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Robbins Pathology-Cardio (Chapters 11 and 12) > Chapter 12-The Heart > Flashcards

Chapter 12-The Heart Flashcards

1
Q

Which patients are more prone to mitral valve prolapse

A

-Female 7:1

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2
Q

What is restrictive cardiomyopathy secondary to

A
  • Deposition of amyloid in the wall

- Fibrosis due to radiation

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3
Q

During a MI, what is the time frame when there is:

-Onset of ATP depletion

A

Seconds

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4
Q

Very generally, what is the clinical presentation of a right to left shunt

A

Cyanosis

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5
Q

What are the increases in VSD

A

Increase in pulmonary pressure and blood flow

*Because some of the pressure and flow from the left ventricle is going into the right ventricle and pulmonary arteries

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6
Q

Which aortic condition will see an accelerated calcification course and subsequent stenosis

A

Bicuspid aortic valve shows an accelerated course

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7
Q

What are the effects of chronic rheumatic fever

A

MITRAL STENOSIS** aka fish mouth appearance
-caused by mitral leaflet thickening, fusion of commissures, thickening of tendinous cords (does not allow valves to open)

-LA enlargement leads to Afib and thromboembolic events

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8
Q

What are the light microscopy features of an MI after:

12-24 hours

A
  • Pkynosis of nuclei
  • Contraction band of necrosis
  • Hypereosinophilia
  • Early neutrophils
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9
Q

What are the gross features of an MI after:

-12-24 hours

A

Dark mottling

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10
Q

What is present in the heart with acute rheumatic fever

A
  • Pancarditis with Aschoff bodies/nodules which are granulomatous inflammation centered around vessels
  • Fibrinoid necrosis of the endocardium and left sided valve with vegetations present
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11
Q

What are the morphological findings in a patient with hypertrophic cardiomyopathy

A
  • myocardial hypertrophy, especially the septal region (produces banana shape, blocks outflow tract)
  • Myocytes are in disarray
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12
Q

What is the treatment for an acute infective endocarditis

A

Surgery and antibiotics

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13
Q

What is the cause of Naxos syndrome

A

Mutations in the gene encoding the desmosome associated protein plakoglobin

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14
Q

What is the qualification for congestive heart failure

A
  • When the heart is unable to meet the peripheral demand for blood
  • Requires increased filling pressure in order to meet the demand for blood
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15
Q

Why is neovasculature seen on the thickening valves during chronic rheumatic fever

A

Because can no longer get the blood via diffusion

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16
Q

Which bacteria tends to affect prosthetic valves

A

S. Epidermidis

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17
Q

Which metabolic issue is strongly associated with dilated cardiomyopathy

A

Hereditary hemochromatosis (HFE) leading to iron overload

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18
Q

What is the prognosis of aortic stenosis

A
  • 5 years after developing angina
  • 3 years after developing syncope
  • 2 years after developing CHF
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19
Q

What is the most common primary cardiac tumor and what is their usual location

A

Myxomas usually in the region of fossa ovalis

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20
Q

Most hereditary conditions of heart arrhythmias are what inheritance

A

Autosomal dominant

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21
Q

What are the organisms commonly involved in infective endocarditis

A
  • S viridans
  • S aureus
  • S epidermidis
  • HACEK (Hemophilus, actinobacillis, Cardiobacterium, eikenella, kingella
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22
Q

How will a myxoma sound upon auscultation

A

Tumor “plop”

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23
Q

What are the clinical complications as a result of a VSD

A
  • Right ventricular hypertrophy

- Pulmonary hypertension, which can lead to reverse flow into a right to left shunt, leading to cyanosis

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24
Q

What is acute infective endocarditis defined by

A

Rapidly progressing destructive infection of a previously normal valve

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25
Q

What is the characteristic of subacute infective endocarditis

A

Infective endocarditis is slower progressing infection of a previously deformed valve

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26
Q

What is the general cause of hypertrophic cardiomyopathy

A

Genetic disorder that leads to myocardial hypertrophy and diastolic dysfunction with reduced SV and outflow obstruction

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27
Q

Which form of VSD is most common

A

Membranous VSD

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28
Q

What are the gross features of an MI after:

