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Medicine Year 1 - Semester 2 - Part 2 > Cell Death > Flashcards

Cell Death Flashcards

1
Q

What is necrosis ?

A

The death of tissues following bioenergetic failure and loss of plasma membrane integrity.

Induces inflammation and repair.

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2
Q

What is apoptosis ?

A

Usually involves DNA fragmentation.

Apoptosis is an active process.

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3
Q

State some features of necrosis

A

Pathological process
Affects cell groups

Cell membrane integrity is lost
Cell swelling and lysis

Inflammatory response

Dead cells are phagocytosed by inflammatory cells

Abnormal ion homeostasis

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4
Q

State some features of apoptosis

A

Physiological or Pathological induced
Affects single cells

Cell membrane integrity is maintained
Cell shrinkage and fragmentation

NO inflammatory response

Dead cells are phagocytosed by neighbouring cells

Energy-dependent fragmentation of DNA

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5
Q

State some features of reversible cell injury

A

REVERSIBLE

Increased intracellular volume
Mitochondrial swelling and calcification

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6
Q

What is key to the homeostasis of a cell ?

A

The mitochondria

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7
Q

Function of the mitochondria

A

They oxidise things, as oxygen is dangerous to the cell.

This process produces free radicals (e.g. hydrogen peroxide), due to burning glucose.

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8
Q

Free radical

A

Any species with an unpaired electron.

Goes to things that like an electron, for example DNA, RNA, membranes. This can cause damage to any of these.

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9
Q

What happens if metabolism (respiration) is not properly controlled ?

A

You can risk further damage to the cell.

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10
Q

Function of mitochondria in reversible injury

A

The mitochondria is important to generate energy, to maintain the cells homeostasis, to keep water out.

Also because the mitochondria can be a potent source of molecules e.g. SOD, which can cause secondary damage.

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11
Q

Describe lethal injury

A

Reversible injury

Not able to restore e.g. membrane pumps to keep water and sodium out

Mitochondria may release oxygen free radicals, causing further damage.

Not enough energy produced.

Cell dies via necrosis.

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12
Q

Causes of necrosis

A

Ischaemia
Metabolic
Trauma

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13
Q

Coagulative necrosis

A

Commonest type

Firm, pale area with ghost outlines in microscopy

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14
Q

Colliquative necrosis

A

Seen in the brain

Dead area is liquefied

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15
Q

Caseous necrosis

A

Seen in tuberculosis

Pale yellow semi-solid material

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16
Q

Gangrene necrosis

A

Necrosis with putrefaction

Follows vascular occlusion or certain infections and is black.

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17
Q

Fibrinoid necrosis

A

Microscopic feature in arterioles in malignant hypertension

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18
Q

Fat necrosis

A

May follow trauma and cause a mass

OR

May follow pancreatitis visible as multiple white spots.

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19
Q

Key feature of necrosis

A

Evokes an inflammatory response
Loss of energy

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20
Q

Why don’t you get inflammation in apoptosis ?

A

As cell membrane integrity is maintained. No cell contents are spilled.

Fragments are phagocytosed and quickly sucked up by adjacent cells.

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21
Q

Give some examples of apoptosis

A

Embryology - lumen of tubules e.g. oesophagus

Inflammation - resolution and death of neutrophils

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22
Q

How to end inflammation ?

A

Acute inflammation can be controlled by neutrophils.

Neutrophils have a limited lifespan, they only stay around for <20hrs and then die.

So after 20hrs there is no inflammation, unless you recruit new cells.

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23
Q

How do neutrophils die ?

A

Apoptosis

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24
Q

What does clearance of apoptotic cells require ?

A

Clearance of apoptotic cells by macrophages requires reorganisation of phosphatidylserine.

25
Q

State the 2 types of causes of apoptosis

A

Extrinsic - receptor triggered

Intrinsic - something from within damage the nucleus/ damage to DNA/ mitochondria

26
Q

Extrinsic causes of apoptosis

A

Receptors
T cells

27
Q

Intrinsic causes of apoptosis

A

Stress
Metabolic
DNA damage and p53

28
Q

State the key features of extrinsic caused apoptosis

A
  1. Receptor interaction
  2. Cytoplasmic signals
  3. Caspase cascade
29
Q

State some examples of extrinsic triggers

A

Tumour necrosis factor - cytokines produced by macrophages

Inflammation

This triggers apoptosis through the receptors.

