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antiinflammatory/DMA
| Question | Answer |
|---|---|
| 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
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