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Clinical Pharmacology - Analgesics
Clinical Pharmacology - Analgesics
Clinical Pharmacology - Analgesics
Clinical Pharmacology - Analgesics
Clinical Pharmacology - Analgesics
Clinical Pharmacology - Analgesics
Clinical Pharmacology - Analgesics
Clinical Pharmacology - Analgesics
Clinical Pharmacology - Analgesics
Clinical Pharmacology - Analgesics
Clinical Pharmacology - Analgesics
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Clinical Pharmacology - Analgesics
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Clinical Pharmacology - Analgesics
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Clinical Pharmacology - Analgesics
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Clinical Pharmacology - Analgesics
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Clinical Pharmacology - Analgesics
Clinical Pharmacology - Analgesics
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Clinical Pharmacology - Analgesics

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  • 1. Clinical Analgesia Clinical Pharmacology PAC 5407 Steve Sager, MPAS, PA-C
  • 2. Objectives Identify non-narcotic and narcotic analgesics by their generic and brand name List appropriate clinical applications for non-narcotic and narcotic analgesics List the different modalities for pain management Write an error free prescription for a non- narcotic and a narcotic analgesic
  • 3. Quiz question #1 Induction of a conformation change in the receptor such that the agonist no longer ―recognizes‖ the agonist binding site is accomplished by which of the following? 1. Non-competitive antagonist 0% 2. Irreversible antagonist 0% 3. Competitive antagonist 0% 4. Partial agonist 0% 5. Inverse agonist 0%
  • 4. Quiz question #2 The concentration of the drug which induces a specified clinical effect in 50% of subjects is called the ____________. 1. Lethal Dose 50% 0% 2. Toxic dose 50% 0% 3. Effective dose 50% 0% 4. Therapeutic index 0% 5. Affinity 0%
  • 5. Quiz question #3 Which of the following statements concerning pharmacodynamics is incorrect? In general, as dose increases, concentration of drug at 1. 0% receptor sites increases The pharmacological response to a drug is proportional 2. 0% to the number of drug receptor interactions that occur The concentration of a drug at the receptor sites 3. 0% determines number of receptors occupied by drug An antagonist is a drug that occupies and activates a 0% 4. receptor, thereby producing a cellular response 0% There are a finite number of receptors on the surface 5. of any given cell
  • 6. PAIN
  • 7. PAIN ―Good‖ Pain (first pain) – mild pain in response to a noxious stimulus ―Bad‖pain (secondary pain) – severe, chronic pain – results from tissue injury, nerve damage, chronic medical conditions
  • 8. Pain: How significant is the problem?
  • 9. Pain: How significant is the problem?
  • 10. Pain Peripheral terminals of primary afferent, somatic, and visceral afferent fibers respond to thermal, mechanical and chemical stimuli. – chemical stimulations are associated with inflammation and tissue injury In the presence of inflammation and tissue damage, kinins are produced and act by stimulating bradykin receptors (B1 and B2) – B1 receptors are induced in response to the pain and inflammatory cytokines IL-1β, TNF-α, IL-2 and IL-9, and to bacterial lipopolysaccharides
  • 11. Pain Conduction of pain signals from the periphery to the spinal cord. – type-Aβ neurons conduct signals rapidly and have a low stimulus threshold to mechanical stimuli. – type-Aδ respond to cold, heat and high-intensity mechanical stimulation and conduct with intermediate velocity. – type-C fibers conduct slowly, responding multimodally (heat, intense mechanical stimuli, or chemical irritants) some type-C afferents only become responsive during inflammation
  • 12. Pain Descending and local inhibitory regulation in the spinal cord – opioid receptors (μ, δ, қ) μ receptors are targeted for morphine (opioid) analgesia – norepinepherine acts on the α2-adrenergic receptor Clonidine can be used for pain treatment At this time, no effective medications are available to treat the transmission of pain through the dorsal horn of the spinal cord
  • 13. Pain Peripheral sensitization: – lowered activation thresholds allodynia – normally innocuous stimuli perceived as painful hyperalgesia – high intensity stimuli are perceived as more painful than usual at the site of injury – complaints of pain out of proportion to the stimulus
  • 14. Migraine Pathophysiologic mechanisms are not completely understood Migraine can be considered the acute manifestation of abnormal intermittent peripheral and central excitability The leading theory involves three events: – 1st : a region of neural activation followed by deactivation travels across the cortex – ―cortical spreading depression” – correlates with the sensory disturbances of migraine auras
  • 15. Migraine 2nd: – neuropeptide release occurs in the dural vasculature possibly evoked by cortical excitation 3rd: – trigeminal afferents from dural vasculature are activated and sensitized by the local release of neuropeptides
  • 16. Pain Treatment Depends on the type of pain: – acute – chronic – neuropathic (ideally) Target the specific receptors on the specific nerves. – How?
  • 17. Pharmacologic classes for treatment of pain There are three broad categories of analgesic drugs: – non-opioid analgesics – adjuvant analgesics – opioid analgesics
  • 18. Pharmacologic classes for treatment of pain Nonsteroidal anti-inflammatory drugs (NSAIDs) DMARDs TCAs SSRIs/SNRIs Anticonvulsants NMDA receptor antagonists Adrenergic agonists 5HT1 receptor agonists (triptans) – for acute treatment of migraine Opioid receptor agonists
  • 19. USP Classification System
  • 20. Acetaminophen Analgesic and antipyretic MOA is unknown – raises pain threshold As effective as NSAIDs in relieving OA pain Acetaminophen is metabolized by the liver Oral dose for adults is 325 to 650 mg every 4 to 6 hours – maximum daily dose is 4 grams Pregnancy cat. B
  • 21. NSAIDs ~ equal in terms of pain relief inhibit both COX-1 and COX-2: Salicylates – aspirin, diflunisal (Dolobid), choline magnesium trisalicylate (Trilisate), and salsalate (Disalcid) – irreversibly bind to COX isoenzymes Proprionic acids – ibuprofen (Motrin), naproxen (Naprosyn), fenoprofen (Nalfon), ketoprofen (Orudis), flurbiprofen (Ansaid), and oxaprozin (Daypro) – relatively lower side effect incidence than salicylates – high incidence of GI discomfort/PUD – naproxen has a longer ½-life
  • 22. NSAIDs: Pharmacodynamics analgesic, anti-inflammatory, antipyretic Inhibit cyclo-oxygenase isoenzymes: – COX-1, COX-2 interfere with the production of prostaglandins – reduce activity threshold at peripheral terminals of nociceptive primary afferent neurons. – reduce inflammatory hyperalgesia and allodynia. – reduce recruitment of leukocytes which produce other inflammatory mediators. prostaglandins act as pain-producing neuromodulators in the dorsal horn of the spinal cord.
