Cellular Responses to Stress

Question 1

Hyperplasia

Answer 1

Increase in number of cells (result of GF-driven proliferation of mature cells - occur in tissues with capacity to divide)

Question 2

Hypertrophy

Answer 2

Increase in size of cells

Question 3

Atrophy

Answer 3

Decrease in size of cells

Question 4

Metaplasia

Answer 4

Change in structure; reversible change in which one cell type is replaced by another cell type

Question 5

Physiologic hypertrophy

Answer 5

Pregnancy, breast tissue from puberty

Question 6

Pathologic hypertrophy

Answer 6

Excessive of inappropriate actions of a stimulus (like a hormone)

Question 7

Physiologic atrophy

Answer 7

Loss/decrease in hormonal stimulation

Question 8

Pathologic atrophy

Answer 8

Decreased workload, loss of innervation, diminished blood supply, inadequate nutrition

Question 9

Causes of cell injury

Answer 9

Oxygen deprivation 
Physical agents
Chemical agents and drugs
Infectious agents
Immunologic reactions
Genetic derangements
Nutritional imbalances

Question 10

Hypoxia

Answer 10

Oxygen deprivation in tissues

Question 11

Hypoxemia

Answer 11

Oxygen deprivation in blood

Question 12

Ischemia

Answer 12

Oxygen deprivation

Question 13

Features of reversible injury

Answer 13

Membrane blebs
Cellular swelling
Mitochondrial changes
Dilation of ER
Nuclear alterations

Question 14

Irreversible cell injury (death)

Answer 14

Necrosis

Apoptosis

Question 15

Necrosis

Answer 15

Result of denaturation of intracellular proteins and enzymatic digestion of the injured cells

Question 16

Biochemical mechanism in necrosis

Answer 16

Mitochondrial damage - less ATP; more ROS
Entry of Ca - increase mitochondrial permeability; activation of cellular enzymes
Membrane damage - Plasma (loss of cell components) or lysosomal (enzymatic digestion of cell components)

Question 17

Coagulative necrosis

Answer 17

Happens in solid organs; firm texture; architecture preserved for days (injury denatures structural proteins AND enzymatic proteins so dead cells won’t lyse until leukocytes come in); caused by ischemia

Question 18

Liquefactive necrosis

Answer 18

Brain; tissue architecture lost; caused by infection; pus

Question 19

Casseous necrosis

Answer 19

Cheese-like appearance; granuloma (injury closed off by activated machrophages); TB infection

Question 20

Fibrinoid necrosis

Answer 20

blood vessel; antigen-antibody complexes are deposited in walls of arteries

Question 21

Fat necrosis

Answer 21

Saponification (calcium formation)

Question 22

Gangrenous necrosis

Answer 22

Usually applied to a limb that has its lost its blood supply; Dry - ischemic; usually coagulative; wet - superimposed infection; liquefactive necrosis

Question 23

Apoptosis

Answer 23

Programmed cell death in which cells destined to die activate intrinsic enzymes that degrade the cells’ own DNA and proteins

Question 24

Morphologic evidence of apoptosis

Answer 24

Cell shrinkage and chromatin condensation
Pyknotic nuclei
Apoptotic bodies

Question 25

Morphologic evidence of necrosis

Answer 25

Increased eosinophilia Myelin figures Karyolysis - loss of nuclear material Pyknosis - nuclear shrinkage and increased basophilia Karyorrhexis - fragmentation of shrunked nucleus

Question 26

Mitochondrial (intrinsic) pathway

Answer 26

Cell injury increases mitochondrial membrane permeability, releasing cytochrome c Cytochrome C binds to APAF forming apoptosome Initiator caspase-9 activated, triggers caspase cascade

Question 27

Death receptor (extrinsic) pathway

Answer 27

Death receptors engage Fas binds to it's ligand and forms a binding site for FADD FADD binds inactive form of caspase -8 Multiple procaspase-8 come together to cleave and activate each other, trigger apoptosis

Question 28

Initiation phase

Answer 28

Some caspases become catalytically active

Question 29

Execution phase

Answer 29

Other caspases trigger degradation of critical cellular components

Question 30

Necrosis characteristics

Answer 30

``` Nuclei digested Loss of membrane integrity - leaky Involves larger area of tissue - many cells Increased inflammation Always pathologic ```

Question 31

Apoptosis characteristics

Answer 31

Nuclei shrink and fragment Membrane blebbing with fragmentation of membrane-bound cytoplasm Involves isolated cells or small groups of cells Decreased inflammation Can be physiologic or pathologic

Question 32

Necroptosis

Answer 32

Like necrosis - swelling of cell and organelles, release of enzymes, rupture of membrane Like apoptosis - triggered by genetically programmed signal transduction similar to extrinsic form DEFENSE AGAINST VIRUSES THAT ENCODE CASPASE INHIBITORS

Question 33

Accumulations

Answer 33

Lipid Protein Glycogen Pigments

Question 34

4 main pathways of intracellular accumulation and examples of each

Answer 34

Abnormal metabolism - fatty liver (steatosis), hemosiderosis (iron accumulation) Defect in protein folding and transport - alpha1-antitrypsin mutation Lack of enzyme that leads to accumulation of endogenous substance - hepatic glycogenosis Ingestion of indigestible substance leads to accumulation of exogenous substance - anthracosis (pigment accumulation)

Question 35

Pathologic calcification

Answer 35

Abnormal tissue deposition of calcium salts, together with smaller amounts of iron, magnesium, and other mineral salts

Question 36

Dystrophic pathologic calcification

Answer 36

Deposition occurs locally in dying tissue (normal serum calcium levels); ex.) atheromas and calcific aortic valves

Question 37

Metastatic pathologic calcification

Answer 37

May occur in normal tissues (almost always due to hypercalcemia); consequence of PTH; widely occurs