Psychiatry medicines

Odongo shadrack
(MbchB)
 Classifications
• Anti psychotics
• Anti depressants
• Mood stabilizers
• Anxiolytics
• Hypnotics
• Psycho stimulants
ANTIDEPRESSANTS
 OVERVIEW OF DEPRESSION
Depression involves clinically significant changes in mood,
behavior, energy, sleep and cognition for at least two weeks
including:
• Depressed mood most of the day
• Markedly diminished pleasure or interest in nearly all daily
activities
• Significant weight loss or gain or significant loss or increase
in appetite
• Hypersomnia or insomnia nearly everyday
• Loss of energy or fatigue nearly everyday
• Feeling of worthlessness or excessive guilt
 DEPRESSION MAY BE SECONDARY TO:
• Organic problems like hypothyroidism,
dementia, anemia
• Psychiatric problem like schizophrenia, drug
abuse and anxiety disorder
• Use of depressant drugs such as alcohol
BIOGENIC THEORY OF DEPRESSION
Depression is due to a deficiency of
monoamines such as norepinephrine and
serotonin, at certain sites in the brain

Antidepressants therefore potentiate, directly or

indirectly the actions of norepinephrine or
serotonin in the brain
 ANTIDEPRESSANTS
• First generation
Tricyclic antidepressants, monoamine oxidase
inhibitors
• Second generation
Selective serotonin reuptake inhibitors,
serotonin-norepinephrine reuptake inhibitors
• Atypical antidepressants
 Selective serotonin reuptake inhibitors
• Antidepressant drugs that specifically inhibit
serotonin reuptake

• They are relatively safe even in overdose

• Have largely replaced TCAs and MAOIs as the

drugs of choice in treating depression
 SSRIs
• Fluoxetine
• Citalopram
• Escitalopram
• Fluvoxamine
• Paroxetine
• sertraline
 Mode of Action
• Block reuptake of serotonin, increasing its
concentrations in the
• synaptic cleft and its postsynaptic neuronal
activity
 SSRIs
• Antidepressants, including SSRIs, takes at least
2weeks to produce significant improvement in
mood

• Maximum benefit may require greater or equal

to 12 weeks

• Do not usually produce CNS stimulation or

mood elevation in normal individuals
 PHARMOKINETICS
• All of the SSRIs are well absorbed after oral administration
• Peak levels are seen in 2-8hours
• Food has little effect on absorption except with
sertraline,food increases it absorption
• Half life 16-36hours: fluoxetine half life 50 hours half life of
active metabolite about 10days
• Its available as sustained-released preparation allowing
once-weekly dosing
• Metabolism by CYP450 enzymes and glucuronide or
sulfate conjugation
 SSRIs
• Fluoxetine and paroxetine are potent
inhibitors of CYP2D6 which is

responsible for the elimination of TCAs,

neuroleptic drugs, and some

antiarrhythmic and beta-adrenergic antagonist

drugs
 ADVERSE EFFECTS
• Headache
• Sweating
• Anxiety and agitation
• Nausea, vomiting, diarrhea
• Weakness and fatigue
• Sexual dysfunction esp. paroxetine and sertraline
• Weight changes: gain esp. paroxetine, loss esp. fluoxetine
• Sleep disturbance (insomnia and somnolence),paroxetine
and fluvoxamine are more sedating, fluoxetine or
sertraline are more activating SSRIs
 ADVERSE EFFECT
• Apathy and emotional blunting
• Irritability
• Akathisia/restlessness
• Nervousness
• QT prolongation
• Palpitation
• Rarely: serotonin syndrome, hyponatremia,
hyperprolactinemia, galactorrhea, seizures
 SEROTONIN SYNDROME
• All SSRIS have the potential of causing
serotonin syndrome when used in the
presence of a MAOI or other serotonergic
drug

• Serotonin syndrome include symptoms of

hyperthermia, muscle rigidity, sweating,
myoclonus, and changes in mental status and
vital signs
 DISCONTINUATION SYNDROME
• All of SSRIs have the potential to cause a
discontinuation syndrome after abrupt withdrawal,

