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what is arachidonic acid? phospholipid found in cell memrbane
what 2 pathways does arachidonic acid lead to? lipoxygenase pathway and cyclooxygenase pathway
what happens if aracidoinic acid goes down the lipoxygenease pathways? it makes inflammatory mediatros called leukotrienes
what happens if aracidonic acid goes down the cyclooxygenase pathway? it makes inflammatory mediatros called prostaglandins and thomboxane
how doe sleukotrienes effect the body? causes smooth muscle contraction, constrict pulmonary airways, increase microvascualr permeability
leukotrienes play an important role in what disorder? asthma
how doe sprostaglanidns work in the body? induce vasodilation and bronchoconstriction, inhibits inflammatory cell funciton
why is thromboxane used for? vasoconstriction, broncoconstriction, promotes platelete function
what is going to happen if a drug inhibits COX? it also inhibits prostaglandins and thromboxane
what mechanisms are prostaglandins used for? vasoconstriciton adn vasodilation. depending on tissue and different types of prostaglandism
mainstay for treatment of inflammation? NSAIDS
most powerfula ntiinflammatory? Corticosteroids
why are corticosteroids so powerful? it blocks the aracidonic acid from even being released
what are some benefits of NSAIDS? supres inflammation, analgesic, antipyretic
what is the implication of NSAIDS being a weak organic acid? I effects, even though out stomach is acidic it absirbs well into the stomach but not the intesitnes
where are nSAIDS metabolized? liver
where are NSAIDS excreted? mainly kidneys some undergo hepatobiliary excretio
features of NSAIDS weak organic acids, well absorbed in GIT, highly emtabolized by CYPs excreted by kidneys, some undergo hepatobiliary recycling, highly portein bound
what is the differnece between COX1 and COX2 COX1 is always present in normal cell funciton, it is always expressed nromally. COX 2 is expressed only when cells become injured or inflammed
describe characteristics of COX1 Constitutive, ubiquitive, major function is cellular protection and maintainence, blocked by NSAIDS
describe characterisitcs of COX2 inducible, only in tissues inflammed or injrued,proinflammatory, this is best to knock out for inflammation, inhibited by NSAIDS and selected COX2 inhibitors
which CO does Aspirin inhibit? nonselective COX1 and COX2
what are characteristics of COX2 inhibitors? may cause gastric ulceration, doesnt inhibit platelet, les hypersensitivity reaction, and possibel impaired renal funciton
characteristis of aspirin nonselective, irreversible inhibitor of COX1 and COX2, mild - mod pain, higher doses for RA, antipyretic, antiplatelet
antipyretic effects is mainly due to what? inhibition of prostoglandins and interlukins
is 81 mg aspirin going to affect inflammation? NO 81 mg effects COX1 which inhibits plateletes but a higher dose is needed ot affct COX2
what is the active componeet of aspirin? salycilate
describe a linear kineti of most drug elimination most drugs the more drugs you give the faster it is eliminated
describe the kinetics of aspirin it is non linear, after giving high dose of aspirin you saturate enzymes in the liver that metabolize it and amount of aspirin accumulates quickly leading ot toxicity
averse effects of aspirin Gi upset, gastric and duodenal ulcers, ptential nephrotoxocity, hypersensitivity black box reyes syndrome
why are prostaglanidns so important? and how does aspirin srew it up helps regulate blood flow to kidney. giving aspirin will knock out prostaglanidns and effect kidney funciton
what is reyes syndrome fatal syndorme with effects on liver and brain. rash, vomiting, liver damage when given aspirin to children after viral illness
WHY does NSADS and aspirins so ulcerative? they are acid and block prostaglandins which normally protects the gut
which pts are sensitive to aspirins? asthmatics - can cause bronchospamss
mechanism why asthmatics are so sensitive to aspirin high levels of arachidonic acid not going down to prostaglandins so it overflows to the lapoxygenease pthway to leukotrene causing bronchospams
what dose causes therapeutic effects of salycilates? 0-10mg/dl
what plasma levels will cause uricosuric effect? 10-30 mg/dl also fo rinflammation
what levels are salycilate intoxication over 50 mg/dl
how can you hasten elimination of aspirin from body following overdose? give sodium bicarb causes the urine to be alkalin and aspirin is acidici so it will become a charged particle less likely to be reabsorbed by kidne and more likely to be exreted
what drugs are propionic acid drivatives? ibuprofin, naproxen, ketoprofen all are nonsecletve COX
if a person is taking aspirin for cardioprotective effect hat other drug should you not give as well? why? ibuprofen and other NSAIDS it is reversible and it displaces the aspirin.
