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21 Cards in this Set
- Front
- Back
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Ibuprofen
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Class: NSAID
MOA: Competitive Inhibitors of COX 1 (Cyclooxygenase), COX2, the enzyme that converts Aas to PGs - some NSAIDS are selective for one isoform Indications: Analgesic for acute pain, Reduce inflammation (takes several days or weeks), Antipyretic, chronic inflammatory diseases (rheumatoid arthritis, lupus, osteoarthritis) Effects: Pre-medication - can pre-medicate with NSAIDS to prevent release of prostaglandins (not stored, released as needed), "Ceiling effect" - There is a maximal effect of NSAIDS because PGs are not the only mediators of inflammation, doses above daily limit lead to renal damage and impairment, COX-2 Inhibitors COX2 catalyses the reaction of AA to PGs that not only cause pain and inflammation, but also PGs that are cardioprotective, Adverse: There is a maximal effect of NSAIDS because PGs are not the only mediators of inflammation. Doses above the daily limits lead to renal damage and impairment. GI upset - All NSAIDS inhibit COX1, which produces PGs that protect GI tissue from protons, Renal Function - renal function is partly dependent on PG synthesis, COX2 inhibitors increase the risk of MI Contraindications: Allergy to NSAIDS, nasal polyps, angioedema, Lithium (seizures), GI bleeding or ulcers, Impaired renal function or renal disease, Pregnancy |
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Aspirin
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Class: Salicylate (a unique NSAID)
MOA: The only NSAID that irreversibly inhibits COX by acetylating serine 530 in the active site, An example of a covalent bond mechanism Indications: Acute pain, max = 4 gms, Rheumatoid arthritis, Fever, Anticoagulation post MI, Prevention of MI in M over 40, Prevention of stroke in F over 40 Effects: Mechanism of platelet inhibition: Prostaglandins (precursor of thromboxane A2), TA2 (inducer of platelet aggregation), platelets (no nucleus, cannot synthesize TA2 for entire lifetime), Adverse: GI upset -COX1 PGs that are involved in the production of mucous protective barrier against stomach acid (protons) Bleeding - COX enzyme is completely inhibited because of the covalent bond mechanism of prostaglandin inhibition, Prostaglandins are precursors of thromboxane A2, Thromboxane A2 is an inducer of platelet aggregation, Platelets - No nucleus, Cannot synthesize TA2 for their entire 10 day lifetime Contraindications: Impaired Renal Function - COX 1 and COX2 PGs reduce water and Na2+ reabsorption at the ascending loop of Henle and maintain dilation of the renal vasculature Gouty arthritis (Competition between uric acid and salicylate in the secretion site in the kidney), Raises or lowers glucose concentrations in the blood, Pregnancy - high doses are teratogenic Asthma- Leukotriene pathway Hypo-coagulation states - bleeding Ulcers or Gastroesophageal reflux disease (GERD), Impaired renal function or renal disease, Pregnancy (doubles the risk for miscarriage in early pregnancy), Allergy to salicylates or NSAIDS aspirin induced asthma, nasal polyps, angioedema Reye’s Syndrome - Children under 16 yo, Viral Infection, Metabolic encephalopathy, liver disease, 80-90 % cases result in death, Symptoms: Delirium, Seizures, Deep coma, Brainstem dysfunction, Even with treatment mortality rate ≈ 30 %, Survivors: permanent brain damage Salicylate Intolerance - Symptoms range from rhinitis to severe asthma, Up to 20 % of patients with, Asthma, Usually intolerant to other NSAIDS, Bronchiole constriction because of more leukotrienes Interactions : Warfarin (increase liklihood of bleeding) Insulin, sulfonylureas (enhanced hypoglycemic effect) Methotrexate, phenytoin, valproic acid (decreases renal clearance, increased risk of toxicity) Drugs for gout (decreased uricosuric effects, exacerbates gout) ACE inhibitors, β blockers, diuretics (decreased antihypertensive effects) ASA and NSAIDS interaction - Low dose ASA therapy for the anti-platelet effect, Competitive inhibtion of the acetylation site of COX in the platelet, Ibuprofen interferes with ASA binding, Ibuprofen leaves the site, but ASA will be excreted because of its short half-life FDA recommends acetaminophen instead of NSAIDS when treating patients for pain who use ASA for anti-platelet effect Increased toxicity - Lithium (Seizures), Digoxin, Cyclosporine, Methotrexate-high dose used in chemo, Oral hypoglycemic Increased risk of GI Bleeding – EtOH Increased Risk of Bleeding – SSRIs, Anticoagulants Antihypertensive drugs whose actions depend on renal prostaglandins - No more than 4 days of treatment of the NSAID Dental: stopping aspirin in patients with heart disease is not recommended |
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Acetaminophen (Tylenol)
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Class: Acetaminophen