• Fluoxetine has the lowest risk of causing an SSRIs

discontinuation syndrome

• Signs and symptoms of SSRIS discontinuation

syndrome include: headache,malaise,flue-like
symptoms, agitation and irritability, nervousness.
 SEROTONIN NOREPINEPHRINE REUPTAKE
INHIBITORS
• MOA
Inhibit the reuptake of both serotonin and
norepinephrine

May be effective in treating depression in

patients where SSRIs are ineffective
 SNRI
• Duloxetine

• Venlafaxine

• Desvenlafaxine

• levomilnacipram
 Duloxetine
• Inhibit serotonin and norepinephrine reuptake at all doses
• Extensively metabolized in the liver, should not be
administered in patients with hepatic insufficiency
• Metabolites are excreted in the urine, and the use of
duloxetine is not recommended in patient with end stage
renal disease
ADVERSE EFFECTS
• Nausea, dry mouth, constipation, insomnia, sexual
dysfunction, risk for increase in either BP or heart rate
• Duloxetine inhibit CYP2D6 and CYP3A4
 Side effects of Venlafaxine and
desvenlafaxine
• Nausea
• Headache
• Sedation
• Dizziness
• Insomnia
• sexual dysfunction
• constipation
 TRICYCLIC ANTIDEPRESSANTS
MOA
• Inhibition of neurotransmitter reuptake: TCAs are potent
inhibitors of neuronal reuptake of norepinephrine and
serotonin in to presynaptic nerve terminal
• Increases concentration of monoamines in the synaptic
cleft, resulting in antidepressant effect
• Maprotiline and desipramine are relatively selective
inhibitors of norepinephrine reuptake
• TCAs also block alpha adrenergic, histaminic, and
muscarinic receptors causing many adverse effects
 TCAs
• Impiramine
• Clomipramine
• Desipramine
• Trimipramine
• Amitriptyline
• Nortriptyline
• Maprotiline
• Protriptyline
• Amoxapine
• doxepin
 Pharmokinetics

• Well absorbed after oral administration

• Lipophilic hence widely distributed and readily
penetrate into CNS
• Long half lives because of lipid solubility e.g. up to
17 hrs for imipramine
• Variable first pass metabolism-; low & inconsistent
bioavailability hence adjust according to patient’s
response
• Initial treatment period is typically 4-8 weeks and
dose gradually reduced
• Metabolized by hepatic microsomal system and
conjugated with glucuronic acid
• Eliminated as inactive metabolites via the kidney
 Adverse effects
• Blockade of muscarinic receptors leads to blurred
vision, dry mouth, urinary retention, constipation
• Affect cardiac conduction which may precipitate life
threatening arrhythmias in overdose
• Blockade of alpha adrenergic receptors causing
orthostatic hypotension,dizziness,and reflex tachycardia
• Sedation especially during first weeks of treatment due
to blockade of histamine H1 receptors
• Weight gain
• Sexual dysfunction
MONOAMINE OXIDASE INHIBITORS
MOA
• Most MAOIs form stable complexes with MAO causing
irreversible inactivation. This results in increased stores
of norepinephrine, serotonin,and dopamine within the
neuron and diffusion of excess neurotransmitter into the
synaptic space
• These drugs also inhibit MAO in the liver and gut that
catalyze oxidative deamination of drugs and potentially
toxic substances, such as tyramine, which is found in
certain foods causing high incidence of drug-food
interactions
 Examples
• Isocarbazide
• Phenelzine
• Tranylcypromine
• selegiline
 Pharmakokinetics
• Well absorbed after oral administration
• Metabolized and excreted in urine
• Individuals on MAO inhibitors are
unable to degrade tyramine in the diet
(Tyramine causes release of stored
catecholamines)
• Phentolamine or prazosin may be used
to manage tyramine induced
hypertension
 Adverse effects
• Orthostatic hypotension
• Drowsiness
• Sexual dysfunction
 ATYPICAL ANTIDEPRESSANT
• Bupropion
Weak dopamine and norepinephrine reuptake inhibitor
Side effects: dry mouth, nervousness, tremor

