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FMS > [FMS] CBS - cell death > Flashcards

[FMS] CBS - cell death Flashcards

1
Q

difference between apoptosis and necrosis

A

Apoptosis = regulated cell death (RCD) / Programmed Cell Death (PCD) : cell dies in a controlled way

Necrosis = Accidental cell death (ACD)

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2
Q

in apoptosis are the triggers intrinsic, extrinsic?

A

both

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3
Q

in apoptosis are the contents of the cell released?

A

no

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4
Q

in apoptosis is there an inflammatory response?

A

no

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5
Q

in necrosis in what 2 ways do the cells die

A
  • Cells die due to lack of ATP (hypoxia or ischemia)
  • Cell death due to physical damage – injury
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6
Q

in necrosis are the contents of the cell released?

A

yes, into extracellular space

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7
Q

in necrosis is there an inflammatory response?

A

yes

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8
Q

2 roles of apoptosis

A
  1. remodelling/development
  2. removing damaged cells
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9
Q

what happens when skin cells are exposed to UVB, how is apoptosis involved?

A
  1. UVB induces chemical bonds between adjacent thymines = thymine dimers
    - dimers disrupt DNA structure and interfere with accurate replication = mutations
    - repaired by Nucleotide Excision Repair (NER) Pathway
    - excessive damage = removed via apoptosis preventing cancer development
    - skin keratinocytes form “sunburn cells” and undergo apoptosis in response to excessive exposure to sunlight
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10
Q

outline the 7 morphological changes during apoptosis

A
  1. smaller cell
  2. cytoskeleton collapse
  3. nuclear envelope disassembles
  4. chromatin condense and fragmented
  5. cell surface bulges (blebs)
  6. cells break up into membrane bound apoptotic bodies
  7. bodies engulfed and destroyed by phagocytosis - macrophages
  8. rapid process
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11
Q

whats the intracellular mediator of apoptosis/ what triggers the intracellular events of apoptosis

A

caspases

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12
Q

what family do caspases come from?

A

proteases

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13
Q

how are caspases synthesised

A

Caspases synthesised as inactive precursors that
are activated by cleavage during apoptosis

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14
Q

2 types of caspases

A

initiator caspases
executor caspases

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15
Q

where are initiator caspases found? what is its apoptotic trigger?

A

found inactive as monomers in cytosol

apoptotic trigger = dimerisation, activation, cleavage

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16
Q

how are executor caspases activated?

A
  • Initiator caspases cleave and activate executor
    caspases
  • Activated executor caspases activate by
    cleavage all the changes in cell biology
    observed in apoptosis
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17
Q

whats the function of a caspase?

A

to increase phosphatidylserine in the outer membrane layer

18
Q

what is CAD?

A
  • a specific endonuclease
19
Q

how is a ladder of fragments formed in DNA fragmentation?

A

DNA fragmentation into discrete chunks occurs due
to activation of CAD

Executioner caspases degrades iCAD – a specific
inhibitor of CAD

DNA is cleaved in the regions between
nucleosomes that result in a ladder of
fragments

20
Q

what is the extrinsic pathway for apoptosis?

A
21
Q

what is the intrinsic (mitochondrial) pathway to trigger apoptosis?

A
22
Q

what activates the caspase cascade in cytotoxic t-cells in the extrinsic pathway for apoptosis?

A

binding of FAS ligand to FAS receptor

23
Q

death receptors are part of which family of receptors

A

TNF (tumor necrosis factor) family of receptors

24
Q

when fas ligand binds to fas receptor what happens

A

activates initiator caspases and forms the death-inducing signalling complex (DISC)

25
Q

which pathway detects DNA damage in the intrinsic pathway (mitochondrial)

A

p53 pathway

26
Q

what does p53 pathway stimulate

A

Bax and Bak aggregation in mitochondrial membrane

27
Q

what does bak/bax aggregation cause?

A

allows for:

  • mitochondrial outer membrane permeabilisation (MOMP)
  • cytochrome c release
28
Q

what does cytochrome c bind to and what does it form?

A

Cytochrome c binds to Apaf1(apoptotic
protease activating factor 1) to form
apoptosome complex

29
Q

what does apoptosome complex do?

A

triggers caspase cascade

30
Q

what do survival factors do? whats an example of a survival factor

A

survival factors BLOCK apoptosis, these proteins interfere with bak/bax complex ie BCl2

31
Q

whats the role of macrophages in cell death?

A

remove apoptotic cells

32
Q

how are apoptotic cells removed by macrophages?

A
  • Composition of outer leaf of plasma membrane is altered
  • Phosphatidylserine (PS) is flipped to the outer leaf of membrane
  • This is detected and triggers phagocytosis
33
Q

for which of these does necrosis take place?

  • hypoxia (lack of O2)
  • Ischemia (leading to hypoxia)
  • Very high temperature
  • Chemical (strong acid/base)
  • High radiation dose
A

all

34
Q

4 stages of necrosis

A
  1. cells swell (oncosis)
  2. leaky membrane = breaks
  3. release of content
  4. inflammatory response triggered
35
Q

whats programmed necrosis called? (another mechanism of cell death)

A

Necroptosis

36
Q

what happens in necroptosis

A
  • Binding of death ligand to death receptor triggers pathway via serine/threonine kinases
    receptor-interacting protein kinase 1 (RIPK1) and RIPK3
  • RIPK1/RIPK2 phosphorylates MLKL
  • Phosphorylated MLKL oligomerises (covalently bonds together) and forms ion channel in the plasma membrane
  • Cell then swells and breaks
37
Q

what 2 things contribute to cancer formation

A
  • increase in cell division
  • decrease in apoptosis
38
Q

what is usually found in the centre of solid tumors?

A

necrotic core in the center of solid tumors due to lack of blood supply - O2

39
Q

what happens in FL (follicular lymphoma)

how can it be treated

what are the symptoms?

A

In follicular lymphoma, there increased BCl2 expression in B cells - the BCl2 then blocks the apoptosis of the cells that have been transformed, leading to the survival and accumulation of abnormal B cells.

It can be treated with venetoclax (inhibitor of BCl2)

the symptoms are:
- shortness of breath
- tiredness
- enlarged spleen/ lymph nodes
- reduced level or RBCs and platelets

40
Q

do keats quiz on cell death

A

https://keats.kcl.ac.uk/mod/quiz/view.php?id=6704964

41
Q

What is used as effective treatment for acute myeloid leukaemia

A

Venetoclax → selective inhibitor of Bcl2 → allow apoptosis

FMS (33 decks)

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