MOA: Possibly an inhibitor of CNS COX, Maybe activation of spinal serotonergic pathways, Maybe inhibtion of nitric oxide synthase, NOT an anti-inflammatory Indications: Pain reliever in patients that cannot take/tolerate ASA or NSAIDS, Ulcer, Asthma, Diabetes, Gout, Children under 16 y/o, Hypo-coagulation states Effects: relief of pain (chronic or acute) Adverse: Hepatotoxicity - At doses > 4 g/day, Alklyation of liver proteins, Nausea and jaundice, Suicide attempts, Accidental overdoses are common because it is an ingredient in many OTC drug combinations Phase 1 (up to 24 hours) - anorexia, nausea, vomiting Phase 2 (24-48 hours) - right upper quadrant pain and tenderness, transaminase elevation Phase 3 (3-4 days) - jaundice, bleeding, encephalopathy, death from cerebral edema Phase 4 (4-14 days) - complete recovery of liver function or death Treatment of Toxicity - Gastric lavage, N – acetylcystine (NAC) – converted to cysteine, which can replenish glutathione stores, detoxifies NAPQI nontoxic metabolites, provide a substrate for sulfation, thereby increasing the capacity for nontoxic metabolism In January of 2014 all tablets and capsules will contain no more than 325 mg of acetaminophen. Contraindications - Liver Disease (proteins are already compromised), Hepatitis (inflammation), Alcoholism (typically have less glutathione) Interactions: Drugs that induce liver enzymes increase toxicity of acetaminophen Increased hepatoxicity - Ethanol, Isoniazid (Nydrazid), phenytoin (Dilantin), carbamazepine (Tegretol) Zidovudine (Retrovir)-reduces zidovudine metabolism resulting in increased bone marrow toxicity Alcohol - P4502E1 metabolizes EtOH, is induced by EtOH, and its preferred substrate is EtOH EtOH is an inhibitor of P4502E1. Chronic ingestion causes a gradual increase in the concentration of P4502E1. Stop EtOH, enzyme is available to transform APAP to toxic metabolite NAPQI |
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Codeine
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Class: Opioid (C-II)
MOA: G-couple protein receptor, Receptor conformation changes, GDP goes to GTP, Activates G-α complex ↓ adenyl cyclase - inhibits Ca conductance, activates K conductance, inhibition of substance P and glutamate release, Hyperpolarization of neurons - make more difficult to excite, Pain seems very distant Indications: mild to moderate pain Effects: analgesia, Cough Suppression-cause depression in the cough center in the medulla in the brain Dextromethorphan (Robitussin), GI tract- increase muscle tone loperamide (Imodium) and diphenoxylate (Lomotil) Opioid induced analgesia involves the sensory-discriminative and the motivational-affective components of pain. More effective against continuous dull aching pain than sharp intermittent pain. Pain is still present but not discomforting Adverse: Moderate addition potential Respiratory Depression- decrease the response of the brainstem respiratory centers to the CO2 tension in the blood, Nausea and Vomiting- directly stimulate the chemo-receptor trigger zone in the medulla, Drowsiness- hyperpolarization of neurons, Constipation- increase smooth muscle tone and decrease propulsive motility, Higher risk of fracture in older adults with short acting and in the first few days of therapy Contraindications: Impaired pulmonary function, Head injuries-CO2 retention results in cerebral vasodilation, Endocrine Disease-prolonged and exaggerated responses to opiates, Hepatic Function Impairment, Seizure Disorders, Pregnancy, History of drug abuse, alcoholism Interactions: Any drug that causes CNS depression – Anticholinergics, Antidepressants, Antihistamines, Sedatives, Alcohol, Benzodiazepines |
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Hydrocodone
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Class: Opioid (C-II)
MOA: G-couple protein receptor, Receptor conformation changes, GDP goes to GTP, Activates G-α complex ↓ adenyl cyclase - inhibits Ca conductance, activates K conductance, inhibition of substance P and glutamate release, Hyperpolarization of neurons - make more difficult to excite, Pain seems very distant Indications: mild to moderate pain Effects: analgesia, Cough Suppression-cause depression in the cough center in the medulla in the brain Dextromethorphan (Robitussin), GI tract- increase muscle tone loperamide (Imodium) and diphenoxylate (Lomotil) Opioid induced analgesia involves the sensory-discriminative and the motivational-affective components of pain. More effective against continuous dull aching pain than sharp intermittent pain. Pain is still present but not discomforting Adverse: Moderate addition potential Respiratory Depression- decrease the response of the brainstem respiratory centers to the CO2 tension in the blood, Nausea and Vomiting- directly stimulate the chemo-receptor trigger zone in the medulla, Drowsiness- hyperpolarization of neurons, Constipation- increase smooth muscle tone and decrease propulsive motility, Higher risk of fracture in older adults with short acting and in the first few days of therapy Contraindications: Impaired pulmonary function, Head injuries-CO2 retention results in cerebral vasodilation, Endocrine Disease-prolonged and exaggerated responses to opiates, Hepatic Function Impairment, Seizure Disorders, Pregnancy, History of drug abuse, alcoholism Interactions: Any drug that causes CNS depression – Anticholinergics, Antidepressants, Antihistamines, Sedatives, Alcohol, Benzodiazepines |
