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OD2 (S1&2) > AED - Cell Injury I - Week 1 > Flashcards

AED - Cell Injury I - Week 1 Flashcards

1
Q

When a cell encounters an injurous agent, what happens?
What happens when the adaptive capacity of a cell is exceeded?

A

The cell adapts to preserve tissue viability.
Cell injury occurs as a result of adaptive capacity being exceeded.

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2
Q

Name 8 common causes of cell injury/stress.

A

Hypoxia
Chemicals/drugs
Physical agents
Microbiological agents
Immunological agents
Genetic defects
Nutritional imbalances
Ageing

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3
Q

Define atrophy.

A

Decrease in cellular size and organelles

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4
Q

Define hypertrophy.

A

Increase in normal cell size

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5
Q

Define hyperplasia.

A

Increase in normal cell number

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6
Q

Define metaplasia.

A

Replacement of one cell type with another by differentation/proliferation

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7
Q

Define dysplasia.

A

Abnormal change in cell shape/size

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8
Q

Give an example of atrophy as it occurs in iris tissue, including the loss of what molecule in which cells, and what condition it results in.

A

Loss of melanosomes in iris pigment epithelial cells
Causes peripupillary atrophy

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9
Q

What does pseudoexfoliation syndrome result in?

A

Deposition of exfoliative deposits in the iris.

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10
Q

What can cause pseudoexfoliation syndrome?

A

Melanosome atrophy in the iris pigment epithelial layer

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11
Q

List 4 common (but not exhaustive) causes of corneal epithelium hyperplasia.

A

Chemical and physical irritants
Microbial infections
Nutritional deficiency

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12
Q

Name a possible cause of conjunctival epithelium dysplasia (a virus).

A

Human papilloma virus

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13
Q

Are dysplasic cells morphologically unique to their original shape, or similar?

A

They retain some semblance to the original cell type

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14
Q

Are dysplasic cells self-limiting?

A

Yesd

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15
Q

Are dysplasic cells invasive?

A

No

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16
Q

Define karyolysis.

A

Chromatin dissolution

17
Q

Define pyknosis.

A

Chromatin clumping

18
Q

Define karyorrhexis.

A

Chromatin fragmentation

19
Q

What happens to the cell and nucleus with cell injury (in general)?

A

The cell swells and nuclear chromatin clumps together

20
Q

Define apoptosis and the two types.

A

Active, programmed process of autonomous cellular dismantling that avoids eliciting inflammation.
Can be pathological or homeostatic.

21
Q

Define necrosis.

A

Passive, accidental cell death resulting from environmental perturbations with uncontrolled release of inflammatory cellular contents.

22
Q

Distinguish briefly between the effects of apoptosis and necrosis.

A

Necrosis can result in the release of inflammatory and degrading agents, causing surround tissue damage and inflammation.
Apoptosis occurs after cellular mechanisms are shut down and disassembled. Breakdown products are enclosed in a membrane, with little tissue disruption.

23
Q

Compare cell size in necrosis vs apoptosis.

A

Shrinks in apoptosis, swells in necrosis.

24
Q

List the four principle biochemical mechanisms of cell injury.

A

Mitochondria and their ability to generate ATP and ROS
Disturbance in calcium homeostasis
Damage to cellular membranes
Damage to DNA and protein misfolding

25
Q

List the two major pathays for apoptosis.

A

Mitochondrial intrinsic pathway
Death receptor extrinsic pathway

26
Q

hat is apoptosis initiated by?

A

Caspases

27
Q

List the passive process by which necrosis occurs.

A

Acute ATP depletion

28
Q

Name a technique to assay cell injury.

A

Detection of DNA fragments by labeling terminal ends.

29
Q

Ho can annexin V be used to image apoptosis?

A

It is exposed with membrane damage, fluorescently labeled annexin V antibodies can be administered.

30
Q

Are apoptosis and necrosis linked or mutually exclusive? Explain.

A

Linked.
Donor corneas show signs of both apoptotic and necrotic cell death after refrigeration, suggesting a link.

31
Q

What happens to the cell membrane in reversible (3) vs irreversible cell injury (2)?

A

Reversible - blebs form, aggregation of intramembranous particles, generalised swelling
Irreversible - myelin figures form, defects occur in cell membrane

32
Q

What happens to lysosomes in reversible (1) vs irreversible cell injury (1)?

A

Reversible - autophagy by lysosomes
Irreversible - rupture of lysosomes and autolysis

33
Q

What happens to mitochondria in reversible (2) vs irreversible cell injury (2)?

A

Reversible - swelling, small densities appear
Irreversible - swelling, large densities appear

34
Q

What happens to ribosomes and the ER in reversible (2) vs irreversible cell injury (2)?

A

Reversible - ER swelling, ribosome dispersion
Irreversible - ER lysis, ribosome dispersion

35
Q

What happens to the nucleus in reversible (1) vs irreversible cell injury (3)?

A

Reversible - chromatin clumps
Irreversible - pyknosis or karyoloysis, or karyorrhexis

36
Q

What strucure might form in cells with irreversible damage and where?

A

Myelin figures near the cell membrane

OD2 (S1&2) (174 decks)

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