• Mirtazapine
Enhances serotonin and norepinephrine
neurotransmission by blocking presynaptic α₂ receptors
and 5-HT₂ receptors
Side effects: increased appetite and weight gain, marked
sedation
• Nefadone and trazodone

Weak inhibitors of serotonin reuptake

Block postsynaptic 5-HT₂ᴀ receptors
Side effects: orthostatic hypertension and
dizziness and hepatotoxicity with nefazodone
ANTIPSYCHOTICS
 PRINCIPLES OF MANAGEMENT OF
FRACTURE
Psychosis is a symptom of mental illness characterized by distorted or
nonexistent sense of reality.

Common psychotic disorders include;

–Mood disorders (major depression or mania) with psychotic features,
–Substance-induced psychosis,
–Dementia with psychotic features,
–Delirium with psychotic features,
–Brief psychotic disorder,
–Delusional disorder,
–Schizoaffective disorder, and
–Schizophrenia

33
Different etiological theories explain psychosis
but inorder to understand how antipsychotics
work, we shall look at the biochemical basis of
psychosis.

With emphasis on Schizophrenia since it is

considered the prototypic disorder for
understanding the psychosis.

34
 Neurochemical abnormality hypotheses
Dopaminergic overactivity

Glutaminergic hypoactivity NMDA receptor antagonists, (e.g. ketamine, PCP) have been shown to
induce both positive and negative symptoms of schizophrenia in healthy volunteers (possibly via
modulation of the DA system) and exacerbate symptoms of patients with schizophrenia.

Serotonergic (5-HT) overactivity

5-HT agonism, associated with sensory distortions and hallucinations.

Alpha-adrenergic overactivity
levels of noradrenaline (NA) have been found in the CSF of patients with acute psychotic symptoms.
Chronic treatment with antipsychotic drugs leads to firing rates in the locus coeruleus (the origin of
the noradrenergic system).

Gamma-aminobutyric acid hypoactivity

Loss of GABA inhibition has been shown to lead to overactivity in other neurotransmitter systems
(e.g. DA, 5-HT, NA).

35
 Dopamine pathways
• Mesolimbic-mesocortical pathway; Related to behavior and
pyschosis. Projects from the ventral tegmentum to the limbic system
and neocortex.
• Nigrostriatal pathway; for coordination of voluntary movement
From substantia nigra to the dorsal striatum (caudate and putamen).
Blockade of D2- receptors in this pathway is responsible for the EPS
• Tuberoinundibular system; Inhibits prolactin secretion into pituitary
portal system. From arcuate nuclei and periventricular neurons to
pituitary portal circulation.
• Medullary-periventricular pathway; Involved in eating behavior;
motor nucleus of the vagus nerve
• Incertohypothalamic pathway From the medial zona incerta to the
hypothalamus and the amygdala. Appears to regulate anticipatory
and motivational phase of copulation behavior in rats 36
37
 Anti psychotic drug classification

1. Typical antipsychotics
• Phenothiazines
➢ Aliphatic derivatives like Chlorpromazine
➢ Piperidine derivatives like Thioridazine.
➢ Piperazine derivatives like Trifluoperazine,
Perphenazine, Fluphenazine

MOA; Block D2 in this pathways.

38
 Anti psychotic drug classification

• Butyrophenones
➢ Haloperidol, Droperidol

• Thioxanthines
➢ Chlorprothixene, Thiothixene

• Miscellaneous;
➢ Pimozide
➢ Molindone 39
 Anti psychotic drug classification

Low Potency:
• Chlorpromazine – Prototype
• Prochlorperizine (Compazine)
• Thioridazine (Mellaril)

High Potency:
• Fluphenazine (Prolixin)
• Haloperidol (Haldol)
• Thiothixene (Navane) 40
 Anti psychotic drug classification
2. Atypical antipsychotics
Sertindole,
Loxapine,
Risperidone,
Olanzapine,
Aripiprazole,
Clozapine,
Quetiapine,
Ziprasidone,

