Acute Cellular Swelling 415s4b

Degeneration ACUTE CELLULAR SWELLING

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 (CCl ). • Impaired lipoprotein secretion from the liver (alcohol). 4

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

Hyaline changes (degeneration)

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

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).

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

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.

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.

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.

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.

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.

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)

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

Pigmentation

• Exogenous:

Carbon Tattooing •Endogenous: Lipofuscin Melanin Hemosiderin Bilirubin

Pathologic calcification • Dystrophic calcification • Metastatic calcification

Dystrophic calcification • Necrotic tissues • Atheroma • Damaged heart valves

• Fig 2-13

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

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