferior part of the left ventricle, AV and SA nodes

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71
Q

What does the left circumflex coronary artery

A

Supplies lateral wall of the left ventricle

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72
Q

Gross order of sequence that occurs in the heart after myocardial infarction

A

<4hrs (none), 4-24hrs (dark discoloration), 1-3days (yellow pallor), 4-7 days (yellow pallor), 1-3 weeks (red border-granulation tissue on edges), months (white scar)

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73
Q

Microscopic changes that occur in the heart after a myocardial infarction

A

<4hrs (none), 4-24hrs (coagulative necrosis-wavy fibers), 1-3days (neutrophils), 4-7 days (macrophages), 1-3 weeks (granulation tissue with collagen, fibroblasts), months (fibrosis)

74
Q

What does reperfusion injury cause on histology

A

Contraction band necrosis - hypercontraction of myofibrils in dying cells (influx of Ca2+ into cytosol)

75
Q

Clinical symptoms of an MI

A

Severe, crushing chest pain for more than 20 minutes that doesn’t relieve with nitroglycerin

76
Q

When does each cardiac enzyme rise and return to normal after myocardial infarction

A

TroponinI elevates 4 hours, peaks at 24 and goes down in 7/10 days
CKMB elevates 4 hours, peaks less at 24 and goes down after 1/3 day

77
Q

Complications of myocardial infarction

A

Contractile dysfunction, arrhythmias, cardiogenic shock (large infarct), myocardial rupture, pericarditis (dressler syndrome, after 3 days), ventricular aneurysms, mitral regurg (papillary muscle dysfunction)

78
Q

What are the arteries affected in MI in decreasing order

A

LAD, Right coronary, LCX

79
Q

What causes sudden cardiac death, and when does death occur

A

A lethal arrhythmia from acute myocardial ischemia Long QT syndrome

80
Q

Most common pre existing condition for sudden cardiac death

A

Atherosclerosis

81
Q

What is required for the diagnosis for hypertensive heart disease

A

Hypertension and left ventricular hypertrophy

83
Q

What does the heart look like with right sided heart failure

A

RVH, dilation, and failure from pulmonary HTN

84
Q

failure of a valve to open completely in the heart

A

stenosis

85
Q

failure of a valve to close completely om the heart

A

insufficiency

86
Q

incompetence of a valve stemming from an abnormality in one of its support structures

A

functional regurgitation

87
Q

2/3 of all cases of valve disease involve what heart valves

A

aortic and mitral

88
Q

valvular stenosis leads to ___ overload of the heart

A

pressure overload

89
Q

valvular insufficiency leads to ____ overload of the heart

A

volume overload

90
Q

most common of all valvular abnormalities

A

acquired aortic stenosis

91
Q

acquired aortic stenosis is commonly a result of

A

wear and tear of anatomically normal valves or congenitally bicuspid valves

92
Q

morphological hallmark of non-rheumatic aortic stenosis

A

heaped up calcified masses within aortic cusps that protrude through the outflow surfaces into the sinuses preventing the opening of the cusps

93
Q

earlier hemodynamically inconsequential stage of calcification found in aortic stenosis

A

aoric vavle sclerosis

94
Q

symptoms associated with aortic valve stenosis

A

angina, CHF, syncope

95
Q

most frequent congenital cardiovascular malformation in humans

A

Congenitally bicuspid aortic valves

96
Q

where does calcium deposit in the mitral valve

A

peripheral fibrous ring

97
Q

histological change found in mitral valve prolapse

A

myxomatous degeneration

98
Q

what is myxomatous degeneration found in MVP

A

attenuation of collagenous fibrosa layer of the valve - dermatan sulfate in the leaflet

99
Q

what genetic disorder is MVP associated with

A

Marfan syndrome - fibrillin-1

100
Q

MVP is most common in what population

A

young women

101
Q

how does a patient with MVP present?

A

asymptomatic and discovered incidentally with a midsystolic click followed by a systolic murmur on physical exam

102
Q

mitral stenosis is seen in what disease

A

rheumatic heart disease

103
Q

dilation of the ascending aorta from htn and aging

A

aortic insufficiency

104
Q

organism involved in rheumatic fever

A

group A stretococcal pharyngitis

105
Q

morphology of rheumatic fever, what type of cells are present? (5)

A

Anitschkow cells, caterpillar cells, small 1-2mm vegetations-verrucae along the lines of closure, MacCallum plaques, aschoff bodies

106
Q

anatomic changes found in the mitral valve in rheumatic heart disease

A

leaflet thickening, commissural fusion and shortening, and thickening and fusion of the tendinous cords (fish mouth/button hole)

107
Q

what are Anitschkow cells and caterpillar cells?

