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USU GSN Pharmacolgy - Pain and Anlagesia
Terms in this set (67)
Pain Is _______________ (Definition)
An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.
What are the two different types of pain.
Discuss what fibers carry Somatic Pain and the stimulus that is conducted.
a) First pain - Sharp, well Localized. a-Delta fibers. Transmitted fast.
b) Second Pain - Dull, diffuse, burning. c fibers. Slow, unmyelinated.
What is Visceral Pain?
Pain is poorly localized. Fewer visceral receptors than somatic receptors.
Pain is referred away from the source of stimulation.
What is a type of Visceral Pain?
Heart Attack. Pain radiates to Jaw, Left Arm, and/or Back. No Somatic receptors on heart. Pain piggybacks on Vagus Nerve
What are some of the local inflammatory mediators?
Kinins; Prostaglandins (E,F); Histamine; 5HT (Serotonin); Substance P; CGRP (Calcitonin Gene Regulated Protein)
Pain from non-noxious stimuli.
Exaggerated pain that is caused by an injury.
What is the Wind-up Process?
When pain is potentiated at the neuronal junction due to the release of enhancers such as Substance P and CGRP.
Explain the Gate Control Theory.
Suggests that pain can be "gated-out" in the Dorsal Horn by other stimuli.
The area in the Dorsal Horn where the afferent pain pathway interacts with the descending inhibitory pathway.
What are neuropeptides?
Endogenous opioids produced by the body. (Endorphin, Dynorphin, Enkephalin, etc.
Where in the brain is pain associated with activity?
What mediators are involved with the descending inhibitory pathway?
Norepinephrine, Serotonin, Endogenous Opioids.
What does an SSRI do for pain?
Alters the response to pain, but does not block it.
What is the Gold Standard for Agonism and Antagonism regarding Opioids?
Agonist - Morphine
Antagonist - Naloxone
What are Opioids. (definition)
Any substance, endogenous or synthetic, that produces morphine-like effects that are blocked by opioid antagonists.
What are the main groups of opioids?
Phenylpeperidines - Fentanyl, Meperidine
Benzomorphans - Pentazocine
Thebaine derivatives - Buprenorphine, Nalbuphine
What Opioid receptor is responsible for most of the analgesic effects of opioids?
What does the Delta receptor do?
Results in analgesia (spinal), Can be proconvulsant
The receptor that contributes to analgesia (spinal), but may also cause sedation, dysphoria, and hullicinations.
What does a partial agonist do?
A partial agonist can competitively displace a full agonist from its receptor. This causes a reduction in the effect of the full agonist.
Why would you want to give a partial agonist or agonist-antagonist vice a full agonist?
A full agonist will block all of the opioid receptors causing respiratory depression whereas the others will not.
Blocking Mu receptors causes what? and what?
Respiratory depression. Pain relief.
Describe general Opioid caharacteristics.
G coupled receptor family.
Significant amino acid sequences.
What is the cellular action of opioids?
Presynaptically closes and blocks a voltage-gated Ca2+ channel.
Postsynaptically opens K+ channels hyperpolarising the cell.
What are CNS effects of opioids?
Mu receptor mediated: Analgesia, Euphoria, Respiratory depression, depression of cough reflex, nausea/vomiting, and miosis.
What effect of opioids is not affected by chronic opioid use?
How will someone on opioids breath?
Slower and deeper pattern in the therapeutic range.
What is the MOA of cough suppression?
Unclear, it does not correlate with analgesic or respiratory doses.
Where is the N/V center in the brain?
What are the cardiovascular effects of opioids?
Normally minimal. Hypotension and bradycardia most common at high doses.
Tolerance is an increase in the amount of dose needed to produce an effect. What action is not affected by tolerance.
Constipation and miosis.
What is the MOA of dependence
Thought to be attributable to opioid-induced changes at the cellular level.
What drug can abstinence syndrome?
Clonidine. (a2 agonist)
What happens to opioids in patients with renal failure or functional issues.
