Myocarditis Flashcards

1
Q

dilated cardiomyopathy: clinical associated

A

-gradual development of cardiac failure
-4-chamber hypertrophy and dilatation
-20% -50% genetic, familial
-myocardial degeneration - defect in force generation,
force transmission and/or signaling
-common end pathway for a variety of myocardial insults
-suspected etiologies:
-alcohol or other toxicities
-previous myocarditis
-pregnancy associated with nutritional deficiency or immunologic

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2
Q

primary abnormality

A

impairment of left ventricular function; end

stage ejection fraction <25% (systolic failure)

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3
Q

dilated cardiomyopathy characteristics

A
  • may occur at any stage age, usually 20-60
  • clinical picture: slowly developing CHF
  • may have precipitous decomposition, 50% die in 2 years
  • need transplant
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4
Q

etiologist for dilated cardiomyopathy

A
  • alcohol, chemotherapeutic agents (doxorubicin/Adriamycin)

- Familial (25-35%): muscular dystrophy, cytoskeletal

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5
Q

morphology of dilated cardiomyopathy

A

large,”globular” dilated hearts 2-3X normal size
-all chambers involved; wall thickness may be = normal
-mural thrombi common, especially near apex of
ventricles, atria
-functional mitral or tricuspid regurgitation
-left ventricle - patchy subendocardial scars; ?ischemic
-histology - most myofibers hypertrophied, stretched,
vacuolization
-interstitial and endocardial fibrosis; REPLACEMENT
fibrosis

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6
Q

alcohol

A

-most common cause of dilated cardiomyopathy
-ETOH or its metabolites (acetaldehyde) has direct toxic
effect
-may be complicated by thiamin deficiency (beriberi heart
disease)

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7
Q

toxic, metabolic, and other

A
alcohol
hyperthyroidism, hypothyroidism
peripartum state (pregnancy) 
adriamycin and other drugs
catecholamines
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8
Q

pregnancy

A
  • globally dilated heart
  • ?due to hypertension, volume overload
  • nutritional deficiency
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9
Q

adriamycin and other drugs

A

-anthracycline chemotherapeutic agents doxorubicin,
daunorubicin - dose dependent
-also lithium, phenothiazines, cocaine
-attributed to lipid peroxidation of myofiber membranes
-myofiber swelling and vacuolization
-usually resolves on discontinuation of drug

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10
Q

catecholamines

A
  • pheochromocytoma - contraction band necrosis

- also dopamine, cocaine

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11
Q

where else are contraction bands necrosis

A

seen with reperfusion injury
cocaine
catecholamines

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12
Q

hypertrophic cardiomyopathy

A

-Idiopathic hypertrophic subaortic stenosis -IHSS
-Hypertrophic obstructive cardiomyopathy
-non-hypertensive heaving muscular hyper-contracting
heart
-100% genetic – defects in sarcomeric proteins
-Autosomal dominant with variable penetrance
-Missense mutations
-sometimes try surgical reduction of septum

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13
Q

problems hypertrophic cardiomyopathy

A

atrial fibrillation, endocarditis, sudden death

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14
Q

what causes the heart failure seen with hypertrophic cardiomyopathy

A

-heart failure due to decrease in chamber size, poor

compliance with decreased stroke volume (diastolic failure)

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15
Q

what is seen with hypertrophic cardiomyopathy

A

-massive myocardial hypertrophy
-IHSS: disproportionate thickening of ventricular septum;
asymmetric hypertrophy (10% symmetric)
-jet lesions
-endocardial thickening/mural plaque formation of left
ventricular outflow tract; thickening of anterior mitral
leaflet 2° to contact with septum during systole

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16
Q

histology of hypertrophic cardiomyopathy

A

-extensive myocyte hypertrophy; myocyte diameter >40 um
(normal 15 um)
-myofiber disarray; interstitial and replacement fibrosis

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17
Q

glycogen storage disease

A

pompe’s disease

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18
Q

pompe’s disease

A
  1. acid alpha-glucosidase deficiency
    - accumulation of normal glycogen in cells
  2. heart failure in infants
    - also juvenile, adult forms
  3. restrictive heart disease
    - left ventricular hypertrophy with outflow obstruction
    - death from heart failure by age 1
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19
Q

restrictive cardiomyopathy: clinical associations

A

-also a diastolic disorder
-diastolic relaxation and left ventricular filling impeded by
inability of myocardium to expand
-contractile (systolic) function of ventricle usually unaffected
-results from infiltrative diseases such as amyloidosis,
hemachromatosis, leukemia, or storage diseases
-also radiation fibrosis, constrictive pericarditis
-endocardial fibrosis

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20
Q

restrictive cardiomyopathy causes

A
amyloidosis 
iron overload (hemachromatosis, hemosiderosis)
21
Q

restrictive cardiomyopathy: amyloidosis

A

-may be part of systemic amyloidosis or only affect
heart, particularly with senile isolated cardiac
amyloidosis
-two forms: ventricular (transthyretin) and atrial

22
Q

restrictive cardiomyopathy: iron overload

A

-more prominent in ventricles than atria
-interferes with metal-dependent enzyme systems
-accumulation of hemosiderin within cardiac myocytes (in
contrast to extracellular amyloid)

