Cology Text Book - Compressed

CBS Confident Pharmacy SerieS
Pharmacology
and Toxicology
Second Edition
ER1991
(0813) Strictly Based on Sylabus as per
for Second Year Diploma in Pharmacy

Question-Answer Type Notesand
Board Question Papers (1996 to 2014)
Salient Features
O Total Confidence and 100 percent Success in
Every Examination.
ORepeatedly Asked Board Questions
Indicated in Brackets.
OChapterwise Collection of Very Important
Questions.
OWriten in Very Simple and Lucid Language.
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CBS Titles by the same Author in
CBS Confident Pharmacy Series
First Year D Pharm

1. Pharmaceutics 1, 2/e
2. Pharmaceutical Chemistry I, 2/e
3. Pharmacognosy, 2/e
4. Biochemistry and Clinical Pathology, 2/e
5. Human Anatomy and Physiology,
2/e
6. Health Education and Community.
Pharmacy,
/e
Second Year D Pharm
1. Pharmaceutics
I,2/e
-2. Pharmaceutical Chemistry
3. Pharmacology I, 2/e
and
4. Pharmaceutical Toxicology, 2/e
. Jurisprudence
Drug Store and Business
Management,
6. Hospital Z/e
and Clinical Pharmacy,
2/e
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Sylabus
(As per ER 1991)
Pharmacology and Toxicology
1. Introduction to Pharmacology, Scope of Pharmacology.

2. Routes of Administration of Drugs, their advantages and
disadvantages.
3. Various processes of absorption of drugs and the factors affecting
them. Metabolism, distribution and execretion of drugs.
4. General mechanism of drugs action and the factors which modify
drug action.
drugs
5. Pharmacological classification of drugs. The discussion of
should emphasise the following aspects:
i. Drugs acting on the Central Nervous System
Intravenous
a. General anaesthetics, Adjunct to anaesthesia,
anaesthetics.
b. Analgesic, Anti-pyretics and
non-steriodal anti-inflamma-
antigout
tory drugs, Narcotic analgesics. Antirheumatic and
remedies. Sedatives and HypnotiCs, Psychopharmacologi-
cal anti-convulsants, analeptics.
antiparkinsonism
c. Centrally acting muscle relaxants and
agents.
i. Local anaesthetics.
iii. Drugs acting on autonomic nervous
system.
Anticholinesterase
a. Cholinergic drugs, Anticholinergic drugs,
drugs.
b. Adrenergic drugs and adrenergic
receptor blockers.
C. Neurone blockers and ganglion
blockers.
myasthenia gravis.
d. Neuromuscular blockers, Drugs used in
e. Drugs acting on eye, mydriatics, drugs used in glaucoma.
. Drugs acting on respiratory system-Respiratory
stimulants,
Bronchodilators, Nasal decongestants, Exceptorants and
Antitussive agents.

X Pharmacology and Toxicology
g. Antacids, Physiological role of histamine and serotonin, His-

tamine, and Antihistamines, Prostaglandins.
h. Cardiovascular drugs, Cardiotonics, Antiarrhythmic agents,
Antianginal agents, Antihypertensive agent, Peripheral
Vasodilators and drugs used in atherosclerosis.
i. Drugs acting on the blood and blood forming organs,
Haematinics, Coagulants and anticoagulants, Haemostatics,
Blood substitutes and plasma expanders.
j. Drugs affecting renal function-Diuretics and antidiuretics.
k. Harmones and hormone antagonists-Hypoglycemic
agents, Antithyroid drugs, Sex harmones and Oral
contraceptives, Corticosteroids.
Drugs acting on digestive system Carminatives Digestants,
Bitters, Antacids and drugs used in peptic ulcer, Purgatives
and Laxatives, Anidiarrhoeals, Emetics, Antiemetics, Anti-
spasmodics.
6. Chemotherapy of microbial disease: Urinary antiseptics,
Sulpho-
namides, Penicillins, Streptomycin, Tetracyclines, and other
antibiotics.
Chemotherapy agents, Antifungal agents, Antirival
drugs
Antileprotic drugs.
7. Chemotherapy of protozoal diseases. Anthelmintic
drugs.
8. Chemotherapy of cancer.
9. Disinfectants and antiseptics.
A detailed study of the action of drugs
on each organ is not necessary.
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Contents
Preface to the Second Edition ..

Introduction and Routes of Administration of Drugs
.. .1
1.
Pharmacology.. 16
2. General *******
.
3. General Anaesthetics...
4. Local Anaesthetics...
. 31
36
5. Analeptics/CNS Stimulants.
******* .. 38
.. 40
6. Drug Abuse
*********..42
7. NarcoticAnalgesics.
8. Hypnotics and Sedatives. ..45
9. Anticonvulsants/Antiepileptics.. ****** .50
Antipsychotics/Tranquillizers. 54
10. ********.
11. Parkinsonism and Antiparkinsonism Agents ... ************e***59
12. Heavy Metal Poisoning. .61

Analgesics, Antipyretics and Anti-inflammatory Agents...
63
13.
14. Drugs Used in Gout and Rheumatism. 68
15. Drugs Acting on Digestive System ... 70
16. Drugs Acting on Respiratory System. ******** ... 74
17. Histamine and Antihistaminics... .77

18. Drugs Acting on Blood
.. . 80
85
19. Hypoglycemic Agents ...
88
20. Antithyroid Drugs.*** *****
21. Drugs Acting on ANS

.. *****************°
.. 89
22. Neuromuscular Blockers/Skeletal Muscle Relaxants.. 99
23. Mydriatics and Miotics. 100
**.
24. Cardiovascular Agents... 102

. 108
25. Diuretics. ********
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xii Pharmacology and Toxicology
26. Chemotherapy.
a. Sulphonamides.. l11
b. Antibiotics .. ****
**** 113
c. Urinary antiseptics.. .. 119
d. Antitubercular agents.. 120
e. Antileproticagents.. .. . 121
f. Antimalarials . 122
g. Antifungal agents...
124
h. Antiviral agents . 124
i. Anticancer/antitumor/antineoplastic/
antimalignant/cytotoxic agents . 124
j. Antiamoebic agents .... 125
k. Anthelmintics. . 126
27. Oxytocics/Echbolics. . 129
28. Hormone and Hormonal Antagonists....
29. Antiseptics and Disinfectants
30. Principles of Drug Interactions.
.. 130
132
135
31. Miscellaneous
.....* 138
a. Reasons .. . 138
b. Antidotes used in poisoning cases ...
156
c. Inhibitors and blockers .. . 157
d. Major adverse/toxic effects
...
e. Drugs and choice. .. .
157
159
f. Contraindications.. 161
Board Question Papers.

162

CHAPTER 1 |
Introduction and Routes of

Administration of Drugs
Definitions
1. Pharmacology: Pharmacology is the branch of science dealing
with the properties of drugs and their effects on living system.
2. General anaesthetics: The drugs which
produce a partial or
are called
total loss of pain sensation and loss of consciousness
general anaesthetics. For example, ether, chloroform,
halo-
thane, nitrous oxide, cyclopropane.
3. Local anaesthetics: The drugs which produce anaesthesia in
anaesthetics. For
limited area of the body are known as local
cinchocaine, cocaine.
example, lignocaine, procaine, benzocaine,
resembling to
4. Hypnotics: The drugs which induce a sleep
phenobar-
natural sleep are known as hypnotics. For example,
bitone, diazepam, nitrazepam, paraldenyde.
and motor
5. Sedatives: The drugs which reduce excitement
inducing sleep
activity and produce a calming effect without
are known as sedatives. For example,
phenobarbitone,
diazepam, nitrazepam.
6. Anticonvulsants (antiepileptics): The drugs which are used
in the treatment of convulsions or epilepsy are
known as
anticonvulsants. For example, phenytoin, ethosuccimide,
carbamazepine.
7. Narcotic analgesics: The drugs which reduce pain sensation
along with loss of consciousness and sleep are known as nar
cotic analgesics. For example, morphine, heroine, codeime,
pethidine, methadone, pentazocin.
8. CNS stimulants/analeptics: The drugs which increase the
or
dcuvity of brain and spinal cord are called CNS stimulants

2 Pharmacology and Toxicology
analeptics. For example, caffeine, theophylline, nikethamide

bemegride.
9. Antipsychotics/psychoactives/psychotropics: The druas
which are used in the treatment of various psychological dis.
orders are known as antipsychoticS. For example, chlorprom-
azine, haloperidol, reserpine.
10. Antianxiety agents: The drugs which are used in the treatment
of anxiety condition are called antianxiety agents. For example,
diazepam, nitrazepam, chlordiazepoxide.
11. Antidepressants: The drugs which improve the moods of
depressed patients are called antidepressants. For example,
imipramine, desipramine, amytryptyline, nor-tryptyline.
12. Tranquillizers: The drugs which produce calming, quietening
effect on the individuals are called tranquilizeS. For example,
chlorpromazine, reserpine, haloperidol.
13. Antiparkinsonism agents: The drugs which are used in the
treatment of parkinsonism are called antiparkinsonism agents.
For example, carbidopa, levodopa.
14. Skeletal muscle relaxants: The drugs which produce
relaxation of skeletal muscles are called skeletal
muscle
relaxants. For example, mephensin, meprobamate,
diazepam.
15. Analgesics: The drugs which reduce
pain sensations are known
as analgesics. For example, paracetamol,
aspirin, analgin,
phenacetin.
16. Antipyretics: The drugs which reduce
elevated body tempera-
ture to normal level are known as antipyretics.
For example,
paracetamol, analgin, aspirin.
17. Anti-inflammatory agents (NSAIDs): The drugs which
reduce inflammation are known as anti-inflammatory
drugs.
For example, aspirin, indomethacin, phenylbutazone,
oxy
phenbutazone.
18. Antigout agents: The
drugs which are used in the treatment
of gout are known as antigout agents. For example,
colchicine,
allopurinol, probencid, aspirin.
19. Antirheumatic agents: The drugs which are used in the
reatment of rheumatism are known as antirheumatics.
example, aspirin, indomethacin, phenylbutazone,
For
gold.

Introduction and Houtes of Administration of Drugs
20. Diuretics: The drugs which increase rate of formation and

excretion of urine are known as diuretics. For example.
acetazolamide, frusemide, chlorthiazide, mersalyl, spiron.
no-
lactone, urea, mannitol.
21. Sympathomimetics/adrenergicS: The drugs which exert an
action similar to actions produced by stimulation of sympa-
thetic nervous system are called sympathomimetics or
adrenomimetics. For example, adrenaline, nor-adrenaline,
ephedrine, amphetamine, dopamine.
drugs which block the
22. Sympatholytics/antiadrenergics: The
actions produced by stimulation of sympathetic nervous sys-
tem, are known as sympatholytics, e.g. propranolol, atenolol,
pindolol, guanethidine.
23. Parasynmpathomimetics/cholinergics: The
drugs which exert
an action similar to actions produced by stimulation of
parasympathetic nervous system are called parasympatho-
mimetics or cholinergics. For example, acetylcholine, physo-
stigmine, neostigmine, pilocarpine.
which block
24. Parasympatholytics/anticholinergics: The drugs
the actions produced by stimulation of parasympathetic ner-
vous system are known as parasympatholytics or anticholin-
ergics. For example, atropine, hyoscine.
25. Ganglionic blockers: The drugs which block or prevent
transmission impulses through the autonomic ganglia are called
ganglionic blocking agents. For example, mecamylamine,
pentolinium.
26. Neurone blockers: The drugs which block the transmission
and conduction of impulses across the neurone are called
neurone blockers. For example, propranolol, atenolol.
27. Antispasmodics: The drugs which are used to reduce spasm
are called antispasmodics. For example, atropine, hyoscine.
28. Antihistaminics/antiallergics: The drugs which reduce
(Dlock) the actions of histamine and give relief from allergic
reactions are known as antihistaminics or antiallergics. For
example, diphenhydramine, chlorpheniramine, pheniramine,
mepyramine.
29. Antithyroiddrugs: The drugs which reduce the secretion of
thyroid hormones and are used in the treatment of thyrotoxi-

cosis are called antithyroid drugs. For

example, carbimazole,
methimazole, propylthiouracil, methylthiouracil.
The drugs which
30. Hypoglycemic agents/antidiabetic agents:
are called
reduce elevated blood sugar level to the normal level
chlorpropamide,
antidiabetic agents. For example, insulin,
tolbutamide, glibenclamide, phenformin, metformin.
31. Antitussives/anticough: The drugs which are
used in the
treatment of cough are known as antitussives. For example,
noscapine, codeine.
32. Expectorants: The drugs which remove
sputums from the
respiratory tract are known as expectorants. For example,
ammonium chloride, potassium iodide.
33. Nasal decongestants: The drugs which are used to relieve
nasal mucosal congestion are called nasal decongestants. For
example, isoprenaline, ephedrine, pseudoephedrine.
34. Bronchodialators: The drugs which dialate the bronchi and
improve breathing are called bronchodialators. For example,
adrenaline, isoprenaline, salbutamol, theophylline.
35. Haematinics: The drugs which increase number of RBCs or
haemoglobin in the blood are known as haematinics. For
example, iron, folic acid, vitamin B12, ferrous sulphate.
36. Haemostatics: The drugs which prevent oozing of blood from
minute blood capillaries are called haemostatics. For example,
thrombin N.F, fibrinogen, aminocaproic acid.
37. Anticoagulants: The drugs which prevent coagulation of blood
are called anticoagulants. For example, wartann, phenindione,
heparin, acenocoumarin.
38. Miotics: The drugs which produce constriction of the pupl
are called miotics. For example, pilocarpine, physostigmine,
acetylcholine.
39. Mydriatics: The drugs which produce dilation of pupil are
called mydriatics. For example, adrenaline, ephedrine, atro-
pine.
40. Antidiuretics: The drugs which suppress urine formation are
called antidiuretics. For example, ADH (vasopressin).
41. Oxytocics/echbolics: The drugs which stimulate the contrac-
tion of smooth muscles of uterus and expel the contents or
uterus are called oxytocics. For example, oxytocin, ergota-
mine, ergometrine.

Introduction and Routes of Administration of Drugs 5
42. Lipid lowering agents: The drugs which reduce excessive

lipid level in the body are called lipid lowering agents. For
example, clofibrate, nicotinic acid.
43. Cardiotonics: The drugs which increase the activity of car-
diac muscles and increase force of contraction of heart are
called cardiotonics. For example, digitalis (digoxin), oubain,
lanatoside-C, Arjuna.
44. Antiarrhythmic agents: The drugs which are used in the
treatment of arrhythmia conditions are called antiarrythmic
agents. For example, quinidine, procainamide, lignocaine.
in the
45. Antihypertensive agents: The drugs which are used
treatment of hypertension are called antihypertensive agents.
For example, methyldopa, clonidine, reserpine, guanethidine.
46. Antianginal agents: The drugs which are used in the
treatment
of angina pectoris are called antianginal agents. For example,
glyceryl trinitnte, amyl nitrite, ethyl nitrite, verapamil.
47. Antacids: The drugs which reduce or neutralize excessive
acidity in the stomach are called antacids. For example, alumi-
nium hydroxide, magnesium hydroxide, sodium bicarbonate.
48. Purgatives: The drugs which promote defaecation are
called
purgatives. For example, senna, castor oil, bisacodyl, dioctyl
sulphosuccinate.
49. EmeticS: The drugs which induce vomiting are called
emetics.
For example, emetin (ipecac) apomorphine, mustard.
50. Antiemetics: The drugs which prevent vomiting are called
antiemetics. For example, metoclopramide, promethazine,
domperidone.
51. Appetizers: The drugs which stimulate appetite are known as
appetizers. For example, alcohol, chirata IP, gention, tonics.
52. Appetite suppressants/anorexiants: The drugs which
suppress or reduce appetite are known as appetite suppressants.
For example, methyl cellulose, amphetamine.
53. Bitters: The drugs which stimulate the flow of saliva and
gastric juice and increase appetite are known as bitters. For
example, alcohol, tincture of chirata, gention.
54. Sulphonamides: The antimicrobial compounds containing
sulphonamide (-S0,NH,) group are called sulphonamides. For
example, sulphamethoxazole, sulphadiazine, trimethoprim.

