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decrease or shrinkage in cellular size |
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an increase in the size of the cells and consequently in the affected organ. |
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an increase in the number of cells resulting from an increased rate of cellular division. |
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refers to abnormal changes in the size, shape, and organization of mature cells. Not considered a true adaptive process but is related to hyperplasia. |
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the reversible replacement of one mature cell type by another |
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muscle cells contain less endoplasmic reticulum and fewer mitochondria and myofilaments. *as a result of chronic malnutrition is often accompanied by a 'self-eating' process called autophagy that created autophagic vacuoles. they fx to bread down substances of the simplest of fat, carbohydrates, or protein. |
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particularly heart and kidneys. associated with an increased accumulation of protein in the cellular components and not with an increase in cellular fluid. *due to 2 hormones that signal (1) mechanical signals such as stretch (2) trophic signals such as growth factors, hormones, and vasoactive agents. (think muscle building) |
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as a response to injury occurs when the injury has been severe and prolonged enough to have caused cell death. 2 typers are (1) compensatory, as and adaptive mechanism that enables certain organs to regenerate [think liver regeneration] (2) hormonal that occurs chiefly in estrogen dependent organs such as the uterus or the breasts [think thickening uterus for egg implantation] |
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thought to be a sign or possible or future cancer. often described as 'high', 'low', 'mild', 'moderate', or 'severe'. may never turn to cancer. predominantly in epithelial tissue of cervix and respiratory tract. |
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develop from a reprogramming of stem cells that exist on most epithelia or of undifferentiated mesenchymal (tissue from embryonic mesoderm) cells present in connective tissue. [think new bronchial cells that do not secrete mucous or have cilia but can be reversed by stopping action that cause mutation in the first place such as smoking] |
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the most common cause of cellular injury |
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mechanism of cellular injury: Hypoxia |
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results from a reduced amount of O in the air, loss of hemoblobin or decreased efficacy of hemoglobin, decreased production of red blood cells, diseases of the respiratory and cardiovascular systems, and poisoning of the oxidative enzymes (cytochromes) with in the cells.
*ischemia- narrowing of arteries,
*anoxia- total lack of O (acute or progressive) |
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mechanism of cellular injury: Reactive Oxygen Species |
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free radical causing oxidative stress that is electrically uncharged atom or group of atoms that has an unpaired electron making it unstable and often looking to form a chemical bond formation with a protein, lipid, or carbohydrate. Highly reactive. Initiated within cells by absorption of extreme energy sources or activation of endogenous reactions by systems involved in e- and O transport. [think second hand smoke] |
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an electrically uncharged atom or group of atomsthat has an unpaired electron that makes the molecule unstable; the molecule becomes stabilized either by donating or by accepting an e- from another molecule. |
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Mechanical injury to body resulting in tearing, shearing, or crushing; most common type of injury seen in healthcare settings. Caused by blows, or impacts; motor vehicle accidents and falls most common *Contusion *Lacerations *Fracture |
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Cutting and piercing injuries. Men have a higher rate. *Incised wound *Stab wound *Puncture wound *Chopping wound |
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Men more likely to die than women. can be penetrating (remains in body) or perforating (exits body). most important factors or appearances are whether it is an entrance or exit and range of fire. |
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Cellular injury due to infection |
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the disease-producing potential of a microorganism depends on its ability to (1) invade and destroy cells (2) produce toxins and (3) produce damaging hypersensitivity reactions. |
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Cellular injury due to inflammation |
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cell membranes are injured by direct contact with cellular and chemical components of the immune and inflammatory response, such as phagocytic cells and substances such as histamine, antibodies, lymphokines, complement, and proteases. Complement is responsible for many of the membrane alterations that occur duruing immunologic injury. |
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cellular injury due to chemicals |
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the site of injury is frequently the liver. (1)direct damage, also called on-target toxicity (2) exaggerated response at the target, including overdose (3) biologic activation to toxic metabolites, including free radicals, (4) hypersensitivity and immunologic reactions, and (5) rare toxicities. |
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direct damage (chemical agents) |
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when chemicals and drugs injure cells by combining directly with critical molecular substances. |
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Liver and nutritional disorders are the most serious consequences of abuse. The major effects involve depressing the CNS. Causes liver cell necrosis due to the fatty build up on the liver. If taken while pregnant can cause FAS. Causes a shortened life span in all if not taken in moderation mostly because of damage to liver. |
