NSAIDs, anticholinergics Flashcards by Jackie Agranat

Ketorolac Class

NSAID

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Ketorolac Use

pain relief and anti-inflammatory

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Ketorolac MOA

reduces inflammatory response by decreasing the activity of cyclooxygenase (COX) 1 and or 2, thus inhibiting prostaglandin synthesis

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Ketorolac Dose

IV 15 - 30 mg, given during emergence

Lower dose for elderly and CKD

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Ketorolac Pharmacokinetics

Onset = 30 min 
DOA = 4 - 6 hours 
Metabolism = hepatic 
Elimination = renal (60% unchanged)

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Ketorolac Contraindications

Ortho surgery due to delay in bone healing

Bleeding risk with intracranial surgery

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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

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Atropine Class

Antimuscarinic (tertiary amine)

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Atropine Use

bradycardia

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Atropine MOA

Competative antagonism of ACh @ muscarinic receptors opposing PSNS

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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

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Atropine Pharmacokinetics

Onset = 1 - 2 min 
DOA = 1 - 2 hours 
Metabolism = liver 
Elimination = renal and hepatic

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Atropine Contraindications

Caution with CAD, pheochromocytoma, hyperthyroidism, and myasthenia gravis

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Atropine Considerations

crosses the BBB

Tachycardia, sedation, anticholinergic syndrome

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Glycopyrrolate Class

antimuscarinic (quaternary ammonium)

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Glycopyrrolate Use

Antisaligogue, often given with Neostigmine for reversal of NMB, bradycardia

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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 MAX ```

Neostigmine 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