15. Cell Adaptation

Question 1

Define “necrosis”.

Answer 1

An irreversible pathological cellular/tissue death, regardless of cause.

Question 2

Define “apoptosis”.

Answer 2

A normal or pathological cell (not tissue) death, characterised by activation of endogenous endonucleases.

Question 3

Define “pyknosis”.

Answer 3

Shrinking of the nucleus caused by the condensation of DNA. Can later go though nuclear dissolution.

Question 4

Define “karyorrhexis”.

Answer 4

Fragmentation of nuclear material combined with the rupture of the nuclear membrane.

Question 5

Define “free radical”.

Answer 5

Chemical radicals with one unpaired electron in the outermost shell. Highly reactive.

Question 6

Define “ischaemia”.

Answer 6

Inadequate blood supply to an organ or part of it.

Question 7

Define “infarction”.

Answer 7

Death of a tissue due to inadequate blood supply (ischaemia).

Question 8

Define “atrophy”.

Answer 8

Decrease in size or number of a cell/tissue/organ either due to physiological (normal) or pathological causes.

Question 9

Define “hypertrophy”.

Answer 9

Increase in cell size (without division*), either caused by physiological or pathological factors.

Question 10

Define “hyperplasia”.

Answer 10

Increase in the number of normal cells.
Hyper = over/beyond, plasia = formation, growth, development

Question 11

Define “metaplasia”.

Answer 11

Reversible replacement of one fully differentiated cell type with another cell type.

Question 12

Define “dysplasia”.

Answer 12

Abnormal growth or differentiation, which can show up as increased cell proliferation, abnormal morphology and decreased differentiation.

Question 13

What are the possible causes of atrophy?

Answer 13

1. Atrophy of disuse
2. Denervation Atrophy
3. Ischaemic Atrophy
4. Malnutrition Atrophy
5. Endocrine-related Atrophy

Question 14

Mechanism of hypertrophy.

Answer 14

Cellular adaptation to an external stressor, e.g. progressive stimulation of the myocytes.

Question 15

Mechanism of hyperplasia

Answer 15

Hyperplasia is the result of:
1. Growth factor-driven proliferation of mature cells
2. Increased output of new cells from stem cells (sometimes)

Question 16

Types of hyperplasia.

Answer 16

1. Physiological
   - Hormonal hyperplasia = under the influence of hormones
   E.g. proliferation of the glandular epithelium of the female breast at puberty and during pregnancy.
   - Compensatory hyperplasia = to compensate for lost cells after damage or partial resection
   E.g. people who donate one lobe of the liver: the organ grows back to its original size.
2. Pathological
   E.g. benign prostatic hyperplasia results from excessive androgen hormones.

Question 17

Mechanism of metaplasia

Answer 17

Metaplasia is the result of:
1. Reprogramming of stem cells
2. Altering the activity of transcription factors that regulate differentiation

Question 18

Define “dystrophic calcification”.

Answer 18

Abnormal accumulation of calcium in degenerated or necrotic tissue, causing the tissue to harden. Occurs as a result of tissue damage.

Tissue damage leads to the release of phosphate-binding proteins by necrotic cells. The proteins bind to phosphate, which results in calcification.

Question 19

Define “metastatic calcification”.

Answer 19

Accumulation of calcium in normal tissues as a result of hypercalcemia and an elevated pH.

Question 20

Mechanism of cell injury by free radicals

Answer 20

Highly reactive free radicals form chemical bonds and tend to initiate/participate in chain reactions. This causes damage to cell membranes and DNA.

Question 21

Mechanism of cell injury by chemicals

Answer 21

Chemical substances can act as metabolic poison. Some can have local effects.

Question 22

Mechanism of cell injury by viruses

Answer 22

Virus enters and uses the host cell’s resources to replicate itself. It then spreads its replica, which then continue on replicating and disrupting the host’s metabolism.

Question 23

Mechanism of cell injury by hypoxia

Answer 23

Reduced oxygen disrupts the oxidative phosphorylation process. There is less ATP.

Less ATP disrupts the Na/K pump. Na+ accumulates inside the cell, causing water to flow in down the water potential gradient. The cell becomes swollen.

Reduced oxygen causes the cell to respire more anaerobically. This causes an accumulation of lactic acid, which leads to metabolic acidosis and denatures proteins.

Ca2+ accumulates in the cytosol, activating enzymes and increasing mitochondrial membrane permeability. The enzymes and the cytochrome C from the mitochondria can then cause cell apoptosis.

Question 24

Mechanism of cell injury by autoimmunity

Answer 24

The body’s immune system mistakenly attacks its own healthy cells, tissues or organs.

Question 25

Mechanism of cell injury by irradiation

Answer 25

Radiation and electrons bombarded by radiation can damage the cell and DNA.

Water can form highly reactive radicals on ionisation, which then interacts with larger molecules.

Rapidly dividing cell populations are most vulnerable. This can cause cancer such as thyroid cancer.

Question 26

Different types of necrosis

Answer 26

1. Coagulative - most common cell death typically caused by ischaemia or infarction. Tissues remain firm and look normal for days after death.
2. Liquefactive - dead cell partially or completely dissolves into pastelike mush or watery debris.
3. Caseous - cell death in which the cell looks like “cheese” - white and soft.
4. Gangrene - cell death caused by lack of blood supply or bacterial infection. Black appearance due to deposition of iron sulphide from degraded Hb.
5. Fibrinoid - cell death of the blood vessel due to platelet activation and fibrin deposition, which causes the formation of a fibrous tissue in the blood vessel.
6. Fat - death of fat tissue due to injury or loss of blood supply.