Psychotropic Drugs
Psychotropic Drugs
Psychotropic Drugs
Typical A typical
Traditional agents Novel agents
Less EPS
Less TD
Effective in R
:Catecholamine-1
Glycine -1 Epinephrine
GABA -2 Nor-epinephrine
Dopamine
Serotonin -2
Absorption, Metabolism and Excretion of Neuroleptics drugs
Absorption
Distribution They
Theyarearehighly
highlylipophilic.
lipophilic.
85%
85% of the drug inplasma
of the drug in plasma
isisbound to albumin.
bound to albumin.
Excretion
Metabolism
Pathophysiology
of
Neuroleptic Agents
-Anti
Neurological Cardiovascular Coma
cholinergic
--11 --22 3-
3- --44
Parkinsonism Akathisia Tardive
Tardive
Parkinsonism Dystonia
Dystonia Akathisia
dyskinesia
dyskinesia
arched back
Torticollis
Investigations:
Toxicological analysis: Non-toxicological
1-Qualitative and semi- investigations:
quantitative 1- Abdominal x-ray
estimation by TLC. radio-opaque
2- Quantitative shadow in the
estimation by the use stomach.
of HPLC. 2- ECG arrhythmia
3- Color test : Forrest
Rapid Urine.
Treatment of Acute Poisoning
3- Decontamination (D):
1- Care of respiration. No emesis (antiemetic ) ?
If the patient is conscious or
2- Care of circulation comatosed: do
gastric lavage
* Hypotension first with warm water
circulatory shock. then with NaHCO3 5%.
* Treat cardiac arrhythmias powdered activated charcoal
repeated dosing)
sodium sulphate as cathartic
3-Treat extra pyramidal manifestations
By the use of antiparkinsonian drugs e.g.
Benztropine Mesylate (cogentin) 1-2 mg IV .
4-If there is cardiac arrhythmias
Treat by phenytoin sodium.
with monitoring for 2 days.
5- No role of elimination (E):
Diuresis, peritoneal or hemodialysis are
ineffective in removing the drug as it is
highly bound to plasma proteins.
Neuroleptic Malignant Syndrome (NMS)
Definition:
Is a serious complication of neuroleptic treatment
Lithium , TCAs , stopping of Levo-dopa or Carbidopa
used in treatment of Parkinsonism .
Cause : diminution of dopamine neurotransmitter.
It is characterized by:
Hyperpyrexia.
Autonomic dysfunction.
(tachycardia, sweating, salivation, hypertension).
Fluctuation of the level of consciousness.
Tremors, Rigidity.
Treatment : Bromocriptine (Parlodel) as it stimulates synthesis
of dopamine.
They have the following effects:
::Therapeutic
Therapeutic effects
effects .. 11
::Anti-
Anti- anxiety
anxiety effect
effect
inin the
the treatment
treatment of
of
.Neurosis
.Neurosis
.Anti-
.Anti- spasmodic
spasmodic effect
effect
Anti-
Anti- convulsant
convulsant effect
effect
.).)Diazepam
Diazepam = = valium
valium((
hypnotic
hypnotic effect
effect
.Lorazepam
.Lorazepam (Ativan)
(Ativan)
Important member of anti-anxiety drugs
I- Meprobamate group
Equanil.
Absorption
Distribution
Excretion
Metabolism
Pathophysiology of Benzodiazepine
GABA
Clinical picture of acute poisoning
1- Care of respiration ( A - B ).
2- Care of circulation (C).
3-Decontamination (D) .
conscious: induce vomiting.
comatosed: endotracheal tube before
gastric lavage.
powdered activated charcoal,
sodium sulphate as cathartics.
4- No role of elimination (E ) :
Diuresis.
peritoneal dialysis.
Hemodialysis are
5- Antidote Flumazenil = Anexate
Mechanism:
It is a Competitive Benzodiazepine Receptor Antagonist
it displaces Benzodiazepines from the receptors and binds
to them).
Dose:
A
the dose is 0.5 mg IV or by I.V infusion
B.R
Time :
After prolonged administration of benzodiazepines.
From 3- 6 days following cessation of Benzodiazepines.
S &S:
Anorexia, nausea, vomiting.
Apprehension, restlessness, insomnia.
Tremors may be convulsions.
To avoid:
Gradual dose reduction over a period of 10-15 days
should be done.