Sedative H ypnotic D rugs
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1 Sedative H ypnotic D rugs H M Bakhriansyah, dr., M.Kes., M.Med.Ed Department of Pharmacology Medical Faculty Lambung Mangkurat University Terminology Sedative state Hypnotic state
2 Sleeping NREM 4 phases Physical processes decreased For relieving physical tiredness Non recalling of and non detail dream Night terror and sleep walking Wakefulness REM 1 phase Physical processes increased For relieving mental tiredness Detail, non logical and bizarre dream nightmare 5HT, adenosin, GABA ACh Wakefulness Driven by formation reticulare brain steam and hypothalamus Neurotransmitters: Excitation: NE, dopamine, histamine Inhibition: 5HT, GABA, adenosine
3 Insomnia Difficultly to fall into sleep or sleep cycle incompletely leading to symptoms and life disturbances diminishing of working ability, social and daily life Classification: Transient insomnia Short term insomnia Long term insomnia : 2-3 days : 3 weeks : > 3 weeks Initial insomnia : difficult to fall into sleep Delayed insomnia : easy to wake up and difficult to gain into sleep again Broken insomnia : multiple awakening
4 Initial insomnia Delayed insomnia Broken insomnia Short acting benzodiazepine Tricyclic and tetracyclic anti depressants agents Long acting benzodiazepine Phenobarbital Anxiety Depression syndrome Psychosocial stress Consideration Given minutes before night sleeping Dose is increased gradually Optimal dose is maintained for 1-2 weeks followed by tapering off Elderly: dose is reduced or given 2-3 times per week
5 SEDATIVE HYPNOTIC AGENTS BENZODIAZEPIN DERIVATES BARBITURATE DERIVATES OTHERS: CHLORALHIDRATE PARALDEHIDE ANTIHISTAMINE: Diphenhidramine, doxylamine NEWER DRUGS: zolpidem, zaleplon, zolpiklon BENZODIAZEPINE DERIVATES Bind to its receptors (close to GABA receptors) inhibitory neurotransmitter within the CNS The receptors-drugs interaction regulates the entrance of Cl into the post synaptic cells. Commonly used: wide range of safety
6 BDZ BARB Intensify Cl conductance mediated by GABA Prolong GABA effects Diminish synaptic transmission Alprazolam Bromazepam Chlorazepate Chlordiazepoxide Diazepam Estazolam Flurazepam Halazepam Lorazepam Midazolam Nitrazepam Oxazepam Prazepam Temazepam Triazolam
7 Pharmacodynamic Depression the CNS Low therapeutic dose Relief of anxiety, drowsiness, sluggishness Increased dose Muscle relaxation, hypnosis Relatively safe: distinctive dose for therapy and death Side effects: minimal related to lacking of GABA neurons in the periphery. Clinical Uses Anxiety Pharmacotherapy accomplished by counseling Using the lowest effective dose and the shortest duration Chosen drug based on half life unless for depression based anxiety (ALPRAZOLAM)
8 Insomnia Altering the normal distribution of REM phase and NREM sleep. Epilepsy and seizures (clonazepam, diazepam) Sedation, retrograde amnesia and anesthesia Muscle relaxant (diazepam) Alcohol and sedative hypnotic withdrawal (diazepam and chlordiazepoxide) Clinical Problems Cross tolerance Dependency (physically and mentally) Drug abuse Withdrawal syndrome particularly for barbiturate rebound insomnia, anxiety
9 Side effects are related to their ability to produce CNS depression: excessive sedation, confusion, impaired motor coordination suppress breathing center, allergy and death. Interaction: alcohol, other CNS depressants BARBITURATES Accidental ingestion suicides Having serious and lethal interaction with other drugs Depressing CNS: sedation general anesthesia Clinical use: insomnia, anxiety, epilepsy, seizure, anesthesia.
10 Side effects : laryngospasm Interaction : oral contraceptive, phenytoin, digitoxin, quinidine etc. Other drugs Azapirones such as buspirone (5HT) Antihistamines such as diphenhidramine, promethazine, hydroxyzine, etc B-adrenergic blocking agents such as propranolol, particularly somatic anxiety controversy. Antipsychotic and antidepressants such as chlorpromazine and amitriptyline.
