Cardiac Pathology Flashcards

1
Q

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

A

Hypertension in the upper extremities and hypotension with weak pulses in the lower extremities

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2
Q

Hypertrophic cardiomyopathy

A

Massive hypertrophy of the left ventricle

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3
Q

Acute Rheumatic fever minor criteria

A

Fever and elevated ESR

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4
Q

Cause of roth spots

A

Due to embolization of septic vegetations

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5
Q

How does myocarditis present in cases of acute rheumatic fever?

A

Myocarditis with Aschoff bodies that are characterized by foci of chronic inflammation, reactive histiocytes with slender, wavy nuclei (Anitschkow cells), giant cells, and fibronoid material

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6
Q

_____________ is chest pain that arises with exertion or emotional stress.

A

Stable angina

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7
Q

Patent ductus arteriosus is associated with congenital _____________.

A

Rubella

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8
Q

Necrosis of cardiac myocytes

A

MI

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9
Q

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

A

Myxoma

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10
Q

Complications of aortic stenosis

A
  • Concentric left ventricular hypertrophy
  • Angina and syncope with excercise
  • Microangiopathic hemolytic anemia
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11
Q

Causes of aortic regurgitation

A

Aortic root dilation

Valve damage

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12
Q

Clinical features of left-sided heart are due to..

A

Decreased forward perfusion and pulmonary congestion

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13
Q

Major complication of atrial septal defects

A

Paradoxical emboli

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14
Q

Which organisms are associated with endocarditis with negative blood cultures?

A

Haemophilus

Actinobacillus

Cardiobacterium

Eikenella

Kingella

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15
Q

Most common arteries infarcted in MI

A

LAD (1st)

Right coronary

Left circumflex

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16
Q

Cause of acute rheumatic fever

A

Molecular mimicry; bacterial M protein resembles proteins in human

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17
Q

What is the cause of syncope with excercise seen with in hypertrophic cardiomyopathy?

A

Subaortic hypetrophy of the ventricular septum results in function aortic stenosis

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18
Q

Jones criteria

A
  • Evidence of prior group A strep infection
    • Elevated ASO or anti-DNase B titers
  • Presence of major and minor criteria
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19
Q

how is aortic stenosis treated?

A

Valve replacement after onset of complications

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20
Q

How is MI treated?

A
  • Aspirin and/or heparin
  • Supplement O2
  • Nitrates
  • B-blockers
  • ACE inhibitor
  • Fibrinolysis of angioplasty
    • Opens blocked vessel
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21
Q

Cause of MI

A
  • Rupture of an atherosclerotic plaque with thrombosis and complete occlusion of a coronary artery (most common)
  • Coronary artery vasospasm
  • Emobli
  • Vasculitis
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22
Q

What is the most common etiology of sudden cardiac death?

A

Acute ischemia

*90% of patients have pre-existing severe atherosclerosis

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23
Q

In what part of the heart does a rhabdomyoma usually arise?

A

Ventricle

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24
Q

Clinical features of right-sided heart failure are due to __________.

A

Congestion

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25
Q

Reperfusion of irreversibly damaged cells results in _______ influx. What is the result of this?

A

Calcium; leading to hypercontraction of myofibrils (contraction band necrosis)

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26
Q

Most common type of atrial septal defect

A

Ostium secundum

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27
Q

How is dilated cardiomyopathy treated?

A

Heart transplant

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28
Q

What trends of elevation does CK-MB follow in infarction?

A
  • levels rise 4-6 hrs after infarction
  • Peak at 24 hrs
  • Return to normal by 72 hrs
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29
Q

How does transposition of the great vessels present?

A

Early cyanosis because pulmonary and systemic circuits do not mix

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30
Q

What distinguishes rheumatic disease from “wear and tear” causing aortic stenosis?

