Injury & Necrosis Flashcards
(30 cards)
Reversible injury
ischemia
- decreas ox phosphorylation
- decrease ATP, increase glycolysis
- decrease Na pump so ER swells, blebs, myelin figures, cell swelling
- detach ribosome- decrease prot syn
Nutritional imbalance
protein calorie def
- found in marasmus, kwashiorkor
- anorexia nervosa
excess calorie intake
- DMII
- metabolic syndrome
Irreversible Injury
Cell death, mem injury
- loss phospholipids
- cytoskeletal alterations
- free radicals
- lipid breakdown
- increase enz leakage
- release lysosomes
Hypoxia
- ischemia
- atheroscelrosis most common cause
- can also be due to resp failure, anemia, CO poisoning
Hypoxia Physical:
Phys:
trauma, temp changes, radiation, electric shock, P changes *Caisson’s disease
Chem agents & drugs
poisons- Arsenic, CN, Hg
alc, tobacco, IV
asbestos, CO, CCL4
infectious agents:
- virus- influenza
- bac- streptococci
- plasmodia- malaria
- rickettsia- Q fever
- fungi- candida
- worms- tape/hookworm
Immunological Rxn
- autoimmune diseases
- hypersensitivity rxn (butterfly rash in systemic lupus)
Genetic Defects
- down syndrome
- sickle cell anemia
Apoptosis
Regulation of cell numbers in development & systems
Also done to kill infectious agents
Cell mem is intact
No adjacent inflammation
Necrosis
Normal post mortem changes
Pathological
Cell mem is disrupted
Enzyme digestion
Frequently w/ adjacent inflammation
LIVING TISSUE
Hydropic Swelling Pathogenesis
- Imparied cell vol reg
- Injurious agents interfere w/ mem regulated process, increase Na+ perm
- damage to pump directly
- reversible
found in kidney= cell swelling
and liver= fatty changes (increase in fat)
EM features of subcellular level of reversible injury
Irreversible Cell Injury
Nucleaus= pyknosis
- nuke shrinks & condenses chromatin
- karyolysis, loss of basophilia
- karyorrhexis, breakup of chromatin into small dense fragments w/ necrotic cell
Cytoplasm of necrotic cell
Hyper eosinophilia
EM features of irreversible injury
clumped nuke chromatin
mitochondrial swelling
Ca2+ deposition
myelin figures present
Injury Review
Reversible
- decrease pH
- increase glycolysis
- decrease prot syn
- failulre of Na+/K+ pump
- hydropic change
Irreversible
- severe ATP depletion
- nuke changes
- mem changes
- ROS
- cytokskeleton abnormal
- influx Ca2+
- mitochondrial densities
Coagulative necrosis
- cell outlines are visible
- no cell organelles
- neutrophils remove these features after few days
- due to ischemia/infarction
- Seen everywhere except BRAIN
- hypoxia blocks proteaolysis & lysosome digestion when it denatures structural prot!
Key: deep eosinophilia, no nuke
Liquefactive Necrosis
- tissue converted into liquied viscous mass
- in brain due to hypoxia- loss CT support & lysosomes
- Form abscess
KEY: look for empty space or inflammatory cells, no cell structure seen
Gangrenous necrosis
- limb or intestine loss of blood supply
- loop of bowel twists,
- dry gangrene
- wet gangrene- w/ liquefactive
- gas gangrene
Gangrene Etiologies
- a.. thromboembolism
- DM vascular disease
- atherosclerosis
- indirect hyperthermic effect like frostbite
Dry gangrene
Key: line of demarcation b/t necrotic tissue & healthy tissue
Wet Gangrene
KEY: bac infectio in patient w/ diabetes
*antibiotics won’t work b/c poor transport in patient
Gas gangrene
KEY: Clostridium perfringens