55. Antibiotics: These are the chemical substances produced by

various species of microorganisms, which in low concentration
destroy or inhibit the growth or otner species of micro-
organisms. For example, penicillins, chloramphenicol,
tetracycline.
56. Antitubercular drugs: The drugs which are used in the
treatment of tuberculosis are called antitubercular drugs. For
example, isoniazid, PAS, ethambutol, pyrazinamide, rifampicin.
57. Antileprotic drugs: The drugs which are used in the treatment
of leprosy are called antileprotics. For example, dapsone,
solapsone, clofazimine, thiacetazone.
58. Antimalarial agents: The drugs which are used in the
treatment of malaria are called antimalarial agents. For
example, chloroquine, amodiaquine, primaquine, quinine.
59. Antiamoebic agents: The drugs which are used in the
treatment of amoebiasis are called antiamoebic drugs. For
example, metronidazole, tinidazole, diloxanide furoate.
60. Antifungal agents: The drugs which are used in the treatment
of fungal infections are called antifungal agents. For example,
nystatin, amphotericin-B, griseofulvin, hamyCin, tolnaftate.
61. Antiviral agents: The drugs which are used in the treatment
of viral infections are called antiviral agents. For example,
idoxuridine, ribavirine, amantidine.
62. Anticancer/antineoplastic agents: The drugs which are used
in the treatment of cancer are called anticancer drugs. For
example, busulphan, cyclophosphamide, methotrexate,
fluorouracil, vinblastin, vincristin.
63. Toxicology: It is the science which deals with the adverse
effects of the drugs and study of poisons.
64. Chemotherapy: Chemotherapy is defined as the use of
chemical compounds in the treatment of infectious diseases
so as to destroy the microorganisms without damaging host
tissues.
65. Pharmacodynamics: The quantitative study of thebiologica
and therapeutic effects of drugs and their mechanism of acion
is termed as pharmacodynamics.
66. Pharmacokinetics: It is the study of absorption, distribution,
metabolism and excretion of drugs and their relationship
to
pharmacological response.

Introduction and Routes of Administration of Drugs
7
67. Pharmacotherapeutics: It means various methods and
systems that are used in prevention and treatment of diseases
68, Bioavailability: The fraction of drug that reaches tbe systemic
circulation in an unchanged rorn and is available at the site of
drug action is known as b:oavailability.
produce loss of power in ciliary
69. Cycloplegics: The dugs which
muscles of the eye or produce paralysis of accommodation
are called cycloplegics. For example, atropine, hyoscine.
70. Anthelmintics/antiworm
agents: The drugs which are used
in the treatment of worm infestation
are called anthelminticS,
piperazine, mebendazole, albendazole, DEC.
O6.g.
of drugs
1 Define pharmacology'. Give the classification
on the basis of source, nature and active constituent
present in it.
Pharmacology
drugs on the living
Pharmacology is defined as the study of effect of
mechanism of action, adverse
organism and its organs along with
effects, and doses of the drugs.
derived from two Greek words,
The word pharmacology is
pharmacon>a drug, "logus> to treat or science
Classification of Drugs
a. As per Source of Drugs
Plants, e.g. morphine, digoxin, reserpine,
vinblastin.
1.
2. Animals, e.g. insulin, heparin, thyroid
extract.
3. Minerals, e.g. liquid paraffin, magnesium
sulphate, kaolin.
4. Synthetic, e.g. aspirin, sulphonamides, corticosteroids.
5. Microorganisms, e.g. penicillins, tetracyclines, rifampicin,
cephalosporins, I-asparginase.
b. As per Nature of Drugs

Tne drugs from plant origin contain pharmacologically active con-
stituents such as:
1. Alkaloids, e.g. reserpine, morphine, emetine, atropine.
2. Glycosides, e.g. digoxin, strophanthin.
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3. Oils:
a. Fixed oils, e.g. olive oil, castor oil, cod-liver oil
b. Volatile oil, e.g. clove oil, eucalyptus oil, turpentine oil.
4. Resins, e.g. podophyllum resin.
5. Gums, e.g. agar, acacia, tragacanth.
6. Tannins, e.g. catechu, tanric acid.
7. Hormones, e.g. insulin, sex hormones.
ROUTES OF ADMINISTRATION OF DRUGS
1 Classification/Types of Routes of Drug Administration
Routes of Administration of Drug
Oral route Sublingual route Parenteral route

(in buccal cavity) (below the tongue) (other than GIT)
Injections Inhalations Local application
a. Intradermal
b. Intravenous (IV)
C. Intramuscular (IM) Enema Other external
d. Subcutaneous (SC) (rectal route) preparations,
e. Intra-arterial e.g. ointment,
f. Intraperitoneal paste
g. Intrathecal
h. dntramedullary
i. Intra-articular
i. lontophoresis
k. Induction
I.
Jetinjection
2 Oral Route
In this route, the drug is placed in oral cavity and is swallowed
along with water or milk, etc.
Advantages
1. It is a common and safe route of drug administration.
2. No special skill is required for administration
of drug.
3. It is very convenient route.
4. Sterilisation is not required for the preparations taken orally

possibilities of adverse reactions.

5. There are low
6. This route is applicable
from infants up to aged patients.
be administered by this route.
7. The large quantity of drug can
8. Preparations like
syrup, mixture, tablet, capsule, pills are
administered by this route.
Disadvantages
1. Onset of action is slow.
2. Absorption of certain
drugs is irregular and negligible.
clinical emergencies.
3. This route is not useful in administered by
cannot be
4. The irritant and unpalatable drugs
this route.
unconscious and incoope-
5. This route is not useful in cases of
rative patients.
and diarrhoea patients.
6. This route is not useful in prevomiting
alimentary canal are not
7. The drugs which are destroyed in
given by this route, e.g. insunn.
interfere with absorption of
8. The presence of food in GIT may
drug.
disturb the microflora
9. Oral administration of some drugs may
of GIT
10. Accurate blood levels of the drug cannot be maintained by
this route.
3 Sublingual Route
this route, tablet is placed below the tongue and allowed
to
In
dissolve in mouth cavity. The active drug gets absorbed through the
sublingual mucus membrane directly into blood circulation.
Examples of Drugs
i. Isoprenaline tablet in the treatment of bronchial asthma.
i. Glyceryl trinitrite in the treatment of angina pectoris.
Advantages
1. Rapid onset of action.
2. Degradation of drug is avoided in stomach.
3. Inactivation of drug in the liver is avoided.
4. If tablet is found to be toxic, it can be spit out easily.
5. Presence of food in GIT does not affect the absorption of drug.
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10 Pharmacology ard Toxicology
Disadvantages
1. Not suitable for large doses and frequent use of drug.
2. Some drugs may cause irritation to buccal
mucosa.
3. Excessive salivation may cause swallowing of
drug.
4. The drugs having direct or toxic etects should be administered
carefully to avoid side effects on heart.
4 Parenteral Route
The routes of administration of drug other than alimentary canal
are called parenteral routes.
In this case, the drug in the form of solution suspension
or is
injected in the body with the help of hollow needle and syringe.
vapour or fine droplets are
In some cases, drugs in the form of
inhaled in respiratory tract or sometimes pastes are rubbed over
the skin.
Advantages
1. Rapid onset of action.
2. The drugs which iritate the GIT, can be given by this route.
3. Accurate dose and accurate blood level of drug can be possible.
4. This route is useful in cases of vomiting and diarrhoea.
5. This route is useful in unconscious and uncooperative patients.
6. The drugs which are destroyed in GIT can be given by this route.
7. The smaller quantity of drugs is required by this route.
8. This route is usefül in clinical emergencies.
9. The large quantities of drug are also administered by this route,
e.g. saline solution.
10. 100% bioavailability is possible by IV route.
Disadvantages
1. This route is inconvenient to the patient and for frequent
administration of drugs.
2. Skilled person is necessary for administration
of drugs
3. Strict aseptic technique is to be followed
during drug adminl-
Stration.
4. The posibility of pain and edema at the
site of application.
5. Self-medication is difficult.
6. The sterilization of syringe and
needle is necessary.

damage.
7.The possibility of nerve
is absorbed in blood circulation, the adverse
8, Once the drug
effects cannot be reversed or
controlled.
Intradermal Route
5 the dermis layer of the skin.
In this route, the drug is injected in
quantity of drug can be administered by this route and
Only a small
the injection is
painful.
Importance
allergy, e.g. penicillin
This route is used for the detection of drug
i) to observe allergic reactions to it.
is injected intradermally
smallpox are administered by this route.
(ii) Vaccines such as BCG,
Intramuscular Route
6 directly into the muscular tissue.
In this route, drug is administered
Advantages
injections with in-
1. Mild irritants, suspensions, colloids and
this route.
soluble oily bases can be administered by
2. The absorption of water
soluble drugs is rapid than subcuta-
neous or oral route.
3. Massaging and application of
heat at the site of injection by
IM route may increase the drug absorption.
4. The drugs administered by this
route form tissue depots from
prolonged
where drug is slowly released and this provides
duration of action.
Disadvantages
1. Sterilization of syringe and needle is essential.
2. Skilled person is required for drug administration.
3. Some drugs may cause tissue iritation and pains by intramus-
cular route.
4. If proper care is not taken there is an injury to the nerves.
5. Total volume of drug injected by IM route is restricted up to
10 ml.
6. Certain intramuscular injections require more time for
absorption as compared to oral route.

Inhalation Route
7 this route, the drug in the form of gas or in can
vapour formcan t
be
In
inhaled, e.g.
Isoprenaline spray is used in bronchial asthma.
() are also given by this route.
(i) Volatile general anaesthetics
Advantages
route is very rapid.
1. The absorption of drug by this
2. The drug given by this route
produces local as well as systemin
effects.
as
3. Blood levels of volatile substances such general
anaesthetics
can be conveniently controlled.
Disadvantages
heart, hence there
1. The drug directly enters the left side of the
is a danger of cardiac toxicity.
2. Certain drugs produce local irritation, may increase respiratory
secretions.
3. Special apparatus such as automizer or nebuliser is needed for
administration of drug.
Intravenous Route route)

8 (IV
In this route, the drug is injected directly into the lumen of vein.
The drug produces rapid action and desired blood concentration can
be achieved by a definite dose of a drug.
Advantages
1. The onset of drug action is very rapid.
2. This route is effectve in clinical emergencies.
3. 100 % absorption of drug is possible by this route.
4. Large quantity of drug can be administered by this route, e.g.
normal saline solution.
5. The drug which produces iritation and pains by IM route can
be given by this route.
6. The hypertonic solutions can be administered intravenously
because the drug is diluted by bloodstream.
7. The accurate blood concentration of drug can be achieved by
this route.

to get a particular
8. Only minimum quantity of drug IS required
routes.
effect as compared to other
9. Adjustment of
additional dose and control on the rate of
administration is possible by IV route.
IV route.
10. Complete bioavailability of drug can be assured by
Disadvantages
Self-medication is difficult.
1. severe
2. Sometimes, leakage of drug outside the vein produces
iritation and abscess formation.
3. Sterilization of needle and syringe is essential.
4. Skilled person is essential for drug administration.
TV set should be slow and
5. Speed of drug entering through
Constant supervision is necessary.
circulation, the
6. Once the drug is absorbed in the systemic
controlled.
adverse effects of drug cannot be reversed or
9 Local Route/Local Application/Topical Route

or to the localized
SIn this route, the drugs are applied administered
or specific areas of the body.
at the site of
These preparations are to be meant for their action
application, e.g. paste, ointment, drops, lotions.
Advantages
1. This route provides an easy administration of drug.
2. Local application is useful when prolonged effect of drug is
required.
3. There is a low possibility of systemic absorption of the
medicament.
4. No special skill or apparatus is required for administration.
Disadvantages
1. The drugs in the form of watery solution are sometimes
absorbed into the blood and may produce undesirable etects.
2. The drugs like eyedrops may penetrate into the anterior
chamber and affect ciliary muscles, e.g. cocaine.
3. Some drugs may show toxic effect at the site of application.

10 Rectal Route
The route of administration in which the drug in the form of
solution is introduced into the rectum is called rectal route, eg. enema
preparation, suppository.
Advantages
1.When the drug produces irritation by oral route, this route
may be used.
2. When patient does not swallow the drug, this route is preferred
3. The children who do not cooperate in taking medicines by
oral route, the rectal route may be recommended.
4. This route is used when local effects in the rectum are required.
Disadvantages
1. The absorption of drug is not complete because less surface
area is available for absorption as compared to oral route.
2. This route is not liked by the patients.
3. A few drugs may produce local irritation of ansal mucosa.
4. Possibility of absorption of drug into blood and dug may be
metabolized in the liver before reaching the target organ.
Questions
1.Enumerate/enlist/give/classify various routes of administration

of drugs. (S. 00, 01, 04, 05, 09; W. 01, 03, 05, 06, 07)
2. Mention the advantages and disadvantages of oral route of
administration of drugs. (S. 96; W. 01, 02, 08)
3. Give advantages and disadvantages of intramuscular route.
(S. 02, 05)
4. Classify parenteral routes of administration of drug. Give
advantages and disadvantages. (S. 03, 09; W. 05, 06)
5. Mention advantages and disadvantages of sublingual route
of.
administration of drugs. Give examples of drugs. (S. 99;
W.96, 98)
6. Give advantages and disadvantages of intravenous route.
(S. 97, 00, 01, 04, 06, 08; W. 98, 03, 07)
7. Which is the most common route of drug administration and
why? When it cannot be employed? (S. 98)

8. Give the examples of drugs administered by inhalation and

comment on their rate of absorption. (S. 98)
pharmacotherapeutics,
9. Define the terms pharmacology,
toxicology. (S. 96; W. 99)
Define the terms 'pharmacokinetics' and pharmacodynamics'.
10.
(S.99; W. 96, 07)
pharmacology. Give sources and nature of drugs.
11. Define
(W. 01)
Mention the factors for deciding the route of choice. (S. 99)
12.

CHAPTER 2 |
General Pharmacology
Definitions
1
Agonist: A drug which combines with receptor and gives a
pharmacological response is called agonist.
Antagonist: A drug which combines with receptor but does not
produce pharmacological action and only blocks the receptor is
called antagonist.
.Affinity: The ability of a drug to get bound to the receptor is
called aftinity of a drug for the receptor.
Efficacy or intrinsic activity: The ability of a drug to give a
pharmacological action after combination with receptor is called
efficacy of a drug.
Receptor: A receptor is a specific functional cellular component
which when combines with drug produces a pharmacological
action.
2 Absorption of Drugs
Definition
The passage of drug from route of administration into blood circula-
tion is known as absorption.
Types/Process/Mechanism/Ways of Absorption
Absorption of drug may be cither directly or indirectly but absorption
involves the passage of drug dose across the cell membrane. This
passage is governed by lipid carriers present at the permeable
membrane. The membrane contains small pores and only water
soluble molecules can pass through them.
16

General Pharmacology 17
The absorption of drug through membrane occurs by following

ways:
a. Simple Diffusion (Passive Diffusion)
This is a bidirectional process where the rate of transfer across
the membrane is proportional to the
concentration ingredient of
the cell membrane.
A water soluble drug of low molecular weight such
as alcohol,
urea, water itself diffuses passively through aqueous
pores of
the membrane.
transfered by
The drugs which are lipid soluble are mainly
simple or passive diffusion after dissolution.
b. Active Transport Process

is a specialised process requiring energy and is independent
This
on physica property of the membrane.
In this process, the carrier molecule combines with drug molecule
and torms a drug carrier complex on one side of the membrane.
This complex then diffiuses through the membrane and dissociates
into carrier and drug molecule when reaches other side of the
membrane.
After that carrier molecule returns to the original surtace to repeat
the process.
The ions which are transported by active transport process
include Na", K",F, amino acids, some dngs, strong acids, strong
bases and wcak electrolytes in ionised fom, glucose, pyrimidines
and some antimetabolites are also transported by this process.
This transport process is rapid than Simple diffusion.
Permeable lipid membrane
Drug molecules (absorbed)
Drug
molecules
' Blood
Drug
carrier complex Carrier
Active transport process

c. Pinocytosis
In this process, the cell
takes up the fluid or micromolecule from its
Surrounding. This process is important for unicellular organisms like
amoeba.