2 months

A

Scarring is complete

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29
Q

What are the conditions that can lead to abnormalities of leaflets and commissures leading to mitral regurgitation

A
  • Postinflammatory scarring
  • Infective endocarditis
  • Mitral valve prolapse
  • Drugs
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30
Q

ASD is most commonly caused by what embryological defect

A

Secundum (90%)

-May be multiple or fenestrated

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31
Q

Which origins of cancers are seen in carcinoid syndrome

A

GI tract
Pancreas
Lungs

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32
Q

What are the common causes for a patent ductus arteriosus

A
  • Hypoxic infants

- Increased pulmonary vascular pressure (commonly seen in VSD)

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33
Q

What is the heritability of arrhythmogenic right ventricular cardiomyopathy

A

Autosomal dominant

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34
Q

What is the morphological changes seen with dilated cardiomyopathy

A
  • Dilation of all chambers
  • Mural thrombi
  • Refurgitation of valves
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35
Q

What must be present for transposition of the great vessels to be compatible with life, and what is the most common forms

A
  • A shunt to mix blood must be present
  • VSD (1/3)
  • ASD or PDA (2/3)
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36
Q

What is the ejection fraction of dilated cardiomyopathy

A

<40%

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37
Q

What are the light microscopy features of an MI after:

1-3 days

A
  • Coagulation necrosis
  • loss of nuclei
  • Interstitial infiltrate of neutrophils
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38
Q

What is the time frame that troponin I will remain in the blood following an MI

A

5-10 days

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39
Q

What correlates with the amount of cardiac lesions seen in carcinoid syndrome

A

-5-hydroxyindoleacetic acid

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40
Q

Which infection and condition can arise as a result of cardiac transplantation

A

EBV associated B cell lymphoma

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41
Q

How is amyloid restrictive cardiomyopathy seen histologically

A

With the Congo red stain, which yields an apple green birefringence

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42
Q

What are the light microscopy features of an MI after:

.5-4 hours

A

Waviness of fibers of infarct border

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43
Q

What is the degree of severity of the tetrology of Fallot dependent on

A

The degree of pulmonary stenosis

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44
Q

Long QT syndrome is commonly caused by which kind of mutations

A
  • Gain of function in sodium current

- Loss of function in potassium current

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45
Q

What does a mitral valve prolapse sound like on auscultation

A

Mid systolic click

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46
Q

What is the presentation of a patient with dilated cardiomyopathy

A
  • Age 20-50
  • progressive CHF
  • Arrhythmias
  • Embolism
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47
Q

What is the major complication with cardiac transplantation

A

Allograft rejection

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48
Q

During a MI, what is the time frame when there is:

-10% of normal ATP levels

A

40 minutes

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49
Q

What is the time frame that CK-MB with peak following an acute MI

A

24 hours

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50
Q

Which patient population is commonly seen or have takotsubo cardiomyopathy

A

Women (90%), between ages 58-75

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51
Q

What are the causes of abnormalities of the leaflets and commissures leading to aortic regurgitation

A

Postinflammatory scarring (rheumatic heart disease)

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52
Q

What is the best way to measure the amount of hypertrophy in the heart

A

Heart weight, because there my be wall thickness increase as well as dilation which will mask the increased thickness

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53
Q

The presence of a contraction band is indicative of what

A

Reperfusion injury

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54
Q

What is Myxomatous mitral valve and what are the physical finding

A

Thickening (proteoglycan deposition) and elastic fiber disruption leading to “hooding” of the valve

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55
Q

What is occurring during a patent foramen ovale and which can complications arise

A
  • Should close permanently by age 2
  • If it doesn’t close, then it can open if there is an increase in right atrial pressure (during bowel movement, pulm HTN, coughing, sneezing)
  • Paradoxical embolus
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56
Q

What are the three types of damage seen to the valves

A

1-Collagen (mitral prolapse)
2-Nodular calcification
3-Fibrotic thickening

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57
Q

What is the most common valve abnormality

A

Calcific aortic stenosis

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58
Q

What are the gross features of an MI after:

2-8 weeks

A

Grey-white scar

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59
Q

What is the findings of myocarditis due to Chagas’ disease

A

Parasitization of myofibers with mixed inflammatory cell infiltrates (PMN, lymph’s, Macros, and eosinophils)

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60
Q

What is the most common cause of death in patients with sudden cardiac death

A

Fatal arrhythmia due to ischemia induced myocardial irritability

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61
Q

What is the most common congenital malformation

A

VSD (42%)

ASD (10%)

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62
Q

What usually precipitates sudden cardiac death

A

Coronary artery disease (80-90%), usually being stenosis of one of the three main arteries (75%)

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63
Q

Which condition leads to anitschkow (caterpillar) cells

A

Acute rheumatic heart disease

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64
Q

What are the gross features of an MI after:

.5-4 hours

A

None

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65
Q

What is the process of calcific aortic stenosis

A

1) Wear and tear due to age HTN, HyperLDL, inflammation
2) Valves contain osteoblasts-like cells, which deposit osteoid-like substance that ossifies
3) Calcifications of cusps prevent complete opening of the valves

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66
Q

Which bacteria tends to affect normal valves, IV drug valves, or abnormal valves

A

S. Aureus

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67
Q

What are the increases in ASD

A
  • Increased Right ventricle and Pulmonary artery outflow volumes
  • No increases in pressure because the ventricle is unaffected
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68
Q

What is unstable or crescendo angina due to and what is a complication

A

Due to rupture of atherosclerotic plaque, with a partial thrombus

*Usually a history of MI necrosis (50%), with another MI being imminent

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69
Q

Mitral valvular calcification commonly occurs with which condition

A

Mitral valve prolapse

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70
Q

What are the complications arising from nonbacterial thrombotic endocarditis (NBTE)

A

Source of emboli because they are only loosely attached

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71
Q

What are the characteristics of stable angina

A
  • Stenotic occlusion of a coronary artery

- Squeeing or burning sensation with physical activity or stree

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72
Q

What does a PDA sounds like upon auscultation

A

Harsh, machinery like murmur

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73
Q

What is the treatment of subacute endocarditis

A

Antibiotics

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74
Q

What are the general findings in an acute MI that was 24+ hours

A
  • Coagulative necrosis
  • pyknotic nuclei
  • loss of cross striations
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75
Q

In the case of eccentric hypertrophy, what is the organization of sacromeres and what is the cause

A

Serial organization (in series so gets longer) as a result of volume overload

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76
Q

What is the hearts response in the left ventricle as a result of pressure overload as in chronic HTN or aortic stenosis

A

Myocytes becomes thicker and there is hypertrophy concentrically

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77
Q

What is the characteristics of mitral valve calcification

A

Calcific deposits on the Fibrous annulus

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78
Q

What are the complications seen with porcine valves

A

Calcification and tearing

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79
Q

What is the portion of the heart that is being supplied by the RCA

A
  • Posterior LV and 1/3 septum

- RV free wall

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80
Q

During a MI, what is the time frame when there is:

-Microvascular injury

A

> 1 hour

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81
Q

What is the most common form of cardiomyopathy

82
Q

What drugs/compounds are strongly linked to dilated cardiomyopathy

A
  • Alcohol strongly strongly

- Iron overload

83
Q

What are the clinical affects seen as a result of left sided heart failure

A
  • Decreased tissue perfusion (due to decreased CO)
  • Congestion of Pulmonary circulation, results in a cough, and dyspnea
  • Left atrial dilation resulting in a fib, stasis and thrombus
  • Decreased glomerular perfusion
84
Q

Which parasite can cause myocarditis

A

Trypanosome Cruzi (Chagas disease)

85
Q

What is the cause of takotsubo cardiomyopathy

A

Excess catecholamines, usually a result of increased stress resulting in the apical balling of the left ventricle

86
Q

What is seen in amyloid restrictive cardiomyopathy

A

Extracellular deposition of proteins in the interstium that form an insoluble Beta pleated sheet aka transthrytin amyloidosis

87
Q

What is the hearts response in the left ventricle as a result of volume overload as a result of decreased ejection fraction

