Medications Individual Flashcards
Albuterol
Short Acting Beta Agonist (SABA) - bronchodilator
MOA: relax airway smooth muscle by direct stimulation of B2 receptors in airway; increase clearance and transport of mucus in airways; stabilize mast cell membranes
AE: tachycardia, tremor, hypokalemia, palpitations, sleep disturbances (more likely in high dose LABAs)
- most effective agent for reversing acute airway obstruction caused by bronchoconstriction
- best at bronchodilating
- 1st line for acute asthma, chronic asthma symptoms, and preventing exercise induced bronchospasm
- used for rescue prn use in COPD
- onset 5 min
- dosed 1-2 puffs per 4-6 hrs
- delivery: inhaler or nebulizer
Lebalbuterol
Short Acting Beta Agonist (SABA) - bronchodilator
- marketed as having fewer side effects as and being more effective than Albuterol, but they are equal
- R-enantiomer of albuterol
MOA: relax airway smooth muscle by direct stimulation of B2 receptors in airway; increase clearance and transport of mucus in airways; stabilize mast cell membranes
AE: tachycardia, tremor, hypokalemia, palpitations, sleep disturbances (more likely in high dose LABAs)
- most effective agent for reversing acute airway obstruction caused by bronchoconstriction
- best at bronchodilating
- 1st line for acute asthma, chronic asthma symptoms, and preventing exercise induced bronchospasm
- used for rescue prn use in COPD
- onset 5 min
- dosed 1-2 puffs per 4-6 hrs
- delivery: inhaler or nebulizer
Terbutaline
Short Acting Beta Agonist (SABA) - bronchodilator
MOA: relax airway smooth muscle by direct stimulation of B2 receptors in airway; increase clearance and transport of mucus in airways; stabilize mast cell membranes
AE: tachycardia, tremor, hypokalemia, palpitations, sleep disturbances (more likely in high dose LABAs)
- most effective agent for reversing acute airway obstruction caused by bronchoconstriction
- best at bronchodilating
- 1st line for acute asthma, chronic asthma symptoms, and preventing exercise induced bronchospasm
- used for rescue prn use in COPD
- onset 5 min
- dosed 1-2 puffs per 4-6 hrs
- delivery: inhaler or nebulizer
Salmeterol
Long Acting Beta Agonist (LABA) - bronchodilator
MOA: relax airway smooth muscle by direct stimulation of B2 receptors in airway; increase clearance and transport of mucus in airways; stabilize mast cell membranes
AE: tachycardia, tremor, hypokalemia, palpitations, sleep disturbances (more likely in high dose LABAs)
- NOT FOR MONOTHERAPY IN CHRONIC ASTHMA- increased risk of severe exacerbation and death
- many in combination with ICS
- 12-24 hr duration; decrease to 5 hr in chronic use
- Onset: salmeterol – 30 min
- delivery: inhaler (alone or w/ ICS) or nebulizer
Formeterol
Long Acting Beta Agonist (LABA) - bronchodilator
MOA: relax airway smooth muscle by direct stimulation of B2 receptors in airway; increase clearance and transport of mucus in airways; stabilize mast cell membranes
AE: tachycardia, tremor, hypokalemia, palpitations, sleep disturbances (more likely in high dose LABAs)
- NOT FOR MONOTHERAPY IN CHRONIC ASTHMA- increased risk of severe exacerbation and death
- many in combination with ICS
- 12-24 hr duration; decrease to 5 hr in chronic use
- Onset:formoterol – 5 min (not approved for SABA)
- delivery: inhaler (alone or w/ ICS) or neb
Indacaterol
Long Acting Beta Agonist (LABA) - bronchodilator
MOA: relax airway smooth muscle by direct stimulation of B2 receptors in airway; increase clearance and transport of mucus in airways; stabilize mast cell membranes
AE: tachycardia, tremor, hypokalemia, palpitations, sleep disturbances (more likely in high dose LABAs)
- NOT FOR MONOTHERAPY IN CHRONIC ASTHMA- increased risk of severe exacerbation and death
- longer lasting
- many in combination with ICS
- 12-24 hr duration; decrease to 5 hr in chronic use
- delivery: inhaler (alone or w/ ICS) or nebulizer
Olodaterol
Long Acting Beta Agonist (LABA) - bronchodilator
MOA: relax airway smooth muscle by direct stimulation of B2 receptors in airway; increase clearance and transport of mucus in airways; stabilize mast cell membranes
AE: tachycardia, tremor, hypokalemia, palpitations, sleep disturbances (more likely in high dose LABAs)
- NOT FOR MONOTHERAPY IN CHRONIC ASTHMA- increased risk of severe exacerbation and death
- longer lasting
- many in combination with ICS
- 12-24 hr duration; decrease to 5 hr in chronic use
- delivery: inhaler (alone or w/ ICS) or nebulizer
Vilanterol
Long Acting Beta Agonist (LABA) - bronchodilator
MOA: relax airway smooth muscle by direct stimulation of B2 receptors in airway; increase clearance and transport of mucus in airways; stabilize mast cell membranes
AE: tachycardia, tremor, hypokalemia, palpitations, sleep disturbances (more likely in high dose LABAs)
