Cardiac Pathology

Front 1

Angina

Back 1

Stable chest pain that arises with exertion or emotional stress; represents reversible injury to myocytes (no necrosis)

Front 2

Cause of angina

Back 2

atheroslcerosis of coronary arteries with >70% stenosis; decreased blood flow is not able to meet the metabolic demands of the myocardium during exertion

Front 3

How does angina present?

Back 3

chest pain (lasting >20 min) that radiates to left arm of jaw, diaphoresis, and shortness of breath; relieved by rest or nitroglycerin

Front 4

What does EKG show in angina?

Back 4

ST-segment depression due to subendocardial ischemia

Front 5

Unstable angina

Back 5

Pain that occurs with rest; usually due to rupture of atherosclerotic plaque with thrombosis and incomplete occlusion of coronary artery

Front 6

Prinzmetal angina

Back 6

episodic chest pain unrelated to exertion; due to coronary artery vasospasm; relieved by nitroglycerin or calcium channel blockers

Front 7

What is found on EKG in prinzmetal angina?

Back 7

ST-segment elevation due to transmural ischemia

Front 8

Clinical features of MI

Back 8

severe, crushing chest pain (lasting > 20 min) that radiates to left arm of jaw, diaphoresis, dyspnea; symptoms not relieved by nitroglycerin

Front 9

Which part of the heart does MI usually involve?

Back 9

Left ventricle

Right ventricle and atria are generally spared

Front 10

Most commonly involved artery in MI

Back 10

LAD; which leads to infarction of anterior wall and anterior septum of LV

Front 11

2nd most commonly involved artery in MI

Back 11

RCA; leads to infarctino of posterior wall, posterior septum, and papillary muscles of LV

Front 12

Which area of the heart becomes infarcted with occlusion of the left circumflex artery?

Back 12

lateral wall of LV

Front 13

EKG finding with MI

Back 13

Initially, ST-segment depression (subendocardial infarction) but ST-segment becomes elevated with transmural infarction

Front 14

Lab tests to detect MI

Back 14

• Troponin I is most sensitive and specific
• CK-MB is useful for detecting re-infarction

Front 15

Treatment for MI

Back 15

1. Aspirin/heparin to limit thrombosis

2. Supplemental O2 to minimize ischemia

3. Nitrates to vasodilate

4. Beta blocker to slow HR and decrease demand

5. ACE inhibitor to decrease LV dilation

6. Fibrinolysis or angioplasty to open blocked vessel

Front 16

Complications within four hours of MI

Back 16

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

Front 17

4-24 hrs post infarction

Back 17

• Dark discoloration
• Coagulative necrosis
• Arrhythmia

Front 18

1-3 days post infarction

Back 18

• Yellow pallor
• Neutrophils
• Fibrinous pericarditis

Front 19

4-7 days post infarction

Back 19

• Yellow pallor
• Macrophages
• Rupture of ventricular free wall (leading to cardiac tamponade), IV septum (leading to shunt), or papillary muscle (leading to mitral insufficiency)

Front 20

1-3 weeks post infarction

Back 20

• Red border emerges as granulation tissue enters from edge of infarct
• Granulation tissue with plump fibroblasts, collagen, and BVs

Front 21

Months post infarction

Back 21

• White scar
• Fibrosis
• Aneurysm, mural thrombus, or Dressler syndrome

Front 22

Dressler syndrome

Back 22

exposure of heart antigens to body leads to production of autoimmune antibodies, leading to autoimmune pericarditis

Front 23

Sudden cardiac death

Back 23

Unexpected death due to cardiac disease, usually due to fatal ventricular arrhythmia due to acute ischemia (less common causes include mitral valve prolapse, cardiomyopathy, cocaine abuse)

Front 24

Causes of Left-sided Congestive Heart Failure

Back 24

Ischemia, hypertension, dilated cardiomyopathy, myocardial infarction, restrictive cardiomyopathy

Front 25

Clinical features of Left-sided Congestive Heart Failure

Back 25

1. Pulmonary congestion leads to pulmonary edema resulting in dyspnea, paroxysmal nocturnal dyspnea, orthopnea, and crackles

2. Small congested capillaries may burst, leading to intraalveolar hemorrhage; marked by hemosiderin-laden macrophages ('heart-failure cells')

3. Decreased flow to kidneys lead to activation of RAAS leading to fluid retention that exacerbates CHF

Front 26

Treatment of Left-sided Congestive Heart Failure

Back 26

ACE-inhibitor

Front 27

Cause of Right-sided Congestive Heart Failure

Back 27

Most commonly due to left-sided heart failure; other causes include left-to-right shunt and chronic lung disease (cor pulmonale)

Front 28

Clinical features of Right-sided Congestive Heart Failure

Back 28

1. Jugular venous distension

2. Painful hepatosplenomegaly with 'nutmeg' liver; may lead to cardiac cirrhosis

3. Dependent pitting edema (due to increased hydrostatic pressure)

Front 29

Which type of shunt, left-to-right or right-to-left, will present as cyanosis shortly after birth? (as opposed to the type of shunt that may be asymptomatic initially)

Back 29

right to left

Front 30

Most common congenital heart defect

Back 30

Ventricular septal defect

Front 31

Which defect is associated with fetal alcohol syndrome?

