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Block 3 Found Sci > 1-Cell Injury and Death > Flashcards

1-Cell Injury and Death Flashcards

1
Q

cell survival
depends on

A
  1. maintain ability to produce energy/ATP
  2. adapt to adverse environmental conditions

injury when stressed beyond adaptation

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2
Q

cell response depends on

A

dose
duration
type of injury

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3
Q

pathway of cell injury

A
  1. healthy cell
  2. stress
  3. adaptation
  4. cell injury if inability to adapt
  5. severe progression
  6. irreversible injury
  7. necrosis or apoptosis
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4
Q

causes of cell injury

A
  1. lack oxygen/hypoxia
  2. physical agents/ trauma
  3. chemical agents and drugs
  4. infectious agents
  5. immunologic rxns
  6. genetic defects
  7. nutritional imbalances
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5
Q

damaged cellular functions

A
  1. aerobic respiration mitochondrial oxidative phosphorylation and ATP
  2. integrity of cell membranes
  3. proteins synthesis
  4. cytoskeleton
  5. genetic apparatus
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6
Q

injurious stimulus

A
  1. membrane damage
  2. protein/cytoskeletal damage
  3. DNA damage

MPD

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7
Q

mitochondrial damage

results

A

-dec ATP
-inc ROS = damage to lipids, proteins, DNA

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8
Q

entry/influx calcium

mechanism

A
  1. inc mitochondrial permeability
  2. binds to activate enzymes
    -phospholipase breaks down phospholipids = membrane damage
    -protease disrupt membrane/cytoskeletal proteins = membrane damage
    -endonuclease breaks down DNA = nuclear damage
    -ATPase break down ATP = dec ATP
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9
Q

membrane damage

mechanism

A

-plasma membrane = loss cellular components
-lysosomal membrane = enzymes digest cellular components

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10
Q

protein misfolding

mechanism

A

activates pro-apoptotic proteins
ER stress

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11
Q

5 major mechanisms

A
  1. influx of calcium into cells, lose calcium homeostasis
  2. mitochondrial damage
  3. depletion of ATP
  4. acc of oxygen free radicals
  5. defects in membrane permeability
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12
Q

sources of calcium

A
  1. extracellular
  2. mitochondria
  3. SER
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13
Q

causes of mitochondrial injury

A
  1. inc Ca in cytosol
  2. oxidative stress
  3. breakdown of phospholipids by phospholipase A2 and sphingomyelin into free FA and ceramides
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14
Q

mitochondrial necrosis pathway

A
  1. dec oxygen, toxins, radiation
  2. mito damage
  3. dec ATP + inc ROS
  4. cellular abnormalities
  5. necrosis
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15
Q

mitochondrial apoptosis pathway

A
  1. survival signals DNA, protein damage
  2. inc pro-apoptotic proteins + dec anti-apop
  3. leakage of proteins
  4. apoptosis
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16
Q

consequences of dec ATP

mitochondrial

A
  1. dec Na/K pump and Ca pump > influx of Ca, H2O, and Na, efflux of K = swelling + blebs
  2. inc anaerobic glycolysis > inc lactic acid > dec pH > clump nuclear chromatin
  3. detachment of ribosomes = dec protein synthesis
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17
Q

ROS

A

O2-, OH, ONOO, lipid peroxidase radicals > membrane damage = cell injury

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18
Q

lipid peroxidation

membranes

A
  1. unsat FA with double bonds attacked by radicals
  2. peroxidases formed
  3. unstable peroxidase react with membrane lipids to make more peroxidases
  4. self sustaining and great damaged until captured by vitamin E, C, A, beta carotene
19
Q

protein oxidation

A
  1. side chains oxidized so change function/structure
  2. formation of disulfide bonds = cross linking
  3. cross links interupt folding
20
Q

DNA damage with radicals

A

radicals interact with thymine = single stranded breaks in DNA = mutations (also shown in carcinogenesis)

21
Q

removal of free radicals

A
  1. SOD (superoxide dismutase) converts superoxide to hydrogen peroxide
  2. glutathione peroxidase converts hydroxyl radical to hydrogen peroxide
  3. catalase converts hydrogen peroxide to water and oxygen
22
Q

neutrophils

A

-do not divide
-multinucleated
-uses ROS to destroy bacteria
-1st line of defense
-can acc with cytokines and cell adhesion molecules