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the leading cause of death for people between the ages of 1 and 34 years. (healthcare mistakes, |
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Ranks between the 2nd and 4th leading cause of death in 1-34 year olds. (suicide, homicide) |
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Manifestations of cellular injury: Oncosis 'hydropic changes' 'vacuolar degneration' |
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When the cisternae of the endoplasmic reticulum become distended, rupture, and then unite to form large vacuoles that isolate the water from the cytoplasm, a process called vacuolation. Progressive vacuolation results in cytoplasmic swelling called... |
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Manifestations of cellular injury: Lipids and Carbohydrates |
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As lipids fill cells, vacuolation pushes the nucleus and other organelles aside. Primarily found in the spleen, liver, and CNS. can cause neurologic dysfunction and severe mental retardation in the CNS. Often they progressive disorders such as when lipids build up in Tay-Sachs disease, Niemann-Pick disease, and Gaucher disease. Mucopolysaccharidoses are when carbohydrates are in excess causing clouding of the cornea, joint stiffness, and mental retardation. |
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Manifestations of Cellular Injury: Proteins |
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Damages cells in two ways (1) metabolites, produced when the cell attempts to digest some proteins, are enzymes that when released from lysosomes can damage cellular organelles. (2) excessive amounts of protein in the cytoplasm push against cellular organelles, disrupting organelle function and intracellular communication. |
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Manifestations of Cellular Changes: pigment changes |
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may be normal or abnormal. can be endogenous (produced within the body) derived from amino acids and include melanin and the blood proteins porphyrins, hemoglobin, and hemosiderin. Exogenous (produced outside the body) include mineral dusts containing silica and iron particles, lead, silver, salts, and dyes for tattoos. |
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sum of cellular changes after local cell death and the process of celllar self-digestion, or autolysis. |
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necrosis apoptosis necroptosis |
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caused by protein denaturation, which causes the protein albumin to change from a gelatinous, transparent state to a firm, opaque state. occurs primarily in the kidneys, heart, and adrenal glands and commonly results from hypoxia |
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cells are digested by their own hydrolases, so the tissue becomes soft, liquefies, and segregates from healthy tissue, forming cysts. Affects dead brain tissue because they are rich in digestive hydrolytic enzymes and lipids and the brain contains little connective tissue. |
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It is a combination of coagulative and liquefactive necroses. The dead cells disintegrate, but the debris is not completely digested by the hydrolases. Tissues resemble clumped cheese in that they are soft and granular. A granulomatous inflammatory wall encloses it. Usually results from tuberculous pulmonary infections, especially Mycobacterium tuberculosis. |
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cellular dissolution caused by powerful enzymes called lipases that occur in the breast, pancreas, and other abdominal structures. lipases break down triglycerides, releasing free fatty acids then combine with calcium, magnesium, and sodium ions, creating soaps (saponification). the tissue appears opaque and chalk-white. |
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an active process of active cellular self-destruction called programmed cell death is implicated in both normal and pathologic tissue changes. Is used in (1)severe cell injury, (2) accumulation of misfolded proteins (3) infections, and (4) obstruction of tissue ducts. Cells that die this way release chemical factors that recruit phagocytes that quickly engulf the remains of the dead cells, thus reducing the chances of inflammation. |
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atrophy, decreased function, and loss of cells, possibly caused by apoptosis. Loss of cellular function from any of these causes initiates the compensatory mechanisms of hypertrophy and hyperplasia of the remaining cells, which can lead to metaplasia, dysplasia, and neoplasia of the remaining cells. All these things can cause changes in the cell. |
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refers to death of tissue and results from sever hypoxic injury, commonly occurring because of arteriosclerosis, or blockage, of major arteries, particularly those in the lower leg. |
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refers to a special type of gangrene casued by infection of injured tissue by one of many species of Clostridium. These anaerobic bacteria produce hydrolytic enzymes and toxins that destroy connective tissue and cellular membranes and cause bubbles of gas in muscle cells. can cause toxic shock resulting in death. |
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The death of the entire person. Involves algor mortis, livor mortis, rigor mortis, and postmortem autolysis. |
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reduction of body temperature after death |
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purple discoloration/settling of blood after death |
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microscopic level, putrefactive changes are associated with the release of enzymes and lytic dissolution (ultimate death) |
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(scrape) results from removal of the superficial layers of the skin caused by friction between the skin and injuring object. |
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tear or rip resulting when the tensile strength of the skin or tissue is exceeded |
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