Cell Death, Injury, And Adaptations.

Question 1

Ischemia

Answer 1

Lack of blood flow. Common cause of hypoxia.

Question 2

Hypoxia

Answer 2

Oxygen deficiency.

Question 3

Reversible injury

Answer 3

Stage of cell injury at which the cell can return to normal function, if the damaging stimulus is removed.

Question 4

Cellular swelling

Answer 4

Commonly seen in cell injury associated with increased permeability of the plasma membrane. Also called hydropic change and vaculolar degeneration.

Question 5

Fatty change

Answer 5

Appearance of triglyceride containing lipid vacuoles in the cytoplasm. Common in liver.

Question 6

Causes of cell death

Answer 6

• inability to restore mitochondrial function
• loss of structure or function of plasma membrane or intracellular membranes.
• Loss of DNA integrity

Question 7

Necrosis

Answer 7

uncontrolled, “accidental” cell death. Usually involves leakage of lysosomes into the cytoplasm.

Question 8

Apoptosis

Answer 8

Controlled cell death. Cells condense and form membrane blebs, chromatin condenses. Phagocytes then consume the cells.

Question 9

Pyknosis

Answer 9

Nuclear shrinkage and increased basophilia. DNA becomes a dark, shrunken mass.

Question 10

Karyorrhexis

Answer 10

Pyknotic nucleus undergoes fragmentation.

Question 11

Karyolysis

Answer 11

The nucleus is digested by DNase activity.

Question 12

Coagulative necrosis

Answer 12

The underlying tissue architecture is preserved for at least several days. Tissue has a firm texture. Proteolysis of the dead cells is blocked. Anucleate cells persist for days to weeks.
Dead cells eventually digested by leukocytes.

Question 13

Liquefactive necrosis

Answer 13

Seen in focal bacterial and fungal infections since they stimulate rapid accumulation of inflammatory cells which digest the tissue.
Hypoxic death of CNS cells results in this.

Question 14

Gangrenous necrosis

Answer 14

Not a distinctive pattern, usually refers to coagulative necrosis of a limb that has lost its blood supply. If it is liquefactive, it is called Wet Gangrene.

Question 15

Caseous necrosis

Answer 15

Cheese-like friable yellow-white appearance of necrotic area. Usually seen in TB infection.
Appears on stain as collection of fragmented cells with amorphous appearance. Often surrounded by a collection of macrophages.

Question 16

Fat necrosis

Answer 16

Focal areas of fat destruction. Lipases leak out of cells and trigger saponification of Ca and fat. Creates visibly chalky deposits.

Question 17

Fibrinoid Necrosis

Answer 17

Complexes of antigens and antibodies are deposited on the walls of blood vessels.

Question 18

Mitochondrial Pathway

Answer 18

Intrinsic pathway, triggered by release of cytochrome c into the cytoplasm by the mitochondria. Starts when mitochondrial membrane becomes permeable.

Question 19

BCL-2

Answer 19

In healthy cells it maintains the integrity of the mitochondrial membrane by keeping Bax and Bak in check.

Question 20

BH3 proteins

Answer 20

Cna activate Bax and Bak to dimerize and insert into the mitochondrial membrane and form channels.

Question 21

Cytochrome C

Answer 21

Triggers the caspase cascade leading to apoptosis.

Question 22

Death receptor Pathway

Answer 22

Surface “death receptors” such as Type 1 TNF receptor and Fas (CD95) receptor.

Question 23

Fas Ligand (FasL)

Answer 23

Expressed on activated T cells. Trigger these cells to kill their target.

Question 24

Hypoxia/Ischemia Mechanism of cell death

Answer 24

In cells deprived of oxygen their energy dependent metabolic pathways fail, leading to death by necrosis. Failure of ATP generation, ATP depletion leads to reduced activity of ATP pumps, increase in glycolysis.
Irreversible damage to mitochondrial and lysosomal membranes.

Question 25

Oxidative stress

Answer 25

Can cause membrane damage, protein misfolding, and mutations.

Question 26

Endoplasmic Reticulum stress

Answer 26

Caused by misfolded proteins. Adaptive unfolded protein response increases production of chaperones and decreases protein translation to decrease the load.
Terminal unfolded protein response can trigger activation of BH3 family proteins to activate the intrinsic apoptosis pathway.

Question 27

Hypertrophy

Answer 27

Enlargement of cells, resulting in increase in size of the organ.

Question 28

Hyperplasia

Answer 28

Increase in the number of cells in an organ. Can take place only if the tissue is capable of replication.

Question 29

Atrophy

Answer 29

Shrinkage in the size of cells by the loss of cell substance.

Question 30

Metaplasia

Answer 30

A change in which one adult cell type (epithelial or mesenchymal) is replaced by another adult cell type. Ex. Smoker’s lungs, chronic GERD

Question 31

Autophagy

Answer 31

Self eating of the cell. Survival mechanism is nutrient deprived. An autophagic vesicle is formed around some cytoplasmic organelles, then it merges with the lysosome and is digested. Can eventually lead to apoptosis.

Question 32

Intracellular accumulations

Answer 32

Cells may accumulate abnormal amounts of various substances by one of four ways:
Inadequate removal of substance
Accumulation as a result of acquired defects
Failure to degrade a metabolite
Deposition of an abnormal exogenous substance.

Question 33

Steatosis

Answer 33

Fatty change. Accumulation of triglycerides within parenchymal cells.

Question 34

Alpha1- antitripsin deficiency.

Answer 34

Mutations in the protein slow folding, resulting in build up of partially folded intermediate, that aggregate in the ER. Resultant deficiency in circulation causes emphysema.

Question 35

Glycogen storage disease

Answer 35

Enzymatic defects in synthesis and breakdown of glycogen result in massive accumulation in the cell.

Question 36

Exogenous material ingestion

Answer 36

Carbon a common air pollutant. Aggregates in lymphnodes and pulmonary parenchyma causing anthracosis and blackening.

Question 37

Pathologic calcification

Answer 37

Abnormal deposition of calcium salts.

Question 38

Dystrophic calcification

Answer 38

Ca metabolism is normal, but it deposits in injured or dead tissues.

Question 39

Metastatic calcification

Answer 39

Associated with hypercalcemia, can occur in normal tissues. Can deposit in layers resulting in psammoma bodies.

Question 40

Major causes of metastatic calcification:

Answer 40

1. Increased secretion of parathyroid hormone.
2. Destruction of bone due to effects of accelerated turnover.
3. Vitamin-D related disorders.
4. Renal failure.