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Pathophysiology > 4 Cell injury, aging, and death > Flashcards

4 Cell injury, aging, and death Flashcards

1
Q

tissue hypoxia

A
  • lack of oxygen
  • causes power failure in cell
  • often caused by ischemia
  • may be caused by heart failure, lung disease, RBC disorders
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2
Q

ischemia

A
  • disrupts blood supply to a tissue> allows metab wastes to accumulate + deprives cell of nutrients for glycolysis>lactic acidosis
  • most common cause of cell injury
  • chronic sublethal ischemia usually results in atrophy
  • injures cells faster than hypoxia alone
  • results in think skin, muscle wasting, hair loss
  • can be due to chronic nutrient starvation
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3
Q

why does hypoxia cause cell injury

A

oxygen is needed to make ATP

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4
Q

how does hypoxia work

A

1 lack of O means no ATP produced
2 w/o ATP, waste accumulates inside cell
3 w/o ATP, Na cannot pump out of cell
4 accumulation of Na in cell, causes water to move in
5 accumulation of Na causes hydropic swelling, which cause 0 protein synth

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5
Q

3 ways cells respond to environmental changes or injury

A

1 reversible cell injury
2 adaptation
3 apoptosis/necrosis

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6
Q

reversible cell injury

A

when change is mild or short lived, the cell may withstand assault + return to normal

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7
Q

which cell response to change/injury is reversible and irreversible?

A

reversible cell injury + adaptation are reversible.

cell death aka apoptosis or necrosis are irreversible

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8
Q

reversible cell injury

A
  • results in cell swelling + accumulation of excess substances in cell
  • changes affect dysfunction in ATP, normal metab functions, or metab enzymes

-once acute stress is removed, the cell returns to its preinjury state

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9
Q

hydropic swelling aka oncosis

A
  • accumulation of water in cell
  • usually due to malfunction in Na-K pumps which is dependent on ATP
  • characterized by large pale cytoplasm, dilates E.R., + swole mitochondria
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10
Q

intracellular accumulations categories

A

1 excessive amt of normal intracellular substances like fat
2 accum of abnormal substances produced by cell bc faulty metab or synth
3 accum of pigments/particles that cell is unable to degrade

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11
Q

normal intracellular substances that tend to accumulate

A

lipid, glycogen, carb, proteins

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12
Q

accum of fat/lipid in liver is associated w…

A

excessive intake of alcohol

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13
Q

2 ways the cell limits accum of abnormal intracellular protein

A

1 chaperone proteins attempt to refold abnormal proteins into its correct shape
2 ubiquitin-proteasome system that digest targeted proteins into fragments

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14
Q

atrophy

A

when cells shrink and reduce their differentiated functions in response to a variety of normal and injurious factors

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15
Q

6 general causes of atrophy

A 
1 disuse
2 denervation
3 ischemia
4 nutrient starvation
5 interruption of endocrine signals
6 persistent cell injury
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16
Q

common form of atrophy that is a result from reduction of functional deman

A

disuse atrophy

ex) immobilization fr bed rest or casting. on resumption of activity, the tissue returns to its normal size

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17
Q

atrophy that results fr persistent cell injury is most commonly related to…

A

chronic inflammation + infection

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18
Q

2 pathways for protein degradation

A 
1 ubiquitin-proteasome systm (degrades to small fragments)
2 autophagy (lysosomes fuse w intracellular structures leading to hydrolytic degradation of components)
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19
Q

hypertrophy

A

increase in cell mass accompanies by an augmented functional capacity

  • response to increased physiologic or pathophysiologic demands
  • subsides when increased demand is removed but may not return to normal
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20
Q

cellular enlargements results primarily from…

A

a net increase in cellular proteins content

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21
Q

organ enlargement may result of…

A

hypertrophy (increase in cell size) and hyperplasia (increase in cell number)

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22
Q

examples of hypertrophy and hyperplasia in muscle cells

A

hypertrophy- increase in skeletal muscle mass fr exercise

hyperplasia - division of satellite cells (muscle stem cells)

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23
Q

example of physiologic hypertrophy

A

breast + uterus due to trophic hormones

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24
Q

hyperplasia

A

increase in number of cells

  • cells that are capable of mitotis division generally increase their functional capacity
  • may also result fr persistent cell injury
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25
Q

an increase in RBC in response to high altitude or liver enlargement in response to drug detox are examples of

A

demand-induced hyperplasia

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26
Q

increase in division of endometrial/uterine cells in response to estrogen is an example of…