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Tramadol
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Class: Non-opioid centrally acting analgesic
MOA: Weak μ receptor agonist, Inhibits reuptake of norepi and serotonin Indications: pain Effects: Dependence liability is low, Not a scheduled drug Adverse: N+V, drowsiness |
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NSAIDs
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Class: NSAIDs
MOA: Competitive Inhibitors of COX 1 (Cyclooxygenase), COX2, the enzyme that converts Aas to PGs - some NSAIDS are selective for one isoform Indications: Analgesic for pain, Reduce inflammation, Antipyretic, Celebrex is only COX-2 on the market - used for artthritis Effects: Pre-medication - can pre-medicate with NSAIDS to prevent release of prostaglandins (not stored, released as needed), "Ceiling effect" - There is a maximal effect of NSAIDS because PGs are not the only mediators of inflammation, doses above daily limit lead to renal damage and impairment, COX-2 Inhibitors COX2 catalyses the reaction of AA to PGs that not only cause pain and inflammation, but also PGs that are cardioprotective, Adverse: GI upset - All NSAIDS inhibit COX1, which produces PGs that protect GI tissue from protons, Renal Function - renal function is partly dependent on PG synthesis, COX2 inhibitors increase the risk of MI Contraindications - Allergy to salicylates or NSAIDS - aspirin induced asthma, nasal polyps, angioedema, Lithium (seizures), GI bleeding or ulcers, Impaired renal function or renal disease, Pregnancy |
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Celebrex
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Class: NSAID (COX-2 selective)
MOA: Inhibits prostaglandin synthesis by decreasing the activity of the enzyme, cyclooxygenase-2 (COX-2), which results in decreased formation of prostaglandin precursors; has antipyretic, analgesic, and anti-inflammatory properties. Celecoxib does not inhibit cyclooxygenase-1 (COX-1) at therapeutic concentrations. Indications: Can be used for acute flare-ups in patients who cannot tolerate ibuprofen or other NSAIDs because of ulcers or GERD. Also, relief of signs and symptoms of osteoarthritis, ankylosing spondylitis, JIA, rheumatoid arthritis, acute pain Effects: antipyretic, analgesic, anti-inflammatory Adverse: |
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Tizanidine (Zanaflex)
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Class: Muscle relaxant – CNS depressant
MOA: α2 receptor agonist that inhibits the release of norepi (inverse agonist) Indications: acute painful muscle conditions of local origin (used with physical therapy, ice, moist heat) Effects: Blocks sympathetic mediated pain, Anti-depressant and sedative properties related to pain relief Adverse: Dry mouth, somnolence, dizziness, orthostatic hypotension, Can lower HR and BP: vital signs monitored during therapy Interactions - CNS depressants Metabolized in liver, baseline liver enzyme levels needed before beginning and during treatment |
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Cyclobenzaprine (Flexeril)
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Class: Muscle relaxant – CNS depressant
MOA: Unknown, may be related to TCA-like structure Indications: acute painful muscle conditions of local origin (used with physical therapy, ice, moist heat) Effects: Muscle relaxation related to antidepressant effects or to normalization of quality of sleep Adverse: Tachycardia, contraindicated in heart disease and elderly patients Interactions - CNS depressants |
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Metaxalone (Skelaxin)
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Class: Muscle relaxant – CNS depressant
MOA: ? - acts on the medulla Indications: acute painful muscle conditions of local origin (used with physical therapy, ice, moist heat) Effects: Anticholinergic and analgesic effects, may not have direct muscle relaxing effects Adverse: Drowsiness, sedation Interactions - CNS depressants Contraindicated - glaucoma, myasthenia gravis, ulcer, angina |
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Steroids
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Steroids
