Life and Death Flashcards

Revision

1
Q

What are the two types of cell death?

A

Necrosis

Apoptosis

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2
Q
When do these Adaptive Responses occur:
Hypertrophy
Hyperplasia
Atrophy
Metaplasia
A

Hypertrophy - if more work is required
Hyperplasia - more work
Atrophy - less work (reduction in cell size and can be physiological or pathological)
Metaplasia - different work

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3
Q

What happens if stress is too severe in terms of quantity of stress?

A

Hyperplasia and hypertrophy only cope so far.
They also take time to happen.
Therefore the cell undergoes cell death in the form of necrosis or apoptosis.

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4
Q

What are the two options for Cell Death?

A

Necrosis or Apoptosis

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5
Q

What is Necrosis?

A

Requires no energy
Always pathological (Abnormal. It does not occur normally).
Never occurs as a physiological phenomenon

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6
Q

What is Coagulative Necrosis?

A

Preservation of cell outline.
Dead cells are consumed by various enzymatic processes and cells.
Microenvironment too toxic for proteolysis etc.
Common.
Often seen in cardia muscle. Myocardial infarction.

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7
Q

What is Liquefactive Necrosis?

A

Liquid viscous mass - no cell structure remains.
Pus.
Associated with localised bacterial and fungal infections.
Necrosis within the brain.

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8
Q

What is Caseous Necrosis?

A

Caseous necrosis (Cheesy necrosis).
Microscopic.
Usually associated with Tuberculosis.
Granulomatous inflammation with central necrosis.
If someone mentions caseous necrosis - think TB
Ask for culture, PCR and look for result of Ziehl Neelson stain.

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9
Q

What is Apoptosis?

A

Programmed cell death in response to specific signals.
Requires Energy (ATP).
Sometimes cell death is physiological and we need cells to die off.
Counter-intuitively it may be a part of normal growth.
Removal of self reactive lymphocytes.
Hormonal-dependent involution.

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10
Q

When does pathological apoptosis occur?

A
In response to injury.
Radiation (including UV light).
Chemotherapy.
Viral infection - hepatitis.
Cancers.
Graft versus host disease.
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11
Q

What do mechanisms rely on?

A

All mechanisms rely on activating caspases.
This can be through 2 pathways:
Extrinsic
Intrinsic

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12
Q

What is an Extrinsic Pathway?

A

Death receptor initiated pathway.
Cell membrane receptors with “death domain”.
Death receptors - Tumour necrosis factor (TNF), Fas.

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13
Q

What is Fas and what can it lead to?

A

Fas - recognition of self
Apoptosis in lymphocytes.
People with Fas mutations often get autoimmune diseases.
TNF - complex but indices apoptosis in association with inflammatory conditions.

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14
Q

What is an Intrinsic Pathway

A

Mitochondrial pathway.
Growth signals promote anti-apoptotic molecules in mitochondrial membrane.
When removed - replaced by Bax, Bak.
Increase permeability of mitochondria.
Release of proteins that stimulate caspases.
Cytochrome C.

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15
Q

What is the role of p53

A

DNA damage.
Cells “sense” damage.
p53 halts cells cycle.
If DNA can’t be repaired then p53 stimulate caspases and induces apoptosis.

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16
Q

What can Apoptotic abnormalities cause?

A
Too little - cancers, autoimmune diseases.
Too much - neurodegenerative disorders.
Ishaemic injury (heart attacks), viral infections (hepatitis).
17
Q

What is Morphology?

A

Cells shrink - pyknosis.
Chromatin condensation - nucleus clumps and breaks up.
Cytoplasmic blebs - cytoplasm breaks up.
Macrophages - come in to hoover everything up.

18
Q

What is Cellular Ageing?

A

Many causes.
Oxidative stress - free radical damage.
Accumulation of metabolism by-products.
- lipofuscin (is sometimes how it is seen down the microscope).