Cellular Adaptation and Cellular Damage

Adult neurons are permanently fixed. There are, of course, exceptions, but the bulk - and certainly the preponderance of clinically relevant neurons - are considered non-convertible.

Neurons cannot undergo hyperplasia.

In patients with aortic stenosis, the left ventricle must work harder to force the blood out. The cells will increase in size and therefore we get hypertrophy. As this is a result of a pathology (stenosis) it is pathological. Hypertension can also cause pathological hypertrophy. Physiological hypertrophy is sometimes seen in athletes.

Denervation is the loss of nerve supply. The vastus medialis is a muscle found in the quadraceps. Loss of innervation to a muscle a commonly recognised cause of muscular atrophy.

This patient has Barrett's oesophagus. In a response to the inflammation from the continued exposure to stomach acid, the cells of the distal oesophagus undergo transformation from squamous cells to gastric columnar epithelium. This is a reversible change from one adult cell type to another. Therefore this a metaplastic change.

This is a dysplastic change - the cells are beginning to lose their function and develop an atypical appearance but their growth is still under neuroendocrine control.

Remember that neoplasia is an abnormal growth of cells that persists after the stimulus has been removed.

Myocardial cells (cells of the heart) would be most at risk from ischaemia as they have a higher rate of glycolytic activity.

ROS: reactive oxygen species are profoundly damaging to cells.

Ultraviolet type B exposure is commonly seen from sunlight.

The stem suggests the patient has tuberculosis. There is a common treatment algorithm and classically a caseous presentation of necrosis found in lung parenchyma.

In states of DNA, organelle damage, intracellular invasion (Eg viral) or pathological atrophy second to infarct/duct occlusion, pathological apoptosis is initiated.