  • 23. NSAIDs: Pharmacokinetics absorption – 80% absorbed from GI tract distribution – highly protein bound metabolism – biotransformation in the liver excretion – excreted primarily in the urine – Some biliary excretion
  • 24. NSAIDs: Indications Mild-moderate pain Osteoarthrtis Rheumatoid arthritis Ankylosing spondylitis Gout Tendonitis Bursitis Dysmenorrhea Fever
  • 25. NSAIDs: Precautions & Contraindications Precautions: – GI, hepatic, renal disease – dehydration – pregnancy cat. B & C Contraindications: – sensitivity to ASA – 3rd trimester of pregnancy – recent CABG
  • 26. NSAIDs: Adverse Reactions non-selective COX inhibitors cause injury to gastric mucosa and the kidneys – the longer the patient uses the medication the greater the potential for adverse side-effects – certain medications have higher incidence of side effects GI upset (nausea) PUD GI bleeding Rash Risk of cardiovascular events Liver failure
  • 27. NSAIDs Acid derivatives – naproxen (Naprosyn) 250-500mg BID – naproxen sodium (Anaprox) 275-550mg BID – fenoprofen (Nalfon) 300-600mg T-QID – flurbiprofen (Ansaid) 200-300mg daily in 2-4 divided doses – ketoprofen (Orudis/Oruvail) 200mg daily – indomethacin (Indocin) 75-150mg daily in 3-4 divided doses – diclofenac potassium (Cataflam) 50mg B-QID – diclofenac sodium (Voltaren) 100mg daily +PGE1 analogue (Arthrotec) – ketorolac (Toradol) 10mg q6h – oxaprozin (Daypro) 1.2g once daily – tolmetin (Tolectin) 600mg-2g daily in 3-4 divided doses – etodolac (Lodine) 600mg-1g daily in 2-3 divided doses
  • 28. NSAIDs Indenes – sulindac (Clinoril) 150mg BID Naphthlyalkanones – nabumetone (Relafen) 1500-2000mg daily Pyrazoles – phenylbutazone Oxicams – piroxicam (Feldene) 20mg daily – meloxicam (Mobic) 7.5-15mg once daily Fenamates – mefenamic acid (Ponstel) 250mg q6h x2-3 days
  • 29. NSAIDs COX-2 selective inhibitors – COX-2 is selectively expressed in inflammation – the criteria used to determine if a medication is COX-2 selective is its thromboxane activity – 50% less incidence of PUD (GI perforation, ulceration, bleed) than ibuprofen – 12-hour pain relief – celecoxib (Celebrex) 100mg BID
  • 30. Adjuvant analgesics Antidepressants Anticonvulsants Alpha-2 adrenergic agonists (clonidine) DMARDs GABA agonists NMDA receptor antagonists Corticosteroids Skeletal muscle relaxants Local anesthetics Topical anesthetics
  • 31. Antidepressants Most are analgesics Can relieve chronic pain even if the patient has no coexisting depression Anti-depressant effects are also important in alleviating chronic depression Potentially capable of relieving all types of pain
  • 32. Antidepressants TCAs = quot;tricyclicquot; antidepressants – amitriptyline (Elavil), imipramine, doxepin , clomipramine , desipramine and nortriptyline SSRIs = serotonin-selective reuptake inhibitors – paroxetine (Paxil) and citalopram (Celexa) SNRIs = serotonin & norepinephrine reuptake inhibitors – venlafaxine (Effexor) bupropion (Wellbutrin) maprotiline (Ludiomil)
  • 33. Anticonvulsants Used to treat neuropathic pain: – painful diabetic neuropathy – postherpetic neuralgia – trigeminal neuralgia Varible effects with: – phenytoin (Dilantin) – carbamazepine (Tegretol) – clonazepam (Klonipin) – oxcarbazepine (Trileptal) – lamotrigine (Lamictal)
  • 34. Anticonvulsants Gabapentin (Neurontin) – most commonly used – side effects: dizziness, somnolence, ataxia, confusion – lowest effective dosing is 900mg / day start with 100mg/day titrate up over several weeks to avoid side effects
  • 35. Adjuvant analgesics DMARDs GABA agonists: – Baclofen interacts with the brain receptor for GABA – used for many years as a treatment for neuropathic pain and trigeminal neuralgia – also used as an SMR NMDA (n-methyl-D-aspartate) receptor antagonists – very important in the treatment of neuropathic pain – dextromethorphan – amantadine (Symmetrel) – Ketamine
  • 36. Adjuvant analgesics Corticosteroids: – Pharmacodynamics: anti-inflammatory & immunosuppressant stimulates the synthesis of enzymes needed to decrease the inflammatory response suppresses the immune system by reducing activity and volume in the lymphatic system causing lymphocytopenia
  • 37. Adjuvant analgesics Corticosteroids: – Pharmacokinetics: absorption – most are readily absorbed with peak onset is 1-2 hours distribution – extensively bound to plasma proteins – only the unbound portion is active – distributed into breast milk and through the placenta metabolism – by the liver into inactive metabolites excretion – excreted in the urine and feces as metabolites and unchanged drug
  • 38. Adjuvant analgesics Corticosteroids: – have the same effects as hormones produced by the adrenal glands – contraindicated in patients with systemic fungal disease (numerous precautions) – adverse reactions: (dosing or duration dependent) GI irritation, increased appetite  weight gain arrhythmias, thromboembolism, heart failure seizures – the adverse effects from these drugs worsen with the duration of treatment – Pregnancy cat. C – acute renal insufficiency may occur with increased stress (i.e. infection, surgery, trauma) or abrupt withdrawal after prolonged therapy
