Injury to Cells Flashcards
1
Q
What is hypertrophy? (Give examples)
A
- Increase in size of cells, resulting in increase in size of organ.
- Physiology - body builders
- Pathological - heart in hypertension
2
Q
What is hyperplasia? (Give examples)
A
- Increase in the number of cells resulting in a larger organ.
- Can occur alongside hypertrophy.
- Physiological - menstrual cycle
- Pathological - endometrial hyperplasia
3
Q
What is atrophy? (Give examples)
A
-
Shrinkage of the size of cells by loss of cell substance caused by:
- Decreased workload
- Reduced blood supply
- Inadequate nutrition
- Ageing
- Loss of hormonal stimulation
4
Q
What is metaplasia? (Give examples)
A
- One adult cell type is replaed by another adult cell type.
- Reversible.
- New type of cells mya be more able to withstand stress (e.g. gastro-oesophageal reflux)
5
Q
What are the 3 types of cell injury?
A
- Hypoxia - low oxygen supply.
- Ischaemia - loss of blood supply, oxygen and nutrients.
- Chemical Exposure - cigarrete smoke, alcohol, paracetamol.
6
Q
What is necrosis?
A
- Damage to membranes allowing enzymes to digest the cell - contents leak out.
- Local inflammation
- Always pathological.
7
Q
What is apoptosis?
A
- Programmed cell death - cell suicide.
- Irreparable damage to cell protein/DNA or deprivation of growth factors.
- Can be pathological or physiological.
- No leakage - dead cells removed by phagocytosis.
8
Q
What are examples of apoptosis?
A
-
Physiological
- Embryogenesis
- Menopause
- Elimination of cells which have served their purpose.
- Elimination of potentially harmful self-reactive lymphocytes.
-
Pathological
- DNA damage.
- Accumulation of misfolded proteins.
- Certain infections
- Direct radiation
- Pathological atrophy in parenchymal organs after duct obstruction.
- Cell death induced by cytotoxic T-cells.
9
Q
What are examples of necrosis?
A
-
Coagulative Necrosis
- Most common - usually after infections and ischaemia.
- Due to loss of blood - MI - blockages.
- Dead tissue is preserved for days.
-
Caseous Necrosis
- Caused by TB
- ‘Cheese-like’ appearance.
-
Liquifactive Necrosis
- Necrosis of big tissue with added putrefaction with black, foul-smelling appearance.
- Digestion of dead cells leads to liquid-mass (infections and hypoxic death in CNS)
- Cerebral infarction and Abscesses.
-
Fat Necrosis
- A focal area of fat destruction forming fatty acids and calcium white deposits.
10
Q
Explain depletion of ATP? (Mechanisms of cell injury)
A
- Energy store of cells - oxidative phosphorylation of ADP within mitochondria.
- Reduced supply of oxygen and nutrients due to mitochondrial damage and poisons.
- Effects:
- ATP dependant on sodium pumps.
- Increased intracellular lactic acid.
- Failure of calcium pumps
- Damage to protein structures.
11
Q
Explain mitochondrial damage? (Mechanisms of cell injury)
A
- ‘mini-factories’ for making ATP
- Sensitive to many types of stress - hypoxia, chemical poisonins and radiation.
- Effects:
- Failure of production of energy
- Failure of free radical production.
12
Q
Explain influx of calcium? (Mechanisms of cell injury)
A
- Ischaemia and certain poisons.
- May trigger apoptosis.
- Effects:
- Leads to activation of enzymes.
- Damage cellular components.
13
Q
Explain oxidative stress? (Mechanisms of cell injury)
A
- Accumulation of reactive oxygen species (free radicals)
- Produced by normal cellular function.
- Some insults increase their production (paracetamol overdose)
- React with and damage proteins, fat, DNA and create more of themselves in the process.
14
Q
Explain defects in membrane permeability? (Mechanisms of cell injury)
A
- Results in necrosis.
- Various sites of damage: mitochondria, membrane, lysosomes.
- Mechanisms of damage:
- Lower phospholipid synthesis - lower amount of ATP.
- Oxygen free radicals.
- Lipid breakdown.
15
Q
Explain damage to DNA and proteins? (mechanisms of cell injury)
A
- May occur after radiation injury/oxidative stress.
- Can result in apoptosis.
