Degeneration

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Degeneration
Section B
ACUTE CELLULAR SWELLING
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FATTY CHANGE

• Excessive entry of free fatty acids into the
  liver
• (starvation, corticosteroid therapy).
• Enhanced fatty acid synthesis.
• Decreased fatty acid oxidation.
• Increased esterification of fatty acid to
• triglycerides (alcohol).
• Decreased apoprotein synthesis (CCl4).
• Impaired lipoprotein secretion from the liver
• (alcohol).

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• Morphology of fatty change
• Sudan III, Oil red O, Osmic acid
• Liver
• Heart
• Kidney

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Hyaline changes (degeneration)

• Intracellular hyaline changes
• Hyaline degeneration of arterioles
• Hyaline degeneration of connective tissue

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Intracellular hyaline changes

• Absorption of protein causing hyaline
• droplets in proximal epithelial cells in
• the kidney.
• Russel bodies in plasma cells.
• Viral inclusions in the cytoplasm or
• the nucleus.
• Masses of altered intermediate filaments
• (Mallory bodies).

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AMYLOIDOSIS

• A heterogeneous group of pathogenic
• fibrillar proteins accumulating in tissues
• and organs.
• Excess synthesis
• Resistance to catabolism

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Chemical nature of amyloid fibrils Two major
forms AL (amyloid light chain protein) AA
(amyloid-associated protein) Derived from serum
AA (12kd) synthesized in liver and elevated
in inflammatory states.
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Minor forms of amyloid fibrils Transthyretin
(TTR) A mutant form of a serum protein in
familial amyloid polyneuropathy. A variant of
TTR in aging. Beta-2-microglobulin (the component
of class I MHC molecules) in long-term
hemidialysis.
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Minor forms of amyloid fibrils Beta-2-amyloid
protein forms the core of cerebral plaques and
deposits within cerebral vessel walls in
Alzheimer disease, deriving from a
transmembrane glycoprotein precursor.
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Minor forms of amyloid fibrils Transthyretin
(TTR) A mutant form of a serum protein in
familial amyloid polyneuropathy. A variant of
TTR in aging. Beta-2-microglobulin (the component
of class I MHC molecules) in long-term
hemidialysis.
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Minor forms of amyloid fibrils Beta-2-amyloid
protein forms the core of cerebral plaques and
deposits within cerebral vessel walls in
Alzheimer disease, deriving from a
transmembrane glycoprotein precursor.
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Clinical forms of amyloidosis Systemic
amyloidosis

• primary (B-cell dyscrasia, AL)
• Secondary or reactive (AA)
• Collagen diseases, bronchiectasis, chronic
• osteomyelitis.
• Hemodialysis-related Beta-2-microglobulin
• deposition.
• Hereditary (AA)

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Localized amyloidosis

• Nodular (tumor-forming deposits,
• B-cell dyscrasia, AL)
• Endocrine amyloidosis (procalcitonin)
• Amyloidosis of aging Heart, lung,
• pancreas, spleen, brain.

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• Exogenous
• Carbon
• Tattooing
• Endogenous
• Lipofuscin
• Melanin
• Hemosiderin
• Bilirubin

Pigmentation
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Pathologic calcification

• Dystrophic calcification
• Metastatic calcification

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Dystrophic calcification

• Necrotic tissues
• Atheroma
• Damaged heart valves

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• Fig 2-13

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Metastatic calcification Hypercalcimia

• Increased secretion of parathyroid
• hormone
• Destruction of bone tissue
• Vitamin D-related disorders
• Sarcoidosis
• Renal failure

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Metastatic calcification Affecting
Interstitial tissue of gastric mucosa Kidneys Lung
s Pulmonary veins Systemic arteries