In this process, cell forms a cavity lIke pseudopodium and particlee

les
are taken inside the cell.
d. Flltration
The passage of drug molecule through the channels is called filtration
Small, soluble and polar drugs are abSOrDed Dy this phenomenon.
e. Facilitated Diffusion
Like passive transfer this process is also not energy-dependant. The
movement of drug is from high concentrao o 1Ow concentration.
There is no involvement of carrier system in this process. The
process
1S rapid than passive transport process.
3 Discuss factors affecting (influencing) the absorption

of drug (bioavailability) from the GiT or gut.
1. Physical state of drug: The liquids are better absorbed than
solid medicaments. Aqueous solutions are more rapidly
absorbed than colloids.
2. Particle size: Smaller the particle size, greater is the absorption
of drugs from gut. Smaller particle size provides greater surface
area for absorption. Thus the dose required to produce an action
is reduced due to smaller particle size.
3. Concentration of drug: Higher the cencentration of drug,
better is the absorption of drug from intestine.
4. Area of absorbing surface: Larger the absorbing
surface area,
greater is the absorption. Thus in small intestine the absorption
of drug Is greater than the stomach.
5. Physical and mental state of the patient:
Disturbed
physiological conditions such as infection,
fever affect the
absorption of drug. Emotional
upset condition also affects
absorption of drug adversely.
6. Functional integrity of GIT:
Increased peristalsis of GIT
decreases absorption of drug, e.g.
in diarrhoea condition,
absorption of drug decreases.
7. pH of drug: Acidic drugs
are rapidly absorbed
while basic drugs are rapidly in stomach
absorbed in intestine due to
respective pHranges.
8. Formulation: Calcium
and magnesium ions
absorption of tetracyclines reduce the
because tetracycline forms

complexes with Ca"" and Mg". Hence such formulation should
not be made.
C increases the absorption
9. Presence of other agent: Vitamin soluble vitamins
of drug from GIT. The absorption of fat
increases in presence of liquid paraffin.
10. Presence of food in GIT: The
presence of food in GIT may
no direct
reduce absorption of drug from GIT because there is
not occur.
contact with walls of GIT. But gastric irritation will
4 Distribution of Drug in the Body

the tissues. The
Distribution of drug involves transport of drug to
majority of drugs for
bodyfluids act as solvents and carriers for the
distribution in the body.
follows:
Drugs may be distributed into body as
i) Extracellular fluid.
(ii) In blood.
(i) Adipose tissue (fat)
(iv) Other body tissues (organs)
GIT, bronchi,
(v)Transcellular fluid compartments, e.g. fluids in
CSF
are simply dissolved in serum
In blood, the majority of drugs to blood proteins such as
water but some of them are bound
albumin, globulin, etc.
acts as a storage site in the
.The plasma protein binding of drugs
blood. Thus plasma protein binding of drug can increase the
duration of action of drugs.
Distribution of drugs into the brain and CSF depends upon the
lipid soluble properties of drugs. Lipid soluble drugs enter in
the brain more easily. Similarly lipid soluble compounds cross
the placental barrier and show similar pharmacological effects
in both mother and foetus.
The enterohepatic circulation is another site of drug distribution.
Some drugs are extracted from the body by liver and then
excreted into the small intestine via bile. Further they are
reabsorbed across the mucosa back into the blood.
Factors affecting distribution of drug in the body are:
) pH
(ii) Protein binding

(ii) Physicochemical properties of drug

(iv) Enterohepatic circulation.
5 Write in brief about protein binding of drugs.
Definition
After absorption, the drug circulates in the blood and binds with
plasma proteins which is known as protein binding of drugs.
Due to protein binding of drug, it is not available for diffusion
into extracellular compartment. Thus, there is no excretion of drug
and prolongs the during of action of a drug.
Importance of Protein Binding
1. Protein binding makes the drug inactive.
2. The drug becomes impermeable to membrane after protein
binding. This reduces metabolism and excretion of drugs.
3. Protein binding acts as a storage of drugs.
4. Protein binding also reduces the amount of drug available
for
filtration at the glomeruli and hence reduces its excretion.
6 Describe biotransformation of drugs/metabolism

of drugs.
Biotransformation
The alteration of drug within a living organism
so as to modify its
activity or its nature, is known as biotransformation
or metabolism.
The enzymes involved in the biotransformation
called microsomal enzymes. of drugs are
Some drugs are biotransformed into more active
compounds, e.g.
) Levodopa (inactive) is converted to dopamine
brain.
(active) in
ii) Conversion of diazepam to oxazepam
which is more active.
ii) Conversion ofphenylbutazone
to oxyphenbutazone which
is more active.
The important pathways of biotransformation
(i) Oxidation: Microsomal of drugs are:
oxidation may involve the
introduction of a hydroxyl
group into the drug molecule,
e.g. converSion of
salicylic acid into gentisic
(ii) Reduction: Many acid.
halogenated compounds
aromatic compounds and nitrated
are reduced by the microsomnal
enzymes, e.g. halothane,
chloramphenicol.

enzymes
i) Hydrolysis: Hydrolysis is usually carried out by
esters.
esterases that hydrolyse the
acetylcholine are hydro-
Drugs like pethidine, procaine,
lysed by esterase.
Conjugation: This is a synthetic process by which a drug
(iv)
combined with an endogenous sub-
or its metabolite is
conjugates such as gluco-
stance, resulting in various
amino acid conjugates, e.g.
ronides, etheral sulphates and
derivative which
phenobarbitone is oxidised to its hydroxy
is conjugated with glucoronic acid.
excretion/disposition of drugs.
Describe routes of
7 as follows:
important channels of excretion of drugs are
The excretion
1. Kidney: The
kidneys act as a primary organ for the
tubular
most of the drugs. The rate of glomerular filtrate,
of influences the rate of
reabsorption and tubular secretion
are quickly eliminated in
excretion of drugs, e.g. weak acids
an alkaline urine while weak
bases are rapidly excreted in an
acidic urine.
2. Lungs: Volatile general anaesthetics
and certain other drugs
excreted by the lungs.
like paraldehyde and alcohol are partially
arsenic and mercury may be partly
3. Skin: Some metals like
excreted through the skin. Arsenic gets deposited in the hair
follicles on prolonged administration. This phenomenon
is
useful for detecting arsenic poisoning.
4. Bile: The drugs such as erythromycin are excreted in the
urine
only in small amounts but appear in high concentration in bile
and are partially excreted into the intestine through the bile.
5. Intestine: Some substances which are not fully absorbed from
the GIT are excreted in the faeces, e.g. purgatives like senna.
6. Milk: Antibiotics are deposited in the milk. Drugs like
chloramphenicol, chlorpromazine, diazepam are deposited in
milk and excreted via milk.
7. Saliva: Certain drugs like iodides and metallic salts are
excreted in the saliva. Lead compounds deposited as lead
sulphide produce blue line on gums.

8 Enlist various factors modifying drug action.

1. Body weight
2. Age
3. Sex
4. Route of administration
5. Time of administration
6. Diet and environmental factor
7. Genetic factor
8. Emotional factor
9. Presence of disease
10. Metabolic disturbances
11. Cumulative effect
1
12. Additive effect
13. Synergism (potentiation)
14. Antagonism
15. Tolerance
16. Dependance.
9 Explain the factors modifying drug action.

1. Body weight: The dose of a drug is related
to body weight.
The dose of drug is usually expressed as mg/kg
2. Age: Infants and old patients need dose
ofbody weight.
different from adults.
In infants, the metabolising enzymes
and excretory process
are not fully developed. Hence doses
of children should be
smaller than adults.
3. Sex: Some drugs which cross the
placental barrier and depress
foetal respiration are avoided in pregnant
women, e.g.
morphine.
4. Route of administration
of drug: As the route of adminis
tration changes, the dose required
for same pharmacological
action varies. Hence IV dose is smaller
than SC dose which15
smaller than oral dose.
IV dose < SC dose < oral dose.
5. Time of administration
of drugs: When the drugs are taken
before meals, the absorption is greater,
but there is irritation
to GIT due to direct contact
of drug with walls of GIT.

poor
When the drugs are taken after meals, the absorption is
drug is mixed
but there is not irritation to GIT. This because
is
with food material hence direct contact of drug with walls of

GIT is avoided.
In the presence of diet, the
6. Diet and environmental factor:
affects
absorption of drug is po0or. Environmental factor also
the variations in the doses of drugs, e.g.
(i) The alcohol is well tolerated in cold environment
than in
summer.
a sleep
ii) The dose of phenobarbitone required to produce
during day time is much more than the dose required
during night.
7. Genetic factor: The patients with hereditary metabolic
disorders rarely show a disturbance in the metabolism of drugs.
This is because of microsomal enzyme systems involved in
the metabolism of drugs. Thus the genetic factor gives
individual variations in response to drugs. Some drugs pass
through genes and modity drug response from generation to
generation, e.g. diabetes mellitus.
8. Emotional factor: The personality of the physician may
influence the drug effect particularly in psychic patients. Hence
nervous patients require smaller doses of drugs as compared
to normal patients.
9. Presence of disease: In diseased conditions, some drugs may
produce unusually prolonged etfects in cirrhotic patients.
Thus drugs like barbiturates and chlorpromazine may
produce unusually prolonged effects in cirhotic patients.
10. Metabolic disturbances: The ckanges in water balance,
electrolyte balance and acid-base balance, body temperature
and other physiological factors may modify the effects of drugs,
e.g. the absorption of iron from the GIT is maximum if the
individual has an iron deficiency anaemia.
11. Cumulation (cumulative effect): When excretion of drug is
slow, repeated administration of drug accumulates in the body
and may lead to toxicity. This is known as cumulation. The
phenomenon is known as cumulative effect, e.g. digitalis,
emetine, heavy metals, chloramphenicol show cumulation.
Cumulation can be avoided by following ways:

() Stop the administration of drug at the appearance offirgt
first
waning symptom.
(i) It must be known that the drug is eliminated slowly or
rapidly.
(ii) Carefully select the dosage form in which the drug isto
be administered.
iv) Check the liver and kidney function before and durino
drug administration.
12. Additive effect: When total pharmacological action of two or
more drugs administered together is equivalent to their
individual pharmacological actions, the phenomenon is known
as additive effect, i.e.
1+1 2 1
For example, combination of ephedrine and aminophylline
shows additive effect in the treatment of bronchial asthma.
13. Synergistic effect (synergism): The increase in pharmacologi.
cal response by the use of two or more drugs at the same time is
called synergism. The effect is known as synergistic effect, i.e.
1+1=3
For example: a. Aspirin and codeine as analgesic.
b. Sulphamethoxazole and trimethoprim as anti
bacterial.
c. Aspirin, phenacetin and caffeine as analgesic.
14. Antagonism: The opposite actions of two drugs on the same
physiological system are termed as antagonism.
.Classification/types of antagonism
() Chemical antagonism: When the biological activity of
drug is totally reduced by a chemical reaction with another
agent, the phenomenon is known as chemical antagonism,
e.g. acid and alkali react with each other for neutralization.
() Competitive/reversible antagonism: In competitive
antagonism, the agonist and antagonist compete for the
same receptor. Hence in such cases, the extent to which
the antagonist opposes the pharmacological action of
agonist depends on the relative number of receptors
Occupied by two compounds, e.g. acetylcholine and
atropine compete for each other at the receptor sites.

eneral Pharmacology 25
is increased, the
If concentration of acetylcholine
Hence
blockade produced by atropine can be overcome.
antagonism is also termed as reversible antagonism.
irreversible antagonism: In this type of
(il) Noncompetitive the receptor by
antagonism, the antagonist inactivates
the effective complex
some mechanism in such a way that
with agonist cannot be formed.
is increased
Hence though the concentration of agonist
at the receptor site, the
receptor is inactive to produce
Hence, there is no any
any combination with agonist.
is called
pharmacological action with agonist. Thus, it
papaverine
irreversible antagonism, e.g. acetyicholine and
noncompetitive antagonism.
on smooth muscles produce
Physiological antagonism: When a drug is administered,
(iv)
it reverses the effects of another dug
by acting on different
physiological
receptors. This phenomenon is known as
reactions are
antagonism, e.g. adrenaline and histamine
of this typ.
interaction of two agonists
(v) Functional antagonism: When
opposite
which act independently of each other but give
functional
effects take place, the reaction is known as
antagonism, e.g. acetylcholine and adrenaline show
functional antagonism.
Importance of antagonism
cases to block the
i) Antagonism is useful in poisoning
actions of poisons.
(ii) Antagonism is useful to control the adverse
effects of the
drugs.
is useful to adjust the doses of the drugs
(i) Antagonism
combined.
15. Drug tolerance: When large dose of a drug is required to get an
effect, produced by the normal therapeutic dose of a drug, the
phenomenon is known as drug tolerance.
Types/classification of tolerance
A. True tolerance: It is seen on both oral and parenteral adminis-
tration.
a. Natural tolerance: It results in difference between species
and races.

i. Species tolerance: Some animal species can

tolerate
large amount of particular drug which may prove
to be
lethal (toxic) to man, e.g. some rabbits can tolerate
laree
amount ofbelladona. This is because of enzyme atropine
esterase present in the rabbits' liver and plasma which
rapidly detoxify the belladona.
Types/classification of tolerance
A. True tolerance B. Pseudotolerance/False tolerance/

Apparent tolerance
Natural Acquired
tolerance tolerance
C. Tachyphylaxis
or acute
Species Racial Tissue Cross tolerance
tolerance tolerance tolerance tolerance
ii. Racial tolerance: When solution of ephedrine is instilled

into the conjunctival sac of the caucasians, it produces
prompt dilation of pupils but in negroes ephedrine does
not produce any dilation at all.
b. Acquired tolerance: Repeated administration of drug produce
a tendency to produce a tolerance. This is known as acquired
tolerance, e.g. the drugs like barbiturates, opiates, alcohol
xanthines, produce acquired type of tolerance. Acquired
tolerance is of two types:
i. Tissue tolerance: In this type, development
of tolerance
is related to certain pharmacological
action and certain
tissues, organs or systems, e.g. morphine
produces
tolerance for its euphoriant effect but pupils
and GIT never
become tolerated. Thus same dose of morphine
invariably
produces constipation but may fail to
"euphoria".
ii. Cross tolerance: When an individual
develops tolerance
to a drug belonging to a particular group,
it also shows
tolerance to other drugs belonging to
the same group
ing, it is known as cross tolerance,
e.g. tolerance to
vasodialator effect of "glyceryl trinitrite' in
an individual
Scanned with camScanner

which
shows tolerance to pentaerythritol tetranitrite'
belongs to same group.
Pseudotolerance/false/apparent tolerance: It is observed only
B.
by oral route.
is taken orally, tolerance is
When small dose of poison
GIT. This is possible after
developed to that poison by the
repeated administration of small
quantity by oral route in the
individual immune to such poison.
administration of drug is probably
This tolerance to the oral
developed by GIT which prevent poison
due to local changes
the systemic circulation.
from getting absorbed into
administration
Tachyphylaxis/acute tolerance: The repeated
C. the pharmaco-
drug within a short interval of time decreases
of progressively. This phenomenon is known as
logical response
tachyphylaxis or acute tolerance.
drug dissociates only
Tachyphylaxis probably can occur if the continuing
with receptor and thus
slowly from its combination
blockade, while loosing its intrinsic activity, i.e. looses
receptor
e.g. repeated administration of
its pharmacological effects,
bronchial asthma decreases the
ephedrine in the treatment of
response to ephedrine.
Difference between:
Pseudotolerance
True tolerance
and 1. It is seen only on oral adminis-
|1. It is seen on both oral tration of drug.
parenteral administration
of drug.
2. Itis observed probably due to
2. It observed naturally
is
local changes developed by
due to presence of certain
enzyme system to tolerate GIT
certain drugs.
3. It is further divided into: 3. It has no further types.
i. Natural tolerence
ii. Acquired tolerance
4. Example, morphine produces 4. Example, if small quantity of
tolerance for its euphoriant poison is taken orally, poisoning
effect but pupils and GIT will not occur.
are not affected.
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16. Drug dependance: It is a psychic or

physical condition ofa
person due to interaction between living ofthe
which includes a compulsion to organism d
and drug
take the drug and tendenc
increase the dose at the cost of
health, e.g.morphine, heroito
alcohol, tobacco. roin,
Dependance is of two types:
i. Physical dependance: It is
the condition in which
the body shows dependant stage
on the drug. If the
drug is withdrawn, the intense
physical disturbance
Occur.
ii. Psychic dependance:
A condition
produces a feeling of satisfaction in which a druo
and
that requires periodic or continuous a psychic drive
administration
the drug to produce pleasure
and to avoid discomfort of
called psychic dependance. is
10 Give the formulae for calculating doses in children.