MOA;
Blockers of serotonin receptors (5HT2A) and to a lesser extent dopamine
receptors (D2)
41
 Pharmacokinetics
Absorption and distribution
• Most are only partly absorbed
• Many undergo significant first-pass metabolism
• Oral chlorpromazine and thioridazine have systemic availability
of 25-35% whereas haloperidol, that has less 1st pass
metabolism has 65% bioavailability
• Most antipsychotics are highly lipid soluble and protein bound
(92-99%).
• Have much longer clinical duration of action that would be
estimated by PK and this parallels prolonged occupancy of D2
receptors

42
 Pharmacokinetics
Metabolism

• Most are completely metabolized by oxidation or demethylation

catalyzed by liver microsomal cytochrome enzymes esp;
CYP2D6. CYP1A2, CYP3A4.

• Potential for interaction with drugs that inhibit the above

enzymes like ketoconazole.

43
44
45
 EPS
1. Parkinsonism: Symptoms resembling Parkinson’s disease can occur, including
bradykinesia (slowness of movement), rigidity (stiffness of muscles), resting tremors,
and postural instability.

2. Akathisia: This condition is characterized by a subjective feeling of inner restlessness

and an urge to move. It can manifest as an inability to sit still or constant pacing.

3. Dystonia: Dystonia refers to involuntary muscle contractions that cause repetitive or

twisting movements or abnormal postures. Commonly affected areas include the face,
neck, tongue, and limbs.

4. Tardive dyskinesia: Tardive dyskinesia is a potentially irreversible condition that can

occur with long-term use of antipsychotic medications. It involves repetitive,
involuntary movements, such as lip smacking, tongue protrusion, grimacing, or rapid
jerking of the limbs. 46
 EPS mgt
Medication adjustments change
Anticholinergic medications: Anticholinergic drugs, such
as benztropine or trihexyphenidyl, can be prescribed to
help alleviate EPS symptoms.
Patient education and support
1. Regular monitoring: Regular follow-up appointments
with the healthcare professional are essential to
monitor the progress of EPS

