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Pathology 3 > quiz 2- CV 3-4 > Flashcards

quiz 2- CV 3-4 Flashcards

1
Q

• what are usual causes of myocardial dysfunction? Cardiomyopathy?

A
  • Common: IHD, HTN, valvular heart dz
  • Less: intrinsic to myocardium itself: heart inflammatory dos of the heart, immunologic dzs, systemic metabolic dos, muscular dystrophies, myocyte genetic abnormalities, dzs of unknown etiology
  • Cardiomyopathy: primary abnormality in myocardium
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2
Q

• What are the 3 major categories of cardiomyopathy, and the relative size of the 4 chambers??

A
  • Dilated (90% of all cases of non-ischemic cardiomyopathy); all 4 enlarged
  • Hypertrophic; very small LV, enlarged LA
  • Restrictive; small LV, enlarged LA
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3
Q

• What causes dilated cardiomyopathy?

A
  • Many unknown etio = idiopathic dilated cardiomyopathy
  • Ischemic CM=most commonly identified (60% pts with sx HF)
  • Common cause in US is chronic alcoholism
  • Viral myocarditis
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4
Q

• What is pathophysiology of DCM? Laplace’s Law?

A
  • <40% EF (despite enlarged LV vol) , may →systolic dysfunction
  • Myocyte injury, necrosis, fibrosis →impaired mechanical function
  • Cell failure → chambers dilate
  • Laplace’s law: ↑diameter → ↑stress → mechanical disadvantage
  • =vicious cycle (adverse ventricular remodeling)
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5
Q

• What is prevalence of DCM? Histology? In vivo?

A
  • 0.4/1000
  • Histo: nonspecific cellular abnormalities, variations in myocyte size, myocyte vacuolation, loss of myofibrillar material, fibrosis
  • flabby, hypo-contracting heart
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6
Q

• What is shape of a very large heart?

A

• Globoid, bc all chambers are dilated

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7
Q

• What is hypertrophic cardiomyopathy (HCM)? Micro?

A
  • Aka idiopathic hypertrophic sub-aortic stenosis, hypertrophic obstructive cardiomyopathy
  • genetic dz, proteins of sarcomere
  • thick-walled, heavy, hyper-contracting
  • massive myocardial hypertrophy w/o ventricular dilation; usu only one ventricle
  • classic: disproportionate thickening of ventricular septum, compared to free wall of ventricle.
  • abnormal diastolic filling, intermittent ventricular outflow obstruction (1/3)
  • Micro: hypertrophy of myocardial fibers (prominent dark nuclei) interstitial fibrosis
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8
Q

• What is restrictive CM? causes?

A
  • Aka: infiltrative CM
  • myocardium usu infiltrated w abnormal tissue → impaired/abn ventricular wall contraction/relaxation
  • most common causes: amyloidosis and hemochromatosis
  • Hemochromatosis (Prussian blue stain for iron): Excessive deposition of iron → heart enlargement and heart failure
  • amyloidosis: amorphous deposits of pale pink material bw myocardial fibers
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9
Q

• what is Infectious endocarditis?

A
  • inflammation on the valve leaflets, or endocardial lining of atrium and ventricles (surgery)
  • begin on lines of closure (greatest P): atrial surfaces of AV valves, ventricular surfaces of the semilunar valves
  • usu left-sided valves, A=M frequency
  • Indwelling devices such as prosthetic valves and pacemakers can also become infected
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10
Q

• When is TC valve IE seen? Pulmonic?

A
  • Suspicious of IV drug use
  • Community-acquired (IV drug abuse)
  • Hospital-acquired (implanted devices)
  • P: rare, confusing sxs
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11
Q

• what are “vegetations” in IE?

A
  • colonization by microbes =bulky masses
  • =collections of infected thrombotic debris deposited on and around affected valve
  • often → destruction of underlying valves and tissue
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12
Q

• What are gross and micro appearance of IE?