  • 39. Adjuvant analgesics Corticosteroids: – prednisone (Deltasone, Orasone) Tabs: – 1mg, 2.5mg, 5mg, 10mg, 20mg, 25mg, 50mg Liquid: – 5mg/5ml dosing: – Adults: 5-60mg QD – Children: 0.14mg/kg/day in four divided dosings – prednisolone (Pediapred) Liquid: 6.7mg/5ml 0.14 – 2mg/kg QD in divided dosings
  • 40. Adjuvant analgesics Corticosteroids: – methylprednisolone (Medrol) Tabs: 2mg, 4mg, 8mg, 16mg, 24mg, 32mg dosing: 2-60mg QD – methylprednisolone acetate (Depo-Medrol) Suspension: 20mg/ml, 40mg/ml, 80mg/ml dosing: 10-80mg IV QD – methylprednisolone sodium succinate (Solu-Medrol) Solution (per vial): 40mg, 125mg, 500mg, 1000mg, 2000mg dosing: 10-250mg IM or IV q4h – dexamethasone sodium phosphate (Decadron) commonly used to treat/prevent cerebral edema also used intra-articular and intra-lesional injection Solution: 4mg/ml, 10mg/ml, 20mg/ml, 24mg/ml dosing: 10mg IV, then 4mg IM q4h x3-4 days then taper
  • 41. Adjuvant analgesics Muscle Relaxants: – marketed as pain relievers for musculoskeletal pain problems – orphenadrine citrate (Norgesic, Norflex) Pharmacodynamics: – atropine-like action on the cerebral motor centers Pharmacokinetics: – ½-life of ~14hours dosing: 100mg po or 60mg IV/IM q12h – cyclobenzaprine (Flexeril) Pharmacodynamics: – unknown MOA but it is a CNS depressant – potentiates the effects of norepinephrine (NE) – exhibits anticholinergic effects similar to TCAs Pharmacokinetics: – ½-life of 1-3 days dosing: 10 - 20mg BID
  • 42. Adjuvant analgesics Muscle Relaxants: – methocarbamol (Robaxin) – chlorzoxazone (Parafon forte) – metaxalone (Skelaxin) – carisoprodol (Soma) high potential for addiction
  • 43. Adjuvant analgesics Local Anesthetic Drugs: – when injected close to a nerve, a local anesthetic produces regional anesthesia in the distribution of the nerve – when taken orally or intravenously, a local anesthetic drug can provide pain relief oral agents – include mexiletine, tocainide and flecainide IV or SC infusion of lidocaine – used to treat neuropathic pain
  • 44. Adjuvant analgesics Topical Agents: – local anesthetics are commonly used in this way – lidocaine (Lidoderm patch) is approved in the U.S. for the treatment of postherpetic neuralgia and is now being used for a variety of other pain problems – lidocaine and prilocaine (EMLA) – capsaicin (Zostrix) – ? analgesic effects from topical antidepressants (i.e. doxepin) – Topical NSAIDs
  • 45. Opioid receptor agonists Used for moderate to severe pain (7-10) Morphine is the standard for comparing narcotic effectiveness All are Schedule II, III, or IV controlled substances Pharmacodynamics: – bind on μ receptors located in: brain and brainstem spinal cord GI tract primary afferent peripheral terminals
  • 46. Opioid receptor agonists Interactions: – potentiation with ETOH, CNS depressants, MAOIs, TCAs, & anticholinergics Common side effects: – respiratory depression – constipation (often a persistent problem) – nausea and vomiting (occurs at onset but resolves quickly) – somnolence (sedation) and fatigue – dizziness and confusion – pruritus – urinary retention – dry mouth – sexual dysfunction – euphoria – hepatotoxicity
  • 47. Opioid receptor agonists Morphine sulfate – oral and parenteral forms – controlled release oral preparations provide extended pain control over 12  24 hours – Patient Controlled Analgesic (PCA) devices are used for post operative, cancer, trauma, sickle cell crisis and burn treatment – epidural administration delivers high concentrations in the dorsal horn of the spinal cord resulting in much longer duration of action – indicated for moderate to severe pain
  • 48. Morphine sulfate Pharmacodynamics – Degree of effects are dosing dependent – CNS analgesia, respiratory depression, sedation, cough suppression – GI decreased gastric, biliary, and pancreatic secretions decreased peristalsis – Cardiovascular peripheral vasodilation  orthostatic hypotension
  • 49. Morphine sulfate Pharmacokinetics – absorption varies according to route of administration onset of analgesia within 15-60 minutes – distribution – metabolism primarily by the liver – excretion excreted in the urine and bile Contraindications: – impaired respiration – paralytic ileus
  • 50. Morphine sulfate Precautions: – head injury or increased ICP – impaired renal, hepatic, thyroid, pulmonary, or adrenal function – elderly & debilitated – Pregnancy cat. C Interactions: – potentiated by ETOH and CNS depressants – do not use within 14 days of MAOIs Adverse reactions: – sedation – constipation – urinary retention – respiratory depression – orthostatic hypotension
  • 51. Morphine sulfate MS Contin – Sustained release – Tabs: 15mg, 30mg, 60mg, 100mg, 200mg – dosing = q12h – MS CONTIN TABLETS ARE TO BE TAKEN WHOLE, AND ARE NOT TO BE BROKEN, CHEWED, OR CRUSHED TAKING BROKEN, CHEWED, OR CRUSHED MS CONTIN TABLETS COULD LEAD TO THE RAPID RELEASE AND absorption OF A POTENTIALLY TOXIC dosing MSIR – Liquid: 15mg, 30mg, 10mg/5ml, 20mg/5ml – dosing = 5-30mg q4h