A

macrophages with abundant cytoplasm and central round nuclei where the chromatin is in the center and is slender wavy ribbon like –> RHD

108
Q

What are aschoff bodies?

A

foci of lymphocytes in rheumatic heard disease post mortem

109
Q

what are MacCallum plaques?

A

subendocardial lesions may produce irregular thickenings

110
Q

manifestations of rheumatic fever (5)

A

migratory polyarthritis of joints, pancarditis, subcutaneous nodules, erythema marginatum of the skin, sydenham chorea (involuntary rapid purposeless movements)

111
Q

Jones criteria for diagnosis of theumatic fever

A

group A strep infection with 2 of the major manifestations or 1 major and 2 minor manifestions (non specific signs)

112
Q

when does acute rhematic fever typically present?

A

10 days - 6 weeks after a pharyngitis

113
Q

what antibodies can be found with rheumatic fever

A

Abs to stretolysin O and DNase B in patient serum

114
Q

first attach of rhematic heart disease at what age group

A

5-15 years old

115
Q

complications of rheumatic fever

A

acute carditis with pericardial friction rubs, weak heart sounds, tachycardia, and arrhythmias

116
Q

what do the vegetations look like in infective endocarditis

A

large irregular masses on the valve cusps that can extend into the chordae

117
Q

what does acute infective endocarditis typically infect

A

a previously normal heart valve by a highly virulent organism

118
Q

what is the difference between acute infective endocarditis and subacute infective endocarditis

A

the organisms are of lower virulence and cause infections of deformed valves

119
Q

most common pathogen for IV drug users in infective endocarditis

A

Staph aureus

120
Q

what pathogen infects previously damaged or otherwise abnormal valves in infective endocarditis

A

Strep viridans

121
Q

what pathogen infects normal valves in infective endocarditis

A

Staph aureus

122
Q

most common pathogen involved in infective endocarditis

A

Strep viridans

123
Q

prosthetic valve endocarditis

A

Staph epidermidis

124
Q

bacteria that don’t fit in a certain category that could be involved in infective endocarditis

A

HACEK –> Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella

125
Q

describe the vegetations in infective endocarditis

A

friable, bulky, destructive vegetations containing fibrin, inflammatory cells, and bacteria on heart valves

126
Q

if the vegetations from infective endocarditis erode into the underlying myocardium, what can result?

A

ring abcess

127
Q

most consistent clinical sign of infective endocarditis

A

fever; murmurs are present in 90% of patients with left sided infective endocarditis

128
Q

long standing infective endocarditis may result in what? (4)

A

microthromboemboli (like splinter hemorrhages), erythematous nontender lesion on the palms or soles (janeway lesions), subcutaneous nodules in digits (osler nodes), and retinal hemorrhages (roth spots)

129
Q

what do the vegetations of nonbacterial thrombotic endocarditis look like?

A

bland small vegetations usually attached at the line of closure (bigger and not as numerous as those of rheumatic fever)

130
Q

what population is associated with nonbacterial thrombotic endocarditis

A

debilitated patients like those wiith cancer or sepsis

131
Q

libman-sacks endocarditis is associated with what disease

A

SLE lupus

132
Q

what do the vegetations look like in libman sack endocarditis and where are they located

A

small single or multiple sterile pink vegetations that have a warty appearance on the undersurfaces of the AV valves, endocardium of atria/ventricles, cords

133
Q

what valve is frequently involved in libman sacks endocarditis

A

mitral valve

134
Q

carcinoid syndrome symptoms

A

flushing of skin, cramps, nausea, vomiting, and diarrhea

135
Q

what valves does carcinoid heart disease usually involve

A

tricuspid (most common) and pulmonary valves

136
Q

what product do carcinoid tumors mostly release

A

serotonin

137
Q

gastrointestinal carcinoid tumors usually induce carcinoid heart disease if…

A

there is extensive hepatic metastases

138
Q

causes of dilated cardiomyopathies

A

genetics (mitochondrial and cytoskeleton proteins), toxins (alcohol-thiamine deficiency, doxorubicin), peripartum, previous myocarditis

139
Q

what is the ejection fraction in dilated cardiomyopathy

A

less than 40%

140
Q

types of cardiomyopathy

A

restrictive, dilated, hypertrophic

141
Q

pathophysiology behind dilated cardiomyopathy

A

decreased contractility leading to enlargement of the heart, systolic dysfunction

142
Q

clinical symptoms found in dilated cardiomyopathy

A

left and right sided heart failure symproms, arrythmias

143
Q

what does the heart look like in people with arrhythmogenic right ventricular cardiomyopathy

A

righ ventricle wall is very thinned due to loss of myocyte and lots of fatty infiltration and fibrosis