23
Q

variant forms of restrictive cardiomyopathy

A

endomyocardial fibrosis
Loeffler’s endomyocarditis
Endocardial fibroelastosis

24
Q

endomyocardial fibrosis

A

-children, young adults in Africa and tropical countries
-fibrosis or ventricular endocardium and
subendocardium
-extends from apex to inflow tract of rt/lt ventricles
-may involve mitral, tricuspid valves
-ventricular mural thrombi

25
Q

Loeffler’s endomyocarditis

A
  • similar to endocardial fibrosis but unrestricted to specific geographic area
  • EOSINOPHILS, leukocytosis
  • involvement of other organs
  • eosinophils appear to be functionally abnormal
26
Q

Endocardial fibroelastosis

A

-focal or diffuse cartilage-like fibroelastic thickening
-first 2 yrs
-often associated with congenital abnormalities (aortic valve
obstruction)
-remove thickened endocardium (“strip out”)

27
Q

myocarditis causes

A

viral

28
Q

who is invulnerable for myocarditis

A

infants
immunosuppressed
pregnant

29
Q

viruses common for myocarditis

A
coxsackie virus B
ECHO
polio
influenza A/B
*occurs days to weeks after primary viral infection
30
Q

morphology of myocarditis

A

-diffuse or patchy involvement; heart may be normal or
dilated
-interstitial mononuclear, predominantly lymphocytic
inflammatory infiltrate; focal necrosis (not typical of
ischemic necrosis): not all myocardial inflammation denotes
myocarditis
-organism-specific lesions, microabscesses

31
Q

variants of myocarditis

A

hypersensitivity myocarditis-> eosinophils

giant cell myocarditis-> associated with poorer prognosis

32
Q

non viral myocarditis

A
chagas
lyme disease
trichinosis
AIDS
Corynebacterium diptheriae
33
Q

myocarditis: chagas

A

-Trypanosoma cruzi; endemic in South America; increasing in North America; myocardial involvement found in 80%; 10% die during acute attack

34
Q

myocarditis: Corynebacterium diptheriae

A

(exotoxin); patchy myocytenecrosis with only sparse lymphocytic infiltrate

35
Q

myocarditis: AIDS

A
  • Inflammation/myocyte damage without a clear etiologic agent
  • ?myocarditis caused directly by HIV or by opportunistic pathogen
36
Q

pericardial sac

A

-potential space, usually hold 50-60 ml serous fluid
-lined on both sides with mesothelial layers of the serous
pericardium
-reflection of pericardium which covers the surface is call
the visceral layer or epicardium
-the layer forming the other side of the sac is called the
parietal layer
-heart and serous pericardium are encased several
layers of the fibrous pericardium

37
Q

pericardial disease

A

-Almost always associated with disease in other
portions of the heart or surrounding structures
-Accumulations of fluid
-normally 30-50 ml thin, clear, straw-colored, translucent
fluid
-pericardial effusions rarely exceed 500 ml
-if slow, little clinical significance
-if rapid, interfere with diastolic filling

38
Q

serous pericarditis

A

-non-infectious inflammation (RF, systemic lupus, scleroderma, tumors); viral infections

39
Q

most frequent type of pericarditis

A

Fibrinous and serofibrinous pericarditis

40
Q

what is seen with Fibrinous and serofibrinous pericarditis

A
  1. myocardial infarction, Dressler’s syndrome (autoimmune conditions
    which appears several weeks after myocardial infarction)
  2. uremia (“bread and butter” pericarditis)
  3. chest irradiation
41
Q

most striking characteristic with fibrinous pericarditis

A

loud pericardial friction rub

42
Q

pericardial disease: purulent or suppurative

A
  • invasion of organisms into pericardial space

- organization may lead to restrictive pericarditis

43
Q

pericardial disease: hemorrhagic

A

-exudate composed of blood mixed with a fibrinous or
suppurative effusion
-Tuberculosis, direct malignant neoplastic involvement of the pericardial space

44
Q

pericardial disease: chronic

A

-misnomer; healed or organized effusions with

fibrosis, adhesive (restrictive) pericarditis

45
Q

pericardial disease: rheumatic heart disease

A

-heart involved in 20-40% or cases; fibrinous pericarditis leading to fibrous adhesions

46
Q

pericardial disease: Hemopericardium

A

-due to rupture of heart wall secondary to myocardial
infarction, traumatic perforation, or rupture of
intrapericardial aorta
-leads to cardiac tamponade
-“electro-mechanical dissociation”
-200-300 ml may cause death if accumulates rapidly

47
Q

neoplastic heart disease

A

myxoma

48
Q

myxoma

A

-most common primary tumor of the heart in adults; 90%
are located in the atria (left to right 4:1)
-almost always single
-sessile or pedunculated masses
-stellate or globular myxoma cells, endothelial cells, sm.
muscle cells with abundant mucopolysaccharide ground
substance; considered benign neoplasia
-Ball-valve obstruction of atrial outflow, embolization,
fever and malaise (?IL-6)