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Chapter 3 – Altered Cellular and Tissue Biology I

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Chapter 3 – Altered Cellular and Tissue Biology I PATHOPHYSIOLOGY Name Chapter 3 – Altered Cellular and Tissue Biology I. Cellular Adaptation A. Physiologic vs. Pathogenic – due to normal demand vs. disease process 1. Atrophy – decrease or shrinkage in cell and organ size. Example – skeletal muscle deprived of innervation. 2. Hypertrophy – increase in the size of cells and organ. Example – skeletal and cardiac muscle (due to increased workload). 3. Hyperplasia – increase in number of cells due to increased mitosis. Examples – liver if part is removed (enlarges to compensate), breasts due to hormonal signals during pregnancy. 4. Dysplasia – abnormal changes in size, shape and organization of mature cells. This is not a true adaptive change. It is due to persistent severe irritation. Often reversible if stimulus is removed. Example – cervical dysplasia due to human papillomavirus. 5. Metaplasia – reversible replacement of one mature cell type by another cell type (sometimes less differentiated). This can be reversible, or it can progress to dysplasia and neoplasia (cancer). Example – in the bronchi pseudostratified ciliated columnar ep. → stratified squamous ep. Match each description with one of the processes above. Circle the letter of those that are pathologic. a) Excessive hormonal stimulation causes cells in the ducts of the breast to change their shape, size and arrangement. b) During childhood, the thymus decreases in size. c) During puberty, the male and female reproductive organs grow and develop into their mature forms. II. Cellular Injury Reversible – cells can recover if injurious stimuli ceases. Irreversible – cells die due to injury. A. Cellular Injury Mechanisms 1. Hypoxic injury – due to lack of sufficient oxygen Ischemia – reduced blood supply; if gradual, then adaptation can occur. Example – a growing thrombus which gradually blocks a vessel. Anoxia – total lack of oxygen. This is not well tolerated by most tissues. Example – an embolus which lodges in a vessel. Cellular responses: o Decrease in ATP, causing failure of sodium-potassium pump and sodium-calcium exchange – Na+ and Ca++ accumulate inside cells, K+ outside cells o Cellular swelling – due to movement of Na+ into cells. This is reversible if oxygen is restored. o Vacuolation – if O2 is not restored, vacuoles accumulate in cytoplasm and organelles swell. 2 Damage is irreversible when there is: o Lack of ATP production due to mitochondrial damage. o Major membrane damage and disturbance of membrane function. Reperfusion injury due to oxidative stress – when O2 is restored, reactive oxygen intermediates damage organelles. Can be prevented using antioxidants. 2. Free radicals and reactive oxygen species Electrically uncharged atom or group of atoms having an unpaired electron that cause damage by: o Lipid peroxidation – damages membranes of cell and organelles, increases permeability. o Alteration of proteins – especially those for ion pumps and transport proteins. o Alteration of DNA – fragmenting of DNA reduces protein synthesis. o Mitochondrial damage – allows liberation of calcium into cytosol. 3. Chemical injury Carbon tetrachloride (CCl4) – the liver converts this to a toxic free radical which causes lipid peroxidation → damage to membranes, release of lysozyme, and mitochondrial damage → fatty liver, cellular autodigestion, and decreased ATP production. Lead – causes neurological problems (interferes with neurotransmitter release), anemia, and renal problems. Carbon monoxide (CO) – prevents oxygen from binding to hemoglobin → hypoxic injury (cherry red coloring of skin). Ethanol → acetaldehyde and free radicals in liver → inflammation, fatty liver, membrane damage; depresses CNS by acting on reticular formation which normally inhibits unacceptable behaviors. Mercury – causes birth defects and brain damage in fetuses and small children. ACTIVITY 2: Indicate whether each of these is primarily associated with a lack of oxygen (–) or with free radicals and oxidative stress (+). a) CO poisoning c) Cellular swelling e) Formation of vacuoles b) Damage by CCl4 d) Damage to DNA f) Decreased ATP production B. Unintentional and Intentional Injuries 1. Blunt force injuries – in ER most are from falls and car accidents Application of mechanical energy to the body resulting in the tearing, shearing, or crushing of tissues Contusion – “bruise” (release of blood into tissues from damaged vessels without break in skin) Hematoma – a collection of blood in soft tissues or an enclosed space (subdural space, etc.) Abrasion – “scrape” (removal of the superficial layers of skin due to friction) Laceration – a rip or tear of the skin; irregular edges. Avulsion – an extreme laceration. May also occur in