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PREMEDICATION DRUGS

PREMEDICATION DRUGS. DR.SUDHIR MUBARAK AL KABEER HOSPITAL. PREMEDICATION- DEFINITION. Premedication refers to the administration of drugs in the period 1 – 2 hours before induction of anaesthesia. OBJECTIVES. Allay anxiety and fear Reduce secretions

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PREMEDICATION DRUGS

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  1. PREMEDICATION DRUGS DR.SUDHIR MUBARAK AL KABEER HOSPITAL

  2. PREMEDICATION- DEFINITION Premedication refers to the administration of drugs in the period 1 – 2 hours before induction of anaesthesia

  3. OBJECTIVES • Allay anxiety and fear • Reduce secretions • Enhance the hypnotic effects of G.A agents • Reduce P.O.N.V • Prodcuce amnesia • Prevent aspiration • Attenuate vagal reflexes • Attenuate sympathoadrenal response

  4. ALLAY ANXIETY & FEAR • The best way to do this is by non –pharmacological means • Psychotherapy – Reassurance • Benzodiazepines- most commonly used drugs

  5. BENZODIAZEPINES • Anxiolytic • Amnesic • Hypnotic • Sedative • Most commonly used premedication drug

  6. Mechanism of action- Site • Modification of emotional response & behaviour – by suppressing the neuronal activity between limbic system and hypothalamus • Decrease in alertness and arousal- by depressing interaction between limbic system and the RAS • Anticonvulsant effect – inhibition of amygdaloid nuclei • Muscle relaxant – suppression of polysynaptic reflexes in spinal cord ( central acting relaxant)

  7. Mechanism of action- Mode • GABA – mediated inhibitory effects • GABAA RECEPTORS • Cortex & Limbic system • GABAB – brain stem & spinalcord – Baclofen • GABAA RECEPTORS – they are mebrane protein pentameric structure associated with chloride channel • Three sububits – ά ,β, γ

  8. GABA binding site Chloride channel Benzodiazepine binding site

  9. GABA binding site Chloride channel Benzodiazepine binding site

  10. Benzodiazepines enhance the efects of GABA on GABA receptor • Thus they increase the frequency of chloride channel opening • Channel opening times are unchanged ( contatrast to barbiturates) • Increased chloride ions cause neuronal hyper polarisation and thus inhibition • Stage 3 sleep is increased • Stage 4 sleep and REM sleep decreased

  11. Classification • Long acting – diazepam • Medium acting – temazepam • Short acting - midazolam

  12. Diazepam • Most commonly used • Insoulble in water so formulated in propylene glycol, which is very irritant to veins. • Diazemulus – lipid emulsion • Bioavailability 100% • Protein binding 90-95%. • Dosage • Premedication 10-15 mg oral 1- 1.5 hrs preop • Sedation- 7-15 mg i.v slowly, increments 1-2 mg • Status epilepticus- 2mg every minute , max 20 mg • Intensive care- not for infusion – 5-10mg 4th hourly

  13. 50 – 120 hrs 4-10 hrs 6-25 hrs

  14. Midazolam • Imidazo – benzodiazepine derivative • It is this imidazole ring which imparts water solubility at pH < 4 • At blood pH, drug becomes lipid soluble due to ring closureand penetrates brain rapidly in 90 seconds – peak effect 2- 5 mins • Bioavailability – 44% • Hepatic elimination( liver blood flow) • Hydroxy-midazolam- active metabolite – 1 hr- clinically important only after prolonged infusion in renal failure

  15. Midazoalm is 1.5 -2 times more potent than diazepam ( ? ) • Dosage: • Premedication: 15mg oral or 5mg I.M,nasal drops • Sedation: 2-7mg I.V incre 0.5 – 1 mg • Status epilepticus : not recommended ( ? ) • Intensive care 0.03 -0.2 mg/kg/hr

  16. Ring open Ring closed

  17. LORAZEPAM • Longer duration(10-20 hrs) • DOC – liver failure • CLONZEPAM • Can be used in status epilepticus • Seizure adjuvant • FLUMAZENIL • Competetive antagonist, reverses all effects • Has slight intrinsic agonist property – so can precipitate seizures ( INVERSE AGONISM ) • Short half life – 1 hr, may need repeated injections or infusion • 0.2 mg ,then 0.1 mg increments ( don’t exceed 3 mg)

