Ebook Viva voce in medical pharmacology: Part 1

Viva Voce
•

zn

Medical Pharmacology

K

Mukhopadhyay

Private General Practitioner
Dhanbad

Former
Senior Resident, Department of Pharmacology
Institute of Medical Sciences, BHU
Medical Officer, Damodar Valley Corporation
Additional Professor, Department of Pharmacology
College of Medical Sciences
Bharat Pur, Nepal

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Viva Voce in Medical Pharmacology

© 2004, K Mukhopadhyay
All rights reserved. No part of this publication should be reproduced, stored in a retrieval system,
or transmitted in any form or by any means: electronic,mechanical, photocopying, recording,
or otherwise,without the prior written pE>rmission of the author and the publisher.
This book has been published in good faith that the material provided by author is original. Every
effort is made to ensure accuracy of material, but the publisher, printer and author will not
be held responsible for any inadvertent error(s). In case of any dlspute,.all legal mattersJo
be settled under Delhi jurisdiction only.

First Edition: 2004
Reprint: 2005
ISBN 81-8061-259-7

Typeset at

JPBMP typesetting unit

Pnnted at

Sanat Printers.


to
my father
Late Tulsi Das Mukherjee
who gave me courage
for my education


Preface

Medical science has rapidly grown and developed in the last
couple

of

decades,

and

so

has

emerged

its

branch

Pharmacology. The real beauty of the subject Pharmacology
is that the clinicians of all specialities and superspecialities
use its knowledge to prevent, diagnose and cure diseases.
This tends to confuse undergraduate students during their
viva-voce exams. Viva-voce examination environment has been
simulated and model questions and their answers have been
provided in this book. Through this book I have attempted
to help students get through their viva-voce exams.
Many people have helped me put together this book. Birds
of the same feather flock together. I am grateful to Dr (Mrs)
Barnali Mukherjee, Dr Jhulan Mukherjee, Dr (Mrs) Shrabani

Mukhopadhyay and Dr Angshuman Mukhopadhyay who
were professional critics outside and loving family near home.
I am also thankful to Smt Bina Mukherjee, Shri Basudeb

Mukherjee, Smt Kajoli Mukherjee, Shri Baladeb Mukherjee,
Shri Abhijit Banerjee, Smt Jayanti Sinha and Shri GCP Sinha
for their blessings and encouragement. I would like to thank
Dr TR Roy and Shri Binod Modi and Dr MM Bandopadhyay
for encouraging me to go ahead with writing this book.
How can I forget to mention my lecturers during my
undergraduate and postgraduate studies. I am indebted to
Prof MS Dey, Prof Robin Chatterjee, Prof BN Das, Prof S
Banerjee, Late Prof AK Sanyal, Prof PK Das, Prof SS Gambhir,
Prof SB Acharya, Prof SK Bhattacharya, Prof RK Goel, Dr BL
Pandey whose lectures were of immense help in preparing
this book. Special thanks go to my department colleagues,
Prof AK Chakraborty, Prof SK Tripathy, Dr Anil Jaiswal for
suggestions and encouragement. Prof JN Neogi and Prof KK
Agarwal of CMS, Nepal also encouraged me to go about
writing this book. My heartfelt thanks to them.


Viva Voce in Medical Pharmacology

viii

I must thank Mr Tarun Duneja, GM (Publishing), Mr Sanjay
Chakraborty, Asstt. Sales Manager of Jaypee Brothers Medical
Publishers to help compile this book.
I would like to mention my cousins Aditi Banerjee, Lakshmi

Chatterjee, Arundhati Banerjee, Nandini Pandit, Anuradha,
Mrinal for their unending enthusiasm.
Finally, kisses and love to my son, Sanak, my niece Esha
and Idrija for their giggles and laughter which always seemed
to tell me: Arise, Awake and Stop not till the goal is achieved..
I must acknowledge my mother, Smt Bedbani Mukherjee
who went through with infinite patience and always stood
by me. Thanks!

K Mukhopadhyay

•

'!>.


Contents

1. General Pharmacology .............. .. . .. .. ............. ........ .. 1
.

2. Autonomic Nervous System .

...

.

.

.

...

..

.

. ..... .. . ... .......... .............. 8
.

.

.

.

3. Central Nervous System ................................................. 19
a.

Drugs used in Gout

... ......... ... ......... ..... ...........................

b. Analeptics, Psychostimulant, Nootropic
c.

Psychopharmacology

d. Alcohol

.............................................. .........

............................................ ................................
.

e. Antiparkinsonian Drugs

f.

Narcotic Analgesic

h. Anti Epileptics
NSAID

......... . ............................... .......

................................................ .........

g. Sedative Hypnotics
i.

..................................... ....................

.................................................... . ..........

......... .. ........ ..........................................................

g. Rheumatoid Arthritis
.

.

.

Local Anaesthetics

.

.

.

.

...

.

..

.....

...

Plasma Kinins, Angiotension

28
30
32
36

39

..

.................... ................. ............... ...

5. Autocoids ........... ... ....

22
27

.... . ..................... 44

........

......... ............................... ................. .

b. General Anaesthetics
.

.

19
20

42

......................................................

4. Anaesthetics .... . ...... . .. . ... ... .

a.

.......................

44
45

......... ...... . ....................... 48

...

.

.

.

.

..............................................

51

6. Prostaglandins . .. .. .. .. .. ...... .... .. .. . ............ ............ 55
.

.

.

...

.

..

..

..

.

.

.

7. Respiratory System ....... ... .............. ........... . ..... ....... 58
.

..

.

.

.

.

.

..

8. Cadiovascular System ........ ........... ......... . . . . ... ... .. . 61
.

a.

Drugs in Heart Failure

b. Antiarrhythmic Drugs
c.

Antianginal Drugs

d. Antihypertensive

.

.

..

..

.

.

.

.

.

............................................... . ...

. ...... ............................................

.

............................................

.....................................

e.

Hypolipoproteinemic Drugs

f.

Plasma Expanders

.

............

...................... .

...........................................

............ ..... . ......................... ... . ............

61
63
65
69
71
72

9. Water, Electrolytes and Drugs Affecting
Renal Function . ..... ..... ...... .......... ...... ............. . .. .. .. 74
..

..

.

..

.

.

.

.

.

x

Viva Voce in Medical Pharmacology

10. Drugs used in Gastrointestinal Tract .......................... 80
11. Haemopoietic System ......................................,............,. 88
12. Endocrine System ........................................................... 98
.

Diabetes mellitus, Insulin, OHG
Corticosteroid

....

.

....

.

............................

......................................................................

Drugs Acting on Calcium Metabolims

..

.

....... . . . . . . .............

Anabolic Steroids ..... . .
..

Androgen
Oestrogen

..

.....................................................

..........................................

........

Contraceptives

109
112
114

; ................................. 116

............................................................................

Progesterone

104

.

......... . ........... ..........................................

.......... .................................................. ........

117
119
120

13. Antimalarial Drugs ........................................................ 124
14. Antiamoebic Drugs .... ..... ............................ ................ 128
.

.

.

15. Antihelmintic Drugs ................
.

16. Anticancer Drugs

.

............................... 131

... .

. ...................................................... 133

... .

.

17. Drugs Acting on Skin and Mucous Membrane

.....

137

18. Sexually Transmitted Diseases .......................... ........ 140
.

19. Antiseptic and Disinfectant ........................................ 142
20. Radioisotopes .............................. .................................. 144
.

21. Therapeutic Gases ....... .................................................. 145
.

22. Immunosuppresant and Gene Therapy .................... 147
23. Vitamins ........................................................................... 149
24. Enzymes in Therapy .......................•...... ....................... 151
,

25. Chelating Agents
26. Vaccines and Sera

........................

.

............. ........ ............ 152
.

.

. ............................................ 154

...... ..... .

27. Antibiotics ..................................

.

.....

............................... 156

28. Sulfonamides ................................................. ................. 160
29. Quinolones ....................................................... . ............ 162
.

.

30. Tetracyclines ................................................. . ................. 168
.

31. Chloramphenicol ..................................;........................ 172
32. Macrolide Antibiotics ................................................... 173


Contents
33. Urinary Tract Infection .

...........................

34. Anti Tubercular Drugs
35. ·Anti Leprotic Drugs .
.

...

