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Pharmacothera py for Common Psychiatric Conditions

by: PGI Ryan Abutazil

General Principles of 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 Drugs must be used in effective doses in

Schizophreni a
Causes alterations in the brain and the way it perceives reality resulting in the hallmark symptoms of hallucinations and delusions Exact etiology is unknown, although several predisposing factors are said to be present

Schizophrenia: Antipsychotic Drugs


1. Dopamine Receptor Antagonists >typical antipsychotic drugs > blocks dopamine receptors in brain nerve cells (D2) which decreases dopaminergic effect

A Synapse

Schizophrenia: Antipsychotic Drugs


1. Dopamine Receptor 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 reality.

Schizophrenia: Antipsychotic Drugs


1. Dopamine Receptor Antagonists Adverse Effects:
Neurologic- dyskenisia (trismus, tongue protrusion, opstothonos, muscular spasms), drowsiness, rigidity, pseudoparkinsonism with akinesia (slow movement) Digestive- mouth dryness, hypersalivation Cardiac- postural hypotension, lengthening of the QT space in ECG

Schizophrenia: Antipsychotic Drugs


1. Dopamine Receptor Antagonists
Haloperidol MOA: blocks postsynaptic dopamine D1 and D2 receptors in the mesolimbic system and decreases the release of hypothalamic and hypophyseal hormones Absorption: Readily absorbed from the GI tract (oral). Distribution: Crosses the blood-brain barrier; Protein-binding: 92% Metabolism: Hepatic via oxidative N-dealkylation

Schizophrenia: Antipsychotic Drugs


1. Dopamine Receptor Antagonists
Chlorpromazine/ Levomepromazine Absorption: 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

Schizophrenia: Anticholinergics
1. Biperiden HCl
Acetylcholine 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 preganglionic 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, which restores the balance between cholinergic and

Schizophrenia: Antipsychotic Drugs


1. Serotonin-Dopamine Antagonists Produces minimal or no EPS Interacts with more subtypes of dopamine receptors + affects serotonin and glutamate receptors
As effective as Haloperidol for

Schizophrenia: Antipsychotic Drugs


1. Serotonin-Dopamine Antagonists
Risperidone for first-break patients who have mild to moderate illness Clozapine most effective for severely ill patients, but with detrimental adverse effects in comparison to other SDAs (agranulocytosis, seizures, high anticholinergic effect) Olanzapine (Zyprexa) more likely to

Mood 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, there are depressive disorders, of which the best known and most researched is major depressive disorder (MDD) commonly called clinical depression or major depression, and bipolar disorder (BD), formerly known as manic depression and characterized by intermittent episodes of mania or hypomania, usually interlaced

Mood Disorders: MDD


Indication for antidepressants: 1 major depressive episode When under medication, first to improve is sleeping pattern and appetite, followed by improvement 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

Mood Disorders: 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 appearing from 6 to 8 hours after oral

Mood Disorders: MDD


SSRIs 1. Fluoxetine Half-life: has a relatively long and highly variable half-life ranging from 1 to 4 days after a single dose and averaging nearly 70 hours Metabolism: in the liver to a desmethyl metabolite, norfluoxetine, which has activity similar to fluoxetine. Peak plasma concentrations of the active metabolite, norfluoxetine, occur around 76 hours after ingestion. Elimination and excretion: The primary route of elimination appears to be further hepatic metabolism to inactive metabolites which are

Mood Disorders: 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 common adverse effects include tremors, sweating, dry mouth, anxiety, drowsiness, and diarrhoea, with a prevalence of 10 to 14 %

Mood Disorders: MDD


Tricyclic antidepressants Tricyclic antidepressants are the oldest class of antidepressant drugs. Tricyclics block the reuptake of certain neurotransmitters such as norepinephrine (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 drugs are often lethal in overdoses, as they may

Mood Disorders: MDD


Tricyclic antidepressants Tertiary amine tricyclic antidepressants: Amitriptyline (Elavil, Endep) Clomipramine (Anafranil) Doxepin (Adapin, Sinequan) Imipramine (Tofranil) Trimipramine (Surmontil)

Mood Disorders: MDD


Monoamine oxidase inhibitors (MAOIs) may be used if other antidepressant medications are ineffective. MAOIs work by blocking the enzyme monoamine oxidase which breaks down the neurotransmitters dopamine, serotonin, and norepinephrine (noradrenaline). Because there are potentially fatal interactions between this class of medication and certain foods (particularly those containing tyramine), as well as certain drugs, classic MAOIs are rarely prescribed anymore.

Mood Disorders: MDD


Monoamine oxidase inhibitors (MAOIs) The MAOI group of medicines include: Isocarboxazid (Marplan) Moclobemide (Aurorix, Manerix) Phenelzine (Nardil) Selegiline (Eldepryl, Emsam) Tranylcypromine (Parnate)

Mood Disorders: Bipolar I 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 best for preventing depressions, while lithium is the only drug proven to reduce suicide in people with bipolar disorder

Mood Disorders: Bipolar I 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. The mechanism of action is unknown. Absorption: completely absorbed from the gastrointestinal tract, complete absorption occurring after about 8 hours. Peak plasma concentrations occur after about 2-4 hours

Mood Disorders: Bipolar I Disorder


Lithium Distribution: initially distributes into extracellular fluid and then to most other tissues. The final volume of distribution equals that 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

Mood Disorders: Bipolar I Disorder


Divalproate (Depakote) MOA- inhibition of the transamination of GABA. 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.

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