PATH1001 Lecture Notes - Lecture 2: Neurapraxia, Spasm, Tendinopathy
Document Summary
A key tenet of pathology is that all disease is a manifestation of cell injury of some sort. Immune reactions-bee sting, asthma: hypoxia-transient ischaemic attack or transient neuropraxia (when leg fall asleep, chemical injury-alcohol, trauma- minor contusions (musculoskeletal) tendinopathy, bone stress reaction, cramp, muscle spasm. However stressed and distressed cells produce more pro-inflammatory mediators. Irreversible (lethal=cell death: hypoxia-stroke, chemical injury-acid burn, alcohol, severe immune reactions- asthma, trauma-(musculoskeletal) muscle and ligament strains, tendon tears, bone fractures, contusions. Inflammatory response is triggered, dead and dying cells release lots of pro-inflammatory mediators to trigger. Caused by too much: volume, magnitude and frequency or no recovery time. You can put high load on your body as long as frequency is low and vica versa. Structural failure occurs when tissue cant handle the load it is put under-this can occur gradually or acutely. Apoptosis=endogenously (internal cause) induced cell death: caused by winding down of cell functionality leading to programmed cell death, occurs due to:
