apoptosis and necrosis Flashcards

1
Q

define apoptosis

A

programmed cell death of a single cell through intracellular sequence of events

Removal of a targeted cell without the release of products harmful to the surrounding cells

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2
Q

list 3 inhibitors of apoptosis

A

Growth factors
Extracellular cell matrix
Sex steroids

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3
Q

list 4 inducers of apoptosis

A

Glucocorticoids
Free radicals
Ionising radiation
DNA damage

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4
Q

what are the 3 types of DNA damage that can cause apoptosis?

A

Single-strand break
Base alteration
Cross-linkage

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5
Q

name a disease caused by a LACK of apoptosis

A

cancer:

lack of apoptosis – mutated p53 gene producing faulty p53 protein so it cannot control apoptosis

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6
Q

name a disease caused by TOO MUCH apoptosis

A

HIV:

too much apoptosis – kills the antibodies in the blood so the body can’t defend itself.

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7
Q

define necrosis

A

traumatic death

death of most or all of the cells in an organ or tissue due to disease, injury, or failure of the blood supply.

There is bioenergetic failure and loss of plasma membrane integrity

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8
Q

give 5 clinical examples of necrosis

A

Toxic spider venom
Frostbite
Cerebral infarction
Avascular necrosis of bone – femur has single arterial supply through the neck of the femoral head
Pancreatitis

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9
Q

what are the 4 types of necrosis

A
  1. coagulative
  2. Liquefactive
  3. Caseous

4.Gangrene

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10
Q

what is coagulative necrosis? (where does it happen, what is its cause)

A

Most common type
Can occur in most organs
Cause by ischaemia

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11
Q

what is liquefactive necrosis? (where does it happen, what is its cause)

A

Occurs in the brain due to its lack of substantial supporting stroma

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12
Q

what is Caseous necrosis? (what is its distance pattern, which disease is characterised by this form)

A

Causes a ‘cheese’ pattern
TB is characterised by this form of necrosis

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13
Q

what is gangrene? what does it look like?

A

Necrosis with rotting of the tissue
Affected tissue appears black due to deposition of iron sulphide (from degraded haemoglobin)

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14
Q

what are the different mechanisms of apoptosis?

A

intrinsic - apoptosis in response to internal stimuli eg. DNA damage

extrinsic - apoptosis in response to external stimuli

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15
Q

what are the 2 groups of modulators involved in intrinsic apoptosis?

A

Bcl-2 family

Bax family

Bcl-2:Bax ratio determines the cell’s susceptibility to apoptotic stimuli

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16
Q

how is the extrinsic pathway of apoptosis carried out?

A

specific ligands binding at ‘death receptors’ on the cell surface, initiate signal transduction cascade

17
Q

what is the execution phase is apoptosis?

A

common to both pathways (intrinsic and extrinsic)

Both pathways results in a cascade activation of caspases

initiator caspases -> executioner caspases -> degrade the cells

18
Q

what happens to a cell structure when it undergoes apoptosis?

A

Nuclear shrinkage (pyknosis)
DNA Fragmentation (karyorrhexis)
Cell shrinks

However - Retains an intact plasma membrane

dead cells are then phagocytosed

19
Q

main differences between apoptosis and necrosis:

  • stimuli
A

apoptosis: physiological, intracellular stimulus

necrosis: pathophysiological, extracellular stimulus (injury, disease)

ie, apoptosis happens in the healthy body all the time, whereas necrosis is often due to a disease

20
Q

main differences between apoptosis and necrosis:

  • inflammation and tissue damage
A

apoptosis: no inflammation, no secondary tissue damage, integrity of cellular structures maintained

necrosis: inflammation and secondary tissue damage, swelling and disintegration of cellular structures

21
Q

main differences between apoptosis and necrosis:

  • ATP dependent?
A

apoptosis - to activate cell death pathway need ATP

necrosis - abnormal pathway, no ATP needed

22
Q

give an example of necrosis

A

renal infarction

23
Q

What is the role of p53 protein?

A

p53 protein looks for DNA damage, if damage is present p53 switches on apoptosis.

24
Q

Activation of which family of protease enzymes can turn on apoptosis?

A

Caspases.

25
Q

Activation of what receptor can activate caspase and therefore apoptosis?

A

FAS receptor