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Immunology + Pathology > Cell injury > Flashcards

Cell injury Flashcards

1
Q

What is reversible cell injury

A

cells adapt to changes in environment​

return to normal once stimulus removed​

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2
Q

What is irreversible cell injury

A

permanent​

cell death as consequence​

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3
Q

What factors decide how the cell reacts to a new environment

A

cell stress
cell vulnerability
Dose intensity

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4
Q

What occurs if a cell cannot adapt

A

Cell injury which could lead to cell death

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5
Q

What determines whether the injury us reversible or irreversible

A

depends on type, duration, severity of injury​

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

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6
Q

What is the aetiology 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 hypoxia

A

deficiency of oxygen​

causes: anaemia, respiratory failure​

disrupts oxidative respiratory processes in cell – decreased ATP​

cells can still release energy via anaerobic mechanisms

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8
Q

What is ischaemia

A

reduction in blood supply to tissue​

caused by blockage of arterial supply or venous drainage, e.g. atherosclerosis ​

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 physical agents can cause cell injury

A

mechanical trauma – affects structure, cell membranes​

extremes of temperature – affect proteins, chemical reactions​

ionising radiation – DNA damage – can often be repared by DNA repair systems (not immediate – may take years to appear usually in form of cancer)​

electric shock - burn​

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10
Q

What chemicals and drugs cause cell damage

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​

Disruption of cell membranes and proteins

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11
Q

What immunological reactions occur to cause cell damage

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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12
Q

How can a nutritional imbalance add to cell damage

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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13
Q

How might someone be more genetically predisposed to cell damage

A

sickle cell anaemia (haemoglobin chain)​

inborn error of metabolism (lack of enzyme causes build up of enzyme substrate)​

also more subtle variations in genetic make up determine susceptibility to cell injury from all of the previous causes​

cancer​

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14
Q

What counts as reversible cell injury

A

disruption to:

aerobic respiration/ATP synthesis (mitochondrial damage)​

plasma membrane integrity​

enzyme and structural protein synthesis​

DNA maintenance​

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15
Q

What is the morphology of reversible cell injury

A

Cloudy swelling
Fatty change

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16
Q

What causes cloudy swelling

A

cells are incapable of maintaining ionic and fluid homeostasis​ (sodium pumps fail)

failure of energy dependent ion pumps in the cell membrane​
-loss of ATP/energy dependent Na pump leads to influx of Na and water ​

there is also a build up of intracellular metabolites

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17
Q

What causes the appearance of fatty change

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.​

occurs with toxic and hypoxic injury (alcohol abuse, diabetes, obesity)​

macroscopically liver enlarged and pale​

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18
Q

What is the point of no return

A

Mitochondrial high amplitude swelling, mitochondrial matrix densities, violent blebbing (breaking off)

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19
Q

What are irreversible changes

A

Membrane rupture, dispersal of organelles
Breakdown of lysosomes - will result in digestion of cells as well as those produced by the neutrophils (leucocytes) which are present as a result of inflammation response
Activation of inflammatory response

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20
Q

What is necrosis

A

cell death​

usually due to pathology​

irreversible cell injury​

intracellular protein denaturation and lysosomal 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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21
Q

What is pyknosis

A

Nucleus shrinks (darker staining in histology)

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22
Q

What is karyolysis

A

the blue staining DNA in nucleus is digested by endonucleases and the blue staining fades away

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23
Q

What is Karyorrhexis

A

Nucleus fragments

24
Q

What cytoplasmic changes occur during necrosis

A

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

25
Q

What are the types of necrosis

A

Coagulative necrosis
Liquefactive necrosis (colliquative) - pus
Caseous necrosis​
Gangrenous necrosis
Fat necrosis
Fibrinoid necrosis​

26
Q

What is coagulative necrosis

A

MOSTCOMMON
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​

27
Q

What is a localised area of coagulative necrosis called

A

Infarct

28
Q

What is 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

29
Q

What is 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​

30
Q

What is gangrenous necrosis

A

coagulative necrosis with superimposed bacterial infection –liquefactive necrosis​

31
Q

What is fat necrosis

A

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

32
Q

What is 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

33
Q

What are the effects of necrosis

A

functional-depends on organ /tissue​

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

34
Q

What are the types of cell death

A

pyknosis
karyorrhexis
karyolysis

35
Q

What is apoptosis

A

Genetically 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​

36
Q

What are the 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

37
Q

What is the purpose 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​

38
Q

What can too much apoptosis lead to

A

Degenerative diseases

39
Q

What can too little apoptosis cause

A

Cancer

40
Q

What is the morphology (appearance) 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​

41
Q

What are the differences between necrosis and apoptosis

A

NECROSIS
-enlarged cells
-disrupted plasma membrane
-nucleus appears as pyknosis - karyorrhexis - karyolysis

APOPTOSIS
-shrinkage of cells
-intact plasma mebrane with disrupted structure
-fragmentation of nucleus into nucleosome size fragments

42
Q

Whar abnormal substances accumulate in cells

A

excessive normal cellular constituent​

   Water, lipid (fatty change), glycogen​

abnormal endogenous/exogenous material​

    Carbon, silica, metabolites, cholesterol
43
Q

What is temporary accumulation called

A

cytoplasmic

44
Q

What is permanent accumulation called

A

Nuclear

45
Q

What is atherosclerosis

A

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

46
Q

What is amyloid

A

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

47
Q

What stimulates amyloid deposits

A

Chronic inflammation
Multiple myeloma
Ageing
Drug abuse

48
Q

Where is amyloid most frequently found

A

Kidneys

49
Q

What are the types of amyloid accumulation

A

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​

50
Q

What is amyloidosis

A

Impairment of degreadation and removal of abnormal protein response

51
Q

What is pathological pigmentation

A

Build up of pigmented substances in cytoplasm​

endogenous pigmentation

exogenous pigmentation​

52
Q

What causes endogenous pigmentation

A

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

53
Q

What causes raised serum calcium

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​

54
Q

What is hypercalcaemia

A

Raised serum calcium

55
Q

What causes exogenous pathological pigmentation

A

Carbon deposition-commonest ​

in macrophages in alveoli of lungs​

black pigment=anthracosis​

inhaled soot/smoke​

in coal workers can be severe and lead to fibrosis=pneumoconiosis​

Tattoos​

Heavy metal salts eg lead​

Pigmentation associated with intravascular drug use​

56
Q

Whar is pathological calcification

A

dystrophic​

-deposits of calcium phosphate in necrotic tissue. Serum calcium is normal

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​

57
Q

What are the types pathologic calcification

A

dystrophic
metastatic

Immunology + Pathology (11 decks)

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