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PATH Final Study Notes

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University of Guelph
PATH 3610
Andrew Vince

Unit 1 CELL INJURY AND CELL DEATHMORPHOLOGY OF CELL AND TISSUE INJURYReversible cell injury if mild or early stage of injury damaging stimulus is removedCellular swelling the result of failure of energydependent ion pumps in the plasma membrane leading to inability to maintain homeostasisFirst manifestation to almost all forms of cell injuryFatty change occurs in hypoxic injury and in various forms of toxic or metabolic injury and is manifested by the appearance of small or large lipid vacuoles in the cytoplasmCell Death Apoptosis when cell deprived of growth factors or cell DNA protein is damaged beyond repair cell kills itselfDoes not elicit inflammatory responseNecrosis severe membrane damage enzymes leak lysosomes entering cytoplasm digesting cellNecrosis MorphologyCoagulative necrosis Liquefactive necrosisGangrenous necrosisCaseous necrosisFat necrosisFibrinoid necrosis Leakage of intracellular proteins through the damaged cell membrane into circulation provides means of detecting tissuespecific necrosisOxygen Deprivation Hypoxia oxygen deficiency distinguished from ischemia loss of blood supplyCellular fxn may be lost long before cell death occursMECHANISMS OF CELL INJURYGeneral principles relevant to most forms of cell injuryCellular response to injurious stimuli depends on type of injury duration and severityConsequence of stimulus depends on type status adaptability and genetic makeupCell injury results from functional and biochemical abnormalities in one or more of several essential cellular componentsPrincipal targets and biochemical mechanisms of cell injury areMitochondria and their ability to generate ATP and ROS under pathological conditionsDisturbance in calcium homeostasisDamage to cellular plasma and lysosomal membranesDamage to DNA and misfolding of proteinsMultple biochemical alterations may be triggered by any one injurious insultDepletion of ATP ATP produced mainly by oxidative phosphorylation of ADP during reduction of oxygen in ETCThe glycolytic pathyway can generate ATP in absence of oxygen using glucose derived either from the circulation or from the hydrolysis of intracellular glycogen Mitochondrial damage and dysfunctionFailure of oxidative phosphorylation leads to progressive depletion of ATP culminating in necrosis of cellAbnormal oxidative phosphorylation also leads to the formation of reactive oxygen species which may have many deleterious effectsDamage to mitochondria is often associated with formation of a highconductance channel in the mitochondrial membrane called the mitochondrial permeability transition poreThe opening of this channel leads to the loss of mitochondrial membrane potential and pH changes further compromising oxidative phosphorylationMitochondria also contain several proteins that when released to cytoplasm tell the cell there is internal injury and activate apoptosis pathwayInflux of calcium 2Increased cytosolic Ca activated a number of enzymes with potential deleterious cellular effectsThese include phospholipases cause membrane damage proteases break down membrane and cytoskeletal proteins endonucleases DNA and chromatin fragmentation ATPases hastening ATP depletionIncreased 2intracellular Ca may induce apoptosis by direct activation of caspases and by increasing mitochondrial permeability Unit 2 Changes in Blood Flow and Body FluidsOsmosis solvent pass from a solution of lesser concentration to one of greater solute concentration Oncotic pressure pressure generated by osmosis Hydrostatic pressure pressure of waternormal tissue hydrostatic and oncotic are near zero Anteriolar capillary end hydrostatic pressure out higher than oncotic pressure ininto tissue Venular capillary end hydrostatic pressure out lower than oncotic pressure ininto blood vessels Ultrafiltrate fluid which has passed out the normal capillary Lymphatic system remaining fluid drains into bloodstreamEDEMA accumulation of fluid in tissue space Localized edema disturbance of the fluid exchange mechanism insect bite Generalized edema fluid accumulation in body cavitieseffusion cognitive heart failure Ascites effusion into peritoneal cavity Anasarca edema of the whole body Pleural space lungs to lining of chest Pericardial sac surrounds heart Peritoneal cavity diaphragm to pelvic floorLocalized edemavenous or lymphatic obstruction acute inflammation acute allergic reaction Case study ten year old male terrier right hind leg swollen below the stifle same temp rule out inflammatory firm round mass at upper limit of swelling normal heart and lungEdema of the skin an subcontaneous tissuesHydrostatic push out force at venular end increasesLymphatic obstruction accumulation of small protein molecules will lead to increased tissue colloid oncotic pressure usually zero o Fluid remains in tissue space pull of plasma colloid osmotic pressure is not sufficient o Fibrosis firm and thicken areaGeneralized edemaeffusion Congestive heart failure right ventricular failure venous blood backs up in systemic circulatory system increases venous hydrostatic pressureDecreases cardiac output by decreasing contractility of heart muscle mechanical abnormalities electrical disturbance Left heart fails forward pump blood builds up in pulmonary circulation increasing venous hydrostatic pressure and fluid remains in lungs
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