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Cardiovascular 2 > Cardiac Pathology 2 > Flashcards

Cardiac Pathology 2 Flashcards

1
Q

2 main types of valvular disease (what are they?)

Both cause what?

A
  • Stenosis (doesn’t open)
  • Insufficiency (doesn’t close)

Both –> Hypertrophy

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2
Q

Chronic stenosis –> ____ overload hypertrophy

A

Pressure

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3
Q

Chronic insufficiency –> ____ overload hypertrophy

A

Volume

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4
Q

Most common valve abnormality

Describe

A

Calcific aortic stenosis

Valves have osteoblast-like cells –> osteoid substance –> mounded calcifications prevent complete opening

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5
Q

Causes of calcific stenosis

A

AGE, chronic HTN, hyperlipidemia, inflammation

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6
Q

Female > 60, benign deposits on mitral valve

A

Mitral annular calcification

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7
Q

Potential dangers of mitral annular calcification (3)

A
  • Thrombus formation
  • Infective endocarditis
  • Mitral valve prolapse
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8
Q

Female, incidental mid-systolic click in L-side of heart

A

Mitral valve prlopase (back into L atrium in systole)

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9
Q

Mitral valve prolapse will show what on the valve?

A

Myxomatous degeneration (thick, rubbery, proteoglycan)

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10
Q

While often incidental, what can secondarily cause mitral valve prolapse?

A

Dilated hypertrophy (valve insufficiency, volume overload, contractility deficit) –> stretches valve, can’t close

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11
Q

Rare dangers of mitral valve prolapse

A
  • Thrombi accumulation –> emboli
  • I.E.
  • Mitral insufficiency
  • Arrhythmias
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12
Q

Typical presentation of mitral valve prolapse

A

Asymptomatic, maybe some angina/dyspnea

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13
Q

Rheumatic fever - description

A

Inflammatory disorder AFTER group A strep pharyngeal infection

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14
Q

Rheumatic heart disease - pathogenesis

A

Immune response to strep M proteins –> cross-react with cardiac (and other) self-antigens

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15
Q

Blood tests to confirm rheumatic fever

A

ASO, anti-DNase B

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16
Q

Symptoms of rheumatic fever

A
  • PANCARDITIS (focus here)
  • Migratory polyarthritis
  • SubQ nodules
  • Rash
  • SYDENHAM chorea
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17
Q

Heart inflammation, random moving joint pains, skin rash and nodules, random unplanned movements

A

Rheumatic fever

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18
Q

Cardiac features of acute rheumatic fever

A
  • Pancarditis w/ Aschoff bodies (T cells and macrophages)

- Fibrinoid necrosis w/ verrucae (vegetations) of valves

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19
Q

Cardiac features of chronic rheumatic heart disease

A
  • Mitral leaflet thickening
  • Fusion/thickening of tendinous cords
  • MITRAL STENOSIS (only cause of this)
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20
Q

See mitral valve STENOSIS…

Think ______

A

Rheumatic heart disease

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21
Q

Potential dangers of rheumatic heart disease

A
  • L atrial enlargement –> A. fib, thrombosis

- Pulmonary congestion –> RIGHT heart failure

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22
Q

Acute infective endocarditis - description
Organism?
Treatment?

A

Rapidly progressing, destruction of normal valve

- Staph. aureus
- Surgery + antibiotics
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23
Q

Subacute infective endocarditis - description
Example of pre-existing condition?
Treatment?

A

Slow-progressing infection of PREVIOUSLY DEFORMED valve

 - Ex. via chronic rheumatic heart disease
 - Treat w/ antibiotics alone
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24
Q

Predisposing factors for infective endocarditis

A
  • Valvular abnormalities
    • RHD, prosthetic valve, MV prolapse, calcific stenosis, bicuspid aortic valve
  • Bacteremia
    • Infection, dental work, needles/drugs, skin scrape
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25
Q

A valve with infective endocarditis will look how?

A
  • Friable (crumply), bulky, vegetations
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26
Q

Vegetations in endocarditis are made of what?

A

Fibrin, inflammatory cells, and organisms

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27
Q

What might a SUBACUTE endocarditis vegetation have as well as fibrin, inflammatory cells, organisms?

A

Granulation tissue

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28
Q

Presentation of infective endocarditis

A
  • NONSPECIFIC symptoms (fever, weight loss, fatigue)

- Murmur

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29
Q

A valve has small, sterile thrombi on cardiac valves along the line of closure. Name of this?

Potential causes?

A

Nonbacterial thrombotic endocarditis

  • Malignancy (mucinous adenocarcinoma)
  • Sepsis
  • Catheter-induced endocardial trauma
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30
Q

2 cardiovascular things associated w/ mucinous adenocarcinomas

A
  • Migratory thrombophlebitis

- Nonbacterial thrombotic endocarditis

31
Q

Describe pathway following dilated L atrium

A

A fib –> mural thrombosis –> thromboembolism

32
Q

L atrial dilation is always present in what class of diseases?

A

Cardiomyopathy

33
Q

3 types of cardiomyopathy

A
  • Dilated
  • Hypertrophic
  • Restrictive
34
Q

Most common type of cardiomyopathy

A

Dilated cardiomyopathy (90%)

35
Q

Dilated cardiomyopathy…
Genetics?
Causes?

