Cardiology Flashcards

(68 cards)

1
Q

Stable Angina

A

= chest pain that arises w/ exertion or emotional stress; represents reversible injury to myocytes (no necrosis)

Due to atherosclerosis of coronary arteries w/ >70% stenosis = ↓ blood flow not able to meet metabolic needs of the myocardium during exertion

Pw/ chest pain (lasting <20 min) that radiates to the left arm or jaw, diaphoresis & SOB

EKG = ST depression due to subendocardial ischemia

Relieved by rest or nitroglycerin (↓ preload = ↓ stress)

**hallmark of reversible injury is cellular swelling

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2
Q

Unstable angina

A

= chest pain that occurs at rest; represents reversible injury of the myocytes (no necrosis)

Usually due to rupture of an atherosclerotic plaque w/ thrombosis & incomplete occlusion of a coronary artery

EKG = ST depression due to subendocardial ischemia

Relieved by nitroglycerin

**high risk of progression to MI

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3
Q

Prinzmetal angina

A

= episodic chest pain unrelated to exertion; represents reversible injury to myocytes (no necrosis)

Due to coronary artery vasospasm

EKG = ST elevation* due to transmural ischemia (cutting blood flow to entire wall for short period of time)

Relieved by nitroglycerin or CCB (relieve vasospasm)

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4
Q

Myocardial Infarction

A

= Necrosis of cardiac myocytes (irreversible injury); usually involves the left ventricle and septum

Usually due to rupture of an atherosclerotic plaque w/ thrombosis & complete occlusion of a coronary artery (other = vasospasm, emboli & vasculitis)

= Severe, crushing chest pain (>20 min) that radiates to the left arm/jaw, diaphoresis & dyspnea
symptoms not relieved by nitroglycerin

Initially ST depression leading to ST elevation and patholigic Q waves as infarction moves from subendocardial to transmural and then tissue death

Labs = Troponin I (rise 2-4 hr, peak 24hr, stay 7-10 day) most sensitive & specific marker (gold standart)
- CK-MB (rise 4-6 hr, peak 24hr, return to normal by 72 hr = useful in detecting reinfarction)

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5
Q

MI Treatment

A

Aspirin &/or heparin - limits thrombosis
Supplemental O2 - minimizes ischemia
Nitrates - vasodilate veins (↓ preload) & coronary arteries
β-blockers - ↓ HR = ↓ O2 demand & arrhythmia risk
ACEI - ↓ LV dilation
Fibrinolysis or angioplasty = open blocked vessels
-reperfusion may lead to contraction band necrosis (from calcium influx) or reperfusion injury (from free radical generation)

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6
Q

MI Morphologic changes

A

< 4 hours = cardiogenic shock, CHF, arrhythmia
2-24 hours = Coagulative necrosis w/ arrhythmia risk = dark discoloration
1-3 days = Neutrophils w/ risk of fibrinous pericarditis = yellow pallor
4-7 days = Macrophages w/ risk or rupture = yellow pallor
1-3 weeks = granulation tissue w/ plump fibroblasts, collagen & blood vessels = Red border from edge
Months = Fibrosis w/ risk or aneurysm, mural thrombosis or Dressler syndrome (pericarditis 6-8 wks post infarction from pericardial Ab formation) = white scar

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7
Q

Sudden Cardiac Death

A

Unexpected death due to cardiac disease; occurs w/out symptoms or < 1 hour after symptoms arise (before biological markers appear)

Usually due to fatal ventricular arrhythmia

Most common etiology = acute ischemia (90% of patients have preexicting severe atherosclerosis); less commonly MVP, cardiomyopathy & cocaine abuse

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8
Q

Chronic Ischemic Heart Disease

A

Poor myocardial function due to chronic ischemic damage (w/ or w/out infarction)

