Pharmacopeia

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Field	NSAIDS – IBUPROFEN Neurology & Sedation · Neurology & Sedation · Level 3	TRAMADOL Neurology & Sedation · Neurology & Sedation · Level 2
Mechanism of action	Reversibly inhibits COX 1 and 2 enzymes causing decreased production of prostaglandin precursors	mod affinity for μ receptors, weak κ, δ -in spinal desc inh pathways by inh of neuronal reuptake of norad&serotonin -presynaptic stim of seritonin release mod affinity for μ receptors, weak κ, δ -in spinal desc inh pathways by inh of neuronal reuptake of norad&serotonin -presynaptic stim of seritonin release
Physiological effects	As an anti-inflammatory, anti-pyretic and mild analgesic	CNS: - Analgesia - Hallucinations - Confusion - Delirium - Agitation - Seizures - Coma (Serotonin syndrome) Respiratory depression and constipation CNS: - Analgesia - Hallucinations - Confusion - Delirium - Agitation - Seizures - Coma (Serotonin syndrome) Respiratory depression and constipation
Absorption	Rapidly absorbed 85% bioavailability	Bioavailability- 75% PO
Distribution	pKa 4.5, weak acid therefore mostly unionised, abs via gut and SB	Crosses placenta Lipid soluble-crosses BBB Crosses placenta Lipid soluble-crosses BBB
Protein binding	99% protein bound (may displace highly protein bound drugs such as warfarin altering PD properties)	Low plasma protein binding, approximately 20%. Prot bind-20% 20%
Volume of distribution	Very small Vd 0.1L/kg	2.9-4.37 L/kg. Vd- 2.5-3L/kg 2.5-3L/kg
Metabolism	hepatic via oxidation	Extensively hepatic via demethylation , glucuronidation, and sulfation; active metabolite by CYP2D6 (M1; O-desmethyl tramadol) Extensively hepatic via demethylation , glucuronidation, and sulfation; active metabolite by CYP2D6 (M1; O-desmethyl tramadol)
Excretion	excreted as metabolites in urine 1% unchanged	Urine 90% (30% unchanged), 10% faeces.
Half-life	half life 2-3 hours	T1/2: ~6-8 hrs; Act metab:7-9hrs; old, hepatic/renal imp. T1/2: ~6-8 hrs; Act metab:7-9hrs; old, hepatic/renal imp.
Adverse Effects Toxicity	Worsen renal function by inhibiting PGE2 and causing vasoconstriction.  risk of thromboembolic events. Increased risk of GI bleeding and ulceration, GORD. Impair platelet function May reduce the beneficial eff¬ects of aspirin	Dysphoria,Euphoria. Miosis (excitation of Edinger-Westphal nucleus) N/V -CTZ stim. Serotonin syndrome with SSRI /SNRI/MAO/TCA Less resp dep than morphine analgesic effect in CYP2D6 deficiency Dysphoria,Euphoria. Miosis (excitation of Edinger-Westphal nucleus) N/V -CTZ stim. Serotonin syndrome with SSRI /SNRI/MAO/TCA Less resp dep than morphine analgesic effect in CYP2D6 deficiency
Class Group	Non-Opiate Analgesic	Opiate Analgesic
Indications Uses	Analgesia Antipyretic Antiinflammatory	Analgesia
Introduction	non selective cycloxygenase inhibitor	Is a synthetic opioid – cyclohexanol derivative Racemic mix. Is a synthetic opioid – cyclohexanol derivative Racemic mix.
Legacy Cicm Level	Level 3	Level 2
Main Action	—	mod affinity for μ receptors, weak κ, δ
Onset Peak Duration	onset 30 mins, duration 6 hours	onset / duration ~1 hour / 9 hours (immediate release)
Presentation	200mg tablets, some formulations in combination with codiene	immediate release, 12 hour release and 24 hour release tablets, IV immediate release, 12 hour release and 24 hour release tablets, IV
Route And Dose	Tablets for PO/PR	Route- PO/IV Dose- 50-100mg QID for all routes (Relative pot 0.2) Route- PO/IV Dose- 50-100mg QID for all routes (Relative pot 0.2)