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Deviation from normal state of health or wellness. Homeostasis not maintained. |
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The study of functional or physiologic changes in the body that result from disease processes. At the organ level-looking at organs. |
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The early stages in the development of a disease |
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disease causing microorganism |
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1. basic science -in lab animals/cells 2. human subjects- small # to see if it is safe 3. only happens if #2 results were positive and most don't make it here. Results of this stage will be EVIDENCE BASED RESEARCH FINDINGS note: money and availability are not taken into account |
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something given to prevent disease |
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he branch of medical science that studies the causes and nature and effects of diseases any deviation from a healthy or normal condition down to cellular level. |
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first line of defense or nonspecific defense mechanism |
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skin mucous membranes (tears, salive) |
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second line of defense including nonspecific |
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the process by which neutrophils (a leukocyte) and macrophages randomly engulf and destroy bacteria, cell debris or foreign matter. |
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nonspecific agents that protect uninfected cells against viruses group of antiviral glycoproteins produced by viral infected cells. |
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treatment, procedure or error cause disease
Physician induced process. Example—wrong medication. Chemotherapy hospital community caused |
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genetic, environmental or other factors increasing risk for a condition |
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development of a disease or sequence of events involved in tissue changes related to specific disease process-course of disease |
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identification of specific disease. more than one factor considered. EX: Pain + X-ray. |
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condition exists with little or no signs or symptoms |
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(or incubation period) time from exposure to time of symptoms-can be contagious during this time. |
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nonspecific signs during early development of disease- fatigue, loss of appetite, usually no positive lab results yet, |
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clinical evidence or effects of disease. EX: swelling, redness. |
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local, specific change in tisue |
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collections of signs and symptoms often affecting more than one organ-occur together |
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condition that triggers an acute episode. EX: angina attack precipitated by shoveling snow |
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potential unwanted outcomes of primary condition. EX: paralysis after stroke |
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rehab period or period of recovery |
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science of tracking pattern of occurrence of a disease. Data used from WHO, CDC. |
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occurrence in a given area |
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occurrence in regions around the globe |
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# of new and old or existing cases |
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decrease in the size of ... |
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increase in the size of... |
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increase in number of cells |
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one cell type replaced by another cell type EX: ciliated columnar replaced by stratified squamous |
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cells vary in size, shape, large nuclei and mitosis increased.
Cell looks and acts ABNORMAL, but not CA...yet!! Chronic irritation or infection causes this. Ex. Pap smear. |
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undifferentiated variable nuclear and cell structures-characteristic of cancer, basis for grading aggressiveness of tumor
Variable: nuclei, cell structure & mitosis. CA. both this and neoplasia are CA but this is localized |
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new growth -tumor can be benign or malignant
Independent growth of cells. Forms tumor. cancer mastisized |
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programmed cell death *abnormal development *excessive number of cells *aged or injured cells enzymatically digests themselves |
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O2 deficit due to respiratory problems or circulatory obstruction- most common cause of injury to cells |
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interferes with energy ATP production in cell-stops NA++ and other functions |
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Too much NA++ in the cell |
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leads to swelling and possibly rupture |
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types of mechanical damage |
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radiation-change in DNA or toxic materials chemicals- alters cell membrane permeability or produce free radicals infectious diseases-uses microorganisms |
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pressure of fluid in a system- higher in arterioles then venules |
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Osmotic pressure is constant, and NOT higher at the venous or arteriole side. The osmotic force is due to the interstitial fluid concentration of protein, which should be fairly conserved. And it is the difference in hydrostatic pressure (higher at the arterial end of the cap. and lower at the venous end of the cap) that allows for the differences in filtration and absorption. |
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albumin, globulin and fibrinogen (normally remain in capillary |
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body's nonspecific response to tissue injury, resulting in redness, swelling, warmth and pain, and perhaps loss of function. -itis |
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direct physical damage caustic chemicals
process the same regardless of cause but timing of events may differ ischemia or infarction allergic reactions extremes of heat or cold foreign bodies (splinters or glass) infection |
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a chemical released in the body during an inflammatory response or immune response. EX: histamine, serotonin, prostaglandins and leukotrienes released by platelets and mast cells in inflammation
complement
histamine
kinins
prostaglandins
leukotrienes
cytokines
tumor or necrosis factor (TNF)
chemotactic factors |
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serve as communicators in tissue and fluids. Send messages to lymphocytes and macrophages, the immune system or the hypothalamus to induce fever. |
