Cardiac Pathology 2 Flashcards

(73 cards)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Chronic stenosis –> ____ overload hypertrophy

A

Pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Chronic insufficiency –> ____ overload hypertrophy

A

Volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Most common valve abnormality

Describe

A

Calcific aortic stenosis

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Causes of calcific stenosis

A

AGE, chronic HTN, hyperlipidemia, inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Female > 60, benign deposits on mitral valve

A

Mitral annular calcification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Potential dangers of mitral annular calcification (3)

A
  • Thrombus formation
  • Infective endocarditis
  • Mitral valve prolapse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

Mitral valve prlopase (back into L atrium in systole)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Mitral valve prolapse will show what on the valve?

A

Myxomatous degeneration (thick, rubbery, proteoglycan)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Rare dangers of mitral valve prolapse

A
  • Thrombi accumulation –> emboli
  • I.E.
  • Mitral insufficiency
  • Arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Typical presentation of mitral valve prolapse

A

Asymptomatic, maybe some angina/dyspnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Rheumatic fever - description

A

Inflammatory disorder AFTER group A strep pharyngeal infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Rheumatic heart disease - pathogenesis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Blood tests to confirm rheumatic fever

A

ASO, anti-DNase B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Symptoms of rheumatic fever

A
  • PANCARDITIS (focus here)
  • Migratory polyarthritis
  • SubQ nodules
  • Rash
  • SYDENHAM chorea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

Rheumatic fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Cardiac features of acute rheumatic fever

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

- Fibrinoid necrosis w/ verrucae (vegetations) of valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Cardiac features of chronic rheumatic heart disease

A
  • Mitral leaflet thickening
  • Fusion/thickening of tendinous cords
  • MITRAL STENOSIS (only cause of this)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

See mitral valve STENOSIS…

Think ______

A

Rheumatic heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Potential dangers of rheumatic heart disease

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

- Pulmonary congestion –> RIGHT heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Acute infective endocarditis - description
Organism?
Treatment?

