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113 Cards in this Set
- Front
- Back
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ABRASION
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a scraping, or rubbing away of a surface, such as skin or teeth, by friction. Abrasion may be the result of trauma such as a skinned knee; of therapy, as in dermabrasion of the skin for removal of scar tissue; or of normal function, such as the wearing down of a tooth by mastication.
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APOPTOSIS
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necrosis of keratinocytes in which the nuclei of the necrotic cells dissolve and the cytoplasm shrinks, rounds up, and is subsequently phagocytized. The term generally refers to "programmed" cell death.
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ATROPHY
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a wasting or decrease in size or physiologic activity of a part of the body because of disease or other influences. A skeletal muscle may undergo atrophy as a result of lack of physical exercise or neurologic or musculoskeletal disease.
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AUTOLYSIS
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the spontaneous destruction of tissues by intracellular enzymes. It generally occurs in the body after death.
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BILIRUBIN
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the orange-yellow pigment of bile, formed principally by the breakdown of hemoglobin in red blood cells after termination of their normal lifespan. In a healthy person about 250 mg of bilirubin is produced daily. The majority of bilirubin is excreted in the stool. The characteristic yellow pallor of jaundice is caused by the accumulation of bilirubin in the blood and in the tissues of the skin.
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CONTUSION
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an injury that does not disrupt the integrity of the skin, caused by a blow to the body and characterized by swelling, discoloration, and pain. The immediate application of cold may limit the development of a contusion.
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DYSPLASIA
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any abnormal development of tissues or organs.
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FREE RADICAL
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an organic compound with at least one unpaired electron. It is unstable and reacts readily with other molecules.
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HEMATOMA
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a collection of extravasated blood trapped in the tissues of the skin or in an organ, resulting from trauma or incomplete hemostasis after surgery. Initially there is frank bleeding into the space; if the space is limited, pressure slows and eventually stops the flow of blood. The blood clots, serum collects, the clot hardens, and the mass becomes palpable to the examiner and is often painful to the patient
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HYPOXEMIA
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an abnormal deficiency in the concentration of oxygen in arterial blood. Symptoms of acute hypoxemia are cyanosis, restlessness, stupor, coma, Cheyne-Stokes respiration, apnea, increased blood pressure, tachycardia, and an initial increase in cardiac output that later falls, producing hypotension and ventricular fibrillation or asystole. Chronic hypoxemia stimulates red blood cell production by the bone marrow, leading to secondary polycythemia.
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PHYSIOLOGIC ATROPHY
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occurs with early development (e.g. the thymus gland undergoes physiologic atrophy during childhood).
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PATHOLOGIC ATROPHY
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occurs as a result of dereases in workload, pressue, use, blood supply, nutrition, hormonal stimulation, and nervous stimulation.
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DISUSE ATROPHY
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experienced by individuals immobilized in bed for a prolonged time.
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AUTOPHAGIC VACUOLES
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membrane-bound vesicles within the cell that contain cellular debris and hyrolytic enzymes (accompanies chronic malnutrition).
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HYPERTROPHY
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an increase in the size of cells and consequently in the size of the affected organ. (OFTEN SEEN IN HEART AND KIDNEY CELLS).
The increase in cellular size is associated with an increased accumulation of protein in the cellular components and NOT with an increase in cellular fluid!!! Can be physiologic or pathologic and is cause by specific hormone stimulatio nor by increased funtional demand. |
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HYPERTROPHY TRIGGERS
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1) mechanical signals, such as stretch;
2) trophic signals, such as growth factors, hormones, and vasoactive agents. |
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HYPERPLASIA
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an increase in the number of cells resulting from an increased rate of cellular division.
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TYPES OF PHYSIOLOGIC HYPERPLASIA
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1) compensatory
2) hormononal |
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COMPENSATORY HYPERPLASIA
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an adaptive mechanism that enable certain organs to regenerate. (e.g. removal of part of the liver leads to hyperplasia of the remaining liver cells-hepatocytes- to compensate for the loss).