A

Myocytes become longer and there is ventricular dilation

88
Q

What is occurring in the transposition of the great vessels

A

-Aorta and pulmonary vessels are musdivided and results in two separate circuits, and is incompatible with life unless there is a shunt present

89
Q

What are the components of a tetralogy of Fallot

A

1) VSD
2) Obstruction of pulmonary vessel (Stenosis)
3) Aorta overrides the VSD
4) RV hypertrophy

90
Q

How common are heart defects in patients with Down syndrome

A

Seen in 40% of patients

91
Q

Most acute MI that result in death occur how long after onset and what is it usually due to

A

-50% occur one hour after onset, usually secondary to an arrhythmia

92
Q

Which gene malformations are seen in those with mitral and aortic valves

93
Q

What are the gross features of an MI after:

-1-3 days

A

Mottling with yellow-tan infarct center

94
Q

What are Roth spots and what are the indicative

A

Spots in the retina and indicative of infective endocarditis

95
Q

What is the time frame following and acute MI that troponins and CK-MB can be seen in the blood and which ones are they

A

Troponins T and I starting about hour 3

96
Q

What are subungual/splinter hemorrhages and what are they indicative of

A

Small hemorrages under the nails and are indicative of infective endocarditis

97
Q

What are the clinical presentations of carcinoid syndrome

A

Flushing, diarrhea, dermatitis, bronchoconstriction

98
Q

What is the leading cause of death in the US and what is the leading cause

A

Ischemic heart disease, with 90% being secondary to atherosclerosis

99
Q

Which condition will have vegetative endocarditis characteristic of warty, line of closure

A

Rheumatic heart disease

100
Q

What is the time frame that troponin T will remain in the blood following an MI

101
Q

During a MI, what is the time frame when there is:

-Irreversible cell injury

A

20-40 minutes

102
Q

Which condition will have vegetative endocarditis characteristic of large and irregular

A

Infective endocarditis

103
Q

What are the characteristics of unstable or crescendo angina

A
  • Pain in increasing frequency, duration, and severity and progressively lower amounts of physical activity and eventually at rest
  • Usually a rupture of atherosclerotic plaque, with a partial thrombus
104
Q

How is prinzmetal angina relieved

A

Vasodilators

105
Q

Which patient group is at a higher risk for developing coarctation of the aorta

A
  • Males

- Turner Syndrome

106
Q

What are the characteristics of prinzmetal angina

A
  • Eposodic coronary artery spasm

- Unrelated to Physical activity, heart rate, or blood pressure

107
Q

What are the changes seen in the valves as the heart ages

A
  • Aortic and mitral valve annular calcification
  • Fibrous thickening
  • Mitral prolapse of leaflets (increases left atrial size)
  • Lambl excrescences
108
Q

What are the light microscopy features of an MI after:

3-7 days

A
  • Disintegration of dead myofibers

- early phagocytosis of fibers by macrophages

109
Q

Valvular insufficiency causes changes in which direction and what does chronic insufficiency lead to

A

Allows reversed flow, where chronic insufficiency causes volume overload hypertrophy

110
Q

What is Naxos syndrome

A
  • Arrhythmogenic right ventricular cardiomyopathy (ARVC)

- Distinct hyperkeratosis of plantar palmar skin surfaces***

111
Q

What is the morphological finding in restrictive cardiomyopathy

A

Both atria are enlarged while the ventricles are normal size

112
Q

What is the clinical presentation of a patient with coarctation of the aorta when there is no PDA present

A

Usually asymptomatic, but will see hypertension of the upper extremities, but hypotension of the lower extremities
-Claudication and cold lower extremities

113
Q

What are the causes of mitral valve regurgitation

A
  • Abnormalities of leaflets and commissures
  • Abnormalities of tensor apparatus
  • Abnormalities of left ventricle and/or annulus
114
Q

Which valves are most commonly affected by infective endocarditis

A

Left sided valves

115
Q

What is the most straining clinical feature of pericardial disease

A

Loud pericardial friction rub upon auscultation

116
Q

In carcinoid heart disease, which portions of the heart tend to be affected

A

Right side endocardium and valves because the left is protected by the lungs degrading the mediators of disease

