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POM (Principles of Medicine) > Cell injury and fate > Flashcards

Cell injury and fate Flashcards

1
Q

The cycle?

A

Normal cell (homeostasis) –(injurious stimulus)–> cell injury to cell death

normal cell (homeostasis) --(stress, increased demand)--> adaptation
--> inability to adapt --> cell injury to cell death
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2
Q

What are the causes of cell injury?

A
  • Oxygen deprivation
  • Chemical agents
  • Infectious agents
  • Immunological reactions
  • Genetic defects
  • Nutritional imbalances
  • Physical agents(injury)
  • Aging
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3
Q

What does the cellular response to injurious stimuli depends on?

A
  • the type of injury
  • its duration
  • its severity
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4
Q

What does the consequence of an injurious stimulus depend on?

A
  • type of cell

- its status

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5
Q

What are the four intracellular systems that are particularly vulnerable?

A
  • cell membrane integrity
  • ATP generation,
  • protein synthesis
  • the integrity of the genetic apparatus
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6
Q

Why do multiple secondary effects rapidly occur?

A

The structural and biochemical components of a cell are so integrally related that multiple secondary effects rapidly occur.

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7
Q

Cellular function is lost before cell death occurs..

A

which in turn occurs before the morphological changes are seen
(cardiac- will stop trying to contract whilst alive- if the injury goes on further, they will die)
- just bc a cell looks normal it doesnt mean its functional

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8
Q

What is lethal cell injury?

A

capable of causing death

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9
Q

What is sublethal cell injury?

A

consequence of exposure to a chemical or physical process that damages but does not kill a cell

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10
Q

What is morphology?

A

structural histological changes

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11
Q

What is atrophy?

A

Shrinkage in the size of the cell (or organ) by the loss of cell substance

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12
Q

What is hypertrophy?

A
  • Increase in the size of cells and consequently an increase in the size of the organ
  • Can be physiological (process that occurs in normal healthy people) or pathological (part of the disease process)
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13
Q

What is the cause of hypertrophy?

A
  • increased functional demand

- specific hormonal stimulation

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14
Q

examples of hypertrophy

A
  • uterus during pregnancy (physiological)
  • muscle fibres( valve abnormality or hypertension) - pathological
    athletes (physiological)
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15
Q

What is hyperplasia?

A
  • increase in the number of cells in an organ

- physiological or pathological

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16
Q

What can physiological hyperplasia be?

A

hormonal or compensatory

17
Q

What can pathological hyperplasia be due to?

A

excessive hormonal or growth factor stimulation.

18
Q

What is an example of hyperplasia?

A
  • menstruation and regrowth of cell wall (physiological)

- cancer (pathological)

19
Q

What is metaplasia?

A
  • A reversible change in which one adult cell type is replaced by another
  • A reversible change in which one adult cell type is replaced by another
20
Q

Examples of metaplasia?

A
  • pregnancy – cervix expands + columnar epithelium of the endocervix which is normally in the canal, becomes visible outside (due to the acidic pH of the vagina the columnar epithelium changes from being columnar into squamous– physiological
  • barretts oesophagus( acid reflux into intestine- squamous epithelium becomes columnar)
21
Q

What is dysplasia?

A

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

22
Q

What is dysplasia associated?

A

with Barretts oesophagus

23
Q

What reversible injuries is the light microscopic changes associated with?

A

Fatty change
Cellular swelling
ballooning degeneration
- degenerative changes

24
Q

What are degenerative changes?

A

changes associated with cell and tissue damage

25
Q

What is necrosis?

A

Confluent cell death associated with inflammation

26
Q

What irreversible injuries is the light microscopic changes associated with?

A

Coagulative necrosis
Liquefactive necrosis
Caseous necrosis
Fat Necrosis

27
Q

What is coagulative necrosis?

A

the structure becomes fixed, in the same way if you fry an egg (muscle fibres)

28
Q

What is liquefactive necrosis?

A

the tissue becomes liquefied (old cerebral infarct)

29
Q

What is Caseous necrosis?

A

cheesy
oozy + structureless
(tuberculosis)

30
Q

What is fat necrosis?

A

in acute pancreatitis( enzymes become active in pancreas and not duodenum)

31
Q

What is apoptosis?

A

programmed cell death/
death of individual cells

theres confluence, sheets of dead cells and a marked inflammatory reaction around

32
Q

What separates apoptosis from necrosis?

A

confluence and inflammatory reaction

33
Q

The apoptotic cells are swallowed up by macrophages

A

in a very neat manner

34
Q

Necrosis

A

a lot of inflammation and inflammatory response

35
Q

What are the causes of apoptosis?

A
  • Embryogenesis.
  • Deletion of auto-reactive T cells in the thymus.
  • Hormone-dependent physiological involution.
  • Cell deletion in proliferating populations.
  • A variety of mild injurious stimuli that cause irreparable DNA damage that, in turn, triggers cell suicide pathways
36
Q

What is mild injury?

A

causes but mild enough to cause irreparable DNA damage, may trigger this kind of suicide pathway by which the cells kill themselves
It cannot be repaired. And because the cells does not want to pass this kind of damage DNA onto the next generation.

37
Q

If some errors remain, and particularly if there’s some additional injury,

A

the cell can no longer repair itself and therefore it will go down and die by apoptotic pathway.

38
Q

What is required for apoptosis?

A

ATP so these cells can maintain cell membrane integrity

package all the organelles and break into little fragments, which can then taken up by the macrophages.

39
Q

What is necroptosis?

A

cell death, programmed cell death associated with inflammation
many causes eg. viral infection

POM (Principles of Medicine) (17 decks)

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