Cardiovascular Pathology Flashcards
(135 cards)
1
Q
T/F: In the case of vasculitis, the etiology is usually unknown, but most cases are not infectious
A
True
2
Q
Large vessel vasculitides affect the aorta or its major branches. What are the 2 types of large vessel vasculitis?
A
Temporal (Giant Cell) Arteritis
Takayasu Arteritis
3
Q
What is the most common form of vasculitis in older adults (>50); usually affects females?
A
Temporal (Giant Cell) Arteritis
4
Q
The classic location for temporal arteritis is branches of the _____ artery, leading to symptoms of headache, visual disturbance, jaw claudication, flu-like symptoms (polymyalgia rheumatica) with joint and muscle pain. Classically, the _____ is elevated to >100
A
Carotid; ESR
5
Q
Temporal arteritis is characterized as a _______ vasculitis, and biopsy will show an inflamed vessel wall wtih giant cells and intimal fibrosis.
Treatment is ________, which must be started promptly because there is high risk of blindness due to thrombosis of ophthalmic artery
A
Granulomatous
Corticosteroids
6
Q
Granulomatous vasculitis that presents in adults <50 that affects aortic arch at the branch points, presenting with visual and neurologic symptoms, weak or absent pulse in upper extremity (“pulseless disease”), elevated ESR, and is treated with corticosteroids
A
Takayasu arteritis
7
Q
Medium vessel vasculitides involve muscular arteries that supply organs. What are the 3 major medium vessel vasculitides?
A
Polyarteritis nodosa
Kawasaki disease
Buerger disease
8
Q
Medium vessel necrotizing vasculitis that involves most organs, but lungs are spared
A
Polyarteritis nodosa
9
Q
Polyarteritis nodosa presents in young adults with ______ (due to involvement of renal artery), abdominal pain with melena (due to involvement of _____ artery), neurologic disturbances, skin lesions, and is associated with serum ______
A
HTN; mesenteric; HBsAg
10
Q
Polyarteritis nodosa presents with lesions of varying stage which have “string of pearls” appearance on imaging. Early lesions will show _______ inflammation characterized by ______ necrosis. These early lesions weaken the wall and can become aneurysms. These lesions will later be replaced by fibrosis.
Treatment for polyarteritis nodosa is _____ and ______
A
Transmural; fibrinoid
Corticosteroids; cyclophosphamide
11
Q
T/F: Polyarteritis nodosa is fatal if not treated
A
True
12
Q
Medium vessel vasculitis that classically affects Asian children <4 y/o, presenting with fever, conjunctivitis, erythematous rash of palms and soles, and enlarged cervical lymph nodes
A
Kawasaki disease
13
Q
The preferential artery involved in Kawasaki disease is the _______ artery, which may lead to complications of thrombosis with myocardial infarction and/or aneurysm with rupture
Treatment is _____ and _____; the disease is self-limited
A
Coronary
ASA; IVIG
[Note that it may seem counterintuitive to give ASA when it appears initially as a viral illness]
14
Q
Medium vessel necrotizing vasculitis involving digits; presents with ulceration, gangrene, and autoamputation of fingers and toes. Raynaud phenomenon is often present. Highly associated with smoking; tx is smoking cessation
A
Buerger Disease
15
Q
Small vessel vasculitides affect the arterioles, capillaries, and venules. What are the 4 major small vessel vasculitides?
A
Wegener granulomatosis
Microscopic polyangiitis
Churg-Strauss syndrome
Henoch Schonlein purpura
16
Q
Small vessel necrotizing, granulomatous vasculitis involving nasopharynx, lungs, and kidneys
A
Wegener Granulomatosis
17
Q
Wegeners granulomatosis presents in middle-aged males with sinusitis or nasopharyngeal ulceration, hemoptysis with bilateral nodular lung infiltrates, hematuria due to _________, and serum _____ levels which correlate with disease activity.