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immune cells that function to detect foreign substances in the tissue spaces and initiate local inflammatory responses against them-found just deep to epithelium release histamine release chemotactic factors produce and release leukotrienes (arichidonic acid) produce and release prostaglandins (arichidonic acid) |
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released from mast cells. immediate vasodilation and increased capillary permeability to form exudate |
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vascular response to injury |
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vasodilation and increased capillary permeability |
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the movement of cells toward or away from an area of the body in response to chemical signals |
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the passage of leukocytes through intact capillary walls to site of inflammation |
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3 ways for tissue to repair |
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regeneration fibrosis resolution-damaged cells recover |
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delicate pink tissue composed of several elements. Highly resistant to infection because it produces bacteria-inhibiting substances. |
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neutrophils-phagocytosis eosinophils- numbers increased in allergic response basophils- release histamine leading to inflammation |
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T-lymphocytes- active in cell mediated immune response B lymphocytes-produce antibodies Monocytes-phagocytosis Macrophages- active in phagocytosis. Mature monocytes that have migrated to tissue from blood |
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first, dilation of capillaries to increase blood flow; second, microvascular structural changes and escape of plasma proteins from the bloodstream; and third, leukocyte transmigration through endothelium and accumulation at the site of injury. |
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collection of interstitial fluid formed in the inflamed area. characteristics vary with cause of trauma |
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watery exudate consisting primarily of fluid with small amounts of protein and white blood cells. |
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thick and sticky and have a high cell and fibrin content. This type increases the risk of scar tissue i the area |
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thick, yellow-green in color, and contain more leukocytes and cell debris as well as microorganims-usually indicates bacterial infection and is referred to as pus |
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localized pocket of purulent exudate or pus in a solid tissue |
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may be present if blood vessels damaged in area of exudate. |
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fever producing substances from WBCs or macrophages. They circulate in the blood and reach the hypothalamus which sets the temp. |
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pyrogens released hypothalamus sets new higher temp shiver, vasoconstriction and cool skin take heat and send it through blood to raise the temp once set temp is reached these halt and high temp remains until cause of pyrexia leaves. |
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increased white blood cells in the blood(esp. neutrophils) |
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ESR-erythrocyte sedimentation rate |
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rate at which plasma proteins settle in a sample. An increase can be sign of inflammation-nonspecific indicator |
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changes in blood in inflammation |
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leukocytosis-wbc differential count-proportion of each type of WBC altered depending on cause plasma proteins-increased fibrinogen and prothrombin c-reactive protein-protein not normally in the blood but appears with acute inflammation and necrosis within 24-48 hours increased ESR-elevated plasma proteins cell enzymes-released from necrotic cells and enter tissue fluids and blood; may indicate the site of inflammation |
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cell enzymes specific to certain organs that differ slightly in structure but have similar functions. Can be helpful in identifying the area of inflammation |
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an open crater-like lesion on the skin or mucous membrane-extensive necrosis may lead to an ulcer or erosion of tissue. |
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a hole through the wall - can be a complication of prolonged inflammation due to cell necrosis and lack of cell regeneration causing erosion of cell tissue in the wall of viscera. |
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potential complications of inflammation |
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infection ulcers -perforation skeletal muscle spasms local complications |
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characteristics of chronic inflammation |
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less swelling and exudate more lymphocytes then in acute (macrophages and fibroblasts) more tissue destruction more collagen produced in the area granuloma may develop |
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small mass of cells with a necrotic center and covered by connective tissue |
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The one thing about the disease that identifies that disease. Ie. HALLMARK of a 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—exposure to asbestos may lead to CA. |
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*Sudden and obvious =‘s acute. The onset could also be insidious (gradual progression w/mild, vague signs) *Acute dz—short-term illness that develops quick *Chronic dz—often milder condition that develops gradually but persists for a long time. Example— |
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Decrease in the number of cells |
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sequestrian of focal injury |
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Body walls off the injured area to keep away from the rest of the body |
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induction of endoplasmic reticulum |
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Grow more ER. Ex-ETOHic—grows more ER to detoxify the alcohol |
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Lack of growth, did NOT form the organ or tisssue such as someone that is born w/o vertebrae—spina bifida. |
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causes of cell injury or death |
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*Hypoxia Lack of oxygen. Stops aerobic respiration. Important for brain, heart & kidney because of high demand of oxygen.* *ischemia—most common cause* Lack of blood/perfusion. Ex. CO poisonhypoxia prior to ischemia *Physical agents (?)—leads to cellular death. Exs. Burns, *extreme cold *Chemicals *Excess of any chemical causes death *Infectious agents *Bacteria, virus *Immune mechanisms *Antibodies attacking antibodies or self attacks self. Example: rheumatoid arthritus *Genetic derangements Ex. Sickle cell anemia-spleen *Nutritional imbalances Obesity—55% of population |
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Following cell death, the nucleus disintegratescells release lysosomes into the tissuecausing inflammation & damage to nearby cells & reduced function.