47
MOOD STABILISERS

48
 MOOD STABILISERS
• Mood; a sustained pervasive emotion or feeling tone that
influence a person’s behavior and colors his or her perception of
being in the world e.g.. Depressed, manic, sad, distressed,
irritable, and euphoric
• Mood disorder; the derangement of mood, sometimes called
affective disorders, and include depressive disorder, bipolar
disorder, and other disorders.
• Mood stabilizers can be classified as:
1. Minerals; Lithium
2. Anti-convulsants
3. Other mood stabilisers (atypical anti-psychotics and
benzodiazepines)
 Lithium
• Lithium is used for the short-term and prophylactic
treatment of bipolar I disorder.
Pharmacokinetics;
• Completely absorbed by the GI tract.
• Serum concentrations peak in 1 to 1½ hours for standard
preparations and in 4 to 4½ hours for controlled-release
preparations.
• Lithium does not bind to plasma proteins, is not
metabolized, and is excreted through the kidneys.
• The half-life of lithium is about 20 hours, and equilibrium is
reached after 5 to 7 days of regular intake.
• The renal clearance of lithium is decreased in persons with
renal insufficiency (common in the elderly)
 Lithium
• Indications for lithium Usage; • Contraindications;
• Acute treatment of mania
• Pregnancy
• Maintenance treatment in
bipolar disorder • Renal failure
• Adjuvant with • Addison’s disease
antidepressants in major • Hypothyroidism
depressive disorder
• Control of aggressive • Cardiovascular
behavior, self-mutilating insufficiency
mannerisms and prevention
of suicide and steroid induced
psychosis.
 Side Effects
• Tremor (C); usually worse • Kidney function
under social scrutiny impairment (UC)
• Gastrointestinal distress (O)
• Psoriasis (O, I)
• Weight gain (O)
• Cognitive impairment (UC) • Acne (O)
• Increased urination (C) • Hypothyroidism (O)
(diabetes insipidus, i.e.,
blockage of vasopressin
receptor response at level of
decreased production of
cyclic adenosine
monophosphate)
 Anti-convulsants;
• Valproate;
Pharmacokinetics;
• All valproate formulations are rapidly and
completely absorbed after oral administration.
• The steady-state half-life of valproate is about 8
to 17 hours
• Clinically effective plasma concentrations can
usually be maintained with dosing once, twice,
or three or four times per day.
 Mechanism of action
• Inhibit sodium and/or calcium channel
function
• thereby boost GABA inhibitory action as well
as reduce glutamate excitatory action.
• Inhibition of T type calcium ion.
• Decrease the release of glutamate in the
brain.
 Indications
• Acute mania and mixed episodes
• First line for bipolar patient’s refractory to lithium
monotherapy
• Focal seizures with impaired awareness
• Prophylaxis in migraine
• Trigeminal neuralgia.
• Tardive dyskinesia.
Contraindications
• Pancreatitis
• Hepatic impairment
• Allergy
 Adverse effects
• alopecia • Common chance of neuro-
• Tremors tube defect in pregnancy.
This is counteracted by co-
• Sedation administration of F/A.
• Cognitive deficit. • Weight gain
• Irreversible hepatic • Menstrual disturbances
necrosis in children < 2 • polycystic ovaries
yrs. • hyperandrogenism
• Acute pancreatitis • Hyperglycemia secondary
• hyperammonemia. to insulin resistance
 Carbamazepine:
• Pharmacokinetics;
• Metabolized in the liver, primarily by CYP450 3A4
• Inducer of CYP450 3A4 thus, induces its own metabolism,
often requiring an upward dosage adjustment
• Initial half-life 26–65 hours
• Renally excreted
• Mechanism of Action
• Blocks voltage‐dependent sodium channels
• thus inhibiting repetitive neuronal firing.
• Also reduces glutamate release and decreases the turnover
of dopamine and noradrenaline.
 Indications
• Acute mania and mixed mania
• Prophylaxis of bipolar2
• Bipolar depression
• Unipolar depression
• Generalized tonic clonic and focal seizure
• Management of alcohol withdrawal symptoms
• To manage aggressive behavior in patients
with schizophrenia.
 Adverse effects:
• dizziness • Dry mouth
• Diplopia • Oedema
• Drowsiness • Sedation
• Ataxia • Confusion
• • generalized erythematous
Nausea
rash (Steven Johnsons’
• headaches syndrome)
• bone marrow suppression
• sexual dysfunction
• hyponatremia
 Lamotrigine
• Pharmacokinetics;
• Completely absorbed, bioavailability of 98%
• Has a steady-state plasma half-life of 25 hours.
• 55% protein-bound in the plasma
• the rate of lamotrigine’s metabolism varies over a sixfold
range, depending on which other drugs are administered
concomitantly.
• Dosing is escalated slowly to twice-a-day maintenance
dosing.
• Food does not affect its absorption
• 94% of its inactive metabolites are excreted in the urine.
 Mechanism of action;
• blockade of voltage-sensitive sodium channels,
• which in turn modulate release of glutamate and
aspartateslight effect on calcium channels.
• Lamotrigine modestly increases plasma serotonin
concentrations possibly through inhibition of
serotonin reuptake
• It is a weak inhibitor of serotonin 5-HT3 receptors.
 Indications
• Bipolar disorder; lamotrigine prolongs time
between depressive and manic episodes in
currently or recently depressed, manic, or
hypomanic bipolar I patients
• Lamotrigine may possess acute
antidepressant effects.
• borderline personality disorder
• various pain syndromes
 Adverse effects
• Dizziness • blurred vision
• Ataxia • Nausea
• Somnolence • cognitive impairment
• joint or back pain are
• Headache
common
• diplopia • The appearance of a rash
(Steven Johnson's
syndrome), which is
common and occasionally
very severe, is a source of
concern
 Other mood stabilisers