  • 52. Opioid receptor agonists meperidine (Demerol) – pharmacodynamics are similar to MS – pharmacokinetics absorption – varies according to route of administration – oral is only half as effective as parenteral distribution – 60-80% bound to plasma proteins metabolism – primarily by hydrolysis in the liver excretion – excreted in the urine as metabolites and unchanged drug – Tabs: 50mg, 100mg – Liquid: 50mg/5ml – Parenteral: 10mg/ml, 25mg/ml, 50mg/ml, 75mg/ml, 100mg/ml – dosing: 50-150mg (po, IM, SC, IV) q3-4h may cause convulsions with large dosings
  • 53. Opioid receptor agonists hydromorphone (Dilaudid) – pharmacodynamics acts directly on the cough center of the medulla similar to MS – pharmacokinetics absorption – varies according to route of administration distribution metabolism – primarily by the liver excretion – excreted in the urine as metabolites and unchanged drug – Tabs: 1mg, 2mg, 3mg, 4mg, 8mg – Liquid: 5mg/ml – parenteral: 1mg/ml, 2mg/ml, 4mg/ml, 10mg/ml – Supp = 3mg – dosing: oral: 2 - 4mg q4-6h parenteral: 1 - 2mg SC or IM q4-6h
  • 54. Opioid receptor agonists Codeine sulfate or phosphate – much less effective for pain control then other opioids – also used as antitussive and antidiarrheal – pharmacokinetics absorption – peak analgesic effect in 30-60 minutes with a 4-6 hour duration distribution – crosses the placenta and enters breast milk metabolism – primarily by the liver through demethylation or conjugation excretion – excreted in the urine as metabolites and free or conjugated morphine – pregnancy Cat. C – numerous interactions
  • 55. Opioid receptor agonists Codeine sulfate or phosphate – Tabs: 15mg, 30mg, 60mg – Sol: 15mg/5ml (phosphate) – Inj: 15mg/ml, 30mg/ml, 60mg/ml (phosphate) – typically in combination with 300mg of acetaminophen (C III) #3 = 30mg of codeine #4 = 60mg of codeine elixir = 12mg codeine + 120mg acetaminophen (C IV) dosing = 1-2 tablets q4h – children 3-6y = 5ml – children 7-12y = 10ml
  • 56. Opioid receptor agonists Oxycodone – semisynthetic – high potential for abuse/addiction more effective for acute pain than chronic pain – several active metabolites – pharmacodynamics are similar to morphine – pharmacokinetics absorption – onset of effect in 15-30 minutes with peak effect in 1 hour and 6 hour duration distribution metabolism – primarily by the liver excretion – excreted in the urine as metabolites and unchanged drug
  • 57. Opioid receptor agonists Oxycodone – Pregnancy Cat. C – + acetaminophen (Percocet, Roxicet, Tylox) 2.5/325, 5/325, 5/325/5ml, 5/500, 7.5/325, 7.5/500, 10/3 25, 10/650 – + aspirin (Percodan) 4.8355/325 – dosing = 1-2 tabs q6h – oxycodone SR (Oxycontin) 5mg, 10mg, 20mg, 40mg, 80mg, 20mg/ml biphasic absorption dosing 1 tab q12h
  • 58. Opioid receptor agonists Hydrocodone – semisynthetic – high potential for abuse/addiction – pharmacodynamics and pharmacokinetics are similar to oxycodone – Interactions: ETOH, MAOIs, TCAs, anticholinergics – + acetaminophen Lortab: 2.5/500, 5/500, 7.5/500, 10/500, 7.5/500/5ml Vicodin: 5/500, ES = 7.5/750, HP = 10/660 dosing: 1 tablet q4-6h – + ibuprofen (Vicoprofen) 7.5/200 dosing: 1 tablet q4-6h
  • 59. Opioid receptor agonists methadone HCl (Dolophine) – qualitatively similar to that of morphine onset of action is slower but more prolonged side effects are less severe – indications: treatment of moderate to severe pain not responsive to non-narcotic analgesics detoxification treatment of opioid addiction (heroin or other morphine-like drugs) maintenance treatment of opioid addiction (heroin or other morphine-like drugs), in conjunction with appropriate social and medical services – pharmacokinetics absorption – peak effect in 1-7 hours metabolism – primarily by the liver excretion – excreted in the urine and feces as metabolites and unchanged drug – 35-hour ½-life – precautions: avoid grapefruit – dosing: 10 - 225mg QD
  • 60. Synthetic opioid receptor agonists Fentanyl – significantly more potent than morphine – short-acting – indicated for patients with chronic/breakthrough cancer pain – pharmacokinetics absorption – varies according to route of administration metabolism – primarily by the liver excretion – excreted in the urine as metabolites and unchanged drug
  • 61. Synthetic opioid receptor agonists Fentanyl – contraindicated for patients taking MAOIs – numerous precautions, interactions, and adverse reactions – availability: lozenge/lollipop for buccal mucosa administration (Fentora) – 100mcg, 200mcg, 400mcg, 600mcg, 800mcg – 1 po B-QID transdermal patch (Duragesic) – 12mcg/hr, 25mcg/hr, 50mcg/hr, 75mcg/hr, 100mcg/hr – 1 Q3D – rotate sites
  • 62. Synthetic opioid receptor agonists propoxyphene HCl (Darvon) propoxyphene napsylate (Darvon N) + acetaminophen (Davocet, Darvocet N) – C IV – considered a ―mild‖ analgesic and a ―bad drug‖
  • 63. Synthetic opioid receptor agonists tramadol (Ultram) – not chemically related to opiate buts binds to opioid receptors – inhibits reuptake of NE and 5-HT – use to treat moderate to moderately severe pain – pharmacokinetics absorption – 75% obsorption distribution – ~20% bound to plasma proteins – can cross the blood-brain barrier metabolism – extensive excretion – excreted in the urine as metabolites (60%) and unchanged drug (30%) – precautions: renal insufficiency (CrCl < 30ml/min) – Tabs: 50mg – + acetaminophen (Ultracet) – 37.5/325 indicated for short-term treatment of acute pain dosing: 1-2 tabs q4-6h