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HORMONAL HYPERPLASIA
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occurs chiefly in estrogen-dependent organs, such as the uterus and breast.
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CELLULAR ADAPTATIONS
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1) atrophy
2) hypertrophy 3) hyperplasia 4) metaplasia 5) dysplasia (atypical hyperplasi) |
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DYSPLASIA
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abnnormal changes in the size, shape, and organization of mature cells. (often called ATYPICAL HYPERPLASIA).classified as mild, moderate, or severe.
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NEOPLASIA
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malignant tumors
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METAPLASIA
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the reversible replacement of one mature cell type by another, sometimes less differentiated, cell type. (e.g., replacement of normal columnar ciliated epithelial cells of the bronchial (airway) lining by stratified squamous epithelial cells from smoking.)
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CELLULAR INJURY
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occurs if the cell is unable to maintain homeostasis in the face of injurious stimuli. Most diseases begins with cellular injury.
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CELLULAR INJURY
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occurs if the cell is unable to maintain homeostasis in the face of injurious stimuli. Most diseases begins with cellular injury.
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TYPES OF PROGRESSIVE CELL INJURY
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Adaptation, Active Cell Injury, Reversible, Irreversible, Necrosis, Apoptosis (programmed cell death), Chronic Cell Injury (subcellular alterations), Accumulations (Infiltrations) Pathologic Calcification
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ADAPTATION
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atrophy, hypertrophy, hyperplasia, metaplasia
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ACTIVE CELL INJURY
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immediate response of "entire" cell
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REVERSIBLE
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loss of ATP, cellular swelling, detachment of ribosomes, autography of lysosomes
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IRREVERSIBLE
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"point of no return" structurally when sever vacuolization of the mitochondria occurs and Ca++ moves into the cell
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NECROSIS
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common types of cell death with severe cell swelling and breakdown of organelles
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APOPTOSIS (programmed cell death)
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cellular self-destruction for elimination of unwanted cell populations
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CHRONIC CELL INJURY (subcellular alterations)
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persistent stimuli response may involve only specific organelles or cytoskeleton (e.g., phagocytosis of bacteria)
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ACCUMULATIONS (INFILTRATIONS)
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water, pigments, lipids, glycogen, proteins
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PATHOLOGIC CALCIFICATION
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dystrophic and metastatic calcification
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FOUR GENERAL MECHANISMS OF CELL INJURY
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1) ATP Depletion; 2) Oxygen and Oxygen-Derived Free Radicals; 3) Intracellular Calcium and Loss of Calcium Steady State; 4) Defects in Membrane Permeability
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ATP DEPLETION
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loss of mitochondrial ATP and decreased ATP synthesis; results include cellular swelling, decreased protein synthesis, decreased membrane transport, and lipogenesis, all changes that contribute to loss of integrity of plasma membrane
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OXYGEN AND OXYGEN-DERIVED FREE RADICALS
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lack of oxygen is key in progression of cell injury in ischemia (reduced blood supply); activated oxygen species (free radicals O2, H2O2, OH·) cause destruction of cell membranes and cell structures
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INTRACELLULAR CALCIUM AND LOSS OF CALCIUM STEADY STATE
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normal intracellular cytosolic calcium concentrations are very low; ischemia and certain chemicals cause an increase in cytosolic Ca++ concentrations; sustained levels of CA++ continue to increase with damage to plasma membrane; Ca++ causes intracellular damage by activating a number of enzymes
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DEFECTS IN MEMBRANE PERMEABILITY
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early loss of selective membrane permeability found in all forms of cell injury
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HYPOXIA
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lack of sufficient oxygen (the single most common cause of cellular injury) usually caused by ischemia
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ISCHEMIA
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reduced blood supply (THE MOST COMMON CAUSE OF HYPOXIA)
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ISCHEMIC INJURY CAUSE
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gradual narrowing of the arteries (arteriosclerosis)
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ARTERIOSCLEROSIS
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gradual narrowing of the arteries
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THROMBIS
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complete blockage of arteries by blood clots
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ANOXIA
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total lack of oxygen caused by a sudden obstruction, usually an embolus (blood clot) or other plug in circulation
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EMBOLUS
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blood clot
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INFARCTION
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myocardial cell death (can be caused by an acute obstruction in a coronary artery)
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MYOCARDIAL ADAPTATION
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caused by gradual onset of ischemia
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REDUCTION OF ATP LEVELS CAUSES…
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the plasma membrane's sodium-potassium pump and sodium-calcium exchange to fail, which leads to an intracellular accumulation of sodium and calcium and diffusion of potassium out of the cell
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WHY DO CELLS BECOME MARKEDLY SWOLLEN WITH HYPOXIC INJURY?
