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Cardiac Pathology Flashcards

1
Q

What happens to the myocytes with unstable angina?

A

Reversible injury to the myocytes (cellular swelling)

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2
Q

What percent of stenosis of the arteries with atheromas does stable angina develop?

A

Greater than 70%

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3
Q

What are the s/sx of stable angina? How long does it last for?

A

Chest pain that lasts less than 20 minutes, and is brought on by exercise

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4
Q

How long does the chest pain last in stable angina? What is the significance of this time?

A

Less than 20 minutes How long that myocytes can tolerate reduced blood flow

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5
Q

Which cell layer of the heart is affected with myocardial ischemia? What are the characteristic EKG findings with this?

A
  • Subendocardial layer

- ST segment depression

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6
Q

What is the MOA by which NTG relieves stable angina?

A

Decreases venous return (preload) via NO production

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7
Q

What are the characteristics of unstable angina?

A

Chest pain at rest due to rupture of an atherosclerotic plaque

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8
Q

What causes unstable angina?

A

Rupture of an atheroscleotic plaque with thrombosis and an incomplete occlusion of a coronary artery

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9
Q

Is the injury to the myocytes in unstable angina reversible?

A

Yes

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10
Q

What are the EKG changes with unstable angina?

A

ST segment depression

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11
Q

What is Prinzmetal angina?

A

Spasm of the coronary artery, causing chest pain that is unrelated to exertion

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12
Q

What are the EKG findings with Prinzmetal angina? Why?

A
  • ST elevation

- Complete loss of blood supply to all layers of the myocardium

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13
Q

What are the meds that are used in Prinzmetal angina, and how do they relieve chest pain?

A

NTG- vasodilation

CCB- vasodilation + stop spasms

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14
Q

What is the cause of an MI?

A

Complete occlusion of a coronary artery by plaque or spasm

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15
Q

How long does the chest pain last with an MI?

A

Greater than 20 minutes

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16
Q

Is the chest pain with an MI relieved by NTG administration?

A

No

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17
Q

What is the most common artery that is occluded in an MI? What does this cause in terms of heart wall damage?

A
  • LAD

- Anterior wall of the LV infarction

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18
Q

What is the artery that supplies the inferior wall of the ventricle?

A

RCA

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19
Q

What is the artery that supplies the left lateral wall of the LV?

A

LCX

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20
Q

Which layer of the heart is undergoes necrosis first in an MI? What will will the EKG show?

A
  • Subendocardium

- ST depression

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21
Q

What is the most sensitive test for an MI? When does this rise, and for how long?

A
  • Troponin I

- Rises 2-4 hours after infarction, peaking at 24 hours, and returning to normal at 7 days

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22
Q

What is the use of CK-MB?

A

Rises 4-6 hours, but returns to normal after 72 hours. Thus can be used to r/o a reinfarction after a recent MI

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23
Q

What is the treatment for an MI?

A
  • ASA/heparin
  • Supplemental O2
  • Nitrates
  • Beta blocker
  • ACEI
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24
Q

What is the use of beta blockers in an MI?

A

Lower oxygen demand by decreasing contractility

Lower BP

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25
Q

What is the basis of using an ACEI in an MI? (2)

A
  • Inhibit volume increase via aldosterone

- Lower BP rise with angiotensin

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26
Q

What causes the contraction band contraction after fibrinolysis?

A

Return of blood flow returns Ca to a dead myocytes, causing contraction

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27
Q

What is the cause of reperfusion injury?

A

Release of oxygenated blood to myocytes that do not have Enzymes to catalyze it

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28
Q

What are the myocyte changes that are seen within four hours after onset of an MI?