36. Antifungal Antibiotic
37. Antiviral Drugs .

Index

...............

. . .. .
.

.

...............

........

.

...............

.

.

.

.

.. ..

.....

. . . .... . .

.

..

..........

.

.

....

. . 175
.

..................

.....

...

.

...

......

.

..

....

.............

.

.........

......

.. ..
.

....

.

..........

.

.......

xi

176

.. . 179

....

.

.

.......

.........

.

..

...................................................................................

181
184

187


General Pharmacology
Q.l. Define pharmacology, drugs, toxicology, therapeutics,
pharmacopeia.

Pharmacology: It is that branch of medical science which
deals with history, source, physical and chemical properties,
compounding, biochemical and physiological effects, mec­
hanism of action, absorption, distribution, biotransformation,
excretion, therapeutic uses and side effects of a drug.

Drug:
i. A chemical substance used for the purpose of diagnosis
prevention, relieve or cure of a disease in man or animals.
ii. WHO has defined drug as "any substance or product
that is used or intended to be used to modify or explore
physiological systems or pathological states for the benefit
of the recipient."

Toxicology: Science of poison. It is the study of measurement,

detection and treatment of poisons.

Therapeutics: It is branch of medicine concerned with cure of a
disease or relief of symptoms.

Pharmacopeia: A book published by recognised authority of
any country containing a list of accepted drugs and formulae
for medical preparations with average dose and description
of their characteristics test for their identity, purity and
potency like IP, BP, USP.
Q.2. What is prescription?

It is written order for one or medical agents along with
direction to the pharmacist for the preparation and to the


2

Viva Voce in Medical Pharmacology

patient for the use of the medicine at a particular time. It has
following parts:
1. Name of patient
2. Superscription

(Rx) Take thou or sign for Jove or Jupiter,

God of healing.
3. Inscription

Body of
prescription

��·.
t

Basis
Adjuvent

c.

Corrective

d.

Vehicle

4. Subscription: Direction of pharmacist for compounding

ingredient.
5. Signa: (Signature) Direction to patient including method

of administration, dose, time of administration.
6. Physicians signature, date, address, registration number.

Q.3. What are the different sources of a drug?
It could be
i. Minerals: Iron
ii. Animals: Thyroid, Insulin
iii. Synthetic: Aspirin

iv. Microbial: Antibiotic
v. Plant: Oils, glycoside, alkaloids, etc.

Q.4. Define bioavailability?
Bioavailability of a drug (Biological active drug) is defined
as percentage of drug absorbed from a given doses form and
reaches systemic circulation following nonvascular adminis­
tration. In case of intravascular administration it is 100%.

Q.S. What is Apparent volume distribution?
Considering body as a single compartment (V) in which drug
(M) is distributed and (C) is the plasma concentration of the
drug in plasma then apparent volume distribution (Vd)

=

M/

C. The apparent volume distribution is governed by
i. Lipid water co-efficient
ii. pka of drug
iii. Protein binding and affinity for other tissues for the drug.
1v. Diseases like CCF, uraemia, cirrhosis and age.


General Pharmacology

3

Q.6. What are the different routes of drug administration?

It may be
Systemic

Local

I
Topical

Deeper
tissues

i. Mouth and Pharynx
ii.

supply

Eye, ear, nose, throat

iii. G.I.T.
iv. Bronchi lungs
v.
vi.

Parenteral

Arterial

Urethra

-Oral

-Subcutaneous

""\ Dermojet
1- Pellet

-Sublingual -Intramedullary

L

-Rectal

- Intra arterial

-Cutaneous

-Intravenous

-Nasal

-Intradermal

Biodegradable and

-Intraperitoneal

non-biodegradable

-Intrathecal

implant

Anal canal

Implantation
Sialistic

Q.7. What are the factors which influence absorption of
drugs?
Absorption of a drug is influenced by the following factors:

Factors in drugs
i. Particle size (smaller particle better absorbed)
ii. pH of drug: Acidic drugs are absorbed in acidic medium
iii. Adjuvents used in drug
iv. Disintegration and dissolution time of drug.

