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OPIOIDS
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TYPES OF OPIOIDS
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Basics Opioid Slides
Barry Basics Opiod Slides
| Question | Answer |
|---|---|
| OPIOIDS | Exogenous substances that specifically bind to several sub-populations of opioid receptors and produce agonist (morphine like) effects.Used during induction to decrease sympathetic response to laryngoscopy and during maitenance and post-op for analgesia. |
| TYPES OF OPIOIDS | Naturally occurringSemi syntheticSynthetic |
| NATURALLY OCCURRING OPIOIDS | Morphine and Papaverine: Derived from opium, an extract of the poppy plant. |
| SEMI SYNTHETIC OPIOIDS | Heroin, Hydrmorphone, Thebain (not used by itself - is a precursor for oxycodone and oxymorphone): Result from simple modifications of the morphine molecule. |
| SYNTHETIC OPIOIDS | Demerol, Methadone, Fentanyl, Butorphanol, Pentazocine: Manufactured by synthesis rather than chemical modification of morphine. |
| CLASSIFICATIONS OF OPIOIDS | AgonistsAgonist-antagonistsAntagonists (Competitive and Non-competitive) |
| AGONISTS | Capable of eliciting full agonist (morphine-like) effects |
| AGONIST-ANTAGONISTS | Bind to Mu receptors and produce limited responses (partial agonist) or no effect (competitive antagonist) But.....may also have agonist effects at other receptors. |
| ANTAGONISTS | Competitive: binds to receptor but can be knocked off if a higher concentration of the agonist is present.Non-competitive: Very strong affinity for receptor. NOT DISPLACED by high concentrations of the agonist. |
| MOA | Bind at receptors to block transmission of pain.Receptors in dorsal horn of spinal cord, the brain (supraspinal), and peripheral tissue.Receptors endogenously activated by: endorphins, enkephalins and dynorphins. |
| WHAT DO OPIOIDS MIMIC? | The actions of endogenous ligands (endorphins, enkephalins and dynorphins) by binding to the opioid receptor which activates pain modulating systems. |
| HOW DO OPIOIDS CAUSE SUPRASPINAL ANALGESIA? | By activating postsynaptic opioid receptors in the midbrain and medulla (results in inhibition of pain pathways. |
| HOW DO OPIOIDS CAUSE SPINAL ANALGESIA? | By activating presynaptic opioid receptors (results in decreased release of neurotransmitters involved with nociception). |
| HOW DO OPIOIDS CAUSE PERIPHERAL ANALGESIA? | By activating opioid receptors on primary afferent neurons (antinociceptive activity). |
| OPIOID RECEPTORS | Discovered: Early 1970'sConstantly revised: intitially thought to be Mu, Kappa and Sigma, NOW Mu, Delta and Kappa which have many subtypes.Each receptor has a different function.Desired effects come mostly from action at Mu receptors. |
| MU-1 RECEPTORS | Primarily supraspinal analgesiaSome spinal analgesiaEuphoriaMiosisUrinary retention |
| MU-2 RECEPTORS | Primarily spinal analgesiaRespiratory depressionBradycardiaPhysical dependenceConstipation N/VItching |
| KAPPA RECEPTORS | Spinal and supraspinal analgesiaSedationDysphoria (psychosis) |
| DELTA RECEPTORS | Mostly spinal analgesiaSome supraspinal analgesiaSome respiratory depressionPhysical dependence |
| CHARACTERISTICS COMMON TO ALL OPIOIDS. | Dose-dependent ventilatory depression (decreased RR with compensatory increased TV)Not reliable at producing LOC: some sedation,but main effect is analgesia.May stimulate chemoreceptor trigger zone.Cause spasm of biliary smooth muscle. |
| HOW IS BILIARY SMOOTH MUSCLE SPASM TREATED? | Nitro, Atropine,Naloxone,Glucagon,and Benadryl (?) |
| MORPHINE | The Prototype: E 1/2 time is 1.5-3hrs.Doseages: Intra-op- 0.1-1 mg/kg IV Post-op- .05-0.2mg/kg IV .03-0.15 mg/kg IV |
| WHAT IS THE MAJOR FEATURE OF MORPHINE? | Histamine release!Signs and symptoms: local redness, itching and hives. Decreased BP and Increased HR and flushing.Slow administration reduces this risk! |
