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

Cell Injury, Death, And Adaptations Flashcards

1
Q

Atrophy

A

Cell shrinking

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2
Q

Hypertrophy

A

Cell getting bigger

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3
Q

Hyperplasia

A

More cells

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4
Q

Metaplasia

A

Changing cells

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5
Q

Dysplasia

A

Always bad, never normal, only pathological

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6
Q

Why would a cell undergo atrophy?

A

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

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7
Q

When would a cell undergo hypertrophy or hyperplasia?

A

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

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8
Q

When would a cell undergo metaplasia?

A

Increased capacity to enable tissue survival - persisting injury

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9
Q

What determines obesity?

A

Size

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10
Q

What determines adipocytes number?

A

Gestational birth weight
Maternal insulin
In utero toxin exposure

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11
Q

Causes of cell injury (10)

A 
Oxygen deprivations
Chemical agents
Infectious agents
Immunologic reactions
Genetic factors
Nutritional imbalances
Physical agents
Radiation
Calcium
Aging
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12
Q

Most common type of cell injury

A

Oxygen depravation

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13
Q

Ischemia

A

Little oxygen to tissues

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14
Q

Hypoxia

A

little oxygen to cells = decrease ATP

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15
Q

Anoxia

A

No oxygen to cells = decrease ATP

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16
Q

What happens to a cell under oxygen depravation?

A 
Decrease in ATP 
= failure of sodium potassium and calcium pump
= cell swelling
= reduce pH
Under extreme conditions, cell can burst
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17
Q

What happens to the ETS under oxidative stress?

A

Electron buildup and the production of a superoxide

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18
Q

SOD

A

Super oxidase dismutase

Will convert superoxide radical into hydrogen peroxide

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19
Q

What can hydrogen peroxide do in a cell?

A

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

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20
Q

When can mitochondrial swelling occur?

A

Hypoxia

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21
Q

Asphyxial cell injuries

A

Suffocation, strangulation, chemical asphyxiates, drowning

22
Q

Chemical agents that can cause cell injury

A

Lead, carbon monoxide, ethanol, Mercury, drugs

23
Q

Immunologic reactions to cell injury

A

Phagocytic cells
Immune and inflammatory substances
Membrane alterations

24
Q

Hypothermic injury

A

Slows cell metabolic processes

25
Q

Hyperthermia injury

A

Heat cramps, heat exhaustion, heat stroke

26
Q

Radiation can affect what type of cells

A

Gastrointestinal cells, fetus, bone marrow (lymph nodes)

27
Q

How can intercellular ca2+ increase?

A

Mitochondria, injurious agent, smooth ER

28
Q

What can happen with increased intracellular ca2+?

A

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

29
Q

What can cause cell aging?

A

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

30
Q

Features of a reversible injury

A 
Cell swelling
Fatty change
Decreased ATP 
Altered ion flux
Mito swelling
Pyknosis
Memb alterations
31
Q

Sings of an irreversible injury

A

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

32
Q

Manifestations of cell injury include cell accumulations like

A 
Lipids
Proteins
Glycogen
Water
Pigments
Calcium
Urate
33
Q

Necrosis

A

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

34
Q

Apoptosis

A

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
Q

Pyknosis

A

Necrosis stage when chromatin condenses

36
Q

Karyorrhexis

A

Necrosis stage when chromatin fragments

37
Q

Karyolysis

A

Necrosis when cell bursts/ nucleus dissolves

38
Q

Eosinophilia

A

Sign of cytoplasmic changes during necrosis

Will take up eosin (h&e stain)

39
Q

Calcification during necrosis

A

Dead cells can be degraded into FA that bind calcium

40
Q

Coagulation necrosis

A

Protein denaturation - albumin turns opaque

Kidneys, heart, spleen, adrenal glands

41
Q

Liquefactive necrosis

A

Hydrologic enzymes

Neurons and glial cells of the brain

42
Q

Caseous necrosis

A

Combo of coagulation and liquefactive

Enclosed within inflammatory border (granuloma)

43
Q

Fat necrosis

A

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

44
Q

Fibrinoid necrosis

A

Arteries

Antigens and antibodies are in walls of arteries

45
Q

Gangrenous necrosis

A

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

46
Q

Pathological causes of apoptosis

A 
Embryogenesis
Hormone depravation
Proliferating populations
End of usefulness
Elimination of wbcs
47
Q

Pathological causes of apoptosis

A

DNA damage
Accrual of misfolded proteins
Injury from infections

48
Q

Mitochondrial apoptosis

A

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

49
Q

Death receptor apoptosis

A

Death receptors activated, will activate capsases

50
Q

Autophagy

A

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

51
Q

Reversible changes of the cells

A

Atrophy, hypertrophy, hyperplasia, metaplasia

DMD 5243 (11 decks)

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