Factors in patient
1.

pH of G.I.T.

ii. Ionization-Non-ionized particle better absorbed.
iii. Gastric hurry decreases absorption.
iv. Prevalence of other substance viz. Vit C enhances
absorption of iron.
v. Area of absorbing surface.
vi. Enterohepatic circulation.
vii. Disease states
viii. Pharmacogenetic.

Q.8. What are different methods of termination of drug
action?
The drug activities are terminated either by biotrans­
formation, excretion or redistribution. By biotransformation
non-polar lipid soluble drugs are transformed into polar lipid
insoluble product. The different methods of biotransformation
are phase !-non-synthetic (oxidation, reduction, hydrolysis,


4

Viva Voce in Medical Pharmacology

cyclization etc.) and phase 11-synthetic (Acetylation, methy­
lation, glucuronide conjugation, etc.)
The Atracurium is inactivated by spontaneous molecular
rearrangements called Hofmann elimination.
Q.9. What is first pass metabolism?

Drug metabolized before reaching systemic absorption either
in gastro-intestinal tract or liver.
Q. 10. Name some drugs that induce enzyme with their

consequence.

Phenobarbitone, Rifampicin et�. they result in:
a. Decrease intensity and duration of action
b. Tolerance;
c. Interfere with dose adjustment;

d. Toxicity.
Q.ll. What are the different routes of drug excretion?

The drug may be excreted through urine, faeces, lungs, saliva,
milk, etc.
Q.12. What are first order and zero order kinetics?

1st order kinetics: Constant fraction of drug eliminated per unit

time.
Zero order kinetics: Constant amount of drug is eliminated per

unit time, e.g. ethyl alcohol is eliminated by zero order kinetics.
Q.13. What are the factors which modify drug action?

1. Body size
2. Age
3. Sex
4. Species race and genetics
5. Routes of administration
6. Environment
7. Pathological states
8. Simultaneous use of other drug
9. Cummulation
10. Tolerance (tachyphylaxis, resistance, �tc.)


General Pharmacology

5

Q.14. What is Young and Dilling formulae?
These are formulae to determine dose in a child:
Young Formula

Dilling Formula
_

Age
=

Age

+

12

Age
=

20

Adult dose

x

x

Adult dose

Q. 15. What is structure action relationship? Why it is
important?
-

Activity of a drug is dependent upon its chemical structure.
It is important for:
a.· Synthesis of newer compounds
b. To know mechanism of action of drug and
c.

Synthesis of competitive antagonist.

Q.16. What is a receptor? What are its functions? What is
against antagonist and partial agonist?
A receptor is a macromolecule on effector cells to produce
effect. It propagates regulatory signals from outside to inside
of the effector cells to integrate various extracellular to
intracellular signals to adopt long and short-term ·changes.
Drug capable of combining receptor to produce effect is
agonist. Affinity is tendency to occupy receptor and efficacy
is ability to produce effect. Antagonist has affinity but without
efficacy. Partial agonist has intermediate efficacy and agonist
has full efficacy.

Q.17. What is dose response curve?
As we increase the dose we get increased drug action till we
achieve the plateau. It is rectangular hyperbola type of graph.
The logarithm of dose produces-sigmoid curve which has four
characteristics:
i. Potency

ii. Slope
iii. Maximal effect and
iv. Variability.


Viva Voce in Medical Pharmacology

6

Q.18. Define Median lethal dose, median effective dose,
therapeutic index.

Median lethal dose: Dose (mg/kg. body wt.) which is expected

to kill half of unlimited population of same species and strain.
Median effective dose: Dose (mg/kg body wt.) which produces

desired response in 50% of population.
Therapeutic index: Ratio of median lethal dose to median
effective dose. It gives indications of margin of safety.
Q. 19. What is ADR? What are the different types of non
dose dependent ADR?

Undesirable clinical manifestation arising as a consequence
of drug administration. It may be dose dependent or dose
independent. The dose independent ADR may be:
i. Side effect
u.

Secondary effect

iii. Toxic effects
iv. Intolerance
v. Idiosyncracy
vi. Allergy
viii. Photosensitivity
ix. Teratogenicity
x. Iatrogenic
xi. Carcinogenic.
Q. 20. What is dosage? and what are its strategies?

