Prescription Pain Management University of Hawaii Hilo Pre - Nursing - PowerPoint PPT Presentation

Prescription Pain Management University of Hawai‘i Hilo Pre - Nursing Program NURS 203 – General Pharmacology Danita Narciso Pharm D 1

2 Objectives  Understand how to preform a pain assessment  Know which medications fit into which pain management classes  Know the general effects and adverse effects of the medications/classes of medications

3 Pain Assessment

4 Pain Assessment  Babies  Respond to changes  Crying  Temperature  Blood pressure  Heart rate  Oxygen consumption  Activity  Scales  CRIES, NIPS, FLACC, CHEOPS

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6 Pain Assessment  P  Provoke – causes, better, worse?  Q  Quality – sharp, dull, stabbing, crushing  R  Radiating – stay in one sport, move to another location  S  Severity – scale of 1-10  T  Time – when start, how long does it last

7 Step treatment strategies - WHO  Mild  Acetaminophen  NSAIDs  ASA  Celecoxib  Moderate  Same as “Mild” + a “Moderate” opioid  Codeine, hydrocodone, oxycodone  Severe  Morphine, hydromorphone, fentanyl

8 Step Treatment - WHO STEP 3 High potency opioids STEP 2 Low potency opioids STEP 1 Aspirin Celecoxib Acetaminophen NSAIDs

9 Opioid Receptor  Agonists  WHO – moderate & severe pain medications  Antagonists  Naltrexone, naloxone  Mixed (agonists & antagonists)  Buprenorphine, nalbuphine  Other  Meperidine, Tramadol, methadone

10 Neuropathic  Anticonvulsants  Pregabalin, gabapentin, carbamazepine, lamotrigine  TCA  Amitriptyline, nortriptyline, doxepin etc.

11 Mild pain  Celecoxib – Celebrex  Selective inhibitor of COX-2  COX-2  Inflammation ARACADONIC ACID  Fever CYCLOOXYGENASE  Pain 2 PGE2 Fever & Pain

12 Celecoxib - Celebrex  Kinetics  ADRs  Distribution – large  Edema, headache, (400 L) dizziness, skin rash, abd pain, diarrhea, cough,  Highly protein bound arthralgia, fever – 97%  Interactions  Metabolized – liver CyP2C9  Other NSAIDs, warfarin, anticoagulants, ACEI,  Half life – 11 hrs ARBs, alcohol, ASA  Time to peak – 3 hrs products  Excretion – feces &  Pregnancy urine (metabolites & unchanged drug)  C (less than 30 weeks) D

13 Opioid Receptors – Pain  Under normal  When opioid receptors circumstances are bound - Agonist P P Presynaptic Presynaptic Receptor Receptor C C

14 Opioid Receptors – Pain  Decrease in  When opioid receptors neurotransmitters are bound - Agonist  Glutamate P  Acetylcholine  NE Presynaptic  Serotonin  Substance P Receptor C

15 Types of opioid receptors  Classic  Mu  Kappa  Delta  Non-classic  ORL-1

16 Mu Receptors - agonists  Endogenous  Exogenous  Endorphins  Morphine Mu receptors are found in: Analgesia Respiratory depression Spinal cord Euphoria Effects Brainstem Sedation Thalamus Decreased GI motility Cortex Miosis Physical dependence

17 Delta Receptors - agonists  Endogenous  Exogenous  Enkephalins  DPDE (used in research) Delta receptors are found in: Analgesia (spinal) Olfactory bulb Decreased gastrointestinal Cerebral cortex motility Effects Nucleus accumbens Respiratory depression? Amygdala Pontine nucleus

18 Kappa Receptors - agonists  Endogenous  Exogenous  Dynorphin  Ketazocine (research) Kappa receptors are found in: Analgesia – Spinal Limbic system Sedation Effects Hypothalamus Dyspnea Brainstem Physical dependence Spinal cord Dysphoria Inhibit ADH release

19 Mu, delta, & Kappa - antagonist  Naloxone  Mu – Greatest Blocks the effects of affinity opioids but does NOT  Delta – Reduced cause the opposite affinity effects!  Kappa – Reduced affinity

20 Opioids - agonists  Uses  Tolerance  Pain  Effects  Cancer, surgical,  Analgesia, sedation, obstetric, trauma, euphoria, nausea, kidney & gall respiratory depression stones, sickle cell  Effects IMMUNE to  Anesthesia tolerance  Adjuvant  Miosis & CONSTIPATION  Others  Dyspnea w/MI  Anti-diarrheal  Cough suppressant