- NOT FOR MONOTHERAPY IN CHRONIC ASTHMA- increased risk of severe exacerbation and death
- longer lasting
- many in combination with ICS
- 12-24 hr duration; decrease to 5 hr in chronic use
- delivery: inhaler (alone or w/ ICS) or nebulizer
Arformoterol
Long Acting Beta Agonist (LABA) - bronchodilator
MOA: relax airway smooth muscle by direct stimulation of B2 receptors in airway; increase clearance and transport of mucus in airways; stabilize mast cell membranes
AE: tachycardia, tremor, hypokalemia, palpitations, sleep disturbances (more likely in high dose LABAs)
- NOT FOR MONOTHERAPY IN CHRONIC ASTHMA- increased risk of severe exacerbation and death
- longer lasting
- many in combination with ICS
- 12-24 hr duration; decrease to 5 hr in chronic use
- delivery: inhaler (alone or w/ ICS) or nebulizer
Ipratropium bromide
Inhaled Anticholinergics
MOA: anti-inflammatory; inhibit the effects of acetylcholine on muscarinic receptors in airways = causes bronchodilation; protect against cholinergic-mediated bronchoconstriction; may decrease mucus secretion
AE: dry mouth; blurred vision, urinary retention, metallic taste, constipation, tachycardia, precipitation of narrow-angle glaucoma, urinary retention, increased CV events
CI: cardiovascular disease
- delivery: inhaler and nebulizer (ipratropium)
- onset: ipratropium – 15 min (too slow for rescue med; tiotropium – 30 min; aclidinium < 30 min
- duration: ipratropium 4-8 hrs
Tiotropium bromide
Inhaled Anticholinergics
MOA: anti-inflammatory; inhibit the effects of acetylcholine on muscarinic receptors in airways = causes bronchodilation; protect against cholinergic-mediated bronchoconstriction; may decrease mucus secretion
AE: dry mouth; blurred vision, urinary retention, metallic taste (ipratropium), constipation, tachycardia, precipitation of narrow-angle glaucoma, urinary retention
CI: cardiovascular disease
- longer lasting
- delivery: inhaler
- onset: tiotropium – 30 min
- duration: tiotropium > 24 hr
Aclidinium bromide
Inhaled Anticholinergics
MOA: anti-inflammatory; inhibit the effects of acetylcholine on muscarinic receptors in airways = causes bronchodilation; protect against cholinergic-mediated bronchoconstriction; may decrease mucus secretion
AE: dry mouth; blurred vision, urinary retention, constipation, tachycardia, precipitation of narrow-angle glaucoma, urinary retention, increased CV events
CI: cardiovascular disease
- delivery: inhaler
- onset: aclidinium < 30 min
- duration: aclidinium < 24 hrs
Umeclidinium bromide
Inhaled Anticholinergics
MOA: anti-inflammatory; inhibit the effects of acetylcholine on muscarinic receptors in airways = causes bronchodilation; protect against cholinergic-mediated bronchoconstriction; may decrease mucus secretion
AE: dry mouth; blurred vision, urinary retention, constipation, tachycardia, precipitation of narrow-angle glaucoma, urinary retention, increased CV events
CI: cardiovascular disease
- longer lasting
- delivery: inhaler
Glycopyrrolate
Inhaled Anticholinergics
MOA: anti-inflammatory; inhibit the effects of acetylcholine on muscarinic receptors in airways = causes bronchodilation; protect against cholinergic-mediated bronchoconstriction; may decrease mucus secretion
AE: dry mouth; blurred vision, urinary retention, constipation, tachycardia, precipitation of narrow-angle glaucoma, urinary retention, increased CV events
CI: cardiovascular disease
- delivery: inhaler
Theophyline
Methylxanthines
MOA: anti-inflammatory and causes bronchodilation by inhibiting phosphodiesterase and antagonizing adenosine; act as a bronchodilator at high concentrations; anti-inflammatory effect at low concentrations
AE: heartburn, restlessness, insomnia, irritability, tachycardia, tremor; with increased dose: nausea, vomiting, seizures, arrhythmias
Target Serum Concentration: 5-15 mg/L
<10 little bronchodilation (more anti-inflammatory)
10-20 bronchodilation
> 15 increased adverse effects (headache, nausea, vomiting, insomnia)
> 20 more serious AE (cardiac arrhythmias, seizures)
CI: many drug interactions (metabolized by CYP1A2, CYP2W1, and CYP3A4) – alcohol, ciprofloxacin, diltiazem, erythromycin, oral contraceptives, phenytoin, propranolol, verapamil
- narrow therapeutic index; life-threatening toxicity
- only for pts who cannot use inhaled meds or if symptomatic despite appropriate use of inhaled meds
- non-linear pharmacokinetics: drug changes, drug interactions, hepatic function, tobacco increases clearance (smokers need higher dose)
Beclomethasone
Inhaled Corticosteroids
MOA: decrease airway inflammation, attenuate airway hyperresponsiveness, minimize mucus production/secretion, improve response to beta 2 agonists
