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Immunity and Pathology 1 > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

What is the difference between reversible and irreversible cell injury?

A

in reversible cell injury - cells adapt to changes in environment and the cells return to normal once stimulus is removed
in irreversible cell injury - the effect is permanent and there is cell death as a consequence

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2
Q

What factors affect whether cell injury is reversible or irreversible?

A

type, duration, severity of injury

the susceptibility/adaptability of the cell: nutritional status, metabolic needs (cardiac vs skeletal muscle).

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3
Q

What can cause cell injury

A
  • hypoxia
  • physical agents (radiation – free radicals)
  • chemicals/drugs
  • infections (bacterial toxins, viruses)
  • immunological reactions
  • nutritional imbalance
  • genetic defects
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4
Q

What can cause hypoxia?

A

anaemia, respiratory failure

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5
Q

What can happen as a result of hypoxia?

A

stops oxidation phosphorylation in cell – decreased ATP

cells can still release energy via anaerobic mechanisms

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6
Q

What is ischaemia?

A
  • reduction in blood supply to tissue
  • caused by blockage of arterial supply or venous drainage, e.g. atherosclerosis
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7
Q

What is atherosclerosis?

A

where your arteries become narrowed, making it difficult for blood to flow through them

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8
Q

Why is ischaemia more dangerous than hypoxia?

A

depletion of not just oxygen but also nutrients, e.g. glucose

more rapid/severe damage than hypoxia- anaerobic energy release will also stop.

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9
Q

What are examples of physical agents that can cause cell injury?

A
  • mechanical trauma – affects structure, cell membranes
  • extremes of temperature – affect proteins, chemical reactions
  • ionising radiation – DNA damage
  • electric shock - burn
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10
Q

What are examples of infectious agents that can cause cell injury?

A
  • bacteria
  • viruses
  • fungi
  • parasites
  • protons
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11
Q

What are examples of chemicals/drugs that can cause cell injury?

A
  • simple chemicals (glucose), in excess cause osmotic disturbance
  • poisons (cyanide blocks oxidative phosphorylation), environmental (insecticides)
  • occupational hazards (asbestos) causes inflammation
  • alcohol, smoking and recreational drug
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12
Q

What are immunological reactions that can cause cell injury?

A
  • anaphylaxis (tp 1 hypersensitivity, IgE mediated)
  • auto-immune reactions (tp 2, antibodies directed towards host antigens, tp 3 – antigen-antibody complexes)
  • damage as a result of inflammation (complement, clotting, neutrophil products, etc)
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13
Q

What are nutritional imbalances that can cause cell injury?

A

Too little (inadequate intake)
Specific nutrient :scurvy, rickets. Generalized: anorexia

Too much (excessive intake) Specific: hypervitaminosis A/D Generalized :obesity

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14
Q

What are genetic defects that can cause cell injury?

A
  • sickle cell anaemia (haemoglobin chain)
  • inborn error of metabolism (lack of enzyme causes build up of enzyme substrate)
  • cancer
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15
Q

What does reversible cell injury disturb?

A

– aerobic respiration/ATP synthesis (mitochondrial damage)
– plasma membrane integrity
– enzyme and structural protein synthesis
– DNA maintenance

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16
Q

Why is there a cloudy swelling of injured cells?

A

– cells are incapable of maintaining ionic and fluid homeostasis
– failure of energy dependent ion pumps in the cell membrane due to loss of ATP/energy dependent Na pump leading to influx of Na and water (water follows sodium due to osmosis)
– there is also a build up of intracellular metabolites.

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17
Q

Why is there fatty changes in injured cells?

A

– accumulation of lipid vacuoles in cytoplasm caused by disruption of fatty acid metabolism so that triglycerides cannot be released from the cell, especially in liver.
– macroscopically liver enlarged and pale

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18
Q

What is a common cause of fatty liver?

A

alcohol consumption, obesity, diabetes

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19
Q

What are the irreversible changes?

A

membrane rupture - organelles released
breakdown of lysosomes
activation of inflammatory response

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20
Q

If necrosis occurs, what will always be present?

A

inflammation

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21
Q

What is necrosis?

A

cell death usually due to pathology after irreversible cell injury (not programmed)

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22
Q

What is the process of necrosis?

A
  • intracellular protein denaturation and lysosomal (from cell) digestion of cell.
  • cell membrane is disrupted leading to leakage of cell contents
  • inflammatory response in surrounding tissue
  • cell remains are removed by phagocytosis
  • histopathological changes may take some time to appear.
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23
Q

What are the microscopic changes of necrosis?

A

pyknosis = nucleus shrinks; darker staining
karyorrhexis = nucleus fragments (K)
karyolysis = the blue staining DNA in nucleus is digested by endonucleases and the blue staining fades away (K)

24
Q

What enzymes digest DNA?

A

endonucleases

25
Q

What are the H&E cytoplasmic changes of necrosis?

A

appears paler, because swollen
more eosinophilic (pinker) because of denaturation of cytoplasmic structural and enzyme proteins

26
Q

What are characteristics of coagulative necrosis?

A

No breakdown of dead cells as enzymes are denatured
Architecture of tissues is preserved for some days
No nucleus; eosinophillic cells.
Firm in texture
Cells digested by lysosomes of leukocytes

27
Q

What is a localised area of coagulative necrosis called?

