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Pathophys > Unit 1a Cell injury and death > Flashcards

Unit 1a Cell injury and death Flashcards

1
Q

Adaptation

A

a change in response to some stimulus or signal

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2
Q

Acute adaptation

A

resolves on its own, once stimulus /signal is removed

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3
Q

Chronic adaptation

A

may deteriorate into dx

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4
Q

Atrophy

A

decrease in cell size, cells have less ER and mitochondria, protein production

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5
Q

Hypertrophy

A

increase in cell size, increased ER, mitochondria, DNA synthesis

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6
Q

Hyperplasia

A

-increase in cell number, more cell division
-can only occur in cells that normally divide

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7
Q

Metaplasia

A

replacement of one mature cell type with another

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8
Q

Dysplasia

A

deranged cell growth, with no benefit/organization

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9
Q

what causes atrophy?

A

from lack of use, nutrition, blood supply, hormones

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10
Q

Atrophy examples

A

-thymus during development, gets smaller as you get older
-Skeletal muscles in bed-ridden ppl

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11
Q

Hypertrophy examples

A

-skeletal muscles in response to incr workload(working out)
-cardiac myocytes in response to high BP

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12
Q

What causes Hypertrophy

A

mechanical or trophic signals

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13
Q

What causes hyperplasia

A

tissue or organ damage

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14
Q

Hyperplasia examples

A

-callus formation from repeated mechanical stimulus
-endometrial hyperplasia-thickening can resolve on its own or develop into cancer

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15
Q

Metaplasia characteristic

A

physiological change if temporary
pathological change if permanent

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16
Q

Metaplasia example

A

-columnar ciliated epithelial cell replaced by stratified squamous epithelial cell in airways=smokers cough

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17
Q

Dysplasia characteristics

A

-Not a true adaptive change
-abnormal shape, size, organization of cells
-cells cant mature
-cells return to normal or progress to cancer
-common in epithelial tissue; cervix, skin, GI tract, respiratory tract.
-differnt fxn

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18
Q

meta=

A

mature

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19
Q

plasia=

A

more cells

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20
Q

dys=

A

disorgainzed

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21
Q

trophy=

A

growth

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22
Q

hyper=

A

increase

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23
Q

cell injury

A

-mild and transient stress, injury is reversible and cell recovers
-severe and progressive stress, injury is irreversible and cell dies

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24
Q

4 organelles most vulnerable to damage

A

nucleus, cell membrane, ribosomes, mitochondria

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25
Q

Hypoxia

A

reduced oxygen availability
most common cause of cell injury

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26
Q

Hypoxia caused by

A

-reduced oxygen content in air
-loss of hemoglobin
-decrease in RBCs production
-respiratory/CV complications
-poisoning of intracellular oxidative enzymes
-ischemia-most common cause

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27
Q

_________can induce inflammations and make inflamed lesions _____

A

Hypoxia, Hypoxic

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28
Q

Ischemia

A

-reduced blood supply
-cell ruptures –> inner components released

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29
Q

Ischemia is caused by

A

-occluded vessels (effects well-studies in cardiac muscle)
-insufficiency in blood supply –> O2 supply –> ATP production

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30
Q

Ischemia inside the cell:

A

-accumulation of Na+ and Ca2+
-water follows Na+, cell swells
cell can recover in O2 restored
-accumulated Ca2+ signals self-destruct cascade
-cell ruptures-inner components released

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31
Q

Helpful diagnostic tool for MI

A

in ischemia after cell ruptures-Troponin released by damaged myocytes after MI-shows up on blood test

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32
Q

Ischemia-reperfusion injury

A

-restoration of O2 supply following ischemia can cause additional injury
-seen most commonly in: tissue transplant, myocardial, hepatic, renal, and cerebral ischemia
-explosion of ROS, (steal e-)

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33
Q

Reperfusion generates _______ that further damages cell

A

ROS- Reactive Oxygen Species

34
Q

ATP consumption leads to build up of purine catabolites____and_______

A

xanthine and hypoxanthine

35
Q

Influx of O2 causes rapid metabolism of hypoxanthine and xanthine to create massive amounts of _______and_______

A

superoxide, hydrogen peroxide

36
Q

Oxidative stress

A

-caused by free radicals and ROS
= Endogenous antioxidant systems are overwhelmed

37
Q

Free radicals

A

-electriclly uncharged atom (s) with an unpaired e-
-highly unstable!
-naturally generated in mitochondria, usually neutralized by endogenous antioxidants
-mitochondria are biggest source of and target ROS

38
Q

Effects of oxidative stress

A

-targets plasma membrane!
-can initiate the destruction of of organelles, entire cell
-fragmentation of proteins/DNA

39
Q

Antioxidants

A

-Vit E, C
-Albumin
-Transferrin
-donate free electron to unstable free radical, neutralizing the threat like ROS

40
Q

Superoxide neutralized by;

A

Superoxide dismutase

41
Q

Hydrogen peroxide neutralized by;

A

Catalase

42
Q

Hydroxy radical neutralized by;

A

Glutathione peroxidase

43
Q

ROS is heavily implicated in..

