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Flashcards in CH8 - Cardiac Pathology Deck (288)
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1

What is ischemic heart disease (IHD)?

Group of syndromes related to myocardial ischemia

2

What is the leading cause of death in the US?

ischemic heart disease (IHD)

3

What is ischemic heart disease (IHD) usually due to?

atherosclerosis of coronary arteries, which decreases blood flow to the myocardium

4

What are the risk factors for IHD?

They are similar to those of atherosclerosis; incidence increases with age.

5

What is stable angina?

chest pain that arises with exertion or emotional stress.

6

What is stable angina due to?

atherosclerosis of coronary arteries with > 70% stenosis;

7

Why does stable angina arise with exertion?

decreased blood flow is not able to meet the metabolic demands of the myocardium during exertion

8

What does stable angina represent?

reversible injury to myocytes (no necrosis)

9

How does stable angina present?

As chest pain lasting < 20 minutes that radiates to the left arm or jaw, diaphoresis, and shortness of breath

10

What does the EKG show in stable angina?

ST-segment depression due to subendocardial ischemia

11

What is stable angina relieved by?

rest or nitroglycerin

12

What is unstable angina?

chest pain that occurs at rest.

13

What is unstable angina usually due to?

rupture of an atherosclerotic plaque with thrombosis and incomplete occlusion of a coronary artery

14

What does unstable angina represent?

reversible injury to myocytes (no necrosis)

15

What does the EKG show in unstable angina?

ST-segment depression due to subendocardial ischemia

16

What is unstable angina relieved by?

Nitroglycerin

17

In unstable angina there is a high risk of what?

progression to myocardial infarction

18

What is prinzmetal angina?

episodic chest pain unrelated to exertion.

19

What is prinzmetal angina due to?

coronary artery vasospasm

20

What does prinzmetal angina represent?

reversible injury to myocytes (no necrosis)

21

What does the EKG for prinzmetal angina show?

ST-segment elevation due to transmural ischemia.

22

What is prinzmetal angina relieved by?

nitroglycerin or calcium channel blockers

23

What is myocardial infarction?

Necrosis of cardiac myocytes

24

What is myocardial infarction usually due to?

rupture of an atherosclerotic plaque with thrombosis and complete occlusion of a coronary artery

25

In addition to atherosclerotic plaque what are some other causes of myocardial infarction?

coronary artery vasospasm (due to Prinzmetal angina or cocaine use), emboli, and vasculitis (e.g., Kawasaki disease).

26

What are the clinical features for myocardial infarction?

include severe, crushing chest pain (lasting > 20 minutes) that radiates to the left arm or jaw, diaphoresis, and dyspnea; symptoms are not relieved by nitroglycerin.

27

In myocardial infarction what does the infarction usually involve?

the left ventricle (LV); right ventricle (RV) and both atria are generally spared.

28

What artery is most commonly involved artery in MI?

LAD; left anterior descending artery ? 45% of cases

29

What does occlusion of the left anterior descending artery (LAD) lead to?

infarction of the anterior wall and anterior septum of the LV

30

What does occlusion of right coronary artery (RCA) lead to?

infarction of the posterior wall, posterior septum, and papillary muscles of the LV;

31

What is the 2nd most commonly involved artery in MI?

RCA, right coronary artery

32

What does occlusion of the left circumflex artery lead to?

infarction of lateral wall of the LV.

33

What does the initial phase of infarction lead to?

subendocardial necrosis involving < 50% of the myocardial thickness (subendocardial infarction);

34

What does the EKG show for the initial phase of infarction?

(subendothelial infarction) ST-segment depression.

35

After the initial phase of infarction, what does continued or severe ischemia lead to?

transmural necrosis involving most of the myocardial wall (transmural infarction)

36

What does the EKG show in transmural infarction?

ST-segment elevation

37

What do the laboratory tests detect for myocardial infarction?

elevated cardiac enzymes.