• atypical anti-psychotics • Benzodiazepines

• Aripiprazole • Benzodiazepines have
anticonvulsant actions, especially
• Olanzapine intravenous diazepam and oral
• Risperidone clonazepam.
• Quetiapine and Quetiapine XR • They are also sedating.
• • These actions have led to the use
Ziprasidone
of benzodiazepines for the
• Paliperidone treatment of mood disorders as
• Asenapine adjunctive treatment for agitation
• and psychotic behavior during the
Lurasidone
phase of acute mania
• Brexpiprazole • Benzodiazepines are also broadly
• Cariprazine used in anxiety and sleep disorders
ANXIOLYTICS AND HYPNOTICS
 ANXIOLYTICS
Anxiolytics are a class of drugs primarily used to alleviate symptoms of anxiety
disorders. They work by modulating the activity of neurotransmitters in the brain,
aiming to reduce excessive neuronal excitability and promote a sense of calmness.
Classifications
1. Benzodiazepines
Short acting: Triazolam, lorazrpam, temazepam, and oxazepam.
Long acting: Diazepam, Chlordiazepoxide, alprazolam, and clobazam.
2. Buspirone: Is a non-benzodiazepine anxiolytic that primarily affects serotonin
receptors. It does not affect GABA receptors.
 Indications
• Generalized Anxiety Disorder (GAD): Persistent and excessive anxiety about
various activities or events.

• -Panic Disorder: Recurrent, unexpected panic attacks.

• - Social Anxiety Disorder: Overwhelming worry and self-consciousness in

everyday social situations.

• - Specific Phobias: Intense, irrational fears of specific objects or situations.

• - Post-Traumatic Stress Disorder (PTSD): Severe anxiety, flashbacks, and

intrusive thoughts following a traumatic event.
 Cont…
Mode of Action:

• - Benzodiazepines:Enhance the inhibitory effects of GABA by binding to

specific receptors on GABA-A receptors. This increases the frequency of
chloride channel opening, leading to membrane hyperpolarization, which
reduces neuronal excitability.

• - Buspirone: Acts as a partial agonist at serotonin (5-HT1A) receptors and

has some affinity for dopamine (D2) receptors. It modulates the activity of
these neurotransmitters in the brain.
 Cont…
Pharmacodynamics:

• - Benzodiazepines primarily enhance the inhibitory effects of GABA, leading

to CNS depression. This results in sedation, muscle relaxation, and anxiolysis.

• - Buspirone modulates serotonin and dopamine receptors, leading to

anxiolytic effects without causing sedation or significant CNS depression.

Pharmacokinetics:

• - Benzodiazepines: Absorbed orally, metabolized in the liver (varies by

specific drug), and excreted through urine. They often have short to
intermediate half-lives.

• - Buspirone: Absorbed orally, metabolized in the liver (CYP3A4 enzyme), and

excreted in urine. It has a delayed onset of action and needs consistent
dosing.
 Cont…
Side Effects:
• Benzodiazepines:Sedation, drowsiness, dizziness, cognitive impairment,
tolerance, dependence, withdrawal symptoms, potential for abuse.
• Buspirone: Nausea, dizziness, headache, nervousness, restlessness, insomnia. It
lacks the sedative and muscle relaxant effects associated with benzodiazepines.
Interaction with Autonomic Nervous System:
• - Benzodiazepines may cause mild autonomic effects such as drowsiness and
sedation, but they primarily exert their effects on the central nervous system.
• Busprone does not significantly affect the autonomic nervous system. It does
not cause sedation or muscle relaxation to the same extent as benzodiazepines.
 Hypnotics
Examples of Drugs:
• 1. Benzodiazepines: Examples include Diazepam, Lorazepam, and
Alprazolam.
• 2. Non-Benzodiazepine Hypnotics: Examples include Zolpidem, Zaleplon,
Zaleplon and Eszopiclone.
• 3. Barbiturates: Examples include Phenobarbital, Secobarbital, and
Pentobarbital.

Indications:
• Hypnotics are primarily used to treat insomnia and other sleep disorders.
They help in initiating and maintaining sleep, promoting relaxation, and
reducing anxiety.
 Cont..