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because if the plasma membrane's barrier to calcium ions is eliminated or damaged, calcium readily enters and accumulates in the mitochondria resulting in mitochondrial swelling and rapid death of the cell, caused by calcium accumulation compromising ATP production by the mitochondria.
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WHEN ARE OXIDATIVE FREE RADICALS DAMAGING TO CELLS?
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when the plasma membrane is damaged and oxygen is restored, high reactive oxygen intermediates are generated (hydroxyl radical OH-, superoxide O2, and hydrogen peroxide H2O2). These radicals can all cause further membrane damage.
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WHEN DOES A CELL BECOME IRREVERSIBLY INJURED?
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when severe vacuolization of the mitochondria occurs and Ca++ moves into the cell
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REPERFUSION INJURY
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restoration of oxygen that generates high reactive oxygen intermediates that can all cause further membrane damage
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ROS
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reactive oxygen species--superoxide (O2)--these are free radicals and are an important mechanism of cellular injury
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FREE RADICAL
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an electrically uncharged atom or group of atoms having an unpaired electron (capable of injurious chemical bond formation with proteins, lipids, and carbohydrates--key molecules in membranes and nucleic acids). Free radicals are difficult to control and initiate chain reactions.
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HOW ARE FREE RADICALS INITIATED?
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1) absorption of extreme energy sources (e.g., ultraviolet light, radiation); 2) endogenous reactions when oxygen is reduced to water created by systems involved in electron and oxygen transport (redox reactions; all biologic membranes contain redox systems important for cell defense, iron uptake, growth, and proliferation and signal transduction); and 3) enzymatic metabolism of exogenous chemicals or drugs (e.g., CCL3, a product of carbon tetrachloride CCL4).
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MOST SIGNIFICANT FREE RADICALS
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ROS (Superoxide O2); Hydrogen Peroxide (H2O2); Hydroxyl Radicals (OH-)
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DAMAGING EFFECTS OF FREE RADICALS
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1) lipid peroxidation; 2) attacking critical proteins that affect ion pumps and transport mechanisms; 3) fragmenting DNA, causing decreased protein synthesis; and 4) damaging mitochondria, causing the liberation of calcium into the cytosol.
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LIPID PEROXIDATION
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the destruction of polyunsaturated lipids (the same process by which fats become rancid) leading to membrane damage and increased permeability
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THREE COMMON FORMS OF CELL INJURY
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1) Hypoxia; 2) Free radicals and reactive oxygen species (ROS) injury; 3) chemical injury
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CHEMICAL INJURY (2 GENERAL MECHANISMS)
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1) direct toxicity caused by combination of a chemical with a molecular component of the cell membrane or organelles; and 2) formation of reactive free radicals and lipid peroxidation.
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COMMON CHEMICAL AGENTS
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1) Lead; 2) Carbon Monoxide; 3) Ethanol; 4) Social or street drugs.
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ORGAN SYSTEMS AFFECTED BY LEAD POISONING
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nervous system, the hematopoietic system (tissues that produce blood cells), and the renal system (specifically the kidneys). Lead inhibits several enzymes involved in hemoglobin synthesis and causes anemia as a result of lysis of red blood cells (hemolysis).