38

What is the most sensitive and specific marker (gold standard) for Ml?

troponin I

39

What are the troponin I levels after 2-4 hours?

Levels rise 2-4 hours after infarction

40

When do troponin I levels peak?

at 24 hours

41

When do troponin I levels return to normal?

By 7-10 days.

42

What is CK-MB is useful for?

detecting reinfarction that occurs days after an initial MI

43

When do creatine kinase MB (CK-MB) levels rise?

4 - 6 hours after infarction

44

When does creatinine kinase MB levels peak?

They peak at 24 hours

45

When does creatinine kinase MB levels return to normal?

by 72 hours.

46

What does treatment for myocardial infarction include?

1) Asprin 2) Supplemental O2 3) Nitrates 4) beta-blockers 5) ACE inhibitor 6)Fibrinolysis or angioplasty

47

How does aspirin and/or heparin help treat MI?

limits thrombosis

48

How does supplemental 02 help treat MI?

minimizes ischemia

49

How do nitrates help treat MI?

vasodilate coronary arteries

50

How does beta-blockers help treat MI?

slows heart rate, decreasing O2 demand and risk tor arrhythmia

51

How does ACE inhibitors help treat MI?

decreases LV dilation

52

How does fibrinolysis or angioplasty help treat MI?

opens blocked vessel

53

What happens in fibrinolysis or angioplasty post-MI?

it opens bloced vessel; 1) contraction band necrosis 2) reperfusion injury

54

What is contraction band necrosis?

After fibrinolysis or angioplasty post-MI there is reperfusion of irreversibly damaged cells resulting in calcium influx, leading to hypercontraction of myofibrils

55

What is reperfusion injury?

After fibrinolysis or angioplasty post-MI, the return of oxygen and inflammatory cells may lead to free radical generation further damaging myocytes

56

< 4 hours from time of infarction what are the gross and microscopic changes?

No gross changes, and no microscopic changes

57

What are the complications < 4 hours from time of infarction?

Cardiogenic shock (massive infarction), congestive heart failure, and arrhythmia

58

4-24 hours from time of infarction what are the gross and microscopic changes?

[Gross] Dark discoloration and [microscopic] Coagulative necrosis

59

What are the complications from 4-34 hours from the time of infarction?

arrhythmia

60

1-3 days from time of infarction what are the gross and microscopic changes?

[gross] Yellow pallor, [microscopic] Neutrophils

61

What are the complications for 1-3 days from time of infarction?

Fibrinous pericarditis presents as chest pain with friction rub

62

What does fibrinous pericarditis present as?

chest pain with friction rub

63

4-7 days from time of infarction, what are the gross and microscopic changes?

[gross] Yellow pallor, [Microscopic] Macrophages

64

What are the complications 4-7 days from time of infarction?

Rupture of ventricular free wall, interventricular septum, or papillary muscle

65

What does rupture of ventricular free wall lead to?

cardiac tamponade

66

What does rupture of interventricular septum lead to?

shunt,

67

What does rupture of papillary muscle lead to?

mitral insufficiency

68

1-3 weeks from time of infarction, what are the gross and microscopic changes?

[gross] Red border emerges as granulation tissue enters from edge of infarct, [microscopic] Granulation tissue with plump fibroblasts, collagen, and blood vessels

69

Months from time of infarction, what are the gross and microscopic changes?

[gross] White scar, [microscopic] Fibrosis

70

What are the complications for 1 Month from the time of infarction?

Aneurysm, mural thrombus, or Dressier syndrome

71

What is sudden cardiac death?

Unexpected death due to cardiac disease, occurs without symptoms or <1 hour after symptoms arise

72

What is sudden cardiac death usually due to?

fatal ventricular arrhythmia

73

What is the most common etiology for sudden cardiac death?

acute ischemia; 90% of patients have preexisting severe atherosclerosis.

74

What are the less common causes for sudden cardiac death?

mitral valve prolapse, cardiomyopathy, and cocaine abuse

75

What is chronic ischemic heart disease?

