Preface

Agam is a group of budding medicos, who are currently doing their under graduation in
various Medical Colleges across Tamil Nadu and Pondicherry. The group was initiated on 18th
November 2017, in the vision of uniting medicos for various social and professional causes.
We feel delighted to present you Agam pharmacology notes prepared by Agam Divide and
Rule 2019 Team to guide our fellow medicos to prepare for university examinations.

This is a reference work of 2017 batch medical students from various colleges. The team
took effort to refer many books and make them into simple notes. We are not the authors of the
following work. The images used in the documents are not copyrighted by us and is obtained from
various sources.

Dear readers, we request you to use this material as a reference note, or revision note, or
recall notes. Please do not learn the topics for the 1st time from this material, as this contain just the
required points, for revision.
Acknowledgement

On behalf of the team, Agam would like to thank all the doctors who taught us Pharmacology.
Agam would like to whole heartedly appreciate and thank everyone who contributed towards the
making of this material. A special thanks to Kareeshmaa H C, who took the responsibility of leading
the team. The following are the name list of the team who worked together, to bring out the
material in good form.

Amritesh K Purushothaman
Rajeswar V
Sabura Misreen Aazam M
Kareeshmaa H C
Anusha Lakshmi Cheetiyar A
Shreevardhan G M
Baskaran S Akash
Rishikkesh Ramana G
Manigandan A
Pavithra J
Monisha T
Ananthapriya G
Snehaa S
Nandhinee A
Sanjay S
Bhargava Ram
Ragha Dharshini K
 INDEX

Chapter 1: General Anaesthetics

Essay
1. General Anaesthesia. 1

Short Notes
2. Stages of Anaesthesia. 4
3. .. 6
4. Pre-
5.
 1

1. GENERAL ANAESTHESIA
CLASSIFICATION:

INHALATIONAL ANAESTHETICS

Nitric Ether Halothane Desflurane Isoflurane Sevoflurane

oxide
Odour - Marked - Mild Mild -
N&V - Mild - Mild Mild Mild
Induction Fast Slow Intermedia Fast Intermediat Fast
te e
Recovery Rapid Slow Rapid Rapid Rapid Rapid
Analgesic Good Good Poor - - -
Inflammabili Nil Inflamm Nil Nil Nil Nil
ty able
Muscle Poor Very Fair Good Good Good
relaxation good
BP changes Nil Nil 20-30 mm
Hg drop
Respiration Nil Nil
Heart Nil Nil Nil mild
Potency Low High High Less 5 times less Intermediate
than
isoflurane.
Cheap Yes Yes Yes Expensive

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PHARMACOKINETICS:
Inhalational anaesthetics are gases or vapours
diffuses rapidly across pulmonary alveoli and tissue barriers.
The depth of anaesthesia depends on the potency of the agent and its partial
pressure in the brain.
Induction and recovery depend on rate of change of PP.
Factors affecting partial pressure (PP) of the anaesthesia obtained in the brain
are
Partial pressure of anaesthetic in the inspired gas
pulmonary ventilation
alveolar exchange
solubility of anaesthetic in blood
solubility of anaesthetic in tissue
cerebral blood flow
Elimination is through the channel of absorption i.e. pulmonary epithelium.
Only halothane is metabolized (<20%) in liver, others are not metabolized.

SECOND GAS EFFECT: This is significant only with nitrous oxide.

In the initial part of induction, diffusion gradient from alveoli to blood is high
and larger quantity of anaesthetic is entering blood. If the inhaled
concentration of anaesthetic is high, substantial loss of gas volume will occur
and the gas mixture will be sucked in, independent of ventilatory exchange gas
flow will be higher than tidal volume.

If another potent anaesthesia is given at the same time it will also be delivered
to blood faster and induction will be faster. This is called second gas effect.

DIFFUSION HYPOXIA: This is significant only with nitrous oxide.

When nitric oxide is discontinued after prolonged anaesthesia, having low
blood solubility, it rapidly diffuses into alveoli and dilutes alveolar air. PP of
oxygen is reduced resulting in diffusion hypoxia.

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COMPLICATIONS OF GENERAL ANAESTHESIA:

During anaesthesia:
Respiratory depression
Hypercarbia
Salivation
Respiratory secretions
mucociliary function
Cardiac arrhythmias
Fall in BP
Laryngospasm and asphyxia
Aspiration of acidic gastric contents
Delirium
Convulsions

After anaesthesia:
Nausea and vomiting.
Persisting sedation.
Pneumonia
Organ damage liver, kidney
Nerve palsies.
Cognitive defects.

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2. STAGES OF ANAESTHESIA

General anaesthesia- reversible depression of CNS function results in loss of

response to and perception of all external stimuli.

Stages of anaesthesia is broadly of 4 types:

Stage of analgesia
Stage of delirium
Surgical anaesthesia
Medullary paralysis

Stage I
This stage starts from beginning of anaesthetic inhalation and lasts upto the loss of
consciousness.

loss of pain sensation.

At the end of this stage analgesia and amnesia are produced

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Stage II

This stage starts from loss of consciousness to beginning of regular respiration.

Excitement - delirium, rise and irregular blood pressure, respiratory rate, risk of
laryngospasm
To shorten and eliminate this stage rapid acting I. V agents are given.

Stage III

Recurrence of regular respiration to complete cessation of spontaneous respiration.

This stage is divided into four planes:

Plane 1 roving eyeballs, ends when eyeballs are fixed.

Plane 2 loss of corneal and laryngeal reflexes.
Plane 3 pupil starts dilating and light reflex is lost.
Plane 4 intercostal paralysis, shallow abdominal respiration, dilated
pupil.

Loss of muscle tone, reflexes, relaxation of skeletal muscles.

Ideal stage for surgery.
Careful monitoring needed.

Stage IV

Cessation of breathing to failure of circulation and death.

Pupils are widely dilated, muscles are totally flabby, pulse is thready and BP is
very low
Ventilation and circulation must be supported to prevent death.

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3. IDEAL ANAESTHETIC DRUG

Properties of an ideal anaesthetic drug should be

For the patient:

Pleasant
less adverse effects nausea, vomiting
induction should be fast
Prompt recovery after its administration is discontinued

For the surgeon:

Good Analgesia.
Amnesia.
Immobility in response to noxious simulation.
Muscle relaxation
Unconsciousness.
Should be non-inflammable and non-explosive.

