Y2S1B2 - Path - Pathoma Cardiac

Front 1

Stable angina is d/t _______ of coronary arteries w/ >____% stenosis.

Back 1

atherosclerosis; >70%

Front 2

Stable, unstable and Prinzmetal angina all represent (reversible/irreversible) to myocytes. What does MI represent?

Back 2

Reversible

MI - irreversible injury

Front 3

In what conditions does an EKG show ST-segment depression?

What does ST depression represent?

Back 3

Stable and unstable angina, and initial phase of MI

subendocardial ischemia/infarction

Front 4

In what conditions does an EKG show ST-segment elevation?

What does ST elevation represent?

Back 4

Prinzmetal angina and continued or severe ischemia in MI.

transmural ischemia/infarction

Front 5

If there is chest pain lasting greater than 20 minutes, what type of ischemic heart disease is likely?

Back 5

MI, because stable angina would be less than 20 minutes (about how long the heart can handle)

Front 6

T/F

Nitroglycerin can be used to relieve stable angina, unstable angina, Prinzmetal angina, and MI.

Back 6

False!

Nitroglycerin can be used to relieve symptoms of all but MI.

Front 7

What is unstable angina due to?

Back 7

rupture of an atherosclerotic plaque w/ thrombosis and incomplete occlusion of coronary artery

Front 8

Which type of angina has a high risk of progression to MI?

Back 8

Unstable angina

Front 9

a) ______ angina occurs w/ exertion or emotional stress.
b) ______ angina occurs at rest.
c) ______ angina is episodic and unrelated to exertion.

Back 9

a) Stable
b) Unstable
c) Prinzmetal

Front 10

Besides nitroglycerin, what else can be used to releive Prinzmetal angina?

Back 10

Calcium channel blockers

Front 11

What is MI usually caused by?

What are some less common causes?

Back 11

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

sometimes:
coronary artery vasospasm (d/t Prinzmetal angina or cocaine use)
Emboli
Vasculitis (ex: Kawasaki dz in children around 5)

Front 12

A patient presents w/ severe, crushing chest pain that has lasted for the past half hour and radiates to the left jaw. He is sweating profusely and is having trouble breathing. Nitroglycerin is not helping to relieve any symptoms.

What does he likely have?

Back 12

Most likely is suffering an MI.

Front 13

What is the most commonly occluded artery (45% of cases) in an MI, and where does it lead to infarction?

What other 2 arteries can be involved?

Back 13

LAD - anterior wall and anterior septum of the LV

2nd MC - RCA - posterior wall, posterior septum, papillary muscles of LV

left circumflex artery - lateral wall of LV

Front 14

a) What is the gold standard marker for MI?
b) When does it rise?
c) When does it peak?
d) When does it return to normal?

Back 14

a) Troponin I
b) 2-4 hrs
c) 24 hrs
d) 7-10 days

Front 15

a) What is CK-MB useful for?
b) When does it rise?
c) When does it peak?
d) When does it return to normal?

Back 15

a) detecting reinfarction that occurs days after an initial MI (while troponin I would still be elevated from the first MI)
b) 4-6 hrs
c) 24 hrs
d) 72 hrs

Front 16

What tx can be given in MI to limit thrombosis?

Back 16

Aspirin and/or heparin

Front 17

What tx can be given in MI to minimize ischemia?

Back 17

Supplemental O2

Front 18

What tx can be given in MI to vasodilate coronary arteries?

Back 18

Nitrates

(arteries + veins -> dec preload -> dec stress)

Front 19

What tx can be given in MI to slow HR? Why does this help?

Back 19

Beta-blockers

decreases O2 demand and risk for arrhythmia (arrhythmia is a feared complication of MI)

Front 20

What tx can be given in MI to decreated LV dilation?

Back 20

ACE inhibitor

(ACE causes increased angiotensin II, which causes arteriole constriction and release of aldosterone -> Na retention -> inc BV)

Front 21

What tx can be given in MI to open the blocked vessel?