Poor myocardial function due to chronic ischemic damage (with or without infarction);

76

What does chronic ischemic heart disease progress to?

congestive heart failure (CHF)

77

What is congestive heart failure?

Pump failure; divided into right- and left-sided failure

78

What are the causes of left-sided heart failure?

ischemia, hypertension, dilated cardiomyopathy, myocardial infarction, and restrictive cardiomyopathy

79

What are the clinical features for left-sided heart failure due to?

decreased forward perfusion and pulmonary congestion.

80

What are the clinical features for left-sided heart failure?

1) decreased perfusion and pulmonary congestion 2) activation of rennin angiotensin system

81

In left-sided heart failure what does pulmonary congestion lead to?

pulmonary edema.

82

In left-sided heart failure why is there paroxysomal nocturnal dyspnea?

Its due to increased venous return when lying flat

83

In left-sided heart failure, pulmonary edema results in what?

dyspnea, paroxysmal nocturnal dyspnea, orthopnea, and crackles

84

How can left-sided heart failure lead to intra-alveolar hemorrhage?

Small, congested capillaries may burst, leading to intraalveolar hemorrhage

85

In left-sided heart failure what is intra-alveolar hemorrhage marked by?

hemosiderin-laden macrophages (heart-failure cells)

86

In left sided heart failure how are the kidneys involved?

Decreased flow to kidneys leads to activation of renin-angiotensin system

87

In left sided heart failure does the kidney affect the rennin angiotensin system?

Fluid retention exacerbates CHF

88

What is the main treatment for left sided heart failure?

treatment is ACE inhibitor.

89

What is right-sided heart failure most commonly due to?

left-sided heart failure;

90

Aside from left sided heart failure what are some other important causes for right sided heart failure?

Left to-right shunt and chronic lung disease (cor pulmonale)

91

What are the clinical features for right sided heart failure due to?

congestion

92

What are the clinical features for right sided heart failure?

1. Jugular venous distension 2. Painful hepatosplenomegaly with characteristic nutmeg liver; may lead to cardiac cirrhosis 3. Dependent pitting edema

93

In right sided heart failure what is the dependent pitting edema due to?

increased hydrostatic pressure

94

What are the congenital heart defects?

Arise during embryogenesis

95

When do congenital heart defects usually arise?

usually weeks 3 through 8

96

In what percentage of live births do you see congenital heart defects?

seen in 1% of live births

97

Most congenital heart defects are?

sporadic.

98

Congenital heart defects often result in?

shunting between left (systemic) and right (pulmonary) circulations.

99

Defects with left-to-right shunting

may be relatively asymptomatic at birth, but the shunt can eventually reverse

100

What does increased flow through the pulmonary circulation result in?

hypertrophy of pulmonary vessels and pulmonary hypertension.

101

What does increased pulmonary resistance eventually result in?

reversal of shunt

102

What does the reversal of shunt in congenital defects with left to right shunt lead to?

late cyanosis (Eisenmenger syndrome) with right ventricular hypertrophy, polycythemia, and clubbing.

103

What do defects with right-to-left shunting usually present as?

cyanosis shortly after birth.

104

What is ventricular septal defect (VSD)?

Defect in the septum that divides the right and left ventricles

105

What is the most common congenital heart defect?

ventricular septal defect (VSD)

106

What is ventricular septal defect (VSD) associated with?

fetal alcohol syndrome

107

What does ventricular septal defect (VSD) result in?

left-to-right shunt,

108

What determines extent of shunting in ventricular septal defect (VSD)?

size of defect and age at presentation

109

What happens with small defects in ventricular septal defect (VSD)?

they are often asymptomatic

110

What happens with large defects in ventricular septal defect (VSD)?

can lead to Eisenmenger syndrome

111

What is the treatment for ventricular septal defect (VSD)?

involves surgical closure; small defects may close spontaneously

112

What is atrial septal defect?