For the anesthetist:

Administration should be easy, controllable and versatile.
Wide margin of safety.
Vital organs should not be affected.
Should be potent under lower concentrations
Rapid adjustments in depth of anaesthesia should be possible
Should be cheap, stable and easily stored
It should not react with rubber tubing or soda lime

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4. PREANAESTHETIC MEDICATION
They refer to use of drugs before anaesthesia to make it safe and less
unpleasant

The aims are:

To relief anxiety and apprehension preoperatively and to facilitate smooth
induction
Amnesia for perioperative events
Supplement analgesic action of the anaesthetics and potentiate it so less
anaesthetic is needed
Decrease secretions and vagal stimulations that may be caused by
anaesthetic
Antiemetic effect extending into post-operative period
Decrease acidity and volume of gastric juice so that it is less damaging if
aspirated

DRUGS:
Sedative antianxiety drugs: They allay anxiety and facilitate amnesia.

Benzodiazepines
diazepam 5-10 mg oral or lorazepam 2mg oral or 0.05 mg/kg i.m. 1
hour before.
Promethazine 50 mg i.m.
(it is an antihistamine with sedative, antiemetic and anticholinergic properties.)
Midazolam i.v. injection can also be used.

H2 blockers/ proton pump inhibitors: to decrease the risk of gastric regurgitation

and aspiration pneumonia. Another advantage is to prevent stress ulcers

famotidine 20 mg
ranitidine 150 mg
omeprazole 20 mg
pantoprazole 40 mg.

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Anticholinergics: to reduce salivary and bronchial secretions.

Atropine or hyoscine 0.6 mg or 10 20 µg/kg i.m. or i.v.

glycopyrrolate 0.2 - 0.3 mg or 5 -10 µg/kg i.m. or i.v.

Neuroleptics: they allay anxiety, smoothen induction and have antiemetic action.

chlorpromazine 25 mg
triflupromazine 10 mg
haloperidol 2-4 mg i.m.

Antiemetics: to prevent post-operative nausea and vomiting

Metoclopramide 10-20 mg i.m.

ondansetron 4-8 mg i.v.
domperidone can also be used.

Antihistamines: diphenhydramine to prevent allergic reaction.

Opioids: fentanyl and non-opioids like acetaminophen for analgesia.

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5. KETAMINE

It produces Dissociative anaesthesia characterized by profound analgesia,

immobility, amnesia with only light sleep.

MECHANISM OF ACTION:

It acts by blocking N-Methyl-D-Aspartate (NMDA) type of glutamate receptors

Primary site of action is cortex and subcortical areas

non- barbiturate anaesthetic - affect reticular activating system

PHARMACOKINETICS:

lipophilic, rapid acting

Route- mostly by i.m.; other routes are i.v., oral
Dose- 0.5-1.5 mg/kg i.v.
3-5 mg/kg i.m.
Metabolism- In liver it is converted into nor-ketamine which has less CNS
activity
Excretion- through bile and urine.
Half-life- 2-4 hours.

Condition makes it suitable for continuous infusion-

Large Volume of distribution
Rapid clearance

ACTIONS:
potent Bronchodilator so it is beneficial in patients with cardio genocide shock,
hypotension, bronchospasm.
Respiration not depressed
muscle tone
CNS - delirium, hallucination, delusion

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CVS - increase in cardiac output, blood pressure, heart rate

ketamine
stimulates

centra sympathetic
outflow

stimulation of heart

output

USES:
For operations of head, neck and face
For dressing burn wounds
Can be used in children and asthmatics who are undergoing short procedures

ADR:
Increases intracranial pressure
Emergence delirium and hallucinations.

CONTRAINDICATION:
Hypertension
Stroke patients
Ischemic heart disease

CNS Agam Pharmacology

 INDEX

Chapter 2: Ethyl and Methyl Alcohols

Essay
1. .. 11

Short Notes
2. Methanol Poisoning 14
3. Alcohol Toxicity .. 16
4.
 11

1. ETHYL ALCOHOL
PHARMACOLOGICAL ACTIONS
Local actions
Ethanol is mild rubefacient and counter-irritant.
If injected it causes intense pain, inflammation and necrosis followed
by fibrosis.
As astringent precipitate surface proteins and hardens the skin.
As antiseptic by precipitating bacterial proteins.

Central nervous system

Neuronal depressant
30-60 ml Euphoria and excitation
50-100ml - individual will be high
100-150ml - Disorganisation, impairment of thought, gait alteration,
drowsiness
150-200ml - Ataxic and drunk, black outs occur.
a dependable hypnotic.
Sleep patterns are disoriented and sleep apnoea is aggravated.
Hangover occurs.

CVS
Small doses - Produces cutaneous and gastric vasodilation.
Moderate doses - Tachycardia and rise in BP.
Large doses - direct as well as Vasomotor centre depression and fall
in BP.

Blood
Increases HDL and decreases LDL oxidation
Lower incidence of coronary artery disease.

Body temperature
Combat cold - Due to cutaneous vasoconstriction but heat loss is
actually increased in cold surroundings.
High doses depress temperature regulatory centre

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Respiration
Respiratory stimulant
Direct action of alcohol on respiratory centre is only a depressant
one.

GIT
Higher concentrations inhibit gastric secretion, cause vomiting,
mucosal congestion and gastritis.
LES tone.

Liver
Fatty liver - Increases fat synthesis and mobilises fat.
Chronic alcoholism causes Cirrhosis, fibrosis, Necrosis of hepatocytes.
Regular alcohol intake induces microsomal enzymes

Skeletal muscle
Fatigue is allayed in small doses.
Weakness and myopathy on chronic alcoholism

Kidney
Diuresis - Alcohol inhibits ADH.

Sex
An aphrodisiac
Chronic alcoholism can produce impotence, testicular atrophy,
gynaecomastia and infertility in both men and women.

Endocrine effects
Hyperglycaemia in normal dose.
Intoxication leads to hypoglycaemic and depletion of glycogen.

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PHARMACOKINETICS
Gastric emptying determines the rate of absorption.
Crosses blood brain barrier effectively.
Crosses placenta.
Alcohol are oxidised by hepatic microsomal enzymes CYP2E1.
Limited 1st pass metabolism.
Zero order kinetics.
Excretion via Kidney and lungs
Concentration in exhaled air is 0.05%of blood concentration.

CONTRAINDICATIONS
Peptic ulcer, hyperacidity, gastroesophageal reflux disease.
Epileptics
Liver disease
Pregnant woman

USES:
Antiseptic
Sprain and joint pains
Prevent bedsores
Reduce body temperature in fever
Neuralgia treatment
Appetite stimulant
Treat methanol poisoning

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2. METHANOL POISONING

A blood level of > 50 mg/dl methanol is associated with severe poisoning.

Even 15 ml of methanol has caused blindness and 30 ml causes death.
Fatal dose is 75 100 ml.

