UNIT 5 - CELLULAR RESPONSE & INJURY Flashcards
Atrophy
decreased cell, tissue, organ size
Hypertrophy
enlarged cell size
- due to increased activity/stimulation
- eg) Hypertension -> heart walls become thicker due to working harder
Hyperplasia
increased cell number
- due to increased stimulation and nutrition
- exact same tissue
Metaplasia
one cell is replaced by another (different tissue)
Dysplasia
disorderly cell growth and tissue structure
- basal cells below basal lamina (sign of cancer)
- irreversible
examples of intracellular accumulations causing cell injury
- silicon particles in lungs
- alcohol-induced fatty liver
- calcification
Dystrophic calcification
accumulation of calcium in dead cells
- eg. atherosclerosis
Metastatic calcification
accumulation of calcium in live cells
what is the key agent that causes injury of most cells
hypoxia
explain hypoxic injury
- less ATP produced
- Na constantly leaks into cell and cannot be removed to due lack of oxygen
- therefore cell swells up
- lactic acid is produced which causes damage to cell structures
explain hydropic change (calcium cascade)
- if cell spends lots of time in hypoxia than ATP levels fall, Na increased so ER/mitochondria rupture which release more calcium causing the cell to rupture and die
Calcium cascade
-release of calcium triggers release of more calcium into the cell (hence cell necrosis)
Reperfusion injury
- cells turn their metabolism to the ‘pilot light’ level when oxygen is lacking
- cells get used to being in minimal circumstances (pilot light level)
Example of reperfusion injury
- heart muscle can survive without oxygen for 20 minutes, but once it gets used to pilot light level and oxygen is restored than free radicals are released and damage the cells
Apoptosis
- programmed cell death/suicide
- cells digest their own proteins and DNA and are then destroyed by WBC
types of necrosis
- coagulative
- liquefactive
- Fat necrosis
- Caseous
Coagulative necrosis
- most common form
- characteristic of hypoxic injury
Liquefactive necrosis
- occurs in brain
- enzymes digest necrotic tissue
Fat necrosis
- occurs in pancreas
Caseous necrosis
- occurs in TB
- results from immune mechanisms
- fibrous capsule around TB area
Gangrene
large areas of necrosis
Dry gangrene
- dry, firm, black, no smell
- most common (no infection)
- eg. frostbite
Wet gangrene
- soggy and infected and smelly
Gas gangrene
- bubbly and smelly