Biopsy shows large necrotizing granulomas with adjacent necrotizing vasculitis. Key treatment is _______ and ________, and relapses are fairly common
A
RPGN; c-ANCA
Cyclophosphamide; corticosteroids
18
Q
Small vessel necrotizing vasculitis involving multiple organs, especially lung and kidney that is similar to wegeners granulomatosis, but nasopharyngeal and granulomas are absent
A
Microscopic polyangiitis
19
Q
With microscopic polyangiitis, ______ levels correlate with disease activity. Similar to Wegeners granulomatosis, treatment is _____ and _____, and relapses are common
A
p-ANCA
Corticosteroids; cyclophosphamide
20
Q
Small vessel necrotizing granulomatous vasculitis with eosinophils involving multiple organs, especially lungs and heart; presents with asthma and peripheral eosinophilia, and p-ANCA levels correlate with disease activity
A
Churg-Strauss syndrome
21
Q
Small vessel vasculitis due to IgA immune complex deposition; most common vasculitis in children. Self-limited but may recur; tx with steroids if severe
A
HSP
22
Q
Clinical presentation of henoch schonlein purpura
A
Palpable purpura on buttocks and legs
GI pain and bleeding
Hematuria (IgA nephropathy)
Usually occurs following a URI
23
Q
Systemic HTN can be divided into primary or secondary types based on etiology. In primary HTN, the etiology is unknown (90%), and risk factors include age, race, obesity, stress, lack of physical activity, and high-salt diet. Secondary HTN is due to an identifiable cause (5% of cases). What is a classic cause of secondary HTN?
A
Renal artery stenosis
24
Q
Renal artery stenosis is associated with an increased plasma _____ and unilateral _____ of the affected kidney
A
Renin; atrophy
25
2 important causes of renal artery stenosis
Atherosclerosis (elderly males)
Fibromuscular dysplasia (young females)
26
HTN can be further subdivided into benign or malignant. Benign HTN involves mild or moderate elevation in BP that is clinically silent; vessels and organs are damaged over time. How does this differ from malignant HTN?
Severe elevation in BP (>200/120 mm Hg); presents with acute end-organ damage — acute renal failure, headache, and papilledema. MEDICAL EMERGENCY!
May arise from preexisting benign HTN or de novo
27
3 pathologic patterns of arteriolosclerosis
Atherosclerosis — thickening of intima in medium and large vessels
Arteriosclerosis — thickening of wall in small vessels (hyaline or hyperplastic)
Monckeberg medial sclerosis — calcification of media of vessel wall
28
Atherosclerosis is characterized as an intimal plaque that consists of a necrotic lipid core with an overlying fibromuscular cap that obstructs blood flow. It involves large and medium-sized arteries — what are the 4 most common arteries involved?
Abdominal aorta
Coronary a.
Popliteal a.
Internal carotid a.
29
Risk factors for atherosclerosis are divided into modifiable (4) and nonmodifiable (3). What are some risk factors in each category?
Modifiable — HTN, hypercholesterolemia, smoking, diabetes
Non-modifiable — age, gender, genetics
30
Complications of atherosclerosis may include stenosis of medium-sized vessels which leads to what clinical features?
Peripheral vascular disease (e.g., popliteal a.)
Angina (coronary a.)
Ischemic bowel disease (mesenteric aa.)
[Note that symptoms don’t tend to arise until there is >70% stenosis]
31
Another complication with atherosclerosis is plaque rupture with thrombosis, leading to what 2 potential events?
Myocardial infarction (coronary a.)
Stroke (middle cerebral a.)
32
Another complication of atherosclerosis is plaque rupture with embolization, characterized by ______ ____ in emboli
Cholesterol clefts
33
Arteriolosclerosis is divided into hyaline and hyperplastic types. Hyaline is caused by proteins leaking into the vessel wall, producing vascular thickening, and is seen as pink hyaline on microscopy.
This is seen in the setting of what 2 conditions?