What are 2 possible complications of doing this?

Back 21

Angioplasty or fibrinolysis

1. Contaction band necrosis - Ca2+ influx in irreversibly damaged cells, leading to hypercontraction of myofibrils
2. Reperfusion injury - O2 and inflammatory cells return and can generate free radicals, further damaging myocytes

Front 22

At <4 hours after an MI, what are the:

a) Gross changes?
b) Microscopic changes?
c) Complications?

Back 22

a) none
b) none
c) Cardiogenic shock (massive infarction; inability to maintain systemic BP -> dec blood to vital organs), CHF, and arrhythmia (if you've damaged the conduction system will likely see it within the 1st 24 hrs)

Front 23

At 4-24 hrs after an MI, what are the:

a) Gross changes?
b) Microscopic changes?
c) Complications?

Back 23

a) Dark discoloration
b) coagulative necrosis (pyknosis, karyorrhexis, karyolysis)
c) arrhythmia (if you've damaged the conduction system will likely see it within the 1st 24 hrs)

Front 24

At 1-3 days after an MI, what are the:

a) Gross changes?
b) Microscopic changes?
c) Complications?

Back 24

a) yellow pallor (same as 4-7 days)
b) neutrophils
c) fibrinous pericarditis (only w/ transmural necrosis); presents as chest pain w/ friction rub

Front 25

At 4-7 days after an MI, what are the:

a) Gross changes?
b) Microscopic changes?
c) Complications?

Back 25

a) yellow pallor (same as 1-3 days)
b) macrophages
c) rupture of ventricular free wall (leads to cardiac tamponade!), interventricular septum (leads to shunt), or papillary muscle (leads to mitral insufficiency, blood regurgitates during systole; only occurs with RCA occulsion).
Rupture is d/t macrophages eating necrotic debris, weakening the wall

Front 26

At 1-3 weeks after an MI, what are the:

a) Gross changes?
b) Microscopic changes?
c) Complications?

Back 26

a) Red border emerges as granulation tissue enters from edge of infarct
b) Granulation tissue w/ plump fibroblasts, collagen, and blood vessels
c) none listed

Front 27

At months after an MI, what are the:

a) Gross changes?
b) Microscopic changes?
c) Complications?

Back 27

a) White scar (weaker than myocardium)
b) fibrosis
c) aneurysm, mural thrombus (can be d/t stasis from aneurysm), or Dressler syndrome (rare, inflam in pericardium can form Abs against own pericardium. occurs 6-8 weeks after MI and is an autoimmune pericarditis)

Front 28

What is the MC type of arrythmia with sudden cardiac death?

Back 28

Fatal ventricular arrhythmia

occurs w/o symptoms or <1 hr after symptoms arise

Front 29

What is the MC etiology of sudden cardiac death? 90% of patients have preexisting what?

What are some less common causes?

Back 29

Acute ischemia; 90% w/ preexisting severe atherosclerosis

Sometimes - mitral valve prolapse, cardiomyopathy, or cocaine abuse

Front 30

Chronic ischemic heart disease is poor myocardial function d/t _______ (w/ or w/o ______). It progresses to ________.

Back 30

chronic ischemic damage (w/ or w/o infarction)

progresses to CHF

Front 31

What are 5 causes of left-sided heart failure?

Back 31

1. ischemia
2. HTN (LV hypertrophy, becomes hard to oxygenate)
3. dilated cardiomyopathy
4. MI
5. restrictive cardiomyopathy (can't fill heart appropriately)

Front 32

Left-sided heart failure can cause what clinical features d/t pulm congestion or decreased forward perfusion?

Back 32

dyspnea, paroxysmal nocturnal dyspnea, orthopnea, and crackles

decreased flow to kidneys

Front 33

What are "heart failure" cells?

Back 33

Hemosiderin-laden macrophages

Front 34

If small, congested capillaries burst in left-sided heart failure, intra-alveolar hemorrhage can occur, marked by what?