MANIFESTATIONS: occurs after accumulation of metabolites

Vomiting
Headache
Epigastric pain
Uneasiness
Disorientation
Tachypnoea
Bradycardia
Hypotension
Acidosis causes retinal damage
Blurring of vision, congestion of optic disc followed by blindness
If left untreated, death is due to respiratory failure.

TREATMENT:

The patient should be kept in dark, quiet room protect the eyes from light.

Gastric lavage with sodium bicarbonate to be given if the patient is

brought within 2 hours of ingestion of methanol.

Combat acidosis so as to thus prevent retinal damage by i.v. sodium

bicarbonate infusion

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Potassium chloride infusion to correct hypokalaemia which occurs due to

alkali therapy.

Ethanol is preferentially metabolized by alcohol dehydrogenase over

methanol. At a concentration of 100mg/dl, it retards alcohol
dehydrogenase metabolism and thus methanol metabolism is inhibited.

Ethanol (10% in water) is administered through a nasogastric tube,

loading dose of 0.7 ml/kg, followed by 0.15 ml/kg/hour. Treatment as to
be continued for several days because methanol will be present for long
in the body.

Haemodialysis clears methanol and its metabolites, hastens recovery.

Fomepizole - a specific inhibitor of alcohol dehydrogenase and drug of

choice in methanol poisoning

A loading dose of 15mg/kg infused i.v. over 30 minutes followed by 10

mg/kg every 12 hours till serum methanol falls below 20 mg/dl.

Folate therapy: Calcium leucovorin 50 mg is injected 6 hourly reduces

formate levels by enhancing its oxidation.

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3. ALCOHOL TOXICITY
Gastric lavage is done, only if the patient is brought soon.
Respiratory airway maintenance
Prevent aspiration of the vomitus
Tracheal intubation and positive pressure are needed
Analeptics is not given because it precipitates convulsions
Fluid and electrolyte balance and correction of hypoglycaemia by
glucose infusion till alcohol is metabolised.
Thiamine (100mg in 500ml glucose solution infused i.v.) to be added.
Haemodialysis to hasten recovery
Insulin + Fructose drip accelerate alcohol metabolism.

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4. WITHDRAWAL SYNDROME
When an alcohol dependent subject abstains himself from alcohol, he develops
withdrawal syndrome.

MANIFESTATIONS:
Anxiety
Sweating
Tachycardia
Tremor
Impairment of sleep
Confusion
Hallucinations
Delirium
Convulsions
Collapse

TREATMENT:
Psychological and medical support
CNS depressants have been used as substitute therapy
Benzodiazepines are preferred drugs.
Naltrexone - dopamine medicated reward function. Reinforcement is
weakened in individuals who are treated with naltrexone.
Naltrexone is used as adjuvant therapy
Acamprosate is a weak NMDA receptor antagonist, Used as
maintenance therapy dose: 666 mg 2 3 times a day.

CNS Agam Pharmacology

 INDEX

Chapter 3: Sedative - Hypnotics

Essay
1. Sedative - Hypnotics.. .. 18

Short Notes
2. Acute Barbiturate Poisoning. 21
3. .. 22
4.

Short Answers
5.
6.
7.
 18

LONG ANSWER

1. SEDATIVE HYPNOTIC

The sedatives and hypnotics are CNS depressants.

Those with quicker onset, shorter duration and steeper dose response
curves are preferred as hypnotics.
slower acting drugs with flatter dose response curves are employed as
sedatives.

CLASSIFICATION:

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NON-BENZODIAZEPINE HYPNOTICS (non BZDs)

These lately developed drugs are chemically different from BZDs but act on
1 subunit containing BZD receptors.
They produce hypnotic, weak antianxiety, muscle relaxant and
anticonvulsant activity.
They have lower abuse potential and due to their short duration of action
are preferred for insomnia.

DRUGS:
Zopiclone
Eszopiclone
Zolpidem
Zaleplon
Etizolam

ZOPICLONE
First drug of non-BZDs
Does not alter REM sleep and tends to prolong stages 3 and 4
Used to wean off insomniacs taking BZD medication.
Metabolized by CYP3A4 and hence dose reduction needed in hepatic
impairment and elderly patients and those taking CYP3A4 inhibitors.
Indicated for short term insomnia
Side effects - metallic and bitter taste, impaired judgement and
alertness, psychological disturbances, dry mouth.

ESZOPICLONE
Active (S) enantiomer of zopiclone
Increases sleep time by prolonging stage 2 with minimal effect on
sleep architecture
No active metabolite produced, t1/2 is 6 hours.
Produces little tolerance and dependence and hence used for short
term and chronic insomnia.

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ZOLPIDEM
Sleep duration is prolonged in insomniacs but anticonvulsant, muscle
relaxant and antianxiety effects not evident
Advantages:
Relative lack of effect on slow wave sleep
Minimal residual day time sedation
Minimal fading of hypnotic action on repeated nightly use
No rebound insomnia on discontinuation
Low abuse potential
Completely metabolised in the liver
Short duration of action (t1/2-2hr)
Used in sleep onset insomnia and intermittent awakenings
Currently most commonly used hypnotic.

ZALEPLON
Shortest acting, rapidly absorbed, oral bioavailability is 30% due to
first pass metabolism.
Only effective in sleep onset insomnia.
Can be taken late in night and does not produce morning sedation.

ETIZOLAM
Produces full range of BZD reaction-anxiolytic, hypnotic,
anticonvulsant, muscle relaxant.
Absorbed rapidly, metabolised by oxidation
Chronic intake produces tolerance and dependence
Indicated for short term management of anxiety, panic and sleep
disorder.

USES
Insomnia, Hypnotic, Anxiolytic
Anticonvulsant (emergency control of status epilepticus and tetanus)
Centrally acting muscle relaxant
Pre-anaesthetic medication
Alcohol withdrawal in dependants
To treat gas or non-specific dyspeptic symptom along with analgesics,
NSAIDs, spasmolytic.

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2. ACUTE BARBITUATE POISONING

Mostly suicidal or accidental

MANIFESTATIONS:

patient is flabby and comatose with shallow and failing respiration

fall in BP
cardiovascular collapse
renal shut down
pulmonary complications
bullous eruptions

TREATMENT: there is no specific antidote

Gastric lavage suspension of activated charcoal

Supportive measures patent airway, assisted respiration, maintenance
of blood volume by infusion
Alkaline diuresis with sodium bicarbonate 1mEq/kg i.v.
Haemodialysis and Hemoperfusion.

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3. BENZODIAZEPINES

Central CNS depressants producing sedation, relief from anxiety, long

sleep, supress seizures and reduce muscle tone.
Higher therapeutic index compared to barbiturates.
Less distortion on sleep architecture and less rebound phenomenon.
.
Low abuse potential.
Has specific antagonist Flumazenil in case of poisoning.