  18. PHENOTHIAZINES • They produce the following effects • Central antiemetic action • Sedation • Anxiolysis • H2 receptor antagonism • ά – adrenergic anatagonism • Anticholenergic properties • Potentiation of opiod analgesia • Side effects : extrapyramidal effects • Promethazine & trimeprazine ( children)

  19. ANTIMUSCURANIC DRUGS • Used for there : • Antisialogue action • Avoid bradycardia due to • anaesthetic agents • surgical stimulus( occulocardiac reflex, mesenteric traction) • Β blocked or digitalised patients • Intermittent suxamethonium • Avoid reflex bronchospasm ( COPD) • Children ( vagal predominance) • Disadvantages : • Dry mouth ,palpitations, arrthymias, blurred vision • Central anticholergic syndrome

  20. GYCOPYRROLATE • Synthetic antimuscuranic drug • Ionised quaternary amine –so doesnot cross BBB & placenta • Prolonged duration of action- 6hrs • No or Less tachycardia • Ideal for cardiac patients ( IHD) • Pupillary and other changes minimal • Antisialagogue action more • Dose 0.1 – 0.4 mg

  21. α2RECEPTOR AGONISTS • Action : they decrease noradrenaline release in both central and peripheral symp. N. • CNS : • tractus solitarius – hypotension & bradycardia • Locus coerulus – sedation • Vagal nuclei • Spinal & supraspinal level(non opioid) - Analgesia • Peripheral : • Decrease cardiac rate • Decrease smooth muscle tone • Increase coronary blood flow • Induce diuresis • Platelet aggregation

  22. Anaesthesia - α2agonists • Decrese MAC requirements • Attenuate sympathoadrenal responses associated with intubation and surgery • CLONIDINE( 100-300 mics orally) • DEXMEDETOMEDINE • AZEPEXOLE • Side effects : dry mouth, sedation,depression, bradycardia, rebound hypertension

  23. Other drugs • NSAIDS • Diclofenac • Ketorolac • TAM mixture – children • ( trimeprazine,atropine,mefenamic acid)

  24. ANTIEMETICS • ANTACIDS • NEXT CALSSES THANK YOU

  25. 8. Atropine: • a) may cause bradycardiab) dilates the pupil in premedicant dosec) has a shorter duration of action than glycopyrrolated) increases the physiological dead spacee) has both muscarinic and nicotinic effects

  26. TTTTF

  27. Flumazenil: • a) may induce panic attacks in susceptible patientsb) has anticonvulsant activity in patients with epilepsyc) has a long duration of actiond) may cause nausea and vomitinge) has inverse agonist action at benzodiazepine receptors

  28. TFFTT

  29. Glycopyrrolate: • a) can act at central cholinergic receptorsb) can increase the physiological dead spacec) can dilate the pupild) is equally effective when given orallye) is five times more potent as an antisialagogue than atropine

  30. FTTFT c) hence use with caution in glaucoma.

  31. Midazolam: • a) is an anticonvulsant b) is lipid soluble at physiological pH c) has no active metabolites d) has an elimination half-life of 2-4 hours e) can be administered as nasal drops for premedication  

  32. TTFTT

  33. Hyoscine: • a) causes tachycardiab) causes sedationc) causes mydriasisd) is an antiemetice) has a weaker antisialagogue effect than atropine

  34. TTTTF

  35. Hyoscine hydrobromide causes:a) antiemesisb) somnolencec) pupillary dilatationd) tachycardia followed by bradycardiae) extrapyramidal symptoms

  36. TTTTF

  37. Chlorpromazine:a) can cause dystonic reactionsb) antagonises apomorphine-induced vomitingc) is a dopamine antagonist at the chemoreceptor trigger zoned) is a weak alpha-adrenergic agoniste) undergoes extensive first-pass metabolism

  38. TTTFT

  39. Clonidine:a) is an alpha-2 receptor agonistb) is a dopamine antagonistc) causes tachycardiad) inhibits salivatione) reduces the minimum alveolar concentration of halothane

  40. TFFTT

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