A
  • Gross: aortic valve has large irregular, reddish tan vegetation
  • Micro: valve has friable vegetations (easily break off, embolize, spread infxn) of fibrin and platelets (pink) mixed w inflammatory cells and bacterial colonies (blue).
  • Gross Mitral: valve destruction and vegetation (destruction at commissure bw anterior and posterior leaflets)
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13
Q

• What organisms can cause IE?

A
  • Many: all bacteria, fungi, Chlamydia and Rickettsiae.

* Most common is bacterial

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14
Q

• What organisms cause IE in community-acquired vs nocosomial?

A
  • Staphylococcus aureus: (30-50%, minority MRSA) vs. (60-80%; majority MRSA)
  • Alpha-hemolytic Strep (S. viridans): 10-35% vs. < 5%
  • Enterococci: 5-10% vs. < 5%
  • Culture negative: 5-30% vs. 5%
  • Staphylococcus epidermidis (coagulase negative): ?? vs. < 5%
  • Misc (Escherichia coli, Klebsiella sp., Corynebacterium) < 5% vs. 5-10%
  • Fungi: < 5% vs. 10%
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15
Q

• What is culture-neg IE?

A
  • 7-33%
  • Hi in community-acquired dt abx tx prior to dx
  • full work-up: serology and culture for esoteric organisms, PCR → etio dounf in >75% cases w initial negative culture (C burnetii and Bartonella species)
  • no assoc bw cult neg and underlying etio
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16
Q

• what are the organisms commonly found in initially culture neg. IE?

A
  • Fungi (10%)
  • Enterococcus (5%)
  • Alpha hemolytic streptococci (<5%)
  • Misc. others including: E coli, Klebsiella, Corynebacterium; 5-10%
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17
Q

• What are portals of entry for organisms that may cause IE?

A
  • Poor dental health, dental procedures, pharyngeal infxn
  • GU infxns, instrumentation the GU tract
  • Skin infections (impetigo)
  • Pulm infxns
  • IV drug use
  • Any infx that can enter blood stream
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18
Q

• What is acute IE?

A
  • rapidly developing, destructive infxn; usu previously normal heart valve
  • usu dt infxn w highly virulent organism
  • mb death in days to weeks in ~50%, even w vigorous tx with abx and surgery
  • fever most common sign
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19
Q

• what is sub-acute IE?

A
  • Mostly dt strep viridens
  • generally slower and less severe course
  • fever common, but not necessarily in elderly (can’t mount fever)
  • valve usu already damaged, usu dt infxn w less virulent organism
  • usu recover after appropriate tx
  • vegetations frequently embolize
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20
Q

• what are splinter hemorrhages? Roth’s spots?

A
  • S: Microemboli to skin, form petechiae I (mouth, under the tongue, feet, nail beds)
  • R: retinal hemorrhages; white center of coagulated firbrin; dt immune complex mediated vasculitis; also seen in leukemia, DM, pernicious anemia, ischemic events, rare HIV
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21
Q

• what are sxs of acute IE?

A
  • Dramatic onset fever, chills, weakness, fatigue
  • Mb new murmur, dt flow over vegetations → commonly embolize
  • abscesses in ring of tissue beneath leaflets of infected valve
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22
Q

• what are risk factors for IE, and corresponding organisms?

A
  • Used to be rheumatic heart dz. Incidence now dec
  • artificial valves- staph epidermitis
  • damaged native valves: step viridens
  • Immunocompromised
  • IV drug abuse- staph aureus
  • Alcoholics- anaerobes, oral cavity bugs
  • indwelling catheters/cystoscopy/prostatectomy: Gram neg like E. coli
  • vascular grafts
  • colon CA: strep bovis
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23
Q

• what is follow-up for strep bovis culture?

A

• Colonoscopy is indicated if cultured from blood, to r/o colon CA

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24
Q

• What is follow-up/sig for culture neg IE?

A
  • Etio not found on blood culture in 5 - 20% of all IE
  • Mb dt abx prior to blood draw, organism not in blood stream at the time, or limitations in culture process in lab
  • Mb an endocarditis that is inflammatory in nature rather than infectious
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25
Q

• What is Libman-Sachs endocarditis?

