3 - Cell injury

Question 1

Aetiology of cell injury

Answer 1

O2 availability
Physical trauma
Chemical agents
Infectious organisms
Irradiation
Others: immunological, lack of nutrients/vitamins, genetic disorders, ageing

Question 2

Difference between hypoxia, anoxia and ischaemia

Answer 2

Hypoxia an anoxia = reduction/loss of O2 to cells

Caused by ischaemia which = lack of blood flow

Question 3

Necrosis vs apoptosis

Answer 3

Necrosis = passive, unprogrammed
Apoptosis = active, programmed

Question 4

Types of necrosis

Answer 4

Coagulative
Caseous
Colliquative
Gangrene
Fat, fibrinoid

Question 5

Coagulative necrosis

Answer 5

Denaturation of intracytoplasmic protein
Dead tissue becomes firm and swollen 
Tissue retains microscopic architecture
Ischaemic injury (except brain)
Cellular proteins may leak into blood

Question 6

Colliquative necrosis

Answer 6

Necrotic neural tissue is liable to total liquefaction and site is eventually marked by a cyst.

Question 7

Caseous necrosis

Answer 7

Characteristic of TB
Cheese like
Cellular detail destroyed in this area, surrounded by granulomatous inflammation
Dead tissue lacks any structure

Question 8

Gangrenous necrosis

Answer 8

Wet or dry
E.g. wet bowel infarct
E.g. dry gangrene in diabetes

Question 9

Physiological apoptosis e.gs

Answer 9

Embryogenesis
Involution
Elimination of self-reacting lymphocytes

Question 10

Pathological apoptosis

Answer 10

DNA/protein damage
Viral infections
Cell killing by cytotoxic T-cells
Chemo/radiotherapy

Question 11

Necrosis vs apoptosis:
No of cells
Cell size
Nucleus
Plasma membrane
Cellular contents
Adjacent inflammation
Physiological/pathologic role

Answer 11

Necro first, apoptosis 2nd
Multiple vs single
Enlarged vs reduced
(pyknosis -> karyorrhexis -> karyolysis) vs (fragmentation -> apoptotic bodies)
Disrupted vs intact
Enzymatic digestion vs intact
Frequent vs no
Invariably pathologic vs physiologic