Enzymes from the damaged cells can diffuse into the blood. This helps with ID’ing the type of cells damaged |
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Process of removal of dead tissue. Lysosomes start process. Macrophages finish process. Coagulative necrosis— Liquefactive necrosis Fat necrosis Caseous necrosis (cheese!) Fibrinoid necrosis Gangrenous necrosis |
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Usually found following ischemia Loss of normal organelle structure Ischemia or infarction |
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Accumulation of PMN’s (pus) Usually found with bacterial infection |
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Usually found with pancreatic disease that leaks lipases. (ex. Acute pancreatitis) or abdo trauma |
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(cheese!) Mostly found with TB; due to resemblance of cottage cheese. CXR—Ca++ deposits because that is what is left after damage. Once TB, always TB. |
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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 & phospholipases—that rapidly can lead to amputation or death. Hemoglobin turns black therefore eschar! |
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1st line—mechanical barrier—blocks entry of bacteria or harmful substances into tissues. Includes tears or saliva to destroy harmful substances. Ex: GI, GU, resp, skin. 2nd line—phagocytosis & inflammation—neutrophils & macrophages to digest harmful substances & debris. Inflammation—limits effects of injury. Interferons protect uninfected cells from viruses 3rd line—immune system. Specific to harmful substance. |
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signs and symptoms of inflammation |
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. Calor (heat) 2. Rubor( redness) 3. Dolor (pain) 4. Edema
-may also see: Functio laeso-loss of function Pus formation—neutrophils that die after engulfing dead tissue |
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1. injury 2. initial vasoconstriction 3. release of chemical mediators 4. vasodilation—increased blood flow (hyperemia) 5. increased capillary permeability 6. WBC’s or leukocytes move to site of injury by chemotaxis. Diapedesis? 7. phagocytosis—removal of debris in preparation for healing |
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endothelial separation leads to... |
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Serous or Transudate—pure water coming across enothelial cells. Example is sunburn Exudate—plasma proteins and water leaking out Serosanginous (blood) exudate—RBC’s, plasma proteins & water present in interstitium Fibrinous—thick & sticky w/high cell & fibrin content—scar is likely to form Purulent—thick yellow-green & contains WBC & cell debris. Typically bacterial infection is present with this type. Pus. Abcess—local pocket of purulent exudate |
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systemic effects of inflammation |
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Malaise—not feeling well Fatigue Ha Anorexia—loss of appetite Pyrexia—fever. Caused by release of endogenous pyrogens from WBC’scirculate in bloodreset hypothalamus |
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Resolution—minimal damage,damaged cells recover & tissue returns to normal Regeneration—tissue is able to heal. Tissues ability to heal is related to cells ability to replicate. Replacement—extensive damage leading to scarring by connective tissue. Scarring impairs the function of the tissue. Ex--MI |
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factors promoting healing of inflammation |
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Youth Good nutrition, vitamin A & C Adequate hemoglobin Effective circulation Clean wound No infection or further trauma to the site |
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factors prohibiting healing |
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Advanced age, reduced mitosis Poor nutrition, dehydration Anemia (low hemoglobin) Circulatory problems Presence of other disorders: DM or CA Irritation, bleeding, or excessive mobility Infection, foreign material, exposure to radiation Chemotherapy Prolonged glucocorticoids |
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Loss of function Contractures & obstruction Adhesions Hypertrophic scar tissue- ex: keloid Ulcerations |
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types and processes of burns |
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Thermal (heat) Non-thermal (chemical or electrical)
Cause acute inflammatory response & release of chemical mediatorsresults in a massive fluid shift, edema & hypovolemia.