  • 64. Opioid receptor agonists Butorphanol (Stadol) – (occasional) competitive antagonist – (occasional) partial μ receptor agonist – available as a nasal spray – pharmacokinetics absorption – IM - onset in <10 min; peaks in 30-60 min. – nasal – onset in <15min distribution – crosses the placenta metabolism – primarily by the liver (hydroxylation) into inactive metabolites excretion – excreted in the urine and feces as metabolites – adverse effects may increase ICP – dosing IM = 1-4mg q3-4h IV = 0.5-2mg q3-4h nasal = one spray in one nostril
  • 65. Opioid receptor agonist-antagonist Nalbuphine (Nubain) – acts on Қ agonist with μ antagonist in CNS – use to treat moderate to severe pain – pharmacokinetics absorption – onset <15 minutes distribution – not protein bound metabolism – primarily by the liver excretion – excreted in the urine and bile – dosing = 10-20mg (IV, IM, or SC) q3-6h (NMT 160mg/day)
  • 66. Naloxone naloxone (Narcan) – μ antagonist – Pregnancy cat. B – pharmacodynamics MOA is unknown (? competitive antagonism of 1+ opioid receptors) – pharmacokinetics absorption – onset of action in 1-2 minutes IV and 2-5 minutes IM metabolism – primarily by the liver (conjugation) excretion – excreted in the urine as metabolites and unchanged drug
  • 67. Naloxone naloxone (Narcan) – adverse reactions: v. fib cardiac arrest – indications: used to reverse side effects of opioids adjunct in the management of opioid overdosing – shorter half-life than morphine – dosing: adult: 0.4 – 2mg (IV, IM, SC) q2-3min (NMT 10mg) child: 0.01mg/kg IV
  • 68. Migraine Various treatment options – acetaminophen – NSAIDs – opioid analgesics – ergotamine – triptans – antiemetics – anticonvulsants – adjuncts Mg sulfate caffeine Combination therapies work best after the headache has started
  • 69. Ergotamines Nonselective 5HT1D agonist Affinity for dopaminergic, cholinergic, and alpha- /beta-adrenergic receptors Adverse effects: – vascular occlusion – toxicity – rebound headaches – pregnancy cat. X Typically combined with phenobarbital, belladonna, and caffeine (Cafergot) dosing: – 2mg SL or po, then 1-2mg q30min (NMT 6mg/24 or 10mg/wk)
  • 70. dihydroergotamine mesylate (DHE 45) Used to prevent, treat, and abort migraines Pharmacodynamics: – vasoconstrictor (peripheral) – alpha-adrenergic blocker – inhibits NE reuptake – 5-hydroxytriptamine (5HT)1D receptor agonist Pharmacokinetics: – absorption onset <5min IV and 15-30min IM – distribution 90% protein bound – metabolism primarily by the liver – excretion excreted in the urine and feces as metabolites
  • 71. dihydroergotamine mesylate (DHE 45) Contraindications: – do NOT take in conjunction with MAOIs, ergotamines, or triptans – elderly – ischemic HD, angina, uncontrolled HTN – Pregnancy Cat X dosing: – 1mg IM or IV qh x3 (x2 IV) – NMT 6mg in one week Works best when combined with an antiemetic
  • 72. Migraine treatments: Triptans 5HT1 receptor agonists – 5HT1B receptors on the vascular smooth muscle of menigeal, dural, and cerebral arteries – 5HT1B/1D receptors in the central trigeminal nerve terminals prevent the release of sensory neurotransmitters Considered an abortive therapy – must be take early in the headache cycle (<90 min.) work best at maximum dosing – approximately ½ of all patients treated require repeat dosing within 24 hours – use long-acting preparations for: delayed intensity, menstrual migraines, frequent recurrence
  • 73. Migraine treatments: Triptans Not recommended for anyone <18 years old Pregnancy cat. C Do not use more than 6-8x per month Adverse effects: – warmth/flushing – ―burning‖ or ―tightness‖ in the chest, face, or limbs Contraindications: – ischemic HD – cerebral or peripheral vascular disease – uncontrolled HTN – concomitant MAOIs or ergotamines No association between triptans and CVA, CV events, and death
  • 74. Triptans Pharmacodynamics – vasoconstriction of the cranial blood vessels – inhibition of pro-inflammatory neuropeptide release Pharmacokinetics – absorption varies according to route of administration – distribution ~ 15 - 25% protein bound – metabolism primarily by the liver – excretion excreted in the urine and feces as metabolites
  • 75. Triptans sumatriptan (Imitrex) – binds to 5HT1B receptors – 2 hour ½-life – oral, nasal, and parenteral preparations – efficacy is 50-85% at 2 hours – interactions: ergots & MAOIs – adverse reactions: a. fib; v. fib; v. tach; MI – dosing: 6mg SC (can repeat after 1 hour prn)
  • 76. Triptans zolmitriptan (Zomig) – high affinity binding to 5HT1B and 5HT1D receptors – 2 hour ½-life – prodrug: converted into active N-demethyl metabolite maximum concentration achieved in 2-3 hours – oral and nasal preparations – efficacy is 60-70% at 2 hours – interactions: cimetidine doubles the ½-life SSRIs may cause weakness, hyperreflexia, incoordination MAOIs increase plasma concentration – dosing: 2.5mg po (can repeat after 2 hours prn)