Benign HTN
Diabetes
34
Hyaline arteriolosclerosis results in reduced vessel caliber with end-organ ischemia. This classically produces what complication?
Glomerular scarring (arteriolonephrosclerosis) — progresses to chronic renal failure
35
Hyperplastic arteriolosclerosis involves thickening of vessel wall by hyperplasia of smooth muscle, which is described as “onion-skin” appearance.
What is this process typically a consequence of?
Malignant HTN
36
Hyperplastic arteriolosclerosis results in reduced vessel caliber with end-organ ischemia. This may lead to fibrinoid necrosis of vessel wall and classically to what complication?
Acute renal failure (with “flea-bitten”) appearance
37
Type of arteriosclerosis characterized by calcification of the media; non-obstructive and not clinically significant — often seen as incidental finding on x-ray or mammography
Monckeberg Medial Calcific Sclerosis
38
Aortic dissection is defined as a tear in the ______ with dissection of blood through the _____ of the aortic wall
Intima; media
39
Aortic dissection occurs in the proximal 10 cm of the aorta with pre-existing weakness of the ______. The most common cause is ______, but it is also associated with inherited defects of connective tissue
Media; HTN
40
The most common cause of death in aortic dissection is _____ _____
Pericardial tamponade
41
A thoracic aneurysm is a balloon-like dilation of the thoracic aorta due to weakness in the aortic wall. This is classically seen in what condition?
Tertiary syphilis (destruction of vasa vasorum results in “tree-bark” appearance of aorta)
42
Complications of thoracic aneurysm
Dilation of aortic valve root with insufficiency —> aortic insufficiency
Compression of mediastinal structures
Thrombosis/embolism
43
AAA is a balloon-like dilation of abdominal aorta, which usually arises below renal arteries but above aortic bifurcation. This primarily occurs due to ________ and is classically seen in male smokers >60 y/o with HTN; presents with pulsatile abdominal mass that grows with time
Atherosclerosis
44
The major complication of AAA is rupture, especially when size is ______ in diameter.
This will present with classic triad of _______, _____, and ______
>5 cm
Hypotension, pulsatile abdominal mass, and flank pain
45
Benign tumor comprised of blood vessels commonly present at birth and often regresses during childhood; most often involves skin and liver
Hemangioma
46
Highly aggressive, malignant proliferation of endothelial cells; common sites include skin, breast, and liver
Angiosarcoma
47
______ angiosarcoma is associated with exposure to PVC, arsenic, and Thorotrast
Liver
48
Low-grade malignant proliferation of endothelial cells associated with HHV-8; presents as purple patches, plaques, or nodules on skin and may involve visceral organs
Kaposi Sarcoma
49
Kaposi sarcoma is classically seen in what 3 patient populations?
Older Eastern European males (usually localized to skin, tx is surgery)
AIDS (spreads early, give anti-retroviral agents)
Transplant recipients (decrease their immunosuppression)
50
Stable angina is chest pain that arises with exertion or emotional stress due to atherosclerosis of coronary arteries with _____% stenosis. It represents _______ (reversible/irreversible) injury to myocytes
Clinically presents as chest pain lasting <20 minutes that radiates to left arm or jaw, diaphoresis, and shortness of breath
>70%; reversible (cellular swelling)
51
EKG findings and treatment for stable angina
EKG shows ST-segment depression (subendocardial ischemia)
Relieved by rest or nitroglycerin (vasodilation of veins, decreasing preload)
52
How is unstable angina different from stable angina?
