Summary Pathology 1 .pdf

1) Cell Injury and Death Necrosis v apoptosis Apoptosis is tactical suicide (may be pathological) Necrosis is always pathological - cell side because they can’t survive in those conditions. Learning objectives Describe the causes and mechanisms of cell injury Explain difference between apoptosis and...

1) Cell Injury and Death Necrosis v apoptosis Apoptosis is tactical suicide (may be pathological) Necrosis is always pathological - cell side because they can’t survive in those conditions. Learning objectives Describe the causes and mechanisms of cell injury Explain difference between apoptosis and necrosis Describe physiological and pathological apoptosis Discuss main pathways of apoptosis Explain different types of necrotic death Ox deprivation = Anoxia Hypoxia = lack of ox Trauma/radiation Poisons Person like apoptosis; 1. Get a disease 2. Palative care before die (initiate dying) 3. The process of dying 4. Burial/removal 1) Ischemia - inadequate blood supply to a region 2) Cardioresp Failure 3) Anaemia Parasites/bacteria Immunodeficiency/Autoimmune/anaphylaxis Down syndrome Obesity/anorexia/Bolemia Increase ROS/mutation/telomere shortening etc Caspases activate DNases in apoptosis (which break up the DNA) 4 main Targets of cell injury: ATP - can be from Mt damage Cell Membrane permeability - Entry of Ca+ /- ROS Protein Syn - enzymes etc DNA Damage - Pro Apoptotic Protein Activation BYg Cytoc FEEL ATP Depletion ER + Cellular Swelling - Loss of microvilli blebs Nuclear Chromatin clumps (with low pH) Lipid Deposition (as decrease in protein syn) Increase intracellular Ca+ Activates 3 things: Phospholipasaes (damage cell mem) Proteases (Damage cell mem + Cytoskeleton) Endonucleases (Damage DNA) 1. Dna damage 2. Protein Misfold 3. GFactor withdrawal Extrinsic - Caspase 8 Intrinsic - caspase 9 EYE ROS generation Caused by absorption of IR/UV Effect 3 ways: Lipid → Membrane Damage Protein → Break+Misfold DNA → Mutations Mitochondrial Damage Caused high conductance channel in my membrane → decreased ATP production Cytochrome c leaks into cytosol → Apoptosis Membrane Damage membrane permeability effects mitochondria ^ , Plasma membrane, lysosomal (leads to necrosis) and all by trauma. When there is an influx of ca - cytoskeletal abnormalities occur rupture in plasma membrane. DNA and protein Damage Extensive dna dames - suicide programmed death apoptosis Non extensive can be progressive and lead to necrosis Executioner caspases 3,6,7 13113 Recognition/phagocytosis phase Cell fragments - eat me apoptotic bodies - macrophages and neighbouring cells eat to avoid inflammatory responses. Necrosis Non programmed - accidental - most common Result = inflammatory reaction Usually as a result of damaged lysosomes who in turn cause denatiration of proteins - a clinical marker of cell death is when these proteins leak out of the cell. ifeng.ucarinbasn. o 70 Tftaed g gangrene Blackesmelly 9EE NIGEL Caseof cottage cheese