A
  • Titin (TTN) mutation
  • Autosomal dominant
  • Alcohol, myocarditis, doxorubicin, iron overload (hemoch.)
36
Q

Titin protein

A

Limits sarcomere stretch

- Deficient in dilated cardiomyopathy (familial)

37
Q

Dilated cardiomyopathy - presentation

A

20-50, dyspnea, exertional fatigue, decreased EF, arrhythmias, mural thromboembolism, functional regurg. murmur

38
Q

Arrhythmogenic RV cardiomyopathy - description and potential result

Genetic?

A
  • Myocardium of RV wall REPLACED by ADIPOSE and FIBROSIS –> V tach. and V fib. –> SUDDEN DEATH

Autosomal dominant

39
Q

Hypertrophic cardiomyopathy - description

Genetic?

A

Genetic disorder –> Myocardial hypertrophy and DIASTOLIC dysfunction –> lower SV, outflow obstruction

Beta-myosin heavy chain

40
Q

MASSIVE left ventricular hypertrophy (including septum), with microscopic MYOCYTE DISARRAY

A

Hypertrophic cardiomyopathy

41
Q

Consequences of long term hypertrophic cardiomyopathy (morphologic, pathologic, presentation)

A
  • Foci of ischemia
  • L atrial dilation –> mural thrombus
  • Pulmonary congestion –> exertional dyspnea
  • Arrrhythmias
  • SUDDEN DEATH
42
Q

A patient has increased stiffness of the ventricle, leading to diastolic dysfunction. BOTH atria are enlarged. What is this? Why are the ventricular walls stiff?

A

Restrictive cardiomyopathy

- Amyloid or post-radiation fibrosis w/in the wall

43
Q

Amyloidosis

A

Restrictive cardiomyopathy

44
Q

Radiation –> diastolic heart dysfunction, atria enlarged

A

Restrictive cardiomyopathy

45
Q

Insoluble beta-pleated sheet deposits

A

Amyloid

46
Q

Causes of amyloid deposits

A
  • Multiple myeloma (systemic deposition)

- Transthyretin mutation (heart-localized deposition)

47
Q

Deposition of transthyretin in the ____ results in a restrictive cardiomyopathy

A

Interstitium of the myocardium (between myocardial cells)

48
Q

See myocarditis (inflammation w/in muscle wall)…

Think _____

A

Coxsackie A/B viruses

49
Q

See myocarditis plus travel history to S. America…

Think _____

A

Trypanosomes (Chagas disease)

50
Q

NON-infectious causes of myocarditis

A

IMMUNE-Mediated Reactions

- Rheumatic fever, SLE, drug hypersensitivity

51
Q

See eosinophilic myocarditis…

Think _____

A

Hypersensitivity reaction

52
Q

See lymphocytic (B/T cells) myocarditis…

Think _____

A

Viral (Coxsackie)

53
Q

Most common cause of congenital heart disease

A

Trisomy 21 (Down syndrome)

54
Q

Atrial septal defect - describe resulting path.

A

L to R shunt –> R side volume overload –> pulmonary hypertension, R heart failure

55
Q

Unique potentially lethal complication w/ atrial septal defect

A

Paradoxical embolization (ex. DVT –> L side –> stroke, etc.)

56
Q

Most common form of congenital heart disease

A

Ventricular septal defect

57
Q

Small vs. large VSD

A

Small - close spontaneously

Large - L to R shunt

58
Q

Morphologic and symptomatic findings w/ large VSD

A
  • R ventricular hypertrophy (via L to R shunt)

- Pulmonary hypertension

59
Q

A patient has a VSD and starts turning blue. Cause?

A

Pulmonary HTN from L to R shunt –> increased R-side pressure –> REVERSED R to L shunt –> CYANOSIS

60
Q

Child w/ harsh, machinery-like murmur

A

Patent ductus arteriosus

61
Q

Cause of patent ductus arteriosus

A

Hypoxic infant and/or increased pulmonary vascular pressure (LIKE W/ A VSD)

62
Q

Effect of a PDA is determined by the _____

Explain.

A

DIAMETER - large shunt = increased pulmonary pressure = shunt reversal = CYANOSIS

63
Q

How is a VSD similar to a PDA?

A

Both are initially L to R shunts, but can reverse to R to L with significant pulmonary HTN and cause CYANOSIS

64
Q

2 types of initial R to L shunts

A
  • Tetralogy of Fallot

- Transposition of great arteries

65
Q

Tetralogy of Fallot

A
  • VSD
  • Obstructed pulmonary valve/outflow
  • Aorta overrides via pumping deox. blood from RV
  • RV hypertrophy
66
Q

Classic description of Tetralogy of Fallot - imaging

A

Boot-shaped (via RVH)

67
Q

Clinical severity of Tetralogy of Fallot depends on ____

A

Degree of pulmonary stenosis

68
Q

What is required for any life w/ transposition of great arteries?

A

A shunt (VSD, PDA, patent FO) - to mix blood btwn circuits

69
Q

Treatment for transposition of great arteries?

A

Corrective surgery - needed for survival

70
Q

Morphology of transposition of great arteries

A
  • RVH

- LV atrophy

71
Q

Coarctation of aorta: infant vs. adult

Which is worse?

A 
Infant = w/ PDA
Adult = w/o PDA

Infant (PDA) –> cyanosis

72
Q

Adult w/ coarctation of aorta - presentation and morphology

A
  • HTN in UEs, hypotension LEs

- Concentric LV hypertrophy, narrowing at lig. arteriosum

73
Q

Why are lower extremities cold and hypotensive w/ coarctation of aorta?

A

Blood flow compromised beyond site of narrowing

Cardiovascular 2 (20 decks)

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