a. Age-based Formulae
1. Young's formula
Child dose =. Age in yrs

-x Adult dose
Age in yrs +12
2. WJ Dilling formula
Child dose =-AgeinyrSxAdult

20
dose
3. Frieds rule for infant
Infant dose = Agein monthsx Adult

dose
150
b. Body Weight-based Formulae

1. Clarks formula
Child dose =.Wt of childin Kg Adult dose

70

nule for infants
2. Clarks
Wt in pouna Adult dose
Dose of infant=- 150
Surface Area
c. As per
Surface area ofchild(mx100=% of adult dose
Surface area of adult (m*)
(1.73 m)
Questions
mean by absorption of drug and mention any
1. What do you 08,
factors affecting the absorption of drugs? (S. 97, 05,
five
08)
09; W. 01, 02, 03, 04,
process can drug cross membranes? Name the
2. By which across cell membrane
commonest process for drug transfer
commonest process. (W. 98)
and explain why it is the
distribution of drugs. (S. 97;
3. Discuss four factors affecting
W.99, 04, 06)
drugs and mention its
4. Describe plasma protein binding of
significance. (S. 96, 03; W, 06, 08)
How does it take place
5. What is biotransformation of a drug?
in the body? (S. 06, 09)
drugs? Or What are
6. Write a note on routes of excretion of
(S. 96, 98, 99, 01, 02,
various channels of excretion of drugs?
04; W. 00)
Enumerate the various
7. What is the mechanism of action?
W. 05, 07)
factors modifying drug action. (S. 01, 02, 03, 04;
is meant by
8. When do drugs cumulate in the body and what
cumulative toxicity. (S. 00)
9. Comment on the following: (W. 98)
) Synergistic action
i) Cumulative toxicity
10. What is drug antagonism? Explain the various types or
antagonism with appropriate examples. (S. 96, 00, 07,
W. 99, 04)

11. Write a note on drug tolerance. (S. 06, 07; W. 96, 98, 02, 03,
07, 08)
12. What is the difference between tolerance' and
tachyphylaxis'.
(S. 99)
13. What is bioavailability of drugs? What do
you mean by drug
metabolism? (W. 96)
14. Write a note on drug dependance. (S.
97, 09; W. 08)
15. Define the term 'dose' and give any two methods
for calculating
the doses for children. (W. 99, 06)
16. Define the term 'dose' and mention
the various factors which
can affect the dose ofa drug. (S. 98)

CHAPTER 3
General Anaesthetics
Definition
1 loss of the pain sensa-
The drugs which produce a total or partial
along with loss of consciousness are called general anaesthetics.
tion
Classification
1. Inhalation general anaesthetics
example, diethyl ether, chloroform,
(a) Volatile liquids: For
halothane.
cyclopropane, nitrous oxide.
(b) Gases: For example,
2. Intravenous anaesthetics
barbiturates: For example, thiopentone,
(a) Ultra-short acting
methohexitone.
(b) Nonbarbiturates: For example,
propandid, ketamine,
althesin.
2 Diethyl Ether
diethyl ether.
Anaesthetic ether contains 96-98%
Advantages
1. It is a safe anaesthetic, can be used by unexperienced anacs
thetist.
2. Preanaesthetic medication is not required.
3. It is an excellent analgesic.
4. Ether produces satisfactory muscular relaxation.
5. Ether does not modify blood pressure during anaesthetic stages.
6. Ether can be employed during delivery to reduce labour pains.
31
32 Phamacology and Toxicology
7. Ether can be administered without a complicated apparatus

8. Ether anaesthesia is economical.
Disadvantages
1. Induction of anaesthesia is slow and is
sometimes associated
with marked excitement.
2. Iritant nature of the ether vapour may increase
and bronchial secretions and induce the salivary
cough and laryngeal
spasms during induction of ether.
3. The heart rate is usually increases during
4.
ether anaesthesia.
Nausea, vomiting appear during recovery
from ether anaesthesia,
5. The motility of GIT is reduced
by ether and secretions are
also depressed.
3 Chloroform
Advantages
1.
It is a highly potent anaesthetic
agent.
2. In very low concentration
it acts as an analgesic.
3. Surgical anaesthesia can
be achieved within 2-3 minutes.
Disadvantages
Chloroform is not a safe anaesthetic
agent due to following toxic
effects:
1..Chloroform depresses the respiratory centre.
2. It may produce arterial
hypotension.
3. It may cause cardiotoxicity,
hepatotoxicity and
4. It also precipitates "delayed cirhosis ofliver.
chloroform poisoning" and
anaesthetic toxemia". "post
5. It also produces cardiac
arrest and arrhythmia.
Differentiate between
ether and chloroform.
Ether
1. It is
Chloroform
a safe anaesthetic
agent. 1. It is nota safe anaesthetic
2. 10 to 15% concentration agent.
of ether is sufficient 2. 1% concentration
to is
produce anaesthesia. sufficient.

General Anaesthetics 33
Contd.
Ether Chloroform
Ether can be used during 3. Itis not used during labour

3. delivery to reduce labour pains. pains due to its high toxicity.
volatile Chloroform is a clear volatile
4. Ether iswithcolourless
pungent odour. liquid having sweet smel.
liquid,
5. Ether, when exposed to air, 5. Chloroform decomposes in the
forms ether peroxides or presence of flame and forms
acetic aldehydes. phosgene gas which is toxic.
5 What is preanaesthetic medication? Name the drugs

commonly used for preanaesthetic medication.
to
The use of drugs before administration of anaesthetic agent
make anaesthesia safer and more aggreable to the patient is called
preanaesthetic medication.
Reasons for Preanaesthetic Medication

1. To reduce anxiety, tension and nervousness.
2. To obtain synergistic effect.
3. To reduce preoperative and postoperative pains.
4. To suppress salivary and respiratory secretions.
5. To counteract adverse effects of anaesthetic agent.
Drugs Commonly Used for Preanaesthetic Medication
1. Narcotic analgesics: These are given due to their sedative
and analgesic properties, e.g. morphine 15 mg by IM.
2. Barbiturates: Drugs like pentobarbitone and secobarbitone
are used to provide sedation and to relieve apprehension.
3. Tranquillizers: These agents produce calming effect and are
safe muscle relaxants. They have less respiratory depression,
e.g. diazepam 5 to 10 mg orally.
4. Anticholinergics: Anticholinergics such as atropine are used
to reduce excessive salivary and respiratory secretions.
5. Antiemetics: These are used to prevent preoperative and post
operative vomiting, e.g. metoclopramide.
6Give the requirements of an ideal general anaesthetic

agent.
An ideal general anaesthetic agent should possess following
properties:

a. For Patient
(i) Anaesthetic agent should be pleasant to
inhale without any
anv
irritation.
(ii) The induction of anaesthesia should be
pleasant and fast.
(iii) The recovery of anaesthesia should
be smooth and rapid.
(iv) It should not produce any toxicity.
b. For Surgeon
i) The anaesthetic agent should produce
good analgesia and
adequate muscular relaxation.
(ii) The capillary bleeding should be
negligible.
11) It should be nonexplosive.
c. For Anaesthetist
i)It should be stable at room temperature.
(ii) It should be easily controllable with a wide
margin of safety
(ii) It should not cause respiratory or circulatory
collapse or
depression.
(iv) It should be easily eliminated from the body.
(v) It should not attack the materials used for anaesthesia
such as
rubber tubing or metal.
d. For Manufacturer
(i) The cost of anaesthetic agent should be cheap.
(ii) It should have no storage problem.
7 Describe mechanism of action of general anaesthetics/

stages of anaesthesia.
Mechanism of anaesthesia is divided into four stages:
a. Stage of Analgesia
This stage starts from begining of inhalation of anaesthetic agent up
to loss of consciousness. It involves sensation of falling, remoteness
and teeling of warmth is observed in some patients. Analgesia 13
produced before consciousness is lost.
b. Stage of Delirium
This stage starts with loss of consciousness to beginning of surgi
anaesthesia. This stage involves marked excitement, shoutng

General Anaesthetics 35
laughing, increased muscular activity, vomiting, pupils may dialate and

patient shows development of marked hypertension and tachycardia.
c. Stage of Surgical Anaesthesia
starts and patient passes
As the more drug gets in, deep breathing
reflexes, regular
into the third stage. This gives gradual loss of
respiration and relaxation of skeletal muscle.
This stage is divided into four different planes:
roving. The pupils
Plane 1: The pupils are normal and eyeballs are
regular. BP
dialate and attain normal size. The respiration is full and
and pulse ate is normal.
respiration is
Plane 2: Eyeballs are fixed and amplitude of
diminished. Adequate muscular relaxation.
muscles are paralysed
Plane 3: The BP begins to fall. Intercostal
completely.
slowly. The pupilary light reflex is lost. Muscles relax
paralysed. The pupils are
Plane 4: Intercostal muscles completely
completely abolished.
further dialated. BP is low. All secretions are
d. Stage of Respiratory Paralysis

vital medullary
This stage is characterised by severe depression of
are irregular.
centres, initially the diaphragmic contractions
Respiratory arrest also leads to vasomotor collapse.
Questions
1.Define and classify general anaesthetics with examples. (S.
97,98, 99, 03, 04, 08; W. 96)
2. Differentiate between ether and chloroform. (W. 96)
3. Write a note on pre-anaesthetic medication. (S. 96, 00, 05, 08;
W. 99, 03)
4. Give a brief account of intravenous anaesthetics. (W. 98).
5. Give the mechanism of action of general anaesthetics. Or
Explain various stages of general anaesthesia. (S. 00, 01, 07;
W.04, 05, 08)
6. Explain the physical signs during surgical anaesthesia in four
different planes. (S. 02)
7. Give the properties of an ideal general anaesthetic? Or In
general what properties should the ideal general anaesthetic
drug possess? (S. 00, 01, 02; W. 07)

CHAPTER 4||
Local Anaesthetics
1 Definition
The drugs which produce anaesthesia in a limited area the
of
body are called local anaesthetics.
Classification
1. Natural, e.g. cocaine, cinchocaine
2. Synthetic compounds
a. Amide type, e.g. lignocaine
b. Ester type, e.g. procaine
3. Miscellaneous, e.g. clove oil, phenol.
2 Give the properties of an ideal local anaesthetic.

i) It should be nonirritating to the tissue.
(ii) It should be stable in water and lipid.
(iii) It should have quick onset of action and sufficient duration
action.
of
iv) It should not cause permanent damage to nerves.
(v) It should not have any little systemic toxicity.
(vi) It should be stable, easily sterilizable and inexpensive and
should be safe.
(vii) It should be cheap and easily available.
3 Give the mechanism of action of local anaesthetics.

Local anaesthetics block both the generation and conduction f
nerve impulses. The blockade results from biochemical changes
caused by the drug on the lipotrophic film of cell membrane
36

Local Anaesthetics 37
The lipophillic activity is essential for migration of drug into the

the drug to
neuronal fibre while water solubility is essential to get
application.
the site of action from site of injection or
4 4 Write a short note on lignocaine.

It is a potent local anaesthetic agent.
Adverse Effects
i) Hypotension
(ii) Bradycardia
(ii) Convulsions intto
(iv) Respiratory paralysis
(v) Skin sensitization
(vi) Allergic dermatitis
(vii) A typical asthmatic attack.
Therapeutic Uses
) It is used for topical anaesthesia
i) For infiltration anaesthesia
(ii) For nerve block anaesthesia
(iv) For spinal anaesthesia
(v) For dental anaesthesia
(vi) As an antiarrhythmic agent.
Preparation and Doses

(i) Lignocaine eyedrops
i) Lignocaine injection.
Trade Names
Xylocaine, Xylocard, Lidocaine.
Questions
1. Define and classify local anaesthetics with examples. (S. 05;
W. 01)
2. Write ideal properties of local anaesthetic. (S. 05; W. 01)
3. What are local anaesthetics? Give an account of commonly
used local anaesthetics. (S. 98)
CHAPTER 5 |
.
Analeptics/CNS Stimulants
1 Definition
The drugs which stimulate the CNS are called
CNS stimulants or
analeptics.
Classification
1. Cortical stimulants, e.g. caffeine,
theophylline,
aminophylline
amphetamine.
2. Medullary stimulants, e.g. nikethamide,
picrotoxin, bemegride.
3. Spinal stimulants, e.g. strychinine.
4. Those which stimulate CNS reflexly,
e.g. lobeline, nicotine.
2 Nikethamide
Adverse Effects
1. Hypertension
2. Tachycardia
3. Vomiting
4. Coughing
5. Hyperpyrexia
6. Arrhythmia
7. Muscular rigidity
8. Convulsions
Therapeutic Uses
1. It is used in cases of respiratory and circulatory failure.
2. It is a safe analeptic drug.
3. It is used in narcotic poisoning.
4. In respiratory failure due to CNS depr e
38

Analeptics/CNS Stimulants 39
5. In respiratory disorders due to lung
disease.
6. Nikethamide have a mild
antipellagra activity.
Preparation
Nikethamide injection IP
Dose: 1 to 4 ml IV
Trand Name
Nikethyl
3 Bemegride
Itis a medullary stimulant.
Adverse Effects
1. Hypertension
2. Tachycardia
3. Convulsions
4. Coughing
5. Hyperpyrexia
6. Arrhythmia
7. Muscular rigidity.
Therapeutic Uses
It is
1. used as a CNS stimulant.
2. It isused for the diagnosis of epilepsy.
3. It is a selective respiratory stimulant.
4. It isused as an antidote for barbiturate poisoning.
5. Itis used to treat respiratory depression caused due to overdose
of CNS depressants.
4 Pharmacological Actions of Xanthines

These are commonly used as mild stimulants and bronchodilators.
Questions
1. What are analeptics? Classify them with examples. (S. 96)
2. Write the classification of CNS stimulant
drugs. Discuss the
pharmacological actions of caffeine. (S. 01))
3. Define analeptics. Classify analeptic drugs.
Write pharmacological
actions of coramine. How is it administered? (S. 07; W.
04)

|CHAPTER 6
Drug Abuse
1 Drug Abuse
The misuse of drug in an excessive manner
wnich is dangerone
to health is known as drug abuse. ous
Classification of Drugs of Abuse

1. Narcotics, e.g. morphine, heroin
2. CNS depressants, e.g. alcohol, barbiturates
3. CNS stimulants, e.g. caffeine, amphetamine
4. Hallucinogens, e.g. mescaline, LSD
5. Cannabis preparation, e.g. charas,
bhang, ganja
6. Banned drugs, e.g. cocaine, heroin
7. Miscellaneous, e.g. nicotine,
ethyl alcohol.
2 Drug Addiction
FA continuous administration of certain
use more doses and produces drugs forces the personto
a tendency to increase
high tendency to withdrawal the dose and
effects is known as drug addiction.
of these drugs are morphine, Some
codeine, heroin, alcohol.
3 Difference
between "drug addiction"
habituation". and "drug
Drug addiction
1. It is a state of Drug habituation
periodic or 1. It is a condition resulting
chronic intoxication
by repeated consumption
produced Trom repeated administrato
drugs. of of drugs.

Drug Abuse 41
Contd.
Drug addiction Drug habituation
there is a
In this condition, 2. No compulsion to take the
2. compulsion to take the drug drugs but continue to take the
and obtain it by any means. drug for sense of well-being.
3. Little or no tendency to
3. A tendency to increase the
dose of a drug.
increase the dose of a drug.
4. Some degree of psychic
4. A psychological as wellis as dependence but absence of
physical dependence
formed. physical dependence.
5. A detrimental effect, any, is
if
is
5. The effect of the drug
detrimental to the individual primarily on the individual.
and to the society.
Questions
and habituation'.
Give the difference between addiction
1.
(S. 02, 08; W. 01)
2. Write a note on 'drug
addiction'.

