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BAMS > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

What is reversible cell injury

A
  • cells adapt to changes in the enviroment
  • return to normal once stimulus removed
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2
Q

What is irreversible cell injury

A
  • permanent
  • cell death as a consequence
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3
Q

What causes cell injury

A

Disease

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4
Q

What are the main factors of cell stress

A
  • dose intensity
  • cell vulnerability
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5
Q

What determines whether cell injury is reversible or irreversible

A
  • depends on type, duration, severity of injury
  • AND susceptibility/adaptability of the cell
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6
Q

What is hypoxia

A

Decreased oxygen supply

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7
Q

Name some causes of cell injury

A
  • hypoxia
  • physical agents
  • chemicals/drugs
  • infections
  • immunological reactions
  • nutritional imbalance
  • genetics
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8
Q

What can causes hypoxia

A

Anaemia, respiratory failure

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9
Q

During hypoxia what can cells do to release energy

A

Cells can release energy via anaerobic mechanisms
Wont last forever

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10
Q

What is ischaemia

A

Reduction of blood supply to tissue

This can be causes by a blockage of arterial supply or venous drainage

More rapid/severe damage than hypoxia no nutrients or oxygen transported

Anaerobic energy release will stop

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11
Q

What can mechanical trauma cause

A

Affects structure, cell membranes

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12
Q

What can extremes of temperature effect

A

Affects proteins, chemical reactoons

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13
Q

What can ionising radiations cause

A

DNA damage

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14
Q

What can electric shocks cause in cell injury

A

Burns

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15
Q

Give some examples of infectious agents

A
  • bacteria
  • fungi
  • viruses
  • parasites
  • protons

Can all produce cell injury

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16
Q

Some chemicals can cause …

A

Osmotic disturbance in excess

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17
Q

Name some immunological reactions that can cause cell injury

A
  • anaphylaxis
  • autoimmune reactions
  • causes damage as a result of inflammation
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18
Q

How can nutrition cause cell injury

A

Too little
- can cause rickets, scurvy
- generalised anorexia
Too much
- hypervitaminosis A/D
- obesity

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19
Q

Name some genetic defects that cause cell injury

A
  • sickle cell anemia
  • inborn error of metabolism
  • cancer
  • subtle variations that can cause cell injury
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20
Q

What happens to cells during reversible injury

A
  • aerobic respiration/ATP synthesis effected
  • plasma membrane integrity
  • enzyme and structural protein synthesis
  • DNA maintaineece
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21
Q

What is cloudy swelling

A

During reversible cell injury ion pumps effected - sodium ion pump when the function is effected sodium and water will move into the cell as a result the cytoplasm and cell organelles will swell up

22
Q

What are the causes of fatty liver

A
  • alcohol abuse
  • diabetes
  • obesity
23
Q

Explain fatty change in response to cell injury

A

Accumulation of lipid vascuoles in cytoplasm caused by disruption of fatty acid metabolism so that triglycerides cannot be released from the cell especially in the liver

24
Q

What is necrosis

A
  • cell death
  • usually due to pathology
  • irreversible cell injury
  • Intracellular protein desaturation and lysosomal digestion of the cell
  • inflammatory response in surrounding tissue
  • histological changes take a while to appear
25
Q

What response occurs in the surrounding tissues in nercosis

A

Inflammation

26
Q

What are some nuclear changes of nercrosis

A

Pykynosis = nucleus shrinks, darker staining
Karyorrhexis = nuclear fragments
Karyolysis= the blue staining DNA in nucleus is digested by endonucleases and the blue staining fades away

27
Q

What is coagulatuev necrosis

A
  • no proteolysis of the dead cell due to the denaturation of enzymes, architecture of tissues is preserved for some days
  • no nucleus, eosinophilic cells
  • cells digested by lysosomes of leukocytes
28
Q

What is liquefactive necrosis (colliquative)

A
  • digestion of dead tissues so tissue in liquid viscous state
  • focal bacteria pr fungal infections
  • pus
  • CNS necrosis as a result of hypoxia often manifested as liquefactive nercrosis
29
Q