Chest pain occurs at rest — and is often due to rupture of an atherosclerotic plaque with thrombosis and INCOMPLETE occlusion of a coronary artery
Still represents reversible injury to myocytes
53
EKG changes and treatment for unstable angina
EKG shows ST segment depression
Relieved by nitroglycerin
54
T/F: unstable angina has high risk of progression to MI
True
55
_______ angina is due to coronary artery vasospasm leading to episodic chest pain unrelated to exertion
Prinzmetal
56
Prinzmetal angina represents reversible injury to myocytes. EKG shows ___________ due to ________ ischemia. This condition is relieved by nitroglycerin or ________
ST-segment elevation; transmural; calcium channel blockers
57
Myocardial infarction results in necrosis of cardiac myocytes due to rupture of atherosclerotic plaque with thrombosis and COMPLETE occlusion of coronary artery. Other causes include coronary artery vasospasm, emboli, and vasculitis (i.e., Kawasaki disease). Symptoms are unlikely to be relieved by nitroglycerin. Infarction usually involves what chamber of the heart?
Left ventricle (usually LAD, RCA, or left circumflex); RV and both atria are generally spared
58
With an MI, the initial phase involves subendocardial necrosis involving <50% of the myocardial thickness. EKG will show ________.
ST segment depression
59
Lab test for most sensitive and specific marker of MI
Troponin I
[Rises 2-4 hrs after infarct, peaks at 24 hours, returns to normal by 7-10 days]
60
______ is a marker most useful for detecting re-infarction days after MI; rises 4-6 hours after infarct and peaks at 24 hours, returning to normal by 72 hours
CK-MB
61
Treatment following MI
```
ASA/heparin
Supplemental O2
Nitrates
Beta-blocker
ACE inhibitor
```
62
A more definitive tx for MI is fibrinolysis or angioplasty. What are 2 potential complications of this tx?
Contraction band necrosis
Reperfusion injury
63
How long after infarction would you see NO gross changes, NO microscopic changes, and complications including cardiogenic shock (massive infarcts), CHF, and arrhythmia?
<4 hours
64
How long after infarction would you see gross changes including dark discoloration, microscopic changes including coagulative necrosis, and complications including arrhythmia?
4-24 hrs
65
How long after infarction would you see gross changes including yellow pallor, neutrophilic microscopic changes, and complications including fibrinous pericarditis?
1-3 days
66
How long after infarction would you see gross changes including yellow pallor, microscopic changes including macrophages, and complications including rupture of ventricular free wall (cardiac tamponade), rupture of interventricular septum (shunt), or rupture of papillary muscle (leads to mitral insufficiency)
4-7 days
67
How long after infarction would you see gross changes including red border emerging as granulation tissue enters from edge of infarct, and microscopic changes showing granulation tissue with plump fibroblasts, collagen, and blood vessels?
1-3 weeks
68
How long after infarction would you see gross changes including white scar (type I collagen), microscopic changes including fibrosis, and complications including aneurysm, mural thrombus, or Dressler syndrome
Months
69
Rupture of the papillary muscle following an MI leads to mitral insufficiency. This occurs if the vessel affected is the ________, as this is the arterial supply to the papillary muscle
RCA
70
Autoimmune pericarditis occurring 6-8 weeks following MI
Dressler syndrome
71
Sudden cardiac death is defined as unexpected death due to cardiac disease occurring without symptoms or <1 hr after symptoms arise. This is usually due to a fatal ventricular arrhythmia. What is the most common etiology?
Acute ischemia; 90% of pts have preexisting severe atherosclerosis
Less common causes include mitral valve prolapse, cardiomyopathy, and cocaine abuse
72
Chronic ischemic heart disease is defined as poor myocardial function due to chronic ischemic damage (with or without infarction) and progresses to _____
CHF
73
Causes of left sided heart failure
```
Ischemia
HTN
Dilated cardiomyopathy
Myocardial infarct
Restrictive cardiomyopathy
```
74
Clinical manifestations of left-sided heart failure are primarily due to ________ congestion
Pulmonary
[Pulmonary edema with dyspnea, PND, orthopnea, and crackles; heart failure cells — hemosiderin-laden macrophages within alveolar air sacs]
75
A consequence of left sided heart failure is decreased forward perfusion, a complication of this is activation of the renin-angiotensin system. The mainstay of treatment is _______
ACE inhibitor
76
Most common cause of right-sided heart failure
Left-sided heart failure
[other important causes include left-to-right shunt and chronic lung disease (cor pulmonale)]
77
Clinical features of right-sided heart failure
JVD
Painful HSM, may lead to cardiac cirrhosis [nutmeg liver]
Dependent pitting edema
78
Congenital cardiac defects typically arise during weeks _____ during embryogenesis and are seen in 1% of live births. Most defects are sporadic.
