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.

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

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 .

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 ,

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

25. Thanks

26.  Reference
 Goodman and Gilman's