ACTIONS:
Anxiolytic
Hypnotic
Muscle relaxant
Anticonvulsant

MECHANISM OF ACTION:

binds to specific BZD

receptor

enhances presynaptic and

postsynaptic inhibition.

BZD receptor is an integral part of GABA A receptor Cl- channel complex.

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DRUGS:
Flurazepam
Diazepam
Nitrazepam
Lorazepam
Alprazolam
Temazepam
Triazolam
Midazolam

PHARMACOKINETICS:
Oral absorption is rapid for some and slow for others.
Plasma protein binding varies markedly
They are widely distributed.
Crosses BBB, placenta and are secreted in milk.
Metabolised in liver by CYP3A4 & CYP2C19 to dealkylated and
hydroxylated metabolites.
Enters entero-hepatic circulation and later excreted in urine.

ADR:
Dizziness
Vertigo
Psychomotor impairment
Blurring of vision
Dry mouth
Urinary incontinence
Sweating
Withdrawal symptoms- anxiety, insomnia, malaise, restlessness, loss of
appetite, bad dreams

INTERACTIONS:
Synergize with alcohol and other CNS depressants
CYP3A4 inhibitors prolong the drug action
Cimetidine, isoniazid, oral contraceptives retard BZD metabolism.

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4. FLUMAZENIL

It is a BZD analogue competing with BZD agonists and inverse agonists

for the BZD receptor and reverse the depressant action.
Abolishes the hypogenic, psychomotor, cognitive and EEG effects of
BZDs.

PHARMACOKINETICS:
Not used orally but as i.v.
Action starts in seconds and lasts for 1-2 hrs
Rapid metabolism and elimination.

USES:
To reverse BZD anaesthesia regain motor control within 1min after iv
dose of 0.3-1mg.
BZD overdose - blocks hypnotic effect of zolpidem like non-BZDs;
flumazenil should not be given in mixed overdosage and BZD dependent
patients.

ADR:
Agitation
Fearfulness
Anxiety
Coldness
Withdrawal seizures

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5. DORA

DORA stands for Dual orexin Receptor antagonist

Suvorexant if the first member of this novel class of insomnia drugs
which blocks both OX1R and OX2R receptors responsible for
wakefulness
Hastens sleep onset, help in sleep maintenance and increase total sleep
time
Absorbed in 1-2 hrs and metabolised by CYP3A4, excreted in faeces.
Does not cause dependence and hence used in chronic insomnia
Elderly are more prone to Adverse effects like somnolence, muscle
weakness, abnormal dreams, etc.

6. FOUR HYPNOTIC BENZODIAZEPINES

Flurazepam
Diazepam
Lorazepam
Alprazolam

7. FOUR ANXIOLYTIC AGENTS

Diazepam
Oxazepam
Lorazepam
Alprazolam
Clonazepam

CNS Agam Pharmacology

 INDEX

Chapter 4: Anti-Epileptic Drugs

Essay
1. Antiepileptic Drugs.. 26

Short Notes
2. . 29
3. Diazepam and its Uses.. .. 30
4.
5.

Short Answers
6. 1st line of drugs for absence seizures
7.
8.
9.
 26

1. ANTIEPILEPTIC DRUGS

CLASSIFICATION:

PHENYTOIN
CNS depressant
Abolishes tonic phase of seizures

MECHANISM OF ACTION:
Phenytoin prevents repetitive detonation of normal brain cells by
Prolongation of inactivated state of voltage sensitive Na + channel.
Depress presynaptic release of glutamate
Facilitating GABA release
Reduce Ca2+ influx

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PHARMACOKINETICS:
Absorption: Oral route, slow
Metabolism: CYP2C9 and 2C19 by hydroxylation as well as glucuronide
conjugation (liver)
The kinetics of metabolism is capacity limited i.e. 1st order to zero order
kinetics (over the therapeutic range)
T1/2 12-24 hours

ADVERSE EFFECTS:
Therapeutic plasma concentration
Gum hypertrophy
Hirsutism
Hypersensitivity
Megaloblastic anemia
Osteomalacia
Fetal hydration syndrome

Over dose toxicity due to higher plasma concentrations

Cerebellar and vestibular manifestations Ataxia, vertigo, diplopia,
nystagmus.
Drowsiness, Hallucination
Nausea, vomiting
i.v. fall in BP

phenytoin sodium i.v.

local vascular injury

damage and thrombosis

of vein

edema and discoloration

of injected limb

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INTERACTIONS:
phenytoin and phenobarbitone unpredictable overall reaction.
Phenytoin and carbamazepine
Valproate displaces protein bound phenytoin plasma level of unbound
phenytoin increases.
Phenytoin competitively inhibits warfarin metabolism.

USES:
Generalized tonic-clonic seizures
Partial seizures
Trigeminal neuralgia (2nd choice)

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2. CARBAMAZEPINE
First line drug for partial seizures and GTCS
Modifies maximal electroshock seizures and raises threshold to PTZ
Inhibits kindling
Lithium like therapeutic effect on mania
Antidiuretic action

MECHANISM OF ACTION: (similar to phenytoin)

It prolongs the rate of recovery of Na+ channels from inactivation, thereby
reduces neuronal excitability.

PHARMACOKINETICS:
Slow absorption.
75% plasma protein bound.
Metabolised by oxidation and hydroxylation in liver.
On chronic medication, plasma half-life decreases due to autoinduction of
metabolism.

ADR:
Sedation
Dizziness
Vertigo
Vomiting
Diarrhea
Seizures
Acute intoxication coma, convulsions, CVS collapse.
Hypersensitivity
Water retention and natriuresis
Minor fetal malformations

USES:
Trigeminal neuralgia
Epilepsy (GTCS)
Mild depression and acute mania

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3. DIAZEPAM AND ITS USES

It belongs to benzodiazepines group of drugs

It has anticonvulsant activity but not used for long term therapy of epilepsy
because of prominent sedative action and rapid development of tolerance
First line drug for emergency convulsions (status epilepticus, tetanus,
eclampsia, convulsant drug poisoning)
0.2-0.3mg/kg doses i.v. followed by repeated doses until 100mg/day

ADR:
Thrombophlebitis
Respiratory depression
Marked fall in BP

USES:
Anxiolytic
Hypnotic
Muscle relaxant
Pre-anaesthetic medication
Emergency control of seizures

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4. VALPROIC ACID

Valproate is more potent in blocking PTZ seizures.

At anticonvulsant doses, valproate produces little sedation or other central
effects.

MECHANISM OF ACTION:
Valproate acts by multiple mechanisms:
A phenytoin-like frequency dependent prolongation of Na + channel
inactivation.