Progresses to CHF

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9
Q

Congestive Heart Failure

A

= pump failure; divided into right- & left-sided failure

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10
Q

Left-sided Heart Failure

A

Causes = ischemia, dilated or restrictive cardiomyopathy, MI, or HTN

  • pulmonary congestion leads to pulmonary edema = dyspnea, paroxysmal nocturnal dyspnea, orthopnea & crackles; congested capillaries may burst resulting in hemosiderin-laden macrophages (“HF cells”)
  • ↓ forward perfusion = ↓ flow to kidneys & activation of the Renin-angiotensin system = fluid retention exacerbates CHF

ACEI = mainstay of treatment

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11
Q

Right-sided Heart Failure

A

Most commonly due to Left-sided heart failure (other causes = L->R shunt & chronic lung disease)

Clinical features due to congestion
= JVD
=Painful hepatosplenomegaly w/ ‘nutmeg’ liver; may lead to cardiac cirrhosis
=Dependent pitting edema (due to ↑ hydrostatic pressure)

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12
Q

Ventricular Septal Defect (VSD)

A

Defect in the septum that divides the ventricles
-Most common CHD; associated w/ fetal alcohol syndrome

= R -> L shunt; small defects often asymptomatic, Large defects can = Eisenmenger syndrome (late cyanosis when shunt reverses w/ RV hypertrophy, polycythemia & clubbing)

Tx = surgical closure; small defects may close spontaneously

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13
Q

Atrial Septal Defect (ASD)

A

Defect in the septum that divides the atria

  • most common type = ostium secundum (foramen ovale)
  • ostium primum associated w/ Down Syndrome

= R -> L shunt & fixedly split S2; Paradoxical emboli (venous thrombus moving into systemic circulation) are an important complication

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14
Q

Patent Ductus Arteriosus (PDA)

A

Failure of ductus arteriosus to close; associated w/ congenital rubella

= L -> R shunt between aorta and pulmonary artery

Asymptomatic at birth w/ continuous ‘machine-like’ murmur; may lead to Eisenmenger syndrome, resulting in lower extremity cyanosis (shunts after branches of the aortic arch)

Tx = indomethacin which ↓ PGE resulting in PDA closure
**PGE maintains patency of ductus arteriosus

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15
Q

Tetralogy of Fallot

A

1 - stenosis of right ventricular outflow tract
2 - right ventricular hypertrophy
3 - VSD
4 - Overriding aorta

= R -> L shunt leading to early cyanosis; degree of stenosis determines the extent of shunting & cyanosis

“boot-shaped” heart on x-ray

Pt learns to squat in response to cyanotic spell (↑ arterial resisitance ↓ shunting & allows more blood to reach lungs)

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16
Q

Transposition of the Great Vessels

A

Pulmonary arises from LV, and aorta arises from RV
-Associated w/ early cyanosis as pulmonary and systemic circuits do not mix
=creation of shunt after birth is required for survival (need to allow blood to mix) - PGE to maintain PDA until definitive surgical repair is performed

= hypertropy of the RV & atrophy of LV

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17
Q

Truncus Arteriosus

A

Single large vessel arising from both ventricles as truncus fails to divide

Pw/ early cyanosis; deoxygenated blood from RV mixes w/ oxygenated blood from LV before circulations separate = mixed blood systemically

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18
Q

Tricuspid Atresia

A

Tricuspid valve orifice fails to develop; right ventricle is hypoplastic

Often associated w/ ASD = R -> L shunt

Pw/ early cyanosis

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19
Q

Coarctation of the Aorta

A

Narrowing of the aorta

Infantile form - associated w/ PDA & coarc lies after the aortic arch, but before PDA
= Pw/ lower extremity cyanosis
- associated w/ Turner syndrome

Adult form - not associated w/ PDA & coarc lies after the aortic arch, associated w/ bicuspid aortic valve
= Pw/ HTN in upper & HoTN/weak pulses in lower extremities; classically discovered in adulthood
- Collateral circulation develops across the intercostal arteries & engorged arteries cause ‘notching’ of ribs on X-ray

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20
Q

Acute Rheumatic Fever

A

systemic complication of pharyngitis due to group A β-hemolytic strep; affects children 2-3 weeks after an episode of strep pharyngitis

caused by molecular mimicry; bacterial M protein resembles proteins in human tissue

