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change from one cell to another type |
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cell looks and acts abnormal but the CA yet. |
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nuclei, cell structure and mitosis are different and considered cancer |
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lack of growth did not form the organ or tissue such as someone that is born w/o vertebrae |
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independent growth of cells- forms tumor |
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lack of oxygen stops aerobic respiration. |
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most common cause of cell injury or death. lack of blood/perfusion ex CO poison- hypoxia prior to ischemia |
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leads to cellular death- burns extreme cold |
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excess of any chemical causes death |
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bacteria viruses cause cell death |
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antibodies attacking antibodies or self attacks self. |
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Steps following cell death |
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the nucleus disintegrates- cells release lysosomes into the tissue- causing inflammation and damage to nearby cells and reduced function. |
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process of removal of dead tissue. lysosomes start process. Macrophages finish process |
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usually found following ischemi. loss of normal organelle structure. ishemia or infaction |
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accumulation of PMN (puss) usually found with bacterial infection |
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usually found with pancreatic disease that leaks lipases. (come and break down the area) |
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cheesy! mostly found with TB due to resemblance of cottage cheese. |
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necrosis that is found in walls of blood vessels w insudation of plasma proteins. Fibrin leaks into the interstitial area |
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caused by infection of ischemic tissue by clostridial perfringens (anaerobic microorganism) this infective agent contains many spreading factors myotoxin, hemolysins and phospholipases that rapidly can lead to amputation or death |
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mechanical barrier, blocks entry of bacteria or harmful substances into tissues includes tears or saliva to destroy harmful substances |
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phagocytosis and inflammation-nerutrophils and macrophages to digest harmful substances and debris. Inflammation limints effects of injury. interferons protect uninfected cells from viruses |
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immune system specific to harmful substance |
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injury initial vasoconstricion release of chemical mediators vasodilation- increased blood flow (hyperemia) increased capillary permiability WBC's move to site of injury by chemotaxis, diapedesis phagocytosis- removal of debris in preparation for healing |
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when cells migrate across the blook into interstitial area |
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pure water coming across enothelial cells. |
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plasma proteins and water leaking out |
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RBC's plasma proteins and water present in interstitium |
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thick and sticky w high cell and fibrin content-scar |
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thick yellow-green and contains WBC and cell debris. Typically bacterial infection is present with this type. Pus |
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minimal damage, damaged cells recover and tissue returns to normal |
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tissue is able to heal. tissues ability to heal is related to cells ability to replicate |
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extensive damage leading to scarring by connective tissue. Scaring impairs the function of the tissue |
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involves the epidermis and part of dermis. superficial partial thickness1st degree burns, damages epidermis and upper dermis |
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deep partial thickness burn |
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destruction of epidermis and part of dermis. red, edematous, blistered, hypersensitive during inflammatory stage. dead skin sloughs off and heals by regeneration |
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destruction of all skin layers and often underlying tissues. dry leathery eschar. |
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dubjective comments made by the patient |
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how the disease manifest itself |
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try to determine what the disease is |
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the identification of a specific dz through evaluation of S&S. Usually more than one factor is used to diagnose. |
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what is the liklihood for the patient to handle the disease. Probability for recovery |
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Varies with prognosis, what we do to intervene with the patient |
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physical observation of the patient |
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the one thing about the disease that identifies that disease Hallmark of disease |
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those things that promote development of a dz in an individual. a predisposing factor indicates a high risk for a dz Example asbestos |
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sudden and obvious acute the onset could also be insidious. gradual progression w mild vague signs |
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short term illness that develops quick |
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often milder condition that develops gradually but persists for a long time. |
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pathology occurs but no obvious manifestations are present |
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silent stage in which no clinical signs are evident. in infection dz, this may be termed the incubation period (time between exposure and onset of S&S) |