Appropriate amount of drug required to produce certain
degree of response. The strategies are:
a. Standard do s e

Same dose appropriate for most of the

-

·patient
b. Regulated dose

-

Dose

adjusted with physiological

parameters.
c. Target level dose

-

Response demonstrated with drug

concentration in plasma
d. Titrated dose

Dose is adjusted by titration by step up or

-

step down.


General Pharmacology

7

Q.21. What are the advantages and disadvantages of fixed
drug combination?
Advantages:
i. Better patient compliance
ii. Some drugs are synergetic
iii. Side effects are concentrated by other.
Disadvantages:
i. Patient may not require all ingredients
ii. Dose of each drug has to be adjusted
iii. Time course of different drugs may vary
iv. Adverse effect cannot be explained by individual drug

v. Altered renal and liver functions affect pharmacokinetics
of individual drug
vi. Contraindication of one component contraindicates whole
combination.
vii. Confusion of therapeutic aim.

Q.22. What are essential and orphan drugs?
The drugs which satisfy health• care of majority of population
are essential drugs.
Drugs which are used to treat prevention, diagnosis and
treatment of a rare disease are orphan drugs.


Autonomic
Nervous System
Q.l. How do autonomic and somatic nervous systems differ?
The autonomic and somatic nervous systems differ in the
following way:

i. Humoral
transmitter
li. Organ supply

iii. Distal most

synaptic junction
iv. Peripheral plexus
formation
v. Myelin sheath
vi. Results of nerve

damage

Autonomic Nr. Sys.

Somatic Nr. Sys.

Acetylcholine, Nor-adrenaline

Acetyl Choline

& Adrenaline

All structures except skeletal muscle
Outside cerebro-spinal axis
i.e.· at ganglia

Skeletal Muscles
Inside cerebro-spinal axis

Present

absent

Preganglionic myelinated,
post ganglionic non-myelinated

Myelinated

Smooth muscles and glands maintain
autonomic activity

Skeletal muscles are
paralysed and atrophied.

Q.2. What are the divisions of A.N.S.? How do they differ?
The ANS has two divisions
i. Sympathetic and
ii. Parasympathetic
Differences between parasympathetic and sympathetic
nervous systems are following:
Parasympathetic

l. Origin
2. Distribution

3. Ganglion

4. Postganglion ganglion
5. Pre to post

Cranial sacral (Ill, VIII, IX, X)
Cr. nerves and sacral nerves
Limited
On or close to organ
short
1:1 except enteric pl�xus

ganglion fibre ratio
6. Transmitter
7. Stability of transmitter

8. Important function

Acetyl choline
Rapidly destroyed
Assimilation of food and
conserve energy

Sympathetic

Thoraco-lumber
Wide
away from organs
long
1:20 to 1:100

Noradrenaline
Diffuses for wider action
Fight and flight emergency
function


Autonomic Nervous System

9

Q.3. What is neurotransmitter?

A neurotransmitter should satisfy the following criteria:

i. The transmitter and the enzyme capable for its synthesis

must be present at the nerve.

ii. The transmitter should be released on nerve stimulation.
m.

Extrinsically applied transmitter should mimic the effect
of nerve stimulation.

·

iv. The enzyme or enzyme system capable of inactivating
the proposed transmitter must be present in the tissues.

v. The drugs altering response to nerve stimulation should
alter the response of proposed transmitter in similar way.

Example Acetylcholine, Noradrenaline, Dopamine.
Q.4 What is neuromodulator?

A nerve on stimulation releases more than one active

substance. For example, apart for acetyl choline and

noradrenaline, autonomic nerve releases ATP, vasoactive
peptides, neuropeptides; prostaglandins, etc. as co-transmitter

acting as neuromodulator. Many abnormal findings of

cholinergic and adrenergic blockade are due to co-tramission
of neuromodulators.

Q.S. What are the different types of cholinoceptors?

The cholinoceptors are of two types:

i. Muscarinic (G-protein coupled receptor) blocked by

atropine present in heart, blood vessels, eye, smooth
muscles, glands, gastrointestinal, urinary, respiratory,
sweat glands, CNS. Their subtypes are Ml, M2, M3, M4,

MS.

ii. Nicotinic (Ligand gated cation channel) blocked by d­

tubocurarine or Hexamethonium. Their subtypes are Nm

and Nn.

