Pharmacology Flashcards
Mu1, Mu2, kappa, delta
inhibit calcium transport presynapitcally and potentiating potassium transport post synaptically , reduce synaptic action potential of central/c pain fibers
Mu1
pain reduction (#1 opioid pain receptor)
Mu2, Kappa side effect
have side effect of respiratory depression “kappa Kills and Mu2 is a character that kills”
codeine metabolism
morphine and hydrocodone –> hydromorphone
morphine and hydrocodone are metabolized into
hydromorphone
side effect of opiates
hypogonadism! Low Testosterone
NMDA antagonists
methadone and ketamine
Buprenorphine
Mixed agonist/antagonist at M1,2, K and delta receptors, often combined with naloxone for opioid detoxification/weaning…8-16 mg sublingual daily
Naloxone
Opioid antagonist, 0.2-2 mg IV
Tramadol
Mu agonist, as well as SNRI reuptake inhibitor, 25 - 100 mg q4-6 hr PRN
Acetaminophen
Phospholipids –PLA2–> AA –COX1,2–> PG, acetaminophen inhibits cox centrally which stop PG formation – helps with fever, pain…bc metabolized centrally no side effects of gastric/renal dz..ceiling effect of pain reduction is at 1,000 mg….4g total daily dose max (out of hospital we rec 3 g total daily dose)
NSAIDs
Cox 2 dont affect platelets
peripherally acting on COX 1&2
Reduces inflammatory pain (bc decr PG)
Ibuprofen 200-800 mg PO q4-6 hrs
Naproxen 220-500 mg PO q12 hrs
Indomethacin 25-50 mg PO BID (good for HO)
Diclofenac 1% gel 2-4 grams topically QID PRN; useful for superficial MSK pain like trochanteric bursitis , hand, wrist, shoulder
Celecoxib (COX2 select) 100-200 mg PO BID
Meloxicam (COX2 select) 7.5-30 mg PO Daily
Steroids
Inhibit PLA2, so inhibit phospholipid to AA transformation
Steroids
Inhibit PLA2, so inhibit phospholipid to AA transformation
Corticosteroids, such as prednisone, function by inhibiting the enzyme phospholipase A2 (PLA-2), which normally produces arachidonic acid. Without arachidonic acid, prostaglandins are also no longer produced. However, the direct effect of prednisone is to inhibit arachidonic acid production, which indirectly leads to decreased prostaglandins. NSAIDs directly inhibit the COX-1 and COX-2 enzymes, the effect of which directly inhibits the production of prostaglandins.
COX2
PG produced by COX1 that protect stomach are still working, inhibit cox 2 PG
COX 2> COX1 inhibitors
meloxicam (once daily dosing) and celecoxib (protect stomach)
COX 2> COX1 inhibitors
meloxicam (once daily dosing) and celecoxib (protect stomach)
Topical meds
fentanyl, diclofenac, lidocaine usually 2% (good for SCI IBD/TID PRN), lido patch 1 patch daily comes in 4-5%
Amitriptyline/NOR
anticholinergic, dry. mouth, constipation, urinary retention, QT prolongation….amitriptyline more potenet than nortriptyline (gentler, possibly less efficiatious)….ami gets metabolized into nortrip
Gabapentin MOA
blocks L type Ca2 in CNS, cleared by kidneys, 3600 mg max daily dose..binds to the alpha 2 delta subunit of calcium channel
Pregabalin
same mechanism, blocks L type Ca2 in CNS, approved for diabetic neuropathic pain, postherpetic neuralgia, and fibromyalgia
Duloxeitine/Venlafaxine
SNRI, antidepp and anti neuropathic pain, FDA approved for diabetic peripheral neuropathic pain and fibromyalgia. 30-60 mg daily , venlafaxine 25 mg PO TID or 37.5-75-150 PO extended release
Carbamazepine
Blocks Na channels on neurons , prevents signal transmission, useful for trigeminal neuralgia, mood stabilizer in TBI, 100-200 mg BID-QID
Lidocaine infusion
Steroid injection
Inhibit sodium channels on C fibers
steroid injection blocks PLA2 so no AA or PGs, also have. DIRECT neuronal inhibition
Capsaicin MOA
depletes substance P, decr pain signal transmission
Baclofen MOA
Gaba B receptor agonist, withdrawal itchy bitchy twitchy, renally cleared
Diazepam MOA
Gaba A receptor agonist
CLACK
gaba A works on Cl
Gaba B1 works on calcium
GabaB2 works on K
tizanidine MOA
alpha 2 agonist (as is clonidine), inhibits spinal reflex arch, hepatically cleared!
dantrolene MOA
peripherally acting, binds to Ryanodine receptor in SR in muscle cells and inhibits calcium release which inhibits muscle contraction.
Botox injections MOA
inhibit presynaptic syntaxin , synaptobrevin and SNP 25 proteins which are full of NTs about to be released into the synapse. By cleaving these proteins, the toxin prevents ACh from being released….3 days onset, 3 week peak, 3 months duration.
Polyethylene glycol
osmotic laxative that pulls fluid into the bowel lumen