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 :
GABA receptor theory
5. ANS of anxious patients- hypersensitive to
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.
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.
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 .
21. Dose : 5-15mg OD –TDS
Rapidly absorb orally , it undergoes first pass
T1/2 is 2-3.5hours
Excreted through urine and faece
22. Dizziness , nausea, headache , rarely
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