Patho 500 Ch 2 Altered cellular & tissue
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| 3 common forms of cell injury | hypoxic---ROS---chemical
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| hypoxic is most common form and leads to | leads to ischemia
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| hypoxic injury is also anoxia | total lack of oxygen
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| ATP depletion, failure of active transport mechanisms (Na/K pump and Na/Ca exchange) all dec pmem permability leads to | cellular SWELLING
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| reperfusion injury | common in heart injury as oxygen is restored to tissue --> ROS species, mem dam, CA++ overload
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| Figure 2-8 in text shows mechanisms of | SHOWS MECH of cellular injury
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| 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
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| 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)
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| cellular injury mechanisms - chemical - damage pmem initially, fig 2-12 for ETOH metab & ETOH dehydrogenase | Lead
Carbon monoxide
Ethanol
Mercury
Social or street drugs
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| 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
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| sharp force injuries | Incised wounds - longer than deep ***
Stab wounds - deeper than long ***
Puncture wounds
Chopping wounds
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| 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
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| Asphyxial injuries caused by failure of cells to receive or use 02 | Suffocation
Strangulation (hanging, ligature, manual strangulation)
Chemical asphyxiants
Drowning
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| infectious injury | Pathogenicity of a microorganism
Virulence of a microorganism
Disease-producing potential
Invasion and destruction
Toxin production
Production of hypersensitivity reactions
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| immunologic & Inflamm injury | Phagocytic cells
Immune and inflammatory substances
Histamine, antibodies, lymphokines, complement, and enzymes
Membrane alterations
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| 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
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| 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
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| Termperature extremes - hypothermic and hyperthermic | Hypothermic injury
Slows cellular metabolic processes
ROS production
Hyperthermic injury
Heat cramps
Heat exhaustion
Heat stroke
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| most common is heat exhaustion | hemoconcentration bwo loss of water and salt. Fainting is compensatory measure
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| heat stroke, life threatening | high env temp & humidity. Core temp to 106 result of thermoreg failure
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| heat crams | mild loss of water, salts
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| Atmospheric Pressure Changes - | Sudden increases or decreases in atmospheric pressure
Blast injury
Decompression sickness or caisson disease
“The bends
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| Atmospheric pressure changes - injury - 2 types | decompression sickness or caisson disease
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| 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
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| cellular injury - illumination (retina) | Eyestrain, obscured vision, and cataract formation
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| Mechanical stresses | physical impact, irritation, overexertion
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| noise | acoustic trauma,noise induced hearing loss
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| manifestations of cellular injury | Cellular accumulations (infiltrations)
Water
Lipids and carbohydrates
Glycogen
Proteins
Pigments
Melanin, hemoproteins, bilirubin
Calcium
Urate
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| cellular death - necrosis | Sum of cellular changes after local cell death and the process of cellular autodigestion (autolysis
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| cellular death - process of necrosis | Karyolysis
Nuclear dissolution and chromatin lysis
Pyknosis
Clumping of the nucleus
Karyorrhexis
Fragmentation of the nucleus
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| 4 types of necrosis - coagulative necrosis | protein denaturation ---heart/kidneys/adrenals
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| liquefactive necrosis | hydrolytic enzymes---neurons/glial in brain
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| Caseous necrosis | combo of coagulative & liquefactive---tuberculosis in lung
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| fat necrosis | lipases----breast/pancreas/abd organs
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| gangrenous necrosis | CLINICAL TERM---Dry vs. wet gangrene
Gas gangrene
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| 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)
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| 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
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| necrosis---apoptosis---autophagic death | 3 types of cell death
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| necrosis has a huger | inflamm resp than apoptosis which is neat
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| Mito pathway ----cell receptor/intrinsic pathways | know these Fig 2-36 - both culminate in EXECUTIONER CASPASES
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| ave life span | 80-100 years
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| Theories of Aging - accumulation of injurious events, genetically controlled program - 3 theories | Genetic/env lifestyle factors---alt of cellular control mechanisms---degenerative EXTRACELLULAR changes
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| cellular aging | atrophy, loss of cell fxn triggering compensatory mechanisms
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| tissue/systemic aging | still, less compliant over time contribue to frailty
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| Theory of aging figure 2-37 | aging damages mito--decreased ATP production---increased radical damage release
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| somatic death | death of entire organism
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| postmortem change - algor mortis | is the reduction in body temperature following death
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| 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
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| hypoxic injury becomes irreversible when | when the membrane is damaged, Ca++ influx---also when swollen lysosomes burst and release their hydrolases = autodigestion
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| ROS & free radical end results | lipid peroxidation---alt of proteins/DNA---set off mechs to inactivate free radicals
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| 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
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| ROS major antioxidant enzymes include | SOD=superoxide dismutase----catalase----glutathione peroxidase
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| free cystolic Ca is a destructive agent that does | phosphorylation of protein/chromatin fragments---membrane damage---damage cytoskeleton---nucleus chromatin damage
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| postmortem change - livor mortis | settling of the blood in the lower (dependent) portion of the body, causing a purplish red discoloration of the skin
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| post mortem change - rigor mortis | chemical change in the muscles after death
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| postmortem autolysis | autolysis after death (I know, right . . .)
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