A
  • =endocarditis of SLE (systemic lupus erythematosus)
  • Inflammatory vegetations can occur w certain collagen vascular dzs like SLE
  • Gross: flat, spreading vegetations over mitral valve surface and chordae tendineae.
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26
Q

• What is Marantic endocarditis?

A
  • culture neg, vegetations dt hypercoagulable state (lung or pancreatic CA)
  • Trousseau’s syndrome= paraneoplastic syndrome assoc w malignancies
  • =not infectious
  • Gross: small pink vegetation on cusp margin; rarely over 0.5 cm
  • very prone to embolize
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27
Q

• what are outcomes of IE?

A
  • successful tx: affected tissue becomes sterilized, valve more fibrotic and scarred
  • cardiac decompensation (CHF dt endocarditis): affected valve must be removed and replaced w artificial/prosthetic valve
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28
Q

What is myocarditis?

A
  • =inflammation of heart muscle

* Dt infxn of heart, or autoimmune (RHD, collagen vascular dzs, SLE, RA, drugs, transplant rejection)

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29
Q

• What Infectious agents can cause myocarditis?

A
  • Viral most common
  • Coxsackie virus (group B)- most common
  • Borrelia burgdorferi (Lyme’s dz)
  • Cytomegalic virus (CMV)
  • HIV
  • Meningococcus
  • Rickettsia typhi (typhus)
  • Toxoplasmosis
  • Trichinosis
  • Trypanosoma cruzi (Chaga’s dz)
30
Q

• What is Coxsackie virus?

A
  • Genus Enterovirus (also poliovirus and echovirus), common, fecal-oral
  • Group A & B: non-specific fever, rash, UR dz, aseptic meningitis
  • A: skin and mucous membrane → herpangia, acute hemorrhagic conjunctivitis, hand foot mouth dz
  • B: heart, pleura, pancreas, liver→pleuritis, myocarditis, pericarditis, pericardial effusion, hepatitis
31
Q

• What is Rickettsia typhi?

A
  • Obligate parasite bacteria

* (Not “typhoid fever”)

32
Q

• What is hallmark of viral myocarditis?

A

• interstitial lymphocytic infiltrates

33
Q

• what is Valvular disease?

A
  • Valves= CT of cardiac skeleton
  • Congetical or acquired; isolated or combined
  • stenosis, insufficiency (regurgitation or incompetence), or both
  • Stenosis: doesn’t open completely, impedes forward flow
  • Insufficiency: doesn’t close completely, allows reverse flow
  • slight and physiologically unimportant to severe and rapidly fatal
  • severe: Sudden destruction of aortic valve cusp by infxn (IE) → severe regurgitant blood flow → rapidly fatal
  • benign: mitral stenosis dt RHD develops over years, well tolerated
  • tx: mb meds, or repair/prosthetic
34
Q

• what are the most common heart valve dzs? Rare?

A
  • aortic stenosis (most common*, or mitral prolapse) and mitral regurgitation or insufficiency.
  • Tricuspid valve dz rare, 2nd to other heart valve dz
  • Mitral stenosis dt rheumatic fever, undeveloped countries
  • Pulmonic valve dz is congenital, dx at birth
  • Aortic and mitral stenosis: 2/3 of all cases
35
Q

• What are sxs of heart valve dz?

A
  • SOB, palpitations (irregular, rapid HR), weakness, dizziness, fainting, edema (ankles, feet), discomfort in chest
  • Can progress slolwly
  • Sxs don’t always reflect severity
  • heart gradually adjusts, sxs may go unnoticed
  • Abd heart sounds: Murmurs and clicks
36
Q

• How is heart valve dz diagnosed?

A
  • W echo

* St CT-angiography, cardiac MRI

37
Q

• What are the murmurs attributable to left sided valvular dz?