describe characteristic of naproxen 20x more potent than aspirin, longer half life, less GI effect then aspirin but 2x risk of GI bleed than iuprofen
which NSAID have the highest risk for GI ulceration? indomethacin
these drugs are acetic acid derivatives indomethacin, diclofenac, ketorolac
characteristic of indomethacin poorly tolerated, alot of GI effects usually requiring disconitnuation, used for rheumatic conditions and gout
which drug is the more potent antiinflamatory than naproxen and indomethacn? Diclofenac
what are charactoristics of ketorolac? potent analgesic effect, can be sed with opiods to decrease opiod dose but must limit use to 3-5 days for its GI effect
what happenes when you increase potency of a drug? increase gi effect
describe acetaminophen not an NSAID, analgesic and antypyretic weak inhibitor of COX1 and OCX 2. it works in the brain, centrally acting, used in pts who are aspirin sensitive, mild - mod pain but not laone for artritis
how does acetaminophen damage liver? uses glucathianoe to emtabolize acetaminophem. it protects your liver form free radicals but its decreased during metabolizm increasing your chances of free radicals to screw up liver
how to treat aetaminophen OD? guthathione, acetylsystene, traps free radicals
COX 2 is mainly involved in inflammation analgesic antypyreticNOT platlete
drugs tat are COX 2 selctiv einhibtros? celecoxcib, meloxicam
what are cox 2 selcetive drugs moslty used for? osteoartritis, RA, Gouty arthritis, musculoskeltal pain
WHAT IS MOST CONCERNING FOR COX 2 inhibitros? high incidence of cardiovascular thrombotic events because it blocks prostacycline release in normal cells, also impair angiogenesis, renal tox CI in renal insuff, hypersensitiv
what is prostacycline prevents platelete aggregation normal tissues release this to prevent platelete aggregatio
why can we see hypersensitivity in cox 2 selective inhibitors? it has a sulfa group
DMARDS can do what? change course of disease but this takes time. in the mean time give NSAIDS to treat symptoms
what is rheumatoid artiritis? autoimmune, mainly in female, synovial membrane in joint cavity is first tissue to be effected, tan spreads to articular cartilage, progressive forms pannus- scar tissue overproduction of cytokines= inflmmation
what is synovial membrane? surround end of long bone, prevents boen from rubbing tigether
what is pannus? scar tissue from long term rheumatoid artritis
what is foren antigen in rhtumatoid artritis? RF factor triggers immune response
Abatacept inhibit activation of T cells which make cytokines. binds and block CD80 and 86 cells
how is abatacept given? IV infusion at 0,2,4wks to slow progression of RA
adverse effect of abatacept? increase risk for infection, infusion reaction.
what drugs should not be given with abatacept? dont use with TNFa blockers due to excess immune supression
how does leflunomide work? inhibits t cell production and antibodies by B cells, inhibits t cells to activate b cells mainly
adverse effect for leflunomide? dont get pregnant, fetal loss and malformation, make sure they have a negativ epregnancy test before therapy and contraception is use
drug of choice for RA? methotrexate
how is methotrexte given? givne orally at low doses then in chemo. at high doses can inhibit cell growth
how does mehtotrexate work? increases adenosine levels in cells. adenosine is antiinflammatory, inhibits neutrophil chemotaxis, free radical release, reduce lympocyte and macrophae activity
what is adenosine? antiinflammatory, inhibit neutrophils chemotaxis and free radical release, reduces lymphocyte and macrophage activity
when given methotrexate we have to monitor what cells? labile cells always turnign over high mitotic tissues
what are side effects of methotrexate? GI, mucosal ulcers, leukopenia, anemia, dose dependant elevated liver enzymes
how do we reduce gi upset and liver effects with methotrexate give folic acid because antiproliferative effect of mtx occurs from blocking folate synthesis. block chemotherapy effects of mtx
monoclonal antibodies-mab at end of name target what? cytokines lik TNF, Interleukins and B lymphocyte
what do TNF-a blockers do? blocks TNF-a which is a ke mediator in joint destruction accompaned with RA, also in chrones disease
what are the 3 differenrt TNF-a blockers? Adalimumab (HUmira), Infliximab (remicade) and etanercept (enbrel)
what does recombinant mean? made from human cells humira is recombinant humana antibodu
what is chimeric? portion of molecule not from humans
whay is rituximab different? direct mainly towards b cells.
