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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
Molecular testing at autopsy includes testing for which conditions
Hypertrophic cardiomyopathy Arrhythmogenic cardiomyopathy QT segment - long or short Brugada syndrome Catecholaminergic polymorphic ventricular tachycardia (CPVT)
26
Causes of constrictive pericarditis
Radiation TB Cardiac surgery Tumor involvement - primary or secondary
27
Clinical signs/symptoms of pericarditis
Chest pain, dyspnea, fever/chills, friction rub, pericardial effusion, ST elevation, decreased QRS amplitude
28
Syndrome of pericarditis presenting late after an MI
Dressler syndrome
29
Causes of fibrinous pericarditis
Viral Drugs Uremia Collagen vascular disease Trauma Tumor MI
30
Clinical manifestations of carcinoid heart disease
Valvular heart disease: tricuspid regurg, pulmonary regurg, pulmonary stenosis Coronary artery vasospasm Arrhythmias Carcinoid tumor mets directly in myocardium MI
31
Why is right sided heart failure more common in carcinoid heart diease
Left side is spared because lungs metabolize vasoactive substances
32
Characteristic pathological findings of carcinoid heart disease
Endocardial plaques - RV, tricuspid valve, pulmonary valve, occasionally vena cava, pulmonary artery, coronary sinus
33
Complications of bioprosthetic and mechanical prosthetic valves
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
34
Regions requiring thorough examination in assessing a coronary artery bypass graft
Bypass graft ostium anastomosis at aorta Bypass graft body Distal anastomosis Distal coronary artery proximal native coronary artery Coronary artery ostium
35
Key features of giant cell arteritis
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
36
Histologic features of giant cell arteritis
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
37
Processing of temporal artery biopsy specimens
Submit entire segment for processing and sectioned at the time of embedding Serially section at 2-3mm, submitted in toto Multiple levels +/- elastin stains
38
Clinical significance of negative temporal artery biopsy
Negative biopsies do not rule out this disease as it is patchy Treatment decisions should be made knowing this
39
Clinical features of mitral valve prolapse
Most commonly in young women Often incidental finding of midsystolic click Associated with marfan syndrome Complications include infective endocarditis, mitral insufficiency, ventricular arrhythmia
40
Pathologic features of mitral valve prolapse
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
41
Clinical complications of mitral valve prolapse
Mitral valve regurg Arrhythmias Endocarditis Chordae tendinae rupture Embolism
42
Pathogenesis of mitral valve prolapse
Degenerative/myxomatous disease
43
Clinical features of angiosarcoma
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
44
Histologic features of angiosarcoma
Anastomosing vascular channels lined by atypical endothelial cells with frequent mitotic figures and necrosis Degrees of differentiation from obviously vascular to undifferentiated
45
3 causes of angiosarcoma
Vinyl chloride Radiation Lymphedema
46
IHC profile of angiosarcoma
CD31+ CD34+ FXIII+
47
Classification of endocarditis
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
Gross and microscopic features of Acute infective endocarditis
Gross - bulky, irregular, friable vegetation on valve cusps; valve destruction; abscess Micro - fibrin, inflammatory cells, bacteria or other organisms
49
Gross and microscopic features of Healing infective endocarditis
Gross - smaller, friable vegetations Micro - granulation tissue at base of vegetations, chronic inflammatory cells
50
Gross and microscopic features of acute rheumatic valvular disease
Gross - row of small, warty vegetations along the lines of closure of valve Micro - Aschoff bodies, Anitschkow cells, fibrin, inflammatory cells
51
Gross and microscopic features of NBTE
Gross - small, bland vegetations, usually attached at the line of valve closure Micro - bland thrombus with no inflammatory reaction or valve damage
52
Gross and microscopic features of Libman-Sacks endocarditis
Gross - small or medium-size vegetations of either or both sides of valve Micro - Fibrin, cellular debris, inflammatory cells without PMNs
53
Predisposing conditions to infective endocarditis
Rheumatic heart disease Myxomatous mitral valve Bicuspid aortic valve Prosthetic valve
54
Gross evaluation of aortic valve
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
Pertinent findings in an autopsy patient with infective endocarditis
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
Risk factors for SLE
Young women Ethnicity: African-Americans, Hispanics, Asians FHx
57
Possible SLE triggers
Cold temperature Fatigue Stress Chemicals exposures Sunlight Certain drugs
58
Cardiac manifestations of SLE
Pericarditis Myocarditis Libman-Sacks endocarditis
59
Systemic associations with berry aneurysms
ADPKD Systemic arterial hypertension Atherosclerosis
60
Histologic features of berry aneurysms
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
Common causes of SAH
Head trauma Rupture of saccular aneurysm Vascular malformations Tumors
62
Clinical findings of GPA
Persistent pneumonitis with bilateral nodular and cavitary infiltrates Chronic sinusitis, mucosal ulceration of nasopharynx Renal disease - hematuria and proteinuria
63
Histologic features of GPA
Acute necrotizing granulomata in resp tract Necrotizing or granulomatous vasculitis affecting small to medium-sized vessels Renal: focal necrotizing and crescentic GN
64
Common site involved in GPA
Upper and lower respiratory tract Kidney Peripheral vessels
65
ANCA subtype associated with GPA
PR3-ANCA
66
Pathogenetic causes of GPA
Hypersensitivity Immune complexes
67
DDx of GPA
Sarcoidosis polyarteritis nodosa
68
Clinical features of EGPA
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
histologic findings of EGPA