Acute attack usually resolves, but may progress to chronic rheumatic heart disease; repeat exposure to group A β-hemolytic strep results in relapse of the acute phase & increases risk for chronic disease

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21
Q

Jones Criteria

A

For diagnosis of acute rheumatic fever1-evidence of prior group A β-hemolytic strep infection2- Minor criteria (nonspecific & include fever, ↑ ESR)3- Major Criteria: Joints (Migratory polyarthritis)
: Pancarditis (does not resolve overtime) = endocarditis involving the mitral valve; Myocarditis w/ Aschoff bodies & Anitschkow cells
: Subcutaneous Nodules
: Erythema marginatum (annular, nonpruritic rash w/ erythematous borders0
:Sydenham chorea - rapid involuntary muscle movement

Major criteria = J<3NES

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22
Q

Chronic Rheumatic Heart Disease

A

Valve scarring that arises as a consequence of rheumatic fever

Results in stenosis w/ a classic ‘fish-mouth’ appearance & almost always involves the mitral valve (leads to thickening of chordae tendinaea & cusps); occasionally involves the aortic valve (leads to fusion of the commissures)

Complications include infectious endocarditis

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23
Q

Aortic Stenosis

A

Narrowing the aortic valve orifice - usually due to fibrosis/calcification from wear & tear

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

Complications include Concentric LV hypertrophy; Angina & syncope w/ exercise; Microangiopathic hemolytic anemia

Bisucpid aorta valve ↑ risk & hastens disease onset; May also arise as a consequence of chronic rheumatic valve disease

Tx = valve replacement after onset of complications

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24
Q

Aortic Regurgitation

A

Backflow of blood from aorta into the LV during diastole

Arises due to aortic root dilation (most common), or valve damage

=Early, blowing diastolic murmur

=hyperdynamic circulation due to ↑ PP; LV dilation & eccentric hypertorphy (due to volume overload)

