Medications Individual Flashcards

Question

Montelukast

Answer 1

Leukotriene Receptor Antagonist MOA: anti-inflammatory; act to antagonize the leukotriene receptor; improve FEV1, decrease asthma symptoms, decreased SABA use, decrease asthma exacerbations, steroid sparing AE: - generally few (esp. Montelukast); sleep disorders, aggressive behavior, suicidal thoughts, eosinophilic granulomatosis with polyangiitis (rare), angioedema, urticartia CI: CYP2C9 drugs

Answer 2

Leukotriene Receptor Antagonist Expensive! MOA: anti-inflammatory; act to antagonize the leukotriene receptor; improve FEV1, decrease asthma symptoms, decreased SABA use, decrease asthma exacerbations, steroid sparing AE: - generally few; hepatotoxicity, sleep disorders, aggressive behavior, suicidal thoughts, eosinophilic granulomatosis with polyangiitis (rare), angioedema, urticartia CI: CYP2C9 drugs (significant)

Answer 3

Leukotriene Receptor Antagonist MOA: anti-inflammatory; act to antagonize the leukotriene receptor; improve FEV1, decrease asthma symptoms, decreased SABA use, decrease asthma exacerbations, steroid sparing AE: - generally few; hepatotoxicity, sleep disorders, aggressive behavior, suicidal thoughts, eosinophilic granulomatosis with polyangiitis (rare), angioedema, urticartia CI: CYP2C9 drugs (significant)

Answer 4

Immunomodulator MOA: anti-inflammatory; inhibits binding of IgE to receptors on mast cells and basophils; results in inhibition of inflammatory mediator release/attenuation of early and late phase allergic response AE: injection site reactions: bruising, redness, pain, stinging, itching, burning; anaphylactic reactions (monitor after injection; give epinephrine prescription); increased risk of CV events and cancer? - subcutaneous q2-4 weeks in office/clinic - expensive

Answer 5

Phosphodiesterase-4 Inhibitor MOA: reduce inflammation by inhibiting breakdown of cAMP - do not cause direct bronchodilation; used for preventing COPD exacerbations or for select chronic bronchitis patients AE: much more likely than other meds; diarrhea, weight loss, nausea, headache, insomnia, decreased appetite, abdominal pain, anxiety, depression, increased suicidality Interaction: theophylline (both inhibit PDE-4) - very expensive - little effect on symptoms and quality of life modest benefit in lung function and preventing exacerbations

Answer 6

broncodilator MOA: decrease bronchospasm through anti-inflammatory effect - not much benefit over placebo - less effective and less cost effective than ICS - reserved for pts who cannot tolerate ICS - 2nd line therapy for exercise induced asthma

Answer 7

Nicotine Replacement Product - provides nicotine at a fixed dose; used prn for cravings AE: irritation in the mouth, sore jaw, hiccups, stomach discomfort Avoid with Dentures - OTC - chew gum until it tingles; park it in the cheek until tingling subsides, repeat until gum no longer tingles - do not eat or drink 30 min after use

Answer 8

Nicotine Replacement Product AE: irritation of mouth and throat, mild coughing, stomach discomfort - prescription/expensive

Answer 9

Nicotine Replacement Product AE: irritation of mouth and throat, sore throat, stomach discomfort - OTC - dissolve in mouth, do not eat or drink 30 minutes after use - contains 25% more nicotine than gum

Answer 10

Nicotine Replacement Product AE: irritation in the nasal passages and throat, runny nose - prescription/expensive

Answer 11

Nicotine Replacement Product AE: rash where the patch is placed, trouble sleeping - can be worn 24 hrs per day; reduces cravings, but doesn’t take them away; can be used in combination with prn nicotine replacement - OTC and prescription - 8-week treatment; longer has no added benefit - change patch q24 hrs - remove patch at night if insomnia or weird dreams

Answer 12

Smoking Cessation Medication MOA: antidepressant; blocks reuptake of dopamine and NE AE: dry mouth, insomnia, lowers seizure threshold, may increase suicidality, esp. in adolescents/young adults - cardiotoxic at high doses; widens QRS complex (caution with CVD) CI: history of seizures or eating disorders (reduces appetite), use of monoamine oxidase within 14 days (risk hypertensive reactions) DI: MAO-Is; drugs that lower seizure threshold (antipsychotics, antidepressants, theophylline, systemic corticosteroids) - can combine with NRT - may benefit in pts w/ history of depression - not 1st line for adolescents - doubles odds of smoking cessation compared to placebo - caution with CVD with immediate post MI or with serious symptoms or worsening angina

