Cardiomyopathy/Pericardial Disease- Melissa (6)* Flashcards
What are the three types of cardiomyopathy?
- Dilated
- Hypertrophic
- Restrictive (as in pericarditis)
5 characteristics associated with Dilated Cardiomyopathy
- Cardiac hypertrophy (2-3 x heavier)
- Dilation of all 4 chambers
- Contractile dysfunction (actin/ myosin overstretch)
- Valvular insufficiency (due to chamber dilation)
- Mural thrombi = common
What are two complications NOT associated with dilated cardiomyopathy?
NO valvular alteration & NO significant CAD
1 cause of dilated cardiomyopathy + 5 others:
"The ABCD&G's of DCM:
Alcohol
Baby-carriers (pregnancy)
Coxsackie
Doxorubicin ("cardiotoxorubicin")
Genetic.... but #1 is idiopathic"
*Love this.2 Histological findings with dilated cardiomyopathy:
- hypertrophied myocardial fibers
2. ^ interstitial fibrosis
When does dilated cardiomyopathy (DCM) occur?
How does it present?
What is the prognosis?
Occurs at any age; presents with insidious CHF
50% dead in 2 years
25% live 5+ years
What are the 3 causes of death induced by DCM?
Progressive CHF; Fatal Arrhythmia; Mural thrombus
What are the treatments for cardiomyopathy of any kind?
Transplant
- If hypertrophic CM, may consider removal of septal tissue, medicines to relax ventricle
What are some characteristics of Hypertrophic cardiomyopathy (HCM) (4)
- Massive hypertrophy, NO DILATION
- Abnormal diastolic filling
- Intermittent LV outflow/ aortic valve obstrxn (30%)
- Hypercontraction (preserved systolic fxn.)
Where in the heart does HCM typically manifest most severely?
Asymmetric septal hypertrophy–most prominent in sub aortic region (LV)
Are the valves involved in HCM? If so, which ones and how?
- septal hypertrophy bulges into aortic valve
(LV outflow obstructed) - thickened anterior mitral valve leaflet
Histological changes associated with HCM (3):
- myocyte hypertrophy
- “haphazard” array of myocyte bundles
- ^ interstitial + replacement fibrosis
Describe the pathogenesis of HCM:
100% genetic!
Briefly describe how HCM will compromise SV (2):
- Smaller chamber + thicker wall–> Poor compliance–> CAN’T FILL LV–> DECREASE SV
- Subaortic septal hypertrophy–> Obstruction of Aortic valve–> DECREASE SV
How will patients with HCM present to the clinic (2)?
Do most patients with HCM have sx?
What causes these sx.?
MOST ARE ASYMPTOMATIC!
- Exertional dyspnia
- Decreased CO
- ^ Pulmonary venous pressure - Anginal Pain
- Focal ischemia
Major complications of HCM (5):
- Sudden Cardiac Death (athletes)***
- A fib–> mural thrombi–> embolism!***
- V ventricular arrythmia
- infective endocarditis in mitral valve
- Intractable CHF
What is the #1 cause of myocarditis in the US?
What is one South American cause?
#1 Viral: Coxackie A, B 2. Trypanosome Cruzi (Chagas Disease)
What is the primary cause of myocardial injury in the case of myocarditis?
Inflammation, of course! (vs. ischemia in cardiomyopathy)
Describe the gross morphology of a heart with myocarditis (3):
- normal or dilated
- flabby myocardium
- mural thrombi (in any chamber)
Describe the microscopic path associated with myocarditis (2):
- mononuclear infiltrate
- focal necrosis
(Reminds me of MI presentation during 1st week)
How does myocarditis present clinically?
What is the prognosis?
- broad spectrum of severity (asymptomatic–> SCD)
- if it clears up, it will leave fibrotic lesions
How much pericardial fluid does a healthy person have?
30-50 ml thin, straw colored fluid
What happens LESS THAN 500ml fluid accumulate slowly in the pericardial sac?
globular enlargment–no tamponade
What is cardiac tamponade and when does it occur (2)?
Restriction of cardiac filling by pericardial pressure!
1. MORE than 500ml fluid accumulate slowly in pericardial sac
- ANY AMOUNT of fluid accumulates rapidly in pericardial sac
Is pericardial inflammation typically primary or secondary?
What is the most common cause of primary pericarditis?
- typically secondary
- most common cause of primary pericarditis = viral infxn.
Describe the morphology of serous pericarditis:
3 cells in infiltrate?
Where are they found?
- serous fluid only (no fibrinous exudate)
- neutrophils, lymphs, histiocytes
- epicardial and pericardial surfaces
BUT this is not infectious, despite presence of neutros.
What type of cellular infiltrate is associated with CHRONIC pericarditis?
JUST lymphocytes (serous)
What is the most common type of pericarditis?
Serofibrinous pericarditis
Describe the morphology of serofibrinous pericarditis
2
Looks like “bread and butter”
- thick, yellow, ~ bloody serous fluid
- fibrinous exudate
Describe the morphology of fibrinous pericarditis:
dry surface with fine granular roughening
What are three clinical exam findings associated with serofibrinous pericarditis?
- Pericardial friction rub
- ST elevation on EKG
- Pain that is relieved by sitting up.
What are 6 causes of serofibrinous pericarditis?
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.
What is the most common cause of purulent pericarditis?
Describe the exudate.
How does it present clinically?
- Caused by infection (mostly bacterial)
- PUS: 400-500ml thin/ creamy yellow (acute inflammation)
- Presents like fibrinous pericarditis + signs of infection (fever, etc.)
Describe the exudate found in hemorrhagic pericarditis.
What are the two diseases that cause this?
How does it present?
- Blood+ fibrinous or suppurative effusion
- CAUSED BY:
1. TB
2. MALIGNANCY - Presents like fibrinous or suppurative pericarditis
What is left when pericarditis heals?
Is cardiac function typically impaired?
- Healed pericarditis–> ADHESIVE pericarditis
- No Hypertrophy/ dilation of the heart
- Causes constrictive pericarditis; RARELY complications
Describe clinical findings of constrictive pericarditis (1).
How is it treated if cardiac function is impaired?
- quiet heart sounds
2. Pericardectomy: surgical removal of pericardium if function is impaired