Nm-Present in skeletal muscle _end plate stimulated by
phenyltrimethylamonium (PTMA) �and blocked by d­

tubocurarine.

Nn-Present in ganglion, adrenal medulla, spinal cord

stimulated by Dimethyl phenyl piperazinium (DMPP) and
blocked by Hemamethonium.

10

Viva Voce in Medical Pharmacology

Q.6. What are the uses of parasympathomimetic drug?

Therapeutic uses of parasympathomimetic drug are limited
i. Methacholine used to treat PSVT;
ii. Bethanecol to treat postoperative retention of urine
iii. Pilocarpine 0.5-4% drops to treat open angle glaucoma.
Q.7. What are the therapeutic uses of choline-esterase
inhibitors?

i. Eye-glaucoma to counter effect of mydriatic, to prevent
adhesion of iris and lens
ii. Myasthenia gravis
iii. Postoperative paralytic ileus and retention of urine
iv. Postoperative decurarization
v. Snake bite cobra

·

vi. Belladona or Atropine poisoning
vii. To treat overdose of antihistaminics tricyclic antidepres­
sants, phenothiazine
viii. Alzheimer's disease.
Q.S. Name some drugs used in Glaucoma.

A. �-Blockers:
a. Timolol (�1, and �2 0.25 - 0.5%)

b. Betaxolol ((�1) 0.5%e) Levobunolol (used once daily)
c. Cartiolol prevent optic nerve damage
d. Metipranolol (has corneal anaesthetic property)
B. Mitotics:
a. Physostigmine;
b. Pilocarpine
c.

a-Adren!frgic

agonist:

1. Adrenaline
2. Phenylephrine
3. Dipivefrine (Pro-drug for Adrenaline),

4. Aprachlonidine 0.5 - 1%. They are used as adjuvants
to miotics or·� blockers.
d. Carbonic Anhydrase inhibitors:
1. Acetazolamide use systematically
2. Dorzolamide used tropically
e. Prostaglandins PGF2a·


Autonomic Nervous System

11

Q. 9. Describe the clinical features of organophosphorus
poisoning and principle of its treatment.

Organophosphorus compounds are irreversable cholinesterase
inhibitors leading to accumulation of acetylcholine at
cholinergic nerve terminals which in turn stimulates
muscarinic and nicotinic receptors.
The action produced by:
A. Muscarinic receptor stimulations are:
a. Miosis;
b. Bradycardia;
c.

Hypotension;

d. Bronchospasm
e. Sweating and salivation
f.

Diarrhoea;

g. Urinary bladder contraction
h. Convulsion
B. The nicotinic receptor stimulation produces skeletal muscle
fasciculation.

Principle of treatment
i. Termination of further exposure by removing cloths and
washing with soap water
ii. Washing of stomach with Ryle's tube
iii. Supportive measure to maintain BP, hydration, control
of convulsion with diazepam
iv. Specific antidote atropine

v. Cholinesterase reactivator PAM; DAM.

Q.lO. Name the drugs used for myasthenia gravis?
i. Neostigmine
ii. Corticosteroid and immunosuppressants
iii. Thymectomy
iv. Ephedrine and potassium chloride as adjuvents.

Q.ll. What are the therapeutic uses of anticholinergic group
of drugs?
1.

Antisecretory
a. Preanaesthetic medication,
b. Peptic ulcer,


12

Viva Voce in Medical Pharmacology

c. Pulmonary embolism
d. Salivation in parkinsonism
ii. Antispasmodic-Renal, abdominal cramps, dysmenorrhoea, pylorospasm, aneuresis
iii. Bronchial asthma and COPD
iv. Mydriatic cycloplegic.
v. Partial heart block
vi. Parkinsonism
vii. Motion sickness
viii. Muscarinic poisoning.

Q.12. Mention the principle of dhatura and belladona
poisoning.
a. Gastric lavage with tanic acid (Potassium permanganate

not eff�ctive);
b. Cold sponging
c. General measures like artificial respiration, blood volume
maintenance, treatment of convulsion with diazepam
d. Physostigmine 1-3 mg SIC or IV

Q.13. Name some skeletal muscle relaxants and their
therapeutic uses.

