Cell Injury, Death, And Adaptations

Question 1

Atrophy

Answer 1

Cell shrinking

Question 2

Hypertrophy

Answer 2

Cell getting bigger

Question 3

Hyperplasia

Answer 3

More cells

Question 4

Metaplasia

Answer 4

Changing cells

Question 5

Dysplasia

Answer 5

Always bad, never normal, only pathological

Question 6

Why would a cell undergo atrophy?

Answer 6

Disuse, inadequate nutrients, lack of endocrine stimulus, poor blood supply, denervation, aging

Question 7

When would a cell undergo hypertrophy or hyperplasia?

Answer 7

Increased work demand, metabolic demand, excess endocrine stimulus, persisting injury

Question 8

When would a cell undergo metaplasia?

Answer 8

Increased capacity to enable tissue survival - persisting injury

Question 9

What determines obesity?

Answer 9

Size

Question 10

What determines adipocytes number?

Answer 10

Gestational birth weight
Maternal insulin
In utero toxin exposure

Question 11

Causes of cell injury (10)

Answer 11

Oxygen deprivations
Chemical agents
Infectious agents
Immunologic reactions
Genetic factors
Nutritional imbalances
Physical agents
Radiation
Calcium
Aging

Question 12

Most common type of cell injury

Answer 12

Oxygen depravation

Question 13

Ischemia

Answer 13

Little oxygen to tissues

Question 14

Hypoxia

Answer 14

little oxygen to cells = decrease ATP

Question 15

Anoxia

Answer 15

No oxygen to cells = decrease ATP

Question 16

What happens to a cell under oxygen depravation?

Answer 16

Decrease in ATP 
= failure of sodium potassium and calcium pump
= cell swelling
= reduce pH
Under extreme conditions, cell can burst

Question 17

What happens to the ETS under oxidative stress?

Answer 17

Electron buildup and the production of a superoxide

Question 18

SOD

Answer 18

Super oxidase dismutase

Will convert superoxide radical into hydrogen peroxide

Question 19

What can hydrogen peroxide do in a cell?

Answer 19

Can turn into a hydroxyl radical and could cause lipid peroxidation, and alter proteins or DNA
Can be turned into water with catalase or glutathione

Question 20

When can mitochondrial swelling occur?

Answer 20

Hypoxia

Question 21

Asphyxial cell injuries

Answer 21

Suffocation, strangulation, chemical asphyxiates, drowning

Question 22

Chemical agents that can cause cell injury

Answer 22

Lead, carbon monoxide, ethanol, Mercury, drugs

Question 23

Immunologic reactions to cell injury

Answer 23

Phagocytic cells
Immune and inflammatory substances
Membrane alterations

Question 24

Hypothermic injury

Answer 24

Slows cell metabolic processes

Question 25

Hyperthermia injury

Answer 25

Heat cramps, heat exhaustion, heat stroke

Question 26

Radiation can affect what type of cells

Answer 26

Gastrointestinal cells, fetus, bone marrow (lymph nodes)

Question 27

How can intercellular ca2+ increase?

Answer 27

Mitochondria, injurious agent, smooth ER

Question 28

What can happen with increased intracellular ca2+?

Answer 28

Activate enzymes like phospholipase, protease, endonuclease, and atpase that can cause membrane damage, nuclear damage, and decreased ATP

Question 29

What can cause cell aging?

Answer 29

DNA damage, decreased cell replication, decreased functional proteins, and altered transcription due to environmental stress

Question 30

Features of a reversible injury

Answer 30

``` Cell swelling Fatty change Decreased ATP Altered ion flux Mito swelling Pyknosis Memb alterations ```

Question 31

Sings of an irreversible injury

Answer 31

Everything like reversible, as well as Increased eosinophilia Greater nuclear changes

Question 32

Manifestations of cell injury include cell accumulations like

Answer 32

``` Lipids Proteins Glycogen Water Pigments Calcium Urate ```

Question 33

Necrosis

Answer 33

Cell death due to loss of memb integrity and leakage of cell contents leading to local damage via inflammation

Question 34

Apoptosis

Answer 34

Cell death where cells activate enzymes that degrade the cells own DNA and nuc/cytoplasmic proteins. Plasma memb stays intact and the cell is phagocytosed. NO INFLAMMATION

Question 35

Pyknosis

Answer 35

Necrosis stage when chromatin condenses

Question 36

Karyorrhexis

Answer 36

Necrosis stage when chromatin fragments

Question 37

Karyolysis

Answer 37

Necrosis when cell bursts/ nucleus dissolves

Question 38

Eosinophilia

Answer 38

Sign of cytoplasmic changes during necrosis | Will take up eosin (h&e stain)

Question 39

Calcification during necrosis

Answer 39

Dead cells can be degraded into FA that bind calcium

Question 40

Coagulation necrosis

Answer 40

Protein denaturation - albumin turns opaque | Kidneys, heart, spleen, adrenal glands

Question 41

Liquefactive necrosis

Answer 41

Hydrologic enzymes | Neurons and glial cells of the brain

Question 42

Caseous necrosis

Answer 42

Combo of coagulation and liquefactive | Enclosed within inflammatory border (granuloma)

Question 43

Fat necrosis

Answer 43

Pancreas, breast, abdominal organs Activation of lipases Free FA and calcium

Question 44

Fibrinoid necrosis

Answer 44

Arteries | Antigens and antibodies are in walls of arteries

Question 45

Gangrenous necrosis

Answer 45

Result of hypoxia, affects limbs Dry - not enough to blood, coagulation, dry, crusty, black Wet - infection, liquefactive, cold, swollen, black, smelly

Question 46

Pathological causes of apoptosis

Answer 46

``` Embryogenesis Hormone depravation Proliferating populations End of usefulness Elimination of wbcs ```

Question 47

Pathological causes of apoptosis

Answer 47

DNA damage Accrual of misfolded proteins Injury from infections

Question 48

Mitochondrial apoptosis

Answer 48

BCL2 (apoptosis inhibitor) controlled Cyt c release= activate apoptosis Activate capsase

Question 49

Death receptor apoptosis

Answer 49

Death receptors activated, will activate capsases

Question 50

Autophagy

Answer 50

Lysosomal digestion of cells own components. A survival mechanism in times of nutrient depravation

Question 51

Reversible changes of the cells

Answer 51

Atrophy, hypertrophy, hyperplasia, metaplasia