Cell Injury, Death, And Adaptations Flashcards Preview

DMD 5243 > Cell Injury, Death, And Adaptations > Flashcards

Flashcards in Cell Injury, Death, And Adaptations Deck (51):
1

Atrophy

Cell shrinking

2

Hypertrophy

Cell getting bigger

3

Hyperplasia

More cells

4

Metaplasia

Changing cells

5

Dysplasia

Always bad, never normal, only pathological

6

Why would a cell undergo atrophy?

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

7

When would a cell undergo hypertrophy or hyperplasia?

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

8

When would a cell undergo metaplasia?

Increased capacity to enable tissue survival - persisting injury

9

What determines obesity?

Size

10

What determines adipocytes number?

Gestational birth weight
Maternal insulin
In utero toxin exposure

11

Causes of cell injury (10)

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

12

Most common type of cell injury

Oxygen depravation

13

Ischemia

Little oxygen to tissues

14

Hypoxia

little oxygen to cells = decrease ATP

15

Anoxia

No oxygen to cells = decrease ATP

16

What happens to a cell under oxygen depravation?

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

17

What happens to the ETS under oxidative stress?

Electron buildup and the production of a superoxide

18

SOD

Super oxidase dismutase
Will convert superoxide radical into hydrogen peroxide

19

What can hydrogen peroxide do in a cell?

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

20

When can mitochondrial swelling occur?

Hypoxia

21

Asphyxial cell injuries

Suffocation, strangulation, chemical asphyxiates, drowning

22

Chemical agents that can cause cell injury

Lead, carbon monoxide, ethanol, Mercury, drugs

23

Immunologic reactions to cell injury

Phagocytic cells
Immune and inflammatory substances
Membrane alterations

24

Hypothermic injury

Slows cell metabolic processes

25

Hyperthermia injury

Heat cramps, heat exhaustion, heat stroke

26

Radiation can affect what type of cells

Gastrointestinal cells, fetus, bone marrow (lymph nodes)

27

How can intercellular ca2+ increase?

Mitochondria, injurious agent, smooth ER

28

What can happen with increased intracellular ca2+?

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

29

What can cause cell aging?

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

30

Features of a reversible injury

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

31

Sings of an irreversible injury

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

32

Manifestations of cell injury include cell accumulations like

Lipids
Proteins
Glycogen
Water
Pigments
Calcium
Urate

33

Necrosis

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

34

Apoptosis

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

35

Pyknosis

Necrosis stage when chromatin condenses

36

Karyorrhexis

Necrosis stage when chromatin fragments

37

Karyolysis

Necrosis when cell bursts/ nucleus dissolves

38

Eosinophilia

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

39

Calcification during necrosis

Dead cells can be degraded into FA that bind calcium

40

Coagulation necrosis

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

41

Liquefactive necrosis

Hydrologic enzymes
Neurons and glial cells of the brain

42

Caseous necrosis

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

43

Fat necrosis

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

44

Fibrinoid necrosis

Arteries
Antigens and antibodies are in walls of arteries

45

Gangrenous necrosis

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

46

Pathological causes of apoptosis

Embryogenesis
Hormone depravation
Proliferating populations
End of usefulness
Elimination of wbcs

47

Pathological causes of apoptosis

DNA damage
Accrual of misfolded proteins
Injury from infections

48

Mitochondrial apoptosis

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

49

Death receptor apoptosis

Death receptors activated, will activate capsases

50

Autophagy

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

51

Reversible changes of the cells

Atrophy, hypertrophy, hyperplasia, metaplasia