A

trophic hormone induced hyperplasia

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27
Q

dysregulation of hormones or growth factors can result in…

A

pathologic hyperplasia

ex thyroid or prostate enlargement

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28
Q

examples of hyperplasia due to chronic irritation of epithelial cells

A

corns + calluses

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29
Q

metaplasia

A

replacement of one differentiated cell type w another

-most often occurs as adaptation to persistent injury w replacement of cell type that can better tolerate injurious stimulation

  • fully reversible when injurious stimuli is removed
  • may become cancerous
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30
Q

5 types of adaptive cellular response

A 
1 atrophy (shrink)
2 hypertrophy (enlargen)
3 hyperplasia (inc in number)
4 metaplasia (conversion of one cell type to another)
5  dysplasia (disorderly growth)
31
Q

common cell type conversion in metaplasia

A

glandular epithelium to squamous epithelium

32
Q

dysplasia

A

disorganized appearance of cells bc of abnormal variations in size, shape, + arrangement

  • occurs more frequently in hyperplastic squamous epithelium
  • may occur in intestinal mucosa
  • significant pot’l to become cancerous; usually regarded as preneoplastic lesions
33
Q

carcinoma in situ

A

severe dysplasia that involves entire thickness of epithelium

34
Q

necrosis vs apoptosis

A
  • both are irreversible cell injury
  • necrosis is usually cell rupture. spilling of contents into ECF, + inflammation; due to ischemia or toxic injury
  • apoptosis usually dont rupture, usually ingested w minimal disruption w/o inflammation; due to injury that doesnt directly kill but triggers intracellular cascades that activate cell suicide, requires adequate ATP
35
Q

morphological changes in necrotic cells

A
  • pyknotic (shrunken nucleus)
  • karyolysis (degraded nucleus)
  • swollen cell vol
  • dispersed ribosome
  • disrupted plasma + organelle membranes
36
Q

critical event in necrosis cell death

A

disruption of permeability barrier of plasma membrane

37
Q

manifestations that indicate necrosis

A
  • inflammation
  • malaise
  • fever
  • inc heart rate
  • inc WBC count
  • loss of appetite
38
Q

presence of specific cellular proteins in the blood is used as an indicator of…

A

the location + extent of necrosis cell death

ex) inc in amylase in serum indicates pancreatic damage
ex) inc in kinase or cardiac troponin indicates myocardial damage

39
Q

4 types of tissue necrosis

A

1 coagulative
2 liquefactive
3 fat
4 caseous

*they differ primarily in type of tissue affected

40
Q

which type of tissue necrosis is most common?

A

coagulative necrosis

41
Q

cascading manifestations of coagulative necrosis

A

*manifestations of coagulative necrosis are the same regardless of the cause of cell death

1 ischemic cellular injury
2 loss of plasma membrane’s ability to maintain electrochem gradients
3 influx of Ca ions + mitochondrial dysfunctions
4 degradation of plasma membranes + nuclear structures

42
Q

coagulative necrosis

A
  • area of coagulative necrosis is composed of denatures proteins + is relatively solid
  • then slowly dissolved by proteolytic enzymes
  • general tissue architecture is preserved for long time (weeks) (unlike liquefactive necrosis)
43
Q

liquefactive necrosis

A
  • dissolution of dead cells occurs v quickly
  • a liquefied area of lysosomal enzymes + dissolved tissue nay result to form an abscess or cyst
  • may be seen in brain (rich in degradative enzymes + little supportive tissue)
  • may result fr bacterial infections that triggers localized collection of WBC (phagocytic WBC contain potent degradative enzymes that digest dead cells + produce liquid debris)
44
Q

fat necrosis

A

death of adipose tissue

-usually results fr trauma or pancreatitis

45
Q

fat necrosis process

A

1 release of activated digestive enzymes fr pancreas or injured tissue
2 enzymes attack cell membrane of fat cells, cause release of stored triglycerides
3 pancreatic lipase can hydrolyze the triglycerides to free fatty acids + glycerol, which precipitate as Ca soaps
-fat necrosis appears as chalky white area of tissue

46
Q

caseous necrosis

A

characteristic of lung tissue damaged by tuberculosis

  • area of dead lung tissue are white, solf, fragile resembling clumpy cheese
  • dead cells are walled off fr rest of lung tissue by inflammatory WBC
  • in center, dead cells lose their cellular structure but are not totally degraded
  • necrotic may persist indefinitely
47
Q

gangrene

A

term used to describe cell death involving large area of tissue
-usually results fr interruption of major blood supply to body part

48
Q

types of gangrene and their type of necrosis

A

dry gangrene is coagulative necrosis

wet gangrene is liquefactive necrosis

gas gangrene infection of necrotic tissue by clostridium

49
Q

in contrast to necrosis, apoptosis is…

A

tidy and does not elicit inflammation.

