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RC > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Modifiable and non-modifiable risk factors for atherosclerosis

A

Modifiable: diet, exercise, smoking, dental hygiene, homocystinemia, T2DM
Nonmodifiable: age, sex, FHx, genetic predisposition, T1DM, coagulation anomalies, primary HTN

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2
Q

Development of atherosclerosis

A

Response to injury hypothesis:
-Endothelial injury causing increased vascular permeability, leukocyte adhesion, thrombosis
- accumulation of lipoprotein in vessel wall
- monocyte adhesion to the endothelium followed by migration into intima, and transformation into macrophages and foam cells
- platelet adhesion
- factors released for smooth muscle cell and macrophage recruitment
- smooth muscle cell proliferation and extracellular matric production, lipid accumulation extracellularly and intracellularly
- inflammatory cell infiltration
- metalloproteinase release
- plaque complication - cap rupture, thrombus adherence, possible stenosis or embolism

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3
Q

List at least 5 benign vascular neoplasms

A

Hemangioma
Angiofibroma
Lobular capillary hemangioma
Glomus tumor
Lymphangioma

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4
Q

List examples of immune complex vasculitis

A

SLE vasculitis
IgA HSP
Cryoglobulin vasculitis
Drug hypersensitivity
Rheumatoid vasculitis

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5
Q

Classification of vasculitidies and examples in each category

A

Chapel-Hill classification
Large vessel: GCA, takayasu arteritis
Medium: polyarteritis nodosa, kawasaki disease
Small: microscopic polyangiitis, GPA, EGPA, HSP

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6
Q

Etiology, cardiac sequelae, gross characteristics, microscopic features of: Mitral stenosis

A

Rheumatic heart disease
Left atrial enlargement and atrial fib
Leaflet thickening and commisural fusion. shortening, thickening and fusion of chordae tendonae
Diffuse fibrosis and neovascularization

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7
Q

Etiology, cardiac sequalae, gross characteristics, microscopic features of: Mitral regurg

A

Mitral valve prolapse
Left atrial enlargment, LVH, atrial fib
Hooding of mitral leaflets, enlarged thickened and redundant leaflets, chordae elongated thinned and occasionally ruptured
Attenuation of fibrosa, marked thickening of spongiosa with myxomatous material

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8
Q

Etiology, cardiac sequalae, gross characteristics, microscopic features of: Aortic stenosis

A

Senile calification
LVH
Calcification within cusps
Fibrosis and calcs

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9
Q

Etiology, cardiac sequalae, gross characteristics, microscopic features of: Aortic regurg

A

Aortic dilatation
LVH, dilated aorta
Cusps from near normal to thickened and calcified with commissural fusion
Near normal to fibrosis, calcification

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10
Q

Common causes of failure of cardiac valve prostheses

A

Thrombosis/thromboembolism
Prosthetic valve endocarditis
Structural deterioration: wear, frature, cuspal tear, calcs
Nonstructural dysfunction: granulation tissue, suture or tissue entrapment, paravalvular leak

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11
Q

Characteristic features of cardiac lesions of rheumatic fever

A

Acute rheumatic fever:
- diffuse pancarditis and aschoff bodies
- verrucae : vegetations due to fibrinoid necrosis within cusps or tendinous cords
-MacCallum plaques: subendocardial lesions, exacerbated by regurgitant jets, can induce irregular thickenings in left atrium
Chronic rheumatic fever:
-valvular leaflet or cusp thickening
- commissural fusion
- shorted, fused, thickened chordae tendonae, fish mouth mitral valve orifice

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12
Q

Borderline myocarditis vs active myocarditis

A

Borderline: inflammation but no myocyte necrosis
Active: inflammation and myocyte necrosis

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13
Q

What to do and what to recommend with a diagnosis of borderline myocarditis

A

Do: cute through block to look for missed myocyte necrosis, stain adjacent sections
Recommend: repeat or follow up biopsy

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14
Q

Features of endomyocardial biopsies to differentiate dilated, hypertrophic, restrictive cardiomyopathies

A

None: all show fibrosis and hypertrophy
Disarray can be a normal finding for endomyocardial right ventricular biopsies and thus not specific for hypertrophic cardiomyopathy

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15
Q

Man causes of aortic valve insufficiency

A

Valve: infective endocarditis, rheumatic valvular disease, congenital bicuspid aortic valce
Aorta: aortic aneurysm, annular dilation, aortic dissection, aortitis

