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USMLE - Pharm

Kaplan Section 4 Chapter 1 CNS Pharm - Muscle Relaxants, Opioid Analgesics

What is the structure of Nm receptors? 5 subunits: 2 alpha - binds Ach (requirement for opening the Na channel)
What is the mechanism of muscle relaxants (MR's)? MR's competitively bind to the alpha subunits of Nm receptors --> prevent depolarization
What is succinylcholine? Muscle relaxant
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
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.
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)
Adverse effects of succinyl choline HyperK and malignant hyperthermia
Name all the muscle relaxants NaM SPAT - Mivacurium, Succinyl choline (dep), Pancuronium, Atracurium, Tubocurarine
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
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)
What does d-tubocurarine do? 1. block ANS ganglia, 2. releases histamine --> dec BP
Adverse effects of d-tubocurarine may cause bronchial secretions and bronchospasms; implicated in malignant hyperthermia
What is malignant hyperthermia? Life-threatening. Muscle rigidity, hyperthermia, HTN, acidosis, and hyperK. Associated with use of muscle relaxants (esp succinyl choline)
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
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)
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.
Mivacurium Very short duration, causes histamine release.
How is mivacurium metabolized? Plasma pseudocholinesterase.
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
Name the spasmolytics that reduce the tonic output of motoneurons BZ's and baclofen
Where do BZ's act? at the BZ receptors in the GABAa/Cl- channel macromolecule
What is Baclofen? Direct agonist at GABAb receptors in spinal cord --> enhance GABA action --> more inhibition
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.
Name the spasmolytics that block Ca release from sarcoplasmic reticulum Dantrolene. Acts directly on skeletal muscle --> decreases contractility
When would you want to use dantrolene? in states of extreme muscle rigidity such as malignant hyperthermia
What drugs can cause malignant hyperthermia? inhaled anesthetics and skeletal muscle relaxants
Name endogenous opioids in our bodies enkephalins, dynorphins, B-endorphins
Opioid receptors are what kind of receptors? G-protein linked
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
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.
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).
Analgesic effects of opioids inc pain tolerance; dec perception and rxn to pain
What opioid will give maximum pain relief? morphine - full agonist at opioid receptors
With which type of pain are opioids most effective? persistent, dull, aching pain responds better than intermittent pain
Can opioids cause short term memory loss? yes
How do opioids affect a patient's breathing? depression of brainstem respiratory center --> dec response to increasing PCO2 --> major problem in OD
How do opioids affect the heart? Minimal effects on heart
How do opioids affect vessels? Head: cerebral vasodilation --> inc intracerebral P; vasculature: histamine release --> hypoTN
What does morphine do to BP? releases histamine --> decrease BP
How do opioids affect the GI tract? decreases GI peristalsis --> constipation (can be used as anti-diarrheal)
What are loperamide and diphenoxylate? Opioids that are used as anti-diarrheal medications
How do opioids affect smooth muscle? inc tone of biliary, bladder, and ureter. Dec tone of vasculature (histamine --> hypoTN) and uterus (slower delivery)
How do opioids affect the pupils? Inc Ach activity --> miosis
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.
How do opioids affect a patient's coughing? Suppresses coughing, independent of the analgesic action. (e.g. dextromethorphan or codeine)
Why do opioids cause nausea and vomiting? stimulates the chemoreceptor trigger zone in the area postrema.
Where is morphine metabolized? Liver - first pass metabolism, so low oral availability
What is morphine-6-glucuronide? highly active metabolite of morphine --> contribute to analgesia
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
Where are opioid analgesics metabolized liver
What is the characteristic triad of acute toxicity from opioid analgesics? 1. pinpoint pupils 2. respiratory depression, 3. comatose state
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)
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
What is pharmacodynamic tolerance? change in receptors
What is pharmacokinetic tolerance? change in elimination rate of drug (e.g. induction of enzymes that break down drug)
What is cross-tolerance? dec response to onedrug due to exposure to another drug (usually of the same class)
What kind of tolerance occurs with opioid analgesics? pharmacodynamic tolerance -- changes in cellular adaptive responses, but the number of receptors stays the same
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)
what kind of drug is heroin? Full agonist opioid
Name 3 opioid mu receptor full agonists Morphine, methadone, meperidine
What is normeperidine? metabolite of meperidine that can cause seizures
Name 3 opioid mu receptor partial agonists buprenorphine > codeine > propoxyphene
Adverse effect of propoxyphene Toxic in OD and has difficult withdrawal
Name two opioids that have both kappa agonist and weak mu antagonist actions 1. nalbuphine, 2. pentazocine
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.
Name a strong mu opioid receptor antagonist Naloxone - used to reverse CNS depressant effects of opioid agonists.
What does naltrexone do? mu opioid receptor antagonist; taken PO; decreases "craving" in alcoholism.
Created by: christinapham