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CVM II > Cardiac Path II > Flashcards

Cardiac Path II Flashcards

1
Q

What is the most common valve abnormality ?

A

calcific aortic stenosis

2% of population

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2
Q

What is calcific aortic stenosis ?

A

affected valves contain osteoblast-like cells, deposit osteoid-like substance ->ossifies
Prevent complete opening of valve
cusp free edges spared

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3
Q

What causes the wear and tear of calcific aortic stenosis and what can show an accelerated course?

A

Wear and tear - hyperlipidemia, chronic HTN, inflammation
Bicuspid valve accelerates; responsible for half of stenosis
usually manifest in 60-80 but with bicuspid, 50-70s

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4
Q

What causes mitral annular calcification?

A

Degenerative, noninflammatory calcific deposits

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5
Q

Describe mitral annular calcificaton

A

Deposits in fibrous annulus
Does not affect valve function
Nodules may become sites fro thrombus formation or IE
Female, older, and with MVP

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6
Q

What is MVP?

A

myxomatous degeneration (PG deposit)
valve leaflets prolapse back into LA during systole
leaflets thick, rubbery due to proteoglycan deposits and elastic fiber disruption
Can cause thrombi to form

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7
Q

Who does MVP usually affect?

A

2-3% adults in US

Female, usually incidental

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8
Q

What are the symptoms and complications of MVP?

A

usually asymptomatic
Some may have angina-like pain or dyspnea
Complications: rare - IE, mitral insufficieny, Thromboemolism, arrhythmias

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9
Q

What is Rheutamic fever?

A

multisystem inflammatory disorder follwoing pharyngeal infection with group A streptococcus
Incidence decreased

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10
Q

What is the only cause of acquired mitral valve stenosis?

A

RHD

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11
Q

What is the pathogenesis of RHD?

A

immune response to streptococcal M proteins cross reacts with cardiac self antigens
T cells/Abs/and Mo

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12
Q

What is acute RF?

A

Acute RF occurs 10 days - 6 weeks after grp A strepinfection
Anti-strep O; anti-DNase B
can include pancarditis, migratory polyarthritis, subcutaneous nodules, rash, syndenham chorea

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13
Q

What are cardiac features of Acute RF?

A

pancarditis, featuring Aschoff bodies (Mo)
Vegetations
Inflammation, fibrinoid necrosis

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14
Q

What are the cardiac features of Chronic RHD?

A

mitral leaflet thickening, fusion, shortening of commisures, fusion and thickening of tendinous cords,
Mitral stenosis -> LA enlargement-> atrial fib/thrombosis; pulm cong/RHF
Fishmouth

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15
Q

What is infective endocarditis?

A

An infection of valves and endocardium

Vegetations consisting of microbes and debris, associated with underlying tissue destruction

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16
Q

What is acute infective endocarditis?

A

rapidly progressing, destructive infection of a previously normal valve
Mainly due to Staph aureus
Requires surgery and Antibiotics

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17
Q

What is subacute IE

A

Slower-progressing infection of a previously deformed valve
Cured with antibiotics alone
Strep viridans

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18
Q

What are the predisposing conditions of IE?

A

valvular abnormalities - RHD, prosthetic valves, MV prolapse, calcific stenosis, bicuspid AV
Bacteremia from another site, dental work, needles

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19
Q

What are the classic features of IE?

A

friable, bulky destructive valvular vegetations
Left-sided valves more common
Septic emboli - can seed at another spot
Invasion of adjacent myocardium or aorta can cause abscesses

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20
Q

What are some classic features of IE in a drug user?

A

Right sided valves involved

Staph aureus

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21
Q

What are symptoms of IE?

A

nonspecific - fever, weight loss, fatigue

Murmur with left-sided lesions

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22
Q

What are the organisms involved in IE?

A

S. viridans - valve abnormal
S. Aureus - normal valves, IV drug, abnormal valves
S. epidermidis - prosthetic valves
HACEK

23
Q

What is nonbacterial thrombotic endocarditis?

A

small, sterile thrombi on cardiac valve leaflets, along the line of closure
May be a source of emboli
Associated with malignancies (especially adenocarcinomas), sepsis, or catheter trauma

24
Q

What is Libman-Sacks disease?

A

endocarditis of SLE

Small fibrinous sterile vegetations on either side of valve leaflets

25
Q

what are the complications of prosthetic valves?

A

IE, occlusion
Mechanical - thromboembolic complications
Bioprosthetic - calcification or tears

26
Q

What is the most common type of cardiomyopathies?

A

dilated - 90%

27
Q

What are some causes of dilated cardiomyopathy?

A

Familial 30-50%: TTN, AD
Alcohol
Myocarditis
Cardiotoxic drugs: doxorubicin, cobalt, iron overload

28
Q

What is the morphology of DCM

A

Dilation of all chambers
Mural thrombi are common - LA and LV
Functional regurgitation of valves

29
Q

what is the clinical presentation of DCM

A

age 20-50
progressive CHF->dyspnea, exertional fatique, decrease EF (less than 40%)
Arrhythmias
Embolism

30
Q

What is takotsubo cardiomyopathy?

