Kaplan Section 4 Chapter 1 CNS Pharm - Muscle Relaxants, Opioid Analgesics
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| What is the structure of Nm receptors? | 5 subunits: 2 alpha - binds Ach (requirement for opening the Na channel)
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| What is the mechanism of muscle relaxants (MR's)? | MR's competitively bind to the alpha subunits of Nm receptors --> prevent depolarization
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| What is succinylcholine? | Muscle relaxant
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| What is so special about the mechanism of succinylcholine? | It's the only MR that bind noncompetitively and instead of preventing depolarization, it opens the Na channel --> excessive depolarization --> desensitization
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| Describe the 2 phases of succinylcholine action | Phase 1 - depolarizing: brief fasciculation --> flaccid paralysis (made worse by AchEi's). Phase 2: - desensitization: end plate repolarizes, but remains unresponsive to Ach some time before recovery.
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| Talk about succinyl choline's duration of action | short duration (metabolized by plasma pseudocholinesterases). However, prolonged effects in people with genotypic variants that have low enzyme activity (less enzyme --> slower breakdown of drug)
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| Adverse effects of succinyl choline | HyperK and malignant hyperthermia
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| Name all the muscle relaxants | NaM SPAT - Mivacurium, Succinyl choline (dep), Pancuronium, Atracurium, Tubocurarine
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| How do you reverse the effects of a competitive muscle relaxant? | Competitive=nondep (decrease the freq of Na channel opening, but don't affect conductance or duration of channels that work). Use AchEi's (PPEND - i.e. neo/pyridostigmine) --> increase Ach at end plate-->overwhelm MR's attached to alpha subunits
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| What is effect of Nm antagonists? | Progressive paralysis, starting with etes and face and progressing via limbs to respiratory muscles. (doesn't affect heart, smooth muscle, or consciousness)
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| What does d-tubocurarine do? | 1. block ANS ganglia, 2. releases histamine --> dec BP
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| Adverse effects of d-tubocurarine | may cause bronchial secretions and bronchospasms; implicated in malignant hyperthermia
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| What is malignant hyperthermia? | Life-threatening. Muscle rigidity, hyperthermia, HTN, acidosis, and hyperK. Associated with use of muscle relaxants (esp succinyl choline)
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| Who is genetically susceptible to developing malignant hyperthermia? | mutations in genes encoding ryanodine receptrs and/or protein of L-type Ca channels in skeletal muscle
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| What is the difference between pancuronium and d-tubocurarine? | pancuronium has more rapid onset and recovery. INCREASES BP (tubocurarine decreases BP) because it is a vagolytic (dec PANS) and sympathomimetic (inc SANS)
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| What stands out about atracurium as a muscle relaxant? | Rapid recovery, safer in hepatic or renal dysfunction because it's spontaneously inactivated --> forms laudanosine. However, this metabolite can enter the CNS and cause seizures.
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| Mivacurium | Very short duration, causes histamine release.
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| How is mivacurium metabolized? | Plasma pseudocholinesterase.
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| What other drugs can help relax skeletal muscles? | spasmolytics - reduce excessive tone or spasm in acute muscle injury and CNS dysfunction (e.g. cerebral palsy, MS, stroke) without loss of muscle strength
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| Name the spasmolytics that reduce the tonic output of motoneurons | BZ's and baclofen
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| Where do BZ's act? | at the BZ receptors in the GABAa/Cl- channel macromolecule
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| What is Baclofen? | Direct agonist at GABAb receptors in spinal cord --> enhance GABA action --> more inhibition
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| Compare Baclofen to Diazepam | Diazepam is the longest acting BZ, and can be used for muscle relaxation. Baclofen is as effective as diazepam in relieving muscle spasticity, but causes much less sedation.
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| Name the spasmolytics that block Ca release from sarcoplasmic reticulum | Dantrolene. Acts directly on skeletal muscle --> decreases contractility
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| When would you want to use dantrolene? | in states of extreme muscle rigidity such as malignant hyperthermia
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| What drugs can cause malignant hyperthermia? | inhaled anesthetics and skeletal muscle relaxants
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| Name endogenous opioids in our bodies | enkephalins, dynorphins, B-endorphins
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| Opioid receptors are what kind of receptors? | G-protein linked
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| What is the mechanism of opioid receptors pre and post-synaptically? | activation of PRESYNAPTIC opioid receptors --> inhibition of Ca influx (voltage-regulated ion channels) --> dec NT release; activation of POSTSYNAPTIC opioid receptors --> increased K OUT --> hyperpolarization --> inhibition
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| What is the mechanism of supraspinal analgesia? | mu opioid receptors in the midbrain (periaqueductal gray region) --> actiavte descending pathways to the Raphe nuclei (ventral medulla) --> dec transmission in pain pathways.