Class: Steroid MOA: 2 Mechanisms – AP-1and NF-κB, Bind and ↓ actions directly through protein-protein interactions, ↑ expression of glucocorticoid induced leucine zipper proteins (GILZ), High concentrations And Chromatin Remodeling of anti-inflammatory genes and pro-inflammatory genes Indications: Preoperative antimicrobial prophylaxis, suppression of signs of inflammation Effects: inhibition of accumulation of macrophages and leukocytes, phagocytosis, lysosomal enzyme release, release of chemical mediators of inflammation Adverse: Must wean of therapeutic dose (even for short duration therapy) – withdrawal symptoms include Joint pain, Muscle pain, Fatigue, Fever, Nausea and vomiting Fluid and Electrolyte - Sodium and fluid retention, CHF, HTN and potassium loss Musculoskeletal - Loss of muscle mass, Osteoporosis, Compression fractures GI - Peptic ulcer, Pancreatitis, Ulcerative esophagitis Dermatologic - impaired and delayed wound healing, Thin fragile skin Neurologic – Convulsions, Vertigo, Headache Endocrine - Development of Cushing's state, Secondary adrenocortical and pituitary, unresponsiveness, Diabetes Ophthalmic – Cataracts, Glaucoma Adrenal insufficiency – increase dose to compensate (Dexamethasone Injection – if pt has relief from pain in the 1st or 2nd week of oral therapy. Dose for a small joint is 0.8 to 1 mg. It does cause tissue degeneration. Only give once.) |
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Amitriptyline (Elavil)
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Class: TCA
MOA: NE and serotonin reuptake inhibitors. Also block muscarinic receptors and α1 adrenergic receptors. Indications: Effects: TCAs downregulate 5-HT2 receptors, Act within a few days, Dose for chronic pain is 10 mg qhs, Anticholinergic adverse effects lead to discontinuation of drug Adverse: Anticholinergic, dry mouth, constipation and urinary retention, sedation. Also cause hypotension and compensatory tachycardia, contraindicated in heart disease Cardiotoxicity is a concern in the elderly Interactions: Increased anticholinergic effects of antihistamines and muscarinic blockers, Increased effects of direct acting sympathomimetics, like epinephrine, IUSD Clinics-epi with TCA used “with restraint and caution,” CNS depressants |
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Duloxetine (Cymbalta)
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Class: SNRI
MOA: NE and serotonin reuptake inhibitor Indications: chronic pain, depression Effects: Adverse: Nausea, constipation, fatigue, drowsiness, dry mouth 5-15% Many drug interactions (the most) |
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Gabapentin (Neurontin)
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Class: Anticonvulsant
MOA: Interacts with voltage dependent Ca2+ channels to reduce activity Indications: migraine, trigeminal neuralgia, diabetic neuropathy and peripheral neuropathy Effects: Therapeutic window is wide: 8 gms/day Adverse: fatigue, dizziness, headache, nausea |
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Carbamazepine (Tegretol)
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Class: anticonvulsant
MOA: Sodium channel blocker inhibiting repetitive neuronal discharge Indications: neuropathic pain, trigeminal neuralgia, and is used for headache Effects: Induces P4503A4 Adverse: Lab values for liver function, blood count and platelets before starting and during therapy |
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Pregabalin (Lyrica)
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Class: Anticonvulsant
MOA: Binds to alpha2-delta subunit of voltage-gated calcium channels Indications: Effects: Inhibits excitatory neurotransmitter release Adverse: May decrease platelet count, Xerostomia up to 15 %, CNS depression |
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Ketamine Patch
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Class: General anesthetic
MOA: Inhibits NMDA receptor activity in the dorsal horn. NMDA activity is present in areas of nerve damage Indications: Induction and maintenance of general anesthesia Effects: sedation Adverse: Not available orally, only IM, IV or Patch |
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Capsaicin
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Class: Topical analgesic
MOA: Reduces C-fiber activity Indications: temporary relief of minor pain, management of PHN, temp relief of pain associated with diabetic neuropathy, topical relief in burning mouth syndrome and oral mucositis Effects: Initially causes a burning sensation, but goes away with time. Available in 0.025 % cream to be applied 5-6 x’s per day Adverse: Erythemia, pain |
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Lidoderm
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Class: Topical analgesic (lidocaine in a patch form)
MOA: Blocks both the initiation and conduction of nerve impulses by decreasing the neuronal membrane's permeability to sodium ions, which results in inhibition of depolarization with resultant blockade of conduction Indications: herpetic lesions, shingles Effects: temporary relief of pain Adverse: |
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Sumatriptan (Imitrex)
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Class: Serotonin 5-HT 1B/1D receptor agonists
MOA: Blocks the release of substance P. Selective agonist for serotonin (5-HT1B and 5-HT1Dreceptors) in cranial arteries; causes vasoconstriction and reduces neurogenic inflammation associated with antidromic neuronal transmission correlating with relief of migraine Indications: Migraine Effects: relief of nausea. Available as PO, IV, nasal spray Adverse: |