A

Mitral stenosis and fusion of the aortic valve commissures

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31
Q

Consequences of patent ductus arteriosus

A

“Machine-like” murmur

Eisenmenger syndrome

  • Lower extremity cyanosis
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32
Q

Clinical features of mitral stenosis

A
  • Opening snap followed by diastolic rumble
  • Volume overload leads to dilation of the left atrium, resulting in:
    • Pulmonary congestion with edema and alveolar hemorrhage
    • Pulmonary hypertension and eventual right-sided heart failure
    • Atrial fibrillation with associated risk for mural thrombi
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33
Q

Benign hamartoma of cardiac muscle

A

Rhabomyoma

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34
Q

Cause of unstable angina

A

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

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35
Q

Migratory polyarthritis

A

Swelling and pain in a large joint that resolves within days and “migrates” to involve another large joint

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36
Q

Major cause of mitral stenosis

A

Chronic rheumatic valve disease

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37
Q

Which chamber of the heart is typically involved in MI?

A

Left ventricle

*Right ventricle and both atria are generally spared

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38
Q

Cause of mitral valve prolapse

A

Myxoid degeneration (accumulation of ground substance) of the valve making it floppy

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39
Q

Occlusion of the left circumflex artery results in infarction of which structures?

A

Lateral wall of the LV

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40
Q

Biopsy seen in hypertrophic cardiomyopathy

A

Myofiber hypertrophy with disarray

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41
Q

Tricuspid atresia is often associated with what defect?

A

Atrial septal defect; resulting in a right-to-left shunt. presents with early cyanosis

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42
Q

Major cause of hypertrophic cardiomyopathy

A

Genetic mutations in sarcomere proteins (autosomal dominant)

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43
Q

Murmur heard in aortic stenosis

A

Cardiac compensation leads to a prolong asymptomatic stage during which a systolic ejection click followed by a crescendo-decrescendo murmur

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44
Q

Acute rheumatic fever major criteria

A
  • Migratory polyarthritis
  • Pancarditis
  • Subcutaneous nodules
  • Erythema marginatum
  • Syndenham chorea
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45
Q

____________ is useful for detecting lesions on valves.

A

Transesophageal echocardiogram

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46
Q

Stable angina is relieved by ________.

A

Nitroglycerin

*Same for unstable angina

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47
Q

Nonbacterial thrombotic endocarditis is due to sterile vegetations that arise in association with a _______________ or _________________.

A

Hypercoagulable state; underlying adenocarcinoma

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48
Q

_____________ is associated with endocarditis in patients with underlying colorectal carcinoma.

A

Strep. Bovis

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49
Q

Complications of mitral valve prolaspe

A

Infectious endocarditis

Arrythmia

Severe mitral regurgitation

*Complications are rare

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50
Q

Does stable angina result from reversible or irreversible injury?

A

Reversible injury to myocytes (no necrosis)

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51
Q

osler nodes

A

Tender lesions on fingers or toes

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52
Q

narrowing of the aorta

A

Coractation of the aorta

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53
Q

Clinical features of right sided heart failure

A
  • JVD
  • Painful hepatosplenomegaly with characteristic nutmeg liver
  • Dependent pitting edema
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54
Q

Mechanism by which strep viridians causes endocarditis

A
  • Damaged endocardial surface develops thrombotic vegetations (platelets and fibrin)
  • Transient bacteremia leads to trapping of bacteria in the vegetations
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55
Q

Laboratory findings in endocarditis

A
  • Positive blood cultures
  • Anemia of chronic disease (Decreased Hb, Decreased MCV, increased ferritin, decreased TIBC, decreased serum iron, and decreased % saturation
    *
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56
Q

Quincke pulse

A

Pulsating nail bed

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57
Q

Clinical features of left-sided heart failure

A
  • Pulmonary edema
    • Dyspnea, paroxysmal nocturnal dyspnea, orthopnea, and crackes
    • Intralveolar hemorrhage
  • Decreased flow to kidneys
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58
Q

Cause of prinzmetal angina

A

Due to coronary artery vasoplasm

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59
Q

Characterized by a single large vessel arising from both ventricles

A

Truncus arteriosus

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60
Q

Loeffler syndrome

A

Endomyocardial fibrosis with an eosionphilic infiltrate and eosinophilia

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61
Q

_________ is the most common cause of endocarditis in IV drug abusers.

A

S.aureus

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62
Q

Treatment for ventricular septal defect

A

Surgical closure

*Small defects may close spontaneously

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63
Q

How does a mitral valve prolapse present?

A
  • Incidental mid-systolic click followed by a regurgitation murmur; usually asymptomatic
64
Q

Infantile form of coarctation of the aorta is associated with ________ and ________.