CHAPTER 7
Narcotic Analgesics
1 Definition
The drugs which reduce pain sensation along with loss of con
sciousness and sleep are called narcotic analgesics.
Classification
a. Natural opium alkaloids, e.g. morphine,
codeine .23
b. Synthetic derivatives, e.g. heroin
c. Synthetic morphine substitutes, e.g.
pethidine, methadone.
2 Morphine
It is an opium alkaloid.
Adverse Effects
1. Dryness of mouth
2. Constipation
5. Nausea, vomiting, headache
4. Mental clouding
5. Increased pressure in biliary
tract
6. Skin rash, contact dermatitis
7. Hypotension
8. Tolerance
9. Dependence, addiction
10. It depresses foetal respiration
if administered in pregnant women.
Therapeutic Uses
1. It is used as a narcotic
analgesic.
2. As a preanaesthetic
medication.
42
Narcotic Analgesics 43
sleep
3. For sedation and
to treat diarrhoea.
4. To produce constipation or
which produce this

3 What is euphoria? Name the drugs
condition.
euphoria. The
condition of feeling of well-being is called
The morphine, heroin, alcohol, etc.
drugs which produce euphoria are
opium poisoning.
4 Acute morphine poisoning/acute
clinical overdosage
Acute morphine poisoning may occur due to
intention.
overingestion in an addict or from suicidal
or accidental
.
Signs and Symptoms

1. Dryness of mouth
2. Pinpoint pupil
3. Respiratory depression
4. Reduced body temperature
5. Reduced urinary output
6. Hypotension
7. Shock and coma
8. Constipation
9. Convulsions may occur in infants
10. Death is usually due to respiratory depression.
Treatments of Morphine Poisoning
A. Drug Treatment
The actions of morphine are antagonised by specific antagonists like
naloxone and nalorphine.
These drugs significantly reverse morphine-induced respiratory
depression.
a. Naloxone: It is usually preferred because of its specific
antagonistic activity. It is given in the dose of 0.4 to 0.8 mg
repeated every 10 to 15 minutes as required.
b.Nalorphine: It is antagonist of morphine and usually
administered intravenously in the dose of 3 to 5 mg repeated
within half an hour if necessary.

B. Other Treatments
a. Gastric lavage: This is done by
administration of emetio
preparation to induce vomiting and
contents. For example, syrup wal of gastric
withdrawal gastric
of ipecac.
b. Supportive treatments: Such as
airway, maintenance of BP, maintenance of patient'
mechanical ventilation,
by intravenous glucose saline nutrition
infection.
and prevention of secondary
c.Anticonvulsants like
paraldehyde are used
Sions, if any. to reduce convul.
. Questions
Define and classify
narcotic analgesics.
cological actions Discuss the pharma-
of morphine on CNS,
W. 01, 02, 03) CVS and GIT. (S.
2. Give the symptoms 04;
and treatments of
morphine poisoning.

CHAPTER S
Hypnotics and Sedatives
1 Hypnotics
The drugs which produce a sleep resembling a natural sleep are
called hypnotics.
2 Sedatives
The drugs which produce calming effect without inducing sleep
are called sedatives.
3 Insomnia
It means lack of sleep or inability to sleep.
Classification of Hypnotics and Sedatives

1. Barbiturates, e.g. phenobarbitone, pentobarbitone
2. Benzodiazepines, e.g. diazepam, nitrazepam, oxazepam
3. Alcohols, e.g. chloral hydrate, ethanol
4. Aldehydes, e.g. paraldehyde
5. Acetylated carbinols, e.g. ethionamate
6. Inorganic ions, e.g. bromides
7. Miscellaneous, e.g. meprobamate, antihistaminics.
4 Barbiturates
Barbiturates are the derivatives of barbituric acid.
The hypnotic activity of barbituric acid is due to replacement of
hydrogen atoms attached to carbon atom at position 5 by alkyl or aryl
radical.
45

Barbiturates are classified according to duration of action:

a. Long-acting barbiturates (action is for 8, hrs or more), eg e.o
phenobarbitone.
b. Intermediate-acting barbiturates (action is for 4 to 8 hrs),
e.ge.
amylbarbitone, butobarbitone, pentobarbitone.
e
c. Short-acting barbiturates (action is less than 4 hrs), e.g.
secobarbitone, hexobarbitone.
d. Ultra short-acting barbiturates (V), eg. thiopentone sodium
methohexitone, kemithal.
Pharmacological Actions of Barbiturates (Phenobarbitone)
I. Effect on CNS
Barbiturates produce depression of CNS.
i. Sedation and hypnosis: The long-acting and intermediate
acting barbiturates are used for sedation and hypnosis.
i. Anaesthetic effect: Ultra short acting barbiturates, when
administered intravenously, produce basal or general
anaesthesia. For example, thiopentone.
ii. Anticonvulsant effect: Phenobarbitone is a selective
anticonvulsant drug and is used for prevention of grand mal
epilepsy.
iv. Analgesic effect: Barbiturates increase the analgesic effect of
salicylates and p-aminophenol derivatives.
v. Respiration: Higher doses of barbiturates depress the respira-
tory centre in medulla oblongata and may lead to respiratory|
collapse.
I. Effect on CVS
Therapeutic doses of barbiturates may cause a slight fall in BP and
decrease the heart rate.
Toxic doses of barbiturates produce sustained hypotension.
I. Effect on GIT
Larger doses of barbiturates retard the peristalsis.
IV.Effect on Kidney
Barbiturates cause decrease in glomerular filtration and hence unn
output decreases.

Hypnotics and Sedatives 47
Adverse Effects of Barbiturates

1. Intolerance-includes excitement, vomiting, headache, diar
rhoea.
2. Megaloblastic anaemia
women, may depress the foetal
3. If administered to pregnant
respiration.
4. Tolerance
5. Drug dependence.
Therapeutic Uses of Barbiturates

1. Used as hypnotics and sedatives
2. Used as an anticonvulsant
Used as a preanaesthetic
medication
3.
thiopentone
4. Used as a general anaesthetics, e.g.
pentobarbitone, thiopentone.
5. The psychiatric uses, e.g.
Preparations and Doses

Phenobarbitone tablet IP
Sedative dose: 15-30 mg daily
daily
Hypnotic dose: 100 to 200 mg
Trade Name
Gardenal, Luminal, Garoin.
5 Acute Barbiturate Poisoning

barbiturate poisoning is caused due to ingestion of an
Acute suicidal intention.
overdose either accidently or with
Signs and Symptoms

shows:
The patient of barbiturate poisoning
i. Weak and rapid pulse
ii. Cold clammy skin
i. Slow or rapid shallow breathing
iv. Constriction of pupils
no v. Paralytic dilation develops initially
vi. Respiratory depression
vii. Peripheral vascular collapse

vii. Urinary retention.
Treatments
1. Gastric lavage
2. Endotracheal intubation
3. Alkalinization of urine
4. IV administration of fluids
. Use of prophylactic antibiotics
6. Dialysis
7. Forced diuresis
1. Gastric Lavage
Ifthe patient is conscious then gastric lavage is carried out by using
syrup of ipecac or salt solution.
If the patient is unconscious then gastric aspiration is
by inserting tube into the stomach.
carried out
2. Endotracheal Intubation
It is performed when respiration
secretions from respiratory tract.
is inadequate and also to remove
Adequate ventilation is of
great importance in barbiturate
poisoning.
3. Forced Diuresis
In this step, diuretics
such as frusemide
barbiturate poisoning and mannitol are used
to increase in
This may lead to increase the flow and excretion
in excretion of barbiturates. of urine.
is most useful in poisoning Forced diuresis
due to phenobarbitone,
barbitone, etc.
4. Alkalinization
of Urine
Alkalinization
of urine prevents
by ionization of filtered tubular reabsorption
barbiturates. ofbarbiturates
barbiturates. This increases the excretion or
Sodium bicarbonate
is used for alkalinization
5. Intravenous
of urine.
Administration
Intravenous fluids of Fluid
are given in
dehydration. They
are also useful
sufficient quantity to preven
for the maintenance
of blood volun

Hypnotics and Sedatives 49
6. Use of Prophylactic Antibiotics

a infection
The antibiotics are used only when there is possibility of
bladder, etc.
due to catheterization of urinary
7. Dialysis
Elimination of barbiturate from the body can be increased by
peritoneal dialysis and haemodialysis.
Benzodiazepines
6
These are the potent and safe hypnotics. For example, diazepam,
nitrazepam, oxazepam, lorazepam.
Therapeutic Uses
1. As hypnotics and sedatives
2. AS anticonvulsants
3. As preanaesthetic medication
4. As antianxiety agents
5. As good muscle relaxants
6. As tranquillizers.
Preparation
Diazepam tablet IP
Dose: 5 to 30 mg in divided doses.
Trade Names
Calmpose, Diazep, Valium.
Questions
1. Define and classify hypnotics and sedatives with examples.
(S. 02, 04, 05; W. 00, 07)
2. Mention the signs, symptoms and treatments of barbiturate
poisoning. (S. 97, 98, 00, 06; W. 99, 00, 07, 08)
3. Explain pharmacological actions of barbiturates. (S. 04;
W.02)
Scanned withCamscanner
CHAPTER 9||
Anticonvulsants/
Antiepileptics
1 Epilepsy
Itis achronic convulsive disorder characterised by sudden distn
bance of consciousness usually but not always with characteristio
body movements and sometimes with autonomic hyperactivity,
Types of Epilepsy
1. Grand mal epilepsy: It involves a sudden loss
ness and major convulsions consisting
of conscious.
of spasms of the whole
body followed by jerky movements.
Convulsions are followed
by generalised CNS depression.
2. Temporal lobe epilepsy:
It consists of sudden
altered behaviour and
emotions. attacks of
Convulsions are absent.
The entire attack consists
of abnormalities
3. Focal cortical epilepsy: of behaviour.
It consists of convulsions
limb or a group of of single
muscles.
4. Minor epilepsy:
It consists of loss
convulsions. of consciousness without
5. Petit mal epilepsy:
associated with It consists of impairment
eyelid blinking of consciousness
6. Myoclonic (insensitivity of light).
epilepsy:
It consists of isolated
7. Infantile epilepsy: clonic jerks.
deterioration. It occurs in infants and consists
of ment
8. Motor epilepsy:
It involves involuntary
angles of mouth, movements of
movements
affected like paralysis. thuni
of half side of the
body may
50
Anticonvulsants/Antiepileptics 51
Antiepileptics/Anticonvulsants
2
The drugs which are used in the treatment of epilepsy/convulsions
are called antiepileptics.
Classification
nts/ 1. Hydantoins, e.g. phenytoin, ethoin, methoin
tics 2.
3.
Barbiturates, e.g. phenobarbitone, mephobarbitone
Iminostilbenes, e-g. carbamazepine
4. Succinimides, e.g. phensuccimide, ethosuccimide
5. Oxazolidine diones, e.g. trimethadione
6. Benzodiazepines, e.g. diazepam
7. Miscellaneous, e.g. bromides, sodium valproate.
a distur-
cteristic
ity.
3 Phenytoin
Itis a primary drug in the treatment of epilepsy.
Mechanism of Action (Antiepileptic Activity)
nscious- Phenytoin exerts selective antiepileptic action. This drug
a
e whole generally inhibits the spread of convulsions in the brain and
ollowed shortens the duration after its discharge.
The phenytoin decreases the neuronal sodium concentration
tacks of which leads to reduction in the post-tetanic potentiation (PTP)
sent. and increase in the neuronal potassium concentration.
our. The reduction in PTP by phenytoin stops the spread ofconvulsive

discharge in the brain.
of single
Adverse Reaction
without 1. Intolerance, skin rash, jaundice
2. Headache, confusion, hallucination
1ousness 3. GIT iritation, nausea, vomiting
4. Megaloblastic anaemia
t).
5. Cardiovascular collapse
rks 6. Severe CNS depression.
of mental
Therapeutic Uses
ofthumb,
be
41. In treatment of grand mal epilepsy n rT
y may 2. In treatment of temporal lobe epilepsy

3. In focal cortical epilepsy
4. In cardiac arrhythmia
or iga
5. In trigeminal neuralgia
Preparation
Phenytoin tablet IP
Dose: 50 to 100 mg twice daily
Trade Names
Eptoin, Epileptin.
4 Write the properties of an ideal antiepileptic agent.

1. It should be effective in all varieties of epilepsy.
2. It should have quick action and
long duration of action.
3. It should have minimum side effects
and non-addicting.
4. It should be orally effective.
5. It must be cheap and easily available.
5 What is status epilepticus?

Give its treatments.
Status epilepticus is a condition in which
follow each other continuously. the epileptic attacks
The term status epilepticus
is used to irdicate
epileptic attacks repeated grand mal
without recovery of
attacks. consciousness
between the
The status epilepticus
must be hospitalized is a medical emergency
for proper treatment. and such patient
Treatment
1. Glucose
saline is given
2. Respiration intravenously.
is supported.
3. Diazepam
is given intravenously
4. Hypotension for controlling convulsions.
and respiratory
carefully. depression may
5. Paraldehyde be watchea
is also given
10 ml by IM. as an alternative
in the dose of 5
to

Anticonvulsants/Antiepileptics 53
6 Mention the anticonvulsant drugs used for each type

of epilepsy.
primidone
1. Grand mal epilepsy: Phenobarbitone, phenytoin,
2. Temporal lobe epilepsy: Phenytoin, primidone, carbamazepine
primidone
3. Focal cortical epilepsy: Phenytoin, phenobarbitone,
diazepamn
4. Petit mal epilepsy: Ethosuccimide, sodium valproate,
5. Myoclonic epilepsy: Sodium valproate
6. Infantile epilepsy: ACTH
7. Motor epilepsy: Phenobarbitone, phenytoin.
Questions
1. Define epilepsy. Mention different types of epilepsy. Mention
adverse effects of phenobarbitone. (S. 07; W. 04, 07, 08)
2. Define and classify antiepileptic drugs with examples. (S. 98,
01,09)
3. What is status epilepticus? Write the treatment for status
epilepticus.
4. Enumerate the types of epilepsy. Discuss mechanism of action
of phenytoin. (S. 05; W. 01)
5. Discuss the mechanism of action of phenytoin, give its adverse
effects. (S. 02)
er9fpns

|CHAPTER 10||
izers
Antipsychotics/Tranquillizers
1 Definition
a. Antipsychotics/Psychotropics/Psychoactive Drugs
The drugs which are used in the treatment of psychic disorders
are
called antipsychotics or psychoactive drugs. For example,
chlorpro-
mazine, reserpine, haloperidol.
b. Antianxiety Agents
The drugs which are used to reduce
anxiety states and nervousness
are called antianxiety agents. For
example, diazepam, nitrazepam,
Oxazepamn.
c. Antidepressants (Mood
Elevators)
The drugs which improve the
moods of depressed
called antidepressants. individuals are
For example, imipramine,
amitryptyline, nor-tryptyline. desipramine,
d. Tranquillizers
The drugswhich produce
calming and quietening
are called tranquillizers.. effect individuals
For example, chlorpromazine,on the
haloperidol.
2 Give classification
of antipsychotics/tranquillizers.
1. Phenothiazines,
e.g. chlorpromazine,
2. Rauwolfia alkaloids, triflupromazine.
e.g. reserpine.
3. Butyrophenone derivative,
4. Diphenyl-butyl piperidine e.g. haloperidol, trifluperidol.
derivative, pimazole.
5. Thiothixene derivative,
thiothixene,
chlorprothixene.
54
Antipsychotics/Tranquillizers 55
3 Chlorpromazine
is a phenothiazine
derivative.
It pharmacological actions, hence it is called
It has large number of
"Larg-actil".
bythe trade name
Pharmacological Actions
1. Chlorpromazine produces
sedation.
causes tranquillizing
2. In psychotic patients, chlorpromazine
effect.
3. Chlorpromazine produces emotional quietening.
4. It has an antiemetic effect.
It reduces the excessive body
temperature.
5.
6. It promotes lactation in women.
7. It has a weak antihistaminic action.
It potentiates the analgesic activity of
morphine.
8.
9. It produces hypotension.
Adverse Effect
1. Skin rash, dermatitis
2. Parkinsonism
3. Excitement, restlessness
4. Tachycardia
5. Constipation
6. Hypotension
7. Aplastic anemia
8. Menstrual irregularities.
Therapeutic Uses
1. of schizophrenia.
In the treatment
2. In sensile psychosis (aged).
3. In the treatment of maniac depressive psychosis.
4. For the treatment of behavioural disorders in children.
5. It acts as an antiemetic by acting on CTZ.