AE: local: oralpharyngeal candidiasis (thrush); cough; dysphonia (hoarse voice; decreases with decreased dose); systemic: reduced linear growth (1/2 cm per year), increased pneumonia
CI: potent CYP34A inhibitors (ritonavir, itraconazole, ketoconazole, etc) + high doses of ICS causes Cushing syndrome and adrenal insufficiency
- smoking decrease response – need higher dose
- onset: 12 hours; 2+ weeks for max effect
- many used in combination with LABAs
- variability in response: age, genetics, smoking (need higher dose), race
- abrupt discontinuation leads to exacerbations
Budesonide
Inhaled Corticosteroids
MOA: decrease airway inflammation, attenuate airway hyperresponsiveness, minimize mucus production/secretion, improve response to beta 2 agonists
AE: local: oralpharyngeal candidiasis (thrush); cough; dysphonia (hoarse voice; decreases with decreased dose); systemic: reduced linear growth (1/2 cm per year), increased pneumonia
CI: potent CYP34A inhibitors (ritonavir, itraconazole, ketoconazole, etc) + high doses of ICS causes Cushing syndrome and adrenal insufficiency
- smoking decrease response – need higher dose
- onset: 12 hours; 2+ weeks for max effect
- many used in combination with LABAs
- variability in response: age, genetics, smoking (need higher dose), race
- abrupt discontinuation leads to exacerbations
Ciclesonide
Inhaled Corticosteroids
MOA: decrease airway inflammation, attenuate airway hyperresponsiveness, minimize mucus production/secretion, improve response to beta 2 agonists
AE: local: oralpharyngeal candidiasis (thrush); cough; dysphonia (hoarse voice; decreases with decreased dose); systemic: reduced linear growth (1/2 cm per year), increased pneumonia
CI: potent CYP34A inhibitors (ritonavir, itraconazole, ketoconazole, etc) + high doses of ICS causes Cushing syndrome and adrenal insufficiency
- smoking decrease response – need higher dose
- onset: 12 hours; 2+ weeks for max effect
- many used in combination with LABAs
- variability in response: age, genetics, smoking (need higher dose), race
- abrupt discontinuation leads to exacerbations
Flunisolide
Inhaled Corticosteroids
MOA: decrease airway inflammation, attenuate airway hyperresponsiveness, minimize mucus production/secretion, improve response to beta 2 agonists
AE: local: oralpharyngeal candidiasis (thrush); cough; dysphonia (hoarse voice; decreases with decreased dose); systemic: reduced linear growth (1/2 cm per year), increased pneumonia
CI: potent CYP34A inhibitors (ritonavir, itraconazole, ketoconazole, etc) + high doses of ICS causes Cushing syndrome and adrenal insufficiency
- smoking decrease response – need higher dose
- onset: 12 hours; 2+ weeks for max effect
- many used in combination with LABAs
- variability in response: age, genetics, smoking (need higher dose), race
- abrupt discontinuation leads to exacerbations
Fluticasone
Inhaled Corticosteroids
MOA: decrease airway inflammation, attenuate airway hyperresponsiveness, minimize mucus production/secretion, improve response to beta 2 agonists
AE: local: oralpharyngeal candidiasis (thrush); cough; dysphonia (hoarse voice; decreases with decreased dose); systemic: reduced linear growth (1/2 cm per year), increased pneumonia
CI: potent CYP34A inhibitors (ritonavir, itraconazole, ketoconazole, etc) + high doses of ICS causes Cushing syndrome and adrenal insufficiency
- smoking decrease response – need higher dose
- onset: 12 hours; 2+ weeks for max effect
- many used in combination with LABAs
- variability in response: age, genetics, smoking (need higher dose), race
- abrupt discontinuation leads to exacerbations
Mometasone
Inhaled Corticosteroids
MOA: decrease airway inflammation, attenuate airway hyperresponsiveness, minimize mucus production/secretion, improve response to beta 2 agonists
AE: local: oralpharyngeal candidiasis (thrush); cough; dysphonia (hoarse voice; decreases with decreased dose); systemic: reduced linear growth (1/2 cm per year), increased pneumonia
CI: potent CYP34A inhibitors (ritonavir, itraconazole, ketoconazole, etc) + high doses of ICS causes Cushing syndrome and adrenal insufficiency
- smoking decrease response – need higher dose
- onset: 12 hours; 2+ weeks for max effect
- many used in combination with LABAs
- variability in response: age, genetics, smoking (need higher dose), race
- abrupt discontinuation leads to exacerbations
Prednisone
Systemic (oral) Corticosteroids
MOA: decrease airway inflammation, attenuate airway hyperresponsiveness, minimize mucus production/secretion, improve response to beta 2 agonists
AE: adrenal suppression, decreased bone mineral density, skin thinning, cataracts, easy bruising, steroid myopathy, insomnia, increased appetite, agitation/ irritation; weight gain (longer term)
- used in acute exacerbation of asthma of asthma or COPD; only used longer-term in serious cases
