pharmacotherapy for common psychiatric conditions

8/6/2019 Pharmacotherapy for Common Psychiatric Conditions

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py for Common

Psychiatric

Conditions

by: PGI Ryan Abutazil


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Psychopharmacology

Use of drug is often the foundation of a

successful treatment

Pharmacotherapy should not be reduced to

a one-diagnosis-one-drug approach

1. drug selection and administration

2. psychodynamic meaning to the patient

3. family & environmental influences


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Antipsychotic Drugs

1. Dopamine Receptor

Antagonists

>typical antipsychotic drugs

> blocks dopamine receptors in

brain nerve cells (D2) whichdecreases dopaminergic effect


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A Synapse


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Antagonists

Effects: sedative effect which results in drowsiness,

diminution of vigilance, agitation and

excitement antideliriant and antihallucinogenic effects:

decrease of delusion and hallucinations

anti-autistic effect: patients become more

communicative and have a better contact with

Antipsychotic Drugs


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Antagonists

Adverse Effects: Neurologic- dyskenisia (trismus, tongue

protrusion, opstothonos, muscular spasms),

drowsiness, rigidity, pseudoparkinsonism withakinesia (slow movement)

Digestive- mouth dryness, hypersalivation

Cardiac- postural hypotension, lengthening of

the QT space in ECG

Antipsychotic Drugs


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Antagonists

HaloperidolMOA: blocks postsynaptic dopamine D1 and

D2 receptors in the mesolimbic system and decreases

the release of hypothalamic and hypophyseal

hormonesAbsorption: Readily absorbed from the GI tract

(oral).

Distribution: Crosses the blood-brain barrier;

Protein-binding: 92%

Antipsychotic Drugs


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Antagonists

Chlorpromazine/ LevomepromazineAbsorption: Only about 32% of the administered

dose is available to the systemic circulation in the

active form. Over time and multiple

administrations, bioavailability may drop to 20%.Peak concentrations are achieved in 1 to 4 hours

Metabolism: degraded by the liver by the action of

cytochrome-P450 family enzymes, usually CYP2D6

Excretion: Less than 1% of the unchanged drug is

Antipsychotic Drugs


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1. Biperiden HClAcetylcholine is secreted by neurons in the following

areas:

a. terminals of large pyramidal cells from motor

cortex b. in the basal ganglia c. motor neurons

that innervates skeletal muscles d. in the pre-

ganglionic neurons of the autonomic nervous system

e. post-ganglionic neurons of the parasympathetic

nervous

MOA: competitive antagonism of acetylcholine at

the cholinergic receptors in the corpus striatum,

Anticholinergics


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1. Serotonin-Dopamine

Antagonists

Produces minimal or no EPS

Interacts with more subtypes

of dopamine receptors +affects serotonin and

glutamate receptors

Antipsychotic Drugs


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1. Serotonin-Dopamine

Antagonists

Risperidone for first-break patients whohave mild to moderate illness

Clozapine most effective for severely ill

patients, but with detrimental adverseeffects in comparison to other SDAs

(agranulocytosis, seizures, high

anticholinergic effect)

Olanzapine (Zyprexa) more likely to

Antipsychotic Drugs


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Disorders

Two groups of mood disorders are broadly

recognized; the division is based on

whether the person has ever had

a manic or hypomanic episode. Thus, thereare depressive disorders, of which the best

known and most researched is major

depressive disorder (MDD) commonly

calledclinical depression ormajor

depression, and bipolar disorder (BD),

formerly known asmanic depression and

characterized by intermittent episodes of


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MDD

Indication for antidepressants: 1 major

depressive episode

When under medication, first to improve is

sleeping pattern and appetite, followed byimprovement in symptoms of agitation,

anxiety, depressive episodes, and

hopelessness. first Choice Antidepressant: The SSRI

antidepressants, fluoxetine (Prozac),

paroxetine (Paxil), fluvoxamine (Luvox), or

sertraline (Zoloft) are excellent choices as


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MDD

SSRIs

1. Fluoxetine

MOA: Fluoxetine specifically inhibits

neuronal re-uptake of serotonin, thus

increasing the concentration of the serotonin

at the synapse and reinforcing of serotonergic

neuronal transmission.Absorption: Fluoxetine hydrochloride is

readily absorbed from the gastrointestinal

tract with peak plasma concentrations


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MDD

SSRIs

1. Fluoxetine

Half-life: has a relatively long and highly variable

half-life ranging from 1 to 4 days after a single doseand averaging nearly 70 hours

Metabolism: in the liver to a desmethyl metabolite,

norfluoxetine, which has activity similar to

fluoxetine. Peak plasma concentrations of the activemetabolite, norfluoxetine, occur around 76 hours

after ingestion.