Chlorpromazine tablet IP
Dose: 200 to 800 mg daily

56 Pharmacology and Toxicolog9y
Trade Name
Larg-actil, Thorazine.
4 Reserpine
It is a principal alkaloid of "Rauwolfia serpentina'"
Mechanism of Action (Tranquillizing Action)

Reserpine produces depletion of 5 HT and catecholamines adrenaline
and nor-adrenaline) from the brain and peripheral sites.
This depletion of monoamines is necessary for its tranquillizing action
Therapeutic Uses
1. As antipsychotic (tranquillizer).
2. As an antihypertensive agent.
3. Used in the treatment of snake bite.
Preparation and Dose

Reserpine tablet IP
Dose: 0.25 mg daily
Trade Name
Serpasil.
5 Antidepressants (Thymoleptics)
The drugs which improve the moods of depressed
individuals
are called antidepressants or mood elevators.
Classification
a. Tricyclic antidepressants, e.g. imipramine,
desipramine,
amitryptyline, nor-tryptyline, doxepin
b. MAO inhibitors, e.g. phenelzine,
pargyline, isocarboxazid,
tranylcypromine
c. Miscellaneous, lithium
carbonate, menaserin.
6 Write a note on "MAO inhibitors".

MAO inhibitors means mono-amino-oxidase
inhibitor.
The drugs which inhibit the actions
mono-amino-oxidase
enzyme are known as mono-amino-oxidaseof
inhibitors. For example
phenelzine, pargyline, 1SOcarboxazid,
tranylcypromine.

Antipsychotics/Tranquillizers 57
is a heterogenous group of drugs which block

.MAO inhibitors
of naturally occurring amines.
Oxidation
. MAO inhibitors have a limited role in
the management of
depression.
Inhibitors
Mechanism of Action of MAO
present intracellularly in
most
mono-amino-oxidase is
The enzyme is found in liver, within the
The highest concentration
ofthe tissues.important function is to oxidise active biogenic amines,
brain and its
nor-adrenaline and dopamine.
5 HT, granules in neurons and are
are normally stored in
These amines
liberated by nerve stimuli.
inhibit the action of MAO enzymes which may
MAO inhibitors
these monoamines in the brain. MAO
lead to accumulation of
prevent oxidation of catecholamine and histamine and
inhibitors brain.
functional availability of these monoamines in the
increase mental depression
effective in the treatment of
MAO inhibitors are pharmacological action by
these drugs prouce their
of man because
increasing the level of active amines like 5 HT
Inhibitors
Adverse Effects of MAO
Headache, excitement
1. Disturbed sleep
2.
3. Hyperthermia
4. Convulsions
5. Sudden increase in BP
6. Constipation
7. Severe jaundice.
Therapeutic Uses of MAO Inhibitors

1. As antidepressants
2. As antihypertensive agents
3. They potentiate the action of
barbiturates, morphine and
anaesthetics.

1. Phenelzine sulphate tablet
Dose: 50 to 60 mg daily orally.

Trade name: Nardil

2. Isocarboxazid tablet
Dose: 10 to 30 mg daily orally
Trade name: Morphan
3. Tranylcypromine tablet
Dose: 10 to 30 mg daily Ato 1o
Trade name: Parnate.
7 Explain the terms and give the drugs of choice.

1. Schizophrenia
- It is a split mind condition characterized by disturbed thinkino
emotional withdrawal from surrounding, delusions, and hallu-
cination.
- The mental functions of schizophrenic patient are sufficiently
impaired to interfere with his capacity to meet the ordinary
demands of life.
Drug treatment
Chlorpromazine, reserpine.
2. Motion Sickness
Motion sickness can develop during any form of travel but is mainly
due to repetitive and rhythmic changes in speed or direction of travel.
It starts with a brief period of euphoria and then followed by un-
easiness.
The face becomes pale and a cold sweat breakout, nausea, saliva-
tion, and vomiting occurs with headache.
Drug treatment
Scopolamine, promethazine, cyclizine, d-amphetamine.
Questions
1. Classify tranquillizers. Write the uses
(W. 98, 00)
of chlorpromazine.
2. Classify psychopharmacological
agents with examples. (W. 01
3. Give adverse effects and therapeutic
uses of phenothiazines:
(S. 02)
CHAPTER 11||
Parkinsonism and
Antiparkinsonism Agents
Parkinsonism
1 and in-
Parkinsonism is caused due to deficiency of dopamine
synapse.
creased acetylcholine at
It is a clinical condition characterised by
symptoms suchas:9
1. Muscular rigidity
2. Tremors (shaking movements/vibrations)
3. Akinesia (inability to move)
4. Excessive salivation.
5. Seborrhoea
6. Liver damage, mood changes may occur
7. Bradykinesia (slowness of movement)
8. Postural instability.
Antiparkinsonism Agents
2 parkinsonism are
The drugs which are used in the treatment of
called antiparkinsonism agents.
Classification
1. Drugs that replace dopamine, e.g. levodopa, carbidopa.
2. Drugs that release dopamine, e.g. amantidine.
3. Anticholinergics, e.g. atropine, benzatropine, procyclidine,
biperiden.
4. Antihistaminics, e.g. diphenhydramine, promethazine,
orphenadrine.
5. Phenothiazines, e.g. ethopropazine
6. Drugs that mimic the action of dopamine, bromocryptine.
59

3 |Levodopa
1. Levodopa gives all manifestations of parkinsonism hence itis
called universal antiparkinsonism agent.
2. Levodopa is converted into dopamine in the brain as well as
in peripheral tissues by the enzyme dopa decarboxylase.
3. The levodopa improves the conditions such as seborrhoea and
also improves the mood, memory and makes the patients more
interested in their surrounding.
4. Levodopa increases psychomotor in-coordination. The young
patients are benefited more than olders.
S. Parkinsonism due to I and mangenise poisoning are also
treated by levodopa.
Preparation
Levodopa tablet IP.
Dose: 125 mg twice daily.
, Trade Names
Levopa, Avopa.
Questions
1. Describe the various drugs used in the treatment
of parkin-
sonism. (W. 98, 08)
2. What is parkinsonism? Mention the
drugs used in parkin-
sonism. Write down the adverse effects
of levodopa. (W. 04)
3. Classify antiparkinsonism agents
with examples.

CHAPTER 12
Heavy Metal Poisoning
Lead Poisoning
1 responsible
Lead compounds are used in various industries and are
for causing chronic lead
poisoning in workers.
Signs and Symptoms

1. Metallic taste in mouth.
2. GIT iritation, vomiting.
3. Blueline on gums.
4. Anorexia, weakness, headache.
5. Severe anemia.
6. Severe haemoglobinuria.
7. Stools appear dark in colour.
8. Constipation.
9. Convulsions, delirium, mild renal damage
Treatments
1. Milk or white of egg is administered.
2. Gastric lavage with magnesium sulphate solution.
3. IV administration of sodium calcium acetate
4. IV administration of 10% solution of calcium gluconate at
intervals of 4 to 6 hrs.
. High calcium and vitamin D diet is given to the pati
6. Sodium citrate is given orally.
7. Chelating agents like EDTA are used as antidotes
Dimercaprol increases excretion of lead from the body.

Antispasmodics like atropine are used to reduce intestinal
spasms.
61

2 Mercury Poisoning
Mercury compounds are toxic. These compounds may
deposi
and may give symptoms of chronic mercurialism.
Signs and Symptoms

.Ash grey appearance to mouth and pharynx
2. Vomiting, diarrhoea.
3. Epigastric pains.
4. Damage to kidney and alimentary canal.
5. Stomatitis.
6. Swelling, ulceration.
7. Loosening of teeth.
8. Marked salivation.
9. It can cause loss of fluids.
10. It may lead to shock.
Treatments
1. Administration of egg white into the stomach to precipitate
the metal.
2. Stomach wash by gastric lavage.
3. BAL is an antidote of mercury, is used.
4. Treatment for collapse is necessary.
EtR.:
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CHAPTER 13||
Analgesics, Antipyretics and

Anti-inflammatory Agents
Analgesics
1 sensation are called analgesics.
drugs which reduce pain
The
ANTIPYRETICS
normal level
which lower elevated body temperature to
The drugs
arecalled antipyretics.
Classification salicylate.
and their derivatives, e.g. aspirin, sodium
Salicylates
1.
paracetamol, phenacetin.
p-aminophenol dervatives, e.g.
2.
ves, e.g. phenylbutazone, oxyphenbutazone.
3. Pyrazolone derivati sulindac.
acid derivatives, e.g. indomethacin,
4. Indole-acetic
e.g. diclofenac.
5. Phenylacetic acid derivatives, fenoprofen.
e.g. 1buprofen, ketoprofen,
6. Propionic acid derivatives,
acid, fluphenamic acid.
7. Fenamates, e.g. mefenamic
8. Oxicams, e.g. piroxicam.
Salicylates (Aspirin)
2 salicylic acid. Saicylates are always
These are the esters or salts of
given orally.
I. On CNS
a. Analgesic action: Salicylates produce relief of pain without
mental activity.
producing hypnosis or marked impairment in
perpheral action.
alicylates relieve pains by central as well as
63

b. Antipyretic action: Salicylates reduce excessive body te

rature to the normal level by heat loss thrOugh sweatine
vasodilation. In fever condition, prostaglandin substance
creased. The salicylates inhibit prostaglandin synthesie th
brain and lowers the body temperature.
in
C. Anti-inflammatory action: Salicylates reduce only the ina
matory component of disease without affecting tlam-
fecting tiss
component. Salicylates reduce the capillary permeabilit
minimising the exudation of fluid and developme t
inflammatory edema. The salicylates inhibit the synthesisOf
prostaglandins and help to prevent pain and intlammation. .
IL. Effect on Respiration
Salicylates stimulate respiration as a result of direct and indirect actiom
ions.
Il. On GIT
The acid pH of stomach leads to unionized form of salicylates. Thi
nonionized form of salicylate is water insoluble hence it sticks
gastric mucosa and produces gastric irritation. To avoid gastrie
imitation, salicylates may be administered after food. Excessive use
of salicylates may cause nausea, vomiting, epigastric distress, peptic
ulceration, GIT haemorrhage, etc.
IV. Antirheumatic Effect
Salicylates have powerful anti-inflammatory action
and are prosta-
glandin inhibitors thus help to prevent pain
and inflammation asso-
ciated with rheumatism.
V.
Antigout Action/Uricosuric Effect
When salicylates are administered in
the dose of more than 5 gm
day, it prevents reabsorption
of uric acid and increases its excretion
Hence due to uricosuric property
they are used in gout.
VI Local Action
Methyl salicylate produces
counterirritant and rubefacient action.
Adverse Effects/Toxic Effects
of Salicylates
1. Allergic reactions:
Skin rash, urticaria, bronchial
2. GIT toxicity: GIT irritation, asthma
nausea, vomiting, GIT blecaus
hyperpyrexia, convulsions, epigastric
tion, deafness, respiratory alkalosis, pains,
coma, deny r

Analgesics, Antipyretics and Anti-inflammatory Agents 65
administration of salicylates produces

Salicylism: Prolonged
3.
mild salicylate intoxication termed as salicylism.
a
headache, deafness, mental
Salicylism is characterised by
diarrhoea.
confusion, vomiting,
(Aspirin)
Therapeutic Uses of Salicylates
analgesic and
antipyretic.
1. As
anti-inflammatory agents.
2. As rheumatiC fever and rheumatoid arthritis.
treatment of
3. In the prevent the formation of platelet
fibrin
has been used to
4. Aspirin
thrombus. fungistatic, mild antiseptic
Salicylic acid also has keratolytic,
5.
activity.
is used as counterirritant and rubefacient.
Methyl salicylate
6.
Preparation
Aspirin tablet IP
to 8 gm daily in divided doses.
Dose: 4
Trade Nanmes
Aspro, Disprin.
Analgesic-Antipyretics
Preparations and Doses of Some
D ose Trade name
Drug
Crocin, Calpol
300 to 600 mg daily
Paracetamol tablet IP Butazolidine
1. Phenylbutazone tablet NF 200 to 400 mg daily
Oxalgin,
2. Oxyphenbutazone tablet 200 to 400 mg daily
3. Flamar
Novalgin
Analgin tablet IP 0.5 to 3 gm daily Zimalgin
4.
Indocin, ldicin,
Indomethacin capsule IP 50 to 150 mg in
5. divided doses Indocap.
Brufen,
Ibuprofen tablet IP 0.4 to 0.6 gm thrice
6. Ibugesic
daily
3Anti-inflammatory Drugs (NSAIDs)

used to reduce
inflammation are called anti-
The drugs which are
phenylbutazone,
nilammatory agents, e.g. aspirin, ibuprofen,
indomethacin, diclofenac.

Therapeutic Uses of Anti-inflammatory Drugs

i. Headache
ii. Rheumatoid arthritis
ii. Rheumatism
iv. Toothache
v. Migraine
vi. Arthritis
vii. Alkaloysing spondylitis
vii. Antigout.
4 Acute Salicylate Poisoning (Salicylism)

A larger dose of salicylate can cause salicylate poisoning.
Symptoms
1. Deep and rapid breathing (hypercapnea)
2. Anorexia
3. Nausea, vomiting, thirst, diarrhoea.
4. Headache, dizziness, deafness, dimness of vision.
5. Confusion, restlessness, disorientation, delirium, mania,
hallucination.
6. Deep coma, respiratory and circulatory collapse.
7. High fever
8. GIT bleeding, epigastric pains, GIT iritation.
Treatment
1. Gastric lavage is done with water or sodium
bicarbonate
(3-5%).
2. Administration of milk or slurry
of universal antidote.
3. Saline cathartics like sodium sulphate
or magnesium sulphate
are used.
4. Checking of acid-base status
of the patient.
5. Sodium bicarbonate is given by
IV as an antidote.
6. To corect dehydration glucose
saline is given.
7. Smaller doses of barbiturates,
paraldehyde may be required
Suppress the restlessness and
convulsions.
8. For hyperpyrexia, use sponge
bath.
9. For CNS depression, caffeine,
nikethamide may be useful.

Analgesics, Antipyretics and Anti-inflammatory Agents 67
Questions
1. Define and classify analgesics-antipyretics with suitable
examples. (S. 01, 02, 09; W. 96, 05, 06)
2. Mention the symptoms
and treatment of acute salicylate
poisoning. (S. 07)
and doses of salicylates.
3. Write therapeutic uses, preparation
(W. 02, 03)
pharmacological actions of
4, What is inflammation? Give
aspirin. (S. 03)
contra-
5. Classify NSAIDs. Mention therapeutic uses and
indications of NSAIDs. (W. 04, 08)
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|CHAPTER 14||
Drugs Used in
Gout and Rheumatisn
1 Gout
The condition in which crystals of sodium urate (uric acid) are

re
deposited in the joints is called gout.
It is caused due to abnormality in purine metabolism resulting in
overproduction of uric acid and causes pains and inflammation
of
joints.
Antigout Agents
The drugs which are used in the treatment of gout are called antigou
agents.
Classification of Antigout Agents

1. In acute stage, c.g. colchicine, indomethacin, phenylbutazone
2. In long-term therapy
a. Uricosuric drugs, e.g. probencid, sulphipyrazone.
b.Metabolic inhibitor, e.g. allopurinol.
2 Rheumatism
It is a disease of connective tissue
usually associated with pa
and swelling of muscles and joints.
Antirheumatic Drugs
The drugs which are used in the treatment rheumatism calle
antirheumatic agents.
of arc
68
Drugs Used in Gout and Rheumatism 69
Classification of Antirheumatics
1, Anti-inflammatory and analgesics, e.g. aspirin, piroxicam,
phenylbutazone.
2. Anti-inflammatory
without analgesic, e.g. glucocorticoids,
ACTH.
azothiopurine.
Immunosuppressants, e.g. cyclophosphamide,
3.
Miscellaneous compounds, e.g. penicillamine, gold salts,
4.
captopril.
ois
CHAPTER 15|
Drugs Acting on
Digestive System
1 Antacid
The drugs which are used to neutralize excessive acidity in the
stomach are called antacids.
Classification
1. Systemic antacids (water soluble), e.g. sodium bicarbonate.
2. Nonsystemic antacids (water insoluble), e.g. magnesium
hydroxide, aluminium hydroxide gel, magnesium trisilicate,
calcium carbonate, MgO.
Properties of an Ideal Antacid
1. It should have a capacity to neutralize excessive acidity.
2. It should have a quick and prolonged action.
3. It should not cause alkalosis.
4. It should be nontoxic, palatable, cheap and easily available.
5. It should not cause constipation or diarrhoea.
6. It should not interfere with digestion and absorption of food.
7. It should not cause evolution of gas.
What are the principles of line of treatment of peptic ulce?

