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187 Cards in this Set
- Front
- Back
what is the first line of defense and give examples
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innate resistance
skin; vomiting; linings of gastrointestinal, genitourinary and respiratory tracts; coughing, sneezing, flushing, mucus and cilia |
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second line of defense
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inflammation
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third line of defense
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adaptive (acquired) immunity
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what is the purpose of inflammation
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to neutralize and wall off the offensive agent and remove dead tissue and establish an environment suitable for healing
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when does inflammation occur
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almost immediately after injury
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what causes the inflammatory response
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infection, mechanical damage, ischemia, nutrient deprivation, temperature extremes, radiation
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what are the key signs of inflammation
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redness, warmth, swelling, pain, loss of function
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is inflammation always present with infection?
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yes
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is infection always present with inflammation
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no
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local response of inflammation
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vascular and cellular stages
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systemic response of inflammation
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white blood cell response and acute-phase response
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etiology of inflammation
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heat, radiation, trauma, allergens, infection
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what determines the intensity of the inflammatory response
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extent and severity of injury; reactive capacity of injured person
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when might someone not show an inflammatory response
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if they are immunocompromised
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list four stages of inflammatory response
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vascular response, cellular response, formation of exudate, healing
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describe vascular response of inflammation
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arterioles undergo transient vasoconstriction; injured cells release histamine and other chemicals causing vasodilation (hyperemia); this results in hyperemia, increased blood flow to the area, raising of filtration pressure
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how does the vascular response appear to us?
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redness and edema in the tissue
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list the effects of vascular and chemical response in inflammation
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endothelial cell retraction, increased capillary permeability, movement of fluid from capillaries into tissues
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plasma protein fibrinogen is activated by products of injured cells to become what
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fibrin
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what is the function of fibrin
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strengthens a blood clot formed by platelets which traps bacteria to prevent spreading
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what is the purpose of the coagulation system at site of injury
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forms fibrinous meshwork at injured/inflamed site that prevents spread of infection, keeps microorganisms and foreign bodies at site of greatest inflammatory cell activity, forms clot that stops bleeding, provides a framework for repair and healing
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describe the first step in the cellular response of inflammation
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neutrophils and monocytes migrate through capillary wall to site of injury
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define chemotaxis and desccribe its purpose
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directional migration of wbcs along concentration gradient of chemotactic factors; mechanism for accumulation of neutrophils and monocytes at site of injury
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what do chemotactic factors do
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act as gps to direct wbc to injured tissue
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define margination
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lining up of wbc along sides of capillary wall
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define diapedesis
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migration out of capillary to site of injured tissue
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where do chemotactic factors originate from
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lipids in walls of cells release chemotactic factors as they break down
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neutrophils are also known as
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polymorphonucleated leukocytes (PMN)
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function of neutrophils in inflammatory response
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phagocytize bacteria, other foreign material and damaged cells
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life span of neutrophils
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24-48 hours
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first leukocytes to arrive at the site of injury
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neutrophils within 6-12 hours
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what does pus consist of
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dead neutrophils, digested bacteria, other cell debris
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what is the correct term for pus filled?
