LEC 3: Cell Injury

Question 1

Principle Adaptive Cellular Responses to Stress

Answer 1

1. Atrophy
2. Hypertrophy
3. Hyperplasia
4. Metaplasia

Question 2

Atrophy

Answer 2

Shrinkage of cell size by loss of substance (organ shrinkage)

Function: gradual decline in effectiveness due to underuse

Cause: decreased protein synthesis, increased protein degradation

Question 3

Hypertrophy

Answer 3

Increase in cell size beyond normal, more cellular organelles and cytoplasm

Function: overuse, increased burden not compensated for

Cause: increased functional demand, growth factor and hormonal stimulation

Question 4

Hyperplasia

Answer 4

Enlargement of organ or tissue cause by increase of cellular reproduction rate

Cause: increased functional demand, growth and hormonal stimulation

Question 5

Metaplasia (conversion)

Answer 5

Adult cell type replaced by another cell type with new function (dependent on cell type)

Cause: differentiation of stem cells along a new lineage

Question 6

Morphology of Cell Injury: Key Concepts

Answer 6

1. All stresses and injuries exert effects first at the molecular or biochemical level
2. Cellular function may be lost long before cell death occurs
3. Morphologic changes lag for behind both (Ultrastructural and Light Microscopic)

Question 7

Reversible Cell Injury: Ultrastructural Changes

Answer 7

Alterations of cell membrane, swelling of RER, detachment of ribosomes

Question 8

Reversible Cell Injury: Microscopic Changes

Answer 8

1. Cell Swelling: increase in cell size d/t increased fluid, causes loss of function of cell membrane Na-K pump
2. Fatty Change: presence of lipid vacuoles in cytoplasm, nucleus displaced to periphery, causes hypotonic, toxic or metabolic injury

Question 9

Biochemical Mechanisms of Cell Injury: ATP Depletion

Answer 9

Causes: inadequate O2, nutrient supply, mitochondrial damage, chemical injury, ineffective ATP dependent pumps

Question 10

Biochemical Mechanisms of Cell Injury: Mitochondrial Damage

Answer 10

Causes: hypoxia, toxins, radiation

Result: abnormal oxidative phosphorylation, formation of mitochondrial permeability transition pore (loss of membrane potential and pH)

Question 11

Biochemical Mechanisms of Cell Injury: Loss of Calcium Homeostasis

Answer 11

Cause: Increased cytosolic Ca2+ activates enzymes

Result: membrane and nuclear damage, decreased ATP

Question 12

Biochemical Mechanisms of Cell Injury: Free Radical Formation/Oxidative Stress

Answer 12

Cause: excessive accumulation of highly reactive oxygen-derived free radicals, attack nucleic acids, proteins and lipids

Result: production of Superoxide, converted to H2O2 and Hydroxyl free radical

Question 13

Biochemical Mechanisms of Cell Injury: Defects in Membrane Permeability

Answer 13

Causes: Ischemia, Free radicals, Cytosolic Ca2+

Result: damage to plasma mitochondrial and lysosome membrane

Question 14

Biochemical Mechanisms of Cell Injury: DNA and Protein Damage

Answer 14

Causes: radiation, oxidative stress, viral, genetic

Result: DNA proof-reading enzyme degraded, leads to proteasomal degradation

Question 15

Irreversible Changes

Answer 15

• Mitochondrial irreversibility
• Irreversible membrane defects
• Lysosomal digestion
• Irreversible mitochondrial dysfunction
• Profound membrane disturbances