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Block 1 Week 2 > Cell Responses to Stress > Flashcards

Cell Responses to Stress Flashcards

1
Q

Regulation of a normal tissue state?

A

=Homeostasis

-means that an effective response to injury/infection etc will restore normal tissue functions

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2
Q

Regulation of a pathological tissue response?

A

-pathological tissue response results in tissue damage and/or tissue remodeling (scaring/altered function)

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3
Q

gross vs microscopic changes in tissue?

A
  • both pathogenic and adaptation (muscle growth) of tissues can be seen both microscopically & grossly
    • in entire tissue vs in individual cells
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4
Q

cell response to altered physiological stimulus or a nonlethal injury stimuli? (ex: decreased nutrients & stimulation; increased demand& stimulation)

A
  • CELL ADAPTATIONS

ex: hyperplasia, hypertrophy, atrophy, metaplasia

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5
Q

cell response to reduced oxygen supply, chemical injury, microbial infection? ( acute & transient, progressive/severe including DNA damage)

A
  • CELL INJURY
  • acute reversible injury= cell swelling; fatty change
  • irreversible injury= apoptosis & necrosis
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6
Q

when does cellular aging occur?

A

-when have a cumulative sublethal injury over long life span

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7
Q

what are cell adaptations?

A

-adaptations to stresses that push tissue one way or other; -are usually reversible if stressor removed

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8
Q

what is cell injury?

A
  • can be pathological or physiological
  • usually progressive; not all cells respond at same time to same thing
  • can see ranges of when stress & death occur in same tissue
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9
Q

Hypertrophy

A
  • ex of cell adaptation
  • an increase in the size of cells w/o cell division
  • see corresponding increase in organ size (ex: uterus)
  • can be pathological or physiological stressors
  • can be selective process
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10
Q

Hyperplasia

A
  • ex of cell adaptations
  • increase in the size of cells w/ cell division too
  • can be pathological or physiological stressors
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11
Q

Hyperplastic

A

-an increase in cell number in response to pathological or physiological stressors

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12
Q

mechanism of cardiac hypertrophy?

A
  • typically from increased workload or from increasing growth factors/vasoactive agents
  • response: increased protein production, changes in gene expression
  • can be SELECTIVE, the same organ can have 2 means of responding the same drug
  • MANY DIFF MECHANISMS
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13
Q

What causes hyperplasia?

A
  • result of cell division
  • can be Physiologic or Pathologic
  • same factors that effect hypertrophy can also affect hyperplasia
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14
Q

Physiologic Hyperplasia? (2 ways)

A

1) Hormonal: increased functional capacity when needed
2) compensatory: increases tissue mass after damage or tissue loss (ex liver regeneration after resection)
- always about returning to homeostasis

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15
Q

Pathologic Hyperplasia?

A
  • most often caused by excess hormones/growth factors
  • also by viral factors (HPV)
  • distinct from cancer but can provide predisposing conditions
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16
Q

atrophy?

A
  • a cell adaptation
  • reduction of organ size due to decreased cell size & number
  • physiological & pathological causes
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17
Q

physiological atrophy?

A

physiological: from malfunction in developmental processes

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18
Q

common causes of pathological atrophy?

A

1) decreased workload
2) loss of innervation
3) ischemia (loss blood supply)
4) malnutrition
5) loss of endocrine stimulation (menopause)
6) pressure; expanding. mass of benign tumor

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19
Q

Mechanisms of Atrophy?

A
  • decreased protein synthesis, increased degradation
  • autophagy
  • early in process, cells may still be alive but cell death soon follows
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20
Q

autophagy

A

-cell cannibalizes its own components

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21
Q

Metaplasia

A
  • a cell adaptation

- when one differentiated cell type is replaced by a different cell type in response to stress

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22
Q

Metaplasia in the respiratory track?

A
  • in response to constant irritation
  • change from Columnar to Squamous
  • change provides a more resistant surface, but loose mucus secretion & ciliary clearance
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23
Q

Metaplasia in the esophogus?

A
  • in response to reflux of gastric acid

- Squamous to Columnar

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24
Q

Connective Tissue Metaplasia

A

-formation of cartilage/bone in muscle in response to injury/hemorrage

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25
Q

Mechanism of Metaplasia

A
  • reprogramming of stem cells to produce a different differentiated cell type
  • is not transdifferentiation of existing cells from one differentiated cell phenotype into another phenotype
  • in stem cells NOT differentiated cells*
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26
Q

why epithelial cells able to do metaplasia?

A
  • because epithelial cells are alive, actively dynamic & constantly undergoing replacement from stem cells
  • instead of correct replacement…do metaplasia & get diff cell type
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27
Q

What types of cells do stem cells produce?