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time in early development of a dz that one is aware of changes but S&S are nonspecific. such as fatigue |
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collection of S&S that occur together in response to a certian condition. |
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manifestations of a dz subside |
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describes the unwanted outcomes of a primary condition |
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the relative number of deaths from a particular dz |
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higher than expected number of cases of an infectious dz w in a given area |
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higher number of cases in many regions of the globe |
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indicated by tracking the prevalence and incidence |
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the number of new and old or existing cases w in a population and time period |
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number of new cases in a population in a time period |
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something that you produce- allergies |
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they dont know the cause of the disease process |
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physician induced process. wrong meds, chemotherapy |
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sense the internal environment by fluid volume and concentration and promote fluid intake |
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antidiuretic hormone. Acts by controlling the amount of fluid leaving the body in urine. ADH promotes resorption of water into the blood from the kidney tubules |
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determines resorption of sodium ions and water from the kidney tubules. acts to conserve more fluid when there is a deficit of fluid in the body. |
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atrial naturietic peptide ,this is released by the heart cells to influence workload on the heart by regulating fluid, sodium and potassium levels. AKA will go from the heart to the kidneys to increase filtration rate by reducing the re-absorption of sodium by inhibiting ADH |
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water wants to move from areas of high concentration to those of low concentration |
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increased capillary hydrostatic pressure loss of plasma proteins obstruction of lymphatic circulation increased capillary permeability |
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controlled by Na/k pump. injested in food lost in feces and urine controlled by the kidneys via aldosterone essential in muscle contraction and in conduction of nerve impulses |
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Na deficient slow nerve conduction velocity cramps fatigue decreased BP confusion headach weakness seizures |
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weakness afitation firm subqutaneous tissue increased thrist dry rough mucous membranes decreased urine because ADH is secreted |
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ingested in foods and excreted in urine under influence of aldoserone bannanas, cirtus insulin helps promote K into the cells important in muscle contraction and NCV |
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dysrhythmias weakness fatigue decreased digestive motility causes anorexia and nausea respiratory muscle weakness when sever loss renal fx impaired concentrated urine polyuria |
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dysrhthmias, muscle weakness progressing to paralysis fatigue, nausea, and parenthesis |
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balance is controlled by the parathyroid hormone and calcitonin but influenced by vitiman D and phosphate food, stored in bone low Ca stimulates secretion of PTH thus increased Ca absorption from digestive tract, kidneys and promotes resorption from bone |
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Definition
muscle twitching, spasms,tetany weak heart contractions arrhythmias mental confusion |
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muscle weakness and tone lethargy stupor personality changes anorexia, mausea dysrhythmias kidney stones polyuria thirst |
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control of acid-base is done by |
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Definition
buffer pairs in blood respiratory system kidney regulation |
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bicarbonate carbonic acid buffer system |
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Definition
controlled by respiratory system and kidneys. lungs can exhale carious amounts of carbon dioxide by changing respiration rate kidneys excrete varying ammounts of hydrogen and retain bicarbonate |
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from carbon dioxide and water |
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pH is below 7.35 causes are due to increased carbon dioxide due to respiratory problems metabolic acidosis due to decreased bicarbonate due to diarrhea, renal disease |
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when pH is above 7.45 respiratory hyperventilation due to anxiety high fever, overdose of asprin, injury metabolic due to increase in bicarbonate due to vomiting or excessive ingestion of antacids |
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Definition
mechanical barrier blocks entry of bacteria or harmful substances into tissues. tears, saliva, skin |
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Definition
phagocytosis and inflammation. neutrophils and macrophages to digest harmful substances and debris. inflammation limits effects of injury. interferons protect uninfected cells from viruses. |
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Definition
immune system. Specific to harmful substance |
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major Histocompatibility complex or Human Leukocyte antigens |
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Definition
membrance proteins on the surface of all cells that tell if self or non-self. Act like a key if it fits then ok, if not then EAT! |
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Definition
-any foreign substance that does not have the characteristic cell surface marker (HLA) of that individual. T |
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aka polymorphonuclear cells. Derived from bone marrow. Increase in response to infection and inflammation. May damage host tisues during destruction. Dead PMN's=pus. Basically they come in and eat up! |
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neutrophils and monocytes Both are WBC's and their function is cell eating. In the lumen it is a monocyte when it is in the interstitial fluid it is a macrophage |