3-8
79
The most common congenital heart defect is a _______, resulting in a ___ to ____ shunt. It is associated with _______ ______ syndrome
VSD; left to right; fetal alcohol syndrome
80
Fetal alcohol syndrome is associated with what congenital heart defect?
VSD
81
VSDs result in a left to right shunt; the size of the defect determines the extent of shunting and age at presentation. Small defects are often asymptomatic, while large defects can lead to _______ syndrome
Eisenmenger
82
The most common type of ASD is ______ ______.
Another type of ASD is ______ ______, this is the type associated with Down syndrome
Ostium secundum
Ostium primum
83
ASDs result in a _____ to _____ shunt and a _________ on auscultation. Paradoxical emboli are an important complication
Left to right; split S2
84
PDA results when there is failure of ductus arteriosus to close; this is associated with what condition?
Congenital rubella
85
Congenital rubella is associated with what congenital heart defect?
PDA
86
PDA results in ____ to _____ shunt between aorta and pulmonary artery. This is asymptomatic at birth with ____________murmur.
Eisenmenger syndrome results in ______ _____ cyanosis. The treatment is indomethacin, which decreases PGE, resulting in PDA closure.
Left to right; holosystolic “machine-like” murmur
Lower extremity
87
4 heart problems in tetralogy of fallot
Stenosis of RV outflow tract
Right ventricular hypertrophy
VSD
Aorta that overrides the VSD
88
Tetralogy of fallot results in a _____ to _____ shunt and classic _____-shaped heart on x-ray
Right to left (leads to early cyanosis); boot
89
What aspect of tetralogy of fallot determines the extent of shunting and cyanosis?
Degree of pulmonary stenosis
90
Why do pts with tetralogy of fallot learn to squat in response to cyanotic spell?
Squatting —> increased arterial vascular resistance —> decreased shunting
Allows more blood to reach lungs
91
____________ is a congenital heart defect in which the pulmonary artery arises from the LV and the aorta arises from the RV. It is associated with maternal ________.
This defect presents with early cyanosis because the pulmonary and systemic circuits do not mix. Creation of a shunt after birth is required for survival, thus _____ can be administered to maintain the PDA until definitive surgical repair is performed
Transposition of the great vessels; diabetes
PGE
92
Congenital heart defect in which single large vessel arises from both ventricles, presenting with early cyanosis because deoxygenated blood from RV mixes with oxygenated blood from LV before the pulmonary and aortic circulations separate
Truncus arteriosus
| occurs when truncus fails to divide
93
______ _____ is a congenital heart defect in which the tricuspid valve orifice fails to develop. This leads to a hypoplastic ______. It is associated with an ASD leading to a _____ to _____ shunt, presenting with early cyanosis
Tricuspid atresia; RV; right to left
94
Coarctation of the aorta = ________ of the aorta. This condition is divided into infantile and adult forms
Narrowing
95
The _______form of coarctation of the aorta is associated with a PDA. The coarctation lies distal to the aortic arch, but proximal to the PDA. It clinically presents as lower extremity cyanosis, and is associated with _____ _______
Infantile; Turner syndrome
96
The _______ form of coarctation of the aorta is not associated with a PDA. The coarctation lies distal to the aortic arch and presents with HTN in the UE and hypotension with weak pulses in LE. This is associated with another heart defect: __________
Adult; bicuspid aortic valve
97
A consequence of coarctation of the aorta is collateral circulation developing across the _______ arteries, leading to what characteristic appearance on x-ray?