A
  • Normal: S1, softer S2
  • Aortic stenosis: long loud systolic
  • Mitral regurgitation: soft, holo-systolic
  • Aortic regurgitation: holo-diastolic
  • Mitral stenosis: S1 and S2 both soft
  • PDA: holo-systolic and diastolic, tapers end diastole
38
Q

• What are the most common of all the valve dzs?

A
  • Most: aortic stenosis
  • MVP
  • Mitral regurg
39
Q

• What causes tricuspid, mitral stenosis, and pulmonic valve dzs?

A
  • T: rare, 2nd to other heat valve dz
  • M: RF (unusual in developed countries)
  • P: congetial, dx at birth
40
Q

• What causes acquired aortic stenosis? Congenital?

A
  • calcification w age; “wear and tear” of either previously anatomically normal aortic valves or congenitally bicuspid valves (3 is normal)
  • 1% in US born w bicuspid aortic valve (raph=cusp w partial fusion at center)
  • incidence increasing w rising avg age of pop
41
Q

• what is mitral annular calcification?

A
  • in fibrous ring (annulus) of mitral valve= hard, irregular, ulcerated nodules behind leaflets
  • usu doesn’t affect valvular fxn
  • but mitral stenosis can occur dt progressive dz
42
Q

• what is Mitral valve prolapse?

A
  • One of the most common forms of valvualr dz
  • one or both mitral leaflets are “floppy” and prolapse, or balloon back into LA in systole
  • ~3% or more of adults in US; F 20-40
  • = “Myxomatous degeneration of the mitral valve”
43
Q

• What is myxomatous degeneration?

A
  • Weak CT, usu in MVP (most common cause of pure M insufficiency)
  • Exact mechanism unknown
  • CT degenerates, glycosaminoglycan accumulates
  • Mb benign, or more severe in Marfan’s, etc
  • In valves: mb insufficiency, regurg
44
Q

• What causes MVP? Ssx? Dx?

A
  • Mb cellular defect in CT
  • Ssx: most asx, mid-sys click; if mitral regurg: late/holo-sys murmur
  • Mb: chest pain (like angina, dyspnea, fatigue)
  • Dx: Usu incidental on PE, Echo
45
Q

• What are possible complications of MVP?

A
  • Mostly benign, 3% develop:
  • IE- high incidence
  • Mitral insufficiency- requires surgery
  • Stroke/other infarct: dt embolism or leaflet thrombi
  • Arrhythmias: A and V (unknown mechanism for V); st sudden death
46
Q

• What is rheumatic fever? Complications?

A
  • acute, immune mediated, multisystem inflammatory dz
  • occurs in few wks after GAS pharyngitis (strep pyogenes)-ONLY
  • Acute rheumatic carditis in active phase may → chronic rheumatic heart disease (RHD)
  • Mb AI response to anti-strep M protein Abs, cross react w cardiac myosin
  • 1/3: →valve insufficiency, HF, pericarditis, or death
47
Q

• What are the major and minor dx criteria for RF?

A
  • Major: Carditis, Polyarthritis, Chorea (Sydenham’s), Subcutaneous nodules, Erythema marginatum
  • Minor: Fever, Arthralgias, Prolonged PR interval on EKG , ↑WBC, ESR, CRP
48
Q

• What is incidence of RHD?

A
  • 100 yrs ago: leading cause of death in US, 5-20 yo
  • markedly dec since 1940s (developed)
  • still common in undeveloped (5-30 million kids, 90,000 die/yr)
  • dt penicillin, change in virulence of strep
  • median age 10 yrs, 20% in adults
  • 2.5 million in US (many contracted 40-50 yrs ago)
49
Q

• how does strep throat progress to RF/RHD?

A
  • GAS spreads by direct contact with oral/resp secretions (↑crowded living)
  • attach to epithelium of upper resp tract, make enzymes to invade and damage local tissue
  • incubate 2-4 d → acute inflammatory response, 3-7 d of sxs (sore throat, fever, malaise, HA)
50
Q

• how is strep throat diagnosed? Tx? Un-tx?