21 Opioid agonists  MOA - Binds to opioid receptors in the CNS, causing inhibition of ascending pain pathways, altering the perception of and response to pain; produces generalized CNS depression  Medication in class  Codeine < hydrocodone < oxycodone < morphine < hydromorphone < fentanyl

22 Opioids - agonists Kinetics  Absorption  Half life  Oral – well  ~2 hours absorbed, subject  Metabolized to first pass effect  Liver  SubQ, IM, IV – well  Excreted absorbed  Urine – mostly  Rectal – moderate metabolites absorption  Decreased in renal  Lipophilic forms – failure, elderly, and nasal, sublingual, & young transdermal

23 Opioids - agonists  ADRs  Interactions  Drugs - Alcohol, CNS  Bradycardia, depressants, MAO dysphoria, inhibitors dependence,  Conditions (CI) – drowsiness, Asthma, constipation, dry emphysema, cor mouth, urinary pulmonale retention,  Pregnancy – C, can tolerance, cross the placenta, can concentrate in breast milk

24 Opioid – antagonists Naloxone/naltrexone  MOA  Pure opioid antagonist that competes and displaces opioids at opioid receptor sites  Naltrexone  Competitive antagonist at mu opioid receptor

25 Opioid - antagonists  Naloxone  Naltrexone  Used in opioid  Differences overdose  Orally bioavailable (respiratory (PO & IM) depression)  Higher potency  Not orally bioavailable  Half life – 3 hours (parenteral  Duration – 24-28 administration) hours  Half life – 30-90  Active metabolite minutes (13 hours)  Duration – 1-2 hours

26 Opioids – mixed agonist/antagonists  Benefits  Pain relief w/o as many addictive qualities  Less respiratory depression & constipation  Risks  Can cause withdrawal symptoms (not for opioid dependent patients)  Types  Buprenorphine, nalbuphine, others

27 Others  Tramadol  MOA – Binds to μ -opiate receptors in the CNS causing inhibition of ascending pain pathways, altering the perception of and response to pain; also inhibits the reuptake of norepinephrine and serotonin, which are neurotransmitters involved in the descending inhibitory pain pathway responsible for pain relief

28 Tramadol  Kinetics  ADRs – Similar to opioid agonists  Onset – 1 hour  CNS – dizziness,  Duration – 9 hrs stimulation,  Absorption – rapid headache, & complete insomnia  Metabolism – liver  Constipation, N&V  Half life  Weakness  Parent – 6-8 hrs  Interactions – MAO  Metabolite – 7-9 inhibitors, alcohol, hrs CNS depressants  Excretion - urine  Pregnancy - C

29  Methadone  Used - addiction Others  Phenylheptylamines – binds to mu receptor  Inhibits NMDA & re-uptake  Meperidine of  Used - Surgery catecholamines/serotonin  Phenylpiperidine – still binds mu receptor  Substances added to  Not cough tablets to prevent abuse suppressant or  Variable kinetics antidiarrheal  Bioavailability – 36-100%  Can accumulate and cause SEIZURES  Half life – 8-59 hrs  Interaction – MAO  Metabolized by CYP3A4 inhibitors & 2B6  ADRs – hyperthermia,  Can prolong QTc interval muscle twitching, (EKG) hallucinations

30 Tricyclic Antidepressants  MOA - Increases the synaptic concentration of serotonin and/or norepinephrine in the central nervous system by inhibition of their reuptake by the presynaptic neuronal membrane pump  Various types of pain (neuropathic pain) – off label  Emotional aspect of pain  Amitriptyline, nortriptyline, doxepin, imipramine

31 Tricyclic Antidepressants  Kinetics  ADRs  Onset 4-8 weeks  Anticholinergic, decrease blood  Absorption – rapid pressure, sedation,  Metabolism – liver EPS  Half life – 13-36  Interactions hours  Anticholinergic  Excretion – urine agents, BP agents,  Can accumulate CNS depressants in elderly  Pregnancy – Risk C

32 Anticonvulsants  MOA – Vary with individual agents  Generally all have CNS effects involving neurotransmitters  Calm the over-activity/excitability of the CNS  Types  Gabapentin, pregabalin, lamotrigine, carbamazepine….

33 Anticonvulsants  Best for neuropathic pain  Select based on adverse drug effect profiles  Drug-drug interactions  Carbamazepine – MAJOR CYP enzyme inducer  Select based on ease of treatment  Dosing schedule

34 Questions  ?????????????????????????????????? ?????????????????????????????????? ?????????????????????????????????? ?????????????????????????????????? ?????????????????????????????????? ?????????????????????????????????? ?????????????????????????????????? ?????????????????????????????????? ??????????????????????????????????