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NURS 500 Patho Ch 2

Patho 500 Ch 2 Altered cellular & tissue

3 common forms of cell injury hypoxic---ROS---chemical
hypoxic is most common form and leads to leads to ischemia
hypoxic injury is also anoxia total lack of oxygen
ATP depletion, failure of active transport mechanisms (Na/K pump and Na/Ca exchange) all dec pmem permability leads to cellular SWELLING
reperfusion injury common in heart injury as oxygen is restored to tissue --> ROS species, mem dam, CA++ overload
Figure 2-8 in text shows mechanisms of SHOWS MECH of cellular injury
Free radicals & ROS species Electrically uncharged atom or group of atoms having an unpaired electron Lipid peroxidation Alteration of proteins Alteration of DNA Mechanisms for inactivation of free radicals
Free Radical injury is the result of oxidative stress To stabilize itself, it gives up an electron or steals one from long chains of phospholipids in cell membranes (lipid peroxidation)
cellular injury mechanisms - chemical - damage pmem initially, fig 2-12 for ETOH metab & ETOH dehydrogenase Lead Carbon monoxide Ethanol Mercury Social or street drugs
Blunt force injuries - application of mechanical energy to tissue Application of mechanical energy to the body resulting in the tearing, shearing, or crushing of tissues Contusion vs. hematoma Abrasion Laceration Fractures
sharp force injuries Incised wounds - longer than deep *** Stab wounds - deeper than long *** Puncture wounds Chopping wounds
gunshot wounds - penetrating within body Entrance wounds Contact-range entrance wound Intermediate-range entrance wound Tattooing and stippling Indeterminate-range entrance wound Exit wounds Shored exit wound
Asphyxial injuries caused by failure of cells to receive or use 02 Suffocation Strangulation (hanging, ligature, manual strangulation) Chemical asphyxiants Drowning
infectious injury Pathogenicity of a microorganism Virulence of a microorganism Disease-producing potential Invasion and destruction Toxin production Production of hypersensitivity reactions
immunologic & Inflamm injury Phagocytic cells Immune and inflammatory substances Histamine, antibodies, lymphokines, complement, and enzymes Membrane alterations
injurious genetic factors (muscular dystrophy for example) Nuclear alterations Alterations in the plasma membrane structure, shape, receptors, or transport mechanisms Examples Sickle cell anemia and muscular dystrophy
Injurious nutritional imbalances - alter cell S/F, nucleus----Vit D (hormone)deficiency---excess would be hyperglycemia Essential nutrients are required for cells to function normally Deficient intake Excessive intake
Termperature extremes - hypothermic and hyperthermic Hypothermic injury Slows cellular metabolic processes ROS production Hyperthermic injury Heat cramps Heat exhaustion Heat stroke
most common is heat exhaustion hemoconcentration bwo loss of water and salt. Fainting is compensatory measure
heat stroke, life threatening high env temp & humidity. Core temp to 106 result of thermoreg failure
heat crams mild loss of water, salts
Atmospheric Pressure Changes - Sudden increases or decreases in atmospheric pressure Blast injury Decompression sickness or caisson disease “The bends
Atmospheric pressure changes - injury - 2 types decompression sickness or caisson disease
ionizing radiation - env is greatest source Any form of radiation capable of removing orbital electrons from atoms X-rays, gamma rays, alpha and beta particles Mechanism of damage Effects of ionizing radiation Somatic, genetic, fetal
cellular injury - illumination (retina) Eyestrain, obscured vision, and cataract formation
Mechanical stresses physical impact, irritation, overexertion
noise acoustic trauma,noise induced hearing loss
manifestations of cellular injury Cellular accumulations (infiltrations) Water Lipids and carbohydrates Glycogen Proteins Pigments Melanin, hemoproteins, bilirubin Calcium Urate
cellular death - necrosis Sum of cellular changes after local cell death and the process of cellular autodigestion (autolysis
cellular death - process of necrosis Karyolysis Nuclear dissolution and chromatin lysis Pyknosis Clumping of the nucleus Karyorrhexis Fragmentation of the nucleus
4 types of necrosis - coagulative necrosis protein denaturation ---heart/kidneys/adrenals
liquefactive necrosis hydrolytic enzymes---neurons/glial in brain
Caseous necrosis combo of coagulative & liquefactive---tuberculosis in lung
fat necrosis lipases----breast/pancreas/abd organs
gangrenous necrosis CLINICAL TERM---Dry vs. wet gangrene Gas gangrene
apoptosis - programmed cell death blebbing occurs where cell contents are neatly contained in apoptotic bodies----no inflamm response --- can be intrinsic or extrinsic pathways BOTH MERGE AT EXECUTIONER CASPASES to deactivate nucleus/cytoskeleton (prior to blebs, apoptotic body)
apoptosis selective programmed cell death figure 2-29 - cells lyse, huge inflamm response. could also form blebs with nuclear fragments and apoptotic bodies----also autophagic death
necrosis---apoptosis---autophagic death 3 types of cell death
necrosis has a huger inflamm resp than apoptosis which is neat
Mito pathway ----cell receptor/intrinsic pathways know these Fig 2-36 - both culminate in EXECUTIONER CASPASES
ave life span 80-100 years
Theories of Aging - accumulation of injurious events, genetically controlled program - 3 theories Genetic/env lifestyle factors---alt of cellular control mechanisms---degenerative EXTRACELLULAR changes
cellular aging atrophy, loss of cell fxn triggering compensatory mechanisms
tissue/systemic aging still, less compliant over time contribue to frailty
Theory of aging figure 2-37 aging damages mito--decreased ATP production---increased radical damage release
somatic death death of entire organism
postmortem change - algor mortis is the reduction in body temperature following death
let's review hypoxic injury induced by ischemia - reversible cell injury--figure 2-8 end result is vacuolization of mito/cellullar sweeling-----dilation of ER, ribosomes detach/lipid deposition-----dec glycolysis/metabolic acidosis/swelling of lysosomes
hypoxic injury becomes irreversible when when the membrane is damaged, Ca++ influx---also when swollen lysosomes burst and release their hydrolases = autodigestion
ROS & free radical end results lipid peroxidation---alt of proteins/DNA---set off mechs to inactivate free radicals
free radical injury is often the result of result of oxidative stress whereby the free rad gives up/steals electrons from long chains of phospholipids in cell membranes = lipid peroxidation
ROS major antioxidant enzymes include SOD=superoxide dismutase----catalase----glutathione peroxidase
free cystolic Ca is a destructive agent that does phosphorylation of protein/chromatin fragments---membrane damage---damage cytoskeleton---nucleus chromatin damage
postmortem change - livor mortis settling of the blood in the lower (dependent) portion of the body, causing a purplish red discoloration of the skin
post mortem change - rigor mortis chemical change in the muscles after death
postmortem autolysis autolysis after death (I know, right . . .)
Created by: lorrelaws