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Cellular Pathology > Cell Damage and Cell Death > Flashcards

Cell Damage and Cell Death Flashcards

1
Q

What are some causes of cell damage/death?

A
  • Genetic
  • Inflammation
  • Physical
  • Chemical
  • Infection
  • Traumatic Damage
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2
Q

Give some examples of Genetic causes which may cause cell death

A
  • Abnormal number chromosomes (aneuploidy)
  • Abnormal chromosomes (deletions/translocations)
  • Increased fragility (Fanconi’s anaemia)
  • Failure of repair (Xeroderma pigmentosa)
  • Inborn errors (Storage disorders ie. Tay Sachs disease)
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3
Q

Give some examples of traumatic damage which may lead to cell death

A
  • Interruption of blood supply
  • Direct rupture of cells
  • Entry of foreign agents
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4
Q

Give some examples of physical causes which may lead to cell death

A
  • Irradiation
  • Heat
  • Cold
  • Barotrauma
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5
Q

Give some examples of chemical causes which may lead to cell death

A
  • Acids/corrosives
  • Specific actions e.g. enzymes
  • Interference with metabolism e.g. alcohol
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6
Q

Give some examples of how infection may lead to cell death

A
  • Toxic agents compete for nutrients
  • During viruses/mycobacteria take over Intracellular replication machinery provoking an immune response, which causes death of that cell
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7
Q

Give some examples of how inflammation may lead to cell death

A
  • Trauma
  • Thrombo-embolism
  • Atherosclerosis
  • Vasculitis
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8
Q

What are the 3 basic mechanism by which cell death can be caused by?

A
  • Necrosis
  • Apoptosis
  • Autophagic cell death
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9
Q

Define Necrosis

A

Necrosis: most common cause of cell death. Occurs after stresses such as ischemia, trauma, chemical injury

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10
Q

Define Apoptosis

A

Programmed cell death. Designed to eliminate unwanted host cells through activation of a co-ordinated, internally programmed series of events effected by a dedicated set of gene products

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11
Q

Define Autophagic cell death

A

Autophagy is responsible for the degradation of normal proteins involved in cellular remodelling found during metamorphosis, ageing and differentiation as well as for the digestion and removal of abnormal proteins that would otherwise accumulate following toxin exposure, cancer, or disease.

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12
Q

what drug can induce cell death of breast cancer cells and what mechanism is involved.

A

An example is the death of breast cancer cells induced by Tamoxifen. The mechanism involved is Autophagic cell death.

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13
Q

Name some causes of Necrosis

A
  • Usually caused by lack of blood supply to cells or tissues
  • injury
  • infection,
  • cancer
  • infarction
  • inflammation
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14
Q

How can a lack of blood supply cause necrosis?

A

Lack of blood supply –>
Lack of oxygen –>
Lack of ATP –>
Lack of OxPhos–>

Note: lack of blood supply can be caused by a lot of reasons

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15
Q

What is the effect of compressing blood vessels on pH?

A

Restricts oxygen supply and therefore lowering pH (makes it acidic)

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16
Q

What are the 3 key principles of necrosis?

A
  1. Whole groups of cells are affected.
  2. Result of an injurious agent or event.
  3. Reversible events proceed irreversible
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17
Q

Describe the mechanism of Necrosis? There are 5 steps

A
  1. As a result of injurious agent or event, which causes oxygen deprivation
  2. Cells unable to produce ATP because of oxygen deprivation
  3. Cells swell due to influx of water (ATP is required for ion pumps to work).
  4. Haphazard destruction of organelles and nuclear material by enzymes from ruptured lysosomes (due to swelling of lysosome membranes).
  5. Cellular debris stimulates an inflammatory cell response
18
Q

Microscopic appearance of Necrosis: Describe the nuclear changes

A
  1. Chromatin condensation/shrinkage.
  2. Fragmentation of nucleus.
  3. Dissolution of the chromatin by DNAse.
19
Q

Microscopic appearance of Necrosis: Describe the cytoplasmic changes

A
  1. Opacification: denaturation of proteins with aggregation.

2. Complete digestion of cells by enzymes causing cell to liquify (liquefactive necrosis).

20
Q

Microscopic appearance of Necrosis: Describe the biochemical changes

A
  1. Release of enzymes such as creatine kinase or lactate dehydrogenase
  2. Release of proteins such as myoglobin
21
Q

What is the clinical application of biochemical changes caused by necrosis?

A

These biochemical changes (concentration of enzymes such as creatine kinase) are useful in the clinic to measure the extent of tissue damage!

22
Q

Astrocytoma is an example of…

A

Necrosis

23
Q

In a H&E cross section of a kidney, how can we identify necrosis?

