Topic 6: Cardiac Histology_Fishbein

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  1. Heart wall consists of what layers from outer to to inner?
    • parietal pericardium
    • pericardial sac
    • epicardium
    • myocardium
    • endocardium
  2. —Parietal pericardium
    • - Fibrous pericardium:
    • * Composed of fibrous tissue
    • * Variable amount of fat toward apex

    • —- Parietal serous pericardium
    • * Thin, inner mesothelial layer
  3. Epicardium
    - AKA visceral serous pericardium

    —- Thin, mesothelial-lined layer continuous with parietal serous pericardium

    - —Invested with variable fat containing blood vessels, lymphatics, nerves, etc.
  4. Periocardial sac
    • - —Potential space between
    • parietal and visceral serous pericardium

    • —- 1 to 30 mL of clear serous fluid
    • allows surfaces to glide over one another
  5. Myocardium
    - Consists of bundles of myocytes separated by fibrous bands


  6. —Cardiac myocytes
    —- mostly single, central, ovoidnucleus, some binucleated —

    - Branching—

    - Cross striations—

    - Intercalated discs—: Usually end-to-endjunctions connecting myocytes

    - —Lipofuscin granules (lysosomes): Increase with age—, product of oxidative stress

    - Contains contractile myofibrils (actin and myosin)
  7. —2 main types of cardiac myocytes
    • —1) Contractile—
    • (Atria & ventricles—)

    • 2) Conductive—
    • (SA node, AV node, bundle of His, Purkinje cells)
  8. Atrial cardiac myocyte

    - secretes what?
    - stimulates what?
    - —Secretes atrial natriuretic peptide (ANP) when blood pressure rises in atrium—

    * ANP  important in controlling volume and strength of contraction of the heart

    - Stimulates diuresis (urine production) by decreasing Na+ resorption in the kidneys
  9. SA and AV nodal tissue
    - conduction system

    —- Small, conductive cells with fewer myofibrils and surrounded by fibrous tissue
  10. —Purkinje cells
    - conductive cells of the heart

    • - Large pale, conductive and contractile cells with fewer myofibrils
    • - no T-tubules on electron microscopy
    • - rich in glycogen
  11. endocardium

    - what is it?
    - name the diff layers
    - —Lines all inner heart surfaces

    —- Left atria thicker than ventricles

    • —1) Innermost layer = endothelium
    • Continuous w/ vascular endothelium

    • 2) —Middle layer
    • —Loose elastic framework, collagen bundles, nerves, and blood vessels

    • —3) Outermost layer = subendocardium
    •  - Merges with myocardium

    - Contains fibrocollagenous tissue and Purkinje cells
  12. endothelium
    —Thin layer consisting of endothelial cells that line blood vessels and all inner heart structures
  13. endothelial cells
    - Flat cells (30 x 5 microns)

    —- Form semi-permeable membrane

    —- Substances can cross this barrier via:

    • —* Intercellular junctions
    • * Pinocytotic vesicles
    • * Fenestrae
  14. functions of endothelium (3)
    - Antithrombotic and prothrombotic properties (blood clotting)

    • —- Play major role in inflammation by providing points of attachment for inflammatory cells (rolling,
    • diapedesis, etc.)

    - —Formation of new vessels (neovascularization) during wound healing and other processes
  15. semilunar valves

    - layers
    • - aortic and pulmonary
    • - layers
    • 1) fibrosa:
    • - Layer of dense collagen and scattered fine elastic fibers
    • —- Major structural component
    • —- Extends to free edge

    • 2) spongiosa:
    • - Subjacent to fibrosa
    • - Best developed in proximal third
    • - Does not extend to free edge
    • - Abundant proteoglycansloosely arranged collagen

    • 3) ventricularis:
    • —- Subjacent to spongiosa
    • - —Extends to free edge
    • - Rich in elastic fibers
  16. atrioventricular valves

    layers?
    - Tricuspid & mitral

    • —- 3 layers
    • 1) —Fibrosa:
    • - —Most consistent layer extending to free edge
    • - —Mostly dense collagen

    • 2) —Spongiosa:
    • - —Extends throughout length of leaflet, but most prominent in free edge

    —- Basal portion has extension of atrial myocardium

    - —Loosely arranged collagen, abundant proteoglycans

    • 3) —Atrialis (auricularis):
    • - —Covers atrial aspect of spongiosa in basal & mid portion of leaflet

    - —Proteoglycans, elastic fibers, occasional smooth muscle cells
  17. Cardiovascular Pathology
    REASONS FOR PUMP FAILURE
    • - Increased peripheral resistance with increased strain & overwork of
    • myocardium (e.g. aortic coarctation)