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16
Q

Main causes of aortic valve stenosis

A

Age related degeneration: calcific degeneration
Congenital bicuspid valve
Postinflammatory disease: rheumatic valve disease

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17
Q

Components of mitral valve apparatus necessary for valve competence

A

Annulus
Leaflets
Chordae
Left venticular papillary muscles
Left ventricle myocardium

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18
Q

How to distinguish tricuspid and mitral valves

A

Septal attachments present on tricuspid valve
Tricuspid and pulmonary valves due to infuldibular spetum
Mitral valve has higher point of insertion on ventricular septum
Mitral as 2 leaflets, tricuspid has 3

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19
Q

Components of tetrology of fallot

A

VSD
Pulmonary stenosis
Overriding aorta
RVH

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20
Q

Systemic or cardiac conditions associated with aortic dissection

A

Bicuspid aortic valve
Systemic arterial hypertension
Trauma - iatrogenic at surgery, iatrogenic at cath, nonpenetrating blunt chest injury
Pregnancy
Connective tissue disease
Giant cell aortitis (really any aortitis)

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21
Q

Complications of acute aortic dissection

A

MI
Coronary artery dissection
Aortic rupture
Aortic valve insufficiency
Stroke
Visceral ischemia
Hemopericardium and cardiac tamponade

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22
Q

Complications of atherosclerotic plaques

A

Thrombosis
Plaque rupture
Plaque hemorrhage
Aneurysm
Embolism (thrombus and athromatous debris)
Plaque erosion
Vessel rupture

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23
Q

Workup of unexpected giant cell inflammation in aortic aneurysm resection

A

History - check for infections (TB, syphilis), cultures, serology etc, any systemic inflammatory disease
Call clinician to report critical value

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24
Q

Stunned myocardium vs hibernating myocardium

A

Stunned: post MI, non-contractile, reversible with time
Hibernating: chronic ischemia related (myocytolysis), noncontractile, reversible with revascularization

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25
Q

Molecular testing at autopsy includes testing for which conditions

A

Hypertrophic cardiomyopathy
Arrhythmogenic cardiomyopathy
QT segment - long or short
Brugada syndrome
Catecholaminergic polymorphic ventricular tachycardia (CPVT)

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26
Q

Causes of constrictive pericarditis

A

Radiation
TB
Cardiac surgery
Tumor involvement - primary or secondary

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27
Q

Clinical signs/symptoms of pericarditis

A

Chest pain, dyspnea, fever/chills, friction rub, pericardial effusion, ST elevation, decreased QRS amplitude

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28
Q

Syndrome of pericarditis presenting late after an MI

A

Dressler syndrome

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29
Q

Causes of fibrinous pericarditis

A

Viral
Drugs
Uremia
Collagen vascular disease
Trauma
Tumor
MI

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30
Q

Clinical manifestations of carcinoid heart disease

A

Valvular heart disease: tricuspid regurg, pulmonary regurg, pulmonary stenosis
Coronary artery vasospasm
Arrhythmias
Carcinoid tumor mets directly in myocardium
MI

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31
Q

Why is right sided heart failure more common in carcinoid heart diease

A

Left side is spared because lungs metabolize vasoactive substances

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32
Q

Characteristic pathological findings of carcinoid heart disease

A

Endocardial plaques - RV, tricuspid valve, pulmonary valve, occasionally vena cava, pulmonary artery, coronary sinus

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33
Q

Complications of bioprosthetic and mechanical prosthetic valves

A

Both:
- Size mismatch
- incorrect positioning
- Suture impingement on disc
- paravalvular leak
- coronary artery ostial occlusion by valve ring
- infective endocarditis
- fibrous pannus
Bioprostheses:
- leaflet degenerative changes with fibrosis and calcification
- leaflet tears and perforation
Mechanical:
- cloth wear
- ball or disc emoboli or erosion
- ball degeneration and cracking
- stent creep
- thrombosis

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34
Q

Regions requiring thorough examination in assessing a coronary artery bypass graft

A

Bypass graft ostium anastomosis at aorta
Bypass graft body
Distal anastomosis
Distal coronary artery
proximal native coronary artery
Coronary artery ostium

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35
Q

Key features of giant cell arteritis

A

Vasculitis involving the temporal artery and aorta
FOund in older patients with headaches, fatigues, fever, vision loss, etc
Associated with PMR
Ophthalmic artery involve may result in irreversible blindness