A

Patent ductus arteriosus and Turner syndrome

65
Q

Gross appearance of a myxoma

A

usually forms a pedunculated mass in the left atrium that cuase syncope due to obstruction of the mitral valve

66
Q

Causes of right sided heart failure

A

Left sided heart failure (most common)

Left-to-right shunt

Chronic lung disease (cor pulmonale)

67
Q

EKG of stable angina

A

ST-segment depression due to subendocardial ischemia

NOTE:Unstable angina presents the same way on EKG

68
Q

Clinical features of hypertrophic cardiomyopathy

A
  • Decreased cardiac output
  • Sudden death due to ventricular arrythmias
  • Syncope with exercise
69
Q

Which valve is more commonly involved in endocarditis?

A

Mitral valve more commonly than the aortic valve

70
Q

__________ maintains patency of the ductus arteriosus.

A

PGE

71
Q

What are the gross changes, mircoscopic changes, and complications months after MI?

A

Gross: White scar

Micro: Fibrosis

Complcations: Aneurysm, mural thrombus, or dressler syndrome

72
Q

Indomethacin mechanism of action

A

Decreased PGE, resilting in PDA closure

73
Q

Ostium primum type of atrial septal defect is associated with __________.

A

Down Syndrome

74
Q

Which valve is mosst commonly affected by S. aureus?

A

Tricupsid

NOTE: S. Aureus infects normal valves

75
Q

What are the gross changes, mircoscopic changes, and complications 1-3 wks after MI?

A

Gross: Red border emerges as granulation tissue enters from edge on infarct

Micro: Granulation tissue with plump fibroblasts, collagen, and blood vessels

76
Q

Treatment for patent ductus arteriosus

A

Indomethacin

77
Q

What are the gross changes, mircoscopic changes, and complications 4-7 days after MI?

A

Gross: Yellow pallor

Micro: Macrophages

Complications: Rupture of ventricular free wall (leads to cardiac tamponade), interventricular septum (leads to shunt), or papillary muscle (leads to mitral insufficiency)

78
Q

Clinical feautures of MI

A
  • Severe crushing chest pain (lasting >20 mins) that radiates to the left arm or jaw
  • Diaphoresis
  • Dyspnea

*Symptoms NOT relieved by nitroglycerin

79
Q

Sudden cardiac death is usually due to ____________.

A

Fatal ventricular arrhythmia

80
Q

Chronic ischemic heart disease progresses to __________.

A

Congestive heart failure

81
Q

Janeway lesions

A

Erthematous nontender lesions on palms and soles

82
Q

Where do vegetations arise in nonbacterial thrombotic endocarditis? What is the result of this?

A

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

83
Q

Ventricular septal defects are associated with ___________.

A

Fetal alcohol syndrome

84
Q

How does the adult form of coarctation of the aorta present on X-ray? Why?

A

“Notching” of ribs, due to engorged arteries from collateral circulation that develops across the intercostal arteries

85
Q

What lab tests are used to detect MI?

A
  • Elevated troponin I
  • CK-MB
86
Q

Symptoms of myocarditis

A

Chest pain

Arrythmia with sudden death, or heart failure

87
Q

How does truncus arteriosus present? Why?

A

Early cyanosis; deoxygenated blood from right ventricle mixes with oxygenated blood from let ventricle before pulmonary and aortic circulations separate

88
Q

What viruses cause myocarditis?

A

Coxsackie A or B

89
Q

Causes of restrictive cardiomyopathy

A

Amyloidosis

Sarcoidosis

Endocardial fibroelastosis

Loeffler syndrome

90
Q

Classic gross apperance of chronic rheumatic heart disease

A
  • Stenosis with a classic “fish mouth” appearance
    • Mitral valve (most common): Results in thickening of chordae tendinae and cusps
    • Aortic valve: leads to fusion of the commissures
91
Q

Criteria for classification of Sudden Cardiac Death

A

Unepected death due to cardiac disease; occurs without symptoms or <1 hr after symptoms arise

92
Q

__________ aortic valve increases risk and hastens onset of aortic stenosis.

A

Bicupsid

93
Q

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

A

Lower extremity cyanosis in infants, often at birth

94
Q

How does fibrinous pericarditis present?

