e. Endogenous pigments i. Lipofuscin

■ Wear and tear pigment

• Perinuclear yellow-brown pigment

■ Indigestible material within lysosomes

■ Common in the liver and heart ii. Melanin

• Black-brown pigment

• Found in melanocytes and substantia nigria iii. Hemosiderin

• Golden yellow-brown granular pigment

■ Found in areas of hemorrhage or bruises

• Systemic iron overload —> hemosiderosis —> hemochromatosis

■ Prussian blue stain Hyaline change a. Definition: nonspecific term used to describe any intracellular or extracellular alteration that has a pink homogenous appearance on H&E stains b. Examples of intracellular hyaline i. Renal proximal tubule protein reabsorption droplets ii. Russell bodies iii. Alcoholic hyaline c. Examples of extracellular hyaline i. Hyaline arteriolosclerosis ii. Amyloid iii. Hyaline membrane disease of the newborn Pathologic forms of calcification a. Dystrophic calcification j. Definition: precipitation of calcium phosphate in dying or necrotic tissues ii. Examples

■ Psammoma bodies = laminated calcifications that occur in meningiomas and papillary carcinomas of the thyroid and ovary

■ Monckeberg's medial calcific sclerosis

■ Atherosclerotic plaques b. Metastatic calcification i. Definition: precipitation of calcium phosphate in normal tissue due to hyper -clacemia (supersaturated solution)

ii. Causes

4 Hyperparathyroidism

■ Parathyroid adenomas

■ Renal failure

• Paraneoplastic syndrome

■ Vitamin D intoxication

• M ilk-alkali syndrome

• Sarcoidosis

• Paget disease

■ Multiple myeloma

• Metastatic cancer to the bone iii. Location o{ calcifications: interstitial tissues of the stomach, kidneys, lungs, and blood vessels

Chapter Summary

Cells can be damaged by a variety of mechanisms.

Hypoxia causes a loss of ATP production secondary to oxygen deficiency and can be caused by ischemia, cardiopulmonary failure, or decreased oxygen-carTying capacity of the blood.

Infections can injure cells directly, or indirectly, via toxin production or host inflammatory response.

Hypersensitivity reactions and autoimmune diseases may kill or injure cells.

Congenital causes of cellular injury include enzyme defects, structural protein defects, chromosomal disorders, and congenital malformations.

Chemical agents, physical agents, and nutritional imbalances can also injure cells.

The response of cells to an insult depends on both the state of the cell and the type of insult The response can range from adaptation to reversible injury to irreversible injury with cell death.

Intracellular sites and systems particularly vulnerable to injury include DNA, ATP production, cell membranes, and protein synthesis.

Reversible cell injury is primarily related to decreased ATP synthesis by oxidative phosphorylation, leading to cellular swelling and inadequate protein synthesis.

Irreversible cell injury often additionally involves severe damage to membranes, mitochondria, lysosomes, and nucleus.

Death of tissues can produce a variety of histologic patterns, including coagulative necrosis, liquefaction necrosis, caseous necrosis, fibrinoid necrosis, and gangrenous necrosis.

Apoptosis is a specialized form of programmed cell death that can be regulated genetically or by cellular or tissue triggers.

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