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purulent (not pussy)
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name for immature neutrophils
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bands, segmented neutrophils, segs
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what does it mean when segs are increased
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demand for neutrophils is so high that bone marrow releases immature neutrophils, or segmented neutrophils
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steps leading to phagocytosis
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pavementing = margination
diapedesis chemotaxis |
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steps of phagocytosis
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adherence, engulfment, phagosome formation, fusion with lysosomal granules/toxic oxygen production, destruction of the target
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what are monocytes
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second type of phagocytic cells to site of injury; biggest type of leukocytes
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when do moncytes arrive to site of inflammation
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3-7 days
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what do monocytes turn into
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macrophages
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functions of macrophages
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assist in phagocytosis of inflammatory debris; clean area so that healing can begin
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what is a multinucleated giant cell
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many macophages fused together; phagocytize particles too big for macrophage; become encapsulated by collagen leading to formation of granuloma
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function of lymphocytes
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cause the immune response; cell-mediated and humoral
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what are eosinophils and what do they do
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released in large quantities during allergic reaction
release chemicals that act to control effects of histamine and serotonin involved in phagocytosis of allergen-antibody complex slow down immune response to allow clean up and wound healing |
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basophils
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carry histamine and heparin that are released during inflammation
limited phagocytic capabilities similar to mast cell |
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what is the most important activator of inflammation
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mast cell degranulation
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where are mast cells located
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throughout loose connective tissue surrounding blood vessels esp in lungs, gi tract and skin
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list the chemical mediators of the inflammatory response
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histamine, serotonin, kinins, complement components, prostaglandins, leukotrienes, cytokines
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describe the complement system
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major mediator of inflammatory response
when activated, components occur in sequential order involving two pathways each activated complex can act on the next component |
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what are the major functions of the complement system
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enhanced phagocytosis
increased vascular permeability chemotaxis cellular lysis |
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functions of the kinin system
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activate and assist inflammatory cells
causes dilation of blood vessels, pain, smooth muscle contraction, vascular permeability, leukocyte chemotaxis |
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primary kinin is
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bradykinin
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function of prostaglandins
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potent vasodilators
inhibit platelet and neutrophil aggregation pro inflammatory contributing to increased blood flow, edema and pain |
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drugs that inhibit the prostaglandin synthesis
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NSAIDs, aspirin, corticosteroids
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what is exudate
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fluid and leukocytes that move from circulation to site of injury
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describe serous exudate
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watery; indicates early inflammation
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describe fibrinous exudate
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thick, clotted exudate; indicates more advanced inflammation
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describe purulent exudate
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pus, indicates bacterial infection
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describe hemorrhagic exudate
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contains blood, indicates bleeding
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clinical manifestations of local response to inflammation
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redness, heat, pain, swelling, loss of function
AKA cardinal signs |
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clinical manifestations of systemic response to inflammation
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increased WBC count with shift to left
malaise nausea anorexia increased pulse and respiratory rate fever |
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what does shift to left mean in reference to wbc
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increased #s of more immature leukocytes
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what are the causes of the systemic response to inflammation
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poorly understood but prob due to complement activation and release of cytokines
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beneficial aspects of fever
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increased killing of microorganisms, increased phagocytosis, increased proliferation of T lymphocytes
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what triggers fever
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release of cytokines --> they initiate metabolic changes in temp regulating center (epinephrine released from adrenal medulla increases metabolic rate)
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signs of fever
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chills and shivering; body is hot yet person seeks warmth until circulating temp reaches core body temp
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describe acute inflammation
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healing occurs in 2-3 wks usually leaving no residual damage
neutrophils are predominant cell at site |
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describe subacute inflammation
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persists longer than acute
similar signs as acute may be cause of vascular damage that leads to atherosclerosis assoc with oral inflammation, pancreatic cancer and alzheimers |
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describe chronic inflammation
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may last for years; injurious agent persists or repeats injury to site; predominant cell types are lymphocytes and macrophages; may result from changes in immune system (autoimmune); assoc with granuloma formation; lasts more than 2-3 weeks
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what are examples of chronic inflammation assoc with autoimmunity
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rheumatoid arthritis and tuberculosis
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final phase of inflammatory response
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healing
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describe regeneration
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replacement of lost cells and tissues with cells of same type
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do skeletal and cardiac muscle regenerate
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no; they are replaced with scar tissue
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describe repair
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healing as a result of lost cells being replaced with connective tissue; more complex than regeneration; most common type of healing; usually results in scar formation
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describe process of repair
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initial phase = 3-5 days
granulation phase = 5 days to 3 weeks maturation phase and scar contraction = 7 days to several months or years |
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what is the most common type of diabetes
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type 2
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where does diabetes rank in causes of death for the US
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5th
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where is insulin released from
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beta cells of pancreas
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where is glucagon released from
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alpha cells of pancreas
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what happens when blood sugar is too high
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insulin produced by the pancreas; liver stores glycogen
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what happens when blood sugar is too low
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glucagon produced by pancreas; liver releases glucose
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list and describe different types of diabetes
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type 1 - autoimmune, insulin absent, pediatric
type 2 - reduced insulin and insulin resistance; some cells produce but not enough type 3 - from pancreatic trauma, drugs, other diseases type 4 - gestational diabetes |
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when does type 1 diabetes generally occur
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before age 30; peak onset between 11 and 13
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etiology of type 1 diabetes
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end result of auto immune process; beta cells destroyed by body's own T cells; related to genetic susceptibility, autoimmunity and environmental triggers
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symptoms of type 1 diabetes
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recent, sudden weight loss
polydipsia polyuria polyphagia |
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why does weight loss occur with type 1 diabetes
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body is no longer able to absorb glucose and starts to break down protein and fat for energy
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types of test for diabetes
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IFG: impaired fasting glucose
IGT: impaired glucose tolerance |
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which test is faster, less expensive and more easily tolerated for diabetes
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impaired fasting glucose
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if positive for pre diabetes, how long before diabetes generally develops
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usually within 10 years
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80 to 90% of people with type 2 diabetes are what?