internal organs due to blunt impact trauma with no external signs on skin. Fractures – breakage of bone tissue 2. Sharp injuries Incised wounds – a cut that is longer than it is deep. 3 Stab wounds – a penetrating sharp-force injury that is deeper than it is long. Puncture wounds – caused by pointed objects without sharp edges. Chopping wounds – caused by axes, hatches, propeller blades, etc. 3. Gunshot wounds Entrance wounds – usually have an abrasion collar o Contact range entrance wound – muzzle touching skin . Blow-back and muzzle imprint – searing of edges by heat of gun o Intermediate range entrance wound – not touching skin; less than 48 inches away . Tattooing and stippling – fragments of gunpowder driven into skin or cause abrasion o Indeterminate range entrance wound – only bullet hits body; may occur through clothes Exit wounds – usually are clean without an abrasion collar, except: o Shored exit wound – abrasion around exit wound as skin pushes against something 4. Asphyxial injuries o Caused by a failure of cells to receive or use oxygen Suffocation – caused by lack of oxygen in environment or blockage of external airways o Choking asphyxiation – blockage of internal airways Strangulation – caused by compression and closure of blood vessels and air passageways by external pressure; death due to lack of blood flow to brain. o Hanging, ligature, and manual strangulation – due to suspension, cord around neck, or hands Chemical asphyxiants – prevent delivery or utilization of oxygen in tissues o Cyanide – CN prevents O2 binding to cytochrome oxidase in mitochondria → cherry red coloring like CO poisoning Drowning – alteration of oxygen delivery due to breathing fluid into lungs; death occurs more rapidly in warm water than in very cold water. C. Infectious Injury Pathogenicity of a microorganism Disease-producing potential depends on an organism’s ability for: o Invasion and destruction o Toxin production o Production of hypersensitivity reactions D. Immunologic and Inflammatory Injury – is caused by: Phagocytic cells Release of immune and inflammatory substances o Histamine, antibodies, lymphokines, complement, and proteases Membrane alterations – cause leakage of K+ out of cell and influx of Na+ and water. o Antibodies can block membrane receptors and intercellular communication. 4 III. Manifestations of Cellular Injury A. Cellular Accumulations (infiltrations) – pathologic accumulations can occur due to: 1) excess production of a normal substance, 2) the substance not being broken down due to lack of an enzyme, or 3) accumulation of harmful exogenous substances. Water – enters cells due to lack of ATP and failure of Na+/K+ pump, causing cellular swelling. o Oncosis (hydropic degeneration) – water accumulates in endoplasmic reticulum forming vacuoles separate from cytoplasm (vacuolation). The organs appear pale as a result. Lipids and carbohydrates – accumulate (usually in spleen, liver and CNS) due to metabolic disorders like Tay-Sachs and Niemann-Pick disease. o Fatty change - can be caused by disruptions of normal lipid metabolism; liver appears yellow. Glycogen – occurs in disorders of glucose and glycogen metabolism, including diabetes mellitus. Proteins – accumulate during pathological change in renal tubules, and B cells (antibodies) Pigments – accumulation may be normal or signal pathological changes (melanoma, jaundice) o Melanin (suntan, melanomas) or hemoproteins, hemosiderin and bilirubin (from RBC breakdown) Calcium – occurs in hypoxic cells due to entry of extracellular Ca2+ into mitochondria Urate – due to increased levels of uric acid from purine catabolism; causes gout. B. Cellular Death Necrosis– cellular dissolution o Sum of cellular changes after local cell death and the process of cellular autodigestion Processes o Karyolysis - nuclear dissolution and chromatin lysis o Pyknosis - clumping of the nucleus o Karyorrhexis - fragmentation of the nucleus C. Necrosis 1. Coagulative necrosis Occurs in kidneys, heart, and adrenal glands, etc. Due to protein denaturation - results from hypoxia caused by chemical injury (for example, mercuric chloride intake). 2. Liquefactive necrosis Occurs in neurons and glial cells of the brain Due to hydrolytic enzymes – from lysozyme in dying cells. Enzymes digest cell contents. Can be caused by bacterial infection - staphylococci, streptococci, and Escherichia coli. 3. Caseous necrosis – “cheese-like” Occurs in a tuberculous pulmonary infection. Combination of coagulative and liquefactive necrosis – cells disintegrate but are not completely digested. 5 4. Fat necrosis Occurs in breast, pancreas, and other abdominal organs that have lipase enzyme. Action of lipases – releases free fatty acids that react with Ca2+, Mg2+ and Na+ → forms soaps 5. Gangrenous necrosis Death of tissue from severe hypoxic injury
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