Back 34

"heart failure" cells (hemosiderin-laden macrophages)

Front 35

What is the mainstay of treatment for left-sided heart failure?

Back 35

ACE inhibitor

Front 36

Besides the MC cause of right-sided heart failure (left-sided heart failure), what are some other causes?

Back 36

left-to-right shunt
chronic lung disease (cor pulmonale)

Front 37

What are some clinical features of right-sided heart failure, d/t congestion?

Back 37

1. jugular venous distention
2. painful hepatosplenomegaly w/ "nutmeg" liver; may lead to cardiac cirrhosis
3. dependent pitting edema (d/t inc hydrostatic pressure)

Front 38

"nutmeg" liver a/w what?

Back 38

painful hepatosplenomegaly in right-sided heart failure

Front 39

During what weeks of embryogenesis do congenital heart defects usually arise?

Back 39

weeks 3 through 8

(seen in 1% of live births)

Front 40

What is the MC congenital heart defect?

Back 40

VSD

Front 41

What is VSD a/w?

Back 41

fetal alcohol syndrome

Front 42

Which congenital heart defects result in a left-to-right shunt?

Back 42

VSD, ASD, and PDA (unless progressed to Eisenmenger syndrome)

Front 43

Which congenital heart defects result in a right-to-left shunt, and therefore cyanosis?

Back 43

PDA (if progressed to Eisenmenger syndrome; pulm HTN leads to reversal of L->R shunt), Tetralogy of fallot, tricuspid atresia (when a/w ASD)

Front 44

What is the presentation/tx of VSD that are
a) small?
b) large?

Back 44

a) often asymptomatic and may close on their own

b) can lead to Eisenmenger syndrome, tx involves surgical closure

Front 45

What is the MC type of ASD?

Back 45

ostium secundum (90% of cases)

Front 46

The ostium primum type of ASD is a/w what disorder?

Back 46

Down syndrome

Front 47

On auscultation, which congenital heart defect is a/w a split S2?

Back 47

ASD

increased blood in right heart delays closure of pulmonary valve

Front 48

Paradoxical emboli are an important complication of what type of congenital heart defect?

Back 48

ASD

embolus from right side can lodge on the left side

Front 49

What disease is PDA a/w?

Back 49

Congenital rubella

Front 50

On auscultation, a holosystolic "machine-like" murmur is a/w what congenital heart defect?

Back 50

PDA

Front 51

What is the tx for PDA?

Back 51

Indomethacin, which decreased PGE resulting in PDA closure (PGE maintains patency of ductus arteriosus)

Front 52

What are the 4 characteristics of tetralogy of Fallot?

Back 52

1. stenosis of right ventricular outflow tract
2. RV hypertrophy
3. VSD
4. aorta that overrides VSD

Front 53

What 2 congenital heart defects can progress to Eisenmenger syndrome?

Back 53

VSD and PDA

Front 54

LE cyanosis is a/w what congenital heart defects?

Back 54

PDA and infantile form of coarctation of the aorta

Front 55

"boot-shaped" heart on xray a/w what congenital defect?

Back 55

tetralogy of fallot

Front 56

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

Back 56

Squat. it increases arterial resistance, decreasing shunting and allowing more blood to reach the lungs

Front 57

What is transposition of the great vessels a/w?

Back 57

Maternal diabetes

Front 58

Which congenital heart defects present w/ early cyanosis?

Back 58

Tetralogy of Fallot, transposition of the great vessels, truncus arteriosus, tricuspid atresia

Front 59

What is the tx for transposition of the great vessels?

Back 59

A shunt must be created after birth for survival, PGE can be given to maintain a PDA until definitive surgical repair can be performed

Front 60

Transposition of the great vessels results in hypertrophy of the ____ and atrophy of the ____.

Back 60

RV; LV

Front 61

_______ is characterized by a single large vessel arising from both ventricles.

Back 61

Truncus arteriosus

Front 62

In tricuspid atresia, the _______ fails to devlop, and the ______ is hypoplastic (b/c blood doesn't go to it).