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GLYCOSURIA
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glucose in urine
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AMINOACIDURIA
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amino acids in urine
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HYPERPHOSPHATURIA
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excess phosphate in the urine
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CAUSES OF CARBON MONOXIDE POISONING
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produces hypoxic injury-- namely, oxygen deprivation--because it directly interferes with cellular respiration (it's a toxic asphyxiant).
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ETHANOL (ALCOHOL) ABUSE
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causes liver and nutritional disorders
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MAJOR EFFECTS OF ACUTE ALCOHOLISM
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affects mainly the CNS but may induce reversible hepatic and gastric changes. The hepatic changes, initiated by acetaldehyde, include inflammation, deposition of fat, enlargement of the liver, interruption of microtubular transport of proteins and their secretion, increase in intracellular water, depression of fatty acid oxidation in the mitochondria, increased membrane rigidity, increased ROS, and acute liver cell necrosis.
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CHRONIC ALCOHOLISM
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causes structural alterations in practically all organs and tissues in the body, especially the liver and stomach.
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ACETALDEHYDE
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a toxin; an end-product of the metabolic detoxification of alcohol. Acetaldehyde damages cellular mitochondria.
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FETAL ALCOHOL SYNDROME
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includes growth retardation, facial anomalies, and ocular malformations (partly due to effect on the L1 cell adhesion molecule--L1 is critical for proper CNS development).
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METHODS CONTRIBUTING TO INACTIVATION OR TERMINATION OF FREE RADICALS
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1) Antioxidants; 2) Enzymes
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TYPES OF UNINTENTIONAL AND INTENTIONAL INJURIES
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1) Blunt Force; 2) Contusion; 3) Abrasion; 4) Laceration; 5) Fractures; 6) Sharp Force Injuries; 7) Gunshot Wounds; 8) Asphyxial Injuries
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BLUNT FORCE INJURY
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caused by the application of mechanical injury to the body resulting in the tearing, shearing, or crushing of tissues. (most common type of injuries seen in most health care settings). May be caused by blows, impacts, or combination of both.
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CONTUSION (bruise)
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bleeding into the skin and/or underlying tissues as a consequence of a blow that squeezes or crushes the soft tissues and ruptures blood vessels without breaking the skin.
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PROGRESSION OF A BRUISE
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red-purple…blue-black…yellow/brown and/or green before disappearing
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HEMATOMA
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a collection of blood in soft tissues or an enclosed space
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SUBDURAL HEMATOMA
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a collection of blood between the inner surface of the dura mater and the surface of the brain, resulting in the shearing of small veins that bridge the subdural space. Can result from blows, falls, or sudden acceleration/deceleration of the head (shaken baby syndrome).
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EPIDURAL HEMATOMA
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a collection of blood between the inner surface of the skull and the dura. It is caused by a torn artery and is almost always associated with a skull fracture.
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ABRASION (scrape)
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results from removal of the superficial layers of the skin that was caused by friction between the skin and injuring object.
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LACERATION
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a tear or rip resulting when the tensile strength of the skin or tissue is exceeded--jagged and irregular and edges are abraded.
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AVULSION
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an extreme laceration in which a wide area of tissue may be pulled away creating a large flap.
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FRACTURE
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broken or shattered bone caused by blunt force blows or impacts
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INCISED WOUND
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cut that is longer than it is deep
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STAB WOUND
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a penetrating sharp force injury that is deeper than it is long.
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PUNCTURE WOUND
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caused by object or instrument with sharp point but without sharp edges
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CHOPPING WOUND
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caused by heavy edged instruments (axes, hatchets, propeller blades)
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CONTACT RANGE ENTRANCE WOUND
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occurs when the gun is held so the muzzle rests on or presses into the skin surface.