Answer 13

Smoking Cessation Medication MOA: nicotinic receptor partial agonist and antagonist; reduces cravings/withdrawal and blocks effects of smoked nicotine AE: - insomnia, nausea, increased risk of CV events; neuropsychiatric symptoms: changes in behavior, hostility, agitation, depressed mood, suicidal thoughts and behavior, attempted suicide (MONITOR) - monotherapy; DO NOT combine with NRT or bupropion - works better than bupropion - begin 1 week before quit date and continue for 12-24 wks - caution with CVD with immediate post MI or with serious symptoms or worsening angina

Answer 14

Conventional Disease Modifying Antirheumatic Drugs MOA: inhibits dihydrofolate reductase, which causes inhibition of inflammatory factors AE: nausea, diarrhea, hepatotoxicity, alopecia (hair loss), new onset cough or SOB, myelosuppression Methotrexate Toxicity (reduced folic acid) – dihydrofolate reductase coverts FH2 to active FH4; methotrexate prevents active folic acid; supplement with 1 gram folic acid; Leucovorin rescue for cancer treatment pts; signs: stomatitis, diarrhea, nausea, alopecia, myelosuppression, elevations in LFTs CI: hepatic impairment, alcohol (increased liver damage risk), pregnancy (even if intended, men and women) - adjust dose in renal impairment - pregnancy – spontaneous abortion, myelosuppression, limb defects, CNS abnormalities); discontinue 3 months before trying to get pregnant - first-line RA treatment - must give folic acid supplements to prevent toxicity - IM, po, or subcutaneously - monitor: CBC, creatine, LFTs ever 6-8 weeks, signs of infection

Answer 15

Conventional Disease Modifying Antirheumatic Drugs MOA: unknown; modify disease process and prevent/reduce joint damage AE: - nausea, diarrhea, headache, vision changes (monitor yearly eye exam), skin pigmentation - OKAY TO USE WITH: renal, hepatic, or bone marrow suppression - slow onset; must use for 6 mo before determining if effective - can combine with either or both methotrexate for RA - oral

Answer 16

Conventional Disease Modifying Antirheumatic Drugs MOA: unknown; modify disease process and prevent/reduce joint damage AE: - nausea, abdominal discomfort, diarrhea (start low, go slow); leukopenia/ myelosuppression (routine blood work); rash, yellow-orange discoloration, photosensitivity (use sunscreen) CI: sulfa-allergy - avoid: hepatic impairment - adjust dose in renal impairment - monitor: CBC every 2-4 wks for 3 months, then every 3 months - slow onset; must use for 6 mo before determining if effective - can combine with either or both methotrexate for RA - oral - drug of choice for pregnancy

Answer 17

Conventional Disease Modifying Antirheumatic Drugs MOA: inhibits t-lymphocyte response which halts inflammatory cascade AE: hepatotoxicity (higher risk if used in combo with methotrexate) - if need abrupt d/c (pregnancy or toxicity), use cholestyramine to speed removal from body - similar efficacy to moderate methotrexate or sulfasalazine doses - long half- life: start with loading dose and follow with maintenance dose - can use with methotrexate

Answer 18

Brand Name: Remicade TNF Antagonists (Biological DMARDs) MOA: prevent action of TNF, causing a reduction in inflammation AE: mouse antibody – infusion related reaction (monitor); rash, urticaria, flushing, headache, fever, chills, nausea; temporarily d/c, slow infusion rate; pre-treat with corticosteroids/ antihistamines if reactions are common - also used in Crone’s, ulcerative colitis, ankylosing spondylitis - screen for TB; could reactivate - screen for hepatitis - avoid in pts with serious infections, demyelinating disorders, hepatitis, and heart failure - ONLY IV