A

-stem cells can produce any type of cell BUT once cell is made & mature…it is terminally differentiated can no longer change its function

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28
Q

cell injury & cell death causes (x7)

A

1) hypoxia (O2 defincency)
2) physical trauma
3) chemical agents & drugs
4) infectious agents
5) immunological rxts
6) genetic effects
7) nutritional imbalances

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29
Q

What is hypoxia? What is the result?

A
  • reduced oxygen availability

- energy production has to go through anaerobic glycolysis

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30
Q

What is ischemia?

A

-reduced blood flow reduced O2, reduced supply of nutrients

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31
Q

what happens during cell injury?

A
  • decreased ATP generation
  • cell cytoskeleton & membrane degeneration
  • mitochondrial swelling
  • is potentially reversible if caught in time*
32
Q

protective response to hypoxia/ischemia? Treatment?

A

1) anaerobic glycolysis
2) production of HIF-1

-transient protection of tissue by induction of hypothermia (92degrees) for brain & spinal cord injuries

33
Q

HIF-1

A
  • Hypoxia-indicble factor
  • trxn factor that promotes blood vessel formation
  • regulates erythropoietin production
34
Q

How HIF-1 regulated?

A

1) HIF-1 is always produced (but never on) so don’t have to waste time w/ trxn&trans when need it
2) HIF-1 constantly being ubiquitnated so is degraded
3) when PHD enzyme senses hypoxia ; halts ubiquitnation causes hydroxylation & activation of HIF-1
4) HIF-1 can make new blood vessels and repair hypoxic damage

35
Q

HIF-1 & tumor angiogenesis?

A
  • angiogeniss= when tumors build blood vessels to feed their growth
  • if inhibit HIF-1; then no blood vessels made
36
Q

HIF-1 inhibited? vs uninhibited?

A
  • inhibited(no hypoxia)=ubiquinated= no blood vessel formation
  • activated (in hypoxic situations)= hydroxylate day PHD= blood vessel formation
37
Q

Potential treatment of anemia?

A
  • blocking HIF-1 degradation

- so are building more blood vessels and organs are receiving more nutrients it needs

38
Q

what is ischemia-reperfusion injury?

A

–when hypoxia/ischema is revered but repercussion causes worse damage

39
Q

How reperfusion cause damage (x3)?

A

1) increased reduced oxygen species (ROS)
2) induction of inflammatory processes
3) activation of complement from IgM deposition in tissue, adding to the activation of inflammatory processes

40
Q

How does reperfusion cause increases reduced oxygen species (ROS)?

A
  • repercussion causes mitochondrial damage& and reduced capacity to reduce oxygen, leading to free radical accumulation
41
Q

How does reperfusion cause inflammatory processes?

A
  • reperfusion causes an incerased production of cytokines & expression of adhesion molecules on endothelium
  • helps recruitment & activation of neutrophils, & macrophages from blood leading to tissue damage
42
Q

What are gross tissue changes?

A

1) changes in tissue integrity ( intact, cheesy, gooey, liquid/slimy)
2) changes in tissue color (hemorrhage, pallor, fibrous scars)

gives clues to microscopic damages

43
Q

What are microscopic/histological changes?

A

changes in:

1) tissue organization
2) cell size & shape
3) cell nuclei (color, size, shape)
4) cytoplasm color
5) infiltrations by inflammatory cells

gives clues to tissue damage

44
Q

what are inflammatory cells?

A

macrophages & neutrophils

45
Q 
Apoptosis:
(cell size?)
(nucleus?)
(PM & cell contents?)
(inflammation?)
(physiological/pathologoical?)
A

1) reduced (shrinkage)
2) DNA fragmentation into 200bp
3) intact PM & cell contents
3) no inflammation
4) usually physiological; removing unwanted cells in development; CAN be pathological after DNA damage

46
Q 
Necrosis:
(cell size?)
(nucleus?)
(PM & cell contents?)
(inflammation?)
(physiological/pathologoical?)
A

1) cell swelling (enlarged)
2) randomly fragmented
3) disrupted; enzymatic digestion may leak out o cell
4) inflammation
5) irresverisbly pathologic

47
Q

Why is loss of PM & cellular contents bad?

A

-occurs in necrosis
-because activates inflammatory response
(macrophages & neutrophils)

48
Q

Coagulative Necrosis

A
  • morophological change due to cell injury
  • integrity of connective tissue is preserved, but loss of nuclei during necrosis
  • inflamamtory cells enter & destroy nuclei, but maintain other structures
49
Q

Liquefactive necrosis

A
  • morophological change due to cell injury
  • digestion of dead cells, with change to liquid viscous mass
  • due to bacteria/fungal infection
  • recuritment of inflammatory cells & enzymatic digestion of tissue (pus)
  • Hypoxic death in CNS often manifests this way
50
Q

Gangrenous necrosis

A
  • morophological change due to cell injury
  • due to lost blood supply
  • can be coagulative or liquefactive necrosis
51
Q

Caseous necrosis

A
  • morophological change due to cell injury
  • seen in TB infections
  • charcateristic of granulomatous inflammation
52
Q

Fat necrosis?