117
Q

The pathogenesis of a patent ductus arteriosus is determined by which factor

A

-Shunts diameter

118
Q

What is the clinical presentation of a patient with coarctation of the aorta when there is a PDA present

A

Manifestation at birth, there is cyanosis of the lower half of the body because the deoxygenated blood from the pulmonary circulation is going into the descending aorta

119
Q

How is stable angina relieved

A

Rest or vasodilators

120
Q

What are the mutations seen with hypertrophic cardiomyopathy

A

Mutations in the sarcometric proteins, especially Beta myosin heavy chain

121
Q

What are the gross features of an MI after:

7-10 days

A

Maximal yellow-tan softening with depressed red/tan margins

122
Q

What are the changes seen in the myocardium and chambers as the heart ages

A
  • Increased left ventricular chamber size
  • Increased epicardial fat
  • Lipofuscin and basophilic degeneration
123
Q

What are the gross features of an MI after:

3-7 days

A

Hyperemic border with central yellow tan softening

124
Q

What are the histological findings in the lungs as a result of heart failure

A

“Heart failure cells” which are hemosiderin laden macrophages as a result of pulmonary congestion leading to high pressure and red cells crossing the vasculature

125
Q

What are the complications seen with artificial valves

126
Q

What is the most common cause of myocarditis

A

Coxsackie A and B virus

127
Q

What is the cause of rhuematic fever

A

Fever and systemic inflammatory disorder 10 days to 6 weeks after a pharyngeal infection with Strep A

128
Q

What are the gross features of an MI after:

10-14 days

A

Red-grey depressed infarct borders

129
Q

What is the immunological cytokine associated with myxomas

130
Q

In the acute MI complication of a myocardial rupture, what is the cause

A

Usually a transmural infarct, leading to weakening of the wall 2-4 days later as a result of the inflammation and necrosis

131
Q

What are the light microscopy features of an MI after:

10-14 days

A

Well established granulation tissue with blood vessels and collagen deposition

132
Q

Which compounds can mimic carcinoid heart disease

A
  • Fenfluramine (appetite suppressant and dieting fab)

- Ergot alkaloids (migraine)

133
Q

What is the genetic component of dilated cardiomyopathy, what is the heritability of it

A
  • Familial 30-50%, with TTN mutation being 20%

- Autosomal dominant

134
Q

During a MI, what is the time frame when there is:

-Loss of contractility

A

<2 minutes

135
Q

What are Jane way lesions and what are they indicative

A

Small, nonpainful hemorrages on the feet and hands indicative of infective endocarditis

136
Q

Myxomas are associated with mutations in which gene and which syndrome

A

GNAS1 in McCune-Albright syndome

PRKAR1A in Carney syndrome

137
Q

What are the most common forms of pericardial disease

A

-Fibrinoid and serofibrinous

138
Q

What is the prognosis with mitral valve prolapse

A
  • Usually does not affect valve function

- Becomes site for thrombus formation or infective endocarditis

139
Q

What are Osler nodes and what are the indicative of

A

Painful raised lesions on the palms and feet that are indicative of infective endocarditis

140
Q

What are the causes of aortic valve stenosis

A
  • Post-inflammatory scarring (rheumatic heart disease)
  • Senile calcific aortic stenosis
  • Calcification of deformed valve
141
Q

What are the classical morphological features of infective endocarditis and complications stemming from it

A

Friable, bulky, destructive valvular vegetations that can lead to septic emboli

142
Q

What is the general order of pathogenesis with left sided hypertensive disease

A

1) Hypertension results in left ventricular hypertrophy
2) LV wall concentrically thickens
3) Diastolic dysfunction results in left astral enlargement
4) Leads to irritation and eventual atrial fibrillation
5) Can lead to CHF and sudden cardiac death

143
Q

Which heart shunt is most common and what are some of the examples

A

Left to right:

  • ASD
  • VSD
  • PDA
144
Q

What is the clinical complication as a result of a PDA

A

-Leads to increase in Pulmonary pressure resulting in reversal of the shunt to a right to left shunt and corresponding cyanosis