Back 31

Ventricular septal defect

Front 32

Eisenmenger syndrome

Back 32

Any untreated congenital cardiac defect with intracardiac communication that leads to pulmonary hypertension, reversal of flow, and cyanosis. The previous left-to-right shunt is converted into a right-to-left shunt secondary to elevated pulmonary artery pressures and associated pulmonary vascular disease.

Front 33

Clinical features associated with Eisenmenger syndrome

Back 33

Right ventricular hypertrophy, polycythemia, clubbing

Front 34

Polycythemia

Back 34

a disease state in which the proportion of blood volume that is occupied by red blood cells increases; can be due to an increase in the number of red blood cells or to a decrease in the volume of plasma

Front 35

Most common type of atrial septal defect

Back 35

ostium secundum

Front 36

Which clinical syndrome is ostium primum associated with?

Back 36

Down syndrome

Front 37

What is heard on auscultation in atrial septal defect?

Back 37

split S2

Front 38

In which condition are paradoxical emboli an important complication?

Back 38

atrial septal defect

Front 39

Which congenital defect is associated with congenital rubella?

Back 39

PDA; left to right shunt between aorta and pulmonary artery

Front 40

How is PDA treated?

Back 40

indomethacin, which decreases PGE, resulting in PDA closure (PGE maintains patency of ductus arteriosus)

Front 41

Characteristics of tetralogy of fallot

Back 41

1. Stenosis of right ventricular outflow tract

2. Right ventricular hypertrophy

3. VSD

4. Overriding aorta

Leads to right-to-left shunt & cyanosis

Front 42

What do patients with tetralogy of fallot learn to do in response to a cyanotic spell?

Back 42

squat

Front 43

What is characteristic of tetralogy of fallot on x-ray?

Back 43

'boot-shaped' heart

Front 44

Which congenital defect is associated with maternal diabetes?

Back 44

Transposition of the great vessels

Front 45

How is transposition of the great vessels treated?

Back 45

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

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

Front 46

Truncus arteriosus

Back 46

Characterized by a single large vessel arising from both ventricles (truncus fails to divide); presents with early cyanosis

Front 47

Tricuspid atresia

Back 47

tricuspid valve orifice fails to develop; right ventricle is hypoplastic; often associated with ASD resulting in R to L shunt; presents with early cyanosis

Front 48

Coarctation of aorta (infantile form)

Back 48

• Associated with PDA
• Coarctation lies after aortic arch but before PDA
• Presents as lower extremity cyanosis
• Associated with Turner Syndrome

Front 49

Coarctation of aorta (adult form)

Back 49

• coarctation lies after aortic arch
• presents as HTN in upper extremities and hypotension with weak pulses in lower extremities
• associated with bicuspid aortic valve

Front 50

What is commonly seen on x-ray in coarctation of aorta (adult form)?

Back 50

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

Front 51

acute rheumatic fever

Back 51

systemic complication of pharyngitis due to group A beta-hemolytic strep; affects children 2-3 weeks after episode; caused by molecular mimicry (bacterial M protein)

Front 52

Jones criteria for diagnosing acute rheumatic fever

Back 52

• J oint - migratory polyarthritis
• O (circle resembles heart) - pancarditis
• N odules - subcutaneous
• E rythema marginatum - rash
• S ydenham chorea - rapid, involuntary movements

Front 53

Pancarditis as seen in acute rheumatic fever

Back 53

• Endocarditis: mitral valve (and sometimes aortic valve) develop small vegetations leading to reguritation
• Myocarditis: Aschoff bodies with Anitschkow cells; most common cause of death
• Pericarditis: friction rub & chest pain

Front 54

Aschoff bodies

Back 54

foci of chronic inflammation, reactive histiocytes with slender, wavy nuclei (Anitschkow cells), giant cells, and fibrinoid material

Front 55

Chronic rheumatic heart disease

Back 55

Valve scarring (usually mitral, sometimes aortic) that arises as consequence of rheumatic fever; results in stenosis with 'fish-mouth' appearance

Front 56

What usually causes aortic stenosis?

Back 56

• 'Wear and tear'; presents >60 years
• Bicuspid aortic valve increases risk and hastens disease onset

Front 57

What kind of murmur is heard in aortic stenosis?

Back 57

Systolic ejection click followed by crescendo-decrescendo murmur

Front 58

Complications of aortic stenosis

Back 58

1. Concentric left ventricular hypertrophy

2. Angina and syncope with exercise

3. Microangiopathic hemolytic anemia

Tx: valve replacement

Front 59

Cause of aortic regurgitation

Back 59

Aortic root dilation (eg syphilitic aneurysm & aortic dissection) or valve damage (eg infectious endocarditis); most common cause is isolated root dilation

Front 60

Clinical features of aortic regurgitation

Back 60

1. Early, blowing diastolic murmur

2. Hyperdynamic circulation due to increased PP (bounding pulse, pulsating nail bed, head bobbing)

3. Results in LV dilation and eccentric hypertrophy

Front 61

Mitral valve prolapse

Back 61

Ballooning of mitral valve into left atrium during systole

Front 62

What causes mitral valve prolapse?