Enhanced release of inhibitory transmitter GABA due to inhibition of its

degradation as well as increasing the synthesis from glutamic acid.
Blockade of NMDA glutamate receptors.

PHARMACOKINETICS:
Good oral absorption
90% plasma protein bound
Completely metabolized in liver
USES:
Excreted in urine
Absence seizures
1st line of drugs in partial
ADR: seizures and GTCS
Myoclonic seizures
Anorexia
Mania and bipolar illness
Vomiting
Prophylaxis in migraine
Loose motions
Heart burn
Drowsiness
Alopecia
Teratogenic spina bifida and other neural tube defects

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5. STATUS EPILEPTICUS
Status epilepticus is a condition in which the seizure activity occur for > 30 min, or
two or more seizures occur without the recovery of consciousness.
Fits have to be controlled as quickly as possible to prevent death and permanent
brain damage.
The first priority is to maintain patient airway. This is followed by 20-50 ml of
50% dextrose injected i.v. to correct hypoglycemia, in case that is responsible
for the seizures.
Other general measures must be taken like fluid and electrolyte balance, BP,
etc.
Lorazepam 4 mg (0.1 mg/kg in children) injected i.v. at the rate of 2 mg/min,
repeated once after 10 min if required.
Diazepam 10 mg (0.2-0.3 mg/kg) injected i.v. at 2 mg/min, repeated once after
10 minutes if required.
Fosphenytoin 100-150 mg/min i.v. infusion to a maximum of 1000 mg (15-20
mg/kg) under continuous monitoring is a slower acting drug which should be
given subsequently irrespective of response to lorazepam. This is useful for
long term seizure treatment.
Phenobarbitone sodium should be used only if Fosphenytoin is not available
because it causes more marked local vascular complications.
Refractory cases who do not respond to lorazepam and Fosphenytoin within
40 mins can be treated with i.v. midazolam/ propofol/ thiopentone
anaesthesia, with or without curarization and full intensive care.

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6. 1ST LINE OF DRUGS FOR ABSENCE SEIZURES

Valproate
Ethosuximide

7. ADR OF ETHOSUXIMIDE

G.i. intolerance
Tiredness
Mood swings
Headache
Inability to concentrate

8. CYCLIC GABA ANALOGUES

Gabapentin
Pregabalin

9. INFANTILE SPASMS

Hypsarrhythmia
Therapy of this condition is unsatisfactory

term due to adverse effects

Clonazepam, valproate and vigabatrin may afford some relief.

CNS Agam Pharmacology

 INDEX

Chapter 5: Anti-Parkinsonian Drugs

Essay
1. Antiparkinsonian Drugs.. 34

Short Notes
2. MAO Inhibitors. . 38
 34

1. ANTIPARKINSONIAN DRUGS

CLASSIFICATION:

LEVADOPA:

MECHANISM OF ACTION:

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PHARMACOLOGICAL ACTIONS:
CNS

Hypokinesia and rigidity resolves first.

Secondary symptoms like posture, gait, handwriting, speech, facial
expression is gradually normalized.
The effect of Levodopa on behavior has been described as a general
alerting response.
It predisposes to emergence of psychiatric symptoms.

CVS
Tachycardia by acting on Beta adrenergic receptors.
Postural hypotension is common.
Impede ganglionic transmission.

CTZ
Activation of CTZ elicits nausea and vomiting.
Tolerance develops further.

Endocrine
Inhibits prolactin release and induces GH release.
Hypoprolactinemia is common in parkinsonism patients while hyper
GH is not seen.

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PHARMACOKINETICS
Bioavailability is affected by
Gastric emptying-
barrier.
Amino acid present in food compete for absorption as it is same carrier.
High first pass metabolism
1% enters brain
Pyridoxine is a cofactor for the enzyme dopa-decarboxylase.

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ADVERSE EFFECTS:
Nausea and vomiting
Postural hypotension
Cardiac arrhythmias
Exacerbation of angina
Alteration in taste sensation
On prolonged therapy
Dyskinesia
Behavioral effects
Fluctuations in motor performance

INTERACTIONS:
Pyridoxine abolishes the therapeutic effect of levodopa
Phenothiazines, butyrophenones, metoclopramide reverses the therapeutic
effect of levodopa.
Non-selective MAO inhibitors
Antihypertensive drugs postural hypotension may happen.
Atropine and antiparkinsonian anticholinergic drugs have additive effect

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2. MAO INHIBITORS

Selegiline
Rasagiline

SELEGILINE
Selective and irreversible MAO-B inhibitor.
Two isoforms of MAO, termed MAO-A and MAO-B are recognized.
MAO -B preferentially oxidizes DA
while
intracerebral degradation of DA is retarded. This is responsible for the
therapeutic effect in PD.
Mild anti-parkinsonism action in early cases
Administered with levodopa, it prolongs the action.
However, advanced cases with on &off effect are not improved.
ADR:
Nausea
Vomiting
Postural hypotension
Insomnia
Agitation
Contraindicated in convulsive disorders
It interacts with pethidine and causes excitement, rigidity, hyperthermia,
and respiratory depression.

RASAGILINE
5 times more potent, longer acting and not metabolized to amphetamine.
Given once a day in the morning
Does not produce excitatory side effects or insomnia.
Preferred over selegiline

CNS Agam Pharmacology

 INDEX

Chapter 6: Antipsychotic and Antimaniac

Drugs
Essay
1. Neuroleptic Drugs.. 39

Short Notes
2. Atypical Antipsychotics. 43
3. .. .. 46
4.

Short Answers
5. Alternatives to Lithium in treating Mania . 49
6.
 39

1. NEUROLEPTIC DRUGS

CLASSIFICATION:

CHLORPROMAZINE

PHARMACOLOGICAL ACTION:

CNS
In non-psychotic individuals, CPZ produces indifference to surroundings,
paucity of thought, psychomotor slowing, emotional quietening,
reduction in initiative and tendency to go off to sleep from which the
subject is easily arousable.
In a psychotic, CPZ reduces irritational behavior, agitation and
aggressiveness and controls psychotic symptomatology.
The disturbed sleep pattern in a psychotic is normalized.
Mechanism of action
They have potent dopamine D2 receptor blocking action.
In untreated persons dopamine receptor population is high.

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ANS
They have varying degrees of alpha-adrenergic blocking activity.
Weak anti-cholinergic action.

Local anaesthetic
Potent local anaesthetic as procaine, but its not used because of its
irritant action.

CVS
They produce hypotension by a central as well as peripheral action in
sympathetic tone.
Reflex tachycardia as a complication.