A
  • Positive throat culture or rapid streptococcal antigen test
  • hi strep Ab titer (antistrepotolysin O, ASO titer) (GAS make cytolytic toxins streptolysin S and O. O induces persistently high Ab titers= good marker)
  • tx: abx shorten strep throat, reduce infectivity, reduce sequelae of heart damage, but don’t change course of acute RF
  • Untx: remain infected/infectious for weeks after symptomatic resolution of pharyngitis
  • 0.3-3% untx cases: get RF
51
Q

• What are Aschoff bodies?

A
  • nodules in heart w RF. dt inflammation in heart muscle, characteristic of RHD
  • granulomatous: collagen, lymphocytes, plasma cells, M0s, surround necrotic center
  • pathognomonic for pan-carditis in RHD (focal inflammation of all 3 layers of heart)
  • found in other tissues in RF, but not called Aschoff
  • M0s may →multinucleated giant cells, or Anitschkow cells (“caterpillar cells”, dt appearance of chromatin)
52
Q

• what is most important cardiac related consequence of RHD?

A
  • Mb chronic valvular deformities, particularly mitral stenosis (65-70%, then aortic valve at 25%)
  • have deforming fibrosis → permanent dysfunction and severe, sometimes fatal, cardiac problems decades later
  • gross: “fish mouth” shape with chronic rheumatic scarring.
  • varying degrees of regurgitation, atrial dilation, arrhythmias, ventricular dysfunction.
  • Chronic RHD= leading cause of MSV and valve replacement
  • Chronic manifestations: 10-40%
  • Fusion of valve develops 2-10 yrs after acute RF, more episodes more damage
53
Q

• What is carditis?

A

o Inflammation of heart muscle
o 2nd most common complication of RF (50%)
o Sxs: like HF, dyspnea, chest discomfort, pleuritic chest pain, cough, pericarditis/rub
o Often w new murmur, tachycardia (out of proportion to fever)

54
Q

• What are sxs of RF?

A 
o	Like HF
o	Difficulty breathing, exercise intolerance
o	Tachycardia (out of proportion to fever)
55
Q

• What are Prosthetic heart valves? Complications?

A
  • older ball and cage variety. last indefinitely, require continual anticoagulant tx because of the exposed non-biologic surfaces.
  • Thrombosis: so need anticoagulant tx, doesn’t entirely precent
  • Infection: vegetations of IE, septic embolization
  • Structural failure: leaflets tend to become stiff and calcify
  • Dehiscence: right after surgery, suture line leaks= valvular leakage
56
Q

• What are non-cardiac ssx of acute RF?

A
  • often diagnostic
  • polyarthritis (most common; transient, large jts, from legs up)
  • chorea (Sydenham’s, St. Vitus’ dance), erythema marginatum, subcutaneous nodules (bx if has Aschoff bodies)
  • abdominal pain, arthralgias, fever, pneumonia
57
Q

• what are subcutaneous nodules?

A
  • Painless, firm, collagen, over bones or tendons
  • back of wrist, outside elbow, front knees
  • have Aschoff bodies w RF
58
Q

• what is erythema marginatum?

A
  • Aka erythema annulare
  • Rash in 5-13% of acute RF
  • Begins trunk/arms 1-3 cm , pink-to-red nonpruritic macules or papules, rarely face
  • spread outward → serpiginous ring w red raised margins and central clearing
  • worse w heat
59
Q

• Describe presentation of 8 yo boy with RF, chorea, subcutaneous nodules:

A
  • Difficulty writing dt chorea in arms
  • Mild sore throat, resolved w/o abx; lo fever, no chills
  • Friction rub over heart
  • subQ nodules over hands
  • bloodword unremarkable, ↑ESR
60
Q

• what are causes of pericarditis/pericardial dz?

A
  • Idiopathic – most common
  • Infectious – all microbes, esp viruses
  • Inflammatory – post-MI, secondary to uremia
  • AI – RF, RA, SLE,
  • Drugs: procainamide, hydralazine
  • Trauma – penetrating/blunt trauma, post-catheterization, post-cardiac surgery
  • Misc. – tumors
61
Q

• What are the types of pericarditis?

