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P > Cell Injury and Fate > Flashcards

Cell Injury and Fate Flashcards

1
Q

2 types of cell injury

A

Lethal and sub-lethal

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2
Q

Lethal cell injury

A

produces cell death

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3
Q

sub lethal cell injury

A

produces injury not amounting to cell death, may be reversible or may progress to cell death

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4
Q

Causes of cell injury

A
  • O2 deprivation
  • Chemical agents
  • Infectious agent
  • Immunological reactions
  • Genetic defects
  • Nutritional imbalances
  • Physical agents(trauma/gunshot wound/radiation)
  • Aging
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5
Q

What do the cellular response to injurious stimuli depend on

A

Type of Injury
Duration
Severity

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6
Q

What do the consequences of an injurious cell depend on

A

type of cell

cell status

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7
Q

Effects to which two systems cause an immediate effect

A

cell membrane integrity and ATP generation

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8
Q

why do effects to protein synthesis and genetic apparatus integrity take time for the effects to become apparent

A

DNA/RNA pathways

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9
Q

what is atrophy

A

shrinkage of cell/organ and by loss of cell substance

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10
Q

hypertrophy

A

increase in size of cell and consequently an increase in the size of the organ. Caused by either increased functional demand or specific hormone stimulation

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11
Q

Pathological vs physiological hypertrophy

A

Physiological (uterus during pregnancy) and pathological ( valve disorders)

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12
Q

Hyperplasia

A

Increase in number of cells in organ

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13
Q

Physiological hyperplasia

A

Hormonal or compensatory (e.g. after menstruation when the lining starts to build up again)

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14
Q

Pathological hyperplasia

A

Due to excessive hormonal or Gf stimulation ( e.g. cancer)

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15
Q

Metaplasia

A

Reversible change in which one adult cell type is replaced by another. Physiological/pathalogical

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16
Q

Physiological metaplasia

A

cervix during change between columnar to squamous epithelium in the cervical canal due to changes in the pH of the vagina

17
Q

Pathological metaplasia

A

Barretts oseophagus - acid reflux leads to metaplasia changing oesophageal cells from sqaumous to columnar. But can be reversed if you lose weights/use antacids

18
Q

Dysplasia

A

Precancerous cells which show genetic and cytological features or malignancy but not invading the underlying tissue

19
Q

How can you distinguish cancer cells microscopically

A

see all the nuclei and most ofthe cell is nucleus. so nucleus:cytoplasmic ratio increases

20
Q

What can you see microscopically in alcoholic fatty changes

A 
fatty change 
Cellular swelling ( associated with cell and tissue damage)
21
Q

What can you see in ballooning degeneration

A

cytoskeleton of hepatocyte is damaged and so rhere is an accumulation of proteins which is causing the cell to swell

22
Q

what occurs in necrosis

A

confluent cell death associated with inflammation

23
Q

coagulative necrosis

A

structure becomes thick/solid and the nuclei disappear

E.g. myocardial infarction

24
Q

liquefactive necrosis

A

where tissue becomes liquefied . Brain is particularly liquefied as not much connective tissue in brain to hold it together.
OCCURS IN BRAIN ONLY

25
Q

caseous necrosis

A

a bit cheesy, granulomas visible

Eg, pulmonary tuberculosis

26
Q

fat necrosis

A

in acute pancreatitis: if enzymes become activated in pancreas instead of duodenum. FFA will bind to calcium and will precipitate out and so will stain blue in microsopic slide

Eg. Acute pancreatitis

27
Q

apoptosis

A

programmed cell death but not associated with inflammation

28
Q

differentiating apoptosis and necrosis

A

apoptosis doesn’t have inflammation, can be physiological and active energy-dependent process

29
Q

causes of apoptosis

A

embryogenesis, deletion of auto-reactive T cells in thymus, hormone-dependent physiological involution, cell deletion in proliferating populations, a variety of mild injurious stimuli that cause irreparable DNA da,age that,in turn, triggers cell suicide pathways

30
Q

Necroptosis

A

Programmed form of cell death associated with inflammation (necrosis)
E.g. associated with viral infections

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