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Drugs acting at the Opiod Receptors

Activators of pain receptors capsaicin, pH < 7 (increase H ions); increased temperature
what are the endogenous pain killers? enkephaline, endorphine, dynorphine
how do the endogenous pain killers work? they are released and act at the synaptic sites in the dorsal horn and thalamus; they interact with endogenous opioid receptors
endorphines (receptor, action, location) mu-opioid receptor; open K channels leading to hyperpolarization; supraspinal/brain
mu-opioid receptor effects spinal and supraspinal analgesia; euphoria, respiratory depression, bradykardia, constipation, urinary retention, miosis, high addiction potential
enkaphalines (receptor, action, location) delta-opioid receptors, modulate mu-receptor activity; everywhere mu is
dynorphines (receptor, action, location) kappa-opioid receptor; inhibit Ca channels (decrease transmitter release); spinal
kappa opioid receptor effects spinal analgesia; dysphoria, psychoto-mimetic effects; low addiction potential
how are the endogenous opioid-peptides metabolized? via neuropeptidases; cleave the amino-terminal tyrosine residue (have ultra short t1/2)
morphine (receptor, effects, metaboilism, t1/2; analgesic potency) mu agonist; histamine release (itching), activates dopamine receptors (emesis); hepatic metab to M6G; t1/2 = 3 h; analgesic potency = 1
piritramid morphine with less SE (less histamine release), 0.8 Mo
codeine hepatic metabolism (3A4 & 2D6) to 10% morphine; analgesic potency 1/10 Mo
tramadol (metabolism, receptor, mode of action) 2D6 metabolism to mu-opioid agonist; NaSRI; alpha-2-agonist (clonidine-like); slows you down
pentazocine kappa agonist, weak mu antagonist; can cause withdrawal syndrome in morphine abuser
methadone mu agonist and NMDA antagonist (double analgesic); slow onset and variable t1/2; active metabolite with long t1/2; accumulation/sedation; 4-12 Mo
what are the i.v. opioids in decreasing order of potency? morphine (10^0); alfentanil (10^1); fentanyl (10^2); remifentanil (10^2); sufentanil (10^3)
what is the mode of action of the i.v. opioids? selective mu agonists
which of the i.v. opioids is the shortest acting? remifentanil is ultra short (infusion)
meperidine/pethidine (analgesic potency, t1/2, metabolite, actions, effects) 1/10 Mo; short t/12; normeperidine (1/20 Mo) is neurotoxic and accumulates (renal insufficiency); anticholinergic, SSRI, alpha-blocker; interacts with MAO-I; post-anesthetic shivering
naloxone opioid antagonist; used for respiratory depression
what are the 3 things that can result in emesis? activation of GIT afferent 5HT3; activation of dopamine receptors in CRTZ zone; activation of vestibular-nucleus which activates muscarin (acts on CRTZ)
what are the 3 ways one can stop emesis? use a 5-HT3 blocker; use a dopamine2 blocker; use a muscarin-blocker
-setron 5-HT2 antagonist
droperidol (DHB) and metoclopramid D2 antagonist; 5-HT3 antagonist, 5-HT4 agonist
scopolamine muscarine antagonist; only good for sea-sickness/ motion induced sickness
atropine ROSA; not useful for vomiting; can induce bradycardia at very low doses
central anticholinergic syndrome occurs from overdose of anticholinergic drug; dry as a bone (lack of perspiration), hot as a hare (body temp increases), red as a beet (periphery dilates), blind as a bat (lose ability to accommodate), mad hatter
poisoning of AChesterase inhibitor Diarrhea, Urination, Miosis, Bronchorrhea/Bronchospasm, Bradykardia, Emesis, Lacrimation, Laxation, Salivation
diphenhydramine H1-blocker (1st gen); anticholinergic; sleeping pill, also used for motion sickness (antimuscarinic)
Created by: cbart004



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