Intercostal
Engorged arteries cause notching of ribs on x-ray
98
Systemic complication of pharyngitis due to group A beta-hemolytic streptococci that may affect children 2-3 weeks after strep throat
Acute rheumatic fever
99
Acute rheumatic fever is caused by molecular mimicry, as the bacterial _________ resembles human tissues
M protein
100
Diagnosis of acute rheumatic fever is made based on Jones criteria. What are these criteria?
Evidence of a prior group A beta-hemolytic strep infection (ASO or anti-DNase B titer)
Minor criteria — fever and elevated ESR
Major criteria — migratory polyarthritis, pancarditis, subcutaneous nodules, erythema marginatum, syndenhams chorea
101
Describe the features of the pancarditis associated with acute rheumatic fever
Endocarditis = vegetations on endocardium of mitral valve (and possibly aortic valve) — leads to mitral valve regurgitation
Myocarditis = Aschoff bodies containing anitchkow cells (MCC of death during acute phase)
Pericarditis = leads to friction rub
102
The acute attack of acute rheumatic fever usually resolves, but may progress to chronic disease. What happens if there is a repeat exposure to group A beta hemolytic strep?
Relapse of acute phase — increases the risk for chronic rheumatic valvular disease (characterized by valve scarring that results in stenosis, almost always involving mitral valve leading to thickening of chordae tendinae and cusps; occasionally involves aortic valve leading to fusion of commissures; complication is endocarditis)
103
Aortic stenosis results in narrowing of aortic valve orifice, usually due to fibrosis and calcifiction from “wear and tear”, so it presents in late adulthood (>60 yrs). ___________ is a heart defect that increases the risk and hastens disease onset
Bicuspid aortic valve
104
Coexisting mitral stenosis and fusion of aortic valve commissures distinguish _____ ____ as the etiology of aortic stenosis from the more common “wear and tear” in older pts
Rheumatic disease
105
Regardless of the cause of aortic stenosis, pts will have a prolonged asymptomatic stage due to compensation. Describe the heart murmur associated with aortic stenosis
Systolic ejection click followed by crescendo-decrescendo murmur
106
3 major complications of aortic stenosis
Concentric LVH
Angina and syncope with exercise
Microangiopathic hemolytic anemia
[note that you don’t proceed with valve replacement until after onset of these complications]
107
Aortic regurgitation is the backflow of blood from aorta into LV during ________ (systole/diastole). This arises due to aortic root dilation (e.g., syphilitic aneurysm) or valve damage (e.g., infective endocarditis)
Diastole
108
Clinical features of aortic regurg, including description of murmur
Early, blowing diastolic murmur
Bounding pulses, pulsating nail bed, and head bobbing (hyperdynamic circulation, widening of pulse pressure)
LV dilation and eccentric hypertrophy
109
Mitral valve prolapse is ballooning of mitral valve into left atrium during _______ (systole/diastole). It is caused by _______ ______ in the valve, making it floppy. The etiology is unknown, but it may be seen in Marfan and Ehler Danlos syndrome
Systole; myxoid degeneration
110
Describe murmur associated with MVP
Mid-systolic click followed by regurgitation murmur
111
Clinical features of mitral regurgitation include ___________ murmur that is _______ with squatting and expiration. It results in volume overload and ____-sided heart failure
Holosystolic “blowing” murmur; louder; left
112
Mitral stenosis is narrowing of the mitral valve orifice, usually due to ________________.
The murmur is characterized as a ________
Chronic rheumatic valve disease.
Opening snap followed by diastolic rumble
113
Mitral stenosis can lead to volume overload resulting in dilatation of the left atrium. What are 3 major complications of this?