Small sized arteries and veins Necrotizing vasculitis with eosinophilic infiltrate and granulomatous reaction
70
Define sudden cardiac death
Unexpected death from cardiac causes that occurs without symptoms or within 1-24h of symptom onset
71
Causes of SCD
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
When should conduction system examination be done
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
Signs at autopsy reflecting heart failure
Right: - Acites - hepatosplenomegaly - peripheral efema - stasis dermatitis Left: - pleural effusion - heavy lungs - pulmonary edema
74
Classification of Kaposi sarcoma
Classic: eastern European and mediterranean males Endemic: people indigenous to central Africa Epidemic: HIV+ Iatrogenic/Immunocompromised - transplant
75
Clinical features of kaposi sarcoma
Erythematous to violaceous cutaneous lesions (macular, patch, plaque, nodular, exophytic), can be solitary, localized, or disseminated Can involve oral cavity, lymph nodes, viscera
76
Histologic features of kaposi sarcoma
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
Cause of Kaposi sarcoma
HHV8
78
DDx of kaposi sarcoma
Benign vascular proliferations: targetoid hemosiderotic hemangioma, fibrous histocytoma Angiosarcoma
79
Intracardiac complications of endocarditis
Valvular destruction Paravalvular destruction/abscess Valvular incompetence Sinus of valsalva aneurysm
80
Common causative organisms of endocarditis in IVDU
S. Aureus Staph epidermidis
81
Poor prognostic features of endocarditis
Acute S. auerus endocarditis Heart failure IVDU (often bilateral disease) Prosthetic valve infection Fungal endocarditis COmplications with or root abscesses or fistulas
82
Common causes of aortic dissection
Inherited syndromes - Marfan, Loey-Dietz, Ehlers-Danlos Systemic arterial hypertension Trauma Infection
83
Pathogenesis of aortic dissection
Occur when a tar of intima of aortic wall causes dissection of blood between and along the laminar planes of the media
84
Classifications of Aortic dissection
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
Clinical features of aortic dissection
Severe pain Dyspnea Limb pain 2' ischemia Organ/visceral pain 2' infarction Stroke signs
86
Effects of chronic systemic arterial hypertension on heart, large vessels, and small vessels
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
Types of ANCA and their associated conditions
PR3-ANCA: GPA MPO-ANCA: microscopic polyangiitis, ANCA-associated GN, EGPA Also associated with UC, ank spon
87
Define ANCA
Antineutrophil cytoplasmic antibody Acts against antigens in cytoplasm of neutrophil granulocytes and monocytes Mostly IgG Particular association with systemic vasculitis
87
2 common subtypes of ANCA
MPO-ANCA and PR3-ANCA MPO-ANCA: myeloperoxidase, perinuclear staining PR3-ANCA: proteinase 3, diffuse, granular cytoplasmic
87
Types of vessels most at risk for ANCA-associated vasculitis
Small arteries Arterioles Venules Veins Capillaries Rarely large elastic arteries
87
How is ANCA measured
ELISA and direct IF
87
Pathogenesis of noninfectious vasculitis
Main pathogenesis is immune complex deposition, ANCA, Antiendothelial cell antibodies
88
5 Immune complex vasculitidies
Cryoglobulinemic vasculitis: cryglobulins (association with HepC) Hypersensitivity vasculitis/leukocytoclastic: meds/drug HSP: IgA-complexes Lupus: Full house Rheumatoid vasculitis
89
Most common primary cardiac neoplasms in adults
Myxoma Papillary fibroelastoma Rhabdomyoma
90
Most common primary cardiac neoplasms in children
Rhabdomyoma Fibroma Sarcoma
91
Origin of myxoma tumor cells
Primitive multipotent mesenchymal cells
92
Most common location for cardiac myxoma
Left atrial septum near fossa ovalis
93
Gross and microscopic features of cardiac myxoma
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
IHC for cardiac myxoma
CD34+ Calretinin+
95
Classification of primary cardiomyopathies
Dilated Hypertrophic Restrictive
96
Etiology, functional impact, gross and microscopic features of dilated cardiomyopathy
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
Etiology, functional impact, gross and microscopic features of hypertrophic cardiomyopathy
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
Etiology, functional impact, gross and microscopic features of restrictive cardiomyopathy
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
Morphologic feature of contraction band necrosis
Eosinophilic bands crossing the short axis of the myocyte
100
Pathogenesis of contraction band necrosis
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
Role of endomyocardial biopsy
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
Approach to endomyocardial biopsy
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
Characteristic findings of arterial and venous diseases of legs
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
Clinical manifestations of cardiac tamponade
Decreased heart sounds, decreased pulse, increased JVP
105
Differentiate constrictive pericarditis and restrictive cardiomyopathy on endomyocardial biopsy
Constrictive pericarditis: atrophic cardiac myocytes or normal myocardium Restrictive cardiomyopathy: fibrosis, myocyte hypertrophy, degeneration
106
What kind of calcification is calcific aortic stenosis
Dystrophic calcs - occurs in degeneration or necrotic tissue Active calcification with cholesterol, inflammation, fibrosis
107
Examples of dystrophic calcification
Leiomyoma Calcification of postinfarct ventricular aneurysm Hyalinized scar Tumor necorsis Old granuloma Fat necrosis
108
Gross features of rheumatic heart disease
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
Elements to report with malignant cardiac tumor
Specimen procedure Specimen integrity Specimen laterality Tumor site Tumor size Histologic type and grade Tumor extension Margins Treatment effect LVI
110
Grading of cardiac tumors
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
pTNM staging for heart tumors
No published staging system

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