Back 62

tricuspid valve orifice; RV

Front 63

Tricuspid atresia is often a/w what other congenital heart defect?

Back 63

ASD

Front 64

The infantile form of coarctation of the aorta is a/w what genetic disorder?

Back 64

Turner syndrome

Front 65

The infantile form of coarctation of the aorta is a/w what other congenital heart defect?

Back 65

PDA (coarctation lies after aortic arch but before the PDA)

Front 66

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

Back 66

HTN in the UE and hypotension w/ weak pulses in the LE

Front 67

"notching" of ribs on xray is a/w what?

Why does this occur?

Back 67

adult form of coarctation of the aorta

b/c collateral circulation develops across the intercostal arteries, and the engorged arteries cause the notching

Front 68

The adult form of coarctation of the aorta is a/w what valve defect?

Back 68

Bicuspid aortic valve

Front 69

A systemic complication affecting children 2-3 weeks after strep throat is what?

Back 69

Acute rheumatic fever

Front 70

Molecular mimicry causes what disease?

Back 70

Acute rheumatic fever

the group A strep's M protein resembles proteins in human tissue

Front 71

In diagnosing acute rheumatic fever, what are the major criteria of Jones criteria?

Back 71

JONES

J - joint (migratory polyarthritis - swelling&pain in large joint that resolves w/i days and migrates to another large joint)
O - <3 (heart) - Pancarditis! Endocarditis involves mitral valve MC than aortic valve, w/ small vegetations along lines of closure that lead to regurgitation. Myocarditis w/ Aschoff bodies are characterized by foci of chronic inflammation, Anitschkow cells, giant cells, and fibrinoid material (degenerated collagen) and is MC cause of death in acute phase.
N - nodules in skin (subQ)
E - erythema marginatum (annular, nonpruritic w/ erythematous borders, commonly on trunk and limbs)
S - sydenham chorea (rapid, involuntary muscle movements)

Front 72

What is the hallmark of myocarditis in acute rheumatic fever?

Back 72

Aschoff bodies

(characterized by foci of chronic inflammation, Anitschkow cells, giant cells, and fibrinoid material)

Front 73

What are Anitschkow cells?

Back 73

reactive histiocytes w/ slender, wavy nuclei

Front 74

Jones criteria for acute rheumatic fever requires what (very generally)?

Back 74

evidence of prior group A strep infection (elevated ASO or anti-DNAse B titers) w/ presence of major and minor criteria

Front 75

Minor Jones criteria are what?

Back 75

nonspecific, such as fever and elevated ESR

Front 76

Acute attacks of rheumatic fever usually resolve, but may progress to chronic rheumatic heart disease, especially when what happens?

Back 76

repeat exposure to group A strep, resulting in relapse of acute phase

Front 77

"fish-mouth" appearance is a/w what?

Back 77

stenosis in chronic rheumatic heart disease

Front 78

a) Chronic rheumatic heart disease stenosis almost always involves which valve? Leading to thickening of what?

b) It sometimes involves what valve, leading to what?

Other valves are less common.

Back 78

a) Mitral valve; thickening of chordae tendinae and cusps

b) Aortic valve; fusion of the commissures

Front 79

What is a complication of chronic rheumatic heart disease?

Back 79

Infectious endocarditis

Front 80

How can you distinguish "wear and tear" aortic stenosis from aortic stenosis that is d/t chronic rheumatic valve disease?

Back 80

If it is d/t chronic rheumatic valve disease, it will usually have coexisting mitral stenosis and fusion of the aortic valve commissures (instead of just unfused, damage to the cusps)

Front 81

When does aortic stenosis typically present?

Back 81

late adulthood (>60) d/t fibrosis/calcification from wear and tear

Front 82

What condition increases risk of and hastens the onset of aortic stenosis?

Back 82

bicuspid aortic valve

Front 83

What are the hallmarks of cardiac compensation in aortic stenosis?

Back 83

prolonged asymptomatic stage w/ a systolic ejection click followed by a crescendo-decrescendo murmur

Front 84

What are 3 possible complications of aortic stenosis?