Answer 19

Brand Name: Humira TNF Antagonists (Biological DMARDs) MOA: prevent action of TNF, causing a reduction in inflammation AE: injection site reaction (rotate sites, topical corticosteroids, antipruritics, analgesics, rotate site) - monitor signs of infection - give subcutaneously or IV - screen for TB and hepatitis; could reactivate - avoid in pts with serious infections, demyelinating disorders, hepatitis, and heart failure

Answer 20

Brand Name: Simponi TNF Antagonists (Biological DMARDs) MOA: prevent action of TNF, causing a reduction in inflammation AE: injection site reaction (rotate sites, topical corticosteroids, antipruritics, analgesics, rotate site); IV infusion reaction - monitor signs of infection - give subcutaneously or IV - screen for TB; could reactivate - screen for hepatitis - avoid in pts with serious infections, demyelinating disorders, hepatitis, and heart failure

Answer 21

Brand Name: Enbrel TNF Antagonists (Biological DMARDs) MOA: prevent action of TNF, causing a reduction in inflammation - screen for TB; could reactivate - screen for hepatitis - avoid in pts with serious infections, demyelinating disorders, hepatitis, and heart failure - SubQ or IV

Answer 22

Brand Name: Cimzia TNF Antagonists (Biological DMARDs) MOA: prevent action of TNF, causing a reduction in inflammation - screen for TB; could reactivate - screen for hepatitis - avoid in pts with serious infections, demyelinating disorders, hepatitis, and heart failure - SubQ or IV

Answer 23

Brand Name: Orencia Costimulation Modulator (Biological DMARD) MOA: blocks T cell signaling and activation (prevents inflammatory response) AE: headache, infection, infusion reaction, injection site reaction - IV or subcutaneous - monitor infection - monotherapy or combo therapy after inadequate response of methotrexate and/or anti- TNF - avoid in pts with serious infections, demyelinating disorders, and hepatitis

Answer 24

Brand Name: Rituxan Anti-CD20 Monoclonal Antibody (Biological DMARD) MOA: causes B lymphocyte depletion in bone marrow and synovial tissue AE: Black Box – fatal infusion reactions, severe mucocutaneous reactions; injection adverse reactions - better response if rheumatoid factor positive RA - also used in non-RA conditions - IV - monitor infection - avoid in pts with serious infections, demyelinating disorders, and hepatitis

Answer 25

Brand Name: Actemra Anti-interleukin-6 Receptor Antibody (Biological DMARD) MOA: blocks interleukin-6, which is implicated in joint damage and disease activity in anemia AE: elevated LFTs, cholesterol, triglycerides, HDL; nasopharyngitis, infection - monitor infection, LFTs - IV, subcutaneous

Answer 26

Brand Name: Xeljanz Targeted Synthetic DMARD MOA: inhibits specific kinases AE: infection, headache, hypertension, elevated LFTs, diarrhea, worsening lipids - adjust dose if renal or hepatic impairment - oral; good choice for patients who prefer oral meds - monitor CBC, hemoglobin, lipids, LFTs, infection

Answer 27

- used for pain and fever MOA: centrally acting analgesic and antipyretic with minimal anti-inflammatory properties - generally well tolerated - renal toxicity (may worsen kidney function), hepatic toxicity, GI upset) - caution with stable chronic liver disease (monitor) - Acetaminophen Toxicity – leading cause of acute liver injury; be cautious of meds that have APAP combo - Signs of Acute APAP OD (200 mg/kg or 10 g): abdominal pain, elevation of ALT and AST about 24 hr after ingestion (peak 2-3 days after), liver failure, renal injury, coma, hyperglycemia, lactic acidosis, death (if serum conc of APA > 500 mcg/mL) - Signs of Chronic Supratherapeutic OD (over 4 g/day): ALT elevation, malaise, N/V, abdominal pain, hepatotoxicity, jaundice, hypoglycemia, coagulopathy, renal failure, fulminant hepatic failure, encephalopathy, death - Mild/moderate toxicity: obtain APAP conc, start acetylcysteine if risk of hepatic injury (>200 mg/kg ingested, > 10g ingested, if conc can’t be measured, or >150 mcg/mL 4 hrs post ingestion) - Severe toxicity: if pt presents >36 hours after ingestion (greater injury/failure), proved emergency care prn (intubation, fresh frozen plasma, vasopressors, dialysis, airway management, fluid resuscitation); acetylcysteine if hepatic injury - avoid alcohol - use for mild-to-moderate pain in general - can be combined with NSADS - effective, inexpensive, favorable risk-benefit profile - same efficacy as NSAIDs - OTC, generally taken prn, but can be scheduled - max daily dose 4000mg per day or less; max dose 1000mg or less – toxicity (know) - onset within 1 hour - one of the safest analgesics; preferred for patients with hypertension of kidney failure