A

None

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29
Q

What are the changes in myocytes that occurs within 4-24 hours? (color, necrosis type)

A

Dark discoloration

Coagulative necrosis

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30
Q

What are the changes in myocytes that occurs within 1-3 days? (color, cellular infiltration)

A

Yellow pallor

PMN infiltration

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31
Q

What are the changes in myocytes that occurs within 4-7 days? (color, cellular infiltration)

A

Yellow pallor with macrophage infiltration

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32
Q

What are the changes in myocytes that occurs within 7+ days? (color, tissue changes)

A

Red border emerges as granulation tissue enters from the edge of infarct

Granulation tissue with plump fibroblasts

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33
Q

What are the myocytes changes that occur months after an MI?

A

White scar

Fibrosis

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34
Q

How long does it takes for arrhythmias to occur during an MI? Why?

A

4-24 hours

If hits the tracts, then will appear in this timeframe

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35
Q

What are the changes that result when macrophages/PMNs infiltrate myocytes?

A

Yellow discoloration

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36
Q

What must happen for pericarditis to occur with an MI, and when does this occur?

A

Transmural infarction

PMN phase–1-3 days

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37
Q

What is the key complication that occurs with the macrophage phase of myocyte infiltration?

A

Rupture of the ventricles or septum

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38
Q

What artery is occluded that risks papillary muscle rupture?

A

RCA

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39
Q

What are the three characteristics of the granulation tissue that forms within myocytes?

A

Plump fibroblasts
Collagen
Blood vessels

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40
Q

What causes the red border of the granulation tissue in dead myocytes?

A

Neovascularization

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41
Q

What is the major long term complication of the white scar left behind from an MI? Why?

A
  • Aneurysm = thombus formation

- Weaker wall

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42
Q

What is Dressler syndrome? When does this occur after an MI?

A

Inflammation of the pericardium, causing an autoimmune pericarditis

6-8 weeks once immune system revs up

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43
Q

What is the collagen type that is found within the white scar post MI?

A

Type I collagen

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44
Q

What causes sudden cardiac death?

A

Fatal ventricular arrhythmia, from severe preexisting atherosclerosis

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45
Q

—What is chronic ischemic heart disease?—

A

—Poor myocardial function d/t chronic ischemic damage, leading to CHF—

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46
Q

What are the major causes of left sided heart failure?

A
  • Ischemia
  • HTN
  • Dilated cardiomyopathy
  • MI
  • Restrictive cardiomyopathy
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47
Q

Why does hypertrophy of the heart lead to damage?

A

Ischemia secondary to lack of oxygenation from increase in muscle tissue

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48
Q

What are heart failure cells? What causes these?

A

Hemosiderin laden macrophages from consuming blood from ruptured capillaries

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49
Q

Why does LV failure lead to congestion failure?

A

Buildup of fluid backward

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50
Q

What happens in the kidney during LV failure?

A

Activation of the renin-angiotensin system leads to increased BP and aldosterone release, causing Na (and water) resorption

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51
Q

What is the mainstay of treatment for CHF? Why?

A
  • ACEI

- Reduces TPR and blood volume

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52
Q

What is the most common cause of RV failure? What are the two other major examples?

A
  • LV failure
  • VSD
  • COPD
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53
Q

How does COPD lead to RV failure?

A

hypoxia throughout the lung causing vasoconstriction, and increased pulmonary resistance

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54
Q

—-What causes cardiac cirrhosis (liver cirrhosis 2/2 HF)? How does this appear grossly?—-

A

—RV failure leads to backup of fluid into the liver

Nutmeg liver—-

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55
Q

When do heart defects generally form in gestation? What percent of births do these occur in?

A

3-8 weeks

1% of live birth

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56
Q

True or false: most congenital heart defects are sporadic

A

True

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57
Q

What is the most common CHD? What is it associated with?

A
  • VSD

- Fetal alcohol syndrome

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58
Q

What is the long term sequale with a VSD?

A

L to R shunt will cause pulmonary HTN until there is lower pressure in the LV, forcing deoxygenated blood to the systemic system

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59
Q

True or false: small VSDs are usually asymptomatic

A

True

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60
Q

What is Eisenmenger syndrome? What may the kidneys do to counteract the hypoxemia

A

RVH from chronic stress of excess blood

Polycythemia d/t chronic hypoxia from a VSD

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61
Q

What is the most common type of an ASD? What genetic disorder is this highly associated with?

