Kaplan Section 6 - Inflammatory Drugs - Gout, Asthma, Steroids, DMARDs
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| What drugs used for the initial treatment of rheumatoid arthritis? | NSAIDs (decrease pain and swelling) | ||||
| For treatment of RA, why wouldn't you want to use NSAIDs long term? | Marked adverse side effects, plus, they have no beneficial effects on the course of the dz or on bone deterioration | ||||
| What are DMARDs | Dz modifying anti-rheumatic drugs | ||||
| What do DMARDs do? | slow dz progression | ||||
| What is DOC for mild arthritis? | Hydroxychloroquine | ||||
| What is DOC for moderate to severe RA? | methotrexate | ||||
| Which RA drug is associated with cinchonism? | Hydroxychloroquine (GI distress and visual dyxfxn) | ||||
| What happens when you prescribe hydroxychloroquine to person with G6PD deficiency? | hemolysis | ||||
| What is the mechanism of hydroxychloroquine? | stabilizes lysosomes and dec chemotaxis | ||||
| What is the mechanism of methotrexate? | cytotoxic to lymphocytes | ||||
| What is sulfasalazine? | DMARD. | ||||
| What is a special adverse side-effect of sulfaxalazine? | can cause SLE-like syndrome | ||||
| What is eternacept? | a recombinant form of the TNF receptor -- binds TNF. Is a DMARD. | ||||
| What is infliximab? | monoclonal antibody to TNF. Is a DMARD. | ||||
| What is anakinra? | IL-1 receptor antagonist. DMARD. | ||||
| Name the DMARDs | HMS is A GIL PEG. Hydroxycloroquine, Methotrexate, Sulfasalazine, Anakinra, Glucocorticoids, Infliximab, Leflunomide, Penicillamine, Gold Salts, Eternacept | ||||
| What are the three DMARDs that can cause injection-site reactions and infections? | Eternacept, infliximab, and anakinra. | ||||
| Name four drugs/drug classes commonly used for acute inflammatory episodes of gout | 1. colchicine, 2. indomethacin, 3. other NSAIDs (naproxen, sulindac), 4.intra-articular steroids | ||||
| What is the mechanism of colchicine | Drug for gout. Binds tubulin --> dec microtubular polymerization, dec LTB4 (activation of integrins, PMNs and chemotaxis), dec leukocyte and granulocyte migration | ||||
| Acute adverse effect of colchicine | diarrhea, GI pain | ||||
| Adverse effect of colchicine due to long term usage | 1. hematuria, 2. alopecia, 3. myelosuppression, 4. gastritis, 5. peripheral neuropathy | ||||
| What is the drug strategy in treating chronic gout? | reduce the uric acid pool | ||||
| What are the three drugs used in the treatment of chronic gout? | 1. allopurinol, 2. probenecid, 3. sulfinpyrazone | ||||
| What is the mechanism of allopurinol | Treat chronic gout. Pro-drug --(xanthine oxidase)--> alloxanthine ----| purine metabolism --> dec uric acid production | ||||
| What are the adverse effects of allopurinol? | 1. GI distress, 2. peripheral neuropathy, 3. rash, 4. vasculitis, 5. stone formation | ||||
| Talk about drug interactions of allopurinol. | inhibits 6-mercaptopurine metabolism. | ||||
| What is the mechanism of probenecid? | inhibits proximal tubular reabsorption of urate --> more urate peed out --> less uric acid in body | ||||
| What is the limitation of probenecid as a gout drug? | ineffective in pts whose GFR is less than 50 mL/min | ||||
| What is the mechanism of Sulfinpyrazone? | inhibits proximal tubular reabsorption of urate --> more urate peed out --> less uric acid in body | ||||
| What is the limitation of Sulfinpyrazone as a gout drug? | ineffective in pts whose GFR is less than 50 mL/min | ||||
| What are the adverse effects of probenecid and sulfinpyrazone | 1. GI distress, 2. nephrotic syndrome, 3. rash, 4. crystallization if high excretion of uric acid | ||||
| What does ASA do to the effects of probenecid and sulfinpyrazone? | decreases its effects | ||||
| Put in order of increasing duration of drug action: betabethasone, dexamethasone, cortisol, prednisone, triamcinolone | cortisol < prednisone < tiamcinolone < dexamethasone/betamethasone | ||||
| List three steroid effects on the cellular level | antiinflammation: 1. dec leukocyte migration, 2. dec capillary permeability, 3. inc lysosomal membrane stability --> dec phagocytosis | ||||
| List four steroid effects on the biochemical level | antiinflammation: 1. inhibit phospholipase A2 --> dec synthesis of prostaglandins and leukotrienes, 2. dec expression of COX2, 3. dec platelet activating factor (causes platelet aggregation), 4. dec production of interleukins (e.g. IL-2) | ||||
| How does steroids affect the production of ACTH? | Steroids suppress ACTH --> cortical atrophy, malaise, myalgia, arthralgia and fever | ||||
| Why should you not abruptly withdraw steroids? | may result in shock state with abrupt withdrawal | ||||