Defect in the septum that divides right and left atria;

113

What is the most common type of atrial septal defect?

It is ostium secundum (90% of cases)

114

What type of atrial septal defect is type is associated with Down syndrome?

Ostium primum

115

What does atrial septal defect result in?

left-to-right shunt and split S2 on auscultation

116

Why is there split S2 on auscultation in atrial septal defect?

increased blood in right heart delays closure of pulmonary valve

117

What is an important complication of atrial septal defect?

Paradoxical emboli

118

What is patent ductus arteriosus?

Failure of ductus arteriosus to close

119

What is patent ductus arteriosus associated with?

congenital rubella

120

What does patent ductus arteriosus result in?

left-to-right shunt between the aorta and the pulmonary artery

121

During development what does the ductus arteriosus normally do?

shunts blood from the pulmonary artery to the aorta, bypassing the lungs

122

What are the symptoms for patent ductus arteriosus?

Asymptomatic at birth with holosystolic machine-like murmur; may lead to Eisenmenger syndrome, resulting in lower extremity cyanosis

123

What does the treatment for patent ductus arteriosus involve?

indomethacin, which decreases PGE2 resulting in PDA closure

124

What is the effect of PGE on patent ductus arteriosus?

PGE maintains patency of the ductus arteriosus

125

What is tetralogy of fallot?

It is characterized by (1) stenosis of the right ventricular outflow tract, (2) right ventricular hypertrophy, (3) VSD, and (4) an aorta that overrides the VSD

126

In tetralogy of fallot what does the right-to-left shunt lead to?

early cyanosis;

127

In tetralogy of fallot what determines the extent of shunting and cyanosis?

the degree of stenosis

128

In tetralogy of fallot what patient behavior is observed?

they learn to squat in response to a cyanotic spell

129

In tetralogy of fallot why does squatting help with the cyanotic spell?

increased arterial resistance decreases shunting and allows more blood to reach the lungs.

130

What is seen on x-ray in tetralogy of fallot?

Boot-shaped heart on x-ray

131

What is transposition of the great vessels characterized by?

pulmonary artery arising from the left ventricle and aorta arising from the right ventricle

132

What is the transposition of the great vessels associated with?

maternal diabetes

133

What does transposition of the great vessels presents with?

early cyanosis; pulmonary and systemic circuits do not mix.

134

In transposition of the great vessels what is required for survival?

creation of shunt (allowing blood to mix) after birth is required for survival.

135

What is the effect of PGE in transposition of the great vessels?

can be administered to maintain a PDA until definitive surgical repair is performed.

136

What does transposition of the great vessels result in?

hypertrophy of the right ventricle and atrophy of the left ventricle

137

What is truncus arteriosus?

Characterized by a single large vessel arising from both ventricles 1. Truncus fails to divide.

138

What does truncus arteriosus present with?

early cyanosis

139

Why is there early cyanosis in truncus arteriosus?

deoxygenated blood from right ventricle mixes with oxygenated blood from left ventricle before pulmonary and aortic circulations separate

140

What is tricuspid atresia?

Tricuspid valve orifice fails to develop; right ventricle is hypoplastic.

141

What is tricuspid atresia often associated with?

ASD, resulting in a right-to-left shunt; presents with early cyanosis,

142

What is coarctation of the aorta?

Narrowing of the aorta,

143

What is coarctation of the aorta classically divided into?

infantile and adult forms

144

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

a PDA

145

In the infantile form of coarctation of the aorta where is the coarctation located?

after (distal to) the aortic arch, but before (proximal to) the PDA

146

What does the infantile form of the coarctation of the aorta present as?

lower extremity cyanosis in infants, often at birth

147

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

Turner syndrome

148

What is the adult form of coarctation of the aorta associated with?