23
Q

membrane permeability damage

A

found in most forms of cell injury
damage = activation of phospholipase in cytosol

no ATP prevents reacylation of phospholipids and dec synthesis so no repair

24
Q

characteristics of necrotic cells

A
  1. swelling of ER and loss ribosomes
  2. lysosome rupture
  3. myelin figures
  4. nuclear condensation/pyknosis > fragmentation
  5. swollen mitochondria
  6. eosinophilic and glassy cytoplasm

necrosis is always pathologic

25
Q

necrosis

definition

A

cell death from exogenous or endogenous damage leading to leaking cellular contents

not controlled so does not require signals

26
Q

apoptosis

definition

A

programmed cell death from external or internal damage, physiologic, or develop

cell fragmentation and phagocytosis

to eliminate unwanted or irreparably damaged cells thru enzymatic degradation so not trigger inflamm

physiologic or pathologic

27
Q

nuclear changes

necrosis

A

pkynosis-condensation
karyorrhexis- break up/fragmentation
karyolysis- dissolved

28
Q

types of necrosis

A
  1. coagulative
  2. liquefactive
  3. caseous
  4. enzymatic fat
  5. fibrinoid
  6. gangrenous
29
Q

coagulative necrosis

A

due to ischemia, hypoxia, reperfusion in organs with significant CT frameworks (except brain)

basic outline of cell preserved but no nuclei

30
Q

liquefactive necrosis

A

usually brain tissue bc only glial cells and not CT

in abscess with pus (enzymatic digested neutrophils)

amorphous, granular, loss of cell and tissue structure

31
Q

caseous necrosis

A

acc of mononuclear/macrophage that mediate chronic inflamm response and granuloma formation

grayish, whitish, yellowish, soft, friable, cheesy appearance

32
Q

enzymatic fat necrosis

A

fatty acids react with calcium to form soap like substance

white, chalky appearance in fat cells or basophilic calcium

usually pancreatitis

33
Q

fibrinoid necrosis

A

injury in blood vessels with acc of plasma proteins (fibrin and debris)

very eosinophilic

34
Q

gangrenous necrosis

A

loss of circulation to a limb or bowel

wet gangrene = combo with superimposed bacterial infection

35
Q

reperfusion

A

blood flow/oxygen restored to ischemic tissues but leads to large amounts of ROS

clot treatment for heart attack and stroke

36
Q

necrosis serum tests

A

creatine kinase or troponin levels elevated in serum after MI = necrosis

37
Q

physiological roles apoptosis

A
  1. embryogenesis
  2. hormone dependent involution
  3. cell celetion in proliferating cell pop
  4. normal immune defense vs viral infections or neoplastic cells aka cytotoxic T cell clearance
  5. removal self reactive lymphocyte clones
  6. removal cells served purpose i.e inflamm cells
38
Q

pathologic conditions apoptosis

A
  1. cell death in tumors
  2. DNA damage from low doses of agents that would cause necrosis in high doses
  3. transplant rejection
  4. atrophy after duct obstruction
  5. some viral diseases
39
Q

stages of apoptosis

A
  1. intrinsic activated (cytochrome c released) or extrinsic (receptor activated)
  2. initiation: intracell signals commit cell to apop by syn/activating initiator caspases
  3. execution: execution caspases catabolize cytoskeleton, activate endonucleases for DNA break down
  4. removal: removal round dead fragments of cells by macrophages
40
Q

intrinsic apoptosis triggers

A
  1. growth factor withdrawal
  2. DNA damage via radiation, toxins, free radicals, p53 will act proapoptic Bcl-2 to stim Bax/Bak
  3. protein misfolding i.e ER stress

cyt c will release thru Bak/Bax dimerized channel in mito membrane

mitochondrial

41
Q

extrinsic apoptosis triggers

A
  1. receptor ligand interactions aka Fas or TNF (tumor necrosis factor) receptor > act adaptor proteins to bind caspases
42
Q

chemicals for cell injury

A
  1. acetaminophen: highly reactive quinone reacts with protein, DNA = oxidative stress
  2. carbon tetrachloride: metabolite reacts w/ membrane and ER
  3. heavy metals/cyanide: mitochondria
  4. phalloidin/paclitaxel: cytoskeleton
  5. chemotherapeutic alkylating agents: DNA
43
Q

SER induction

aka hypertrophy

A

adaptive response to become more efficient if metabolizing or detoxing barbituates + p-450 mixed function oxidase system

Block 3 Found Sci (60 decks)

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