A

Chest pain with friction rub

95
Q

What ailment is transposition of the great vessels associated with?

A

maternal diabetes

96
Q

Valve scarring that arises as a consequence of rheumatic fever

A

Chronic rheumatic fever

97
Q

What part of the heart most commonly involved in metastasis? What is the result?

A

Metastasis to the heart, commonly involve the pericardium, resulting in a pericardial effusion

98
Q

Adult form of coarctation of the aorta is associated with _____.

A

Bicupsid aortic valve

99
Q

What condition is rhabdomyoma associated?

A

Tuberous sclerosis

100
Q

Dilation of all four chambers of the heart

A

Dilated cardiomyopathy

101
Q

Cause of stable angina

A

Due to atherosclerosis of coronary arteries with >70% stenosis, results in decreased blood flow that is unable to meet the metabolic demands of the myocardium during exertion

102
Q

Most common cause of endocarditis

A

Strep viridans: results in small vegetations that do not destroy the valve (subacute endocarditis)

*Infects previously damaged valves

103
Q

How does stable angina present?

A

Chest pain that radiates tot he left arm or jaw

Diaphoresis

Shortness of breath

104
Q

Prinzmetal angina is relieved by ____________

A

Nitroglycerin or calcium channel blockers

105
Q

Where does the coartication of the aorta lie in the infantile form?

A

After the aortic arch but before the PDA

106
Q

What are the gross changes, mircoscopic changes, and complications <4hrs after MI?

A

Gross: none

Micro: none

Complications

  • Cardiogenic shock
  • Congestive heart failure
  • Arrhythmia
107
Q

How does restrictive cardiomyopathy present?

A

Congestive heart failure

Low-voltage EKG with diminished QRS amplitude

108
Q

____________ is useful for detecting reinfarction that occurs days after and initial MI.

A

Creatine kinase MB (CK-MB)

109
Q

Complications of chronic rheumatic heart disease

A

Infectious endocarditis

110
Q

How is endocarditis characterized?

A

Small vegetations along lines of closure that lead to regurgitation

111
Q

Hypertrophic cardiomyopathy is a common cause of sudden death in young _______.

A

Athletes

112
Q

What are the gross changes, mircoscopic changes, and complications 4-24 hrs after MI?

A

Gross: Dark discoloration

Micro: Coagulative necrosis

Complications: Arrythmias

113
Q

Which congenital defects are associaed with right-to-left shunts?

A

Tricuspid atresia

Tetralogy of Fallot

114
Q

What causes an increase in pulse pressure?

A
  • Diastolic pressure decreases due to regurgitation
  • Systolic pressure increases due to increased stroke volume
115
Q

Acute rheumatic fever is based on ___________.

A

Jones criteria

116
Q

Lymphocytic infiltrate in the myocardium

A

Myocarditis

117
Q

Cause of paroxysmal nocturnal dyspnea

A

Due to increased venous return when lying flat

118
Q

How is aortic regurgitation treated

A

Valve replacement once LV dysfunction develops

119
Q

____________ angina is episodic chest pain unrelated to exertion.

A

Prinzmetal

120
Q

_____________ is associated with endocarditits of prostetic valves.

A

S. epidermidis

121
Q

Common cause of aortic stenosis

A

Fibrosis and calcification from “wear and tear”

122
Q

During development, the ductus arteriosus normally shunts blood from the _________ to the _________, bypassing the lungs.

A

Pulmonary artery; aorta

123
Q

Does unstable angina result from reversible or irreversible injury?

A

Reversible injury to myocytes (no necrosis)

124
Q

Common metastases to the heart

A

Breast and lung carcinoma

Melanoma

Lymphoma

125
Q

Heart sounds of atrial septal defects

A

Split S2

126
Q

__________ angina is chest pain that occurs at rest.

A

Unstable

127
Q

Decreased compliance of the ventricular endomyocardium that restricts filling during diastole

A

Restrictive cardiomyopathy

128
Q

Which chambers of the heart are effected by transposition of the great vessels?