145
Q

What are the common complications seen following an MI

A
  • Arrhythmia
  • Contractile dysfunction
  • Fibrinoid pericarditis
  • Myocardial rupture
  • Infarct expansion leading to thrombosis
  • Ventricular aneurysm
146
Q

What is the morphological changes seen in carcinoid heart disease

A

Glistening White intima plaque-like thickening of the endocardial surfaces and valves

*Plaques are acidmucopolysaccaride rich

147
Q

When are fibrinous and serofibrinous pericardial diseases seen

A
  • Following an acute MI or postinfarction(aka Dressler’s)

- Uremia

148
Q

What are the characteristics of nonbacterial thrombotic endocarditis (NBTE)

A

-Small, sterile thrombi loosely attached on the cardiac valve leaflets along the line of closure

149
Q

What is the time frame the CK-MB will remain in the blood following an MI

A

48-72 hours

150
Q

What is the blood supply to the myocardium

A

Coronary arteries during diastole

151
Q

What is the portion of the heart that is being supplied by the LCX

A

Lateral wall of LV

152
Q

What are the causes of abnormalities if tensor apparatus leading to air tic regurgitation

A

Marfan*
Syphillitic aortitis*
RA
Degenerative aortic dilation

153
Q

What are the effects of right sided heart failure

A

Aka cor pulmonale causes venous congestion leading to:

  • Liver congestion and nutmeg liver
  • splenic congestion and splenomegaly
  • Peritoneal, pleural and pericardial effusion
  • Renal congestion
  • Distended jugular vein
  • ascites and edema
154
Q

What are the light microscopy features of an MI after:

2-8 weeks

A

Increased collagen deposition

155
Q

What is the most common inherited arrhythmias

A

Long QT syndrome

156
Q

If you are looking at a histological slide of a patient with myocarditis, and there a excess numbers of eosinophils, what is the likely cause

A

Hypersensitivity reaction

157
Q

Which bacteria tends to be involved in endocarditis of valve abnormalities

A

S. Viridans

158
Q

What is the only cause of mitral valve stenosis

A

Postinflammatory scarring (rheumatic heart disease)

159
Q

How are the valves of the heart nourished

A

Via diffusion

160
Q

What are the gross features of an MI after:

4-12 hours

A

Start of dark mottling

161
Q

What are lambl excrescences

A

Small filliform processes forming on the closure lines of the aortic and mitral valves, usually from small thrombi

162
Q

What is the greatest limitation to cardiac transplantation

A

Allograft arteriolar as a result of intima proliferation leading to stenosis

163
Q

What is the cause of carcinoid syndrome

A

Serotonin release from carcinoid tumors, which will be seen excreted in the urine

164
Q

What is the time frame that troponin I will peak

165
Q

What are the complications seen in the kidney as a result of left sided heart failure

A

Decreased ejection fraction results in decreased glomerular perfusion. Leads to increased renin production and can lead to prerenal azotemia

166
Q

What is occurring in arrhythmogenic right ventricular cardiomyopathy

A

Right ventricular wall is replaced with adipose and fibrosis leading to ventricular tachycardia/fibrillation and subsequent death

167
Q

What is the portion of the heart that is being supplied by the LAD

A
  • Apex

- Anterior LV and 2/3 septum

168
Q

What is the pathogenesis of acute rheumatic fever causing cardiac isssues

A

Immune cross reacts the streptococcal M protein with cardiac self antigens

169
Q

What is the pathogenesis that accompanies the increased hypertrophy of the heart

A

While there is an increased thickness of myocytes, there is no corresponding increase in blood supply to match the increased energy demand

170
Q

What are the two common reasons that congestive heart failure occurs

A
  • Loss of myocardial contractile functions (systolic dysfunction)
  • Loss of ability to fill the ventricles during diastole (diastolic dysfunction)
171
Q

What are the usual morphological findings in myxomas

A

Pedunculated or sessile structure:

  • “Wrecking ball” causing damage to leaflets on valve
  • “Ball-Valve” obstruction
172
Q

IN those patients with Down syndrome, was is the most common source of their heart detects

