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DT3- EXAM 1 > Cardiomyopathy/Pericardial Disease- Melissa (6)* > Flashcards

Cardiomyopathy/Pericardial Disease- Melissa (6)* Flashcards

1
Q

What are the three types of cardiomyopathy?

A
  1. Dilated
  2. Hypertrophic
  3. Restrictive (as in pericarditis)
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2
Q

5 characteristics associated with Dilated Cardiomyopathy

A
  1. Cardiac hypertrophy (2-3 x heavier)
  2. Dilation of all 4 chambers
  3. Contractile dysfunction (actin/ myosin overstretch)
  4. Valvular insufficiency (due to chamber dilation)
  5. Mural thrombi = common
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3
Q

What are two complications NOT associated with dilated cardiomyopathy?

A

NO valvular alteration & NO significant CAD

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4
Q

1 cause of dilated cardiomyopathy + 5 others:

A 
"The ABCD&G's of DCM:
Alcohol
Baby-carriers (pregnancy)
Coxsackie
Doxorubicin ("cardiotoxorubicin") 
Genetic.... but #1 is idiopathic"
*Love this.
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5
Q

2 Histological findings with dilated cardiomyopathy:

A
  1. hypertrophied myocardial fibers

2. ^ interstitial fibrosis

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6
Q

When does dilated cardiomyopathy (DCM) occur?
How does it present?
What is the prognosis?

A

Occurs at any age; presents with insidious CHF
50% dead in 2 years
25% live 5+ years

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7
Q

What are the 3 causes of death induced by DCM?

A

Progressive CHF; Fatal Arrhythmia; Mural thrombus

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8
Q

What are the treatments for cardiomyopathy of any kind?

A

Transplant

- If hypertrophic CM, may consider removal of septal tissue, medicines to relax ventricle

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9
Q

What are some characteristics of Hypertrophic cardiomyopathy (HCM) (4)

A
  1. Massive hypertrophy, NO DILATION
  2. Abnormal diastolic filling
  3. Intermittent LV outflow/ aortic valve obstrxn (30%)
  4. Hypercontraction (preserved systolic fxn.)
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10
Q

Where in the heart does HCM typically manifest most severely?

A

Asymmetric septal hypertrophy–most prominent in sub aortic region (LV)

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11
Q

Are the valves involved in HCM? If so, which ones and how?

A
  1. septal hypertrophy bulges into aortic valve
    (LV outflow obstructed)
  2. thickened anterior mitral valve leaflet
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12
Q

Histological changes associated with HCM (3):

A
  1. myocyte hypertrophy
  2. “haphazard” array of myocyte bundles
  3. ^ interstitial + replacement fibrosis
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13
Q

Describe the pathogenesis of HCM:

A

100% genetic!

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14
Q

Briefly describe how HCM will compromise SV (2):

A
  1. Smaller chamber + thicker wall–> Poor compliance–> CAN’T FILL LV–> DECREASE SV
  2. Subaortic septal hypertrophy–> Obstruction of Aortic valve–> DECREASE SV
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15
Q

How will patients with HCM present to the clinic (2)?
Do most patients with HCM have sx?
What causes these sx.?

A

MOST ARE ASYMPTOMATIC!

  1. Exertional dyspnia
    - Decreased CO
    - ^ Pulmonary venous pressure
  2. Anginal Pain
    - Focal ischemia
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16
Q

Major complications of HCM (5):

A
  1. Sudden Cardiac Death (athletes)***
  2. A fib–> mural thrombi–> embolism!***
  3. V ventricular arrythmia
  4. infective endocarditis in mitral valve
  5. Intractable CHF
17
Q

What is the #1 cause of myocarditis in the US?

What is one South American cause?

A 
#1 Viral: Coxackie A, B 
2. Trypanosome Cruzi (Chagas Disease)
18
Q

What is the primary cause of myocardial injury in the case of myocarditis?

A

Inflammation, of course! (vs. ischemia in cardiomyopathy)

19
Q

Describe the gross morphology of a heart with myocarditis (3):

A
  • normal or dilated
  • flabby myocardium
  • mural thrombi (in any chamber)
20
Q

Describe the microscopic path associated with myocarditis (2):

A
  • mononuclear infiltrate
  • focal necrosis

(Reminds me of MI presentation during 1st week)

21
Q

How does myocarditis present clinically?

What is the prognosis?

A
  • broad spectrum of severity (asymptomatic–> SCD)

- if it clears up, it will leave fibrotic lesions

22
Q

How much pericardial fluid does a healthy person have?

A

30-50 ml thin, straw colored fluid

23
Q

What happens LESS THAN 500ml fluid accumulate slowly in the pericardial sac?

A

globular enlargment–no tamponade

24
Q

What is cardiac tamponade and when does it occur (2)?

A

Restriction of cardiac filling by pericardial pressure!
1. MORE than 500ml fluid accumulate slowly in pericardial sac

  1. ANY AMOUNT of fluid accumulates rapidly in pericardial sac
25
Q

Is pericardial inflammation typically primary or secondary?

What is the most common cause of primary pericarditis?

A
  • typically secondary

- most common cause of primary pericarditis = viral infxn.

26
Q

Describe the morphology of serous pericarditis:
3 cells in infiltrate?
Where are they found?

A
  • serous fluid only (no fibrinous exudate)
  • neutrophils, lymphs, histiocytes
  • epicardial and pericardial surfaces

BUT this is not infectious, despite presence of neutros.

27
Q

What type of cellular infiltrate is associated with CHRONIC pericarditis?

A

JUST lymphocytes (serous)

28
Q

What is the most common type of pericarditis?

A

Serofibrinous pericarditis

29
Q

Describe the morphology of serofibrinous pericarditis

2

A

Looks like “bread and butter”

  • thick, yellow, ~ bloody serous fluid
  • fibrinous exudate
30
Q

Describe the morphology of fibrinous pericarditis:

A

dry surface with fine granular roughening

31
Q

What are three clinical exam findings associated with serofibrinous pericarditis?

A
  1. Pericardial friction rub
  2. ST elevation on EKG
  3. Pain that is relieved by sitting up.
32
Q

What are 6 causes of serofibrinous pericarditis?

A

acute MI (2-3 days later); uremia (aka renal disease); SLE; rheumatic fever; surgery/ trauma; chest radiation

**BASICALLY: anything but infection is possible– this isn’t infectious!!– & know uremia/renal disease. That’s high yield.

33
Q

What is the most common cause of purulent pericarditis?
Describe the exudate.
How does it present clinically?

A
  • Caused by infection (mostly bacterial)
  • PUS: 400-500ml thin/ creamy yellow (acute inflammation)
  • Presents like fibrinous pericarditis + signs of infection (fever, etc.)
34
Q

Describe the exudate found in hemorrhagic pericarditis.
What are the two diseases that cause this?
How does it present?

A
  • Blood+ fibrinous or suppurative effusion
  • CAUSED BY:
    1. TB
    2. MALIGNANCY
  • Presents like fibrinous or suppurative pericarditis
35
Q

What is left when pericarditis heals?

Is cardiac function typically impaired?

A
  • Healed pericarditis–> ADHESIVE pericarditis
  • No Hypertrophy/ dilation of the heart
  • Causes constrictive pericarditis; RARELY complications
36
Q

Describe clinical findings of constrictive pericarditis (1).
How is it treated if cardiac function is impaired?

A
  1. quiet heart sounds

2. Pericardectomy: surgical removal of pericardium if function is impaired

DT3- EXAM 1 (26 decks)

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