Peptic ulcer is one of the common diseases of adult male.
It is caused as a result of digestive action of pepsin and diluu
HCI against which the normal stomach and deod: numa
protected by their mucus secretions.
In peptic ulcer, there is an excessive secretion of gasuricac
The treatment of peptic ulcer consists of
i. Controlling gastric acidity, hypermotility and spasms
ii. Promoting ulcer healing.
70
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Drugs Acting on Digestive System
71
ii. Use of antacids, milk or ion exchange resin.
iv. Withdrawal of stimulants of gastric acid like alcohol,
tobacco, etc.
v. Surgical removal of acid producing gastric mucosa.
Drug treatments
i. Aluminium hydroxide gel
i. Magnesium hydroxide
ii. Aluminium trisilicate
iv. Magnesium oxide
v. Ranitidine
vi. Cimetidine
vii. Famotidine.
Emetics
2
The drugs which induce vomiting are called emetiCs.
to:
Emesis: It is the process of vomiting. It can be caused due
i. Stimulation of CTZ
i. Local iritation in GIT
ii. Vestibular stimulation
iv. Psychological
Drugs: Apomorphine, ipecac, mustard,

sodium chloride solution.
Uses of emetics:
i. In poisoning cases for gastric lavage
ii. As expectorants.
Antiemetics
e.g.
The drugs which prevent vomiting are called antiemetics,
metoclopramide, promethazine, domperidone.
Uses of antiemetics
i. In vomiting due to poisoning
11. Preanaesthetic medication
ii. To prevent vomiting of pregnancy

iv. In motion sickness.
itx
B Purgatives and Laxatives
Purgatives: The drugs which promote defaecation are called
purgatives.

Toxicology
72 Pharmacology and
Classification
e.g. senna, castor oil, phenol
Stimulant/irritant purgatives,
i.
phthalein, biacodyl.
Osmotic
purgatives/saline
purgatives, e.g.
magnesium sulphate ,
11.
potassium phosphate. agar-agar.
methyl cellulose,
11. Bulk
purgatives, e.g. e.g. liquid paraffin
purgatives/lubricant purgatives,
iv. Emollient
a purgative?
How does senna act as
purgative.
Senna is a stimulant stimulation
anthraquinone glycosides which act by
Senna contains
probably by inhibiting NaCl and water
of large bowel and also increase evacuation of faecal
matter
reabsorption in the colon. Hence
from the colon and produce purgation.
How does castor oil act as a purgative?

When castor oil is ingested orally, it is hydrolysed by pancreatic lipase
to glycerol and ricinoleic acid.
stimulates the peristaltic
This ricinoleic acid, by its irritant action,
movements of intestine and produces purgation.
Full dose of castor oil produces purgation within 2-6 hrs.
O Write a note on saline purgative/osmotic purgative.
Saline Purgatives
These drugs act by maintaining a volume
of fluid in the bowel
by osmosis.
These drugs increase the osmotic pressure
fluid in the intestinal tract by secreting additional
resulting in increase
stimulate the peristalsis in bulk and
of GIT, hence they are used
constipation. in
Examples
i. Magnesium sulphate:
5 to 15 gm before
ii. Magnesium breakfast.
carbonate: 2 to 4 gm
as required.
ii. Magnesium hydroxide:
2 to 4 gm as required.

Drugs Acting on Digestive System 73
Therapeutic Uses of Saline Purgatives

1. In constipation.
suffering from painful
For easy evacuation in patients
2.
haemorrhoids or other rectal disorders.
3. To remove radiopaque
solid prior to X-ray analysis.
pressure during evacuation of bowel.
4. To avoid rise in blood
Indications of Purgatives/Therapeutic Uses

1. In treatment of constipation.
purgatives are used.
2 In food or drug poisoning saline purgatives are given.
3. During anthelmintic therapy,
4. Used before preoperative
abdominal surgery and X-ray
examination.
5. In patients with anal fissures, pile
and in pregnant women in
defaecation, the
order to avoid excessive straining during
purgatives are given.
Questions
examples. (S. 96;
1. Define and classify gastric antacids with
W. 98, 05)
(S. 07; W. 02)
2. Give the properties of an ideal/good antacid.
and
3. Mention the drugs used in peptic ulcer along with doses
route of administration. (S. 98)
4. Write a note on emetics. (S. 99)
5. Write a note on antiemetics. (S. 07; W. 99)
6. What is the difference between laxative and purgatives.
(S. 06; W. 99, 00)
7. Give the classification of laxatives with examples. (S. 06, 09;
W. 99, 00, 03, 06)
8. Define diarrhoea. Classify antidiarrhoeal agents. Mention
mechanism of antidiarrhoeal drugs. (W. 04)

CHAPTER 16
Drugs Acting on
Respiratory System
1 Bronchodilators
drugs which dilate the bronchi and improve the rate af
The
breathing are known as bronchodilators.
Classification
1. Sympathomimetics, e.g. adrenaline, ephedrine, isoprenaline
salbutamol, terbutaline.
2. Phosphodiesterase inhibitors, e.g. theophylline, aminophyline,
3. Anticholinergics, e.g. methyl atropine.
2 Bronchial Asthma
Asthma is a chronic disease in which the patient
has difficulty in
breathing. Bronchial asthma is a clinical
syndrome characterised by:
i. Paroxysmal dyspnoea (breathlessness)
ii. Cough due to increased air
resistance due to bronchoconstriction.
ii. Narrowing of brorchi is due to bronchospasm,
chial mucosa and thick sticky edema of bron-
mucus in the bronchial
iv. Hyperreactivity of lumen.
bronchi which constrict
v. Hypoxemia (decreased due to allergens.
arterial O tension)
VI. Hypercapnea
(increased arterial
CO, tension)
Treatments of Bronchial
Asthma
1.Drug treatment: Adrenaline,
isoprenaline, terbutaline,
costeroids. corti-
2. Supporting treatments:
i. Avoiding
respiratory irritants
chemicals. such as tobacco
smoking,
74

Drugs Acting on Respiratory System 75
ii. Psychological treatment.

factors, e.g. allergens.
ii. Elimination of trigger air.
iv. Ventilation by supply of pure
v. Supervision of patient
for the physiological parameters
like BP, heart rate, pulse, etc.
3 Nasal Decongestants
congestion are called
drugs which are used to reduce mucosal
The naphazoline, ephedrine.
nasal decongestants, e.g.
Expectorants
4 which increase the bronchial secretions and help to
The dugs mucosa are called expectorants, e.g.
ammonium
protect the irritated
iodide.
chloride, codeine, potassium
5 Antitussives (Anticough)
are used in the treatment of cough are called
which
The drugs noscapine, tincture of opium, heroin, methadone.
antitussives, e.g.
Classification
Pharyngeal demulscent, e.g. syrups and linctus (codeine
1.
linctus)
e.g. ammonium chloride, ipecac ammonium
2. Expectorants,
bicarbonate.
3. Central cough
suppressants, e.g. noscapine.
6 Status Asthmaticus
urgent hospitalisation
It is aserious medical emergency requiring
and vigorous therapy.
Signs and Symptoms

1. Marked dyspnoea
2. Exhaustion
3. Dehydration
4. Tachycardia
5. Respiratory infections
6. Hypoxemia
7. Hypercapnoea.

Treatments
1.
Hydrocortisone and its derivatives are life-saving drugs in this
case. Hydrocortisone 100 to 200 mg is given parenterally
Tepeated every one to two hrs.
and
2. Adrenaline and aminophylline are also used.
3. Oxygen is administered in high dosage for
the treatment of
hypoxemia.
4. Administration öf 5% glucose is essential.
5. Isoprenaline aerosol by positive pressure
ventilation is applied
when all treatments have been failed.
6. The use of antibiotics to overcome
associated infections.
Questions
1. What are cough suppressants
and expectorants? Mention two
examples of drugs used for expectorants.
2. Write a note on expectorant. (S. 98, 04; W. 00, 07)
(S. O1; W. 98)
3. Write a treatment of
status asthmaticus. (S. 02,
02, 08) 04, 05; W. 01,
4. What is bronchial asthma?
Give the drug therapy
(S. 07, 09; W. 05) on asthma.

CHAPTER 17
Histamine and
Antihistaminics
1 Define autacoids. Give classification.

The substances which have self-regulating power in the body are
called autacoids.
Classification
1. Endogenous amines, e.g. histamine, 5-hydroxy tryptamine
(serotonin) (5 HT)
2. Polypeptides, e.g. bradykinins, kinins, kallidin, angiotensin.
3. Lipids, e.g. prostaglandins, prostacyclins.
2 Discuss physiological role of histamine and serotonin.

A. Role of Histamine in the Body
1. Histamine may play an important role in gastric secretion with
hormone gastrin.
2. It also plays a part in tissue growth and repair.
3. It helps in antigen-antibody reaction.
4. It contracts all plain muscles including muscles of uterus,
bronchi, intestine.
. Intradermal injection of histamine produces "triple response".
6. Histamine dilates blood capillaries and thereby causing fall in
BP.
B. Role of Serotonin (5 HT) in the Body

. It gives constriction of peripheral blood vessels.
2. It has stimulant action on heart.
77
3. It stimulates smooth muscles.

4. It plays important role in neurohumoral transmission.
3 Explain "triple response" produced by histamine.

Intradermal administration of 10-20 gm of histamine
inTDan
produces a characteristic effect described by
Lewis as a
response".
The "triple response" consists of:
1. Reddening at the site
of injection described as a 'flush'
2. The flush is followed by development
of bright flare, i.e.
irregular outline. an
3. Development of localised
edema ('wheal' which is dueto
escape of fluid from the capillary) to
4 Antihistaminics
The drugs which block the actions
called antihistaminics. produced by histamine are
Classification
1. Amino-alkyl ether
type, e.g. diphenhydramine,
nate. dimenhydr-
2. Alkylamine derivatives,
e.g. chlorpheniramine,
3. Ethylene diamine derivatives, pheniramine.
4.
e.g. mepyramine,
Piperazines, e.g. meclizine, antazoline.
buclizine, chlorcyclizine.
5. Phenothiazines, e.g.
promethazine.
5 Write a note on Hz-receptor

antagonists.
The drugs which block
the actions of histamine
by competitive inhibition
antihistaminics. are called H-receptor on H-receptors
H-receptor antagonists antagonists or H
and prevent ulcers. reduce gastric acid secretion
For example:
i. Cimetidine
ii. Ranitidine
ii. Famotidine
iv. Metiamide
v. Burimamide.

Histamine and Antihistaminics 79
Cimetidine
6 Ha-receptor antagonist.
It is a
Cimetidine markedly inhibits the basal and meal stimulated gastric
secretion.
reduces the gastric secretion of
On oral administration, cimetidine
acid to about 20% within an hour.
Adverse Effects
i. Skin rash
ii. Diarrhoea
ii. Muscle pain
iv. Hepatotoxicity
v. Sexual disturbances
Preparation and Dose

Cimetidine tablet IP
Dose: 200 mg twice daily orally
Trade Names
Cimetigate, Lock-2.
Therapeutic Uses
i. In treatment of peptic ulcer.
ii. In treatment of duodenal ulcers.
Questions
1. What are autacoids? Mention the physiological role of hista-
mine. (S. 96, 07, 09; W. 04, 05, 08)
2. What is triple response? Explain it. (S. 07, 08, 09; W.
O1, 04,
08)
3. Write a note on histamine. (W. 03)
4. Classify antihistaminics with examples. (W. 04, 08)

CHAPTER 18
A
.
Drugs Acting on Blood
1 Haematinics
The drugs which increase the formation of RBCs (HB)
as haematinics, e.g. iron, folic acid, are know
vitamin B12, ferrous sulphate
Iron
It has a medicinal value in the treatment
-
-
Iron requirements are greatly of anemia.
increased during growth, preg.
nancy, menstruation and haemorrhage
-
In iron deficiency anemia,
condition.
the iron requirement is
or more per day. up to 60 me
-Oral dose of iron is 100-200 mg daily.
Side Effects
i. GIT imitation
i. Nausea
ii. Epigastric pains
iv. Diarrhoea
Uses of Iron
i. In iron deficiency
anemia
ii. In haemorrhage condition
Preparations of Iron
i. Ferrous sulphate
dried 200-300
ii. Ferrous gluconate mg daily
1.2-1.8 gm in
ii. Ferrous fumarate divided doses daily
iv. Ferrous succinate 200-400 mg in divided doses
200-400 mg in
divided daily dose
80

Drugs Acting on Blood 81
Colloidal iron
v. 200-400 mg daily
vi. Ferrous ammonium citrate 200-400 mg daily
150 mg daily
vii. Sodium ironedetate
Iron dextran injection (50 mg/ml)
1
ml by IM (Inferon)
vii.
1.5 mg/kg IM (Jectofer)
ix. Iron sorbitol injection (50 mg/ml)
Intoxication)
Iron Poisoning (Acute Iron
more than 50 gm of iron.
Iron poisoning may result from ingestion of
Signs and Symptoms

i. Abdominal pain
ii. Vomitingg
ii. Acidosis
iv. Cardiovascular collapse
v. Coma and finally death.
Treatment
i. Gastric lavage
(antidote)
ii. IV administration desferroxamine
replacement.
ii. Fluid and electrolyte
2 Haemostatics
the oozing of blood from the
The drugs which are used to control
minute blood vessels are known as
haemostatics, e.g. thrombin NF
thromboplastin, fibrinogen, oxidized cellulose.
3 Anticoagulants
The drugs which prevent coagulation of blood are called
anticoagulants.
Classification
i. In vivo anticoagulants
a. Rapid-acting (parenteral), e.g. heparin and derivatives.
b. Slow-acting (oral), e.g. warfarin, phenindione
11. In
vitro anticoagulants, e.g. oxalic acid, sodium citrate.