Severity of burn depends on cause of burn, temperature, duration of contact as well as extent of burn surface (rule of 9’s) & site of injury. Young & old are more susceptible. |
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Partial thickness burn involves the epidermis & part of dermis. Superficial partial thickness aka 1st degree burns, damages epidermis & upper dermis. Ex-sunburn Deep partial thickness burn—destruction of epidermis & part of dermis. Red, edematous, blistered, hypersensitive during inflammatory stage. Dead skin sloughs off & heals by regeneration. Full-thickness burn—destruction of all skin layers & often underlying tissues. Dry, leathery eschar. Many burns are mixed. |
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complications of burn injuries |
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Shock Respiratory problems Pain Infection Metabolic needs |
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burns front arm 4.5 total arm 9 front leg 9 total leg 18 trunk 18 front 18 back total head 9 groin 1 |
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bands of scar tissue joining two surfaces that are normally separated. |
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interstitial fluid formed in the inflamed area. collection of interstitial fluid formed in the inflamed area |
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wound clean, free of necrosis, edges close together: like surgical incision |
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large break in tissue and more inflammation, longer heal more scar tissue |
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produce collagen-basic component of scar tissue |
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no function but a filler up. loss of function contractures and obstructions-stenosis adhesions hypertrophic ulceration |
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leukocytes (white blood cells) |
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neutrophil eosinophil basophil lymphocyte monocyte |
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most numerous wbc chemically (chemotaxis) attracted to sites of inflammation active phagocytes especially effective with bacteria and some fungi have granules considered lysosomes that specifically digest bacteria |
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attack against parasitic worms that are too large to be phagocytized reside in loose connective tissues at body sites have complex role in allergy and asthma |
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rarest wbc contain histamine similar to mast cells; both bind to IG E that causes the cells to release histamine contain heparin an anticoagulant |
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mount immune response by direct cell attack or via antibodies t-cells b-cells natural killer cells second most numerous leukocytes in the blood |
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phagocytosis; develop into macrophages in the tissues largest leukocyte |
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monocytes that have gone into the tissues active phagocytes crucial in defense against viruses, intracellular bacterial parasites and chronic infections such as TB important in activating lymphocytes to mount the immune response
process and present antigens to lymphocytes for the immune response |
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released from necrotic cells and enter tissue fluids and blood: may indicate the site of inflammation |
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proportion of each type of wbc altered, depending on the cause |
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the process that occurs when there is minimal tissue damage. The damaged cells recover and tissue returns to normal. |
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the steroid hormones from the adrenal cortex that increase blood glucose levels and act to decrease inflammation and allergic reactions |
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like pus (microbes wbcs and cell debris) thick, yellowish material in tissue often resulting from bacterial infection |
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narrowing of a tube, valve or opening |
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(corticosteroids, steroidal anti-inflammatory drugs) synthetic related to naturally occurring hydrocortisone produced by adrenal cortex short tem treatment decrease capillary permeability-enhancing effectiveness of hormones epinephrine and norepinephrine which stabilized vascular system
reducing the number of leukocytes and mast cells at the site-reduces histamine and prostaglandin blocks the immune response-the cause of inflammation |
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adverse effects of glucocorticoids |
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prednisone-oral, triamcinolone-topical,methylprednisone-inra-articular, dexamethasone-intramuscular,IV injections and inhalers also
*atrophy of lymphoid tissue and reduced # WBCs leading to increased risk of infection and decreased immune response
*catabolic effects, increased tissue breakdown and reduced protein synthesis and tissue regeneration, including osteoporosis *delayed healing *delayed growth in children *retention of sodium and water leading to high blood pressure and edema |
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process by which neutrophils and macrophages randomly engulf and destroy bacteria, cell debris or foreign matter. |
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replacement of destroyed tissue with the same kind of tissue |
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proliferation of fibrous connective tissue called scar tissue |
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delicate pink tissue composed of several elements. it contains capillaries that grow in from nearby areas and lay down a new capillary bed. destined to become scar tissue. produces bacteria inhibiting substances |
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