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Pathology > Cell injury > Flashcards

Cell injury Flashcards

1
Q

what are causes of cell injury?

A
  • oxygen deprivation
  • physical damage
  • microbial (like infection?)
    -immunological (like autoimmune?)
  • chemical
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2
Q

How is cell harmed by
a) ionising radiation?
b) contact with strong acid?
c) carbon monoxide inhalation?
d) trauma?

A

a) damage to DNA
b) coagulates tissue proteins
c) prevents O2 transportation
d) mechanical disruption of tissue

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3
Q

how can cells be damaged? (what ways?)

A
  • ATP depletion →multiple downstream effects
  • mitochondria damage →leakage of pro-apoptotic proteins
  • intra-cellular calcium →increased mitochondrial permeability & activation of multiple cellular enzymes (as calcium = cofactor)
  • free radical (ROS) damage → damage to lipids, proteins, DNA (accumulation of reactive oxygen species - different from oxidative burst which is intentional release of recative oxygen species by neutrophils)
  • defective membrane permeability →loss of cellular components
  • protein misfolding →activation of pro-apoptotic protiens
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4
Q

what is hypoxia?

A

a state in which oxygen is not available in sufficient amounts at the tissue level to maintain adequate homeostasis

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5
Q

what is hypoxia caused by?

A
  • ischaemia →most common cause & is when reduced blood flow so reduced delivery of O2 to tissues - comprimises delivery of glycogen substrates too
  • Reduction in oxygen carrying capacity of the blood e.g anaemia, CO poisoning
  • Inadequate blood oxygenation e.g pneumonia
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6
Q

what happens to cells in hypoxic injury?

A

=reduced intra-cellular ATP which means Na+ pump reduced so NA+ accumulates which causes iso-osmotic gain of water & acute cellular swelling

= increased anaerobic glycolysis (bc of decreased ATP) →rapid depletion in glycogen stores

= ribosomes detach from RER
= polysomes dissociate into monomers →reduced protein synthesis

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7
Q

what happens if hypoxia persists?

A
  • cytoskeleton breaks down & loss of ultra structural features
    -last point of return before irreversible injury or death
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8
Q

what can result in cell recovery?

A

restoration of blood flow

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9
Q

what is reperfusion injury?

A

sometimes restoration of blood flow can result in cell recovery

but sometimes reperfusion into ischaemic tissues can cause paradoxical further injury

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10
Q

what do high ROS levels cause?

A

membrane damage & promotes mitochondrial permeability damage

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11
Q

what is free radical induced cell injury?

A

it’s when free radicals damage cells by producing reactive oxygen species (ROS)

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12
Q

what are forms of mechanical injury? (how mechanic of cell injured)

A
  • direct mechanical damage = cell membranes rupture, cytoplasm spills out
  • Freezing = Intracellular and cell membranes perforated by ice crystals
  • Osmotic imbalance = Rupture as a result of rapid change in osmotic pressure
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13
Q

what are forms of microbial injury?

A

Bacteria
= Metabolic products/secretions which then harm the host cells
= Host inflammatory response causing further damage

Viruses
= Intracellular – can cause physical rupture of host cells
= Again, host inflammatory response can cause further damage

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14
Q

what are forms of chemical damage to the cell?

A

-drugs & poisons
- systemic Vs local toxicity
- caustic substances = rapid local death from extreme alkalinity or acidity = corrosive effect on tissue (protein digestion)

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15
Q

what is atrophy?

A

shrinkage in the size of cell by the loss of cell substance

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16
Q

what is hypertrophy?

A

increase in the size of the cells and consequently an increase in the size of an organ

17
Q

what is hyperplasia?

A

increase in number of cells in an organ or tissue

18
Q

what is metaplasia?

A

reversible change in which one adult cell type is replaced by another adult cell type (like squamous epithelial cells?)

19
Q

what are 2 forms of irreversible cell death?