Elimination and excretion: The primary route of

elimination appears to be further hepatic


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MDD

SSRIs

1. Fluoxetine

Main adverse effects The major adverse

effects reported with therapeutic doses of

fluoxetine are primarily those of headache,

insomnia, nausea, and nervousness, with a

prevalence of 15 to 23 %. Less commonadverse effects include tremors, sweating, dry

mouth, anxiety, drowsiness, and diarrhoea,

with a prevalence of 10 to 14 %


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MDD

Tricyclic antidepressants

Tricyclic antidepressants are the oldest class of

antidepressant drugs. Tricyclics block the

reuptake of certain neurotransmitters such asnorepinephrine (noradrenaline) and serotonin.

They are used less commonly now due to the

development of more selective and safer drugs.

Side effects include increased heart rate,drowsiness, dry mouth, constipation, urinary

retention, blurred vision, dizziness, confusion,

and sexual dysfunction. Toxicity occurs at

approximately ten times normal dosages; these


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MDD

Tricyclic antidepressants

Tertiary amine tricyclic antidepressants:

Amitriptyline (Elavil, Endep)

Clomipramine (Anafranil) Doxepin (Adapin, Sinequan)

Imipramine (Tofranil)

Trimipramine (S

urmontil)


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MDD

Monoamine oxidase

inhibitors (MAOIs)

The MAOI group of medicines include:

Isocarboxazid (Marplan)

Moclobemide (Aurorix, Manerix)

Phenelzine (Nardil) Selegiline (Eldepryl, Emsam)

Tranylcypromine (Parnate)


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Disorder

Lithium, divalproex, and olanzapine

are the standard treatment for the

manic phase

Carbamazepine is also well established

as a standard treatment

Lamotrigine has been found to be bestfor preventing depressions, while

lithium is the only drug proven to

reduce suicide in people with bipolar


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Disorder

Lithium

MOA- Lithium carbonate provides a source of

lithium ions that may act by competing with

sodium ions at various sites in the body.

Therapeutic concentrations of lithium have

almost no discernible psychotropic effects in

normal volunteers but considerable effectin

patients suffering from affective disorders. Themechanism of action is unknown.

Absorption: completely absorbed from the

gastrointestinal tract, complete absorption

occurring after about 8 hours. Peak plasma


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Disorder

Lithium

Distribution: initially distributes into

extracellular fluid and then to most other

tissues. The final volume of distribution equalsthat of total body water

Elimination: occurs via the kidneys but

lithium can also be detected in

sweat and saliva

Half-life:The biological half-life is variable

ranging from 7-20 hours and may be longer at

night


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Disorder

Divalproate (Depakote)

MOA- inhibition of the transamination ofGABA.

By inhibiting GABA transaminase, GABA would

increase in concentration

Absorption: Valproic acid is rapidly absorbed in

the GI tract. Divalproex and valproic acid

dissociates into valproate ion in the GI tract.

Metabolism: Metabolized primarily in the liver. Elimination 30% to 50% excreted as glucuronide

conjugate in the urine.

The half-life is 9 to 16 h for valproate.


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Anxiety Disorders

Panic Disorder SSRIs, Benzodiazepines

Phobias Pharmacotherapy with

benzodiazepines can be helpful

social phobia SSRIs, benzodiazepines,tricyclic drugs, MAOIs

OC disorder SSRIs, Clomipramine

(tricyclic) PTSD SSRIs, sertraline, paroxetine

Generalized Anxiety Disorder Buspirone,

benzodiazepines, SSRIs

pharmacotherapy for common psychiatric conditions

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