Myocardial Disease Flashcards

1
Q

Dilated Cardiomyopathy causes

A

Caused by myocarditis
-Coxsackie virus B

EtOH and metabolites are toxic to myocardium

Thiamine deficiency can cause DCM

Doxorubicin (chemo agent)

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2
Q

Gene mutations causing dilated cardiomyopathy

A

Mitochondrial genes

dystrophin genes

Genes encoding enzymes involved in beta oxidation of FAs

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3
Q

DCM clinical

A

Slowly progressive CHF

50% die within 2 yrs
25% survive longer than 5 years

Death due to progressive cardiac failure or arrhythmia

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4
Q

Hypertrophic Cardiomyopathy

A

Massive myocardial hypertrophy

Abnormal diastolic filling

In 1/3of cases: intermittent LV outflow obstruction

Hypercontracting

  • systolic function is preserved
  • primarily a diastolic disorder
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5
Q

HCM morphology

A

Massive myocardial hypertrophy without ventricular dilation

Classic: asymmetrical septal hypertrophy

Usually most prominent in subaortic area

Endocardial thickening of LV outflow tract and thickening of ant mitral leaflet

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6
Q

HCM microscopic morphology

A

Myocyte hypertrophy

Haphazard disarray of bundles of myocytes

Interstitial and replacement fibrosis

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7
Q

HCM pathogenesis

A

Mutations in genes that encode sarcomeric proteins

Autosomal dominant with variable expression

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8
Q

HCM clinical

A

Reduced chamber size

Poor compliance, reduced SV due to:

  • impaired diastolic filling of LV
  • massively hypertrophied LV

Exertion also dyspnea due to decreased CO and increased pulmonary venous pressure

Harsh systolic ejection murmur due to ventricular outflow obstruction

Angina pain

SUDDEN DEATH IN ATHLETES

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9
Q

Myocarditis

A

Inflammatory process plays a primary role in development of myocardial injury

Coxsackie viruses A and B

Trypanosoma Cruzi

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10
Q

Myocarditis morphology

A

Heart normal or dilated

Lesions diffuse or patchy

Ventricular myocardium is flabby

Mural thrombi may be present in any chamber

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11
Q

Myocarditis microscopic

A

Interstitial infiltrate and injury (lymphocytes)

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12
Q

Hypersensitivity myocarditis

A

Perivascular infiltrate- lymphocytes, macrophages and eosinophils

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13
Q

Giant Cell myocarditis

A

Giant cells are present

Poor prognosis

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14
Q

Pericardial effusion

A

Fluid in pericardium

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15
Q

Hemopericardium

A

Blood in pericardium

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16
Q

Purulent pericarditis

A

Pus in pericardium

17
Q

Globular enlargement

A

Due to slow accumulation of fluid and is < 500 ml

18
Q

Cardiac Tamponade

A

Due to a large chronic effusion (> 500ml) or accumulate rapidly

Restricts cardiac filling

19
Q

Serous pericarditis

A

Non infectious inflammation

  • rheumatic fever
  • systemic lupus erythematosus
  • scleroderma
  • tumors
  • uremia
20
Q

Serous pericarditis morphology

A

Neutrophils, lymphocytes, and histiocytes on epicardial and pericardial surfaces

21
Q

Acute pericarditis morphology

A

Fibrinous: surface is dry with a fine granular roughening

Serofibrinous: thick yellow to bloody fluid and fibrin

FIBRINOUS DEVELOPS A LOUD PERICARDIAL FRICTION RUB

22
Q

Purulent pericarditis clinical

A

Active phase is similar to fibrinous along with signs of systemic infection- spiking temps, chills, fever

23
Q

Hemorrhagic pericarditis

A

TB or malignant neoplasm ( most common)

bacterial infections

Bleeding diathesis

Cardiac surgery

24
Q

Healed pericarditis

A

Healing causes adhesive mediastinopericarditis

Pericardial sac in obliterated

Heart adheres to surrounding structures

  • systolic retraction of the rib cage and diaphragm
  • pulsus paradoxus
  • hypertrophy and dilation of heart
25
Q

Constrictive Pericarditis

A

Encased in dense fibrous or fibrocalcific scar

  • limits diastolic expansion
  • restricts CO