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36
Q

Histologic features of giant cell arteritis

A

Granulomatous inflammation with destruction of internal elastic lamina
Mixed inflammatory infiltrate consisting of lymphocytes, eos and histiocytes
Intimal proliferation
Medial fibrosis
Healed stage: collagenous scar and neovascularization of vessel wall

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37
Q

Processing of temporal artery biopsy specimens

A

Submit entire segment for processing and sectioned at the time of embedding
Serially section at 2-3mm, submitted in toto
Multiple levels +/- elastin stains

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38
Q

Clinical significance of negative temporal artery biopsy

A

Negative biopsies do not rule out this disease as it is patchy
Treatment decisions should be made knowing this

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39
Q

Clinical features of mitral valve prolapse

A

Most commonly in young women
Often incidental finding of midsystolic click
Associated with marfan syndrome
Complications include infective endocarditis, mitral insufficiency, ventricular arrhythmia

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40
Q

Pathologic features of mitral valve prolapse

A

Interchordal ballooning (hooding) of mitral leaflets
enlarged redundant, thick, and rubbery leaflets
Elongated and thinned tendinous cords
Annular dilatation
Microscopic features - attenuated fibrosa layer of valve and thickened sponsiosa layer with myxomatous degeneration

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41
Q

Clinical complications of mitral valve prolapse

A

Mitral valve regurg
Arrhythmias
Endocarditis
Chordae tendinae rupture
Embolism

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42
Q

Pathogenesis of mitral valve prolapse

A

Degenerative/myxomatous disease

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43
Q

Clinical features of angiosarcoma

A

Often in older adults, may be secondary to radiation therapy
Most commonly in skin, soft tissue, breast, liver
Characterized by rapid growth, leading to ulcers and hemorrhage

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44
Q

Histologic features of angiosarcoma

A

Anastomosing vascular channels lined by atypical endothelial cells with frequent mitotic figures and necrosis
Degrees of differentiation from obviously vascular to undifferentiated

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45
Q

3 causes of angiosarcoma

A

Vinyl chloride
Radiation
Lymphedema

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46
Q

IHC profile of angiosarcoma

A

CD31+ CD34+ FXIII+

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47
Q

Classification of endocarditis

A

Infective endocarditis:
- native valve endocarditis
- prosthetic valve endocarditis, early and late
- Intravenous drug abuse endocarditis

Noninfective:
- nonbacterial thrombotic endocarditis
- endocarditis of SLE (Libman-Sacks)
-verrucous endocarditis

48
Q

Gross and microscopic features of Acute infective endocarditis

A

Gross - bulky, irregular, friable vegetation on valve cusps; valve destruction; abscess
Micro - fibrin, inflammatory cells, bacteria or other organisms

49
Q

Gross and microscopic features of Healing infective endocarditis

A

Gross - smaller, friable vegetations
Micro - granulation tissue at base of vegetations, chronic inflammatory cells

50
Q

Gross and microscopic features of acute rheumatic valvular disease

A

Gross - row of small, warty vegetations along the lines of closure of valve
Micro - Aschoff bodies, Anitschkow cells, fibrin, inflammatory cells

51
Q

Gross and microscopic features of NBTE

A

Gross - small, bland vegetations, usually attached at the line of valve closure
Micro - bland thrombus with no inflammatory reaction or valve damage

52
Q

Gross and microscopic features of Libman-Sacks endocarditis

A

Gross - small or medium-size vegetations of either or both sides of valve
Micro - Fibrin, cellular debris, inflammatory cells without PMNs

53
Q

Predisposing conditions to infective endocarditis

A

Rheumatic heart disease
Myxomatous mitral valve
Bicuspid aortic valve
Prosthetic valve

54
Q

Gross evaluation of aortic valve

A

Assess number of cusps, size, and consistency
Describe any abnormalities - distribution, surface, location
Describe any vegetations
Submit representation sections taken from free edge to annulus

55
Q

Pertinent findings in an autopsy patient with infective endocarditis

A

Vegetations on aortic and mitral valve
Vegetations on pulmonary and tricuspid valve for IVDU
Any valve abnormalities eg perforation, indentation, rupture chordae
Ring abscess
Septic emboli