A

apoptosis and necrosis

20
Q

what is apoptosis?

A

pre-programmed, contained killing of cell = no surrounding damage

21
Q

what is necrosis?

A

causes surrounding damage & leakage of cellular contents
- much less contained and more explosive than apoptosis

22
Q

what is the difference in affects to the following features with necrosis & apoptosis?
a) cell size
b) nucleus
c) plasma membrane
d) nearby inflammation
e) physiological/pathological

A

a) necrosis = increased, swollen cell and apoptosis skrink
b) necrosis= pyknosis (going), kayohexis (going), karyolysis (gone)
apoptosis = fragmentation/condensation
c) N = disrupted, A = intact
d) N = almost always, A = never
e) N= pathological, A = physiological but may be pathological

23
Q

what are types of necrosis?

A
  • coagulative necrosis (caused by ischaemia)
  • colliquative/liquefactive necrosis (liquifies -> pus)
  • caseous necrosis (type of coagulative - unrecognizable chunks)
  • gangrenous necrosis (wet & dry)
  • fat necrosis (from lipases & trauma)
24
Q

what is coagulative necrosis?

A

tissue with connective tissue → basic arrangement preserved

  • Caused by ischemia→ results in decreased ATP, increased cytosolic Ca++, and free radical formation, which each eventually cause membrane damage
    e.g. Infarct: localized area of ischemic necrosis - myocardial infarct
25
Q

what is caseous necrosis?

A

cheese-like necrotic debris

  • Distinct form of coagulative necrosis
  • Coagulated tissue no longer resembles the cells, but is in chunks of unrecognizable debris
  • Usually giant cell and granulomatous reaction

Example: Tuberculosis

26
Q

what is colliquative necrosis?

A

tissue with minimal connective tissue

  • Often in brain because lack of supporting stroma predisposes to total liquefaction when necrotic
  • Usually caused by focal bacterial infections, because they can attract polymorphonuclear leukocytes (neutrophils)
  • The enzymes in the neutrophils are released to fight the bacteria, but also dissolve the tissues nearby, causing an accumulation of pus effectively liquefying the tissue
27
Q

what is gangrenous necrosis?

A

= Dry –sterile coagulative necrosis (doesn’t involve bacterial infection) e.g. distal limb - GI tract & bacterial

= Wet – coagulative necrosis with superimposed infection - limbs (diabetic)

  • often associated with lack of blood supply
28
Q

what is fat necrosis?

A
  • Release of enzymes from pancreas or gut or traumatic
  • Enzymes (lipases) release free fatty acids, which with calcium produce soapy deposits in tissues
  • Histology: shadowy outlines of fat cells, calcium deposits, foam cells, surrounding inflammatory reaction
29
Q

what is autolysis?

A
  • rotting of tissue
  • lysis of tissue by their own enzymes, following death of the organism
  • “ no vital reaction (i.e., no inflammation)”
  • Early autolysis is indistinguishable from early coagulative necrosis due to ischemia, unless the latter is focal
30
Q

why is apoptosis physiologically important? (i.e what is apoptosis important for)

A
  • Embryogenesis
  • Menstrual cycle (shedding of endometrium)
  • Immune system = Death of post-inflammatory neutrophils & Removal of self-reactive lymphocytes & Death of virally infected cells
31
Q

a) what is healing by primary intention?
b) what is healing by secondary intention?

A

a) Restitution with no – or minimal – residual defect(surgical context = sewn up minimal)
b) Organisation and repair where there is tissue loss & Granulation tissue (scar) (surgical context = left open to heal itself and scar formed)

32
Q

what is labile cell group?

A

cells that have good capacity to regenerate (like surface epithelial cells)

33
Q

what is stable cell group?

A

cells that divide at a slow rate, but can regenerate if needed (eg hepatocytes in liver)

34
Q

what is permanent cell group?

A

cells with no means of effective regeneration eg nerve cells, striated muscle cells

Pathology (10 decks)

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