Skeletal muscle relaxants can be classified as:
a. Directly acting (Dantrolene, Quinine)
b. Centrally acting mephenasine group (Carisoprodol,
Mephenesin, Chlomerzanone), Diazepam and GABA
derivative-Beclofen.
c. Pheripheral acting i. Depolarizing blockers (Succinylcholine, Decamethonium)
ii: Nori.-depolarising blockers- d(d tubocurarine, Gallamine,
Pancuronium, Doxacurium, Vecuronium, Atracurium,_
etc.)
The skeletal muscle relaxation requires in the following.
conditions:
i. Adjuvant to anaesthesia in orthopaedic manipulation and
abdominal surgery
ii. In spastic disorders like tetanus athetosis, status epilepticus
m.

In electroconvulsive therapy

iv. Centrally acting skeletal muscle relaxants used for torto­
colis, anxiety, ECT, tetanus, orthopaedic manipulation.


Autonomic Nervous System

13

Q.14. What is malignant hyperthemia? What is its treatment?
Sudden rise of temperature may occur in some genetically
susceptable individuals with fluorinated anaesthesic due to
release of calcium from sarcoplasmic reticulum of skeletal
muscles. Treatment:
i. Discontinuation of anaesthesia
ii. Oxygen inhalation
iii. Maintenance of acid-base balance
iv. Dantrolene

25,50, 100 mg caps or IV (1 mg/kg)

Name some mast cell degranulators. Why d•tubo­

Q.15.

curarine can precipitate bronchial asthma?

Tubocurarine is mast cell degranulators may release histamine
from mast cells producing bronchospasm and asthma. Other

mast cell degranulators are histamine itself, heparin.

Q.16. What

happens if d-tubocurarine and aminoglycosides

or tetracycline given together?

Aminoglycosides reduce acetylcholine release and tetracycline
chelates calcium and potentiate competitive blocking.

Q.17.

What is Hoffman elimination, which skeletal muscle

relexant eliminated by this process?

It is non-enzymatic degradation. Atracuraium eliminated by
this process so can be used in hepatic and renal insufficiency.

Q.18.

What is Dales Vasomotor Reversal?

Adrenaline acts on both

a.

receptor. By stimulating

and � receptors but more on �
a.

receptor it ra ises BP and by

stimulating � receptor it decreases BP; which is more
prolonged, i.e. produces biphasic response. Dale noticed that
prior administration of ergot (an

a.

receptor blocker) it

produces only depressor response.

Q.19.
Tachy

What is tachyphylaxis?
=

Quick; phylaxis

=

protection

It has been observed that after repeated administration of
indirectly acting sympathomimetic their effect gradually
decreases; the phenomenon is known as tachyphylaxis.

14

Viva Voce in Medical Pharmacology
The mechanism proposed for tachyphylaxis are

i. Gradual depletion of presynaptic stores
ii. Prior occupation of receptors.

Q.20. What are the types of adrenergic receptors?
The adrenergic receptors are G protein coupled receptors act
by production of second messenger c AMP. Ahlquist classified
it as stimulatory a and inhibitory p receptors which are
further classified as al, a2, pl, p2, depending upon agonistic
activity. al are further cloned into ala; alb; and a2 into
three subtypes a2A, a2B, a2C.

Q.21. What are the therapeutic uses of the sympathomimetic
group of drugs?
They are used for the following clinical conditions:
A. As pressor agent-Noradrenaline, Ephedrine, Dopamine,
Phenylephrine, Methoxamine, Metaraminol, Mephen­
teramine.
B. Cardiac stimulant-Adrenaline, Isoprenaline, Dobutamine
C. Bronchodilator: Orciprenaline, Salbutamol, Terbutaline,
Salmeterol.
D. Anorectics-Ampehtamine, Fenflurarnine
E. CNS stimulants-Amphetamine in Narcolepsy, Parkin­
sonism, Hyperkinetic children.