A

-focal areas of fat destruction
-from release of lipases into pancreas & peritoneum
-Fatty acids combine w/ calcium to produce calcium soaps
(saponification)

53
Q

saponification

A

-fatty acids combine with calcium to produce calcium soaps

54
Q

Fibrinoid necrosis

A

-vascular lesions in vasculitis from immune complex deposition in arterial wall

55
Q

Mechanisms of Cell Injury? (x6)

A

1) ATP depletion
2) mitochondrial damage
3) Ca+ influx
4) oxidative stress (ROS)
5) membrane permeability
6) DNA/protein damage

56
Q

Depletion of ATP & cell injury ?

A
  • associated w/ hypoxic chemical injury
  • affects many systems since loosing cell’s energy source
  • can lead to necrosis due to mitochondrial damage
57
Q

Mitochondrial Damage & cell injury?

A

2 consequences

1) mito. permeability increase, loose membrane potential, depletion of ATP–> necrosis
2) leakage of apoptosis-inducing proteins; activation of caspases & initation of apoptosis

58
Q

Calcium Influx & cell injury?

A
  • intracellular Ca2+ (normal=low) is then increased. Causes:
    1) mito. permeability increased, loss of ATP production, necrosis
    2) Ca dependent enzymes (phosphatases, ATPases, proteases) are activated w/ bad outcomes
    3) activation of caspases & apoptosis
59
Q

how do reactive oxygen species (ROS) cause cell injury?

A

1) peroxidation of membrane lipids
2) oxidation of protein amino acid side chains
3) DNA damage (strand breaks)

60
Q

How does peroxidation of membrane lipids occur?

A

1) O2 converted to superoxide by oxidative enzymes in the ER& mito;
2) then converted to H202
3) results in peroxidation of lipids, protein & DNA

61
Q

how does membrane permeability cause cell damage?

A
  • cell membrane permeability occurs by ROS, toxins, phospholipase
  • causes damage by effecting 3 targets
    1) mito-loss of ATP/apoptosis induction
    2) PM- loss of osmotic balance
    3) lysosome- Leake of degradative enzymes leading to necrosis
62
Q

What could intracellular accumulation be due to?

A

1) increased accumulation/production of normal cell products
2) defective metabolism due to increased accumulation of abnormal proteins/ genetic defect in degradative enzyme
3) ingestion & accumulation of abnormal exogenous substances (ex. silica)

63
Q

what is Steatosis? where is it at? what causes it?

A
  • triglyceride accumulation in the liver due to excessive entry of fatty food or defective metabolism caused by (ethanol)
64
Q

what is Cholesterolosis? What called in wall of large blood vessel?

A
  • accumulation of cholesterol-laden macrophages in the wall of the gall bladder
  • if in the wall of large blood vessels is called: ATHEROSCLEROTIC PLAGUES
65
Q

intracellular Protein Accumulations?

A
  • intracellular accumulation of protein appears as eosinophilic material
  • accumulation of cytoskeletal proteins can be normal (keratin in skin) or abnormal (Alzheimers disease)
66
Q

Extracellular protein accumulations?

A
  • protein accumulations can also happen extracellular

- ex: amyloid

67
Q

Two types of pigment accumulation?

A

1) exogenous pigments

2) endogenous pigments

68
Q

exogenous pigments example?

A
  • coal dust accumulating in lung tissue

- tattoo pigments on skin

69
Q

endogenous pigments examples?

A

1) lipofuscin
2) melanin
3) hemosiderin

70
Q

lipofuscin

A
  • polymers of lipids & phospholipids w/ protein
  • sign of free radical injury & lipid peroxidation
  • seen in cells undergoing slow regressive changes
71
Q

melanin?

A
  • brown-black pigment by tyrosinase in melanocytes
72
Q

hemosiderin?

A
  • golden yellow/brown granular pigment, derived from hemoglobin
  • serves as iron storage from RBC breakdown
73
Q

two types of calcification?

A

1) dystrophic:

2) metastatic

74
Q

dystrophic calcification

A
  • in areas of necrosis & in foci of enzymatic necrosis of fat
  • seen in advanced atheromatous plaques & aging/damaged hart valves
  • bone can form from them
75
Q

metastatic calcification due to (x4)?

A
  • can occur in normal tissue w/ hypercalcemia
    1) increased secretion of parathyroid hormone (PTH) w/ bone resorption due to parathyroid tumor
    2) destruction of bone tissue, due to bone marrow tumors
    3) vitamin D disorders
    4) renal failure, cause retention of phosphate & secondary hyperparathyroidism

Block 1 Week 2 (9 decks)

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