  • 77. Migraine naratriptan (Amerge) – high affinity binding to 5HT1B and 5HT1D receptors – 6 hour ½-life – oral form only – efficacy is 40-50% at 2 hours – adverse reactions: abnormal ECG changes – prolonged PR and QT intervals – ST/T wave changes – a. flutter; a. fib; PVCs – dosing: 1 - 2.5mg po (can repeat after 4 hours)
  • 78. Triptans rizatriptan (Maxalt) – high affinity binding to 5HT1B and 5HT1D receptors – 2 hour ½-life – pharmacodynamics/–kinetics are similar to zolmitriptan – oral preparations only (completely absorbed) mean absolute bioavailability is about 45% mean peak plasma concentrations are reached in ~ 1 - 1.5 hours efficacy is 60-75% at 2 hours – dosing: 5 - 10mg po (can repeat after 2 hours)
  • 79. Triptans almotriptan (Axert) frovatriptan (Frova) 26 hour ½-life eletriptan (Relpax) high affinity binding to 5HT1B/5HT1D/5HT1F receptors oral preparations only – well absorbed with peak plasma levels after ~1.5 hours – mean absolute bioavailability is ~ 50% 90% non-renal clearance dosing: 20 – 40mg po (can repeat after 2 hours)
  • 80. Migraine treatments Other agents: – butalbital, acetaminophen & caffeine 50/325/40 (Fioricet, Esgesic) 50/500/40 (Esgesic-plus) – butalbital, aspirin & caffeine 50/325/40 (Fiorinal) CIII – dosing: 1 or 2 po q4h – isometheptene 65mg, dichloralphenazone 100mg, acetaminophen 325mg (Midrin) indicated for tension & vascular headaches contraindications: – glaucoma – severe cardiac, renal, or hepatic disease – uncontrolled HTN – concomitant MAOIs dosing: 2 po stat, then 1 qh prn x3 (NMT 5 per 12 hours)
  • 81. Migraine Other options: – Botox – trigger point injections – occipital nerve block – sphenopalatine ganglion block – olanzapine (Zyprexa) ―rescue‖ drug thienobenzodiazepine derivative DA1-4 and 5HT2A/2C agonist
  • 82. Migraine Prophylaxis – Propranolol (Inderal) – Topiramate (Topamax) OTC meds – APAP (500mg) + ASA (500mg) + Caffeine (130mg) Oxygen
  • 83. Quiz question #4 A 19-year-old male arrives to the ED via EMS. He is unconscious but responds to painful stimuli. His pupils are constricted and respirations are depressed. You not several needle marks on his arms. Which of the following medications should you order? 1. Propoxyphene 0% 2. Naloxone 0% 3. Tramadol 0% 4. Carbamazepine 0% 5. Nalbuphine 0%
  • 84. Quiz question #5 After administering the Naloxone the patient immediately regains consciousness. This medication was effective because _____. 1. The patient was suffering from a cocaine 0% overdose 2. Naloxone binds to the opiate and inactivates 0% it 3. Naloxone is a CNS stimulant 0% 4. Naloxone antagonizes opiates at the receptor 0% site 5. Naloxone immediately activtes μ, κ, and δ 0% receptors
  • 85. Quiz question #6 NSAIDs act primarily by which of the following mechanisms? 1. They inhibit cyclooxygenase 0% 2. They antagonize μ receptors 0% 3. They reduce prostoglandin synthesis 0% 4. They block neurotransmission 0% 5. They produce vasodilatation 0%
  • 86. Case Study #1 45-year-old female with a long-standing history of chronic pain walks into your emergency department in ―severe‖ generalized pain (10+/10). She denies any trauma or other reason for the exacerbation of her chronic symptoms. She has taken 1-2 Percocet every 4 hours for the past two days without relief. She is a 1½ ppd smoker and consumes moderate quantities of EtOH. She denies other drug use. VSS. Every place you palpate is tender but she has no obvious signs of injury. The remainder of your exam is unremarkable. She demands IV narcotics. What factors are influencing this pt’s pain control? What do you prescribe?
  • 87. Case Study #2 23-year-old female college student presents with her ―worst headache ever‖ (10/10) that started this morning. She has associated nausea & photophobia. PMH is significant for periodic migraine headaches which have been the same as this headache but not as severe. She is under a lot of stress at school and from her fiance’. Non- smoker and rare EtOH. VSS. PERRLA with moderate photophobia. CN II-XII are grossly intact. Equal strength bilaterally. What is your Dx? What is your next recommendation?
  • 88. Which of the following medications would be the best first line treatment for this patient (Case #2)? 1. Ibuprofen 600mg orally 0% 2. Sumatriptan 6mg SC 0% 3. Sertraline 50mg orally 0% 4. Zolmitriptan 2.5mg orally 0% 5. Meperidine 50mg IM 0%
  • 89. Case #3 A 32-year-old woman complains of daily headaches. The headaches vary in severity, but she usually has severe headaches (8/10 on a visual analog scale) once or twice a week; she describes the latter as severe throbbing or pounding pain on the top of the head but also involving the occipital and frontal areas—and occasionally one or the other temple. These episodes, which are usually associated with some nausea and sensitivity to bright light and loud noises, typically last up to 48 hours if untreated. The patient also has headaches that are not nearly as severe (3-4/10 on the VAS) but are almost constant. She describes them as mild to moderate, dull, pressure-like pain located primarily on the top of her head and occipital area bilaterally. She is able to function with these headaches more easily than with the severe ones, although she sometimes needs to use over-the-counter (OTC) medications to lessen the intensity of the pain.