30
Q

Caspases function

A

Chew up the cell, chew up/ lead to the chewing up of DNA into chunks.

Help fragment the cytoskeleton, membrane is flipped inside out.

31
Q

Describe some key features of T cell mediated apoptosis

A
  1. Touch the target cell and inject enzymes
  2. Perforin and granzymes
  3. Cytoplasmic activation, caspase activation
32
Q

Examples of T cell mediated apoptosis

A

Viral infection

Transplantation rejection

Tumour cell destruction

33
Q

State some key features of intrinsic apoptosis

A
  1. Endogenous activation
  2. Mitochondrial involvement
  3. Caspase activation which breaks up the cell

(response to DNA damage/ damage to the mitochondria)

34
Q

What is a key step in intrinsic pathway of apoptosis ?

A

Release of cytochrome C from the mitochondria.

35
Q

Apoptosome

A

A whole series of proteins which speeds up the biochemistry that chews up the cell into smaller parts.

AUGMENTS, AMPLIFIES, SPEEDS up the whole process.

Releases activated caspases, causing the cell to fragment.

36
Q

Cells response to DNA damage

A
  1. Stop proliferating, cell doesn’t grow anymore, cell doesn’t die
  2. Sequence of events, hitting the mitochondrion, causing apoptosis
37
Q

Control of apoptosis

A

Bcl2 family

  • family of factors that either stick to each other, or stick to other members of the family
38
Q

Describe the BCL-2 family

A

A. Anti-apoptotic Bcl2 protein

B. Pro-apoptotic BH123 protein

C. Pro-apoptotic BH3-only protein

39
Q

BH3-only protein

A

Pro-apoptotic

39
Q

Bcl2 protein

A

Anti-apoptotic
Stabilises the mitochondria

40
Q

BH123 protein

A

Pro-apoptotic

41
Q

What does abnormal Bcl2 expression lead to ?

A

Can contribute to cancer

  • translocation and rearrangement
  • too much Bcl2
  • cell doesn’t die
  • too much B cells
42
Q

State the multiple layers of control of apoptosis

A

Caspases
Mitochondria
Bcl2 + family
Inhibitors of apoptosis (IAP proteins)

43
Q

Describe caspase structure

A

Cysteine in the active site: ‘C’
Cleavage after aspartate: ‘asp’
Protease: ‘ase’

44
Q

What are caspases ?

A

Key effectors of apoptosis

45
Q

Function of cleaving ICAD

A

Destroy genetic information

46
Q

Function of cleaving PARP

A

Prevents DNA repair

47
Q

Function of cleaving lamin

A

Breaks down nuclear architecture

48
Q

Function of cleaving keratin

A

Breaks down cytoplasmic architecture

49
Q

Importance of apoptosis in carcinogenesis

A

Apoptosis is :

  • discrete
  • specific
  • targeted
  • a morphological diagnosis
50
Q

State the 3 survival factors to block apoptosis

A
  1. Increased production of the anti-apoptotic Bcl2 protein
  2. Inactivation of pro-apoptotic BH3-only Bcl2 protein
  3. Inactivation of anti-IAPs
51
Q

What lengthens the lifespan of cells ?

A

Calorie restriction

52
Q

State some examples when apoptosis goes wrong

A

Autoimmune disease
Cancer
Neurodegeneration

53
Q

Can pathway components be drug targets ?

A

Bcl2 in lymphoma

Caspase 3 in Alzheimer Type Dementia

IAP in cancer

54
Q

State some other variants of cell death

A

Anoikis
Pyroptosis
Ferroptosis
Necroptosis

55
Q

Trigger of pyroptosis

A

Microbial trigger

e.g. Salmonella

56
Q

Pyroptosis

A

Features similar to apoptosis and necrosis

  • Caspase 1 activation not 3
  • nuclear fragmentation
  • no cytoplasmic blebbing
  • pro-inflammatory
57
Q

Anoikis

A

Death after losing contact with basement membrane / extra-cellular matrix

Medicine Year 1 - Semester 2 - Part 2 (53 decks)

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