Endocrine
They increase prolactin release by blocking the inhibitory action of DA
on pituitary lactotropes.
Gynecomastia and galactorrhea can occur.

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PHARMACOKINETICS:

Oral absorption is somewhat unpredictable.

Bioavailability is low.
i.m. or i.v. administration.
Highly bound to plasma as well as tissues proteins.
The metabolites are excreted in bile and urine.

ADVERSE EFFECTS:

CNS drowsiness, lethargy, mental confusion.

CVS postural hypotension, palpitation, inhibition of ejaculation.
Anti-cholinergic dry mouth, blurring of vision, constipation, urinary
hesitancy.
Endocrine Hyperprolactinemia.
Metabolic effects blood sugar elevation, raised triglyceride level.
Extra pyramidal disturbances Parkinsonism, acute muscular dystonia,
Akathesia, Malignant neuroleptic syndrome, tardive dyskinesia.
Miscellaneous weight gain.
Hypersensitivity reactions like skin rashes, urticaria, contact dermatitis,
photosensitivity among others.

INTERACTIONS:
Neuroleptics potentiate all CNS depressants-overdose symptoms occur.
Blocks actions of levodopa and direct DA agonists in parkinsonism.
Antihypertensive action of clonidine and methyldopa is reduced due to
central alpha 2 adrenergic blockade.

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USES:
Schizophrenia
Gilles de la Tourette syndrome
Acute mania
Bipolar disorder
Organic brain syndrome
Anxiety
Anti-emetic
Tetanus
Alcoholic hallucinosis

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2. ATYPICAL ANTIPSYCHOTICS

Second generation antipsychotics.

Has weak D2 blocking but potent 5-HT2 antagonistic activity.
Advantages:
Extrapyramidal side effects are minimal.
They tend to improve the impaired cognitive function in
psychotics.

DRUGS:
Clozapine
Risperidone
Olanzapine
Quetiapine
Aripiprazole
Ziprasidone
Amisulpiride
Zotepine

CLOZAPINE:
First atypical antipsychotic.
Both positive and negative symptoms of schizophrenia are
improved.
It is the most effective drug in refractory schizophrenia when
typical neuroleptics are ineffective.
Quite sedating, moderately potent anticholinergic.
Metabolised in CYP1A2, CYP2C19 and CYP3A4.
Higher incidence of agranulocytosis is a limiting factor.
Other limiting factors are
Metabolic complications weight gain, hyperlipidaemia and
precipitation of diabetes.
Other side effects are sedation, unstable BP, tachycardia
and urinary incontinence.

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RISPERIDONE:
More potent D2 blocker than clozapine.
Weight gain and incidence of new onset of diabetes are less
compared to clozapine.
Major side effect is postural hypotension.
Increased risk of stroke in elderly is noted.
It is often used as 1st line of drug in schizophrenia.

OLANZAPINE:
Both positive and negative symptoms of schizophrenia are
improved.
It is approved for use in mania.
Metabolized by CYP1A2 and glucuronyl transferase.
Side effects:
diabetes and serum triglyceride levels.

QUETIAPINE:
Short acting
Used in maintenance therapy in acute mania as well as bipolar
disorder.
Metabolised in CYP3A4.
Risk of arrhythmia in high doses.
ADR: postural hypotension, urinary retention, weight gain, etc.

ARIPIPRAZOLE:
Risk of arrhythmia in high doses.
ADR: nausea, dyspepsia, constipation and light-headedness.
Metabolised by CYP3A4 & CYP2D6.
Indicated in schizophrenia with positive and negative symptoms.
It is also used as an augmenting agent in resistant depression and
as maintenance drug in bipolar disorder.

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ZIPRASIDONE:
Can cause arrhythmias.
Nausea and vomiting are common side effects.
Indicated in mania.

AMISULPIRIDE:
It is similar to typical psychotics.
Side effects are hyperprolactinemia, insomnia, anxiety and
agitation.
Used in schizophrenia.

ZOTEPINE:
Used in schizophrenia
Lowers seizure threshold.
Side effects are weakness, headache

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3. LITHIUM CARBONATE

Anti-manic
Mood stabilizing drug

MECHANISM OF ACTION:
Exact mechanism is unknown, the most accepted hypothesis is phosphatidyl
inositol hydrolysis.

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lithium inhibits inositol monophosphatae

prevents hydrolysis of IP

free inositol is

regeneration of membrane phosphatidyl inositides

IP3 and DAG is

dampening of signal transduction in overactive receptors

PHARMACOKINETICS:

Absorption oral.
Neither protein bound nor metabolised.
Distribution - total body water, slowly enters into intracellular
compartment.
Penetrates brain, secreted in milk.
Excretion - kidney.

USES:

Acute mania
Bipolar disorder
Unipolar depression antidepressant + Lithium
Recurrent neuropsychiatric illness

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ADVERSE EFFECTS:

Nausea, vomiting, thirst, polyuria, fine tremors

Cns toxicity occurs plasma concentration more than 2mEq/L.
Muscle twitching
Drowsiness
Delirium
Coma
convulsions
Cardiac arrhythmias
Treatment:
It is symptomatic. No specific antidote.
Osmotic diuretic and sod. Bicarbonate infusion to promote
excretion.
Hemodialysis is recommended when serum levels are > 4mEq/L.
Hypoglycemia.
Goitre - interfere in release of thyroid hormone, fall in t3, t4 cause increase
in TSH, enlargement of thyroid.

DRUG INTERACTIONS:

Diuretics (furosemide / thiazide) - increase proximal Na+ & Li+

reabsorption - increase lithium level
Tetracyclines, NSAIDs, ACE inhibitors - lithium retention

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4. DRUG INDUCED PARKINSONISM

Caused due to anti-psychotics.

MANIFESTATION:
Rigidity
Tremor
Hypokinesia
Mask like face shuffling gait

Appears between 1-4 weeks of therapy persists unless dose is reduced.

Central anticholinergics should be given if dose reduction is not sufficient.
Changing to atypical antipsychotic might help.
Routine administration of anticholinergics with anti-psychotics tend to
worsen memory, impair intellect, cause dry mouth and urinary retention.

5. Alternatives to Lithium in treating Mania.

Sodium valproate (Divalproex) - First line of treatment.
Carbamazepine - long term prophylaxis of bipolar.
Olanzapine
Risperidone
Aripiprazole

6. Four indole amines.

LSD (lysergic acid diethyl amide)
Lysergic acid amide.
Psilocybin
Harmine
Bufotenin.

