NSAIDs, anticholinergics Flashcards
Ketorolac Class
NSAID
Ketorolac Use
pain relief and anti-inflammatory
Ketorolac MOA
reduces inflammatory response by decreasing the activity of cyclooxygenase (COX) 1 and or 2, thus inhibiting prostaglandin synthesis
Ketorolac Dose
IV 15 - 30 mg, given during emergence
Lower dose for elderly and CKD
Ketorolac Pharmacokinetics
Onset = 30 min DOA = 4 - 6 hours Metabolism = hepatic Elimination = renal (60% unchanged)
Ketorolac Contraindications
Ortho surgery due to delay in bone healing
Bleeding risk with intracranial surgery
Ketorolac Considerations
- Decreases postop opioid requirements
- Low incidence of N/V
- Lack of respiratory depression
- Communicate with surgeon prior to admin
- Ok to use with stable and healing bone fracture
- Caution with asthma d/t bronchoconstriction d/t decrease in leukotriene production
- Caution with renal disease d/t renal vasoconstriction d/t decrease in leukotriene production
Atropine Class
Antimuscarinic (tertiary amine)
Atropine Use
bradycardia
Atropine MOA
Competative antagonism of ACh @ muscarinic receptors opposing PSNS
Atropine Dose
With edrophoniuim = 7 mcg/kg
Non-symptomatic bradycardia = titrate to effect with small doses
Sympomatic bradycardia in ACLS = 0.5 - 1 mg bolus, 3mg max
Atropine Pharmacokinetics
Onset = 1 - 2 min DOA = 1 - 2 hours Metabolism = liver Elimination = renal and hepatic
Atropine Contraindications
Caution with CAD, pheochromocytoma, hyperthyroidism, and myasthenia gravis
Atropine Considerations
- crosses the BBB
Tachycardia, sedation, anticholinergic syndrome
Glycopyrrolate Class
antimuscarinic (quaternary ammonium)
Glycopyrrolate Use
Antisaligogue, often given with Neostigmine for reversal of NMB, bradycardia
Glycopyrrolate MOA
Competitively antagonizes ACh at postganglionic muscarinic receptors
Blockade at postsynaptic muscarinic receptors leads to: mydriasis, blurred vision, tachycardia, decreased salivation/pharyngeal secretions/bronchial secretions, bronchodilation, decreased tone/motility of lower esophageal sphincter, decreased bladder tone
Glycopyrrolate Dose
With neostigmine= 0.2mg glyco for 1mg neo
Concentration 0.2mg/mL (neo concentration 1mg/mL) therefore, 1mL of glyco per 1 mL of neo
Glycopyrrolate Pharmacokinetics
Onset = 2 min DOA = 2 - 4 hours Metabolism = portion by liver Elimination = renally, larger portion unchanged
Glycopyrrolate Contraindications
Caution with CAD, pheochromocytoma, hyperthyroidism, and myasthenia gravis
Glycopyrrolate Considerations
Tachycardia & Does not cross BBB
Scopolamine Class
antimuscarinic (tertiary amine)
Scopolamine Use
Antiemetic, antisialagogue, and sedation
Scopolamine MOA
Competitively antagonizes ACh at muscarinic receptors
Peripheral tissues innervated by parasympathetic postganglionic nerves
Tertiary amine = crosses BBB
Blockade at postsynaptic muscarinic receptors leads to: mydriasis, blurred vision, tachycardia, decreased salivation/pharyngeal secretions/bronchial secretions, bronchodilation, decreased tone/motility of lower esophageal sphincter, decreased bladder tone
Scopolamine Dose
Patch = 1.5mg
Scopolamine Pharmacokinetics
Onset = 4 hours DOA = 24 hours Metabolism = liver Elimination = renal and hepatic *crosses BBB
Scopolamine Contraindications
Caution with CAD, pheochromocytoma, hyperthyroidism, and myasthenia gravis
Scopolamine Considerations
Patch is most effective if placed 4 hours before induction
Pt education = patch can cause dry mouth, blurred vision, dilated pupils, can stay on for 24 hours, and after removal wash hands before touching eyes
Tachycardia, sedation, anticholinergic syndrome
Neostigmine Class
Anticholinesterase
Neostigmine Use
Reversal of non-depolarizing neuromuscular blockade
Other: glaucoma, paralytic ileus, atonic bladder, myasthenia gravis
Neostigmine MOA
Antagonizes postsynaptic acetylcholinesterase at the NMJ, increasing the concentration of ACh in the synaptic cleft.
Excess ACh displaces nondepolarizing NMBAs bound to nicotinic receptors & binds to nicotinic receptors
Note: the excess ACh also binds to muscarinic receptors throughout the body
Neostigmine Dose
Dosing based on twitches on TOF
1 twitch = no reversal
2-3 twitches = 50 mcg/kg
4 twitches w/ fade = 40 mcg/kg
4 twitches w/o fade = 15-25 mcg/kg
Often administered with an antimuscarinic (glycopyrrolate)
5mg MAXNeostigmine Pharmacokinetics
Onset: 5 - 15 minutes
DOA: 45 - 90 minutes
Metabolism: pseudocholinesterases (50%)
Elimination: kidneys (50% unchanged)
Neostigmine Contraindications
Brady-arrhythmias & certain respiratory pathologies
Neostigmine Considerations
May cause bradycardia (r/f asystole) when paired with antimuscarinic
Side effects: salivation, bronchoconstriction, peristalsis, miosis, enhanced gastric secretions
Sugammadex Class
Selective relaxant binding agent
Sugammadex Use
reversal of steroidal NMBAs
Sugammadex MOA
Irreversibly encapsulates (binds to) steroidal NMBAs
Sugammadex Dose
Reversal of profound block: Post tetanic count <2: 16 mg/kg Post tetanic count >2: 4 mg/kg TOF 0: use post tetanic TOF 1: 4 mg/kg TOF 2+: 2 mg/kg
Sugammadex
Onset: 3 minutes
DOA: 15 min
Metabolism: NOT metabolized
Elimination: kidneys
Sugammadex Contraindications
ESRD
Anaphylaxis
Sugammadex Considerations
If paralysis desired after sugammadex administration, must use succinylcholine or a bezylisoquinolone (cis/atra)
Patients using hormonal contraceptives must use an additional, non-hormonal method of contraception for the next 7 days