Its not associated with a PDA

149

Where is the coarctation for the adult form of coarctation of the aorta?

coarctation lies after (distal to) the aortic arch

150

How does the adult form of coarctation of the aorta present?

as hypertension in the upper extremities and hypotension with weak pulses in the lower extremities; classically discovered in adulthood

151

In the adult form of coarctation of the aorta what is seen on x-ray?

Notching of ribs

152

Why is there notching of the ribs seen on x-ray for the adult form of coarctation of the aorta?

Collateral circulation develops across the intercostal arteries; engorged arteries cause notching of ribs on x-ray

153

What is the adult form of coarctation of the aorta associated with?

bicuspid aortic valve

154

What is the purpose of heart valves?

To prevent back flow

155

What are the has four valves of the heart?

tricuspid, pulmonary, mitral, and aortic

156

What does valvular lesions generally result in?

stenosis (decreased caliber of the valve orifice) or regurgitation (backflow)

157

What is acute rheumatic fever?

Systemic complication of pharyngitis due to group A beta-hemolytic streptococci

158

Who does acute rheumatic fever affect?

children 2-3 weeks after an episode of streptococcal pharyngitis strep throat

159

What is acute rheumatic fever caused by?

molecular mimicry, bacterial M protein resembles proteins in human tissue

160

What is diagnosis of acute rheumatic fever based on?

Jones criteria.

161

What evidence is needed for the Jones Criteria?

Evidence of prior group A beta-hemolytic streptococcal infection with the presence of major and minor criteria

162

What would indicate prior group A beta-hemolytic streptococcal infection?

Elevated ASO or anti-DNase B titers

163

What is the minor Jones criteria?

Minor criteria are nonspecific and include fever and elevated ESR.

164

What is the major Jones criteria?

1) migratory polyarthritis 2) pancarditis 3) subcutaneous nodules 4) erythema marginatum 5) Sydenham chorea

165

What is Migratory polyarthritis?

In Jones criteria, swelling and pain in a large joint (e.g., wrist, knees, ankles) that resolves within days and migrates to involve another large joint

166

What is Pancarditis?

a) endocarditis b) myocarditis c) pericarditis

167

In endocarditis which valve is involved more commonly?

Mitral valve is involved more commonly than the aortic valve.

168

How is endocarditis characterized?

by small vegetations along lines of closure that lead to regurgitation

169

What is myocarditis in pancarditis?

its with Aschotf bodies that are characterized by foci of chronic inflammation, reactive histiocytes with slender, wavy nuclei (Anitschkow cells), giant cells, and fibrinoid material

170

What is the most common cause of death during the acute phase?

myocarditis

171

What is pericarditis in pancarditis lead to?

friction rub and chest pain

172

What is involved with erythema marginatum in the major criteria of Jones criteria

annular, nonpruritic rash with erythematous borders, commonly involving trunk and limbs

173

What is Sydenham chorea in the major criteria of Jones criteria?

It is rapid, involuntary muscle movements

174

What usually happens to an acute attack of rheumatic fever?

usually resolves, but may progress to chronic rheumatic heart disease;

175

What does repeat exposure to group A beta-hemolytic streptococci result in?

relapse of the acute phase of rheumatic fever and increases risk for chronic disease.

176

What is chronic rheumatic heart disease?

Valve scarring that arises as a consequence of rheumatic fever

177

What does chronic rheumatic heart disease result in?

stenosis with a classic fish mouth appearance

178

What does chronic rheumatic heart disease almost always involve?

the mitral valve

179

What does the involvement of the mitral valve in chronic rheumatic heart disease lead to?

thickening of chordae tendineae and cusps

180

What does chronic rheumatic heart disease occasionally involve?

the aortic valve

181

What does the involvement of the aortic valve in chronic rheumatic heart disease lead to?

fusion of the commissures

182

What do complications in chronic rheumatic heart disease include?

infectious endocarditis

183

What is aortic stenosis?

Narrowing of the aortic valve orifice

184

What is aortic stenosis usually due to?

fibrosis and calcification from wear and tear

185

When does aortic stenosis present?

in late adulthood (> 60 years)

186

What does a bicuspid aortic valve increase the risk for?

aortic stenosis and hastens disease onset.