Answer 28

NSAID - Nonselective MOA: has analgesic (aspirin not advised for pain) and antipyretic activities by blocking COX1 and COX2, which causes inhibition of prostaglandins - COX1 = gastric mucosa (increase mucus, bicarb), kidney (dilate afferent arteriole), platelets (promote normal function) - COX 2 – normally undetectable, but increases at sites of inflammation and local tissue injury AE: - Salicylism: toxic syndrome that occurs due to excessive doses of aspirin, salicylic acid, or consumption of oil of wintergreen (5mL); mixed respiratory alkalosis and metabolic acidosis (anion gap); can occur due to acute overdose or chronic overdose; signs: severe headache, nausea, vomiting, tinnitus, confusion, increased pulse, increased respiratory rate; can progress to seizures, coma, cerebral/pulmonary edema, death; treatment: urine alkalization (sodium bicarb), hemodialysis, emergency care prn - GI (COX1 related; add gastroprotection to nonselective NSAID or use lower GI risk NSAID: celecoxib), renal insufficiency (drink water), hepatic dysfunction, increased cardiovascular risk (COX2 related), CNS effects, increased blood pressure, fluid retention, rarely cause tubulointerstitial nephropathy renal papillary necrosis - COX 1 related: adverse effects on gastric mucosa – asymptomatic gastric and duodenal mucosal ulceration (15-45%); direct irritant effect on GI (10-60%) – nausea, dyspepsia, anorexia, abdominal pain, flatulence, diarrhea; perforation, gastric outlet obstruction, GI bleeding (1.5-4%) - COX2 related: degree of COX2 selectivity dictates CV risk; celecoxib (selective COX2 inhibitor) has strongest association with CV events; diclofenac and ibuprofen have strong association with CV events CI: - at risk/current peptic ulcers or GI risk; bleeding risk; renal insufficiency, uncontrolled hypertension, heart failure, caution if NSAID/aspirin sensitive asthma - caution women of childbearing age/pregnant women: risk of fetal bleeding; possible CI – some potential association with miscarriage in 1st trimester; CI after 30 wks (3rd trimester); may promote premature closure of ductus arteriosus in fetus - renal insufficiency; esp in chronic renal insufficiency, LV dysfunction, elderly, diuretics, RAAS drugs; causes decreased glomerular filtration, hyperkalemia, sodium/water retention - interaction: aspirin, warfarin, oral hypoglycemic, antihypertensives, lithium, other drugs that bind to proteins, drugs that affect renal efficiency, drugs that have antiplatelet activity (monitor efficacy and AE) - use for mild-moderate pain in general - can be combined with APAP - OTC - oral - similar APAP efficacy - onset of pain relief = 1 hr - onset of inflammatory response = 2-3 wks of continuous therapy

Answer 29

NSAID - Nonselective

Answer 30

NSAID - Nonselective

Answer 31

NSAID - Nonselective topical; minimizes systemic exposure; only for superficial joints (dosing depends on joint); gel solution or patch AE – NSAID specific AE are low; application site dermatitis, pruritus, phototoxicity high association with CV events

Answer 32

NSAID - Nonselective

Answer 33

NSAID - Nonselective

Answer 34

NSAID - Nonselective

Answer 35

NSAID - Nonselective OTC lowest CV risk and low GI risk

Answer 36

NSAID - Nonselective

Answer 37

NSAID - Nonselective

Answer 38

NSAID - Nonselective

Answer 39

NSAID - Nonselective -strong NSAID CI: CV disease, GI risk, peptic ulcer risk, advanced renal impairment, high bleeding risk, contaminant NSAIDs; short term only (max 5 days); only for adults; initiate in office with IM or IV - significant risk of potentially fatal GI adverse events, CV events, acute renal insufficiency; not common for OA (osteoarthritis)