Back 84

1. concentric LV hypertrophy (may progress to cardiac failure)
2. Angina and syncope w/ exercise (dec perfusion of myocardium and brain)
3. Microangiopathic hemolytic anemia (RBCs damaged, producing schistocytes, while crossing calcified valve)

Front 85

When would you replace the valve in aortic stenosis?

Back 85

After the onset of complications

Front 86

Aortic regurgitation occurs during ______ while mitral regurgitation occurs during ________.

Back 86

Diastole

Systole

Front 87

What can cause aortic regurgitation?

Back 87

aortic root dilation (syphilitic aneurysm and aortic dissection)

valve damage (infectious endocarditis)

*MC cause is isolated root dilation

Front 88

Aortic regurgitation has what type of murmur?

Back 88

early, blowing diastolic murmur

Front 89

Why is there hyperdynamic circulation (d/t increased pulse pressure) with aortic regurgitation?

Back 89

diastolic pressure decreases d/t regurgitation
systolic pressure increases d/t increased stroke volume

Front 90

A bounding pulse (water-hammer pulse), pulsating nail bed (Quincke pulse) and head bobbing are characteristic of what?

Back 90

Hyperdynamic circulation

(seen in aortic regurgitation)

Front 91

When does aortic stenosis typically present?

Back 91

late adulthood (>60) d/t fibrosis/calcification from wear and tear

Front 92

What condition increases risk of and hastens the onset of aortic stenosis?

Back 92

bicuspid aortic valve

Front 93

What are the hallmarks of cardiac compensation in aortic stenosis?

Back 93

prolonged asymptomatic stage w/ a systolic ejection click followed by a crescendo-decrescendo murmur

Front 94

What are 3 possible complications of aortic stenosis?

Back 94

1. concentric LV hypertrophy (may progress to cardiac failure)
2. Angina and syncope w/ exercise (dec perfusion of myocardium and brain)
3. Microangiopathic hemolytic anemia (RBCs damaged, producing schistocytes, while crossing calcified valve)

Front 95

When would you replace the valve in aortic stenosis?

Back 95

After the onset of complications

Front 96

Aortic regurgitation occurs during ______ while mitral regurgitation occurs during ________.

Back 96

Diastole

Systole

Front 97

What can cause aortic regurgitation?

Back 97

aortic root dilation (syphilitic aneurysm and aortic dissection)

valve damage (infectious endocarditis)

*MC cause is isolated root dilation

Front 98

Aortic regurgitation has what type of murmur?

Back 98

early, blowing diastolic murmur

Front 99

Why is there hyperdynamic circulation (d/t increased pulse pressure) with aortic regurgitation?

Back 99

diastolic pressure decreases d/t regurgitation
systolic pressure increases d/t increased stroke volume

Front 100

A bounding pulse (water-hammer pulse), pulsating nail bed (Quincke pulse) and head bobbing are characteristic of what?

Back 100

Hyperdynamic circulation

(seen in aortic regurgitation)

Front 101

Aortic regurgitation results in LV dilation and ________ hypertrophy d/t volume overload.

Back 101

Eccentric

Front 102

When would you replace the valve in aortic regurgitation?

Back 102

once LV dysfx develops

Front 103

Myxoid degeneration (accumulation of ground substance) of the mitral valve causes what?

Back 103

Mitral valve prolapse, by making it floppy

Front 104

The etiology of mitral valve prolapse is unknown, but it may be seen in what disorders?

Back 104

Marfan syndrome and Ehlers-Danlos syndrome

Front 105

A patient comes in for a regular check-up and on exam, you find a mid-systolic click followed by a regurgitation murmur near the mitral valve. She reports that she has not had any symptoms.

What do you suspect she has?

To test your theory, you ask your patient to do something that should make the click and murmur become louder. What is it?

Back 105

Mitral valve prolapse (click is d/t parachute snapping shut, regurg murmur usually present)

Squat! increased systemic resistance decreases LV emptying

Front 106

What are some RARE complications of mitral valve prolapse?

