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BDS1 Pathology > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

What is reversible cell injury?

A
  • Cells adapt to changes in the environment
  • Once change has gone wrong the cell returns to normal once the stimulus is removed as cells live in a state of equilibrium - many factors can affect this
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2
Q

What is irreversible cell injury?

A
  • Even if factor is removed cannot return back to original state
  • Permanent
  • Cell death as a consequence
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3
Q

What determines whether cell injury is reversible or irreversible?

A
  • Depends on type, duration and severity of injury

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

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4
Q

What are the possible causes of cell injury?

A
  • Hypoxia
  • Physical agents (radiation)
  • Chemicals/drugs
  • Infections (bacterial toxins, viruses)
  • Immunological reactions
  • Nutritional imbalance
  • Genetic defects
  • Heat and cold
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5
Q

What is hypoxia and what does it cause?

A
  • Deficiency of oxygen
  • Causes: anaemia, respiratory failure
  • Disrupts oxidative respiratory processes in cell - decreased ATP
  • Cells can still release energy via anaerobic mechanisms (only for a limited amount of time)
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6
Q

What is ischaemia and what does it cause?

A
  • Reduction to blood supply to tissue (so reduction in nutrients and oxygen)
  • Caused by blockage of arterial supply or venous drainage, e.g. atherosclerosis
  • More rapid/severe damage than hypoxia - anaerobic energy release will also stop
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7
Q

What are examples of physical agents and what do they cause?

A
  • Mechanical trauma: affects structure and cell membranes
  • Extremes of temperature: affect proteins, chemical reactions
  • Ionising radiation: causes DNA damage
  • Electric shock - burns
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8
Q

What are examples of infectious agents and what do they cause?

A
  1. Bacteria
  2. Viruses
  3. Fungi
  4. Parasites
  5. Prions

All associated with inflammation and produce various degrees of injury by different mechanisms

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9
Q

What are examples of chemicals and drugs and what do they do?

A
  • Simple chemical (glucose), in excess cause osmotic disturbance
  • Poisons (cyanide blocks oxidative phosphorylation), environmental (insecticides)
  • Occupational hazards (asbestos) causes inflammation in the lungs
  • Alcohol, smoking and recreational drugs
  • Causes disruption of cell membranes and proteins
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10
Q

What are examples of immunological reactions and what do they cause?

A
  • Anaphylaxis (type 1 hypersensitivity, IgE mediated)
  • Auto-immune reactions (type 2, antibodies directed towards host antigens, type 3 - antigen-antibody complexes)
  • Cause damage as a result of inflammation (complement, clotting, neutrophil products etc)
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11
Q

What are the 4 different types of hypersensitivity reaction?

A

Type 1 - Anaphylaxis - severe reaction - swelling of the face and lips

Type 2 - Basis behind autoimmunity - treats self-cells as if they were something foreign

Type 3 - Antigen/antibody complex - can cause damage

Type 4 - cell mediated

All of these will bring about damage to the cell

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12
Q

What are the specific and generalised conditions cause by an inadequate intake of nutrients?

A

Specific - Scurvy, Rickets

Generalised - anorexia

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13
Q

What are the specific and generalised conditions caused by an excessive intake of nutrients?

A

Specific - Hypervitaminosis A/D

Generalized - Obesity

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14
Q

What are examples of genetic defects and what do they cause?

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 makeup determine susceptibility to cell injury from all of the pervious causes
  • Cancer
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15
Q

What happens to cells during mechanisms of reversible injury?

A

Disruption to:

  • Aerobic respiration/ ATP synthesis (mitochondrial damage)
  • Plasma membrane integrity
  • Enzyme and structural protein synthesis
  • DNA maintenance
  • Some affects ion channels
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16
Q

What is the morphology of the cell during the mechanism of reversible injury?

A
  • Cloudy swelling

- Fatty change

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17
Q

What is the morphology of cloudy swelling in cells and what causes this?

A
  • Mainly due to hypoxia
  • 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 leads to influx of Na and water
  • There is a build up of intracellular metabolites
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18
Q

What is the morphology of fatty change in cells and what causes this?

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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19
Q

What is the ‘point of no return’?

A

Does not matter if factor is or isn’t there, cell cannot return back to normal

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20
Q

What is necrosis and what is it usually caused by?

A
  • Cell death

- Usually due to pathology

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21
Q

What is the process of necrosis?

A
  • Intracellular protein denaturation and lysosomal digestion of cell
  • Cell membrane is disrupted leading to leakage of cell contents
  • Inflammatory response in surrounding tissues
  • Cell remains are removed by phagocytosis
  • Histopathological changes may take some time to appear
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22
Q

What is a useful histological sign that a cell is necrotic?

