Cell death

Question 1

Cellular Atrophy

Answer 1

Cellular shrinkage due to stress/environmental factors. Part of adaptation. Reversible change. Due to reduced function and demand.

Question 2

Cellular response to adaptation

Answer 2

Atrophy, hypertrophy, hyperplasia, metaplasia. All are reversible changes.

Question 3

Cellular involution

Answer 3

Reduce cell numbers in response to stressful adaptations. Due to reduced function and demand of organ.

Question 4

Hypertrophy

Answer 4

Increase in cell size, resulting in increase size of organ. Increased demand from organ

Question 5

Hyperplasia

Answer 5

Increase number of cells resulting in increase size of organ. Increased demand from organ.

Question 6

Metaplasia

Answer 6

Replacement of one cell type for another cell type. This is abnormal change-usually changed with less varying cell type. Loss of some function but better than none and in response to persisting injury. This is maintained after loss of stimulus.

Question 7

Dysplasia

Answer 7

patholigical disorder of cellular overgrowth. Results from persistent severe injury or irritation

Question 8

At what percentage does hyperplasia of adipose cell occur?

Answer 8

170%

Question 9

Ischemia

Answer 9

Tissue not getting enough oxygen, caused by hypoxia and anoxia

Question 10

Hypoxia

Answer 10

Cell oxygen levels getting low. Results in decrease ATP, cell swelling, reduced pH and failure of sodium-potassium pump plus calcium pump. Can also cause mitochondria swelling. Causes ischemia

Question 11

Anoxia

Answer 11

No oxygen present in cells. Results in decrease ATP, cell swelling, reduced pH and failure of sodium-potassium pump plus calcium pump. Causes ischemia.

Question 12

Reperfusion injury

Answer 12

Rapid restoration of blood flow to ischemic tissue. Results in free radical formation in the mitochondria and forms peroxides. Results in oxidative stress.

Question 13

Oxidative Stress

Answer 13

Results in reactive oxygen species what damage DNA, lipids, and proteins. Ketogenic diets increase mitochondrial glutathione levels.

Question 14

Chemical agents

Answer 14

Damage cellular walls by altering membrane permeability, osmotic homeostasis, enzyme function.

Question 15

Infectious agents

Answer 15

Invasion and destruction of cells, toxin production, production of hypersensitivity reactions.

Question 16

Immunologic Reactions

Answer 16

phagocytic cells, histamine, antibodies, cytokines, complement, and enzymes. Changes in ion/water permeability.

Question 17

Genetic factors

Answer 17

Alterations in the plasma membrane structure, shape, receptors, or transport mechanisms.

Question 18

Hypothermic cell injury

Answer 18

slows cellular metabolic process and is physical injury.

Question 19

Hyperthermic cell injury

Answer 19

From heat cramps, to heat exhaustion, to heatstroke with increasing loss of salt and water.

Question 20

Cellular radiation damage

Answer 20

Any form of radiation capable of removing orbital electrons from atoms. Results in chromosomal aberrations, Does not affect lymph nodes.

Question 21

Calcium cellular damage

Answer 21

Agents that increase cytosolic calcium from mitochondrial and smooth ER. This can activate other cellular activities.

Question 22

Manifestation of cellular damage

Answer 22

Cellular accumulations of triglycerides, cholesterol, protein, glycogen, water, melanin, hemoproteins, bilirubin, calcium, urate.

Question 23

Fatty change

Answer 23

Accumulation of triglycerides in cells from excessive cellular intake or defective transport. Common sign of reversible injury.

Question 24

Necrosis

Answer 24

Loss of membrane integrity and leakage of cell contents, causing local damage and inflammation.

Question 25

Apoptosis

Answer 25

Cells activate enzymes that degrade cells own dna and nuclear/cytoplasmic proteins. Plasma membrane remains intact and is phagocytosed. No inflammation. Fragments to apoptotic bodies.

Question 26

Necrosis process

Answer 26

pyknosis-clumping of chromatin, karyorrhexis-fragment of nucleus, karyolysis-nuclear dissolution and chromatin lysis.

Question 27

Dystrophic calcification

Answer 27

Happens in areas of necrosis. Not related to hypercalcemia. Fatty acid products from necrosis bind calcium.

Question 28

metabolic calcification

Answer 28

Result of hypercalcemia.

Question 29

Coagulative necrosis

Answer 29

Albumin changes to opaque state. Kidney, heart, spleen, and adrenal glands.

Question 30

Liquefactive necrosis

Answer 30

neuron gland and glial cell of brain. Hydrolytic enzymes

Question 31

Caseous necrosis

Answer 31

Combination of coagulation and liquefactive.

Question 32

Fat necrosis

Answer 32

Free fatty acids and calcium. Pancreas, breast, abdominal organs

Question 33

fibrinoid necrosis

Answer 33

Arteries. Antigen and antibodies deposited in walls.

Question 34

Dry gangrenous necrosis

Answer 34

Occurs in limbs, insufficient blood, coagulative, dry, crusty, black

Question 35

Wet gangrenous necrosis

Answer 35

infection, liquefactive, cold, swollen, black, foul odor from puss.

Question 36

Apoptosis

Answer 36

Cell shrinkage, pyknosis (chromatid condense), apoptotic bodies.

Question 37

Mitochondrial apoptosis (intrinsic)

Answer 37

Depends on mitochondrial membrane permeability. Release cytochrome C to activate apoptosis from mitochondrial. Activates caspases and is stimulated by cellular injury.

Question 38

Death receptor apoptosis (extrinsic)

Answer 38

Activated by TNF then activates adaptor proteins that activates caspases.

Question 39

Autophagy

Answer 39

Lysosomal digestion of cell own components to survive nutrient deprivation. Allows for ATP production. Can cause apoptosis.