A

Ostium secundum

Down syndrome (THIS IS PRIMUM, thus this card is half-incorrect)

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62
Q

What is the treatment for small and large VSDs?

A

Large need surgical closure, small usually regress on their own

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63
Q

What is the cause of a paradoxical embolus?

A

ASD allows a thrombus to cross over to the systemic circulation as opposed to the pulmonary

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64
Q

What infectious disease is PDA associated with? What are the other s/sx of this congenital infection?

A

Congenital rubella

  • PDA
  • Cataracts
  • Sensorineural deafness
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65
Q

What is the natural history of a PDA (specifically before and after the pulmonary artery changes occur)?

A

shunting of blood from the pulmonary artery to the aorta initially causes pulmonary overload, and pHTN.

The shunt reverses when this gets high enough, causing deoxygenated blood to flow to the aorta, resulting in peripheral cyanosis

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66
Q

What is the murmur that is found with PDA?

A

Holosystolic, machine-like murmur

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67
Q

What is the basis for using indomethacin for closing a PDA?

A

Decreases PGE, resulting in PDA closure

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68
Q

What are the four components of the TOF?

A
  1. VSD
  2. Pulmonary stenosis
  3. Overriding aorta
  4. RVH
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69
Q

What is the way in which kids with TOF increase blood flow to the pulmonary circuit? How does this work?

A
  • Squat down

- Increasing arterial vascular pressure increases afterload

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70
Q

What determines that degree of shunting in TOF?

A

Degree of pulmonary artery stenosis

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71
Q

What is the classic finding on CXR with TOF?

A

Boot-shaped heart

72
Q

What is transposition of the great vessels?

A
  • Aorta connects to the RV

- Pulmonary artery connects to the LV

73
Q

What is the drug that can be administered to maintain an open PDA?

A

PGE

74
Q

Transposition of the great vessels is associated with what maternal condition?

A

Maternal DM

75
Q

How do kids with TGA present?

A

Pulmonary and systemic circuits do not mix, thus fast onset of cyanosis

76
Q

What is the immediate treatment for transposition of the great vessels?

A

PGE to maintain PDA

77
Q

What is the pathophysiology of persistent truncus arteriosus?

A

Single large vessel arising from both ventricles d/t failure of the truncus to divide.

This causes inappropriate mixing of blood = cyanosis

78
Q

What occurs in the heart with tricuspid atresia?

A

Failure of the tricuspid valve to develop, leading to RV hypoplasia. ASD leads to a R to L shunt

79
Q

What is the infantile form of coarctation of the aorta?

A

Coarctation lies distal to the aortic arch, but proximal to the PDA

80
Q

What genetic disease is the infantile form of coarctation of the aorta associated with?

A

Turner syndrome

81
Q

How does the infantile form of coarctation of the aorta usually present?

A

Lower extremity cyanosis

82
Q

What is the major cause of cyanosis in infantile coarctation of the aorta?

A

Lower pressure after the coarctation allows PDA to shunt deoxygenated blood to the systemic circuit

83
Q

What is the adult form of coarctation of the aorta?

A

Not associated with a PDA, but coarctation lead to HTN in the upper extremities, and hypotension in the lower extremities

84
Q

What is the classical sign of the adult form of coarctation of the aorta?

A

Major SBP difference between upper and lower extremities d/t coarctation cutting off blood to the lower part of the body

85
Q

What other congenital condition of the adult form of coarctation of the aorta associated with?

A

Bicuspid aortic valve

86
Q

—What is the classical findings on CXR with the adult form of coarctation of the aorta?—

A

—Engorged arteries cause notching of ribs—

87
Q

What is the agent that causes acute rheumatic fever? When does it occur?

A

Group A strep pharyngitis complication that occurs 2-3 weeks after strep throat

88
Q

How does Strep cause rheumatic fever?