What is Caseous necrosis

A
  • white appearance
  • Tuberculous infection
  • formation of granuloma as a result of mass apoptosis surrpunded by inflammatory cells
30
Q

What is fibrinoid necrosis

A
  • special type of necrosis in blood vessels
  • immune complexes are deposited in artery walls together with fibrin (clotting factor) that leaks out of the vessels
31
Q

Name some effects of necrosis

A
  • functional depends on organ/tissue
  • inflammation
  • release of cell contents activates inflammation
  • cell remains phagocytosed
  • necrotic area replaced by a scar
  • if remains not removed calcium salts may be deposited in the area
32
Q

Why may calcium salts be deposited in the remains of necrotic tissue

A

If all the remains of the cell are not removed

33
Q

What is apoptosis

A

Programmed cell death
Requires energy
Does not cause inflammation
Gets rid of unwanted cells

34
Q

What enzyme causes apoptosis

A

Capsases

35
Q

Name some physiological roles of apoptosis

A
  • deletion of cell populations during embryogenesis
  • hormone change
  • cell deletion in proliferating cells - epithelial cells
  • deletion of inflammatory cells
  • deletion of self reactive lymphocytes
36
Q

What can too much apoptosis cause

A

Degenerative diseases

37
Q

What can too little apoptosis cause

A

Cancer

38
Q

What is gangrenous necrosis

A

Coagulative necrosis with superimposed bacterial infection - liquefactive nercosis

39
Q

What is fat necrosis

A

Focal areas of fat destruction, fat cells may be liquefied by activate pancreatic enzymes (acute pancreatitis)

40
Q

What are some pathological triggers of apoptosis

A
  • Hypoxia/ischemia
  • viral infection
  • DNA damage - if unrepairable p5£ triggers apoptosis
  • caspases are activated enzymes that trigger apoptosis
  • cell contents are degraded by enzymes activated by the cell
41
Q

What affects does apoptosis have on cells

A
  • cell shrinkage
  • fragmentation into nucleoside size fragments
  • interact, altered structure especially orientation of lipids
  • interact- may be released in apoptic bodes
  • no adjacent inflammation
  • often physiologic
42
Q

What is atherosclerosis

A

Accumulation of cholesterol in macrophages and smooth muscle cells in blood vessel walls

43
Q

What are the macrophages called that accumulate around cholestrol

A

Foam cells

44
Q

What is amyloid

A

Amyloid is a fibrillar protein material that is deposited as a result of pathologic processes leading to increased production of these proteins

Deposited in extracellular location (mostly on basement membrane) in various tissues and organs

45
Q

What are the types of Amyloid

A

AL (amyloid light chain)
AA (amyloid associated)
Abeta

46
Q

What is AL

A

Amyloid light chain, derived from light chain immunoglobulins from plasma cells

47
Q

what is AA

A

Amyloid associated - derived from proteins synthesised in the liver

48
Q

What is A beta

A

Amyloid beta causes Alzheimer’s disease

49
Q

What is the stimuli for Alzheimer’s disease

A

Chronic inflammation, multiple myeloma, ageing, drug abuse

50
Q

What is exogenous pathological pigmentation

A
  • carbon deposition-commonest
  • in macrophages in alveoli of lungs
  • black pigment = anthracosis
  • inhaled soot/smoke
  • in coal workers
  • tattoos
  • heavy metal salts
  • pigmentation associated with intravascular drug use
51
Q

What is pathologic calcification

A
  • dystrophic - deposits of calcium in necrotic tissue
  • metastatic - deposits of calcium salts in normal, vital tissue with raised serum calcium levels, often seen in connective tissue of blood vessels, can compromise function of tissue
52
Q

What are some causes of raised serum calcium

A

1) increased level of PTH (hyperparathyroidism) parathyroid gland tumour
2) destruction of bone tissue - leukaemia, metastasis to bone, immobilisation
3) excess vitamin D
4) renal failure

BAMS (41 decks)

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