- onset: 4-12 hours; start early in exacerbation, continue for 3-10 days
- taper only necessary if used long-term
- avoid long-term use
Prednisolone
Systemic (oral) Corticosteroids
MOA: decrease airway inflammation, attenuate airway hyperresponsiveness, minimize mucus production/secretion, improve response to beta 2 agonists
AE: adrenal suppression, decreased bone mineral density, skin thinning, cataracts, easy bruising, steroid myopathy, insomnia, increased appetite, agitation/ irritation; weight gain (longer term)
- used in acute exacerbation of asthma of asthma or COPD; only used longer-term in serious cases
- onset: 4-12 hours; start early in exacerbation, continue for 3-10 days
- taper only necessary if used long-term
- avoid long-term use
Methyprednisolone
Systemic (oral) Corticosteroids
MOA: decrease airway inflammation, attenuate airway hyperresponsiveness, minimize mucus production/secretion, improve response to beta 2 agonists
AE: adrenal suppression, decreased bone mineral density, skin thinning, cataracts, easy bruising, steroid myopathy, insomnia, increased appetite, agitation/ irritation; weight gain (longer term)
- used in acute exacerbation of asthma of asthma or COPD; only used longer-term in serious cases
- onset: 4-12 hours; start early in exacerbation, continue for 3-10 days
- taper only necessary if used long-term
- avoid long-term use
Montelukast
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
Zileuton
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)
Zafirlukast
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)
Omalizumab
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
Roflumilast
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
Cromolyn
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
Nicotine Gum
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
Nicotine Inhaler
Nicotine Replacement Product
AE: irritation of mouth and throat, mild coughing, stomach discomfort
- prescription/expensive
Nicotine Lozenge
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
Nicotine Nasal Spray
Nicotine Replacement Product
AE: irritation in the nasal passages and throat, runny nose
- prescription/expensive
Nicotine Patch
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
Bupropion SR
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
Varenicline
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
Methotrexate
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
Hydroxychloroquine
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
Sulfasalazine
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
Leflunomide
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
Infliximab
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
Adalimumab
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
Golimumab
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
Etanercept
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
Certolizumab
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
Abatacept
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
Rituximab
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
Tocilizumab
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
Tofacitinib
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
Acetaminophen
- 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
Aspirin
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
Solsalate
NSAID - Nonselective
Etodolac
NSAID - Nonselective
Diclofenac
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
Indomethacin
NSAID - Nonselective
Nabumetone
NSAID - Nonselective
Ibuprofen
NSAID - Nonselective
Naproxen
NSAID - Nonselective
OTC
lowest CV risk and low GI risk
Meloxicam
NSAID - Nonselective
Prioxicam
NSAID - Nonselective
Sulindac
NSAID - Nonselective
Kerorolac
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)
Celecoxib
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
Colchicine
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)
Allopurinol
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)
Febuxotat
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
Probenecid
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
Pegloticase
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
- $$$
Oxycodone
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.)
Hydrocodone
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.)
Methadone
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.)
Hydromorphone
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.)
Fentanyl
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.)
Tramadol
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.)
Codeine
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.)
Duloxetine
Anti-depressant
Use: pain relief in OA
Capsaicin
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