144
Q

arrhythmogenic right ventricular craiomyopathy and hyperkeratosis of plantar palmar skin surfaces

A

Naxos syndrome

145
Q

what is the gene mutation in Naxos syndrome

A

plakoglobin

146
Q

most common cause of death in young athletes

A

hypertrophic cardiomyopathy, diastolic dysfunction

147
Q

genetics of hypertrophic cardiomyopathy

A

most are autosomal dominant in young people, less commonly sporadic; involves mutations in proteins of the sarcomere

148
Q

what does the heart look like on gross examination in hypertrophic cardiomyopathy

A

thick interventricular septum

149
Q

on histology of hypertrophic cardiomyopathy, you would see

A

myofiber disarray

150
Q

auscultation in hypertrophic cardiomyopathy reveals

A

a harsh systolic ejection murmur

151
Q

restrictive cardiomyopathy is most commonly caused by

A

amyloidosis, myocardial fibrosis after surgery, radiation, sarcoidosis, metastasis, metabolite deposition from errors of metabolism, hemochromatosis, endocardial fibroelastosis, loeffler syndrome

152
Q

the ventricles are ____ in restrictive cardiomyopathy

A

noncompliant

153
Q

what is endomyocardial fibrosis and where is it found

A

disease of kids and young adults in africa and tropics by fibrosis of ventricular endocardium

154
Q

what is loeffler syndrome

A

endomyocardial fibrosis with eosinophilic infiltrate and mural thrombi

155
Q

what is endocardial fibroelastosis

A

where a dense layer of fibrosis and elastic tissue is in the endocardium

156
Q

most common cause of myocarditis

A

virus –> coxsackievirus A and B & enteroviruses, less common are HIV,CMV`

157
Q

protozoan infection with what organism can cause myocarditis

A

Trypanosoma cruzi - Chagas disease

158
Q

most common helminthic infection associated with myocarditis

A

Trichinosis

159
Q

bacteria associated with myocarditis

A

Corynebacterium diphteriae, Borrelia

160
Q

Illness associated with myocarditis

A

rheummatic fever, lupus, sarcoidosis

161
Q

hypersensitivity myocarditis results from

A

drugs like antibiotics, diuretics, antihypertensives

162
Q

during active myocarditis, what does the heart look like on gross examination

A

dilated and enlarged

163
Q

name type of myocarditis: myocyte injury with lymphocytic infiltrate

A

Viral myocarditis

164
Q

name type of myocarditis: interstitial inflammatory inflitrate with a high proportion of eosinophils

A

hypersensitivity myocarditis

165
Q

name type of myocarditis: widespread inflammatory infiltrate with giant cells

A

giant cell myocarditis (myocarditis of uncertain cause)

166
Q

name type of myocarditis: myocyte distended with trypanosomes

A

myocarditis of chagas disease

167
Q

type of pericarditis associated with noninfectious inflammatory diseases like SLE

A

serous pericarditis

168
Q

most frequent type of pericarditis

A

fibrinous and serofibrinous pericarditis

169
Q

causes of fibrinous and serofibrinous pericarditis

A

post MI, also same causes as serous pericarditis

170
Q

syptoms of fibrinous pericarditis

A

pericardial friction rub!!, signs of congestive heart failure

171
Q

type of pericarditis from microbes

A

purulent/suppurative pericarditis

172
Q

symptoms of suppurative pericarditis

A

same as fibrinous but increased signs of systemic infection

173
Q

common cause of hemorrhagic pericarditis

A

spread of a malignant neoplasm into pericardial space

174
Q

pericarditis caused by TB

A

caseous - spread from tuberculous foci within the tracheobronchial nodes

175
Q

heart is encased in a dense fibrous/fibrocalcific scar

A

constrictive pericarditis

176
Q

what is restricted physiologically in restrictive pericarditis

A

limited diastolic expansion and cardiac output; heart can’t increase its output in response to increased peripheral needs

177
Q

most common primary tumor of the heart in adults; benign/malignant

A

myxomas; benign

178
Q

most myxomas are located

A

in the left atrium

179
Q

morphology of myxomas

A

sessile or pedunculated

180
Q

if the myxoma tumor is mobile what may result

A

wrecking-ball efefct causing damage to the valve leaflets

181
Q

major clinical manifestations of myxoma tumors are…

A

due to valvular ball-valve obstruction, embolization, or syndrome with constitutional symptoms

182
Q

most frequent primary tumor of the heart in infants and children

A

rhabdomyomas

183
Q

rhabdomyomas of the heart are often associated with which disease and what mutation

A

tuberous sclerosis, TSC1 or TSC2

Pathology (9 decks)

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