Acute Pain Flashcards
This drug is a relatively inexpensive synthetic opioid considered to be a broad-spectrum opioid because it is a (1) μ receptor agonist, (2) NMDA antagonist, and (3) inhibitor of monoamine transmitter reuptake, making it potentially useful for the treatment of neuropathic pain. It is generally not necessary to adjust the dosage of methadone in patients with renal insufficiency.
Methadone
This drug is a highly lipophilic partial μ opioid receptor (MOR) agonist, κ receptor (KOR) antagonist, and ORL1 agonist. It is a lipophilic opioid with moderate intrinsic activity and a high affinity for the μ opioid receptor. It also produces less constipation and less cognitive dysfunction than other μ opioid receptor agonists and does not prolong the QTc interval like methadone.
Buprenorphine
This drug is an excellent alternative for the treatment of acute pain in the patient who cannot tolerate morphine secondary to allergy or other sensitivity.
Buprenorphine
In the adult patient the parenteral dose of buprenorphine is 300 μg, which is equivalent to 10 mg of morphine.
A novel (off-label) route of administration of buprenorphine is the PERINEURAL application of the drug with local anesthetic. Referred to as multimodal perineural analgesia.
These drugs are orally active, centrally acting synthetic analgesics possessing a novel mechanism of action which combines μ receptor agonist activity with monoamine reuptake inhibition.
Tramadol (inhibits reuptake of NE & serotonin) (MILD-MOD pain)
Tapentadol (inhibits reuptake of NE) (does not require enzymatic conversion to an active drug) (MOD-SEVERE pain)
Advantages of tapentadol over tramadol include
- lack of CYP450 drug interactions
- lower risk of seizures and serotonin syndrome
- superior analgesia
- fewer GI side effects
- less variation in individual drug response secondary to genetic polymorphism
Serotonin Syndrome
- mental status changes
- autonomic instability
- neuromuscular aberrations
Is the constitutive enzyme that produces prostaglandins, which are important for general “house-keeping” functions such as gastric protection and hemostasis.
COX-1
Is the inducible form of the enzyme that produces prostaglandins that mediate pain, inflammation, fever, and carcinogenesis.
COX-2
Is the key mediator of both peripheral and central pain sensitization.
PGE2
Peripherally, prostaglandins do not directly mediate pain; rather, they contribute to hyperalgesia by sensitizing nociceptors to other mediators of pain sensation such as histamine and bradykinin.
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Unlike the opioids, NSAIDs exhibit a “ceiling effect” with respect to maximum analgesic effects.
The optimal dose of ketorolac for postoperative pain control is 15 to 30 mg intravenously every 6 to 8 hours, not to exceed 5 days.
This drug inhibits prostanoid synthesis. It does not enter the active site COX but reduces Fe IV to Fe III and prevents activation of the peroxide catalytic moiety and therefore inhibits PGH2 synthesis.
Paracetamol
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NSAIDs and COX-2–selective inhibitors should not be administered to patients with known hypersensitivity to the drugs or to patients with Samters triad (aka aspirin triad), which is a medical condition
characterized by asthma, aspirin insensitivity, and nasal polyposis.
Finally, avoid celecoxib and valdecoxib in patients with allergic-type reactions to sulfonamides.
This drug has both analgesic and antipyretic properties, similar to aspirin, but is devoid of any anti-inflammatory effects. The drug is primarily a centrally acting inhibitor of the COX enzyme with minimal peripheral effects. Acetaminophen neither enters the active site of the COX enzyme nor binds to the COX site, but instead it prevents COX activation by reducing heme at the peroxidase site of the enzyme.
Paracetamol
In adults, 2 g of oral acetaminophen is equivalent to 200 mg of celecoxib.
MC side effect of dextromethorphan?
Nausea and vomiting
Because the intravenous administration of large doses can lead to hypotension and tachycardia, the intramuscular route may be the preferred route of delivery.
An NMDA receptor antagonist which has been shown to both inhibit secondary hyperalgesia following peripheral burn injury and cause a reduction in temporal summation of pain.
Dextropmethorphan
Side effects from clonidine include sedation, hypotension, and bradycardia if the dose exceeds?
150 ug
This drug is a potent and highly selective α2-adrenoreceptor agonist which demonstrates cardioprotective, neuroprotective, and renoprotective effects against hypoxic/ischemic injury.
Dexmedetomidine
The drug does not decrease gut motility and prevents postoperative nausea and vomiting and shivering.
Has no anticholinergic effects and promotes more physiological sleep pattern attributes
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The most frequently observed adverse effects associated with the use of dexmedetomidine are bradycardia and hypotension, which can be adequately treated with atropine, glycopyrrolate, and ephedrine.
Compared to traditional analgesics, which decrease afferent input from the site of tissue injury, these drugs decrease the hyperexcitability of dorsal horn neurons caused by tissue damage.
Gabapentinoids
Although structurally similar to GABA these drugs are not GABAergic and do not bind GABAA GABAb GABAc radioligand sites or allosteric GABA receptor sites.
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Although structurally similar to GABA these drugs are not GABAergic and do not bind GABAA GABAb GABAc radioligand sites or allosteric GABA receptor sites.
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The antinociceptive mechanism of action of the gabapentinoids has two aspects: modulation of the calcium-induced release of glutamate centrally in the dorsal horn, and activation of descending noradrenergic pathways in the spinal cord and brain.
The gastrointestinal absorption of gabapentin occurs only in the?
Duodenum through a SATURABLE transport system resulting in bioavailability that decreases with increasing doses.
Preoperative dosing of gabapentin as high as 1,200 mg orally has been recommended
In the opioid-naive patient, the preoperative dose of gabapentin should rarely exceed 300 mg orally.
Pregabalin, on the other hand, is absorbed in?
small intestines through a NONSATURABLE transport system and has a linear pharmacokinetic profile (dose-independent absorption), and is more potent than gabapentin.
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However, because it takes gabapentin and pregabalin 4 to 6 hours and 8 hours, respectively, to reach peak cerebrospinal fluid levels dosing of the drug the evening prior to surgery may ultimately prove to be the most beneficial method of administration.