it is usually a normal physiologic process that regulate normal system function

50
Q

necrosis and apoptosis portion of tissue death after a myocardial infarction (heart attack)

A

20% necrosis

80% apoptosis

51
Q

when the rate of apoptosis is ___ than the rate of cell replacement, tissue/organ function may be impaired

A

GREATER

52
Q

EXTRINSIC SIGNALS that cause apoptosis

A
  • may be triggered by withdrawal of “survival” signals that normally suppress apoptotic pathways
  • -if contacts/signals are removed, cell death cascade is activated
  • extracellular signals (like Fas ligand) that bind to the cell + trigger the death cascade thru activation of death receptors
53
Q

P53

A

protein that governs an INTRINSIC apoptosis pathway

  • TUMOR SUPPRESSOR GENE
  • normally low amt but inc in response to severe cellular DNA damage
  • high levels cause apoptosis
54
Q

caspases

A

family of enzymes that are the main components of proteolytic cascade that degrades key intracellular structures leading to cell death.

-proenzymes that are activated in a cascade

55
Q 
type of tissue necrosis for each organ:
1 heart
2 brain
3 lung 
4 pancreas
A

1 heart -COAGULATIVE
2 brain -LIQUEFACTIVE
3 lung -CASEOUS
4 pancreas -FAT

56
Q

anaerobic respiration

A
  • due to hypoxia
  • pyruvate end products fr glycolysis are converted into LACTATE
  • lactate released in bloodstream results in LACTIC ACIDOSIS
  • as pH falls, cellular proteins + enzymes become more dysfunctional
57
Q

reperfusion injury

A

most cellular damage occurs after the blood supply to tissues has been restored

58
Q

3 components of ischemia-reperfusion

A

1 Ca overload fr blood
2 formation of free radicals
3 subsequent inflammation

59
Q

free radicals

A

reactive O molecules bc of unpaired electrons on outer orbital

  • they steal H atoms + form abnormal bonds
  • damage cell membrane, denature proteins, disrupt cell chromosomes

ex superoxide (O2 -), peroxide (H2O2), hydroxyl radicals (OH-)

60
Q

why can’t ischemic cells tolerate Ca overflow?

A

depleted ATP means they are unable to control ion flux across the cell membrane
-accumulation of Ca may trigger apoptosis or activate enzymes that degrade lipids in the membrane

61
Q

when is ischemic injury nonreversible?

A

cell death occurs when plasma, mitochondrial, + lysosomal membranes are critically damaged.

62
Q

what causes cell injury via nutrient deficiency?

A
  • poor intake
  • altered absorption
  • impaired distribution by circulatory systm
  • inefficient cellular uptake
63
Q

what causes cell injury via nutrient excess?

A

BMI > 27kg/m2: health risk

BMI > 30kg/m2: obesity

64
Q

infectious + immunologic cell injury

A

DIRECT: bacteria/virus itself cause virus

INDIRECT: added injury may occur indirectly by triggering body’s immune response

65
Q

examples of DIRECT infectious/immunologic cell injury

A
  • clostridium perfrinogens produce enzymes that eat meat and cause gangrene
  • microbes that secrete exotoxins + attack nervous system
  • endotoxins are in gram neg like e.coli
66
Q

chem injury

A

-toxic chem or poisons can cause cellular injury both DIRECTLY or by BECOMING METABOLIZED INTO REACTIVE CHEMS by the body

67
Q

physical/mechanical injury

A
  • extreme temp
  • abrupt changes in atmospheric pressure
  • mech deformation
  • electricity
  • IONIZING RADIATION (breaks chem bonds)
68
Q

extreme temp cell injury

A

COLD: vasoconstriction, less flow due to inc viscosity

HEAT: vasodilation, more flow due to dec in viscosity (more fluid)

69
Q

mechanisms of radiation-induced injury

A
  • heat
  • radiolysis
  • free radicals
70
Q

order of radiation-induced injury

A

radiant energy either cause
1a direct hit on DNA
2a DNA damage that causes
3a genetic mutations + apoptosis

or 1b ionization (which can also caught DNA damage)
2b free radical damage cell structure
3 acute cell destruction + necrosis

71
Q

first manifestation of most form of reversible cell injury….

A

hydropic swelling

72
Q

any injury that results in loss of ATP will also result in…

A

hydropic swelling

73
Q

intracellular accumulation that leads to cellular injury

A
  • toxicity
  • immune response
  • taking up cellular space
74
Q

fas ligand

A

binds to receptors to activate caspase and apoptosis

Pathophysiology (32 decks)

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