  • 90. Case Study #3 She started having severe episodic headaches in her early 20s; these became progressively more frequent. In addition to the increasingly frequent severe headaches, about 5 years ago, she began having milder headaches as well. These also became gradually more frequent—and eventually occurred daily. She has had daily headaches for about 2 years. She has been using oral sumatriptan, 100 mg, for her severe headaches and notes that this reduces the severity of the pain significantly within 1 to 2 hours when she is able to take the medication shortly after pain onset. However, she seldom takes it early enough to have this effect. She uses OTC acetaminophen or ibuprofen for her milder headaches once or twice a day, about 2 days a week. Results of physical and neurologic examinations and MRI and CT scans of the head are all normal.
  • 91. Case Study #3 Dx? Tx?
  • 92. Case Study #4 26-year-old male presents via EMS in full spinal immobilization secondary to a high-speed MVA. He is obtunded but responds to verbal stimuli. He had a brief LOC at the scene. He ―hurts all over‖ (8-9/10) but sensory and motor function are intact. VS: B/P – 108/70 mmHg; P – 96bpm, regular; R – 20, shallow; T – 98.9 F orally; SpO2 – 96% RA PE reveals a fracture of the right femur, 2 fractured ribs, and a dislocation of the left shoulder. What is your recommendation for pain management?
  • 93. A 24-year-old female G1P0 at 36 weeks gestation complains of back pain (3-4/10) and generalized muscle aches. She admits that she ―over did it‖ yesterday working around the house. She has taken two 650mg doses of acetaminophen without relief. She denies any problems with her pregnancy and has had regular pre-natal checkups. VSS. P.E. is unremarkable except for some mild paravertebral tenderness in the L4-S1 region. Which of the following treatments should you prescribe to control her pain? Acetaminophen 1000mg every four hours prn pain 1. 0% Ibuprofen 600mg every six hours prn pain 2. 0% Tylenol w/ codeine #3 two every six hours prn pain 3. 0% Orphenadrine citrate 100mg one every 12 hours 4. 0% Methylprednisolone 8mg daily 5. 0% Vicodin one every fours hours prn pain 6. 0%
  • 94. Case Study #5 Bob is a 52-year-old salesman at Lowe’s. He has mild, generalized osteoarthritis. He has been previously evaluated on a couple of occasions, but you don't remember the full details, apart from him having had back pain. When you arrive in the exam room, Mr Jones is lying supine on the exam table with his knees bent. He states he was changing the TV channel when he felt a ―click‖ in his back and was immediately unable to move. He is currently experiencing lumbosacral back pain, spreading up into his dorsal region and down into his buttocks. He takes 600mg of Ibuprofen BID for his OA NKDA
  • 95. Case Study #5 VSS On examination he lies stiff and motionless and he is anxious and diaphoretic. Neurological examination of his lower extremities reveals slightly diminished strength (5+) bilaterally, normal sensation, and severe back pain on straight leg raising. Reflexes are 2+ bilaterally. Next step? Rx?
  • 96. If you were going to give him painkillers, what might you consider? 1. Acetaminophen 0% 2. NSAIDs 0% 3. COX-2 inhibitors 0% 4. Tramadol (Ultram) 0% 5. Opioids 0% 6. None of the above 0%
  • 97. If you were going to give her painkillers, what else might you consider? 1. Anticonvulsants 0% 2. Amitriptyline (Elavil) 0% 3. Hypnotics 0% 4. Skeletal muscle relaxants 0% 5. None of the above 0%
  • 98. Case Study #6 Julie Smith is a 45-year-old female with a long history of mild chronic low back pain. She is in the clinic today because it has got a lot worse in the last 6 months. Past medical history is significant for irritable bowel syndrome, a sero-negative arthritis, and chronic headaches. In the past she has suffered from alcoholic abuse and was also addicted to Diazepam. However, she has been successfully weaned off both alcohol and Diazepam. The back pain is now debilitating and she cannot do some of her household jobs and cannot drive for more than 5 minutes. There is no radiation into the legs. She is stiff in the morning when she wakes and the pain then gets worse over the day with activity. It remains throughout the night, and keeps her awake.
  • 99. Case Study #6 She weighs 192 pounds and is 66‖ tall. On examination she has marked tenderness throughout the back, her paravertebral muscles are extremely tight and tense, and she has a mild scoliosis to the left. Pain is present on axial loading and on straight leg raising to 45 degrees bilaterally but she can sit to 90 degrees. She puffs and pants throughout the examination. Next step?
  • 100. Case Study #6 A straight X-ray of her lumbar spine shows disc degeneration at L4/5 and L5/S1. ESR is normal. She has a mild iron deficiency anemia. Other bloodwork is normal. Next step? – does she require further investigation? MR scan shows disc bulging at S1 without neural encroachment.
  • 101. What is your primary management of this patient? 1. Tell her to ―work through the pain‖ 0% 2. Tell her to lose weight 0% 3. Prescribe analgesics 0% 4. Refer her to a neurosurgeon 0% 5. Refer her for physiotherapy for TENS 0% 6. Get a psychological opinion 0% 7. Carry out a nerve block 0%
  • 102. If you were going to give her painkillers, what would you prescribe? 1. Acetaminophen 0% 2. NSAIDs 0% 3. COX-2 inhibitors 0% 4. Tramadol (Ultram) 0% 5. Opioids 0% 6. None of the above 0%
  • 103. If you were going to give her painkillers, what else might you consider? 1. Anticonvulsants 0% 2. Amitriptyline (Elavil) 0% 3. Hypnotics 0% 4. Skeletal muscle relaxants 0% 5. None of the above 0%
  • 104. Case Study #7 Barbie Dawl is a 35-year-old female who presents to a walk- in clinic with ―severe‖ (8/10) neck pain. She is in ―good‖ general health. At the clinic, Miss Dawl was observed lying on the bed, grimacing in pain, and looking very stiff. She states that she was involved in a minor car accident two days earlier when she was driving home from work. She did not seek treatment and was fine until yesterday morning when her neck pain began and continued to get worse throughout the day. The pain is now spreading up into the back of the head and over the eyes and is both constant and severe. She feels dizzy when she tries to get up to go to the bathroom, and has pains shooting down the left arm and into the ring and little finger. A divorced mother of two, she has a part time checkout job at a local supermarket. Her stress levels are ―fairly high‖ particularly in association with her unsatisfactory marriage and her financial difficulties since the divorce.