A

infarct

28
Q

What are characteristics of liquefactive necrosis (colliquative)?

A

Digestion of dead tissues so tissue in liquid viscous state
Focal bacterial or fungal infections (abscess)
Necrotic material is thick, pale yellow in colour (pus)

29
Q

What is CNS necrosis as a result of hypoxia often characterised as?

A

liquefactive necrosis

30
Q

What are characteristics of caseous necrosis?

A

Crumbly white appearance (like cheese)
Microscopically; granuloma-fragmented cells and granular debris ( mass apoptosis) surrounded by inflammatory cells

31
Q

Where is caseous necrosis mostly seen?

A

tuberculous infection

32
Q

What are characteristics of fat necrosis?

A

limited areas of fat destruction.
Fat cells may be liquefied by activated pancreatic enzymes -lipases (acute pancreatitis)

33
Q

What are characteristics of gangrenous necrosis?

A

coagulative necrosis with bacterial infection –liquefactive necrosis

34
Q

What are characteristics of fibrinoid necrosis?

A

-special type of necrosis seen in immune reactions in blood vessels
-immune (antigen –antibody) complexes are deposited in artery walls together with fibrin that leaks out of the vessels.
- bright pink and amorphous substance in H&E

35
Q

What are the effects of necrosis?

A
  • release of cell contents activates inflammation
  • cell remains are then phagocytosed
  • finally the necrotic area is replaced by a scar-i.e. it undergoes organisation or repair
  • if remains are not removed then calcium salts may be deposited in necrotic tissue
36
Q

What is apoptosis and what are the characteristics of it?

A

Programmed cell death which can be physiological and pathological

Requires energy and does not cause inflammation

Cells shrink not swell

37
Q

What are pathological triggers for apoptosis?

A
  • hypoxia/ischaemia (protein misfolding)
  • viral infection – cytotoxic T-lymphocytes contain enzymes which can induce apoptosis.
  • DNA damage- if unrepairable p53 triggers apoptosis
  • Caspases are activated enzymes that trigger apoptosis.
  • Cell contents are degraded by enzymes activated by the cell.
38
Q

What are the physiological roles of apoptosis?

A
  • deletion of cells during embryogenesis
  • hormone change dependent involution –uterus, breast, ovary
  • cell deletion in proliferating cell populations to maintain constant number of cells - epithelium
  • deletion of inflammatory cells after an inflammatory response
  • deletion of self reactive lymphocytes in the thymus
39
Q

What does too much apoptosis and too little apoptosis cause?

A

too much - degenerative disease
too little - cancer

40
Q

What is the morphology of apoptosis?

A
  • cell shrinkage
  • chromatin condensation – packaging up of nucleus
  • cell membrane remains intact, with formation of cytoplasmic blebs
  • phagocytosed, but no widespread inflammation
41
Q

What are the types of accumulation that can occur?

A

excessive normal constituents - glycogen, lipids, water
abnormal endo/exogenous material - carbon, silica, cholesterol

42
Q

What condition occurs due to high cholesterol accumulation?

A

atherosclerosis

43
Q

What is atherosclerosis?

A

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

44
Q

What are foam cells?

A

lipid ingested macrophages

45
Q

What is amyloid?

A

Amyloid is a fibrillar protein that is deposited as a result of pathologic processes

46
Q

What are the types of amyloid?

A

AL -(amyloid light chain) derived from light chain antibodies from plasma cells.
AA -(amyloid associated): derived from proteins synthesized in the liver
Aβ -Alzheimer’s disease

47
Q

What can cause amyloid accumulation?

A

chronic inflammation, multiple myeloma, ageing, drug abuse

48
Q

What does amyloid accumulation cause?

A

The build-up of amyloid proteins (deposits) can make it difficult for the organs and tissues to work properly - organ failure (amyloidosis)

49
Q

What are examples of endogenous pigmentation accumulation?

A

Lipofuscin
Melanin
Haemosiderin-localised bruising
Bilirubin

ALL APPEAR BROWN

50
Q

What are examples of exogenous pathological pigmentation?

A

Carbon deposition-commonest
Tattoos
Heavy metal salts eg lead
Pigmentation associated with intravascular drug use

51
Q

Where is carbon deposited?

A

in macrophages in alveoli of lungs

52
Q

What is dystrophic pathologic calcification?

A

-deposits of calcium phosphate in necrotic tissue.

Serum calcium is normal.

53
Q

Where is dystrophic pathologic calcification seen?

A

valvular heart disease

54
Q

What is metastatic pathologic calcification?

A

deposits of calcium salts in normal, vital tissue

Raised serum calcium levels

55
Q

Where is metastatic pathologic calcification seen?

A

connective tissue of blood vessels
nerve fibres

56
Q

What are causes of hypercalcaemia?

A

1-increased levels of parathyroid hormone (hyperparathyroidism) parathyroid gland tumour
2-destruction of bone tissue- leukaemia, metastasis to bone, immobilization
3- excess vitamin D
4- renal failure- causes secondary hyperparathyroidism

Immunity and Pathology 1 (13 decks)

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