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
Hypoxia
reduced oxygen availability most common cause of cell injury
26
Hypoxia caused by
-reduced oxygen content in air -loss of hemoglobin -decrease in RBCs production -respiratory/CV complications -poisoning of intracellular oxidative enzymes -ischemia-most common cause
27
_________can induce inflammations and make inflamed lesions _____
Hypoxia, Hypoxic
28
Ischemia
-reduced blood supply -cell ruptures --> inner components released
29
Ischemia is caused by
-occluded vessels (effects well-studies in cardiac muscle) -insufficiency in blood supply --> O2 supply --> ATP production
30
Ischemia inside the cell:
-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
31
Helpful diagnostic tool for MI
in ischemia after cell ruptures-Troponin released by damaged myocytes after MI-shows up on blood test
32
Ischemia-reperfusion injury
-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-)
33
Reperfusion generates _______ that further damages cell
ROS- Reactive Oxygen Species
34
ATP consumption leads to build up of purine catabolites____and_______
xanthine and hypoxanthine
35
Influx of O2 causes rapid metabolism of hypoxanthine and xanthine to create massive amounts of _______and_______
superoxide, hydrogen peroxide
36
Oxidative stress
-caused by free radicals and ROS = Endogenous antioxidant systems are overwhelmed
37
Free radicals
-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
Effects of oxidative stress
-targets plasma membrane! -can initiate the destruction of of organelles, entire cell -fragmentation of proteins/DNA
39
Antioxidants
-Vit E, C -Albumin -Transferrin -donate free electron to unstable free radical, neutralizing the threat like ROS
40
Superoxide neutralized by;
Superoxide dismutase
41
Hydrogen peroxide neutralized by;
Catalase
42
Hydroxy radical neutralized by;
Glutathione peroxidase
43
ROS is heavily implicated in..
Heart disease and neurodegeneration
44
chemical injury
toxic substance injures cell directly (plasma membrane or other organelle) or with a toxic metabolite
45
chemical injury examples
-lead/mercury/arsenic-poison -ethanol -cyanide -carbon monoxide
46
Lead poisoning
-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
Stored in blood (weeks), soft tissues( mouth) and bone (years)can continuously be released into blood long after exposure
Lead poisoning
48
Ethanol
-readily absorbed into the blood, easily crosses blood-brain barrier BBB -needs to be ingested
49
Acute intoxication
-drunkness -depression of CNS fxns -Sedation, drowsiness, loss of coordination, altered behavior,loss of consciousness -extreme amounts lead to coma, respiratory come, death
50
Chronic intoxication
-alcoholism -ALTERS NEARLY EVERY ORGAN TISSUE -CELL INJURY TO OXIDATIVE STRESS -fatty live disease, liver cirrhosis, live cancer
51
Cyanide
-lethal, kills fast -targets electron transport chain in mitochondria, impairs formation of ATP -Cytochrome oxidase -without ATP, cells dysfunction and die quickly
52
Carbon monoxide
-CO binds to hemoglobin molecules of RBCs -tissue becomes hypoxic -treated with hyperbaric oxygen chamber
53
Infectious agents
Microorganisms invade the body and proliferate, causing damage to cells and tissues
54
Disease-producing potential of a microorganism depends on its ability to:
-invade and destroy cells -produce toxins -produce damaging hypersensitive reactions
55
Nutritional imbalances
-too much/too little (protein, carbs, lipids, vitamins, minerals)
56
Protein malnutrition
-most common worldwide -deficiency reduces absorptive fxn of gut, diminishes hormone secretion, can lead to edema
57
Vit deficiency
-13 essential vitamins identified -required for fxn of cells example: Vit B1 thiamine def--> encephalopathy; presents as psychosis,delusional, common in alcoholics
58
Immunological rxns
-cell membranes injured by direct contact with components of immune system- ex allergies
59
Genetic factors
-disorders or dysfunction in genetic info harms cells -inherited: sickle cell anemia -acquired-cancer
60
physical trauma
-mechanical stress -temp extremes -sound -radiation -atmospheric pressure -illumination
61
Cell accumulations
Manifestation of cell injury
62
Four mechanisms of accumulation
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
water
cell swelling, most common degenerative change
64
lipids and carbohydrates
-accumulate dues to insufficient enzymes ex, fatty liver dx from alc abuse
65
proteins
-disrupts organelle fxn ex. albumin in kidney
66
calcium
Ca2+ is essential for signaling but too much is cytotoxic -apoptosis ex; atherosclerosis, tumor
67
systemic manifestations of cell injury
-fatigue/malaise -altered apetite -pain -fever
68
Apoptosis
cell is degraded with minimal effect to surrounding tissue, no inflamm
69
2 phases of apoptosis
-initiation-activation of caspases (cleaves DNA) -execution- ACTION OF CAPASES CAUSES DEATH
70
Necrosis
disorganized, unregulated, cell death and dissolution (autolysis) -always pathologic, inflammatory -explosion, burst open
71
Types of necrosis
-coagulative -liquefactive -caseous -fat -gangrenous
72
Coagulation
-kideny, heart, adrenal glads -protein degranulation -albumin coagulates-turns opaque like cooked egg
73
Liquefactive
-neuron, glial cells -dead brain cells digested by their own hydrolytic enzymes -tissue liquefies
74
Caseous
-result of TB so in lungs -dead cells not completely digested, resembles clumped cheese
75
fat
-breast, pancreas, other abdominal organs -lipases dissolve cells into free fatty acids which combine with Ca2+, Mg2+, Na+ -creates soaps, saponification
76
Gangrenous
-not distinct type of necrosis: larger areas of tissue death -result of sever hypoxic injury -dry=frostbite -wet= bacterial infection
77
somatic death
-death on entire person
78
algor mortis
reduced temp
79
livor mortis
purple skin discoloration
80
rigor mortis
muscle stiffening
81
postmortem autolysis
breakdown of cell membranes leads to release of enzymes