    —- Lost of viable myocardium (e.g. myocarditis)

    —- Disturbance of intrinsic electrical circuit (e.g. arrhythmia)

    —- Primary abnormality of myocardium (e.g. cardiomyopathy)

    - —Decreased blood supply to myocardium (e.g. coronary artery disease leading to myocardial infarction)

    —- Decreased blood return to heart (e.g. pulmonary embolism)

    • - —Abnormal development resulting in physiologically suboptimal function
    • (e.g. congenital heart disease)
  18. Cardiovascular Pathology:

    Classifications of Heart Disease by???
    • - pathophysiology
    • - structure
    • - pathogenesis
  19. cardiomyopathy

    - def
    - how is it classified?
    • Diseases of myocardium associated w/ cardiac dysfunction and/or arrhythmias

    • classified by dominant pathophysiology or by etiologic/pathogenetic factors
  20. dilated cardiomyopathy

    - what is it?
    - possible etiologies?
    - prognosis?
    - —Most common type of cardiomyopathy characterized by progressive CHF w/ 4-chamber dilatation affecting individuals  of all ages, mostly between 20- 50

    • —Possible etiologies:
    • - —Idiopathic (30% or more)
    • - Postviral myocarditis (30%)
    • - Peripartum (1/1300-1/15000)
    • - Alcohol and other toxicities
    • - Familial (30%)

    • Prognosis:
    • —- 50% dies within 2 years
    • - often cause of sudden death
    • - Cardiac transplantation often recommended
  21. dilated cardiomyopathy: Gross Findings
    - Increased heart weight (up to 1 kg) with dilation & hypertrophy

    - —Mural thrombi (blood clots) in chambers

    - —Minimal or absent structural diseases (looks like normal heart)
  22. dilated cardiomyopathy: histopathology
    - Myocyte hypertrophy & interstitial fibrosis

    —- Occasional minimal mononuclear inflammatory infiltrates
  23. ARRHYTHMOGENIC RIGHT VENTRICULAR
    CARDIOMYOPATHY

    - what is it?
    - clinical presentation
    • - type of nonischemic cardiomyopathy that involves primarily the right ventricle
    • - uncommon, young adults
    • - Caused by genetic defects of the heart

    • —Clinical presentation:
    • —- Right-sided heart failure

    - —Exercise-induced arrhythmias

    —- Sudden death

    —- Left-sided involvement w/ heart failure may occur
  24. ARRHYTHMOGENIC RIGHT VENTRICULAR
    CARDIOMYOPATHY:

    Gross findings
    - Dilated and thinned right ventricle

    —- Myocardial replacement by fibroadipose tissue
  25. ARRHYTHMOGENIC RIGHT VENTRICULAR
    CARDIOMYOPATHY:

    histopathology
    - —Replacement of RV free wall with fibro-adipose tissue ± scattered mononuclear cells
  26. HYPERTROPHIC CARDIOMYOPATHY

    - characterized by?
    - inheritance pattern?
    - clinical manifestations
    • Disease characterized by:
    • - myocardial hypertrophy
    • - LV diastolic failure due to loss of distensibility & increased rigidity
    • - intermittent LV Outflow Tract obstruction in ⅓ of cases

    - Autosomal Dominant

    • —Clinical manifestations i
    • - sudden death
    • - syncope (fainting)
    • - exertional dyspnea (difficult breathing)
    • - angina (chest pains)
  27. forms of Hypertrophic cardiomyopathy
    • 1) Asymmetric form
    • - Disproportionate thickening of IVS compared to LVFW (ratio > 1.2:1)

    • 2) —Symmetric form
    • - Hypertrophy symmetric throughout heart
  28. hypertrophic cardiomyopathy:

    gross findings
    - Increased wt with significant mural (blood clot) hypertrophy

    —- Bulging IVS into lumen produces small, banana-shaped ventricular cavity

    —- Fibrous plaque in LV outflow tract due to systolic motion of anterior leaflet of mitral valve (Venturi effect)
  29. hypertrophic cardiomyopathy:

    histopathology
    - Marked myocyte hypertrophy with myocyte & myofibril disarray

    - —Fibrointimal thickening of intramyocardial arteries

    —- Ischemic changes in myocardium
  30. restrictive cardiomyopathy
    • —Disorder characterized by
    • primary decrease in ventricular relaxation resulting in diastolic dysfunction

    —- Systolic function usually unaffected
  31. —Idiopathic restrictive cardiomyopathy

    - gross findings
    - histopathology

    *note: idiopathic = spontaneous
    • Gross findings:
    • —- Normal sized ventricular cavities