A

Rapidly progressing, destruction of normal valve

- Staph. aureus
- Surgery + antibiotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
A valve with infective endocarditis will look how?
- Friable (crumply), bulky, vegetations
26
Vegetations in endocarditis are made of what?
Fibrin, inflammatory cells, and organisms
27
What might a SUBACUTE endocarditis vegetation have as well as fibrin, inflammatory cells, organisms?
Granulation tissue
28
Presentation of infective endocarditis
- NONSPECIFIC symptoms (fever, weight loss, fatigue) | - Murmur
29
A valve has small, sterile thrombi on cardiac valves along the line of closure. Name of this? Potential causes?
Nonbacterial thrombotic endocarditis - Malignancy (mucinous adenocarcinoma) - Sepsis - Catheter-induced endocardial trauma
30
2 cardiovascular things associated w/ mucinous adenocarcinomas
- Migratory thrombophlebitis | - Nonbacterial thrombotic endocarditis
31
Describe pathway following dilated L atrium
A fib --> mural thrombosis --> thromboembolism
32
L atrial dilation is always present in what class of diseases?
Cardiomyopathy
33
3 types of cardiomyopathy
- Dilated - Hypertrophic - Restrictive
34
Most common type of cardiomyopathy
Dilated cardiomyopathy (90%)
35
Dilated cardiomyopathy... Genetics? Causes?
- Titin (TTN) mutation - Autosomal dominant - Alcohol, myocarditis, doxorubicin, iron overload (hemoch.)
36
Titin protein
Limits sarcomere stretch | - Deficient in dilated cardiomyopathy (familial)
37
Dilated cardiomyopathy - presentation
20-50, dyspnea, exertional fatigue, decreased EF, arrhythmias, mural thromboembolism, functional regurg. murmur
38
Arrhythmogenic RV cardiomyopathy - description and potential result Genetic?
- Myocardium of RV wall REPLACED by ADIPOSE and FIBROSIS --> V tach. and V fib. --> SUDDEN DEATH Autosomal dominant
39
Hypertrophic cardiomyopathy - description Genetic?
Genetic disorder --> Myocardial hypertrophy and DIASTOLIC dysfunction --> lower SV, outflow obstruction Beta-myosin heavy chain
40
MASSIVE left ventricular hypertrophy (including septum), with microscopic MYOCYTE DISARRAY
Hypertrophic cardiomyopathy
41
Consequences of long term hypertrophic cardiomyopathy (morphologic, pathologic, presentation)
- Foci of ischemia - L atrial dilation --> mural thrombus - Pulmonary congestion --> exertional dyspnea - Arrrhythmias - SUDDEN DEATH
42
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?
Restrictive cardiomyopathy | - Amyloid or post-radiation fibrosis w/in the wall
43
Amyloidosis
Restrictive cardiomyopathy
44
Radiation --> diastolic heart dysfunction, atria enlarged
Restrictive cardiomyopathy
45
Insoluble beta-pleated sheet deposits
Amyloid
46
Causes of amyloid deposits
- Multiple myeloma (systemic deposition) | - Transthyretin mutation (heart-localized deposition)
47
Deposition of transthyretin in the ____ results in a restrictive cardiomyopathy
Interstitium of the myocardium (between myocardial cells)
48
See myocarditis (inflammation w/in muscle wall)... Think _____
Coxsackie A/B viruses
49
See myocarditis plus travel history to S. America... Think _____
Trypanosomes (Chagas disease)
50
NON-infectious causes of myocarditis
IMMUNE-Mediated Reactions | - Rheumatic fever, SLE, drug hypersensitivity
51
See eosinophilic myocarditis... Think _____
Hypersensitivity reaction
52
See lymphocytic (B/T cells) myocarditis... Think _____
Viral (Coxsackie)
53
Most common cause of congenital heart disease
Trisomy 21 (Down syndrome)
54
Atrial septal defect - describe resulting path.
L to R shunt --> R side volume overload --> pulmonary hypertension, R heart failure
55
Unique potentially lethal complication w/ atrial septal defect
Paradoxical embolization (ex. DVT --> L side --> stroke, etc.)
56
Most common form of congenital heart disease
Ventricular septal defect
57
Small vs. large VSD
Small - close spontaneously | Large - L to R shunt
58
Morphologic and symptomatic findings w/ large VSD
- R ventricular hypertrophy (via L to R shunt) | - Pulmonary hypertension
59
A patient has a VSD and starts turning blue. Cause?
Pulmonary HTN from L to R shunt --> increased R-side pressure --> REVERSED R to L shunt --> CYANOSIS
60
Child w/ harsh, machinery-like murmur
Patent ductus arteriosus
61
Cause of patent ductus arteriosus
Hypoxic infant and/or increased pulmonary vascular pressure (LIKE W/ A VSD)
62
Effect of a PDA is determined by the _____ Explain.
DIAMETER - large shunt = increased pulmonary pressure = shunt reversal = CYANOSIS
63
How is a VSD similar to a PDA?
Both are initially L to R shunts, but can reverse to R to L with significant pulmonary HTN and cause CYANOSIS
64
2 types of initial R to L shunts
- Tetralogy of Fallot | - Transposition of great arteries
65
Tetralogy of Fallot
- VSD - Obstructed pulmonary valve/outflow - Aorta overrides via pumping deox. blood from RV - RV hypertrophy
66
Classic description of Tetralogy of Fallot - imaging
Boot-shaped (via RVH)
67
Clinical severity of Tetralogy of Fallot depends on ____
Degree of pulmonary stenosis
68
What is required for any life w/ transposition of great arteries?
A shunt (VSD, PDA, patent FO) - to mix blood btwn circuits
69
Treatment for transposition of great arteries?
Corrective surgery - needed for survival
70
Morphology of transposition of great arteries
- RVH | - LV atrophy
71
Coarctation of aorta: infant vs. adult Which is worse?
``` Infant = w/ PDA Adult = w/o PDA ``` Infant (PDA) --> cyanosis
72
Adult w/ coarctation of aorta - presentation and morphology
- HTN in UEs, hypotension LEs | - Concentric LV hypertrophy, narrowing at lig. arteriosum
73
Why are lower extremities cold and hypotensive w/ coarctation of aorta?
Blood flow compromised beyond site of narrowing