Uploaded byKamran Afzal, PhD.
Cell injury
This document discusses cell injury and cell death. It defines cell injury as a change in cell structure, metabolism or function that impairs its vital activity. Causes of cell injury include internal stresses like metabolic imbalances and external stresses such as physical agents, toxins, and chemicals. Cell injury can be reversible or irreversible and lead to cell death through mechanisms like necrosis, autolysis, or apoptosis. Signs of cell injury include morphological changes, functional impairments, and metabolic derangements. Specific types of cell injury discussed include fatty change, pigmentation, calcification, amyloidosis, and various forms of necrosis.
More Related Content
Cell injury
- 1. Cell Injury Dr KamranAfzal MBBS, FCPS, PhD
- 2.
- 3. Cell Physiology Cellmembrane: Semi-permeable membrane with pumps for ionic / osmotic homeostasis Nucleus: Nucleolus (synthesis of ribosomal RNA) Mitochondria: Oxidative phosphorylation (main source of ATP) Endoplasmic reticulum (ER), Ribosomes and Golgi Apparatus: Protein synthesis and transport Lysosome: Endocytosis, phagocytosis and pinocytosis followed by degradation Peroxisome: Catalase and oxidase enzymes, metabolism of H2O2 fatty acid
- 4. Cellular Functions Movement Conductivity Metabolic absorption Secretion Excretion Respiration (oxidation) Reproduction Communication
- 5. Cell Injury Achange in cell structure, metabolism, physico-chemical properties and function which leads to impairment of its vital activity
- 6. Main Causes ofCell Injury Internal stresses: Metabolic imbalances, nutritional deficiencies or excesses Genetic abnormalities Hypoxia ˃ impairment in aerobic tissue respiration, ischemia ˃ decrease in blood supply External stresses: Physical agents (mechanical injury, high and low temp, radiation, electrical shock, sudden fluctuations of the barometric pressure, acceleration, etc) Natural toxins, venoms, infections Drugs and chemicals, abundant oxygen, increase in glucose, high doses of dietary salt, poisons, insecticides, carbon monoxide, asbestos, social stimulators, e.g. alcohol, narcotics
- 7. Stages in CellInjury
- 8. Reversible Cell Injury Occurs when environmental changes exceed the capacity of the cell to maintain normal homeostasis But if the stress is removed or the cell withstands the assault the injury is reversible
- 9. Irreversible Cell Injury If the stress remains severe, the cell injury becomes irreversible and leads to cell death
- 10. Reversible And IrreversibleCell Injury
- 11. Mechanisms of CellInjury Defects in membrane permeability Mitochondrial damage ˃ Depletion of ATP Accumulation of oxygen-derived free radical (Oxidative stress) Influx of intracellular calcium and loss of calcium homeostasis
- 12. Mechanisms Of CellDeath Physiological, as in cell life cycle Necrosis: Morphologic changes seen in dead cells within living tissue Autolysis: Dissolution of dead cells by the cells own digestive enzymes Apoptosis: Programmed cell death “Apoptosis is a pathway of cell death that is induced by a tightly-regulated suicide program in which cells destined to die activate enzymes that degrade the cell’s own nuclear DNA and nuclear and cytoplasmic proteins”
- 13. Cell Injury Signs Morphological Swelling Dystrophy Dysplasia Necrosis Autolysis Functional Decrease in function Cellular Increase in permeability Cytoplasmic enzymes leakage to the blood Metabolic derangements Injury mediators Synthesis impairments Electrolyte balance disorders
- 14. Fatty Change Occursin: Hypoxic injury Toxic or metabolic injury Appearance of lipid vacuoles in the cytoplasm Swelling of cells is reversible In cells involved in and dependent on fat metabolism Hepatocytes Myocardial cells
- 15. Pigmentation Endogenous Lipofuscin– ageing pigment Melanin – in melanocyte Hemosiderin – aggregates of ferritin Accumulation of bilirubin Too much produced (e.g., hemolysis) Not processed (e.g., cirrhosis) Outflow blocked (e.g., choledocholithiasis) Exogenous Anthracosis (cigarette smoking; urban living) Tattoo
- 16. Calcification Abnormal tissuedeposition of calcium salts Dystrophic • Patients have a normal calcium level • Calcification affects previously damaged tissue (Ageing or damaged heart valve) Metastatic • Patients have an elevated level of serum calcium Causes: Hyperparathyroidism, bony metastases, RF Atherosclerosis (common) Aortic stenosis (uncommon) - Calcification is not routinely reversible Tricuspid valve - Calcification
- 17. Amyloidosis A groupof diseases characterised by extracellular depostion of fibrillar proteinaceous substance called amyloid Has morphological appearance, staining properties and physical structure but with variable protein or biochemical composition Deposits intracellularly and extracellularly
- 18. Amyloidosis of Heart Heart is involved in systemic amyloidosis Advanced cases.. restrictive cardiomyopathy, arrhythmias Gross: heart enlarged, surface pale, translucent and waxy Epicardium, endocardium and valves show tiny nodular deposits of amyloid Microscopy: Amyloid deposits in and around coronaries In primary amyloidosis, deposits of AL are seen around myocardial fibres in ring like formations (ring fibres) In localised form, deposits are seen in left atrium and interatrial septum
- 19. Necrosis Result ofdenaturation of intracellular proteins and enzymatic digestion of the lethally injured cell Necrotic cells are unable to maintain membrane integrity Lysosomal enzymes digest the necrotic cells Dead cells may ultimately become calcified Coagulative Liquefactive Caseous Fat Gangrenous Fibrinoid
- 20. Coagulative Necrosis –Kidney A localized area of coagulative necrosis is called an infarct Gangrene - Coagulative necrosis involving multiple tissue planes
- 21. Caseous Necrosis –Tuberculosis collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border Fat Necrosis – Mesentry Focal areas of fat destruction, typically resulting from release of activated pancreatic lipases
- 22. Fibrinoid - Artery Whencomplexes of antigens and antibodies are deposited in the walls of arteries Liquifactive Necrosis – Cerebrum Digestion of the dead cells, resulting In transformation of the tissue into a liquid viscous mass