A

molecular mimicry from the bacterial M protein

89
Q

What is the criteria (eponym) for rheumatic fever infection?

A

Evidence of a prior group A strep infection
Fever + elevated ESR
And a major criteria

90
Q

What are the two lab markers of a prior group A strep infection?

A

ASO

Anti-DNase B titer

91
Q

What are the major criteria for the Jones criteria of acute rheumatic fever?

A
  • Joint infection (migratory)
  • O (pancarditis)
  • Nodules of skin
  • Erythema marginatum
  • Sydenham chorea
92
Q

What is the preferential area affected with endocarditis secondary to rheumatic fever?

A

Endocardium (usually Mitral valve or sometime Aortic)

93
Q

What is the key histological finding of rheumatic fever affecting the mitral valve? What are these made of?

A

Aschoff bodies

Collagen, giant cells, and Anitschkow cells

94
Q

What are Aschoff bodies?

A

Collections of collagen, giant cells, and anitschkow cells found in rheumatic fever

95
Q

What are Anitschkow cells?

A

Histiocytes with slender, wavy nuclei in the center found in myocarditis in acute rheumatic fever

96
Q

What happens with chronic rheumatic fever upon reexposure to strep A?

A

results in relapse of the acute phase, and increases the risk for chronic valvular disease

97
Q

What is chronic rheumatic valve disease?

A

Valve scarring that results from rheumatic fever that usually results in stenosis with a “fish-like” appearance

98
Q

What is the hallmark appearance of the aortic valve stenosis in chronic rheumatic fever?

A

“fish-like”

99
Q

What happens to the chordae tendineae and cusps of the mitral valve in chronic rheumatic fever?

A

Thickening

100
Q

What happens if the mitral valve is affected in chronic rheumatic fever?

A

Fusion of the commissures, causing stenosis

101
Q

What is the cause of aortic stenosis?

A

Wear and tear on the valve

102
Q

When does aortic stenosis usually present?

A

Late adult life

103
Q

What particular congenital disorder increases the risk of developing aortic stenosis? Why?

A

Bicuspid aortic valve

now two cusps are doing the work of three

104
Q

How do you differentiate aortic stenosis secondary to rheumatic valve disease, and the “wear and tear” etiology?

A

Rheumatic valve disease has coexisting mitral valve stenosis

Aortic valve with have fusion of the commissures with rheumatic heart disease

105
Q

What does the compensation of aortic stenosis (of any etiology) lead to?

A

Systolic ejection click, crescendo-decrescendo followed by a murmur.

LV hypertrophy

106
Q

Why are angina and syncope common with aortic stenosis?

A

Inability to get blood across the valve to the heart and coronaries

107
Q

What is the anemia that is caused by aortic stenosis? How does it cause this?

A

Microangiopathic hemolytic anemia

Rupture of the RBCs as they pass the stenotic area

108
Q

What is the treatment for aortic stenosis? When is this performed?

A

Valve replacement after the onset of complications

109
Q

When in the heart cycle does aortic regurgitation occur?

A

Diastole

110
Q

What are the two causes of aortic regurgitation?

A

Aortic root dilation (increases space between the valves) or valve damage

111
Q

What are the sounds of an aortic regurg murmur?

A

Early, blowing diastolic murmur

112
Q

What are the hyperdynamic findings of aortic regurgitation? Why does these occur?

A

bounding pulses, pulsating nail bed, head bobbing

Large increase in SBP

113
Q

What causes the increase in wedge pressure with aortic regurg?

A

Large increase in SBP d/t LVH, lower DBP d/t backflow of blood

114
Q

What happens to the LV in aortic regurgitation?

A

Dilation and eccentric hypertrophy

115
Q

What is the treatment for aortic regurg?

A

Valve replacement when LV dysfunction develops

116
Q

What is the cause of mitral valve prolapse?

A

Degeneration of the mitral valve, making it more floppy than usual

117
Q

What inherited diseases is mitral valve prolapse associated with?

A

Ehlers-Danlos syndrome or Marfan’s

118
Q

What causes the click heard in mitral valve prolapse?

A

Ballooning back of the mitral valve into the atrium

119
Q

What are the characteristics of the murmur produced from mitral valve prolapse?

A

Mid-Systolic click

120
Q

What are the complications of mitral valve prolapse?

A

Infectious endocarditis
Arrhythmia
Severe mitral regurg

121
Q

What is the treatment for mitral valve prolapse?

A

Valve replacement

122
Q

What, usually, is the cause of mitral regurg?

A

Complication secondary to mitral valve prolapse

Or can be from LV dilation

123
Q

What muscles, when damaged during an MI, can lead to mitral valve prolapse?

A

Papillary muscles

124
Q

What are the characteristics of the murmur found in mitral valve regurgitation? What can increase the intensity of the sound?

A

Holosystolic “blowing” murmur, with squatting and expiration increasing the sound

125
Q

What causes the increase in intensity of a mitral regurgitation murmur with expiration?

A

Expiration leads to increased venous return to the LA and LV, meaning more blood is regurgitated

126
Q

What is the usual cause of mitral stenosis?

A

Chronic rheumatic valve disease

127
Q

What are the characteristics of the murmur heard in mitral stenosis?

A

Opening snap, followed by a diastolic rumble

128
Q

—What are the three major complications associated with mitral stenosis?—-

A
  • Pulmonary congestion
  • Pulmonary HTN
  • A-fib
129
Q

What is endocarditis?

A

Inflammation of the endocardium that lines the cardiac valves, usually due to a bacterial infection

130
Q

What infectious agent is the most common overall cause of endocarditis? How virulent is this and why?

A
  • Strep viridans

- Low virulence, since it only infects previously damaged valve

131
Q

What is the end result of endocarditis infection with Strep Viridans?

A

Small vegetations that do not destroy the valve

132
Q

What about damaged valve leads to the development of endocarditis?

A

Damaged endocardial surface develops thrombotic vegetations, allowing for the trapping of bacteria within the vegetations

133
Q

What is the most common infectious agent that causes endocarditis in IV drug abusers? How virulent is this and why?

A
  • Staph Aureus

- High virulence, since it can infect normal valve, and results in large vegetations that destroy the valve

134
Q

Which valve is the one classically infected by staph Aureus?

A

tricuspid

135
Q

What is the key bacteria that causes endocarditis of prosthetic valves?

A

Staph Epidermidis

136
Q

What is the infectious agent that causes endocarditis in patient with underlying colorectal carcinoma?

A

Strep Bovis

Bovis in the blood, cancer in the colon

137
Q

What are the HACEK organisms that cause endocarditis? What is characteristic of the blood cultures of these organisms?

A
  • Haemophilus
  • Actinobacillus
  • Cardiobacterium
  • Eikenella
  • Kingella

All will grow negative blood cultures

138
Q

What are the clinical features of endocarditis?

A
  • Fever
  • Murmur
  • Janeway lesions
  • Osler nodes
  • Anemia of chronic disease
139
Q

What causes the murmur in endocarditis?

A

Vegetation of the valves disrupts flow

140
Q

What causes the emboli found with endocarditis?

A

break off pieces of the vegetations

141
Q

What are Janeway lesions?

A

Erythematous, non-tender lesions on the palms and soles of the feet due to septic emboli

142
Q

What are Osler nodes?

A

Painful lesions on the fingers or toes secondary to septic emboli from endocarditits

143
Q

What hematologic abnormality may occur with endocarditis?

A

-Anemia of chronic disease

144
Q

What type of anemia is the anemia of chronic disease?

A
  • Microcytic anemia

- Hepcidin release, forcing Fe into storage ferritin

145
Q

What is the best method to diagnose endocarditis?

A

Transesophageal echocardiogram (TEE)

146
Q

What is nonbacterial thrombotic endocarditis? What valve do the vegetations usually form on?