187

How many cusps does a normal aortic valve have?

three cusps,

188

What is the effect of fewer cusps on the aortic valve?

it results in increased wear and tear on each cusp

189

What is the relationship between aortic stenosis and chronic rheumatic fever?

aortic stenosis may arise as a consequence of chronic rheumatic valve disease;

190

What distinguishes rheumatic disease from wear and tear in aortic stenosis?

coexisting mitral stenosis and fusion of the aortic valve commissures

191

In aortic stenosis what happens during cardiac compensation?

it leads to a prolonged asymptomatic stage during which a systolic ejection click followed by a crescendo-decrescendo murmur is heard

192

What does the complications of aortic stenosis include?

1) Concentric left ventricular hypertrophy 2) angina and syncope with exercise 3) microangiopathic hemolytic anemia

193

In aortic stenosis what does concentric left ventricular hypertrophy lead to?

It may progress to cardiac failure

194

In aortic stenosis what does angina and syncope with exercise lead to?

Limited ability to increase blood flow across the stenotic valve leads to decreased perfusion of the myocardium and brain

195

In aortic stenosis what does microangiopathic hemolytic anemia lead to?

RBCs are damaged (producing schistocytes) while crossing the calcified valve

196

In aortic stenosis what does treatment involve?

valve replacement after onset of complications.

197

What is aortic regurgitation?

Backflow of blood from the aorta into the left ventricle during diastole

198

Aortic regurgitation arises due to what?

aortic root dilation (syphilitic aneurysm and aortic dissection) or valve damage (infectious endocarditis)

199

What is the most common cause of aortic regurgitation?

isolated root dilation

200

What are the clinical features for aortic regurgitation?

1. Early, blowing diastolic murmur 2. Hyperdynamic circulation due to increased pulse pressure

201

What is pulse pressure?

it is the difference between systolic and diastolic pressures

202

What is the relationship between pressure and aortic regurgitation?

Diastolic pressure decreases due to regurgitation, while systolic pressure increases due to increased stroke volume

203

How does aortic regurgitation present?

with bounding pulse (water-hammer pulse), pulsating nail bed (Quincke pulse), and head bobbing

204

What does aortic regurgitation result in?

LV dilation and eccentric hypertrophy (due to volume overload)

205

What is the treatment for aortic regurgitation?

valve replacement once LV dysfunction develops

206

What happens in mitral valve prolapse?

Ballooning of mitral valve into left atrium during systole

207

What is the incidence of mitral valve prolapse in US adults

Seen in 2-3% of US adults

208

What is mitral valve prolapse due to?

myeloid degeneration (accumulation of ground substance) of the valve, making it (loopy)

209

What is the etiology for mitral valve prolapse?

Unknown

210

What might mitral valve prolapse be seen in?

Marfan syndrome or Ehlers-Danlos syndrome

211

What does mitral valve prolapse present with?

an incidental mid-systolic click followed by a regurgitation murmur that is usually asymptomatic

212

With mitral valve prolapse, when does the mid-systolic click get louder?

Click and murmur become louder with squatting

213

Why does squatting make the mid-systolic click get louder in mitral valve prolapse?

increased systemic resistance decreases left ventricular emptying

214

What are the complications for mitral valve prolapse?

they are rare, but include infectious endocarditis, arrhythmia, and severe mitral regurgitation.

215

What is the treatment for mitral valve prolapse?

valve replacement.

216

What is mitral regurgitation?

Reflux of blood from the left ventricle into the left atrium during systole

217

Mitral regurgitation usually arises as a complication of what?

mitral valve prolapse

218

Aside from mitral valve prolapse, what are some other causes of mitral regurgitation?

Left ventricular dilatation (left-sided cardiac failure), infective endocarditis, acute rheumatic heart disease, and papillary muscle rupture after a myocardial infarction.

