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BDS1 BAMS pathology and immunity > cell injury > Flashcards

cell injury Flashcards

1
Q

what is meant by reversible cell injury?

A

cells adapt to changes in the environment then return to normal once stimulus is removed

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2
Q

what is meant by irreversible cell injury?

A

permanent and the consequence is cell death

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3
Q

what does cell injury cause?

A

disease

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3
Q

what dos cell injury give?

A

disease

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4
Q

what are factors which are involved in cell injury?

A
  • dose intensity
  • cell stress
  • cell vulnerability
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5
Q

what is the reversiblility of the cell dependant on?

A
  • cell type
  • duration
  • severity of injury
  • susceptibility of the cell
  • adaptability of the cell
  • nutritional status
  • metabolic needs (cardiac vs skeletal)
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6
Q

what is the aetiology (causes) of cell injury?

A

hypoxia (=decreased oxygen supply)
physical agents (radiation – free radicals)
chemicals/drugs
infections (bacterial toxins, viruses)
immunological reactions
nutritional imbalance
genetic defects

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7
Q

what is the aetiology (causes) of cell injury?

A

hypoxia (=decreased oxygen supply)
physical agents (radiation – free radicals)
chemicals/drugs
infections (bacterial toxins, viruses)
immunological reactions
nutritional imbalance
genetic defects

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8
Q

what is hypoxia?

A
  • oxygen deficiency
  • causes include anaemia and respiratory failure
  • disrupts oxidative respiratory processes in the cell giving decreased ATP
  • cells can still release energy via anaerobic mechanisms
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9
Q

what is ischaemia?

A
  • reduction in blood supply to tissue
  • caused by a blockage of arterial supply or venous drainage eg atherosclerosis
  • depletion or oxygen and nutrients
  • faster rate of damage than hypoxia as anaerobic energy release also stops
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10
Q

what are examples of physical agents which cause cell injury?

A
  • mechanical trauma
  • extreme temperatures
  • ionising radiation
  • electrical shock
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11
Q

what are examples of infectious agents which can cause cell injury?

A

bacteria
viruses
fungi
parasites
protons

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12
Q

what are examples of chemicals/drugs which can cause cell injury?

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

all disrupt cell membranes and proteins

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13
Q

what are examples of immunological reactions which 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)
    cause damage as a result of inflammation (complement, clotting, neutrophil products, etc)
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14
Q

what are examples of nutritional imbalances which can cause cell injury?

A
  • too little nutrients eg scurvy, rickets, anorexia
  • too much eg hypervitaminosis A/D, obesity
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15
Q

what are genetic defects which can cause genetic defects?

A
  • sickle cell anaemia
  • inborn error of metabolism- lack of enzyme causes substrate build up
  • cancer
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16
Q

what happens to the cells which undergo reversible injury?

A
  • aerobic respiration/ATP synthesis (mitochondrial damage)
  • plasma membrane integrity
  • enzyme and structural protein synthesis
  • DNA maintenance
  • cloudy swelling/fatty change
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17
Q

what is cloudy swelling?

A
  • failure of the cells energy dependant ion pumps in the cell membrane
  • influx of sodium and water
  • build up of intracellular metabolites
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18
Q

what is fatty change?

A
  • accumulation of lipid vacuoles in the cytoplasm caused by disruption of fatty acid metabolism so that triglycerides cannot be released from the cell esp in liver
  • occurs with toxic and hypoxic injury (alcohol abuse, diabetes, obesity)
  • macroscopically the liver appears enlarged and pale
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19
Q

when is the point where a cells damage becomes irreversible?

A
  • mitochondrial highly swollen
  • voilent blebbing
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20
Q

what is necrosis?

A
  • cell death
  • due to pathology
  • irreversible cell injury
  • intracellular protein denaturation
  • lysosomal digestion of cell
  • cell membrane disrupted due to leakage
  • inflammatory response in the surrounding tissue
  • remains removed by phagocytosis
  • hustopathological responses can take a while to appear
21
Q

what are the microscopical changes of necrosis?