| What is iatrogenic cushingoid syndrome? | result of steroid use --> fat deposition, muscle weakness/atrophy, bruising, acne | ||||
| Why would steroids produce a hyperglycemic state? | cortisol --> gluconeogenesis --> inc insulin demand and other adverse effects | ||||
| How do steroids affect bone? | Can cause osteoporosis --> vertebral fractures and aseptic hip necrosis (poor blood supply to bone --> bone death) | ||||
| Why do steroids cause ulcers? | increased GI acid and pepsin release --> ulcers and GI bleeding | ||||
| Do steroids cause high vol or low vol state? | Na/water retention --> edema and HTN | ||||
| How do steroids affect K+ and Ca2+ levels? | hypoK+ alkalosis, hypoCa2+ | ||||
| How do steroids affect skeletal growth in children? | retards skeletal growth | ||||
| How do steroids affect infections and wound healing? | Increases chance for infection; slows wound healing | ||||
| How do steroids affect the eye? | increases glaucoma and cataracts | ||||
| What are the three most common causes of toxicity in children under 3 yo? | 1. ASA (Reye's), 2. Acetominophen, 3. supplementary Fe | ||||
| T or F: Asthma is an inflammatory dz | True. It's an inflammatory dz associated with bronchial hyperactivity, bronchospasm, inc mucus secretion, edema, and cellular infiltration | ||||
| Early asthmatic responses | 30 to 60 min. Histamine and leukotrienes --> bronchospasm | ||||
| Late asthmatic responses | infiltration of eosinophils and lymphocytes into airways --> bronchoconstriction and inflammation with mucus plugging | ||||
| How to provide short term relief to asthmatics? | broncohdilators (reduce bronchial hyperactivity) and anti-inflammatory agents (protect against cellular infiltration) | ||||
| In asthma, what are B2-selective agonists used for? | Albuterol, metaproterenol, terbutaline. Used for relief of acute bronchoconstriction. Also used for prophylaxis of exercise-induced asthma (like Annie and Pat). | ||||
| What asthma medication can I use to decrease nighttime attacks prophylactically? | Salmeterol (longer-acting drug) | ||||
| Why would you want to use M receptor blockers for asthmatics who have CV disease? | B2 agonists can cause CV toxicity if overused. M blockers like ipratropium are safter in pts with CV dz and still cause bronchodilation in acute asthma. | ||||
| If an asthmatic pt had bronchospasm due to B-blockers, what is the DOC? | Ipratropium or other M blockers (minor atropine-like effects) | ||||
| What is theophylline and why would you use it in asthmatics? | A bronchodilator. Inhibits phosphodiesterase --> inc cAMP --> bronchodilation; antagonize adenosine (a bronchoconstrictor) | ||||
| Toxicity for thoephylline is increased by what drugs? | erythromycin, cimetidine, and fluororquinolones | ||||
| What is aminophylline? | IV. Sometimes used in bronchospasm or status asthmaticus. | ||||
| What do cromolyn and nedocromil do? | Prevent degranulation of pulmonary mast cells | ||||
| What do cromolyn and nedocromil release from mast cells? | histamine, platelet activating factor, LTC4 | ||||
| Can cromolyn and nedocromil be used prophylactically? | yes -- dec sx's and bronchial hyperactivity (esp responses to allergens) | ||||
| What are the adverse effects of cromolyn and nedocromil? | throat irritation and cough (relieved by B2 agonist) | ||||
| Why would you use adrenal steroids for asthma? | block mediator release; inhibit prostaglandins, leukotrienes, and interleukins --> dec bronchial hyperactivity. | ||||
| What type of drugs are beclomethasone and flunisolide? | Adrenal steroids. Surface-active drugs - can be inhaled. Used for acute attacks as well as prophylactically. | ||||
| What happens with excessive use of adrenal steroids? | 1. Oropharyngeal candidiasis, 2. dec long bone growth in children | ||||
| What would you use for severe acute asthma attacks? | Oral prednisone or IV steroids. | ||||
| What type of drug is zafirlukast? | antagonists at LTD4 receptors. Slow onset. | ||||
| What are the adverse effects of zafirlukast? | diarrhea, headache, increased infections | ||||
| What is zileuton? | selective inhibitor of lipo-oxygenases, decreasing formation of leukotrienes. | ||||
| Which has faster onset? Zafirlukast or zileuton? | Zileuton (1 to 3 hrs) | ||||
| What are the adverse effects of zileuton? | asthenia (feeling of weakness without actual loss of strength), headache, and inc LFTs | ||||
| What would you use for acute asthma in the ER? | 1. O2, 2. aerosolic B agonists, 3. IV steroids |
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Created by:
Christina Pham
on 2008-03-20