Barbiturates:
• Barbiturates are a class of central nervous system depressant drugs that act as
sedatives and hypnotics. They were commonly used in the past for their sedative and
anesthetic properties, but their use has decreased due to their high potential for
overdose and addiction.
Examples: Phenobarbital, Pentobarbital and Secobarbital
Mode of Action:
• - Barbiturates work by enhancing the inhibitory effects of the neurotransmitter
gamma-aminobutyric acid (GABA) in the central nervous system. They bind to specific
GABA-A receptors, leading to an increase in the frequency of chloride channel
opening. This results in membrane hyperpolarization, reducing neuronal excitability.
Pharmacodynamics:
• - They produce sedation, muscle relaxation, and can induce sleep at higher doses.
Their effects range from mild sedation to anesthesia, depending on the specific
barbiturate and dosage.
 Cont…
Pharmacokinetics:
• - Absorbed orally, but can also be administered intravenously.
Metabolized in the liver and excreted primarily through urine.

Indications:
• - Historically, barbiturates were used as sedatives, hypnotics, and
anesthetics. They were also employed in the treatment of epilepsy.

Side Effects:
• - Barbiturates can cause drowsiness, sedation, dizziness, impaired
coordination, and respiratory depression. They can also lead to tolerance,
dependence, and withdrawal symptoms upon discontinuation
 Interaction with ANS
• Barbiturates impact the autonomic nervous system.
• They may lead to reduced sympathetic activity, respiratory depression,
changes in cardiovascular responses, pupillary reflex alterations, and
effects on gastrointestinal motility and vasomotor tone

• Zolpidem, a non-benzodiazepine hypnotic, enhances the effects of the

inhibitory neurotransmitter GABA. This leads to sedation, reduced sleep
latency, and preservation of natural sleep stages. Zolpidem has a shorter
half-life, minimizing daytime drowsiness.
 Pyscho- stimulants
Examples of Drugs:
• 1. Amphetamines: Examples include Amphetamine, Dextroamphetamine
(Adderall), and Methamphetamine.
• 2. Methylphenidate: Examples include Methylphenidate (Ritalin, Concerta)
and Dexmethylphenidate (Focalin).
• 3. Modafinil and Armodafinil
• 4. Anticholinesterase inhibitors e.g. Donepezil, rivastigmine, galantamine.

Psycho Stimulants: Indications

• 1. Amphetamines:
• - ADHD: Manages symptoms like inattention, hyperactivity, and
impulsivity.
• - Narcolepsy: Treats excessive daytime sleepiness and sudden sleep
attacks.
• 2. Methylphenidate:
• - ADHD: Improves focus, impulse control, and behavior.
• - Narcolepsy: Helps manage symptoms of narcolepsy.
• 3. Modafinil and Armodafinil:
• - Narcolepsy: Keeps individuals awake during the day.
• - Sleep Disorders: Treats excessive sleepiness in conditions like sleep
apnea and shift work sleep disorder

Pharmacokinetics:
• - Absorption: These drugs are often administered orally and are rapidly
absorbed from the gastrointestinal tract.
• - Distribution: They are distributed widely in the body, including the brain,
due to their lipophilic nature.
• - Metabolism: Most psycho stimulants are metabolized in the liver through
various enzymatic pathways.
• - Excretion: Metabolites are primarily excreted through the kidneys.
Pharmacodynamics:
• - Dopamine and Norepinephrine Reuptake Inhibition: Psycho stimulants
block the reuptake of dopamine and norepinephrine, leading to increased
levels of these neurotransmitters in the brain.
• - Increased Release of Neurotransmitters: Some stimulants increase the
release of dopamine and norepinephrine from nerve endings, further
enhancing their effects.

Side Effects:
• - Common Side Effects: Increased heart rate, elevated blood pressure,
reduced appetite, restlessness, insomnia, and increased alertness.
• - Less Common but Serious Side Effects: Irregular heartbeat, high blood
pressure, hallucinations, paranoia, and, in the case of amphetamines,
potential for addiction and substance abuse.
 Cont….
Interaction with the Autonomic Nervous System:
• - Sympathetic Nervous System Activation: Stimulants increase SNS
activity, leading to increased heart rate and blood pressure.

• - Parasympathetic Nervous System Inhibition: They inhibit

parasympathetic activity, reducing activities that promote relaxation and
calmness.
 References
• Oxford text of psychiatry 4th edition
• Osmosis
• Katzungu