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overweight
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symptoms assoc with type 2
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fatigue, blurred vision, unexplained weight loss
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what factors contribute to development of type 2 diabetes
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age, genetic basis, race (higher in blacks, asians, hispanics and natives), obesity, genetic mutations
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what are the metabolic abnormalitites assoc with type 2 diabetes
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insulin resistance
decreased ability to produce insulin inappropriate glucose production alteration in production of hormones (adipokines) |
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where do adopokines come from?
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belly fat (cytokines of adipose tissue)
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what causes the pancreas to have decreased ability to produce insulin
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worn out beta cells; beta cells decrease in mass
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what are the two main adipokines
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adiponectin and leptin
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what is metabolic syndrome and what does it increase risk for
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cluster of abnormalities that increase risk for cardiovascular disease and diabetes; characterized by insulin resistance; abdominal obesity, high triglycerides, low HDL cholesterol, hyperglycemia, hypertension
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risk factors for metabolic syndrome
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central obesity, sedentary lifestyle, urbanization, certain ethnicities
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acute complications of diabetes
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hypoglycemia, diabetic ketoacidosis, hyperglycemic hyperosmolar syndrome (more common in older persons)
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common manifestations of hypoglycemia
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confusion, irritability, diaphoresis, tremors, hunger, weakness, visual disturbances
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what happens if hypoglycemia is not treated
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loss of consciousness, seizures, coma, death
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clinical manifestations of type 2 diabetes
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fatigue, recurrent infections, recurrent vaginal yeast or monilia infections, prolonged wound healing, visual changes (blurred vision)
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chronic hyperglycemia causes what
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micro and macrovascular disease and neuropathies; nonenzymatic glycosylation, shunting of glucose to polyol pathway, activation of protein kinase C
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describe nonenzymatic glycolysation
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reversible attachment of glucose to proteins, lipids w/o enzyme action; glucose can become permanently bound; leads to creation of AGEs which cause tissue injury
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how do AGEs cause injury
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procoagulant changes (clotting), production of free radicals, binding to macrophages inducing inflammation, thickening basement membranes which result in increased vascular permeability
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how does shunting of glucose to polyol pathway affect tissues
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polyol pathway is for tissues that do not require insulin for glucose transport; when glucose is shunted this increases osmotic pressure leading to tissue damage
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what tissues use polyol pathway
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RBCs, blood vessels, nerves, eye lens
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how does activation of protein kinase c injure tissues
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result in insulin resistance due to increased cytokines and increased permeability
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chronic complications of diabetes
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angiopathy, diabetic retinopathy, diabetic nephropathy, diabetic neuropathy, infection
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describe angiopathy
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blood vessel damage; a major effect of diabetes; macrovascular and microvascular; symptoms usually appear 10-20 years after diagnosis
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which vascular changes are specific to diabetes
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microvascular
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areas most noticeably affected by microvascular angiopathy
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eyes, kidneys, skin
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what is the most common cause of new cases of blindness in people 20-74 years
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diabetic retinopathy (microvascular damage to retina as a result of chronic hyperglycemia)
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2 forms of diabetic retinopathy
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nonproliferative = most common, partial occlusion of small blood vessels in retina causing microaneurysms and retinal edema intraretinal hemorrhages
Proliferative = most sever form, retinal capillaries become occluded leading to retinal detachment |
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leading cause of end stage renal disease
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diabetic nephropathy
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critical factors for prevention/delay of diabetic nephropathy
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tight glucose control
blood pressure management yearly urine screening |
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what is diabetic neuropathy
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nerve damage due to metabolic changes
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describe sensory neuropathy
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usually worse at night; can cause atrophy of small muscles of hands/feet; most common form is distal symmetric affecting hands and/or feet bilaterally; characterized by loss of sensation, abnormal sensation, pain and paresthesias (numbness)
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describe autonomic neuropathy
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complications include gastroparesis, sexual dysfunction, neurogenic bladder
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what is the most common cause of hospitalization with diabetes
