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NURS 500 Patho Ch 2
Patho 500 Ch 2 Altered cellular & tissue
| Question | Answer |
|---|---|
| 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 . . .) |
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lorrelaws
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