A

Hypertrophy of the right ventricle

Atrophy of the left ventricle

129
Q

Treatment for left-sided heart failure

A

ACE inhibitor

130
Q

What are the diff phases of MI? What are the characteristics of each?

A

Early

  • Subendothelial necrosis involving <50 % of the myocardial thickness
  • EKG: ST-segment depression

Severe

  • Transmural necrosis involving most of the myocardial wall (transmural infartion)
  • EKG: ST- segment elevation
131
Q

Clinical features of bacterial endocarditis

A
  • Fever
    • Due to bacteremia
  • Murmur
    • Due to vegetations on heart valve
  • Janeway lesions
  • Osler nodes
  • Splinter hemorrhages in nail bed
  • Roth spots
  • Anemia of chronic disease
132
Q

Most commonly involved artery in MI. What is the consequence of this?

A

LAD

  • Occlusion of LAD leads to infarction of the anterior wall and anterior septum of the left ventricle
133
Q

Erythema marginatum

A

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

134
Q

Concentric left ventricular hypertrophy, due to aortic stenosis, may progress to __________.

A

Cardiac failure

135
Q

What are the gross changes, mircoscopic changes, and complications 1-3 days after MI?

A

Gross: Yellow pallor

Micro: neutrophils

Complications: Fibrinous pericarditis; presents as chest pain with friction rub

136
Q

Histo sign of intraalveolar hemorrhage

A

Hemosiderin-laden macrophages

137
Q

EKG on prinzmetal angina?

A

ST-segment elevation due to transmural ischemia

138
Q

_________ is the most sensitive and specific marker for MI

A

Troponin I

139
Q

Why is a split S2 seen in atrial septal defects?

A

Increased blood in right heart delays closure of pulmonary valve

140
Q

Aside from acute ischemia, what are other causes of sudden cardiac death?

A

Mitral valve prolapse

Cardiomyopathy

Cocaine abuse

141
Q

Occlusion the right coronary artery results in infarction of which structures?

A

Posterior wall, posterior septum, and papillary muscles of the LV

142
Q

What causes the click and murmur seen in mitral valve prolaspe to become softer?

A

Squatting (increased systemic resistance decreases left ventricular emptying)

143
Q

Complications of dilated cardiomyopathy

A
  • Results in systolic dysfunction (ventricles cannot pump), leading to biventricular CHF
  • Mitral and tricupside valve regurgitation and arrhythmia
144
Q

Which congenital defects are associaed with left-to-right shunts?

A

Ventricular septal defect

Atrial septal deect

Patent ductus arteriosus

145
Q

Why is CO decreased in hypertrophic cardiomyopathy?

A

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

146
Q

Clinical features of mitral regurgitation

A
  • Holosystolic “blowing” murmur
    • Louder with squatting and expiration
  • Volume overload
  • left sided heart failure
147
Q

Causes of dilated cardiomyopathy

A
  • Genetic mutation (usually autosomal dominant)
  • Myocarditis
  • Alcohol abuse
  • Drugs
  • Pregnancy
  • Hemochromotosis
148
Q

Where do vegetations arise in Libman-Sacks endocarditis? What is the result of this?

A

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

149
Q

Decreased flow to ________ leads to activation of renin-angiotensin system.

A

Kidneys

*Fluid retention exacerbates CHF

150
Q

Large ventricular septal defects can lead to __________.

A

Eisenmenger syndrome

151
Q

What trends of elevation does troponin follow in MI?

A
  • Levels rise 2-4 hrs after infarction
  • Peak at 24 hrs
  • Return to normal by 7-10 days
152
Q

What does left-sided heart failure lead to?

A

Ischemia

Hypertension

Dilated cardiomyopathy

MI

Restrictive cardiomyopathy

153
Q

Causes of mitral regurgitation

A

Mitral valve prolapse (most common)

LV dilation

Infective endocarditis

Acute rheumatic heart disease

Papillary muscle rupture after a MI

154
Q

Clinical features of aortic regurgitation

A
  • Early, blowing diastolic murmur
  • Hyperdynamic circulation due to increased pulse pressure
  • Bounding pulse
  • Pulsating nail bed
  • Head bobbing
  • LV dilation
  • Eccentric hypertrophy
155
Q

Ballooning of mitral valve into left artium during systole

A

Mitral valve prolapse