A

Heart disease and neurodegeneration

44
Q

chemical injury

A

toxic substance injures cell directly (plasma membrane or other organelle) or with a toxic metabolite

45
Q

chemical injury examples

A

-lead/mercury/arsenic-poison
-ethanol
-cyanide
-carbon monoxide

46
Q

Lead poisoning

A

-Absorbed through skin or mucous membranes (eyes, nose, throat, stomach)
-mimics other metals (Ca2+, Fe 2+, Zn 2+) in biological processes
-interferes with the production of heme- severe anemia
-toxic to nerve cells

47
Q

Stored in blood (weeks), soft tissues( mouth) and bone (years)can continuously be released into blood long after exposure

A

Lead poisoning

48
Q

Ethanol

A

-readily absorbed into the blood, easily crosses blood-brain barrier BBB
-needs to be ingested

49
Q

Acute intoxication

A

-drunkness
-depression of CNS fxns
-Sedation, drowsiness, loss of coordination, altered behavior,loss of consciousness
-extreme amounts lead to coma, respiratory come, death

50
Q

Chronic intoxication

A

-alcoholism
-ALTERS NEARLY EVERY ORGAN TISSUE
-CELL INJURY TO OXIDATIVE STRESS
-fatty live disease, liver cirrhosis, live cancer

51
Q

Cyanide

A

-lethal, kills fast
-targets electron transport chain in mitochondria, impairs formation of ATP
-Cytochrome oxidase
-without ATP, cells dysfunction and die quickly

52
Q

Carbon monoxide

A

-CO binds to hemoglobin molecules of RBCs
-tissue becomes hypoxic
-treated with hyperbaric oxygen chamber

53
Q

Infectious agents

A

Microorganisms invade the body and proliferate, causing damage to cells and tissues

54
Q

Disease-producing potential of a microorganism depends on its ability to:

A

-invade and destroy cells
-produce toxins
-produce damaging hypersensitive reactions

55
Q

Nutritional imbalances

A

-too much/too little (protein, carbs, lipids, vitamins, minerals)

56
Q

Protein malnutrition

A

-most common worldwide
-deficiency reduces absorptive fxn of gut, diminishes hormone secretion, can lead to edema

57
Q

Vit deficiency

A

-13 essential vitamins identified
-required for fxn of cells
example: Vit B1 thiamine def–> encephalopathy; presents as psychosis,delusional, common in alcoholics

58
Q

Immunological rxns

A

-cell membranes injured by direct contact with components of immune system- ex allergies

59
Q

Genetic factors

A

-disorders or dysfunction in genetic info harms cells
-inherited: sickle cell anemia
-acquired-cancer

60
Q

physical trauma

A

-mechanical stress
-temp extremes
-sound
-radiation
-atmospheric pressure
-illumination

61
Q

Cell accumulations

A

Manifestation of cell injury

62
Q

Four mechanisms of accumulation

A

1.excess of normal endogenous substances
2. abnormal substance as result of gene or protein defect
3. endogenous ( in cell) substance not effectively catabolized
4. harmful exogenous (not normally found in the cell) material

63
Q

water

A

cell swelling, most common degenerative change

64
Q

lipids and carbohydrates

A

-accumulate dues to insufficient enzymes
ex, fatty liver dx from alc abuse

65
Q

proteins

A

-disrupts organelle fxn
ex. albumin in kidney

66
Q

calcium

A

Ca2+ is essential for signaling but too much is cytotoxic -apoptosis
ex; atherosclerosis, tumor

67
Q

systemic manifestations of cell injury

A

-fatigue/malaise
-altered apetite
-pain
-fever

68
Q

Apoptosis

A

cell is degraded with minimal effect to surrounding tissue, no inflamm

69
Q

2 phases of apoptosis

A

-initiation-activation of caspases (cleaves DNA)
-execution- ACTION OF CAPASES CAUSES DEATH

70
Q

Necrosis

A

disorganized, unregulated, cell death and dissolution (autolysis)
-always pathologic, inflammatory
-explosion, burst open

71
Q

Types of necrosis

A

-coagulative
-liquefactive
-caseous
-fat
-gangrenous

72
Q

Coagulation

A

-kideny, heart, adrenal glads
-protein degranulation
-albumin coagulates-turns opaque like cooked egg

73
Q

Liquefactive

A

-neuron, glial cells
-dead brain cells digested by their own hydrolytic enzymes
-tissue liquefies

74
Q

Caseous

A

-result of TB so in lungs
-dead cells not completely digested, resembles clumped cheese

75
Q

fat

A

-breast, pancreas, other abdominal organs
-lipases dissolve cells into free fatty acids which combine with Ca2+, Mg2+, Na+
-creates soaps, saponification

76
Q

Gangrenous

A

-not distinct type of necrosis: larger areas of tissue death
-result of sever hypoxic injury
-dry=frostbite
-wet= bacterial infection

77
Q

somatic death

A

-death on entire person

78
Q

algor mortis

A

reduced temp

79
Q

livor mortis

A

purple skin discoloration

80
Q

rigor mortis

A

muscle stiffening

81
Q

postmortem autolysis

A

breakdown of cell membranes leads to release of enzymes

Pathophys (11 decks)

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