Summary General Pathology, covers every topic in a simpler way, read this and you'll pass your exams

Injury to cell membranes: Receptor defects – e.g. familial hypercholesterolemia Complement related injury – e.g. immunological reactions that activate complement, opening transmembrane channels that alter ionic homeostasis Free radical injury – atoms/molecules with unpaired e- (usually O2 intermediates): O2 therapy Æ Excess O2 PMNs, macrophages Æ inflammation PMNs, xanthine oxidase Æ reperfusion injury after ischaemia Mixed function oxidation, cyclic redox reactions Æ drug-induced/chemical toxicity Radiotherapy Æ ionising radiation Initiators, promoters Æ chemical carcinogenesis Æ O2 - , H2O2, ●OH – reactive oxygen intermediates Æ membrane damage (lipid peroxidation) Viruses – direct membrane injury (e.g. polio – viral proteins inserted into membrane forming pores or channels) or indirect membrane injury (e.g. hepatitis B – viral release from the cell exposes viral proteins at the cell surface leading to immune response) Another example is the alpha toxin produced by Clostridium perfringens – this disrupts membrane function. Lysosomes and cell injury: Intracellular ‘storage’ diseases – inherited deficiency of lysosomal enzymes leading to failure to degrade particular substrates that accumulate Abnormal intracellular release – e.g. gout and silicosis where the ingestion by phagocytic cells of uric acid/silica leads to rupture of phagosomes Abnormal extracellular release – e.g. rheumatoid arthritis Cell injury and energy production: Hypoxia or ischaemia compromise energy-dependent process like contraction, and transmembrane ionic exchange is affected Reactions of cells to stress and energy: Adaptation Abnormalities of growth – atrophy, hypertrophy, hyperplasia, metaplasia Abnormal storage – accumulation of products in cytoplasm (e.g. lipofuscin) Reversible cell damage Irreversible cell injury – typically cell death by necrosis Note that there is evidence of reversible cell injury: Cell and organelle swelling – due to failure of energy-dependent ionic exchange and/or membrane injury, also known as intracellular oedema Fat accumulation – fatty change in the parenchymal cells of the liver, heart and kidney due to failure to utilize or convert the NEFA arriving at the cell (e.g. inadequate synthesis of lipid-acceptor protein in