A

Sterile vegetations that arise with hypercoagulable state or underlying adenocarcinoma

Mitral valve along the lines of closure

147
Q

—What is Libman-Sacks endocarditis?—

A

—Sterile vegetations associated with SLE, the results on vegetations present on both sides of the mitral valve—

148
Q

What is the most common form of cardiomyopathy?

A

Dilated cardiomyopathy

149
Q

What is dilated cardiomyopathy? What type of dysfunction does it cause (systolic or diastolic)?

A
  • Dilation of all four chambers of the heart

- Systolic dysfunction, leading to biventricular CHF

150
Q

What are the complications of dilated cardiomyopathy?

A

Mitral and tricuspid valve regurgitation and arrhythmia d/t stretching of valves

151
Q

What causes the regurgitation in dilated cardiomyopathy?

A

Stretching of the valves

152
Q

What are the factors that are thought to play a role in the development of dilated cardiomyopathy? (5)

A
  • Genetic mutations
  • Myocarditis
  • Alcohol abuse
  • Drugs
  • Pregnancy
153
Q

What virus is the most common cause of myocarditis?

A

Coxsackie virus

154
Q

What is the treatment for dilated cardiomyopathy?

A

Transplant

155
Q

What is the most common cause of hypertrophic cardiomyopathy?

A

AD mutations in sarcomere proteins

156
Q

What is the most common form of hypertrophic cardiomyopathy?

A

LVH

157
Q

Why is there decreased CO with hypertrophic cardiomyopathy?

A

-Decreased compliance of the ventricle walls

158
Q

What are the clinical features of hypertrophic cardiomyopathy?

A
  • Sudden death
  • Decreased CO
  • Syncope with exercise
159
Q

What is the classic histological finding with hypertrophic cardiomyopathy?

A

Fibrillar and myocyte disarray

160
Q

What is restrictive cardiomyopathy?

A

Decreased compliance of ventricular endocardium

161
Q

What type of dysfunction is seen with restrictive cardiomyopathy (systolic or diastolic)?

A

Diastolic

162
Q

What are the causes of restrictive cardiomyopathy? (5)

A
  • Amyloidosis
  • Sarcoidosis
  • Hemochromatosis
  • Endocardial fibroelastosis
  • Loeffler syndrome
163
Q

What is Loeffler syndrome? What type of cardiomyopathy does it cause?

A
  • Eosinophilic infiltration of the endo and myocardium

- Leads to restrictive cardiomyopathy

164
Q

What is Endocardial fibroelastosis? Who does this usually occur in?

A

Fibrous and elastic tissue build up in the heart–usually in children

165
Q

How do patients with restrictive cardiomyopathy present (what late complication)? EKG findings?

A
  • CHF

- Low voltage EKG with diminished QRS amplitudes

166
Q

What is a myxoma? Where is this usually found?

A

Benign mesenchymal proliferation with a gelatinous appearance that grows as a pedunculated mass in the LA

167
Q

What are the histological characteristics of a myxoma?

A

Abundant ground substance

168
Q

What is the most common primary cardiac tumor in adults? Children?

A

Myxoma -adults

Rhabdomyomas - children

169
Q

What causes the syncope commonly seen with a myxoma?

A

Syncope d/t obstruction of the mitral valve

170
Q

What are rhabdomyomas? Where do they usually arise? What are they associated with?

A

Benign hamartoma of cardiac muscle that usually arise in the ventricles, and are associated with tuberous sclerosis

171
Q

True or false: mets to the heart are more common than primary tumors

A

true

172
Q

What are the common mets that go to the heart? (4)

A

Breast and lung carcinoma, melanoma, and lymphoma

173
Q

Metastases that go to the heart usually involve what layer? What does this result in?

A

Pericardium

Pericardial effusion

174
Q

What type of cardiac hypertrophy is had with chronic HTN? (concentric or eccentric)

A

Concentric

175
Q

What happens to the heart sounds with ASDs? Why?

A

Fixed splitting of S1 and S2, since LA has a consistent volume, regardless of inspiration or not

All the things (36 decks)

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