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| What is the mechanism of spinal analgesia? | activation of mu & kappa opioid receptors in dorsal horn of spinal cord --> do not release substance P (NT that causes excitatory actions in pain pathways). Receptors located PREsynaptically on primary afferent fibers (C & A-delta).
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| Analgesic effects of opioids | inc pain tolerance; dec perception and rxn to pain
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| What opioid will give maximum pain relief? | morphine - full agonist at opioid receptors
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| With which type of pain are opioids most effective? | persistent, dull, aching pain responds better than intermittent pain
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| Can opioids cause short term memory loss? | yes
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| How do opioids affect a patient's breathing? | depression of brainstem respiratory center --> dec response to increasing PCO2 --> major problem in OD
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| How do opioids affect the heart? | Minimal effects on heart
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| How do opioids affect vessels? | Head: cerebral vasodilation --> inc intracerebral P; vasculature: histamine release --> hypoTN
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| What does morphine do to BP? | releases histamine --> decrease BP
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| How do opioids affect the GI tract? | decreases GI peristalsis --> constipation (can be used as anti-diarrheal)
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| What are loperamide and diphenoxylate? | Opioids that are used as anti-diarrheal medications
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| How do opioids affect smooth muscle? | inc tone of biliary, bladder, and ureter. Dec tone of vasculature (histamine --> hypoTN) and uterus (slower delivery)
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| How do opioids affect the pupils? | Inc Ach activity --> miosis
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| How does meperidine differ from the rest of the opioids? | Meperidone blocks M receptors --> no smooth muscle contraction and no miosis. Doesn't increase the tone of biliary, bladder, and ureter.
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| How do opioids affect a patient's coughing? | Suppresses coughing, independent of the analgesic action. (e.g. dextromethorphan or codeine)
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| Why do opioids cause nausea and vomiting? | stimulates the chemoreceptor trigger zone in the area postrema.
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| Where is morphine metabolized? | Liver - first pass metabolism, so low oral availability
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| What is morphine-6-glucuronide? | highly active metabolite of morphine --> contribute to analgesia
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| In what patient population would you want to reconsider the administration of morphine? | 1. Head injuries(cerebral vasodil-->inc intracranial P), 2.pulm dysfxn(resp depression), 3.hepatic/renal dysfxn: morphine-6-glucuronide-->toxicity w accumulation, 4.adrenal/thyroid def (exaggerated responses to opioids), 5. preg (dependence/neonatal depre
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| Where are opioid analgesics metabolized | liver
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| What is the characteristic triad of acute toxicity from opioid analgesics? | 1. pinpoint pupils 2. respiratory depression, 3. comatose state
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| How to manage a pt with toxicity from opioid analgesics? | 1. maintain airway, 2. assist ventilation (do NOT give O2 --> decreases breathing by patient), 3. UC naloxone (opioid receptor antagonist)
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| How to manage a pt with withdrawal from opioid analgesics? | 1. oral methadone (full mu-opioid agonist), buprenorphine (partial agonist activity at μ-opioid receptors, κ-opioid receptor antagonist), or clonidine (a2 agonist - combat SANS response to wdrawal - tachy & HTN) 2. gradual dose tapering
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| What is pharmacodynamic tolerance? | change in receptors
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| What is pharmacokinetic tolerance? | change in elimination rate of drug (e.g. induction of enzymes that break down drug)
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| What is cross-tolerance? | dec response to onedrug due to exposure to another drug (usually of the same class)
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| What kind of tolerance occurs with opioid analgesics? | pharmacodynamic tolerance -- changes in cellular adaptive responses, but the number of receptors stays the same
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| Describe withdrawal from opioid dependence | 1. anxiety, 2. lacrimation, 3. rhinorrhea, 4. sweating, 5. yawning, 6. goosebumps (cold turkey), 7. hot/cold flashes, 8. muscle cramps/spasms (kicking the habit), 9. GI (cramps & diarrhea), 10. perception of pain (originating in CNS)
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| what kind of drug is heroin? | Full agonist opioid
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| Name 3 opioid mu receptor full agonists | Morphine, methadone, meperidine
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| What is normeperidine? | metabolite of meperidine that can cause seizures
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| Name 3 opioid mu receptor partial agonists | buprenorphine > codeine > propoxyphene
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| Adverse effect of propoxyphene | Toxic in OD and has difficult withdrawal
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| Name two opioids that have both kappa agonist and weak mu antagonist actions | 1. nalbuphine, 2. pentazocine
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| What stands out about nalbuphine? | good analgesic with less abuse liability than most strong opioids; if OD, however, naloxone may be less effective in reversing its effects because of nalbuphine's kappa activity.
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| Name a strong mu opioid receptor antagonist | Naloxone - used to reverse CNS depressant effects of opioid agonists.
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| What does naltrexone do? | mu opioid receptor antagonist; taken PO; decreases "craving" in alcoholism.
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