  • 105. Case Study #7 Meds: None Allergies: Tylenol #3, Penicillin, Aspirin VSS Examination reveals a very stiff neck but she can be coaxed into moving it. The pupils are equal, round, and react to light. Range of motion is decreased in BUE but seems restricted only by pain. Muscle strength in the LUE is 4+ and in the RUE is 5+. Reflexes are 2+ bilaterally. Next step?
  • 106. What is the management of this patient? Do you: 1. Tell her to ―work through the pain‖ 0% 2. Send her for X-rays of the neck 0% 3. Prescribe analgesics 0% 4. Refer her to a neurosurgeon 0% 5. Refer her for physiotherapy for TENS 0% 6. Get a psychological opinion 0% 7. Carry out a nerve block 0%
  • 107. Case Study #7 She is sent to your Emergency department by ambulance. X-rays are taken of her cervical spine which are read as normal. After three or four hours waiting for an assessment and X-rays, her pain has begun to settle somewhat. Next step?
  • 108. If you are going to give her painkillers, what would you prescribe? 1. Acetaminophen 0% 2. NSAIDs 0% 3. COX-2 inhibitors 0% 4. Tramadol (Ultram) 0% 5. Opioids 0% 6. None of the above 0%
  • 109. If you are going to give her painkillers, what else might you consider? 1. Anticonvulsants 0% 2. Amitriptyline (Elavil) 0% 3. Hypnotics 0% 4. Skeletal muscle relaxants 0% 5. None of the above 0%
  • 110. Case Study #7 She is given a cervical collar and analgesics, and advised to go home and rest for two days. Miss Dawl comes back to the walk-in clinic to see you a week later, complaining of ongoing neck pain, headache, and a heavy feeling in the left arm. She is continuing to use the collar and asks for more pain killers and a release from work. Next step?
  • 111. What is the management of this patient? Do you: 1. Tell her to ―work through the pain‖ 0% 2. Prescribe analgesics 0% 3. Refer her to a neurosurgeon 0% 4. Refer her for physiotherapy for TENS 0% 5. Get a psychological opinion 0% 6. Carry out a nerve block 0%
  • 112. If you are going to give her painkillers, what would you prescribe? 1. Acetaminophen 0% 2. NSAIDs 0% 3. COX 2 inhibitors 0% 4. Tramadol (Ultram) 0% 5. Opioids 0% 6. None of the above 0%
  • 113. Case Study #8 An 88-year-old retired lawyer comes to see you complaining of severe (6/10) lower back pain spreading down the back of his legs to his feet when he walks. He denies any trauma but notes that the pain began after playing in a golf tournament. He denies urinary or fecal incontinence. In the last 3 weeks, he has been unable to play even 9 holes and the pain is now so severe that he has to drive a golf cart instead of walking the course. He is a very keen golfer who plays and lives locally. He tells you that he lives for his golf, and he wants to get back to it, and if this is impossible his life really isn’t worth continuing on with. There is no quality to his life as all of his interests revolve around golf, including his social circle.
  • 114. Case Study #8 He was widowed 10 years ago, but is of sound mind and in ―good‖ general health. PMH is significant for HTN, OA, cirrhosis, and CRI (CrCl = 40ml/min). He is 6 months S/P 3-vsl CABG. Ex-smoker. 3-4 alcoholic beverages QD. Meds: – Vaseretic 10-25 one QAM – Excedrin two tablets QAM – MVI NKDA
  • 115. Case Study #8 VS: B/P = 108/60mmHg RUE, sitting; P = 60 bpm; R = 12 breaths/min On examination he moves stiffly. Spine is midline but he has mild kyphosis. Paravertebral tenderness is present at L4-S1. Neurological examination of his lower extremities reveals diminished strength (4+) bilaterally, normal sensation, and severe back pain on straight leg raising. Reflexes are 1+ bilaterally. Next step? Rx?
  • 116. If you choose pain-relieving techniques, what do you think would be appropriate? 1. TENS or acupuncture 0% 2. NSAIDs 0% 3. Cox-2 inhibitors 0% 4. Acetaminophen 0% 5. Opioids 0% 6. Nerve block 0% 7. Surgery 0%
  • 117. You decide to prescribe non-narcotic analgesics. Which of the following should you choose? Ibuprofen 800mg three times daily 1. 0% Celecoxib 200mg twice daily 2. 0% Diclofenac 50mg three times daily 3. 0% Tramadol 100mg every morning 4. 0% Acetaminophen 1000mg four times daily 5. 0% None of the above 0% 6.
  • 118. You decide to prescribe a narcotic analgesic. Which of the following would you choose? Darvocet N-100 one every four hours prn 1. 0% Meperidine 50mg one every four hours prn 2. 0% Fentanyl 75mcg/hr transdermal Q3D 3. 0% Percocet 5/325 one every six hours prn 4. 0% Vicodin 7.5 one every six hours prn 5. 0% Tylenol #3 two every six hours prn 6. 0%
  • 119. Thought for the day… If you have a lot of tension and you get a headache, do what it says on the aspirin bottle: ―Take two aspirin‖ and ―Keep away from children.‖ --Author Unknown

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