56
Q

Risk factors for SLE

A

Young women
Ethnicity: African-Americans, Hispanics, Asians
FHx

57
Q

Possible SLE triggers

A

Cold temperature
Fatigue
Stress
Chemicals exposures
Sunlight
Certain drugs

58
Q

Cardiac manifestations of SLE

A

Pericarditis
Myocarditis
Libman-Sacks endocarditis

59
Q

Systemic associations with berry aneurysms

A

ADPKD
Systemic arterial hypertension
Atherosclerosis

60
Q

Histologic features of berry aneurysms

A

Deficiency of elastic and muscled tissues with dilatation of vessel wall
Arterial wall adjacent to neck of aneurysm shows intimal thickening and attenuation of media
Smooth muscle and intimal elastic lamina do not extend into the neck and are absent from aneurysm sac itself

61
Q

Common causes of SAH

A

Head trauma
Rupture of saccular aneurysm
Vascular malformations
Tumors

62
Q

Clinical findings of GPA

A

Persistent pneumonitis with bilateral nodular and cavitary infiltrates
Chronic sinusitis, mucosal ulceration of nasopharynx
Renal disease - hematuria and proteinuria

63
Q

Histologic features of GPA

A

Acute necrotizing granulomata in resp tract
Necrotizing or granulomatous vasculitis affecting small to medium-sized vessels
Renal: focal necrotizing and crescentic GN

64
Q

Common site involved in GPA

A

Upper and lower respiratory tract
Kidney
Peripheral vessels

65
Q

ANCA subtype associated with GPA

A

PR3-ANCA

66
Q

Pathogenetic causes of GPA

A

Hypersensitivity
Immune complexes

67
Q

DDx of GPA

A

Sarcoidosis
polyarteritis nodosa

68
Q

Clinical features of EGPA

A

Associated with asthma, allergic rhinitis, lung infiltrates, peripheral hypereosinophilia
Skin lesions - urticaria and palpable purpura
Young adults
MPO-ANCA
May present with GI bleeding
Renal disease - FSGS
Cardiomyopathy - half of syndrome-related deaths

69
Q

histologic findings of EGPA

A

Small sized arteries and veins
Necrotizing vasculitis with eosinophilic infiltrate and granulomatous reaction

70
Q

Define sudden cardiac death

A

Unexpected death from cardiac causes that occurs without symptoms or within 1-24h of symptom onset

71
Q

Causes of SCD

A

Ischemic heart disease (80-90%)
Congenital structural or coronary arterial abnormalities
Aortic valve stenosis
Mitral valve prolapse
Myocarditis
Dilated or hypertrophic cardiomyopathy
Pulmonary hypertension
Arrhythmia
Isolated LVH

72
Q

When should conduction system examination be done

A

Sudden death with normal heart examination
Cardiomyopathies
AV block
Arrhythmias with condition system anomalies
Sarcoidosis
Conduction problems post aortic valvular surgery
Post cardiac ablation

73
Q

Signs at autopsy reflecting heart failure

A

Right:
- Acites
- hepatosplenomegaly
- peripheral efema
- stasis dermatitis
Left:
- pleural effusion
- heavy lungs
- pulmonary edema

74
Q

Classification of Kaposi sarcoma

A

Classic: eastern European and mediterranean males
Endemic: people indigenous to central Africa
Epidemic: HIV+
Iatrogenic/Immunocompromised - transplant

75
Q

Clinical features of kaposi sarcoma

A

Erythematous to violaceous cutaneous lesions (macular, patch, plaque, nodular, exophytic), can be solitary, localized, or disseminated
Can involve oral cavity, lymph nodes, viscera

76
Q

Histologic features of kaposi sarcoma

A

Slit-like space, extravasated RBCs, plasma cells
Proloeration of spindle shaped cells arranged as short fascicles and diffuse proliferation of blood vessels
Later stage: greater degrees of cytological atypia, high mitotic rate

77
Q

Cause of Kaposi sarcoma

A

HHV8

78
Q

DDx of kaposi sarcoma

A

Benign vascular proliferations: targetoid hemosiderotic hemangioma, fibrous histocytoma
Angiosarcoma

79
Q

Intracardiac complications of endocarditis

A

Valvular destruction
Paravalvular destruction/abscess
Valvular incompetence
Sinus of valsalva aneurysm