describe th MAB drugs they are all antibodies ust target a diffetne cytokine
how do we administer MABS? they are all protein so not oral given subq or iv and have high half life so they can be dsoed weekly
what are adver effcts of MABs? risk for infection, TB, opportunistic infection, URTI possibly risk for lymphoma and solid tumor malignancy
mainline drug for RA? corticosteroids short term use
initial dx of RA NSAID, education, within 3 months give DMArD
first DMARD a person gets with RA? methotrexate
what is gout inflammatory respone to excess levels of URiC acid in blood and tissue
what is uric acid? metaboite of purine, adenine and guanine so body always makses this
how do they get gout? clearance of uric acid is reduced rare for increase production mostly because of clearance
how is uric acid eliminated? urine kidney anythign that affects renal clearace can effect uric acid levels
risk factors for gout? diet high meat diet, decreae renal function, age 40-50 for men
what is hyperuiciemia characterized by? 7.0mg/dl
main source of uric acid? breakdown of purines ( from neuclotides DNA and RNA breakdown) small amout from Diet
what forms can uric acid come in? Urate or Uric acid
significance of having urate in blood musch more soluble in tissues than uric acid
where does uric acid tend to accumulte? joint tissue and synovial tissues
significance of high uric acid uric acid reaches high levels in the lood it crystalizes and forms precipitates it can aggregate in joints and cause inflammation
what are tophi small white nodiles of uric acid that are vissible subcutaneously
why they synovial fluid bad for uric acid? thick viscous not water souluble, acid doesnt dissovle , temp of joints is lower then central body meaning urates are less soluble
what other conditions cnagout lead to? uric acid 2/3 are eliminated in kidneys . pH of kidneys is low causes uric acid to precipitate in kidneus
how to treat gout? NSAID, uricosuric agent, allopurinol, febuxosat, pegloticase
first line treatment for gout nsaids- naproxen, indomethaxin- high potency have better effect in gout, inhibit prostaglandins and inhibit phagocytosis of urate crystals
why are nsaids good for gout? antiinflammation but GI effect
why is aspirin bad for gout? acid in renal tubules it effects clearance of uric acid. higher doses of aspirin
which drugs are uricosuric agents? probenecid, sulfinpyrazone
how do uricosuric agents work inhibits reabsorption of uric acid b kidney tubules and increase secretion of uric acid by kids
how does allopurinal works inhibits synthesis of uric acid. it inhibits xanthine oxidase by being converted to oxypurinol- inhibits xanthine oxydase
what is xanthine oxidase enzyme in the body that makes uric acid in body
how do we make uric acid? start with purine then we release hypoxanthine, it is converted by xanthine oxydase to xanthine and than again by xanthine oxydase to uric acid
why is allopurinol iused in chronic treatment of gout? it prevents uric acid formation, in acute exacerbation if uric acid is already made it has no effect
what drugs do allopurinol interact with? azathioprine and 6-mercaptopurine because azathiprine is broken down to mercaptopurine is activated by xanthine oxidase. our levels of mercapropurine will rise and it is very toxic
what is febuxostat like similar to allopurinol potent and selective inhibitor of xanthine oxidase better than allopurinol, greater potency, less side effects
what is pegloticase (krystexxa) recombitant urate oxidase (uricase) attached to PEG giveng them an enzyme that will break down uric acid. we have genes but its not active
adverse effects of peglotcase? infusionreacton, kidneystone, mainly used for refractory gout
2 things you want ot do for pt with gout? 1. reduce uric acid thats there 2. prophylactically prevent accumualtion of uric acid
Created by: Cherry5301