| WHAT ARE THE ACTIVE METABOLITES OF MORPHINE? | Morphine 3-glucuronideMorphine 6-glucuronideMorphine 6-glucuronide is a more potent and longer acting agonist than morphine! |
| HOW IS MORPHINE METABOLIZED? | It undergoes biotransformation in the liver.Excreted by the kidneys (problem for pts. who have renal dx.) |
| HYDROMORPHONE | Pharmacokinetic profile similar to morphine.8-10X more potent than morphine.Similar SE profile (less n/v, itching, and dysphoria).No active metabolite. |
| MEPERIDINE | 1st synthetic opioid.1/10 the potency of morphine.E 1/2 time: 3-5hrsDose: 0.5-1 mg/kg IM and 0.2-0.5 mg/kg IVStructure: Similar to atropine. Increases HR, Mydiasis (eyes dilate) and dry mouth. |
| WHICH OPIOID IS GIVEN IN PACU FOR SHIVERING? | Meperidine: Mechanism is unclear, but it is believed that meperidine stimulates the kappa receptors which decreases the shivering threshold. Is an agonist at alpha-2 receptors. |
| WHAT IS THE METABOLITE OF MEPERIDINE? | Normeperidine: Excreted by the kidneys. Is neurotoxic at high concentrations causing myoclonus and seizures. |
| WHICH OPIOID IS UNSAFE TO GIVE TO PATIENTS ON MAOI'S LIKE NARDIL? | Meperidine:Causes a severe excitatory state: signs and symptoms include: Increase in HR, BP and Temp. Delerium, seizures and possible death. |
| FENTANYL | Structurally related to meperidine.100x more potent than morphine.E 1/2 time: 3-6 hours.Doseages: Intra-op- 2-10 mcg/kg. CT surgery- 30-50 mcg/kg. Post-op-0.5-1.5 mcg/kg.Minimal CV depression: may decrease HR.1cc = 50 mcg. |
| WHICH OPIOID CAUSES CHEST WALL RIGIDITY? | Fentanyl |
| SUFENTANYL | 7-10x more potent than fentanyl.Intra-op dose: 0.2-0.8 mcg/kgCT surgery: 10-30 mcg/kgE 1/2 time: 2.5-3.5 hours |
| ALFENTANYL | 1/5-1/10 As potent as fentanyl.Intra-op dose: 10-100 mcg/kgE 1/2 time: 1.5 hrs.More rapid onset and shorter duration of action then fentanyl and sufentanyl. |
| REMIFENTANYL | Similar potency as fentanyl.Extremely rapid onset, clearance and recovery.E 1/2 time: 15-30 min.Dose: 1 mcg/kg IV over 60-90sec then 0.25-1mcg/kg or 0.05mcg/kg/min. |
| HOW IS REMIFENTANYL METABOLIZED? | By non-specific plasma and tissue esterases. |
| WHAT ARE THE OPIOID ANTAGONISTS? | Naloxone and Naltrexone |
| NALOXONE | Also known as Narcan.Most frequently used.Great affinity for Mu receptors and is a competitive antagonist.Used to reverse unconciousness from narcotic overdose.Reverses respiratory depression: give in 20-40mcg increments. |
| HOW LONG DOES NARCAN LAST? | Peaks in 1-2 min and lasts 30-45 min.May require redosing. |
| HOW IS NARCAN MIXED? | Mix 1 amp (0.4mg) in 9cc of NS. Give one cc at at a time (20 mcg). |
| WHAT HAPPENS WITH ABRUPT REVERSAL OF OPIOIDS? | Execessive sympathetic stimulation!Arrythmias, Inc HR, Inc BP, N/V, and Pulmonary edema. |
| NALTREXONE | Also known as Trexan.Longer acting anatagonist given in PO form for addicts.May last up to 24 hoursPatients who take this may have a temporary resistance to narcotics. |
| WHAT ARE THE OPIOID AGONISTS-ANTAGONISTS (PARTIAL-AGONISTS)? | Butorphanol (Stadol)Nalbuphine (Nubain) |
| BUTORPHANOL | Partial AgonistProduces analgesia and respiratory depression similar to 10mg of morphine.More sedation than Nubain.Incidence of dysphoris is low.Does not increase biliary pressure.Can be used to tx post-op shivering.Dose: 0.5-3mg IV. |
| NALBUPHINE | Partial agonist at kappa and Mu recceptors.Like morphine analgesia.Less sedative than Stadol.Will reverse respiratory depression but not analgesia.Used for itching from morphineCan be given IV or IMDose: 5-10mgCan cause withdr |
| WHICH PARTIAL AGONIST CAUSES WITHDRAWL IN ADDICTS? | Nubain (nalbuphine) |
| WHAT IS FLUMAZENIL? | A BENZODIAZEPINE ANTAGONIST!!!!! (competitive)Reversal can be total or partial, depends on dose.High affinity for Benzo receptors but minimal intrinsic activity.Dose: usually 0.2mg increments titrated to effect. Not to exceed 1mg. |
Created by:
Christine.scott1
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