CNS Agam Pharmacology

 50

CNS Agam Pharmacology

 INDEX

Chapter 7: Antidepressant and Antianxiety

Drugs
Essay
1. Antidepressant Drugs 50

Short Notes
2. . 54

Short Answers
3. . 56
4.
5.
 50

1. ANTIDEPRESSANT DRUGS

CLASSIFICATION:

TRICYCLIC ANTIDEPRESSANTS
MECHANISM OF ACTION:

inhibit NET & SERT

initial stimulation of 5HT1A/ 2

receptors

later receptor desensitization

occurs

mediation of negative feedback

control on transmitter release

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PHARMACOLOGICAL ACTIONS:
CNS:
NORMAL INDIVIDUAL:
Peculiar clumsy feeling
Tiredness
Light-headedness
Difficulty in concentrating and thinking
Unsteady gait

DEPRESSED INDIVIDUAL:
After 2-3 weeks of continuous treatment, the mood is
gradually elevated, patients become more communicative and
start taking interests in themselves and their surroundings.

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ANS:
Potent anticholinergic.
Potentiate exogenous and endogenous NA by blocking uptake.

CVS:
Tachycardia
Postural hypotension
ECG changes T wave suppression or inversion
Arrhythmia - NA POTENTIATING + CHOLINERGIC BLOCKADE along
with direct myocardial depression compound the pro- arrhythmic
potential.

TOLERANCE AND DEPENDENCE:

Tolerance develops gradually.
Addiction to these drugs are rare.
Gradual withdrawal is recommended.

PHARMACOKINETICS:
Absorption oral route, good
Highly plasma bound
Large volumes of distribution
Extensively metabolised in liver
Metabolised are excreted in urine
They exhibit an unusual therapeutic window phenomenon.

ADVERSE EFFECTS:
Dry mouth
Constipation
Epigastric distress
Urinary retention
Sedation
Mental confusion
Weight gain
Sweating
Fine tremors

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Postural hypotension
ACUTE POISONING:
Manifestations: excitement, delirium, respiratory
depression, fall in BP and body temperature,
tachycardia, ECG changes and ventricular arrhythmias.
Treatment: primarily supportive therapy with gastric
lavage, respiratory resistance, fluid infusion,
maintenance of vitals. Acidosis must be corrected by
bicarbonate infusion.

INTERACTIONS:
TCAs potentiate directly acting sympathomimetic amines.
TCAs potentiate CNS depressants.
Phenytoin, phenylbutazone, aspirin can displace TCAs.
Phenobarbitone competitively inhibits as well as induces imipramine
metabolism.
SSRIs inhibit metabolism of TCAs.
TCAs delay gastric emptying.
MAO inhibitors when given with TCAs cause dangerous hypertensive
crisis.

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2. SSRI
Selective serotonin reuptake inhibitor.

DRUGS:
Fluoxetine
Fluvoxamine
Paroxetine
Sertraline
Citalopram
Escitalopram
Dapoxetine

ADVANTAGES:

Little or no sedation.
Does not interfere with cognitive and psychomotor function.
No anti-cholinergic side effect.
-blocking, hence no Postural hypotension.
No seizure precipitating propensity.
do not inhibit cardiac conduction.
No weight-gain.

USES:

Prophylaxis of recurrent depression.

OCD 1st choice of drugs.
Panic disorder
Social phobia
Eating disorders
PMDD
PTSD
Kleptomania

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MECHANISM OF ACTION:

Inhibit SERT

block uptake of 5HT into

neuron

receptors

enhance serotoninergic
activity

ADVERSE EFFECTS:

Gastrointestinal - nausea, loose motions.

CNS - nervousness, insomnia, headache.
Systemic - epistaxis and ecchymosis

DRUG INTERACTION:

Inhibits the drug metabolizing iso-enzyme CYP2D6, CYP3A4. Hence elevated

-blocker, BZD and
carbamazepine.
Serotonin syndrome manifesting as agitation, restlessness, rigidity,
hyperthermia, delirium, sweating, etc when any serotonergic drugs are taken
along with SSRIs.

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3. SNRI

Venlafaxine
Desvenlafaxine
Duloxetine

4. ATYPICAL ANTIDEPRESSANT

Mianserin
Mirtazapine
Amoxapine
Bupropion

5. DRUGS FOR OCD

Fluoxetine
Fluvoxamine
Clomipramine
Buspirone

CNS Agam Pharmacology

 INDEX

Chapter 8: Opioid Analgesics and Antagonists

Essay
1. 57

Short Notes
2. 61
3. Complex Action 62
4. 64

Short Answers
5. Endogenous Opioids . 66
6. 66
7. Contraindications of Morphine. 66
8.
 57

1. OPIOID ANALGESICS:

CLASSIFICATION:

MORPHINE:

Morphine is the principal alkaloid in opium.

Morphine is an agonist which has 3 receptors namely µ,
All three receptors on stimulation cause analgesia.

PHARMACOLOGICAL ACTIONS:
CNS
Analgesia
It is a strong analgesic.
Morphine suppress both perception of pain and its emotional
component.

Sedation
Drowsiness, mental dullness and indifference to the
surroundings is noted.
High doses progressively induce sleep and then coma.

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Subjective effects and euphoria

Prominent calming effect
Loss of apprehension
Feeling of detachment
Mental clouding
Inability to concentrate.

Respiratory Depression
Morphine depresses respiratory centre.
Death in morphine poisoning is due to respiratory failure.

Antitussive Actions
Suppression of the cough reflex.

Temperature regulation
Hypothalamic thermostatic centre is depressed.

Nausea and Vomiting

Nausea and vomiting are caused by activation of the chemoreceptor trigger
zone and are increased by ambulation.
GIT
Constipation.

CVS
Vasodilatation
Decreased cardiac work
Intracranial pressure rises due to retention of CO2 leading to cerebral
vasodilatation.

NEURO-ENDOCRINE ACTIONS
Hypothalamic activation by afferent collaterals is dampened.
Hypothalamic influence on pituitary is reduced.

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SMOOTH MUSCLE

spasm of sphincter of oddi

biliary colic

PHARMACOKINETICS:
Oral absorption is unreliable.
High and variable 1st pass metabolism.
30% plasma protein bound.
Wide distribution.
Small fraction crosses BBB.
Freely crosses placenta.
Affects foetus more than the mother.
Excreted by kidney.

ADVERSE EFFECTS:
Sedation
Mental clouding, Lethargy
Vomiting
Constipation
Respiratory depression
Blurring of vision
Urinary retention
Allergic reactions
Apnoea of new born naloxone 10 µg/kg injected in the umbilicus cord is
treatment of choice.
Acute morphine poisoning
Tolerance and dependence

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USES:
Analgesia
Pre-anaesthetic medication
Balanced and surgical anaesthesia
Relief of anxiety and apprehension
Acute LVF / pulmonary edema
Cough
Diarrhoea

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2. ACUTE MORPHINE POISONING

Accidental, suicidal or seen in drug abusers.