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foot complications
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risk factors for complications of foot and lower extremity
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sensory neuropathy, peripheral artery disease
other contributors include smoking, clotting abnormalities, impaired immune function, autonomic neuropathy |
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how is infection affected by diabetes
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diabetics are more susceptible; defect in mobilization of inflammatory cells; impairment of phagocytosis by neutrophils and monocytes; loss of sensation may delay detection; treatment must be prompt and vigorous
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when did modern antimicrobials first appear
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in the 1930s and 40s
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host
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any organism capable of supporting the nutritional and physical growth requirements of another
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infection
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presence and multiplication of a living organism on or within the host
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colonization
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bacteria present at site of entry; not necessarily in tissues
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microflora
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microorganisms normally living in or on your body; some are useful; many have no effect
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what are disease causing organisms called
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pathogens
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opportunistic pathogens
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those that normally would not cause disease but seize an opportunity provided by a person's decreased immune or inflammatory responses
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stages of infection
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colonization, invasion, multiplication, spread
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colonization
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presence of pathogen at portal of entry
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invasion
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may be aided by production of bacterial extracellular substances that break down primary or secondary defenses
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multiplication
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# of organisms increase
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spread
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movement to other tissues of the body
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stages of infectious disease
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incubation period
prodromal stage acute stage convalescent period |
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incubation period
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pathogen begins active replication without producing recognizable symptoms in host
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prodromal stage
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inital appearance of symptoms in host
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acute stage
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host experiences maximum impact of infectioius process
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convalescent period
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containment of infection, progressive elimination of pathogen, repair of damaged tissue, resolution of associated symptoms
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insidious disease
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protracted prodromal phase
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fulminant illness
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abrupt onset of symptoms with little or no prodrome
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factors affecting infection
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mechanism of action, infectivity, pathogenicity, virulence, immongenicity, toxigenicity
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mechanism of action for infection
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direct damage of cells, interference with cellular metabolism, rendering a cell dysfunctional bc of accumulation of pathogenic substances and toxin production
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infectivity
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ability of pathogen to multiply in the individual
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pathogenicity
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ability of an agent to produce disease; depends on speed of reproduction, extent of tissue damage and production of toxins
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virulence
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potency of pathogen measured in terms of number of microorganisms or micrograms of toxin required to kill a host
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toxigenicity
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factor important in determining virulence such as production of soluble toxins or endotoxin
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kinds of infectious agents
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prions, viruses, bacteria, mycoplasmas, rickettsiae, chlamydiae, fungi, parasites
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prions
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small modified infectious proteins
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mechanism of action for prions
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cause normal proteins to change their shape and become new prions
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viruses
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protein coat surrounding nucleic acid core
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mechanism of action for viruses
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insert their genome into host cells' DNA and use that metabolic machinery to make new viruses
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cellular effects of viruses
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inhibition of host cell dna, rna or protein synthesis; disruption of lysosomal membranes, promotion of apoptosis, fusion of infected adjacent host cells; alteration of antigenic properties; transformation of host cells into cancerous cells; promotion of secondary bacterial infections
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bacteria
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cells without membrane bound organelles (prokaryotes)
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what feature of bacteria is important to antibiotic use
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cell wall that eukaryotes dont have