A
  • pyknosis = nucleus shrinks; darker staining
  • karyorrhexis = nucleus fragments
  • karyolysis = the blue staining DNA in nucleus is digested by endonucleases and the blue staining fades away
  • end result is loss of the blue staining nucleus – a useful sign that a cell is necrotic
  • cytoplasm paler and pinker
22
Q

what are the types of necrosis?

A
  • coagulative
  • liquefactive
  • caseous
  • fibrinoid
  • gangrenous
  • fat
22
Q

what are the types of necrosis?

A
  • coagulative
  • liquefactive
  • caseous
  • fibrinoid
23
Q

describe coagulative necrosis?

A
  • No proteolysis of the dead cells due to denaturation of enzymes
  • Architecture of tissues is preserved for some days
  • No nucleus; eosinophillic cells.
  • Grossly, firm in texture
  • Cells digested by lysosomes of leukocytes
  • Localised area of coagulative necrosis is called an infarct.
24
Q

what is the type of necrosis in the CNS?

A

liquefactive as a result of hypoxia

25
Q

describe liquefactive necrosis

A
  • Digestion of dead tissues so tissue in in liquid viscous state
  • Focal bacterial or fungal infections (abcess)
  • Grossly, necrotic material is thick, pale yellow in colour
  • CNS necrosis as a result of hypoxia often manifested as liquefactive necrosis.
26
Q

describe caseous necrosis

A
  • Grossly, friable white appearance (like cheese)
  • Mostly seen in tuberculous infection
  • Microscopically; granuloma-fragmented cells and granular debris ( mass apoptosis) surrounded by inflammatory cells
27
Q

what type of necrosis is seen in tuberculous infection?

A

caseous

28
Q

what is gangrenous necrosis?

A

coagulative necrosis with superimposed bacterial infection –liquefactive necrosis

29
Q

what is fat necrosis?

A

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

30
Q

describe 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
31
Q

what are the effects of necrosis?

A
  • functional
  • inflammation:
    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
32
Q

what organelle within the cell can tell you whether the cell has died?

A

nucleus

33
Q

what organelle within the cell can tell you how the cell died?

A

cytoplasm

34
Q

what is apoptosis and how does it differ from necrosis?

A
  • programmed cell death
  • orderly elimination of unwanted cells
  • important physiological role
  • can occur in pathological situations
  • requires energy
  • distinct pathways involved
  • does not cause inflammation
  • different morphology from necrosis
35
Q

what are potential pathological triggers of 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.
36
Q

what are the physiological roles of apoptosis?

A
  • deletion of cell populations 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
37
Q

what happens if there is too much apoptosis?

A

degenerative disease

38
Q

what happens if there is too little apoptosis?

A

cancer

39
Q

describe the morphology of apoptosis

A
  • cell shrinkage
  • chromatin condensation – packaging up of nucleus
  • cell membrane remains intact, with formation of cytoplasmic blebs
  • break off to form apoptotic bodies
  • phagocytosed, but no widespread inflammation
40
Q

intracellular accumulation

A
41
Q

what is one of the most common materials to accumulate in the cell?

A

cholesterol

42
Q

what happens when cholesterol accumulates in the cell (atherosclerosis)?

A
43
Q

what is commonly accumulated in the basement membrane of cells?

A

amyloid

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.

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

45
Q

what stimuates amyloid accumulation?

A
  • chronic inflammation
  • multiple myeloma
  • ageing
  • drug abuse
46
Q

what does amyloid look like under a microscope?

A

pale pink

47
Q

what are common causes of endogenous pigmentation?

A

Lipofuscin-cellular lipid breakdown products
Melanin
Haemosiderin-localised bruising
Bilirubin

All appear brown

48
Q

what are the most common causes of exogenous pigmentation?

A
  • carbon deposition in alveoli of lungs
  • black pigment from tattoos
  • inhaled smoke and soot
49
Q

what is pathologic calcification?

A
  • dystrophic, valves in heart become thick
  • metastatic, can compromise tissue function (BV and CT)
50
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

BDS1 BAMS pathology and immunity (12 decks)

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