Lecture 2 Flashcards
Cellular response to stess
depends on type, duration and severity of injury.
Adaptation, Reversible injury, Irreversible injury -> Necrosis/Apoptosis
Hyperplasia
Increase in cell number resulting in a larger organ
Hypertrophy
Increase in size of cells, resulting in an increase in size of the organ.
Atrophy
Shrinkage in the size of the cell caused by: Decreased workload Reduced blood supply Inadequate nutrition Loss of hormonal stimulation Ageing
Metaplasia
One adult cell type is replaced by another. Reversible. Barrett’s oesophagus
Hypoxia
Low oxygen supply
Ischaemia
Loss of blood supply, therefore oxygen and nutrients
Cell death
Necrosis- causes local inflammation, always pathological
Apoptosis- programmed cell death, cell internally digested with enzymes, no inflammation
Mechanisms of apoptosis
Result from the activation of enzymes call caspases
Mitochondrial pathway/Intrinsic pathway
Fas(death) pathway/Extrinsic pathway
Coagulative necrosis
After infection, loss of blood supply, infarction of organs
Caseous (cheesy) necrosis
TB unless proved otherwise
Liquefactive necrosis
Typical of brain. Results in a hole in the brain. Can get a secondary infection and form an access.
Fat necrosis
White chalky appearance. Typical in breast injuries. Can mimic tumours.
Intracellular accumulation if abnormal material
Fat in hepatocytes (liver cells) - due to alcohol misuse. Also can be due to hepatitis and diabetes.
Cholesterol in smooth muscles in atherosclerosis
Protein in alzheimers and parkinsons disease
Dysplastic
abnormal growth