Answer 40

NSAID - Selective COX2 Inhibitor for pts with high risk for GI complications and low risk for CV events - COX2 related: degree of COX2 selectivity dictates CV risk; celecoxib (selective COX2 inhibitor) has strongest association with CV events; diclofenac and ibuprofen have strong association with CV events

Answer 41

Gout Treatment MOA: anti-inflammatory; interferes with migration of neutrophils to sites of inflammation that have been induced by deposits of monosodium urate crystals in synovial fluid; NOT analgesic or uricosuric AE: - common: nausea, vomiting, diarrhea, abdominal pain - more serious: myopathy, bone marrow suppression (neutropenia) - caution: toxicity more likely if renal insufficiency (adjust dose) - low therapeutic index - interactions: p-glycoprotein or strong CYP3A4 inhibitors: clarithromycin, verapamil, ritonavir, cyclopsporine, ranolazine - used to stop attack; do not used for acute attack if already on or if have used colchicine in the last 14 days - only works if given right away (<36 hours); 2/3 of people respond if given within 24 hrs of attack - used to be generic; now only brand name – more expensive, proper labeling and safety data, FDA approved, dosing changed (less used now, just as effective)

Answer 42

Urate Lowering Therapy First Line MOA: both drug and primary metabolite (oxypurinol) reduce uric acid concentrations by inhibiting xanthine oxidase (preventing production of uric acid) - adjust dose based on renal function (cleared by kidneys) - interactions: theophylline (may lower T dose); warfarin (may need to lower W dose); azathioprine (muse reduce Az dose); ampicillin (increased risk of skin rash) - AE: generally well tolerated, nausea, diarrhea - Stevens-Johnson Syndrome: can be caused by a variety of meds; characterized by severe expression of erythema multiforme, top layer of affected skin dies and sheds off, often hospitalized in burn unit, potential for severe morbidity or death, may occur 1-2 weeks after initiation; do not take med again! Allopurinol Hypersensitivity Syndrome: presents as sever desquamating skin lesions, high fever (>39*C), hepatic dysfunction, leukocytosis with predominant eosinophils, renal failure; highest risk in first months; rare (20-25% mortality); screen: HLA BS801 for pts at elevated risk – Koreans with stage 3+ CKD, Han Chinese or Thai descent; do not give allopurinol if AHS history - commonly used - generally effective when titrated properly - oral - half-life: allopurinol – 2-3 hrs; oxypurinol 24 hrs (once daily dosing) - important to give anti-inflammatory (low dose colchicine or NSAID) if initiated during acute attack – rapid uric acid concentration changes can cause crystals, so it is important to prevent inflammation and therefore crystals - dosing: decrease dose if renal impairment, start with low dose, increase 2-5 wks prn and tolerated, titrate dose to reach goal uric acid level (<6mg/dL) or max dose (800 mg daily) - monitor serum uric acid levels (2-5 wks during titration, 6 mo after target is achieved)

Answer 43

Urate Lowering Therapy First Line MOA: xanthine oxidase inhibitor that acts to decrease uric acid; structurally different than allopurinol CI: CrCL <30 – can cause kidney stones AE: nausea arthralgias, rash, transient elevation of hepatic transaminases Monitor: liver function tests (baseline, 2mo, 4mo, periodically) - important to give anti-inflammatory (low dose colchicine or NSAID) during initiation and titration to prevent gout attack - expensive – only use if allopurinol is not tolerated or if additional therapy is needed to reach uric acid goal

Answer 44

Urate Lowering Therapy Alternate MOA: uricosuric; blocks reabsorption of uric acid, increasing its excretion CI: history of urolithiasis or urate nephropathy AE: nausea, fever, rash, hepatic toxicity - less effective as renal function declines; avoid if CrCl <50 - counsel pts to drink a lot of water – reduces risk of stone formation - not recommended for urate overproducers

Answer 45

Urate Lowering Therapy Refractory IV MOA: recombinant form of uricase, an enzyme that exists in nonprimates to convert uric acid into soluble product that is easily excreted AE: gout flares, infusion reactions, anaphylaxis (5%) CI: G6PD deficiency (due to risk of hemolysis and methemoglobinemia; screen for this) - use when other therapies don’t work - reserve for sever gout with tophi or nephropathy that is refractory - $$$

Answer 46

Opioid Use: last resort for OA pain relief AE: - MAJOR ADDICTION POTENTIAL - nausea, constipation, sedation, addiction - respiratory depression/arrest esp at high dose, in combo with other opioids, in combo with alcohol - do not drive - start with low doses and use lowest possible dose for shortest duration possible - APAP combos reduce opioid need (oxy-APAP; hydrocodone-APAP) - reserve for special patients: those who have severe pain; if other options are inadequate; if other conditions make other meds CI (like NSAIDS and renal failure, heart failure, anticoagulation, etc.)