11 Status Epilepticus SE : Continues seizures occuring 30 minutes (epilepsi foundation) More than 30 minutes of continues seizures activity or 2 or more sequential seizures without full recovery of consciousness between seizures (Dodson, 1993). Systemic and primary brain changes related to morbidity and mortality rates Decreasing GABA inhibition. Increasing blood pressure (early stage) decreasing Acidosis (+) Pulmonary edema Hyperthermia Mild leukocytosis GABAergic mechanism fails
12 Goal of therapy: to treat the epilepsy and to minimalise the side effects Principal therapy: Monotherapy is better than polypharmacy Dosage is increased until the therapeutic effect or toxicity effect are met. Polypharmacy is introduced when monotherapy does not work Avoiding the sudden withdrawal Treatment flowchart for status epilepticus
13 Medications Fenitoin Karbamazepin Lamotrigin Na Glutamate STATUS EPILEPTICUS GABA Ca Barbiturat Benzodiazepin Asam valproat Gabapentin Fenitoin Karbamazepin Asam valproat Etosuksimid Karbamazepin Stabilize neural membrane by decreasing Na, Ca and K flows through it. avoid to be given with MAO inhibitor consecutively Fenitoin Difenilhidantoin derivate Mechanism of actions are similar to Karbamazepin Could be given orally, intra venous and intra muscular
14 Valproic Acid Increasing GABA transmission Sedation effect is minimal Etosuksimid Mechanism of action is unknown Probably by inhibiting Ca channel Phenobarbital Stimulating GABA receptor SE: sedation, nistagmus, ataxia and allergy Inducing enzym P450 Primidon Mechanism of actions are unknown Its active metabolit has long half life
15 Gabapentin GABA agonist Adjuvant therapy Lamotrigin Stabilizing neuron and affecting glutamate release Adjuvant therapy SE: rash (prominent) Klonazepam Stimulating GABA receptor Felbamat Stimulating GABA receptor and inhibiting NMDA receptor Used un-frequently
16 Parkinson disease A progressive neurodegenerative disorder associated with loss of dopaminergic nigrostriatal neurons. Distinctive features: Resting tremor, rigidity, bradikinetia, and postural instability Principle therapy To facilitate action of dopaminergic To suppress action of cholinergic Increasing the synthesis and release of dopamine (Ldopa+karbidopa, amantadin) Inhibiting dopamin metabolism (selegilin/deprenil) Activating dopamine receptor (bromocriptine, pergolide) Blocking muscarinic/ cholinergic receptor (trihexiphenidile, benzathropine, diphenhidramine)
17 Protocol of therapy Anti cholinergic Amantadine L-dopa+karbidopa Dopamine agonists drugs MAO B inhibitors L-dova (levodopa) Dopamine precursor inactive form Activated by decarboxilase enzyme; Brain Lever & kidneys can not pass through BBB bioavailability countered by karbidopa/benserazide. Interaction: piridoxine increases decarboxilated reaction. On/off phenomenon (+) after 3-5 years application mechanism??? Desensitization of dopamine receptor Not a first line therapy
18 Selegiline (deprenil) Instead of inhibiting metabolism of dopamine: Stimulating dopamine release. Neuro-protective effect + MOA inhibitors crisis of hypertension. Bromociptine & Pergolide Dopamine receptor agonists Action: Lesser than L- dopa As a single therapy at the early stage Combination with L- dopa at the moderate and late stage. Tapering dose Trihexiphenidile & benzotropine Action: less than L- dopa Adjuvant therapy Tapering dose Diphenhidramine Anti cholinergic effect at central level Anti histamine
19 Amantadine Anti virus Mechanism:??? May be by facilitating dopamine release Action: Less than L-dopa Better than anti cholinergic Early stage: Anti cholinergic or Amantadine When early stage therapy is not effective, L- dopa+karbidopa are started. Final stage: dopamine agonists medications and MAO inhibitors.
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