A

The second heart field aka arterioventricular space

-Most commonly defects of the endocardial cushions, which include ostium primum, ASD,AV valves, VSDs

173
Q

What is the time frame that troponin T will peak

A

12-48 hours

174
Q

What are the clinical complications as a result of left to right shunting

A
  • Pulmonary Hypertension
  • Right sided heart failure
  • Paradoxical embolization
175
Q

What is the most common cause of left sided heart failure

A

Left sided heart failure

176
Q

What are the major causes of congenital heart disease

A

Sporadic genetic abnormalities

  • Turner syndrome
  • *Trisomies 13,18,21
  • Trisomies are the single most common genetic cause
177
Q

In the case of concentric hypertrophy, what is the organization of sacromeres and what is the cause

A

Parallel organization as a result from pressure overload

178
Q

During an acute MI, what is the first indicator is the blood

A

Myoglobin, but is not specific

179
Q

Which gene malformations are seen in those with alagille syndrome- which include pulmonary stenosis or tetralogy of Fallot

A

Jag1

Notch2

180
Q

What is the general process of restrictive cardiomyopathy

A

Increased ventricular stiffness (decreased compliance) leading to diastolic dysfunction with normal systolic function

*Atria are enlarged while ventricles are normal

181
Q

What are the light microscopy features of an MI after:

7-10 days

A
  • Well developed phagocytosis by macrophages

- Granulation tissue(vessels between fibers) at Margins

182
Q

What are the causes of restrictive endocarditis

A

Amyloidosis, radiation induces fibrosis

183
Q

What are the light microscopy features of an MI after:

>2 months

A

Dense collagenous scar

184
Q

For mitral valve prolapse, what is the cause of leaflets becoming thickened and rubbery

A

Myxomatous degeneration (proteoglycan deposits) and elastic fiber disruption

185
Q

What type of calcification is seen in the mitral valve

186
Q

During a MI, what is the time frame when there is:

-ATP reduction of 50%

A

10 minutes

187
Q

What are the serum markers that are present in a rheumatic fever

A
  • Antistreptolysin O

- Anti-DNAase B

188
Q

What are the histological findings in a patient with dilated cardiomyopathy

A

Myocytes hypertrophy with interstitial fibrosis

189
Q

What are the light microscopy features of an MI after:

4-12 hours

A

Edema, hemorrhage

190
Q

What is angina pectoris

A

Transient, recurrent chest pain induced by myocardial ischemia leading that is insufficient to cause a myocardial infarction

191
Q

What is the cause of Mitral valve stenosis

A

Post-inflammatory scarring due to rheumatic heart disease

192
Q

Which condition will have vegetative endocarditis characteristic of small, line of closure

A

Nonbacterial thrombotic endocarditis (NBTE)

193
Q

Which valves are most commonly affected by IV drug use

A

Right sided valves

194
Q

What type of calcification is seen on the aortic valve

195
Q

What are the causes of hypertrophic cardiomyopathy

A

100% genetic causes with myofiber disarray being the most common

196
Q

What is sick sinus syndrome

A

SA node damage leading to bradycardia

197
Q

What condition is nonbacterial thrombotic endocarditis (NBTE) associated with

A

Malignancy, especially mucinous adenocarcinomas

198
Q

During an MI, which portion of the endocardium is first to undergo necrosis

A

The farthest from the vessel and closest to the lumen of the chamber

199
Q

Valvular stenosis impedes which direction of flow and what is a common result of chronic stenosis

A

Impedes forward flow, chronic stenosis causes pressure overload hypertrophy

200
Q

What is the day break up between different immune cell types following an MI

A

Neutrophils dominate days 3-4

Macrophages dominate days 7-10

201
Q

What are the physiological changes seen as a result of the transposition of the great vessels

A

-Since the aorta and systemic circulation is now supplied by the RV, then the RV will become hypertrophic and the LV will atrophy

202
Q

What are the increases in PDA

A

Increase in pulmonary pressure and blood flow

*Because some of the pressure and flow from the left ventricle is going into the right ventricle and pulmonary arteries

Robbins Pathology-Cardio (Chapters 11 and 12) (4 decks)

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