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exotoxins
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proteins released by bacteria that damage or kill host cells
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endotoxins
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parts of bacterial cell wall that cause host immune reactions
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what must bacteria have to multiply
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iron
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bacteremia or septicemia
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presence of bacteria in blood as a result of a failure of body's defense mechanisms; usually caused by gram negative bacteria; toxins released in blood cause widespread vasodilation resulting in seriously low blood pressure
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mycoplasmas, rickettsiae, chlamydiae
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smaller than bacteria; mycoplasmas lack cell walls; R and C have to live inside cell like virus
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fungi
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most fungal infections on body surface bc core temp is to high; deep fungal infections are life threatening and commonly opportunistic
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mechanism of action for fungal infections
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adapt to host environment; suppress immune defenses allowing fungi to grow
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diseases caused by fungi are called
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mycoses
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fungi that invade skin, hair or nails
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dermatophytes
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diseases produced by dermatophytes
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tineas
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types of parasites
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protozoa, helminths, arthropods
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examples of protozoan diseases
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malaria, amoebic dysentery, giardiasis
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examples of helminths
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roundworms, tapeworms, flukes
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examples of arthropods
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ticks, mosquitoes, mites, lice, fleas, itchmite, scabies, RMSF (rickettsiae)
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chain of infection
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causative organism, reservoir, portal of exit, mode of transmission, portal of entry, susceptible host
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antibiotic
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chemical produced by one microbe and has ability to harm other microbes
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antimicrobial drug
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any agent, natural or synthetic, that has the ability to kill or suppress microorganisms
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selective toxicity
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ability of a drug to injure a target cell or target organism without injuring other cells or organism that are in intimate contact with the target
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what makes antibiotics valuable
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selective toxicity
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how do we achieve selective toxicity
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disruption of bacterial cell wall; inhibition of an enzyme unique to bacteria; disruption of bacterial protein synthesis
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antibiotics kill bacteria by targeting what?
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cell wall synthesis; protein synthesis; nucleic acid synthesis; bacterial metabolism
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antiviral agents kill viruses by
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blocking viral rna or dna synthesis; blocking viral binding to cells; blocking production of the protein coats (capsids) of new viruses
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defense mechanisms of pathogens
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surface coats, viral-antigenic variation (mutation and recombination), parasites
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how bacteria acquire resistance to antimicrobials
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develop drug metabolizing enzymes; cease active uptake of the drug; drug receptors undergo changes decreasing the uptake; synthesize compounds that antagonize actions
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how do antibiotics promote resistance
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kill non resistant bacteria reducing the competition for resources which allows the resistant ones to flourish; promote overgrowth of normal flora that possess mechanism for resistance
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what can we do to help prevent antibiotic resistance
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culture and sensitivity tests; avoid casual use of antibiotics; use more narrow spectrum antibiotics
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MIC
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minimum inhibitory concentration; lowest concentration of abx that produces complete inhibition of bacterial growth (does NOT kill bacteria)
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MBC
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minimal bacterial concentration; lowest concentration to produce 99.9% decline in # of colonies indicating bacterial kill
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things we as nurses can do to delay emergence of drug resistance
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vaccinate, get the catheters out, target the pathogen, access the experts, practice antimicrobial control, use local data, treat infection not contamination, treat infection not colonization, know when to say no to vanco, stop treatment when infection is cured or unlikely, isolate the pathogen, break the chain of contagion
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things to consider when selecting antibiotics
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identify organism, drug sensitivity of organism, host factors, allergy, penetration to site of infection, patient variables
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misuses of antimicrobial drugs
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untreatable infection, fever of unknown origin, improper dosage, unidentified organism, omission of surgical drainage
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interfeurons
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protect against viruses and they also enhance the inflammation process
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