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ADVANCE PHARMACOLOGY AND
TOXICOLOGY-1
Department of pharmacology
PRESENTATION TOPIC :
Anxiety
Submitted to : Dr Raju Koneri
Prepared by : Diana Moria
 Anxiety is an emotional state characterized by
an unpleasant nature of inner turmoil, often
accompanied by nervous behaviour ,
uneasiness and concern about some define or
undefined future threat.
 Neurotransmitters like GABA, noradrenaline,
serotonin abnormalities – anxiety.
 Amygdala, temporal lobe, hippocampus and
hypothalamus - involved in anxeity
 Neurochemical theories :
 Noradrenaline theory
 Serotonin theory
 GABA receptor theory
 ANS of anxious patients- hypersensitive to
stimuli.
 Locus cerulus – activates epinephrine release
 Anxiogenics – stimulate locus cerulus firing
 Anxiolytics- inhibits locus cerulus firing and
decrease noradrenaline activity.
 GABA – inhibitory neurotransmitter in brain.
 Has inhibitory and regulatory effects on
serotonin, noradrenaline and dopamine.
 GABAA receptor involved in anxiety;
decreases neuronal excitability
 Patients suffering from anxiety disorders have
less level of GABA in cortex
 Abnormalities in serotonin function i.e., release
and uptake plays role in anxiety.
 Greater serotonin activity – reduces
norepinephrine activity in locus cerulus.
 SSRIs – increases serotonin levels post
synaptically – blocks symptoms of anxiety.
 Panic disorder
 Generalised anxiety disorder
 Social anxiety disorder.
 Obsessive compulsive disorder.
 Post traumatic stress disorder
 Anxiolytics are also known as minor
tranquilizers. The term is less common in
modern texts and was originally derived from
a dichotomy with major tranquilizers, it is the
medication or other intervention that inhibits
anxiety or antipsychotics.
1 ) Benzodiazepines
 clonazepam, diazepam
2 ) Azapirones
 Buspirone, tandospirone, gapirone
3) Sedative antihistaminics
 Hydroxyzine
4) Beta blockers
 Propranalol
5) carbamates
 meprobamate
 At lower doses they acts as anxiolytics ,
by enhancing GABA transmission of
neurons having the alpha subunit in their
GABAa receptor , thereby inhibiting
neuronal circuits in the limbic system of
the brain .
 Dizziness, vertigo , ataxia , amnesia, weakness,
dry mouth , CNS depressant , restlessness
Agitation
 Interaction
 With alcohol produces excessive impairment
 Oral contraceptives retards its metabolism
 5-10mg tab daily
 Quickly absorb , t1/2 of 1 hour ,
 Dose : 5-15mg OD –TDS
 Rapidly absorb orally , it undergoes first pass
metabolism
 T1/2 is 2-3.5hours
 Excreted through urine and faece
 Dizziness , nausea, headache , rarely
excitement.
 CONTRINDICATION
 MOA inhibitors causes increase in Bp
 Propranolol/ atenolol
 They acts by blocking peripheral
sympathetic system .
 Reduces somatic symptoms of anxiety
 Decrease BP and slows HR
 Mainly use in performance anxiety bt
less effective in other forms
Thanks
 Reference
 Goodman and Gilman's

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Anxiety ppt

  • 1. ADVANCE PHARMACOLOGY AND TOXICOLOGY-1 Department of pharmacology PRESENTATION TOPIC : Anxiety Submitted to : Dr Raju Koneri Prepared by : Diana Moria
  • 2.  Anxiety is an emotional state characterized by an unpleasant nature of inner turmoil, often accompanied by nervous behaviour , uneasiness and concern about some define or undefined future threat.
  • 3.
  • 4.  Neurotransmitters like GABA, noradrenaline, serotonin abnormalities – anxiety.  Amygdala, temporal lobe, hippocampus and hypothalamus - involved in anxeity  Neurochemical theories :  Noradrenaline theory  Serotonin theory  GABA receptor theory
  • 5.  ANS of anxious patients- hypersensitive to stimuli.  Locus cerulus – activates epinephrine release  Anxiogenics – stimulate locus cerulus firing  Anxiolytics- inhibits locus cerulus firing and decrease noradrenaline activity.
  • 6.  GABA – inhibitory neurotransmitter in brain.  Has inhibitory and regulatory effects on serotonin, noradrenaline and dopamine.  GABAA receptor involved in anxiety; decreases neuronal excitability  Patients suffering from anxiety disorders have less level of GABA in cortex
  • 7.  Abnormalities in serotonin function i.e., release and uptake plays role in anxiety.  Greater serotonin activity – reduces norepinephrine activity in locus cerulus.  SSRIs – increases serotonin levels post synaptically – blocks symptoms of anxiety.
  • 8.  Panic disorder  Generalised anxiety disorder  Social anxiety disorder.  Obsessive compulsive disorder.  Post traumatic stress disorder
  • 9.
  • 10.
  • 11.
  • 12.
  • 13.
  • 14.  Anxiolytics are also known as minor tranquilizers. The term is less common in modern texts and was originally derived from a dichotomy with major tranquilizers, it is the medication or other intervention that inhibits anxiety or antipsychotics.
  • 15. 1 ) Benzodiazepines  clonazepam, diazepam 2 ) Azapirones  Buspirone, tandospirone, gapirone 3) Sedative antihistaminics  Hydroxyzine 4) Beta blockers  Propranalol 5) carbamates  meprobamate
  • 16.  At lower doses they acts as anxiolytics , by enhancing GABA transmission of neurons having the alpha subunit in their GABAa receptor , thereby inhibiting neuronal circuits in the limbic system of the brain .
  • 17.
  • 18.  Dizziness, vertigo , ataxia , amnesia, weakness, dry mouth , CNS depressant , restlessness Agitation  Interaction  With alcohol produces excessive impairment  Oral contraceptives retards its metabolism
  • 19.  5-10mg tab daily  Quickly absorb , t1/2 of 1 hour ,
  • 20.
  • 21.  Dose : 5-15mg OD –TDS  Rapidly absorb orally , it undergoes first pass metabolism  T1/2 is 2-3.5hours  Excreted through urine and faece
  • 22.  Dizziness , nausea, headache , rarely excitement.  CONTRINDICATION  MOA inhibitors causes increase in Bp
  • 23.  Propranolol/ atenolol  They acts by blocking peripheral sympathetic system .  Reduces somatic symptoms of anxiety  Decrease BP and slows HR  Mainly use in performance anxiety bt less effective in other forms
  • 24.