Back 106

infectious endocarditis
arrhythmia
severe mitral regurgitation

Front 107

What is the MC cause of mitral regurgitation?

other causes?

Back 107

complication of mitral valve prolapse

sometimes - LV dilation (left-sided heart failure), infective endocarditis (weakens valve leaflets), acute rheumatic heart disease, and papillary muscle rupture (keeps it closed in systole normally) after an MI

Front 108

A patient presents w/ a holosystolic "blowing" murmur that gets louder with squatting and with expiration.

What do you suspect she has?
What can this result in?

Back 108

Mitral regurgitation (squatting increases systemic resistance/decreases LV emptying; expiration increases return to LA)

results in volume overload and left-sided heart failure

Front 109

Mitral stenosis is usually d/t what?

Back 109

chronic rheumatic valve disease

Front 110

A patient presents w/ an opening snap followed by a diastolic rumble. This is characteristic of what?

This can lead to what 3 things?

Back 110

Mitral stenosis

Volume overload leads to:
1. pulm congestion w/ edema and alveolar hemorrhage
2. pulm HTN and eventual right-sided heart failure
3. atrial fib w/ risk for mural thrombi (d/t stasis)

Front 111

Endocarditis is inflammation of endocarduyn that lines the surface of __________.

Back 111

cardiac valves

Front 112

____________ is the MC cause of endocarditis, and it is a low-virulence organism that infects previously damaged valves (ex: chronic rheumatic heart disease, mitral prolapse).

Back 112

streptococcus viridans

Front 113

_______ endocarditis results in small vegetations that don't destroy the valve (subacute), while _______ endocarditis leads to large vegetations that do destroy valve (acute).

Back 113

strep viridans

staph aureus

Front 114

Damaged endocardial surface develops thrombotic vegetations composed of ____ and ____.

Then, transient bacteremia leads to trapping of bacteria in the vegetations. What can be given prophylactically to decrease the risk of endocarditis?

Back 114

platelets and fibrin

antibiotics

Front 115

________ is the MC cause of endocarditis in IV drug abusers, and it is a high-virulence organism that infects normal valves, most commonly the _______ valve.

Back 115

staph aureus; tricuspid

Front 116

What organism is a/w endocarditis of prosthetic valves?

Back 116

staph epidermidis

Front 117

What organism is a/w endocarditis in patients w/ underling colorectal carcinoma?

Back 117

strep bovis

Front 118

What organisms are a/w endocarditis in negative blood cultures?

Back 118

HACEK organisms (haemophilus, actinobacillus, cardiobacterium, eikenella, kingella)

Front 119

What clinical feature of bacterial endocarditis is d/t bacteremia?

Back 119

Fever

Front 120

What clinical feature of bacterial endocarditis is d/t vegetations on the heart valve?

Back 120

Murmur

Front 121

What clinical features of bacterial endocarditis is d/t embolization of septic vegetations?

Back 121

Janeway lesions (erythematous nontender lesions on palms and soles)
Osler nodes ("Ouch" erythematous tender lesions on fingers and toes)
Splinter hemorrhages in nail bed

Front 122

What clinical feature of bacterial endocarditis is d/t chronic inflammation?

Back 122

Anemia of chronic disease

Front 123

What are some lab findings of endocarditis?

Back 123

Positive blood cultures
Anemia of chronic disease (decreased Hb, MCV, TIBC, serum iron and % saturation; increased ferritin)
Transesophageal echocardiogram is useful for detecting lesions on valves

Front 124

What are 2 forms of endocarditis that are caused by sterile vegetations on the mitral valve, resulting in mitral regurgitation?

Back 124

Nonbacterial thrombotic endocarditis and Libman-Sacks endocarditis

Front 125

What type of endocarditis is a/w a hypercoagulable state or underlying adenocarcinoma?

Back 125

Nonbacterial thrombotic endocarditis

Front 126

Vegetations in nonbacterial thrombotic endocarditis arise where on the mitral valve?