80
Q

Common causative organisms of endocarditis in IVDU

A

S. Aureus
Staph epidermidis

81
Q

Poor prognostic features of endocarditis

A

Acute S. auerus endocarditis
Heart failure
IVDU (often bilateral disease)
Prosthetic valve infection
Fungal endocarditis
COmplications with or root abscesses or fistulas

82
Q

Common causes of aortic dissection

A

Inherited syndromes - Marfan, Loey-Dietz, Ehlers-Danlos
Systemic arterial hypertension
Trauma
Infection

83
Q

Pathogenesis of aortic dissection

A

Occur when a tar of intima of aortic wall causes dissection of blood between and along the laminar planes of the media

84
Q

Classifications of Aortic dissection

A

Stanford:
- Type A involved either ascending only or ascending and descending
- Type B descending only

DeBakey:
- I involved ascending and rest of aorta
- II involves ascending aorta only
- III arises after ascending aorta

85
Q

Clinical features of aortic dissection

A

Severe pain
Dyspnea
Limb pain 2’ ischemia
Organ/visceral pain 2’ infarction
Stroke signs

86
Q

Effects of chronic systemic arterial hypertension on heart, large vessels, and small vessels

A

Heart: LVH, cardiac myocyte hypertrophy, interstitial myocardial fibrosis
Large vessels: increased atherosclerosis, aortic aneurysms and dissection
Small vessels: retinopathy, nephropathy, nephrosclerosis, cerebral infarct, hemorrhage

87
Q

Types of ANCA and their associated conditions

A

PR3-ANCA: GPA
MPO-ANCA: microscopic polyangiitis, ANCA-associated GN, EGPA
Also associated with UC, ank spon

87
Q

Define ANCA

A

Antineutrophil cytoplasmic antibody
Acts against antigens in cytoplasm of neutrophil granulocytes and monocytes
Mostly IgG
Particular association with systemic vasculitis

87
Q

2 common subtypes of ANCA

A

MPO-ANCA and PR3-ANCA
MPO-ANCA: myeloperoxidase, perinuclear staining
PR3-ANCA: proteinase 3, diffuse, granular cytoplasmic

87
Q

Types of vessels most at risk for ANCA-associated vasculitis

A

Small arteries
Arterioles
Venules
Veins
Capillaries
Rarely large elastic arteries

87
Q

How is ANCA measured

A

ELISA and direct IF

87
Q

Pathogenesis of noninfectious vasculitis

A

Main pathogenesis is immune complex deposition, ANCA, Antiendothelial cell antibodies

88
Q

5 Immune complex vasculitidies

A

Cryoglobulinemic vasculitis: cryglobulins (association with HepC)
Hypersensitivity vasculitis/leukocytoclastic: meds/drug
HSP: IgA-complexes
Lupus: Full house
Rheumatoid vasculitis

89
Q

Most common primary cardiac neoplasms in adults

A

Myxoma
Papillary fibroelastoma
Rhabdomyoma

90
Q

Most common primary cardiac neoplasms in children

A

Rhabdomyoma
Fibroma
Sarcoma

91
Q

Origin of myxoma tumor cells

A

Primitive multipotent mesenchymal cells

92
Q

Most common location for cardiac myxoma

A

Left atrial septum near fossa ovalis

93
Q

Gross and microscopic features of cardiac myxoma

A

Gross: soft, gelatinous, papillary to firm, smooth
- cut surface variegated with areas of hemorrhage and degeneration, calcified changes
Microscopic: myxoma cells are stellate, ovoid, or polygonal with inconspicuous nucleoli, eosinophilic cytoplasm and indistinct cell borders
- cells may form rings, ribbons, glandular structures, and cords
- background of myxoid and loose fibrous tissue with scatters lymphs, hemosidering-laden macrophages, and a capillary network

94
Q

IHC for cardiac myxoma

A

CD34+ Calretinin+

95
Q

Classification of primary cardiomyopathies

A

Dilated
Hypertrophic
Restrictive

96
Q

Etiology, functional impact, gross and microscopic features of dilated cardiomyopathy

A

Etiology: 30-40% gene mutations, other causes include myocarditis, toxic, peripatum, idiopathic
Functional impact: ventricular systolic dysfunction
Gross: 4 chamber dilation, bilateral ventricular hypertrophy or thinning, mural thrombi, endocardial fibrosis
Micro: variable myocyte hypertrophy, interstitial and endocardial fibrosis

97
Q

Etiology, functional impact, gross and microscopic features of hypertrophic cardiomyopathy