A

broken heart syndrome
Excess catecholamines following extreme emotional or psychological stress
Mostly women 58-75
Symptoms similar to MI
Apical ballooning of LV with abnormal wall motion and contractile dysfunction

31
Q

what is arrhythmogenic right ventricular cardiomyopathy?

A

right ventricular failure and arrhytmias
Myocardium of RV wal replaced by adipose and fibrosis
Desmosome gene involved at intercalated disc
Causes ventricular tachycardia and fibrillation, SCD
Familial - AD

32
Q

What is hypertrophic cardiomyopathy ?

A

genetic disorder leading to myocardial hypertrophy and diastolic dysfunction, leading to reduced SV and ventricular outflow obstruction
Mutation: b-myosin
collapse of young athlete

33
Q

What is the morphology of hypertrophic CM?

A

massive myocardial hypertrophy
Marked septal hypertrophy
Myocyte disarray
banana like ventricle

34
Q

What are the consequences of extensive hypertrophy with HCM?

A 
foci of myocardial ischemia 
left atrial dilation and mural thrombus
Diminished CO and Increased pulmonary congestion - extertional dyspnea
Arrhythmia 
SCD
35
Q

What is restrictive cardiomaypathy?

A

decreased ventricular compliance leading to diastolic dysfunction
may be secondary to deposition of material in wall (amyloid) or increased fibrosis (radiation)
Ventricles normal size but atria can be enlarged

36
Q

What is amyloid?

A

extracellular deposition of proteins which form an insoluble beta-pleated sheet
May be systemic (myeloma) or restricted to heart (transthyretin)
When in interstitium of myocardium->RCM
green in plain polarized light (congo red)

37
Q

What is myocarditis? what is it most commonly due to?

A

Inflammation of myocardium
Due to virus - Cox A and B
Lymphocyte infiltration
Other infections: trypanosomes (chagas), bacteria or fungi

38
Q

What is the single most common genetic cause of congenital HD. what are they at increased risk for?

A

Trisomy 21
40% of pts with own syndrome have at least 1 heart defect

Chronic illness and IE

39
Q

Describe atrial septal defect

A

L->
usually asymptomatic until adulthood
Most common congenital cardiac anomalies seen in adults
Fossa ovalis most common

40
Q

What can left to right shunting cause?

A

volume overload on right side -> pulmonary HTN, RHF, paradoxial embolization

41
Q

Describe ventricular septal defect/

A

L->R
most common form of congenital heart disease
Many small VSDs close spontaneously
Large VSDs may cause shunting -> RV hypertrophy, Pulm HTN which may reverse flow through shunt-> cyanosis

42
Q

Describe patent ductus arteriosis

A

L->R
may fail to close when infants are hypoxic, and/or have defects associated with increased pulmonary vascular pressure (VSD)
Harsh, machinery-like murmur
Large shunts increase pulmonary pressure and eventually shunt reversal and cyanosis

43
Q

What happens with persistent Left to right shunting?

A

pulmonary HTN forms
Causes Right to left shunting then cyanosis
= eisenmenger syndrome

44
Q

What causes cyanosis to be seen soon postnatally?

A

Right to left shunt

45
Q

Tetrology of Fallot?

A

VSD
Obstruction of RV outflow tract
Aorta overrides the VSD
RV hypertrophy

Boot shaped heart
Severity depends on subpulmonary stenosis

Right to left shunt with cyanosis

46
Q

What is transposition of great arteries?

A

results in two separate circuits when aorta goes to right atrium and pulmonary artery to left

1/3 have VSD
2/3 have PDA, or patent foramen ovale

right ventricle become hypertrophy

Left ventricle atrophies

Dies w/i few months

47
Q

What is coarctation of the aorta?

A

Narrowing of the aorta, generally seen with PDA in infants or w/o PDA in adults
M>F
Common in Turners syndrome
Cyanosis in lower half of body

48
Q

Coarctation without PDA

A

usually asymptomatic
HTN in upper extremities, Hypotension in LE
Claudication in cold LE
may see LV hypertrophy

49
Q

Myxomas

A

most common primary cardiac tumor in adults
Left atria
benign
mostly single

50
Q

Lipomas

A

well-circumscribed benign accumulation of adipose tissue

Left venticle, righ atrium or septum

51
Q

Papillary fibroelastomas

A 
sea-anemone-like lesions 
On valves 
can cause emboli 
usually incidental 
Core of myxoid
52
Q

Rhabdomyomas

A

most common primary heart tumor in children
Valvular or outflow tract obstruction
Half associated with tuberous sclerosis (TSC1/2)
spider clls

53
Q

Angiosarcoma

A

malignant neoplasm

Not distiinctive from counterparts in other locations

CVM II (4 decks)

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