Answer 47

Opioid Use: last resort for OA pain relief AE: - MAJOR ADDICTION POTENTIAL - nausea, constipation, sedation, addiction - respiratory depression/arrest esp at high dose, in combo with other opioids, in combo with alcohol - do not drive - start with low doses and use lowest possible dose for shortest duration possible - APAP combos reduce opioid need (oxy-APAP; hydrocodone-APAP) - reserve for special patients: those who have severe pain; if other options are inadequate; if other conditions make other meds CI (like NSAIDS and renal failure, heart failure, anticoagulation, etc.)

Answer 48

Opioid Use: last resort for OA pain relief AE: - MAJOR ADDICTION POTENTIAL - nausea, constipation, sedation, addiction - respiratory depression/arrest esp at high dose, in combo with other opioids, in combo with alcohol - do not drive - start with low doses and use lowest possible dose for shortest duration possible - APAP combos reduce opioid need (oxy-APAP; hydrocodone-APAP) - reserve for special patients: those who have severe pain; if other options are inadequate; if other conditions make other meds CI (like NSAIDS and renal failure, heart failure, anticoagulation, etc.)

Answer 49

Opioid Use: last resort for OA pain relief AE: - MAJOR ADDICTION POTENTIAL - nausea, constipation, sedation, addiction - respiratory depression/arrest esp at high dose, in combo with other opioids, in combo with alcohol - do not drive - start with low doses and use lowest possible dose for shortest duration possible - APAP combos reduce opioid need (oxy-APAP; hydrocodone-APAP) - reserve for special patients: those who have severe pain; if other options are inadequate; if other conditions make other meds CI (like NSAIDS and renal failure, heart failure, anticoagulation, etc.)

Answer 50

Opioid Use: last resort for OA pain relief AE: - MAJOR ADDICTION POTENTIAL - nausea, constipation, sedation, addiction - respiratory depression/arrest esp at high dose, in combo with other opioids, in combo with alcohol - do not drive - start with low doses and use lowest possible dose for shortest duration possible - APAP combos reduce opioid need (oxy-APAP; hydrocodone-APAP) - reserve for special patients: those who have severe pain; if other options are inadequate; if other conditions make other meds CI (like NSAIDS and renal failure, heart failure, anticoagulation, etc.)

Answer 51

Opioid Use: last resort for OA pain relief AE: - MAJOR ADDICTION POTENTIAL - nausea, constipation, sedation, addiction - respiratory depression/arrest esp at high dose, in combo with other opioids, in combo with alcohol - do not drive - start with low doses and use lowest possible dose for shortest duration possible - APAP combos reduce opioid need (oxy-APAP; hydrocodone-APAP) - reserve for special patients: those who have severe pain; if other options are inadequate; if other conditions make other meds CI (like NSAIDS and renal failure, heart failure, anticoagulation, etc.)

Answer 52

Opioid Use: last resort for OA pain relief AE: - MAJOR ADDICTION POTENTIAL - nausea, constipation, sedation, addiction - respiratory depression/arrest esp at high dose, in combo with other opioids, in combo with alcohol - do not drive - start with low doses and use lowest possible dose for shortest duration possible - APAP combos reduce opioid need (oxy-APAP; hydrocodone-APAP) - reserve for special patients: those who have severe pain; if other options are inadequate; if other conditions make other meds CI (like NSAIDS and renal failure, heart failure, anticoagulation, etc.)

Answer 53

Anti-depressant Use: pain relief in OA

Answer 54

Topical Pain Relief MOA: stimulates the release of a compound believed to be involved in communicating pain between the nerves in the spinal cord and other parts of the body - element of hot pepper - may increase pain during first application before relieving it

Medications Individual Flashcards

(78 cards)