BY Click to edit Master subtitle style VAMSI KRISHNA M.PHARMACY


associated with uneasiness.   treatment is needed when it is disproportionate to the situation and excessive. unpleasant in nature. Def: it is defined as an emotional state .  4/22/12 . TREATMENT OF ANXIETY: Anxiety is a universal phenomenon. if anxiety symptoms are frequent and persist in a severe form. discomfort and concern or fear about some defined future threat. they are a cause of distress/ suffering and markedly impair performance.

 The established drugs are BZDS which should be used in smallest possible dose.  The anxiolytic-sedative drugs differ markedly from antipsychotics .    ill -defined group of Antianxiety drugs: These are drugs. and more closely resemble sedative – hypnotics. produced a restful state with out interfering with normal mental or physical functions. the dose has to be found out for each patient by titration with symptoms of anxiety . which are aimed to control the symptoms of anxiety . They are 4/22/12 . mostly mild CNS depressants.

Have anticonvulsant property . Do not produce extra pyramidal side effects.v Have no therapeutic effect to control through disorder of schizophrenia. Produce physical dependence and carry abuse liability Do not selectively block conditioned avoidance response in animals 4/22/12 v  v v v .

Gepirone. Ispapirone 3) Sedative antihistaminic : Hydroxyzine 4) β blocker : Propranolol 4/22/12 . CLASSIFICATION OF DRUGS: : Diazepam 1) BENZODIAZEPINES  Oxazepam 2) Azapirones chlordiazepoxide lorazepam.alprazolm : Buspirone.

which leads to an increase in chloride conductance. The influx of chloride ions causes small hyperpolarization that moves the post synaptic potential away from its firing threshold and thus inhibit the formation of action potential.   Approximately 20 benzodiazepine derivatives are currently available.   4/22/12 . BENZODIAZEPINES: These are the most widely used anxiolytic drugs. Mode of action : Binding of GABA to its receptor on the cell membrane triggers an opening of chloride channel . They have largely replaced barbiturates and meprobamate in the treatment of anxiety. since the benzodiazepine are more effective and safer.

but may be noted if large 4/22/12 are used. resulting in a more frequent opening of adjacent chloride channels .impairment of psychomotor skills . The binding of benzodiazepines enhances the affinity of GABA receptors for this neurotransmitter. Adverse effects : It causes vertigo. ataxia. Hangover is less common . amnesia. This in turn results in enhanced hyperpolarization and further inhibition of neuronal firing. prolongation of reaction time . especially of longer acting drugs.which are separated from but adjacent to the receptor for the GABA. Benzodiazepines bind to specific . disorientation. doses       . high affinity sites on the cell membrane .

dry mouth and urinary incontinence are sometimes complained. blurring of vision. irritability and sweating my some patients experience increase in night mares and behavioral alterations. Administration during labour may cause flaccidity    4/22/12 . especially with nitrazepam. especially with flurazepam.   paradoxical stimulations. older individuals are more susceptible to psychomotor side effects. weakness. but there is little tendency to increase the dose.   occur in an occasional patient. Tolerance to the sedative develops gradually. An earlier report of increased birth defects on use of diazepam during pregnancy has been disputed.

valproate has provoked psychotic symptoms. INTERACTIONS: BZDs synergise with alcohol and other CNS depressants leading to excessive impairment. erythromycin and others. Since CYP 3A4 isoenzyme plays important role in metabolism of several BZDs . their action can be prolonged by CYP 3A4 inhibitors like ketoconazole. concurrent use with sod.     4/22/12 . drug interactions due to displacement from protein binding or microsomal enzyme induction are not significant.

     4/22/12 . distinctly different from BZDs Does not produce significant sedation or cognitive/ functional impairment. Does not suppress BZD or barbiturate with drawl syndrome. Does not produce tolerance or physical dependence. anew class of antianxiety drugs. Does not interact with BZD receptor or modify GABAergic transmission. Buspirone: It is the first azapirone .

 It relieves mild to moderate generalized anxiety. By stimulating presynaptic   5-HT 1A autoreceptors. undergoes extensive first pas metabolism. t1/2 is 2-3. The mechanism of anxiolytic action is not clearly known. The therapeutic effect develops slowly maximum benefit may be delayed up to 2 weeks. but may be dependent on its selective partial agonistic action on 5-HT 1A receptors. rapidly absorbed . adaptive reduction in cortical 5-HT2 receptor may occur A mild mood elevating action has been noted occasionally – may be due to facilitation of central nor adrenergic system.  After chronic treatment. it reduces the activity of dorsal raphe serotonergic neurons.5 hrs   4/22/12 It is .

by cutting the vicious cycle and provide symptomatic relief.and these symptoms reinforce anxiety. etc ) are due to sympathetic overactivity. headache. rarely ecitment.    β Blockers: Many symptoms of anxiety(palpitation. but does not potentiate CNS depressants. propranolol and other non selective β blocker helps anxious patients troubled by these symptoms . they do not affect psychological symptoms such as   4/22/12 . It may cause rise in BP in patients on MAO inhibitors. rise in BP. shaking tremor gastrointestinal hurrying . Side effects are minor : dizziness nausea. light headedness.

it shows its action in short term stressful situvation.   4/22/12 . but this is due to peripheral rather than a specific central action . they may be used for performance/situvational anxiety or as adjuvant to BZDs .

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