219

What are the clinical features for Mitral regurgitation?

1. Holosystolic [blowing] murmur;

220

In mitral regurgitation why is the holosystolic murmur louder with squatting?

increased systemic resistance decreases left ventricular emptying and expiration, increased return to left atrium

221

What does mitral regurgitation result in?

Volume overload and left-sided heart failure

222

What is mitral stenosis?

Narrowing of the mitral valve orifice

223

What is mitral stenosis usually due to?

chronic rheumatic valve disease

224

What are the clinical features for mitral stenosis?

1. Opening snap followed by diastolic rumble 2. Volume overload leads to dilatation of the left atrium

225

In mitral stenosis what does the dilation of the left atrium leading to volume overload result in?

i. Pulmonary congestion with edema and alveolar hemorrhage ii. Pulmonary hypertension and eventual right-sided heart failure iii. Atrial fibrillation with associated risk for mural thrombi

226

What is endocarditis?

Inflammation of endocardium that lines the surface of cardiac valves

227

What is endocarditis usually due to?

bacterial infection

228

What is the most common overall cause of endocarditis?

Streptococcus viridans

229

What is streptococcus viridans?

it is a low virulence organism that infects previously damaged valves (chronic rheumatic heart disease and mitral valve prolapse).

230

What does streptococcus viridans result in?

small vegetations that do not destroy the valve (subacute endocarditis)

231

How does streptococcus viridans affect the endocardial surface?

develops thrombotic vegetations (platelets and fibrin) on damaged endocardial surface, transient bacteremia leads to trapping of bacteria in the vegetations, prophylactic antibiotics decrease risk of endocarditis.

232

What is the most common cause of endocarditis in IV drug users?

Staphylococcus aureus

233

What is Staphylococcus aureus?

High-virulence organism that infects normal valves, most commonly the tricuspid.

234

What does Staphylococcus aureus result in?

large vegetations that destroy the valve (acute endocarditis)

235

What is Staphylococcus epidermidis associated with?

endocarditis of prosthetic valves

236

What is Streptococcus bovis associated with?

endocarditis in patients with underlying colorectal carcinoma

237

What are HACEK organisms associated with?

are associated with endocarditis with negative blood cultures.

238

HACEK

Haemophilus, Actinobacius, Cardiobacterium, Eikenella, Kingella

239

What are the clinical features of bacterial endocarditis?

1) Fever 2) Lesions 3) Janeway lesions 4) anemia of chronic disease

240

What is the fever in bacterial endocarditis due to?

bacteremia

241

What is the murmur in bacterial endocarditis due to?

vegetations on heart valve

242

What are the Janeway lesions, splinter hemorrhages in nail bed and osier nodes in bacterial endocarditis due to?

embolization of septic vegetations

243

What are Janeway lesions?

erythematous nontender lesions on palms and soles.

244

What are Osier nodes?

tender lesions on fingers or toes

245

What is anemia of chronic disease due to?

chronic inflammation

246

What are the laboratory findings for endocarditis?

1. Positive blood cultures 2. Anemia of chronic disease 3. Transesophageal echocardiogram is useful for detecting lesions on valves

247

What are the general lab findings of anemia of chronic diseae?

low Hb, low MCV; high ferritin, low TIBC, decreased serum iron, and decreased l% saturation

248

What is the transesophageal echocardiogram useful for?

detecting lesions on valves

249

What is non-bacterial thrombotic endocarditis due to?

sterile vegetations that arise in association with a hypercoagulable state or underlying adenocarcinoma.

250

What does non-bacterial thrombotic endocarditis result in?

Vegetations arise on the mitral valve along lines of closure and result in mitral regurgitation.

251

What is Libman-Sacks endocarditis due to?

sterile vegetations that arise in association with SLE.

252

What does Libman-Sacks endocarditis result in?

Vegetations are present on the surface and undersurface of the mitral valve and result in mitral regurgitation

253

What is cardiomyopathy?