Back 62

myxoid degeneration (accumulation of ground susbstance) of valve, making it floppy

*may be seen in Marfan/Ehlers-Danlos syndrome

Front 63

What is heard on auscultation in mitral valve prolapse?

Back 63

Incidental mid-systolic click following by a regurgitation murmur

Front 64

Clinical features of mitral regurgitation

Back 64

1. Holosystolic 'blowing' murmur; louder with squatting and expiration

2. Results in volume overload and left-sided heart failure

Front 65

What does mitral stenosis sound like on auscultation?

Back 65

Opening snap followed by diastolic rumble

Front 66

Consequences of volume overload in mitral stenosis?

Back 66

• pulmonary congestion with edema and alveolar hemorrhage
• pulmonary HTN and eventual right-sided heart failure
• atrial fibrillation with associated risks for mural thrombi

Front 67

Most common cause of endocarditis

Back 67

Strep. viridans; low virulence organism that infects previously damaged valves (eg chronic rheumatic heart disease and mitral valve prolapse); results in small vegetations that do not destroy the valve (subacute endocarditis)

Front 68

Most common cause of endocarditis in IV drug users

Back 68

Staph. aureus; high virulence organism that infects normal valves (often tricuspid) resulting in large vegetations that destroy valve (acute endocarditis)

Front 69

Which organism is associated with endocarditis of prosthetic valves?

Back 69

Staph. epidermidis

Front 70

Which organism is associated with endocarditis in patients with underlying colorectal carcinoma?

Back 70

Strep. bovis

Front 71

Which organisms are associated with endocarditis with negative blood cultures?

Back 71

HACEK organisms:

Haemophilus

Actinobacillus

Cardiobacterium

Eikenella

Kingella

Front 72

Clinical features of bacterial endocarditis

Back 72

1. Fever

2. Murmur

3. Janeway lesions, osler nodes, splinter hemorrhages in nail bed and Roth spots (on fundoscopy)

4. Anemia of chronic disease

Front 73

Lab findings in bacterial endocarditis

Back 73

1. Positive blood cultures

2. Anemia of chronic disease (↑ferritin, ↓Hb, ↓MCV, ↓TIBC, ↓serum Fe, ↓%saturation)

3. Transesophageal echocardiogram useful for detecting lesions on valves

Front 74

Nonbacterial thrombotic endocarditis

Back 74

due to sterile vegetations that arise in association with a hypercoaguable state or underlying adenocarcinoma; vegetations arise on mitral valve along lines of closure and results in regurgitation

Front 75

Libman-Sacks endocarditis

Back 75

due to sterile vegetations that arise in association with SLE

Front 76

Dilated cardiomyopathy

Back 76

Dilation of all four chambers of the heart; most common form of cardiomyopathy; results in systolic dysfunction leading to biventricular CHF

Front 77

Causes of dilated cardiomyopathy

Back 77

1. Genetic mutation

2. Myocarditis (usually due to coxackie A or B)

3. Alcohol abuse

4. Drugs (eg doxorubicin, cocaine)

5. Pregnancy

6. Hemochromatosis

Tx: heart transplant

Front 78

Cause of hypertrophic cardiomyopathy

Back 78

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

Front 79

Clinical features of hypertrophic cardiomyopathy

Back 79

1. Decreased cardiac output

2. Sudden death due to ventricular arrhythmias (young athletes)

3. Syncope with exercise

Front 80

What is seen on biopsy in hypertrophic cardiomyopathy?

Back 80

Myofiber hypertrophy with disarray

Front 81

Restrictive cardiomyopathy

Back 81

Decreased compliance of ventricular endomyocardium that restricts filling during diastole

Front 82

Causes of restrictive cardiomyopathy

Back 82

• Amyloidosis
• Sarcoidosis
• Endocardial fibroelastosis
• Loeffler syndrome (endomyocardial fibrosis with an eosinophilic infiltrate and eosinophilia)

Front 83

How does restrictive cardiomyopathy present?

Back 83

Congestive heart failure; classic finding is low-voltage EKG with diminished QRS amplitude

Front 84

Myxoma

Back 84

Benign mesenchymal tumor with a gelatinous appearance and abundant ground substance on histology; usually forms a pedunculated mass in L atrium that causes syncope due to obstruction of mitral valve

Front 85

Most common primary cardiac tumor in adults

Back 85

myxoma

Front 86

Rhabdomyoma

Back 86

Benign hamartoma of cardiac muscle; usually arises in ventricle; associated with tuberous sclerosis

Front 87

Most common primary cardiac tumor in children

Back 87

rhabdomyoma

Front 88

Common metastases to heart

Back 88

breast/lung carcinoma, melanoma, lymphoma

Front 89

Which species make up the Viridans strep group that cause endocarditis?

Back 89

S. mutans

S. Sanguinis

S. oralis

S. mitis