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BLOW BACK
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hard contact (gun shot wound) of the head where the large amount of gas and explosive energy sent into the wound may cause severe tearing and disruption of the tissues, giving the wound a large, gaping, and jagged appearance.
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INTERMEDIATE (DISTANCE) RANGE ENTRANCE WOUNDS
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a wound surrounded by gunpowder tattooing or stippling (tattooing results from fragments of burning or unburned pieces or gunpowder exiting the barrel and striking the skin surface…stippling results when fragments of powder strike with enough force to abrade the skin but not actually penetrate the surface).
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INDETERMINATE RANGE ENTRANCE WOUND
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occurs when flame, soot, or gunpowder does not reach the skin surface and the only thing striking the body is the bullet (range of fire cannot be determined from the appearance of the wound).
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PENETRATING GUN SHOT WOUND
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bullet retained in the body
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PERFORATING GUN SHOT WOUND
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bullet exits the body
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SHORED EXIT WOUND
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exiting bullet pushes against the supporting surface, causing rubbing and scraping around the exit defect
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ASPHYXIAL INJURY
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caused by a failure of cells to receive or utilize oxygen. Deprivation may be partial (hypoxia) or total (anoxia).
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FOUR CATEGORIES OF ASPHYXIAL INJURY
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1) Suffocation; 2) Strangulation; 3) Chemical; and 4) Drowning.
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SUFFOCATION
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oxygen failing to reach the blood, can result from a lock of oxygen in the environment (entrapment in an enclosed space of filling of the environment with a suffocating gas) or blockage of the external airways.
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STRANGULATION
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caused by compression and closure of the blood vessels and air passages resulting from external pressure on the neck.
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HANGING STRANGULATIONS
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a noose is placed around the neck; leaves a distinct inverted V mark on the neck, with the base of the V pointing toward the suspension.
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LIGATURE STRANGULATION
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the mark on the neck is horizontal without the inverted V pattern seen in hangings. Petechiae may be more common.
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CHEMICAL ASPHYXIANTS
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either prevent the delivery of oxygen to the tissues or block its utilization.
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COMMON CHEMICAL ASPHYXIANTS
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1) Carbon Monoxide; 2) Cyanide (combines with the ferric iron atom in the cytochrome oxidase, thereby blocking the intracellular utilization of oxygen). Victims of both have a cherry-red appearance. 3) Hydrogen Sulfide (sewer gas).
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DROWNING
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an alteration of oxygen delivery to tissues resulting from the breathing in of fluid, usually water. Hypoxemia caused by airway obstruction is the major cause of death rather than excessive fluid/water in lungs and cells.
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INFECTIOUS INJURY
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caused by micro organisms
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IMMUNOLOGIC AND INFLAMMATORY INJURY
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cellular membranes are injured by direct contact with cellular and chemical components of the immune and inflammatory responses, such as phagocytic cells and substances such as histamine, antibodies, lymphokines, complement, and protease. Complement is responsible for many of the membrane alterations that occur during immunologic injury.
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CELLULAR ACCUMULATIONS (INFILTRATIONS)
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the accumulation of normally present substances (fluids and electrolytes, lipids, glycogen, etc.) that can occur in the cytoplasm (often the lysosomes) or in the nucleus if 1) the normal, endogenous substance is produced in excess or at an increased rate; 2) an endogenous substance (normal or abnormal) is not effectively catabolized; or 3) harmful exogenous materials, such as heavy metals, mineral dusts, or microorganisms, accumulate because of inhalation, ingestion, or infection.
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CELLULAR SWELLING
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the most common degenerative change, caused by the shift of extracellular water into the cells--reversible and considered sublethal.
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FATTY CHANGE
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intracellular lipid accumulation most commonly found in the liver
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LIPID AND CARBOHYDRATE ACCUMULATION SITES
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may accumulate throughout body but found primarily in the spleen, liver, and CNS.
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GLYCOGEN ACCUMULATION CAUSE
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the disorder of glucose metabolism, diabetes mellitus
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