Tx - Valve replacement once LV dysfunction develops

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25
Mitral Valve Prolapse
Ballooning of mitral valve into LA during systole Due to myxoid degeneration of the valve making it floppy Pw/ incidental mid-systolic click followed by a regurgitation murmur (usually asymptomatic) **Click/murmur become SOFTER w/ squatting (↑ systemic resistance = ↓ LV emptying) Complications rare = infectious endocarditis, arrhythmia & severe mitral regurge Tx = valve replacement
26
Mitral Regurgitation
Reflux of blood from the LV into the LA during systole Usually arises as a complication of MVP; other causes include LV dilation, Infective endocarditis, Acute rheumatic heart disease, papillary muscle rupture after MI = Holosystolic 'blowing' murmur; louder w/ squatting & expiration = results in volume overload and left-sided HF
27
Mitral Stenosis
Narrowing of the mitral valve orifice usually due to chronic rheumatic valve disease = Opening snap followed by diastolic rumble Volume overload leads to dilatation of the LA = - Pulmonary congestion w/ edema & alveolar hemorrhage - Pulmonary HTN & right-sided HF, - A Fib w/ associated risk for mural thrombi
28
Endocarditis
Inflammation of the endocardium that lines the surface of cardiac valves; usually due to bacterial infection = Fever (due to bacteremia), Murmer (due to vegetations), Janeway lesions (erythematous nontender lesions on palms & soles), splinter hemorrhages in nail bed & Roth spots (seen fundoscopically) (both due to embolization of septic vegetations) Labs - + Blood Cultures; Anemia of chronic disease - transesophageal endocardiogram is useful for detecting lesions on valves
29
Streptococcus viridans Endocarditis
= most common, infects previously damaged valves, resulting in small vegetations that do not destroy the valve
30
S. Aureus Endocarditis
most common in IV drug abusers = affects normal valves (tricuspid most commonly), results in large vegetations that destroy the valve
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S. Epidermidis Endocarditis
associated w/ endocarditis of prosthetic valves
32
Streptococcus bovis endocarditis
associated w/ endocarditis in Pt w/ underlying colorectal carcinoma
33
HACEK organisms endocarditis
(Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella) Associated w/ endocarditis w/ negative blood cultures
34
Nonbacterial thrombotic endocarditis
due to sterile vegetations that arise in association w/ a hypercoagulable state or underlying adenocarinoma Vegetations arise on the mitral valve along lines of closure & result in mitral regurgitation
35
Libman-Sacks endocarditis
due to sterile vegetations that arise in association w/ SLE Vegetations are present on the surface & undersurface of the mitral valve & result in mitral regurgitation **vegetation present on both sides of the valve**
36
Dilated Cardiomyopathy
Dilation of all 4 chambers; most common cardiomyopathy Most commonly idiopathic; Genetic mutation (AD), myocarditis (coxsackie A/B), Alcohol abuse, Drugs, Pregnancy (late), or Hemochromatosis are also possible causes = systolic dysfunction leading to biventricular CHF -complications = mitral & tricuspid valve regurgitation & arrhythmia Tx = heart transplant
37
Hypertrophic Cardiomyopathy
Massive hypertorphy of the Left Ventricle Usually due to genetic mutations in sarcomere proteins (most common form is AD) = diastolic dysfunction & ↓ CO; Sudden death due to ventricular arrhythmias; syncope w/ exercise (subaortic hypertrophy of septum = functional aortic stenosis) **common cause of sudden death in young athletes** *Biopsy shows myofiber hypertrophy w/ disarray
38
Restrictive Cardiomyopathy
↓ compliance of the ventricular endomycardium that restricts filling during diastole Causes = amyloidosis, sarcoidosis, endocardial fibroelastosis & Loeffler syndrome (=endocardial fibroelastosis w/ eosinophilic infiltate & eosinophilia) Pw/ CHF; classic finding = low-voltage EKG w/ diminished QRS amplitude
39
Myxoma
Benign mesenchymal tumor w/ gelatinous appearance & abundant ground substance on histology Most common primary cardiac tumor of adults Usually forms as a pedunculated mass in the LA that causes syncope due to obstruction of the mitral valve
40
Rhabdomyoma
Benign hamartoma of cardiac muscle Most common primary cardiac tumor in children (associated w/ tuberous sclerosis) Usually arises in the ventricle
41
Metastasis
Metastatic tumors are more common in the heart than primary tumors Most commonly involve the pericardium, resulting in pericardial effusion Common metastases to the heart include breast & lung carcinoma, melanoma, & lymphoma
