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2. Hypertrophy نمو في الحجم العضلات *عضلة القلب
3. Hyperplasia ازدياد في عدد الخلايا - عند الحوامل
4. Metaplasia تحول
dysplasia
Free radicals are highly reactive and can injure cells through:
1. Peroxidation of membrane lipids.
2. Damage of cellular proteins.
3. Mutation of cellular DNA.
protease enzymes - calsium dependent
* Apoptosis may be a mechanism to eliminate worn-out or
genetically damaged cells. (Epstein–Barr virus)
2) Necrosis : Involves the unregulated, enzymatic digestion (“autolysis”) of a cell
and its components
Three main types of necrosis have been identified:
Liquefaction necrosis : Digestive enzymes released by necrotic cells soften and liquefy dead tissue. (brain), that are rich in hydrolytic enzymes
Caseous necrosis : “cheese like” tuberculosis , prolonged inflammation and immune activity.
Coagulative necrosis : appear firm, gray and slightly swollen. The acidosis denatures cellular
proteins and hydrolytic enzymes. (myocardial infarction) caused by : ischemia and hypoxia
Types of pathologic calcification:
Dystrophic 1. calcification caseous necrosis.
Metastatic 2. calcification because an abnormal concentration of calcium
Repair by regeneration : labile cells - stable cells
.Proud flesh:
Keloid : abnormality in collagen
Hernia : فتق ربما يقود الى غرغرينا
4.Stricture : scar encircle a tubular structure
.Contracture : scar tissue is shorten and more dense and compact انكماش
Adhesions : serosal sufaces are inflamed and not resolve serosalsurfaces may bind
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