    -—Marked bi-atrial dilatation

    • —Histopathology:
    • Patchy or diffuse interstitial fibrosis
  32. CARDIAC AMYLOIDOSIS

    3 types
    • 1) Systemic amyloidosis
    • - Primary AL
    • - Secondary AA

    • —2) Senile cardiac amyloidosis
    • - Involves ventricles & atria of elderly pts
    • - Derived from transthyretin

    • 3) —Isolated atrial amyloidosis
    • - —Limited to atria
    • - Derived from ANP
    • - —Most often presents as restrictive cardiomyopathy
  33. SARCOIDOSIS
    - Disease that is not understood very well

    systemic involvement-Can affect any organ in the body

    —Cardiac involvement reported in 20-30% of pts with sarcoidosis at autopsy

    —Only <5% w/ sarcoidosis have cardiac symptoms including heart block, CHF, arrhythmias, sudden death, & pericarditis

    -Some are asymptomatic

    • —Base of IVS & LVFW typically involved
    • (RV) endomyocardial biopsies often negative due to sampling error
  34. Sarcoidosis histopathology
    - —Well-formed, non-necrotizing granulomas replacing myocardium w/variable interstitial fibrosis
  35. MYOCARDITIS

    - what is it?
    - 3 requirements to be called myocarditis
    inflammation of myocardium

    • 1) Inflammatory infiltration AND
    • 2) damage to myocytes
    • 3) not typical of ischemic damage associated with coronary artery disease
  36. 3 Major causes of Myocarditis
    • 1) infection (viruses are most common)
    • 2) immune-mediated rxns
    • 3) idiopathic
  37. LYMPHOCYTIC MYOCARDITIS
    - Most common myocarditis

    —- Most cases are presumed viral in origin

    • —Most frequently implicated:
    • —Coxsackieviruses A & B
    • —Echoviruses
    • —Adenoviruses
    • —Influenza viruses
    • —Parvovirus
  38. LYMPHOCYTIC MYOCARDITIS : Histopathology
    - Interstitial mononuclear inflammatory infiltrate, predominantly lymphocytic

    - —interstitium is widened by the inflammatory infiltrate and edema

    —- Myocyte damage
  39. GIANT CELL MYOCARDITIS

    - occurence
    - prognosis
    - population affected
    - effects
    - —Rare, idiopathic form of myocarditis with fulminant & frequently fatal clinical course

    —Affects young adults who present acutely with florid CHF ± arrhythmias

    —Reported to be associated with thymoma, myasthenia gravis, thyrotoxicosis, & collagen vascular diseases

    —Immunosuppression followed by transplantation

    disease r—eoccurs in 25% of heart transplants
  40. Giant Cell Myocarditis: Histopathology
    - —Diffuse geographic necrosis

    - key feature: multi-nucleated giant cells

    - —Polymorphous inflammatory infiltrate (including eosinophils & multinucleated giant cells)

    —ABSENCE of sarcoid-like granulomas
  41. EOSINOPHILIC MYOCARDITIS

    - 3 general categories
    - note about eosinophils
    1. —Hypersensitivity myocarditis

    2. Hypereosinophilic syndrome

    —3. Parasitic infections

    • Eosinophils are TOXIC:
    • -When they degranulate, it can damage the host tissue and causes damage to the heart
  42. HYPERSENSITIVITY MYOCARDITIS

    - causes
    - Reaction to drugs (antibiotics, antihypertensives, diuretics, anti-epileptics) that involve myocardium

    - disease goes away if you remove the drug

    • - —Not dose dependent and may occur at any time during or after use of drug

  43. HYPERSENSITIVITY MYOCARDITIS: Histopathology
    - Patchy inflammatory infiltrate (lymphocytes, plasma cells, histiocytes, & increased eosinophils)

    —- Myocyte necrosis not prominent

    - —Fibrosis & granulation tissue are typically absent
  44. CONSTRICTIVE PERICARDITIS

    - what is it?
    - effects?
    - therapy used
    - —Dense fibrotic or fibrocalcific scar tissue within pericardium resulting in reduced compliance of pericardium

    —- May develop slowly over many years or subacutely over weeks to months

    • —Severe restriction results in:
    • limited diastolic expansion & filling
    • shortness of breath
    • reduced exercise tolerance
    • abdominal distension
    • palpitations (heart pounding)
    • syncope (fainting)

    - NO —Cardiac hypertrophy & dilatation

    —Mainstay of therapy is pericardiectomy

Card Set Information

Author:
jlyip89
ID:
255845
Filename:
Topic 6: Cardiac Histology_Fishbein
Updated:
2014-01-16 00:43:09
Tags:
Cardiac Histology
Folders:
systems 1
Description:
Systems1: Fishbein lecture 1.5
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