Pulmonary congestion
Pulmonary HTN
Atrial fibrillation
114
Most common overall cause of endocarditis; low-virulence organism that infects previously damaged valves resulting in small vegetations that do not destroy valve
S viridans
115
Pathogenesis of endocarditis due to S viridans
Damaged endocardial surface develops thrombotic vegetations (platelets and fibrin)
Transient bacteremia leads to trapping of bacteria in vegetations
116
_________ is the most common cause of endocarditis in IV drug-abuse; high virulence organism that can infect normal valves, particularly the _______ valve, resulting in large vegetations that destroy the valve (acute endocarditis)
S aureus; tricuspid
117
_______ causes endocarditis of prosthetic valves
S epidermidis
118
_______ causes endocarditis in pts with underlying colorectal carcinoma
S bovis
119
Group of organisms that may cause endocarditis with negative blood cultures
HACEK organisms — Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella
120
Clinical features of endocarditis, regardless of bacterial cause
```
Fever
Murmur
Janeway lesions (painless)
Osler nodes (painful)
Anemia of chronic disease
```
121
Lab features of endocarditis include positive blood cultures (usually), anemia of chronic disease, and _____________ is useful for detecting lesions on valves
Trans-esophageal echo
122
Pathogenesis of nonbacterial thrombotic endocarditis
Sterile vegetations that arise with hypercoagulable state or underlying adenocarcinoma
Vegetations arise on mitral valve along lines of closure and result in regurgitation
123
Sterile vegetations associated with SLE present on surface AND undersurface of mitral valve, resulting in mitral regurgitation
Libman-Sacks Endocarditis
124
Most common form of cardiomyopathy
Dilated cardiomyopathy — dilation of all 4 chambers of the heart
125
Dilated cardiomyopathy results in systolic dysfunction leading to biventricular CHF; complications include mitral and tricuspid regurgitation and arrhythmia.
T/F: dilated cardiomyopathy is typically due to an identifiable cause
False — most commonly idiopathic
[other causes include genetic mutation (AD), myocarditis (coxsackievirus), alcohol abuse, drugs (doxorubicin, cocaine), pregnancy]
126
Treatment for dilated cardiomyopathy
Transplant — there is no way to fix that dilated heart
127
Hypertrophic cardiomyopathy is characterized by massive hypertrophy of the left ventricle due to genetic mutations in _____ proteins, typically _____ _____ inheritance pattern
Sarcomere; autosomal dominant
128
Clinical features of hypertrophic cardiomyopathy include _____ cardiac output, sudden death due to ______ ______ (common cause of sudden death in young athletes), and _______ with exercise
Decreased; ventricular arrhythmias; syncope
129
T/F: Biopsy of hypertrophic cardiomyopathy shows myofiber hypertrophy with disarray.
True
130
Restrictive cardiomyopathy is characterized by decreased compliance of ventricular endomyocardium, which restricts filling during diastole. What are some causes of restrictive cardiomyopathy?
```
Amyloidosis
Sarcoidosis
Hemochromatosis
Endocardial fibroelastosis (children)
Loeffler syndrome (eosinophilic infiltrate leading to fibrosis of endomyocardium)
```
131
Pts with restrictive cardiomyopathy present with CHF, and the classic finding is a ____-voltage ECG with _______ QRS amplitudes
Low; diminished
132
Most common primary cardiac tumor in adults, due to benign mesenchymal proliferation with a gelatinous appearance and abundant ground substance on histology
Myxoma
133
Cardiac myxomas develop as pedunculated mass in the _____ _____, and cause syncope due to obstruction of the _____ _____
Left atrium; mitral valve
134
_______ is the most common primary cardiac tumor in children and develops as a benign hamartoma of cardiac muscle; associated with _____ ______. It usually arises in the ventricle
Rhabdomyoma; tuberous sclerosis
135
Cardiac metastases are more common than primary tumors. What are some common primary tumors that metastasize to the heart, and what parts of the heart are typically affected?
Breast and lung carcinoma, melanoma, lymphoma
Most commonly involves pericardium, resulting in a pericardial effusion