Group of myocardial diseases that result in cardiac dysfunction

254

What are the types of cardiomyopathy?

Dilated cardiomypathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy

255

What is dilated cardiomyopathy?

Dilation of all four chambers of the heart

256

What is the most common form of cardiomyopathy?

Dilated cardiomyopathy

257

What does dilated cardiomyopathy result in?

Results in systolic dysfunction (ventricles cannot pump),

258

What does the systolic dysfunction resulting from dilated cardiomyopathy lead to?

biventricular CHF

259

What are the complications of dilated cardiomyopathy?

mitral and tricuspid valve regurgitation and arrhythmia.

260

What is the most common cause of dilated cardiomyopathy?

Its idiopathic

261

What are some other causes of dilated cardiomyopathy?

1. Genetic mutation (usually autosomal dominant) 2. Myocarditis (usually due to coxsackie A or B) 3. Alcohol abuse 4. Drugs (doxorubicin) 5. Pregnancy

262

In pregnancy, when is dilated cardiomyopathy?

Its seen during late pregnancy or soon (weeks to months) after childbirth

263

What characterizes myocarditis leading to dilated cardiomyopathy?

characterized by a lymphocytic infiltrate in the myocardium

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What does dilated cardiomyopathy from myocarditis result in?

chest pain, arrhythmia with sudden death, or heart failure. Dilated cardiomyopathy is a late complication.

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What is the treatment for dilated cardiomyopathy?

heart transplant.

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What is hypertrophic cardiomyopathy?

Massive hypertrophy of the left ventricle

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What is hypertrophic cardiomyopathy usually due to?

genetic mutations in sarcomere proteins; most common form is autosomal dominant

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What are the clinical features for hypertrophic cardiomyopathy?

1. Decreased cardiac output 2. Sudden death due to ventricular arrhythmias 3. Syncope with exercise

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How does hypertrophic cardiomyopathy lead to syncope with exercise?

Subaortic hypertrophy of the ventricular septum results in functional aortic stenosis

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What is a common cause of sudden death in young athletes?

hypertrophic cardiomyopathy

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In hypertrophic cardiomyopathy what does the decreased cardiac output lead to?

Left ventricular hypertrophy leads to diastolic dysfunction (ventricle cannot fill).

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In hypertrophic cardiomyopathy, what does biopsy show?

myofiber hypertrophy with disarray

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What is restrictive cardiomyopathy?

Decreased compliance of the ventricular endomyocardium that restricts filling during diastole

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What are the causes of restrictive cardiomyopathy?

amyloidosis, sarcoidosis, hemochromatosis, endocardial fibroelastosis (in children), and Loeffler syndrome (endomyocardial fibrosis with an eosinophilic infiltrate and eosinophilia).

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What does restrictive cardiomyopathy present as?

congestive heart failure;

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What is the classic finding in restrictive cardiomyopathy?

low-voltage EKG with diminished QRS amplitude.

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What are the cardiac tumors?

Myxoma, rhabdomyoma

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What is myoxma?

Benign mesenchymal tumor with a gelatinous appearance and abundant ground substance on histology

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What is the most common primary cardiac tumor in adults?

myxoma

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What does myxoma usually form?

a pedunculated mass in the left atrium

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What does the pedunculated mass in the left atrium due to myxoma cause?

syncope due to obstruction of the mitral valve

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What is rhabdomyoma?

Benign hamartoma of cardiac muscle

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What is the most common primary cardiac tumor in children?

rhabdomyoma

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What is rhabdomyoma associated with?

Tuberous sclerosis

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Where does rhabdomyoma usually arise?

in the ventricle

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Which type of tumors are more common in the heart?

Metastatic tumors more than primary tumors

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What does common metastases to the heart include?

breast and lung carcinoma, melanoma, and lymphoma

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What does metastatic tumors in the heart most commonly involve? What does this result in?

the pericardium, resulting in a pericardial effusion