42
Vasculitis
Inflammation of the blood vessel wall Etiology usually unknown, most causes are not infectious =Nonspecific Sx of inflammation (fever, fatigue, weight loss, myalgias) =Sx of organ ischemia (due to luminal narrowing or thrombosis of the inflamed vessel) Large vessel = aorta & its major branches Medium vessel = Muscular arteries that supply organs Small vessel = arterioles, capillaries & venuoles
43
Temporal (Giant Cell) Arteritis
LVV = Granulomatous vasculitis that classically involves branches of the carotic artery Most common form in older adults (>50), usually females Pw/ headache (temporal a.), visual distrubances (ophthalmic a.), & jaw claudification. Flu-like Sx w/ joint & muscle pain often present ESR is elevated (>100) Biopsy = inflamed vessel wall w/ giant cells & intimal fibrosis (lesions are segmental = negative biopsy doesn't exclude disease) Ts = corticosteroids; *high risk for blindness w/out Tx
44
Takayasu Arteritis
LVV = Granulomatous vasculitis that classically involves the aortic arch at branch points In adults ) ESR is elevated Tx = corticosteroids
45
Polyarteritis Nodosa
MVV = necrotizing vasculitis involving multiple organs (lungs are spared) Classically in young adults; Pw/ HTN (renal a.), ab pain w/ melena (mesenteric a.), neurologic disturbances & skin lesions. Associated w/ serum HBsAg Lesions of varying stages are present. Early lesion consists of transmural inflammation w/ fibrinoid necrosis; eventually heals w/ fibrosis, producing 'string-of-pearls' appearance Tx - corticosteroids & cylcophosphamide (fatal if not Tx)
46
Kawasaki Disease
MVV - classically affects Asian children < 4 yo Pw/ nonspecific signs including fever, conjunctivitis, erythematous rash of palms & soles, and enlarged cervical lymph nodes Coronary artery involvement is common and leads to risk for thrombosis w/ MI, & aneurysm w/ rupture Tx = aspirin** and IVIG; disease is self-limited **need to make sure it is not viral infection before giving aspirin (due to risk of Reye's syndrome)
47
Buerger Disease
MVV - Necrotizing vasculitis involving digits Pw/ ulceration, gangrene, autoamputation of fingers & toes; Raynaud phenomenon is often present Highly associated w/ heavy smoking; and classically seen in younger males Tx = smoking cessation
48
Wegener Granulomatosis
SVV = Necrotizing granulomatous vasculitis involving nasopharynx, lungs & kidneys Classic presentation is a middle-aged male e/ sinusitis/nasopharyngeal ulceration, hemoptysis w/ bilateral nodular lung infiltrates, & hematuria due to rapidly progressive glomerulonephritis Biopsy reveals reveals large necrotizing granulomas w/ adjacent necrotizing vasculitis Serum c-ANCA levels correlate w/ disease activity Tx = cyclophosphamide & steroids; relapses are common WeCener Granulomatosis - c-ANCA, Cyclophsphamide
49
Microscopic Polyangiitis
SVV - necrotizing vasculitis involving multiple organs, especially lung & kidney Pw/ similar to Wegener (but nasopharyngeal involvement & granulomas are absent) Serup p-ANCA levels correlate w/ disease activity Tx - corticosteroids & cyclophosphamide; relapses are common
50
Churg-Strauss Syndrome
SVV - necrotizing granulomatous inflammation w/ eosinophils involving multiple organs, especially lungs & heart *Asthma & peripheral eosinophilia are often present Serum p-ANCA levels correlate w/ disease activity
51
Henoch-Schonlein Purpura (HSP)
SVV - due to IgA immune complex deposition; most common vasculitis in children Pw/ PALPABLE purpura on buttocks & legs, GI pain & bleeding, & hematuria (IgA nephropathy); usually occurs following an URTI Disease is self-limited, but may recur; Tx w/ steroids if severe
52
Hypertension
↑ blood pressure; may involve pulmonary or systemic circulation Systemic HTN is defined as pressure > 140/90 mm Hg (normal < 120/80) - can have isolated systolic or diastolic HTN Divided into primary and secondary types based on etiology
53
Primary HTN
HTN of unknown etiology (95%) Risk factors include: - age, race (↑ AA, ↓ Asian), obesity, stress, lack of physical activity & high-salt diet
54
Secondary HTN
HTN due to an identifiable etiology (5%) Renal artery stenosis is a common cause (renovascular HTN) - ↓ blood flow to glomerulus = JGA secretes renin = ANGI -> ANGII (by ACE) -> ANGII ↑ BP by contracting arteriolar AM (↑ TPR) & promoting adrenal release of aldosterone (↑ Na reabsorption = expanding plasma volume) =↑ plasma renin & unilateral atrophy of affected kidney (neither seen in primary HTN) - Atherosclerosis (elderly males) & fibromuscular dysplasia (young females) = important causes