A

Dark purple dots = DNA

In necrotic kidney DNA is completely damaged so there is less dark purple dots, but cell membrane is still visible.

These cells can be referred to as ghost cells

24
Q

What is the function of Necrosis?

A

Removes damaged cells from an organism

Failure to do so may lead to chronic inflammation

25
Q

What is the function of apoptosis?

A

-Selective process for the deletion of superfluous, infected or transformed cells.

This is Involved in:

  • Embryogenesis
  • Metamorphosis
  • Normal tissue turnover
  • Endocrine-dependent tissue atrophy
  • A variety of pathological conditions
26
Q

Try and give 8 examples of apoptosis?

A
  1. Cell death in embryonic hand to form individual fingers
  2. Apoptosis induced by growth factor deprivation (neuronal death from lack of NGF).
  3. DNA damage-mediated apoptosis. If DNA is damaged due to radiation or chemo therapeutic agents, p53 (tumour suppressor gene product) accumulates. This arrests the cell cycle enabling the cell repair the damage. If repair process fails, p53 triggers apoptosis.
  4. Cell death in tumours causing regression.
  5. Cell death in viral diseases (ie viral hepatitis).
  6. Cell death induced by cytotoxic T cells (ie. Cellular immune rejection or graft vs. host disease).
  7. Death of neutrophils during an acute inflammatory response
  8. Death of immune cells( both T and B lymphocytes) after depletion of cytokines as well of death of autoreactive T cells in the developing thymus..
27
Q

Name some factors that effect the balance of survival or apoptosis of cell by favouring survival?

A
  • (high) growth factors
  • cytokines
  • disruption of cell-cell and or cell-matrix contacts
28
Q

Name some factors that effect the balance of survival or apoptosis of cell by favouring
apoptosis?

A
  • Lack of growth factors
  • Death domain ligands
  • DNA damaging agens
  • Disruption of cell-cell and or cell-matrix contacts
29
Q

There are two types of apoptosis, what are these?

A

Intrinsic

Extrinsic

30
Q

Name some (intrinsic) factors which induce intrinsic apoptosis?

A

DNA damage – p53-dependent pathway

Interruption of the cell cycle

Inhibition of protein synthesis

Viral Infection

Change in redox state

31
Q

Name some (extrinsic) factors which induce extrinsic apoptosis?

A

Withdrawal of growth factors (e.g. IL-3)

Extracellular signals (e.g. TNF)

T cell or NK (Natural Killer) (e.g. Granzyme

32
Q

What are Caspases?

A

(Cysteine Aspartate-specific Proteases)

Caspases are Cysteine Proteases that play a central role in the initiation of apoptosis.

Most proteases are synthesised as inactive precursors requiring activation (usually partial digestion by another protease).

33
Q

Caspase activation leads to characteristic morphological changes of the cell such as:

A

shrinkage, chromatin condensation, DNA fragmentation and plasma membrane blebbing (bulge)

34
Q

what are the 8 key ideas of apoptosis?

A
  1. Single or few cells selected.
  2. Programmed cell death.
  3. Irreversible once initiated.
  4. Events are energy driven.
  5. Cells shrink as the cytoskeleton is disassembled.
  6. Orderly packaging of organelles and nuclear fragments in membrane bound vesicles.
  7. New molecules expressed on vesicle membranes stimulate phagocytosis, no inflammatory response.
35
Q

Microscopic appearance of apoptosis: Nuclear changes

A
  1. Nuclear chromatin condenses on nuclear membrane.

2. DNA cleavage.

36
Q

Microscopic appearance of apoptosis: cytoplasmic changes

A
  1. Shrinkage of cell. Organelles packaged into membrane vesicles.
  2. Cell fragmentation. Membrane bound vesicles bud off.
  3. Phagocytosis of cell fragments by macrophage and adjacent cell.
  4. No leakage of cytosolic components.
37
Q

Microscopic appearance of apoptosis: biochemical changes

A
  1. Expression of charged sugar molecules on outer surface of cell
    membranes (recognised by macrophages to enhance phagocytosis)
  2. Protein cleavage by proteases, caspases
38
Q

Apoptosis = “Death by a thousand cuts”, Expand on this:

A

Hundreds of substrates for activated caspases. Substrates fall into most classes of important genes

39
Q

How do we activate the initiator caspases?

A

By induced proximity.

For example:
In response to receptor dimerization upon ligand binding or
Cytochrome C release from the mitochondria.

40
Q

what can mutations in the p53 gene lead to?

A

Mutations in the p53 gene are the most common mutations
in cancer. Some mutations destroy the ability of p53 to induce
Apoptosis.

Cellular Pathology (13 decks)

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