Back 126

along lines of closure

Front 127

Vegetations in Libman-Sacks endocarditis arise where on the mitral valve?

Back 127

surfance AND undersurface... both sides!

Front 128

What type of endocarditis is a/w SLE?

Back 128

Libman-Sacks endocarditis

Front 129

What is the MC form of cardiomyopathy?

Back 129

Dilated cardiomyopathy, which is dilation of all 4 chambers

Front 130

Dilated cardiomyopathy results in (systolic/diastolic) dysfx, leading to what?

Back 130

Systolic (ventricles can't pump); biventricular CHF

This stretches the valves and conduction system, possibly causing mitral/tricuspid regurgitation and arrhythmia.

Front 131

While most cases of dilated cardiomyopathy are idiopathic, what are 5 possible causes?

Back 131

1. Genetic mutation (usually AD)
2. Myocarditis (usually d/t coxsackie A or B; characterized by lymphocytic infiltrate in myocardium resulting in chest pain, arrhythmia w/ sudden death, or heart failure. dilated cardiomyopathy is a late complication)
3. Alcohol abuse
4. Drugs (ex: doxorubicin and cocaine)
5. Pregnancy (late pregnancy or soon (wks-mos) after childbirth)

Front 132

What is the tx for dilated cardiomyopathy?

Back 132

Heart transplant

Front 133

Myocyte disarray (myofiber hypertrophy w/ disarray) is a classic biopsy finding in what?

Back 133

Hypertrophic cardiomyopathy

Front 134

Hypertrophic cardiomyopathy is massive hypertrophy of the ____ and leads to (systolic/diastolic) dysfx.

Back 134

LV

diastolic dysfx, b/c ventricle can't fill

Front 135

What disorder is d/t genetic mutations in sarcomere (usually AD)?

Back 135

Hypertrophic cardiomyopathy

Front 136

Common cause of sudden death in young athletes?

Back 136

ventricular arrhythmias d/t Hypertrophic Cardiomyopathy

Front 137

Syncope w/ exercise, a/w hypertrophic cardiomyopathy, is d/t what?

Back 137

subaortic hypertrophy of the ventricular septum, resulting in functional aortic stenosis

Front 138

Restrictive cardiomyopathy is decreased compliance of the ventricular endomyocardium that restricts filling during (systole/diastole).

Back 138

Diastole

Front 139

What are possible causes of restrictive cardiomyopathy?

Back 139

Amyloidosis
Sarcoidosis
Hemochromatosis
Endocardial fibroelastosis (children)
Loeffler syndrome (endomyocardial fibrosis w/ eosinophilic infiltrate and eosinophilia)

Front 140

What cardiomyopathy presents as CHF?

Back 140

Restrictive cardiomyopathy

Front 141

The classic finding of what condition is low-voltage EKG w/ diminished QRS amplitude?

Back 141

Restrictive cardiomyopathy

Front 142

A benign mesenchymal tumor w/ gelatinous appearance and abundant ground substance is called what?

Back 142

Myxoma

Front 143

What is the MC primary cardiac tumor in adults?

Back 143

Myxoma

Front 144

What is the MC primary cardiac tumor in children?

Back 144

Rhabdomyoma

Front 145

What condition typically forms a pedunculated mass in the LA that causes syncope d/t obstruction of mitral valve?

Back 145

Myxoma

Front 146

A rhabdomyoma is a ____________ of cardiac muscle.

Back 146

benign hemartoma

Front 147

Rhabdomyoma usually arises where?

Back 147

In the ventricle

Front 148

What condition is rhabdomyoma a/w?

Back 148

Tuberous sclerosis

Front 149

T/F

Primary tumors are more common in the heart than metastatic tumors.

Back 149

False!

Metastatic are more common.

Front 150

Common metastases to the heart come from where?

What part of the heart do they most commonly affect?

Back 150

breast and lung carcinoma, melanoma, lymphoma

pericardium -> pericardial effusion