F. Uterine relaxants-Isoxsuprine, Ritodrine.
G. Nasal decongestants-Oxymetazoline, Xylometazoline,
Naphazoline.

Q.22. What are therapeutic uses of

a

Adrenergic blocking

-

agents?
They are used in following clinical conditions:
i. Pheochromocytoma: Phentolamine, Phenoxybenzamine
n.

Hypertension: Prazosin

·

iii. Secondary shock
iv. Peripheral vascular diseases-Tolazine, Prazosin
v. Congestive cardiac failure-Prazosin
vi. Benign hypertrophy of prostrate-Prazosin, Terazosin,
Doxazosin
vii. Migraine-Ergotamine


Autonomic Nervous System

15

viii. To induce penile erection-Papavarine and Phentolamine
induce penile erection.

Q.22. How the action of catecholamine are terminated?
The catecholamine after being released are reuptaken by
presynaptic nerve terminals called uptake I and metabolized
by mono-amine oxidase. It is also uptaken by extraneuronal
other cells called uptake II. The portion diffuses in circulation
is acted upon by enzyme catechol-ortho methyl trasferase
producing metanephrine and nor-metanephrine which are
excreted by glucuronide or sulfate conjugation.
The uptake I mechanism can be blocked by tricyclic anti­
deprassants (imipramine) or cocaine producing potentiation
of action of catecholamine.

Q.24. How the a and � receptors are distributed? Discuss
broadly.
The a receptors are excitatory except in G.l. tract and �
receptors are inhibitory except in heart. The al receptors are
present in vascular smooth muscle. a2 receptors are
responsible for inhibition of renin release from kidney.
�1 receptors are responsible for myocardial stimulation
lipolysis. �2 receptors are responsible for smooth muscle
relaxation, vasodilatation and uterine relaxation.

Q.25. How does True (Acetylcholinesterasd and pseudo
(Butyryl cholinesterase) differ?

The true and pseudocholinesterase differ in th� following
ways:
True cholinesterase

Distribution

Pseudocholinesterase

All cholinergic sites, RBC,

Plasma, liver, intestine, white

gray matter

matter

Hydrolysis

Very fast

Slow

Methacholine

Slower than Acetylcholine

Not hydrolysed

Benzoylcholine

Not hydrolysed

Hydrolysed

Butyrylcholine

Not hydrolysed

Hydrolysed

Inhibited by

Physostigmine

by organophosphorous

Function

Terminate action of

compounds
acety!choline

Terminate ingested esters


16

Viva Voce in Medical Pharmacology

Q.26. What do you mean by direct, indirect and mixed acting
sympathomimetic drugs?

Directly acting sympathomimetic drugs act directly on a

and 13 receptors like Phenylephrine, Salbutamol. The indirectly

acting sympathomimetics are generally non-catecholamine act
on presynaptic adrenergic nerve terminals to release

catecholamine. NAd which then acts on target receptors viz.

Tyramine. They produce tachyphylaxis.
Mixed acting sympathomimetics are Ephedrine, Amphe­
tamine act both directly and indirectly.

Q.27. How al and a2 receptors differ?
The a1 and a2 receptors differ in following ways:
al

Location

Post-junctional

a2

Prejunctional mainly also in post­
junctional pancreatic, platelet
and certain blood vessels..

Function

Smooth muscle

Autoregulatioin and inhibition.

contraction, secretion

Noradrenaline release,

from glands,

platelet, aggregation, decrease

GI relaxation

insulin release, vasoconstriction

heart stimulation
Agonist

Phenylephrine

Clonidine

Methoxamine
Antagonist

Prazosin

Acts through

IP3/increases DAG

Yohimbine
·decreases cAMP, close Ca
channel and opens K channel

Q.28. What is Sildenafil? What is its popular trade name?
It is FDA approved drug for treatment of erectile dysfunction

popularly known as VIAGRA available as 25,50, 100 mg
capsules. It acts by selectively inhibiting phosphodiesterase 5

Nitric oxide causes vascular smooth muscle relaxation through

cGMP. Selective inhibition of phosphodiesterase-S by
Sildenafil enhances Nitric oxide action, Generally given 1 hour

before intercourse in the dose of 50-100 mg (below 65 years

of age). The common side effects are headache, dizziness,

visual disturbances, loose motion and nasal congestion.