55
Benign HTN
mild or moderate elevation in BP = Clinically silent; vessels & organs are damaged slowly over time Most causes of HTN are benign
56
Malignant HTN
severe elevation in BP (>200/120) May arise from preexisting benign HTN or de novo Pw/ acute end-organ damage (acute renal failure, headache, & papilledema) **Is a medical emergency** comprises <5% of cases
57
Atherosclerosis
Intimal plaque that obstructs blood flow (in medium & large sized vessels) Modifiable RF = HTN, hypercholesterolemia (LDL), smoking & diabetes Nonmodifiable RF = age, gender (estrogen is protective), & genetics Damage to endothelium allows lipids to leak into the intima, lipids are oxidized & then consumed by macrophages via scavenger receptors = foam cells =Results in fatty streaks that progress to atherosclerotic plaques
58
Complications of Atherosclerosis
account for >50% of disease in Western countries Stenosis of medium-sized vessels results in impaired blood flow and ischemia, leading to = Peripheral vascular disease, Angina, Ischemic bowel disease Plaque rupture w/ thrombosis results in MI & stroke Plaque rupture w/ embolization results in atherosclerotic emboli, **characterized by cholesterol crystals w/in the embolus Weakening of vessel wall results in aneurysm
59
Arteriolosclerosis
Narrowing of small arterioles diveded into hyaline & hyperplastic types
60
Hyaline Arteriolosclerosis
caused by proteins leaking into the vessel wall, producing vascular thickening; proteins are seen as pink hyaline on microscopy *Consequence of long-standing benign HTN or Diabetes = reduced vessel caliber w/ end-organ ischemia; classically produces glomerular scarring (arteriolonephrosclerosis) that slowly progresses to chronic renal failure =reason that Pt w/ HTN or Diabetes get renal failure
61
Hyperplastic arteriolosclerosis
Thickening of vessel wall by hyperplasia of smooth muscle ('onion-skin' appearance) * Consequence of malignant HTN = reduced vessel caliber w/ end-organ ischemia May lead to fibrinoid necrosis of the vessel wall w/ hemorrhage; classically causes acute renal failure w/ a characteristic 'flea-bitten' appearance (pin-point hemorrhages from blowing out small vessels)
62
Monckeberg Medial Calcific Sclerosis
Calcification of the media of muscular (medium-sized) arteries **nonobstructive** Not clinically significant; seen as an incidental finding on x-ray or mammography
63
Aortic Dissection
Intimal tear w/ dissection of blood through media of the aortic wall Most common cause is HTN; also associated w/ inherited defects of CT (Margan or Ehlers-Danlos Syndrome) Occurs in the proximal 10cm (high stress region) w/ preexisting weakness of the media Pw/ sharp, tearing chest pain that radiates to the back Complications = pericardial tamponade (most common cause of death), rupture w/ fatal hemorrhage, & obstruction of branching arteries w/ resultant end-organ ischemia
64
Thoracic Aortic Aneurysm
Balloon-like dilation of the thoracic aorta Due to weakness in the aortic wall *Classically seen in tertiary syphilis; endarteritis of the vasa vasorum results in luminal narrowing, ↓ flow & atrophy of the vessel wall = 'tree bark' appearance of the aorta Complications = dilation of the aortic valve root resulting in aortic valve insufficiency; compression of mediastinal structures; & thrombosis/embolism
65
Abdominal Aortic Aneurysm
Balloon-like dilation of the abdominal aorta; usually arises below the renal arteries, but above the aortic bifurcation Primarily due to atherosclerosis; classically seen in male smokers >60yo w/ HTN Pw/ a pulsatile abdominal mass that grows w/ time Complications = rupture (esp when >5cm) (pw/ triad of HTN, Pulsatile ab mass & flank pain); compression of local structures & thrombosis/embolism
66
Hemangioma
Benign tumor comprised of blood vessels Commonly present at birth; often regresses during childhood Most often involves skin & liver **will blanch when pressed on (vs a bleed into the skin (ex a purpura))
67
Angiosarcoma
Malignant proliferation of endothelial cells; highly aggressive Common sites include skin, breast & liver - Liver angiosarcoma is associated w/ exposure to polyvinyl chloride (PVC), arsenic, & Thorotrast
68
Kaposi Sarcoma
Low-grade malignant proliferation of endothelial cells; associated w/ HHV-8 Pw/ purple patches, plaques, & nodules on the skin; may also involve visceral organs Classically seen in: - Older Eastern European males - tumor remains localized to skin; Tx w/ surgical removal - AIDS - tumor spreads early; Tx - antiretroviral agents - Transplant recipients - tumor spreads early; Tx - ↓ immunosuppression