Prolonged 1/2 life due to accumulation of metabolites.
What is the metabolite of morphine that may be more potent than morphine?
What is the metabolite in Demerol and what patient population does it affect?
Normeperidine effects neonates, infants, and the elderly. CNS excitation
What are phenanthrenes?
Morphine, hydromorphone, codeine, hydrocodone, and oxycodone.
What is methadone typically prescribed for and why is it not normally used as a primary pain control adjunct.
Typically prescribed for chronic, heroin addiction. Unpredictable 1/2 life. >24 hours.
What is a side effect of Demerol and why?
Tachycardia. Has antimuscarinic (anticholinergic) properties. Contraindicated in underlying tachycardia.
Describe the potency of the Fentanyl group of phenylpiperidines in descending order.
Sufentanyl (5-10 times) > Remifentanyl (2 times) > Fentanyl (100 times more potent than morphine) > Alfentanyl.
What is the MOA of Pentazocine?
Kappa agonist and Mu antagonist. associated with dysphoria (Kappa receptor)
What is an advantage of Buprenorphine?
Partial Mu agonist. Has a respiratory depressant ceiling.
What occurs if Naloxone is given to a patient with chronic pain and why?
Hyperalgesia and pain intensifies because Naloxone is antagonizing endogenous opioids.
What is the order of antagonism for Naloxone?
Opiod antagonists do what?
a) Respiration b) Level of Consciousness c) Pupil Size d) GI Motility
What does COX-1 and COX-2 inhibit?
COX-1, Platelet stickiness
COX-2, Inflammatory response
What inflammatory stimuli is produced after an injury.
Arachidonic Acid. Also IL-1, Prostacyclin.
Cyclooxygenase-1 is inducible. True/False.
False. COX-1 is found in most tissues, whereas COX-2 is induced by injury, infection, or activation by inflammatory cytokines (IL-1, TNF-a, etc.)
COX-2 produces what?
Prostaglandins in the inflammatory response.
Name the three major functions of NSAIDs.
Analgesia, Anti-Inflammatory, Antipyretic.
What is the prototypical NSAID?
Aspirin. Non-specific COX enzyme inhibitor.
What is the MOA of ASA?
Irreversibly blocks platelet COX. Lasts for 8-10 days (the life of a platelet)
What are some of the unwanted effects of NSAIDs?
GI effect (Most common), skin reactions, adverse renal effects, CV.
What drug can be given with NSAIDs to combat GI side effects?
Misoprostol (Oral prostaglandin analogue)
Renal effects of NSAIDs occur in what patient population and why?
Acute renal insufficiency, extremes of age, hypovolemia. Due to inhibition of PGE2, PGI2, and prostacyclin.
NSAIDs can oppose the effects of hypertensive medications. True/False.
What are the CNS effects of Aspirin?
Salicylism. Tinnitus, decreased hearing, vertigo.
What is a concerning ASA interaction with warfarin?
Warfarin in conjunction with ASA increases the effect of displacement & inhibition of platelet aggregation.
ASA can make gout worse because of what?
Inhibiting uricosuric effect of Probenecid and Sulfinpyrazone.
NSAIDs are more likely to cause gastric ulceration in what dosage ranges and what is the recommended length of dose?
Anti-Inflammatory doses. Not recommended for longer than 10 days without concurrent administration of Misoprostol.
What are the side effects of COX-2 inhibitors?
Rash, edema, headache, dizziness.
What is the effect of Paracetamol?
Non NSAID analgesic and antipyretic. Inhibits prostaglandin synthesis.
What is the toxic dose of Acetaminophen.
10-15 grams. Not to be used for > 4 g/day due to increased risk of hepatotoxicity.
What are Amitryptylene and Gabapentin used for?
Chronic Neuropathic pain. Phontom limb pain. Trigeminal neuralgia.
What do NMDA antagonists do?
Theorized to interfere with the "Wind-up" Phenomenon in the Dorsal Horn.
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