A

Etiology: 100% gene mutations in sarcomere, AD inheritance
Function: diastolic dysfunction
Gross: LVH, banana-like config of left ventricular cavity, asymmetrical septal thickening, endocardial thicking of aortic outflow tract and anterior mitral leaflet
Micro: extensive myocyte hypertrophy, haphazard disarray of bundles, myocytes, and fibres, interstitial fibrosis

98
Q

Etiology, functional impact, gross and microscopic features of restrictive cardiomyopathy

A

Etiology: amyloid, sarcoid, endomyocardial fibrosis, loeffler endomyocarditis, endocardial fibroelastosis, radiation, metabolic diseases, idiopathic
Function: diastolic dysfunction
Gross:
- amyloid: firm, rubbery, thick walls
- sarcoid: firm, parenchymal scarring/fibrosis
Micro: appearance of amyloid, sarcoid, or interstitial fibrosis

99
Q

Morphologic feature of contraction band necrosis

A

Eosinophilic bands crossing the short axis of the myocyte

100
Q

Pathogenesis of contraction band necrosis

A

Irreversible myocardial injury
May occur in setting of reperfusion injury
Mediated by fluctuations in calcium concentration causing sarcomere hypercontraction
Can be an artifact seen in endomyocardial biopsy specimen

101
Q

Role of endomyocardial biopsy

A

Gold standard for surveillance of cardiac transplant rejection and for diagnosing myocarditis
Helpful for diagnosis or monitoring of primary cardiomyopathies, amyloidosis, sarcoidosis, drug toxicities, fabry disease, endocardial fibrosis, neoplasia

102
Q

Approach to endomyocardial biopsy

A

Requires clinical history
Adequacy: at lest 4 good pieces of myocardium
Evaluation of endocardium, myocardium, interstitium, vasculature
Report should include biopsy site, type of biopsy, diagnosis, grade, microscopic description

103
Q

Characteristic findings of arterial and venous diseases of legs

A

Arterial disease: deep distinct ulcers, gangrene, muscular atrophy, hair loss, toenail thickening, mottling
Venous disease: congestion, varices, shallow medial malleolar ulcer, stasis dermatitis with skin flaking and brownish discolouration

104
Q

Clinical manifestations of cardiac tamponade

A

Decreased heart sounds, decreased pulse, increased JVP

105
Q

Differentiate constrictive pericarditis and restrictive cardiomyopathy on endomyocardial biopsy

A

Constrictive pericarditis: atrophic cardiac myocytes or normal myocardium
Restrictive cardiomyopathy: fibrosis, myocyte hypertrophy, degeneration

106
Q

What kind of calcification is calcific aortic stenosis

A

Dystrophic calcs - occurs in degeneration or necrotic tissue
Active calcification with cholesterol, inflammation, fibrosis

107
Q

Examples of dystrophic calcification

A

Leiomyoma
Calcification of postinfarct ventricular aneurysm
Hyalinized scar
Tumor necorsis
Old granuloma
Fat necrosis

108
Q

Gross features of rheumatic heart disease

A

Acute - small verrucous vegetations along lines of valve closure
MacCallum patch - thickening of left atrial endocardium proximal to base to posterior mitral valve leaflet
Leaflets thickened with commissural fusion
Chordae thickened, shortened, fused
Fibrosis and calcs create fish mouth orifice of mitral valve

109
Q

Elements to report with malignant cardiac tumor

A

Specimen procedure
Specimen integrity
Specimen laterality
Tumor site
Tumor size
Histologic type and grade
Tumor extension
Margins
Treatment effect
LVI

110
Q

Grading of cardiac tumors

A

Mostly sarcomas so FNCLCC used:
Tumor diff:
- Score 1: sarcomas closely resembling normal adult mesenchymal tissue
- Score 2: sarcomas for which histologic typing is certain
- Score 3: undifferentiated, angiosarcoma
Mitosis:
- Score 1: 0-9/10 hpf
- Score 2: 10-19/10 hpf
- Score 3: >19/10 hpf
Tumor necrosis:
- Score 0: none
- Score 1: <50% tumor necrosis
- Score 2: >50% tumor necrosis
Histologic grade:
- Grade 1: total score 2-3
- Grade 2: total score 4-5
- Grade 3: total score 6-8

111
Q

pTNM staging for heart tumors

A

No published staging system

RC (20 decks)

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