DOSE:
In non-tolerant adult 50 mg i.m. produces serious toxicity
Human lethal dose 250 mg

MANIFESTATONS:
Stupor or coma
Flaccidity
Shallow and occasional breathing
Cyanosis
Pinpoint pupil
Fall in BP
Shock
Convolutions may be seen
Pulmonary edema occurs at terminal stage
Death due to respiratory failure

TREATMENT:
Respiratory support
Maintenance of BP
Gastric lavage with KMnO4 to remove unabsorbed drug.
Lavage is indicated even when morphine has been injected.
Specific antidote: naloxone 0.4 0.8 mg i.v. every 2 3 minutes till respiration
picks up, due to short duration of action, it should be repeated every 1 4
hours, according to response.

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3. COMPLEX ACTION OPIOIDS:

Nalorphine:

ceiling analgesia.
It is not used clinically because of dysphoric and psychotomimetic effects.

Pentazocine:
It is the first agonist-antagonist to be used as an analgesic.
The profile of action is similar to morphine; important differences are:

different character than that caused by morphine.

Sedation and respiratory depression are 1/3 to 1/2 of morphine at
lower doses.
Tachycardia and rise in BP are produced at higher doses due to
sympathetic stimulation.
Biliary spasm and constipation are less severe.
Vomiting is less frequent.
Subjective effects are pleasurable (morphine-like) at lower doses:
recognised by post-addicts as an opiate.

Used for postoperative and moderately severe pain in burns, trauma,

fracture, cancer.

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 63

Butorphanol:
. Likewise,
analgesia and respiratory depression have a lower ceiling than morphine.
Sedation, nausea, cardiac stimulation and other side effects are similar to
pentazocine, but subjective effects are less dysphoric.
Withdrawal can be precipitated by high dose of naloxone, but the
syndrome is mild.
The abuse potential of butorphanol is low.
It has been used for postoperative and other short-lasting (e.g. renal colic)
painful conditions.

Buprenorphine:
It is a synthetic thebaine congener
Sedation, vomiting, miosis, subjective and cardiovascular effects are similar to
morphine, but constipation is less marked.
Postural hypotension is prominent.
Respiratory depression (and analgesia) exhibit ceiling effect.
Lower degree of tolerance and physical as well as psychological dependence
develops with buprenorphine on chronic use.
Its withdrawal syndrome resembles that of morphine, but is delayed for
several days, is milder and longer lasting.
Use: Buprenorphine is indicated for long-lasting painful conditions requiring an
opioid analgesic, e.g. cancer pain. It has also been recommended for
premedication, postoperative pain, in myocardial infarction and in the
treatment of morphine dependence.

Nalbuphine:
More potent analgesic than pentazocine.
No cardiovascular effects
Drug seeking behaviour is minimal
Can precipitate morphine withdrawal in dependent subjects
Indicated in postoperative and other moderately severe pain

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4. TRAMADOL

Atypical synthetic opioid

Centrally acting analgesic

MECHANISM OF ACTION:

tramadol inhibits

re-uptake of NA & 5HT

activates monoaminergic
spinal inhibition of pain.

PHARMACOKINETICS:
Oral bioavailability is good
t½ - 5-6 hours and effect lasts for 4-6 hours

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ADR:
Insignificant respiratory depression
Sedation
Constipation
urinary retention
nausea
Dizziness
Sleepiness
Dry mouth
Sweating
Lowering of seizure threshold

CONTRAINDICATION:
Epileptics because of lowered seizure thresholds
Patients on SSRI therapy - because of rise serotonin syndrome

USES:
Mild to moderate short-lasting pain due to injury, surgery, etc.
Chronic pain including cancer pain

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5. ENDOGENOUS OPIOIDS
Endorphin
Endorphin
Enkephalin
Dynorphins

6. OPIOID ANTAGONISTS
Naloxone
Naltrexone
Nalmefene

7. FOUR CONTRINDICATIONS OF MORPHINE

patients with respiratory insufficiency (emphysema, pulmonary
fibrosis, cor pulmonale).
Infants and elderly.
patients with head injury.
undiagnosed acute abdominal pain.

8. FOUR SYNTHETIC OPIOIDS

Pethidine
Methadone
Fentanyl
Tramadol

CNS Agam Pharmacology

 INDEX

Chapter 9: CNS Stimulants and Cognition

Enhancers

Short Notes
1. 67

Short Answers
2. Drugs for night shift workers... . 68
3. 68
4. . 68
5. Miscellaneous 69
 67

1.

Cognition Drugs Route of Mechanism of ADR

enhancers administration action
Cholinergic Rivastigmine Oral AntiChEs GI
activators Donepezil inhibit true and disturbances
Galantamine pseudo ChEs

transmission in
brain
cognitive
function.
Glutamate Memantine Oral Inhibits Constipation,
antagonist glutamate dizziness,
transmission etc.
Miscellaneous Piracetam Oral, i.m. Insomnia,
drugs microcirculation. headache.
Neuroprotective
effect.
Citicoline Oral, i.m., i.v. 2 and blood Headache
supply to brain.
Piribedil Oral Dopamine Nausea and
agonist. vomiting
Ginkgo biloba Oral Neuroprotective GI
disturbances

bleeding.

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1. Four drugs for night shift workers:

Modafinil
Amphetamine
Dextroamphetamine
Methamphetamine

2. Four Convulsants

Strychnine
Picrotoxin
Bicuculline
Pentylenetetrazol (PTZ)

3. Why is Tacrine not in use?

It is hepatotoxic

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Miscellaneous

1. Drugs for Attention deficit-hyperactivity disorder (ADHD)

Methylphenidate
Atomoxetine
Amphetamine
Dexamphetamine

2. Balanced Anaesthesia:
The combined use of inhalational and IV Drugs produce the following features
in patients:
Loss of all sensation - especially pain
Sleep (unconsciousness)
Amnesia
Immobility
Muscle relaxation
Abolition of somatic and autonomic reflexes

3. Neuroleptic in Anaesthesia:
Useful in pre-anaesthetic condition.
Chlorpromazine (25 mg)
Triflupromazine (10 mg)
Haloperidol (2 4 mg) i.m.
They allay anxiety, smoothen induction and have antiemetic action.

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4. Hepatotoxic Drugs
Those Drugs, when taken in overdoses and sometimes even when
introduced within therapeutic ranges, may injure the liver.

Tacrine
Atomoxetine
Naltrexone
Flutamide

Isoniazid, rifampicin, pyrazinamide, halothane, paracetamol are other

hepatotoxic drugs.

CNS Agam Pharmacology