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circulate in the blood. after neutrophols kill the invading organism, macrophages clear up the debris. both neutrophils and macrophages have receptors for antibodies and complememnt so coating of bugs occurs |
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derived from bone marrow. multiply in both allergic disorders and parasite infestations. when bugs are to big, eosinophils get into close contact and release their contents of granules to kill the bugs |
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leukocutes that circulate in the blood and function similarly to mast cells in allergic disorders. mast cells release histamine that dilates blood vessels when released.(mast cells in blood vessels, and called basophils in tissue) |
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Definition
Helper T lymphocytes carry microscopic markers located on their surface that identifies them, T4 are helper cells and T8 are the cytotoxic T cells. T4 turns on killer cells and B cells. THey kill nonself by insertion of a protein channel. Suppressor T cells limit immune response. Memory T cells are activated during initial exposure, and can be activated quick with re-exposure. |
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tupe of cytokine protein released by macrophages to trigger the immune response. is released by macrophages to help the T cells. They function to increase the temperature set point in the hypothalamus. increase serotonin in Bstem and duodenum to cause sleep and nausea. stimulate production of prostaglandins thus leading to decrease in pain threshold. increase systhesis of collagenases reslutes in destruction of cartilage. KICKS THE T4 CELLS INTO ACTION. |
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migrage throughout the body to increase interaction with antigens. antibody churning machine. |
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large granular lymphocytes that function to kill viruses, other intracellular microbe-infected cells and tumor cells. Kill w/o prior sensitization or activation. |
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nonspecific line of defense |
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Definition
reacts the same every time. no memory of type of invader. |
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specific and involves memory. its job is to recognize and destroy foreign invaders. results when a pathogen enters the body and the body produces a specific response to the invader. So the next time that pathogen tries to invade thy body, it remembers and reacts stronger. |
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Definition
protection by natural or artificial(vaccine) introduction of an antigen into a responsive host. |
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passive acquired immunity |
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antibodies or sensitized lymphocytes produced by 1 person are transferred to another. mom via breast milk to kid. |
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Definition
or immunoglobulins. antibodies attach to an antigen and destroy it. Allows us to immune to various dzs. divided into 5 classes "MADGE" |
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Definition
largest immunoglobulin that predominated in initial immune response. involved in blood incompatibility rxn. |
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Definition
defends external body surfaces, mucus membrane. found in saliva, colostrum, urine, seminal fluid, tears, nasal fluids, respiratory, GI and GU secretions. |
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attached to B cells and activates B cells |
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is the major antibacterial and antiviral antibody and is the predominant antibody in the blood. |
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primary for parasitic infections. also fxs by activating mast cells and releasing histamine in allergic rxn's anaphylaxis, asthma, urticaria |
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1 part of body to another |
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type I hypersensitivity rxn |
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immediate. allergies, asthma, anaphylaxis, IgE sits on outside of mast cell or basophil, allergen comes into contact and causes IgE to react. if throughout the body then we get an all over body rxn. (anaphalaxis, anasarga) |
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type II hypersensitivity rxn |
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Definition
cytotoxic IgM or IgG formed against self specifically on surgace of own body, myasthenia gravas, graves disese (autoimmune) |
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anaphaylaxis signs and symptoms |
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Definition
general- malaise, weakness and sense of illness dermal-hives erythema mucosal-periorbital edema, nasal congestion and pruititus, flushing, pallor or cyanosis. respiratory- sneezing, rhinorrhea, dyspnea upper airway- hoarsness, stridor, tongue and pharyngeal edema lower airwayp dyspnea, asthma GI- incresased peristalsis, vomiting, dysphagia, nausea CV-tachycardia, dysrthymia hypotension, cardiac arrest CNS- anxiety, seizures. |
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efects females more. pathogenesis this is a type II hypersensitivity. Antibody formed against acetylcholine receptors in skeletal muscles, Prognosis-slow progressive disease with exacerbation and remissions |
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Definition
immune complex dzs forms antibodies on something floating in the body not on the surgace. Antibody attaches to another antibody. leads to inflammation. RA, lupusm glomarular nephritis, vasculitis |
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nothing to do with B cells, related to T cells and macrophages. The body overreacts to antigen Latex |
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etiology unknown. type three hypersensitivity. Primarily IgM-IgG comlex. Wherever this complex lands, destruction of tissue |
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etiology, unknown but factors known are related to hormones, genetic, and environmental. Tupe III hypersensitivity develop antibodies against DNA which damage cells via complement activation. |
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Definition
antigen processed in macrophage, antigen recognition and t cell activation. Amplification and recruitment of MAC's and T cells. Damage to area where antigen is present. (poison ivy) |
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cell mediated cytotoxicity type IV |
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Definition
target antigens recognition of antigen by T cells, activation of T helper and killer cells. destruction of target cells and adjacent tissue |
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