A
  • Serous
  • Fibrinous
  • Hemorrhagic
  • Purulent
  • Caseous
62
Q

• What are features of Serous pericarditis?

A
  • Usu non-infectious, mb viral
  • Uremia (acute)
  • AI – RA, SLE
  • Normally, minimal fluid in pericardium and less inflammatory response. Often has complete resolution.
63
Q

• What is Fibrinous pericarditis?

A
  • Post-MI or Dressler’s syndrome; Post-cardiac surgery; Trauma; Uremia (chronic); AI– RA, SLE
  • Pericardial fluid is mixture of fibrinous exudate in serous fluid
  • Pericardial friction rub mb audible
  • Gross: surface looks rough, not normal glistening (dt fibrin strands)
  • “bread and butter” pericarditis
64
Q

• What is Hemorrhagic pericarditis?

A
  • TB; Tumor; Bacterial; Bleeding dos; Trauma
  • =fibrinous pericarditis w blood (w/o inflammation, would be called hemopericardium)
  • Pericardial fluid w blood mixed with fibrin, st pus exudate
  • Gross: rough and red surface
  • usu with metastatic tumors, TB
65
Q

• what is Purulent pericarditis?

A
  • from adjacent infection, septic embolism, septicemia, iatrogenic after heart procedure
  • exudative, yellow pericardial fluid, w pus and fibrin.
  • Resolution w scarring, may → constrictive pericarditis.
66
Q

• What is incidence of heart tumors?

A
  • Primary: rare, 70% benign, 30% malignant
  • Metastatic also uncommon, but most common malignancy in heart
  • most common: atrial myxoma (benign)
67
Q

• what are the types of benign and malignant heart tumors?

A
  • B: Fibroma, Hemangioma, Lipoma, Lymphangioma, Myxoma, Neurofibroma, Rhabdomyoma, Teratoma,
  • M: Angiosarcoma, Extraskeletal Osteosarcoma, Fibrosarcoma, Leiomyosarcoma, Liposarcoma, Neurogenic Sarcoma, Rhabdomyosarcoma, Malignant Lymphoma, Malignant Teratoma, Mesothelioma, Thymoma,
68
Q

• What is atrial myxoma? Dx?

A

o benign masses, attached to atrial wall, or valve, ventricle (in chambers)
o usu LA, 80-90%l usu septum
o 1-15 cm, usu 5-6
o 29% all heart tumors
o “ball valve” effect: intermittently occlude valve orifice
o Can embolize (metastasize); esp be careful on surgical removal
o Dx: echo, further confirmation by MRI

69
Q

• What is gross and micro appearance of atrial myxoma?

A

o Gross: gelatinous ball into LA
o Hypocellular myxoid mass, polygonal/elongated cells
o Mono- or multinuclear
o finely vacuolated eosinophilic cytoplasms.

70
Q

• What is Cardiac rhabdomyoma?

A

o most common primary pediatric tumor of the heart.
o benign, can’t metastasize, but certain position may cause lethal arrhythmias, chamber obstruction.
o spontaneous regression.
o Mild atypical histology
o Gross: clear cells (not normal myocardium, dt glycogen loss in staining), round/polygonal, enlarged

71
Q

• Which neoplasm has greatest propensity to metastasize to heart? Others?

A

o Melanoma (64%), but not most common cardiac malig
o Dt hematogenous invasion (like lymphoma, dt myocardium involvement)
o Gross: See brown-black pigment
o Met to heart: 10-12% of autopsies w malignancy, dt hematogenous dissemination
o Bronchogenic 36%, nonsolid 20%, breast 7%, esophagus 6%

72
Q

• What is the most common cardiac malignancy?

A

o Carcinoma of lung (bronchogenic, 36%)
o involves heart dt proximity/extension or hematogenous spread
o dt lymphatic invasion (dt peri/endocardium involvement)
o Also bc lung CA is so common

Pathology 3 (6 decks)

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