A

The loss of a blue staining nucleus

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23
Q

How can you identify coagulative necrosis

A
  • No proteolysis of the dead cells due to denaturation of enzymes
  • Architecture of tissues is preserved for some days
  • No nucleus; eosinophilic cells
  • Grossly firm in texture
  • Cells digested by lysosomes of leukocytes
24
Q

What is a localised area of coagulative necrosis called?

A

An infarct

25
Q

How can you identify liquefactive necrosis?

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

How can you identify caseous necrosis?

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

What is gangrenous necrosis?

A

Coagulative necrosis with superimposed bacterial infection - liquefactive necrosis

28
Q

What is fat necrosis?

A

Focal areas of fat destruction. Fat cells may be liquefied by activated pancreatic enzymes

29
Q

What is fibrinoid necrosis?

A

Special type of necrosis seen in immune reactions in blood vessels

30
Q

How can you identify fibrinoid necrosis?

A
  • 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 possible 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
  • If remains are not removed then calcium salts may be deposited in necrotic tissue
32
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
33
Q

What are the pathological triggers of apoptosis?

A
  • Hypoxia/ischaemia (protein misfolding)
  • Viral infection
  • DNA damage - if unrepairable p53 triggers apoptosis
  • Caspases are activated enzymes that trigger apoptosis
  • Cell contents are degraded by enzymes activated by the cell
34
Q

What are a few physiological roles of apoptosis?

A
  • Deletion of inflammatory cells after an inflammatory response
  • Deletion of self-reactive lymphocytes in the thymus
35
Q

What can result from too little apoptosis?

A

Cancer

36
Q

What can result from too much apoptosis?

A

Degenerative diseases

37
Q

What is the morphology of apoptosis?

A
  • Cell shrinkage
  • Packaging up of nucleus
  • Cell membrane remains intact
  • Phagocytosed but no widespread inflammation
38
Q

What is pyknosis?

A

Nucleus shrinks; darker staining

39
Q

What is karyorrhexis?

A

Nucleus fragments

40
Q

What is karyolysis?

A

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

41
Q

What are examples of excessive normal cellular constituents in the accumulation of abnormal substances in cells?

A
  • Water
  • Lipid
  • Glycogen
42
Q

What are examples of abnormal endogenous/exogenous material in the accumulation of abnormal substances in cells?

A
  • Carbon
  • Silica
  • Metabolites
  • Cholesterol
43
Q

What is atherosclerosis?

A

Accumulation of cholesterol in macrophages and smooth muscle cells in blood vessel walls
- Also found at sites of haemorrhage and necrosis

44
Q

What are foam cells?

A

Macrophages ingested lipid

45
Q

What is amyloid?

A

A fibrillar protein material that is deposited as a result of pathologic processes leading to an increased production of these proteins
- Deposited in extracellular location in various tissues and organs

46
Q

What are the 3 different types of amyloid?

A
  1. AL (amyloid light chain) - derived from light chain immunoglobins from plasma cells
  2. AA (amyloid associated) - Derived from proteins synthesised in the liver
  3. A-beta - Alzheimer’s disease
47
Q

What causes amyloid?

A

Chronic inflammation, multiple myeloma, aging and drug abuse

48
Q

What is the microscopical appearance of amyloid?

A
  • Pink hyaline appearance
  • Difficult to identify with H&E
  • Special stain: Congo red (easier to identify)
49
Q

What 2 types of pathological pigmentation are there?

A
  • Endogenous

- Exogenous

50
Q

What is endogenous pigmentation?

A
  • Lipofuscin-cellular lipid breakdown products
  • Melanin
  • Haemosiderin-localised bruising - breakdown of RBC
  • Bilirubin

ALL APPEAR BROWN

51
Q

What is exogenous 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 e.g. lead
  • Pigmentation associated with intravascular drug use
52
Q

What is pneumoconiosis?

A

Excessive amounts of carbon deposited in the lungs - clotting up and closing of the alveoli

53
Q

What is dystrophic pathologic calcification?

A
  • Deposits of calcium phosphate in necrotic tissue. Serum calcium is normal - no relation to level of calcium in the body
54
Q

What is metastatic pathologic calcification?

A
  • 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
55
Q

What are the 4 causes of raised serum calcium (hypercalcemia)

A
  1. Increased levels of parathyroid hormone (hyperparathyroidism) parathyroid gland tumour
  2. Destruction of bone tissue - leukaemia, metastasis of bone, immobilization
  3. Excess vitamin D
  4. Renal failure - causes secondary hyperparathyroidism

BDS1 Pathology (14 decks)

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