Oral Anticoagulants
4
The drugs which are effective by oral route as anticoagulant are
arekn.
known
as oral anticoagulants.
They take about 36 to 48 hrs for anticoagulant effect to devat
Nelop
Hence called oral anticoagulants.
Oral anticoagulants act by competitiveiy antagonising the
of vitamin K as they have structural similarities, e.g. warfar
acti
acenocoumarin.
rfarin
Warfarin
It is readily and completely absorbed by oral route. It is
nsively
bound to plasma albumin and, therefore, it has relatively long plasm
sma
half-life.
Side effects
i. Haemorrhage
ii. Anorexia, nausea, vomiting, diarrhoea.
Therapeutic uses
i. In treatment of venous thrombosis and pulmonary embo-
lism.
ii. In myocardial infarction.
ii. In rheumatic heart disease.
iv. In artificial heart valve to prevent emboli.
Preparations
i. Warfarin sodium tablet 5 mg twice daily (Uniwartin)
ii. Acenocoumarin tablet 15 to 20 mg/day orally (Acitrom.
Sintro.
O
5 Plasma Volume Expanders
The plasma expanders are the substances of relatively hig"
molecular weight, when infused into bloodstream, they remain long8
time to increase the volume of circulating fluid by increasing8
osmotic pressure.
They are used where reduced blood volume is the main causeo
shock.
ume
Therefore, it is essential to restore the intravascular blood
as quickly as possible.
vo
The blood volume is generally maintained by IV fluid ther

Drugs Acting on Blood 83
Types of
Plasma Expanders
Polymerised carbohydrates Acacia, dextran
1.
substitute Gelatin, oxypolygelatin
2. Protein
Methyl cellulose PVP
3. Plastics
Electrolytes Physiological saline, glucose,
4.
etc.
Requirements of an ldeal Plasma

Expander
colloidal particles should remain in the circulation until its

1. Its
original proteins.
place can be taken by the
osmotic pressure, pH and viscosity of the solution must
2. The
be same as that of the
plasma.
composition of plasma substitute must be constant.
3. The
must be nontoxic and apyretic.
4. It
over a long period of storage.
5. It should be stable act as a
be retained along in the tissue and must not
6. It must
diuretic.
suitable for
should be easily sterilized and have viscosity
7. It
infusion.
interfere with blood grouping and should be
8. It should not
fluids/drugs.
compatible with other IV
Therapeutic Uses of Plasma Expanders

blood volume and in shock
after
1. It is used for restoration of
severe haemorrhage.
increase oxygen-carrying capacity of blood.
2. It is also used to
hypoproteinemia.
3. It is used to treat infectious
immune bodies in the treatment of
4. Itis used to supply
etc.
diseases like scarlet fever, polio,
Questions
megalo-
haematinics? Describe the drugs used for
.What are
blastic anemia. (W. 98, 00)
examples. (S. 03)
haemostatics? Explain with three
2.What are (S. 07)
Give different types of anemias.
5, What is anemia?
4. Define haematinics. Describe role of iron as haematinio

(W. 06) ic.
5. What are the causes of anemia? Give the treatment of anemio
(W. 01) ia.
6. Write short note on oral anticoagulants. (W. 96)9
7. What are anticoagulants? Describe the mode of action oe
warfarin sodium. (S. 00)
8. Write a note on plasma expander. (S. O2,
04, 09)
tt

CHAPTER 19
Hypoglycemic Agents
Definition
1 which decrease elevated blood sugar to normal
level
The drugs
called hypoglycemic agents.
are
Classification
1. Parenteral
hypoglycemic agents, e.g. insulin.
2. Oral hypoglycemic
agents
e.g. chlorpropamide,
tolbuta-
urea derivative,
a. Sulphonyl
mide, glibenclamide.
e.g. phenformin, metformin.
b. Biguanide derivative,
agar-agar.
3. Plant source, e.g.
2 Insulin
a polypeptide hormone secreted by B-cells of
islets of
Insulin is
Langerhans of pancreas.
leads to diabetes
insulin synthesis and secretion
Deficiency of
mellitus.
Mechanism of Action
1. Insulin enhances the
conversion of glucose to glycogen in
skeletal muscle.
glucose from fats, proteins
2. Insulin inhibits the conversion of
and amino acids.
Preparations
1. Insulin injection IP (by IV)
2. Insulin zinc suspension
85

3. Isophane insulin suspension

4. Protamine zinc insulin suspension.
Adverse Effects/Toxic Effects of Insulin

1.Hypoglycemia.
2. Headache, blurred vision, diplopia, mental contusion, convul.
vul
sions.
3. Local reaction at the site of injection.
4. Insulin allergy.
Uses of Insulin
1.In the treatment of diabetes mellitus
2. For the diagnosis of hypopituitarism
3. Glucose insulin IV drip is used to treat hypercalcemia
4. To treat patients with myocardial infarction.
3 Oral Hypoglycemic Agents/Oral Antidiabetic Agents

These drugs are effective by oral route. The insulin therapy gives
its inactivation in GIT. Hence oral preparations are prepared. These
preparations are alternatives or substitutes to insulin therapy.
The current available oral hypoglycemic agents belong to
following:
1. Sulphonyl urea derivatives, e.g. chlorpropamide, tolbutamide
2. Biguanides, e.g. phenformin, metformin
3. Plant source, e.g. agar-agar.
Mechanism of Action
1. Sulphonyl ureas: These drugs stimulate the release of insulin
by the B-cells of islets of Langerhans.
2. Biguanides: These dugs stimulate the peripheral utilization
of glucose.
Therapeutic Uses
1.To treat symptomatic maturity onset type of diabetes
2. In insulin-resistant patients
3. Chlorpropamide has been used in diabetes insipidus

Hypoglycemic Agents 87
ABiguanides may be added to a sulphonyl urea in cases of

secondary failure.
Adverse Effects
Nausea, vomiting, epigastric discomfort, weakness, paraesthesia,
fever, rash,
jaundice.
Preparations of Oral Hypoglycemic Agents

Chlorpropamide tablet 500 mg daily Diabenese
1.
Tolbutamide tablet 0.5 to 1.5 gm daily Rastinonn
2. Daonil
3. Glibenclamide tablet 5 to 15 mg daily
4. Glipizide tablet 5 to 20 mg daily Glynase
75 mg daily DBI, chlorformin
5. Phenformin tablet
6. Metformin tablet 0.5 to 2 gmday Glyciphage
Questions
1. Write a note on hypoglycemic agents. (S. 97, 01, 06; W. 98,

05, 08)
2. Discuss various preparations of insulin. (S. 07; W. 01, 03,
04, 07)
3. Write a note on oral hypoglycemic agents

CHAPTER 20
Antithyroid Drugs
DEFINITION
The drugs which prevent excessive secretion ofthyroid hormoneo

from thyroid gland and are used in thyrotoxicosis are
called antithyroid
drugs.
Classification
1. Goitrogens, e.g. propylthiouracil,
methylthiouracil, carbi
mazole, methimazole.
2. lodine and iodides, e.g. radio
iodine (31)
3. Lithium.

CHAPTER 21|
Drugs Acting on ANS
Drugs acting on ANS
Sympathetic nervous system

Parasympathetic nervous system
B
D
Sympathomimetics Sympatholytics Parasympathomimetics Parasympatholytics
(Adrenergics) (Antiadrenergics) (Cholinergics) (Anticholinergics)
e.g. adrenaline, e.g. tolazoline e.g. acetylcholine, e.g. atropine,
isoprenaline, la betalol, carbachol, hyoscine,
ephedrine, propranolol, physostigmine, benzatropine,
amphetamine atenolol neostigmine homatropine
A Sympathomimetics/Adrenergics
The drugs which exert an action similar to actions produced by
stimulation of sympathetic nervous system are called sympathomi-
metics.
Classification
On basis of catechol nucleus
i. Catecholamines, e.g. adrenaline, nor-adrenaline, isoprena-
line.
i. Non-catecholamines, e.g. ephedrine, amphetamine,
salbutamol.
On therapeutic basis
i. Those used for raising BP, e.g. nor-adrenaline.
i. Those used as central stimulant, e.g. amphetamine.
89

ii. Those used as smooth muscle relaxants, e.g. adrenaline

salbutamol.
iv. Those used in allergic condition, e.g. adrenaline, ephedrine
ffect, e.g.
v. Those used for local vasoconstrictor effect, e.g. adre
adrer
line, naphazoline.
vi. Those used for suppressing the appetite (anorexiants
phenfluramine, phenteramine.
1. Adrenaline (Epinephrine)
1. On heart: Adrenaline increases heart rate, force of contraction
and cardiac output, i.e. it produces +ve and -ve chronotropie
effect.
2. Blood vessel and BP: Adrenaline increases the BP
due to its
direct effect on heart and vasoconstriction of blood vessels.
3. On smooth muscles: Adrenaline relaxes the bronchial
smooth
muscles and produces bronchodilation. Adrenaline reduces
GIT
motility.
4. On eye: Adrenaline produces dilation of
pupils, 1.e. mydriasis.
Adverse Effects of Adrenaline
. Severe hypertension
2. Palpitation
3. Cardiac arrhythmia
4. Acute pulmonary edema
5.. Fear, anxiety, restlessness
6. Headache, tremors.
Therapeutic Uses of Adrenaline

1. In bronchial asthma
2. In allergic reactions
3. In cardiac arrest
4. To control the haemorrhage
5. It is added to local anaesthetic injections.
Preparation
Adrenaline injection (1:1000) IP 0.2 to 0.5 ml by SC/IM.

Drugs Acting on ANS 91
Contralndications
Hypertension
1. Thyrotoxicosis
2. Arteriosclerosis
3.
Spinal anaesthesia.
4.
Explain "Dale's vasomotor reversal" phenomenon.
2. Explain
Adrenaline is a mixed agonist which produces an increase in systolic
but decrease
in diastolic blood pressure.
A secondary fall occurs when the concentration of adrenaline
decreases.
The drugs like ergotoxin reverses the actions of adrenaline which
is called "Dale's vasomotor reversal".
The vasoconstrictor action of adrenaline is blocked by ergot
alkaloids. This may lead to stimulation of both receptors by adrenaline
and thus causing a fall in blood pressure.
The high dose of adrenaline with ergot extract also blocks the
effects of adrenaline.
Adrenaline Ergot
V
Adrenaline
-Persistant B, action
Dale's vasomotor reversal
3. Ephedrine
Adverse Effects
1. Palpitation
2. Tachycardia
3. Headache, confusion, agitation
4. Insomnia
5. Emotional disturbances
6. Habituation, tolerance, dependance
7. Delirium, suicidal tendencies after larger dose.

Therapeutic Uses
1. In bronchial asthma
2. As a nasal decongestant
3. In heart block
4. As a mydriatic
5. In narcolepsy
6. In whooping cough
1. In dysmenorhoea
8. In hypotension during spinal anaesthesia.
BSympatholytics/Antiadrenergics
The drugs which block the actions produced
by stimulation
sympathetic nervous system are
called sympatholytics. of
Classification
1. Alpha-adrenergic
blockers (a-blockers),
tolazoline, e.g.
ergot alkaloids, phenoxybenzamine.phentolamine,
2. B-adrenergic blockers
(B-blockers), e.g.
labetalol. propranolol, metoprolol,
3. Adrenergic neuron
blockers, e.g. guanethidine,
bretylium.
4. P-Blockers
The drugs which block
the actions on B-receptor
are called B-blockers.
Classification
1. Specific B-blockers,
e.g. sotalol, timolol
2. B-blockers with membrane
sympathormimetic stabilizing activity
and intrinsic
activity, e.g. dichloroisoprenaline
3. B-blockers with membrane (DCI)
4. B-blockers with stabilizing activity,
additional o-blocking e.g.propranolol
activity, e.g. labetalol.
Adverse Effects
1. Bradycardia
2. Sudden hypotension
3. Heart failure
4. Nausea, vomiting
5. Bronchospasm
6. Mental depression
7. Cold extremities,
absent pulses.

Drugs Acting on ANS 93
Therapeutic Uses
1. In angina
pectoris :
infarction
2. In myocardial
arrhythmias
cardiac
3. In hypertension
4. In thyrotoxicosis
5. In
Preparations of B-Blockers
Inderal
1. Propranolol
20 mg to 2 gm daily in
divided doses
Lopressor
Metaprolol 150 to 300 mg once daily
2. Normadate
3. Labetalol 80 to 400 mg twice daily
Visken
4. Pindolol I to 45 mg daily Aten
5. Atenolol 50 to 100 mg daily
Parasympathomimetics/Cholinergics
c
Definition stimu-
drugs which exert an action similar to actions produced by
The parasympatho-
parasympathetic nervous system are called
lation of
mimetics or cholinergics.
Classification
acetylcholine, methacholine, carbachol.
1. Ester of choline, e.g.
2. Cholinomimetic
alkaloids, e.g. pilocarpine.
inhibitors/anticholinesterases, e.g. physostig-
3. Cholinesterase
pyridostigmine.
mine, neostigmine,
5. Acetylcholine
It is an ester of choline with acetic
acid. Its actions are divided into:
a. Muscarinic actions: By
stimulation of muscarinic receptors
muscarine.
which are similar to mushroom alkaloid
nicotinic receptors which
b. Nicotinic actions: By stimulation of
tobacco.
are similar to nicotine alkaloid from
Muscarinic Actions of Acetylcholine

1. On heart: Acetylcholine depresses
the activity of SA node
and reduces the heart rate and may
produce cardiac arrest.
and auto-
Acetylcholine decreases the cardiac contractility
maticity, rhythmicity and conductivity.
h
Scanned with camscanner

Toxicology
94 Pharmacology and
2. On blood vessels: Acetylcholine dilates the blood vessel

el and
causes decrease in peripheral resistance and output and
to hypotension.
eads
3. Smooth muscles of GIT: Acetylcholineiincreases the
rhy
activity of smooth muscles of GIT and increases peristaleamic
Acetylcholine contracts smooth muscles alsis
of gallbladdero
urinary bladder. and
4. Secretions: Acetylcholine increases
the gastric, intestinat
bronchial, salivary, lacrimal secretions.
Acetylcholine increases sweating.
5. On eye: Acetylcholine
produces constriction of pupil
Nicotinic Actions (miosis
of Acetylcholine
Acetylcholine
produces nicotinic
adrenal medulla, actions on autonomic
motor end plates ganglia
1. Acetylcholine of skeletal muscles.
stimulates the
adrenaline and adrenal medulla
nor-adrenaline. to release
2. Acetylcholine
induces contraction
of skeletal muscles.
6. What is myasthenia
gravis? Give
Myasthenia gravis: its treatments.
skeletal muscle It is a chronic disease
weakness and characterised
It is now considered fatigability. by abnormal
deficiency as
ofthe postsynapticautoimmune disease
complex. neuromuscular caused by the
acetylcholine
Signs and Symptoms receptor
1. Weakness
of muscles
2. Diplopia of eye
3. Difficulty
4. Slurring in chewing, swallowing
of
5. Respiratoryspeech
failure
due to weakness
Drugs of Choice of respiratory
Neostigmine, muscles.
physostigmine,
7. Organophosphorus pyridostigmine.
The poisoning Poisoning
with organophosphorus
a. Occupational,
as in persons compounds
engaged may be
in spraying due
inseri Camsca to
Drugs Acting
on ANS
95
b. Accidental, by consumption of agricultural
with insecticide. products sprayed
C. Suicidal, due to intentional ingestion.
Signs and Symptoms

1.Miosis
2. Headache
3. Bronchospasm
4. Hypotension
5. Respiratory depression
6. Convulsions
7. Nausea, vomiting
8. Abdominal cramps
9. Anorexia
10. Diarrhoea.
Treatments
1. If ingestion is by mouth, rapid gastric lavage is advised.
2. Mouth and pharyngeal secretions are removed by suction.
3. For removal of secretions and maintenance of patient's airway,
place the patient in a proper position. .
4. Endotracheal intubation is necessary for proper respiration.
5. If the body is soiled with insectides, remove clothes and give
medicated bath.
6. Drug treatment
a. Atropine sulphate 2 to 4 mg initially up to 50 mg
parenterally to block all secretions.
b. Enzyme reactivators such as pralidoxamine (2-PAM) I to
2 gm by slow IV injection.
C. Convulsions may be controlled by injecting trimethadione
I gm after every 15 minutes.
Parasympatholytics/anticholinergics/cholinergic
antagonists
Definition
The drugs by stimulation of
urugs which block the actions produced
sym parasympatholytics.
pathetic nervous system are called

96 Pharmacology and 1Oxicology
.Classification
1. Belladonna alkaloids: Atropine, hyoscine (scopolamine
2. Semisynthetic derivative: Homatropine, ipratropine bromid
3. Synthetic compounds: Propantheline, oxyphenonium, dieu
clomine, cyclopentolate. y-
8. Atropine
It is an alkaloid obtained from "Atropa belladonna'".
1. On GIT: Atropine reduces tone, motility or peristalsis
of GIr
and produces constipation.
2. On CVS: In larger doses, atropine increases heart rate
(tachycardia).
3. Urinary tract: Atropine reduces the movements of ureters
and urinary bladder and tends to produce urinary retention.
4. On CNS: In larger doses, atropine produces marked
CNs
stimulation which may cause restlessness, irritability
disorientation.
5. On eye: Atropine has two primary effects on the
eye, i.e.
mydriasis (dilation of pupil) and cycloplegia (paralysis
of
accommodation).
6. On secretions: Atropine reduces all exocrine secretions
including lacrimal, salivary, gastric, intestinal, laryngeal,
pharyngeal and causes dryness of mouth and intense thirst.
Hence also called antisecretory agent.
On local instillation, atropine produces mydriasis
by
blocking the cholinergic nerve supply. The ciliary
muscles of
the eye are likewise paralysed by atropine which causes
increase in focal length of the lens. Thus individual
can see
the things only at long distance. This is termed as "cycloplegia"
As the muscles of sphincter of iris are paralysed, individual
cannot constrict the pupil in response to bright light. Because
of mydriasis and cycloplegia, person fails to
respond to brignt
light, this is known as "photophobia".
Adverse Effects of Atropine

1. Dryness of mouth and intense thirst.
2. Blurring of vision (photophobia)

Drugs Acting on ANS
97
Constipation.
3. swallowing. hpe
Difficulty in
Retention of urine.
5. itation, tachycardia.
Palpitati 221e3
6.
Hyperpyrexia.
7. Dermatitis.
8.
TherapeuticUses of Atropine
1. As antispasmodics.
peptic ulcer.
2. In
3. As a preanaesthetic medication.
4, mydriasis and cycloplegia.bhto
To produce 1
5. In myasthenia graVIS
along with neostigmine.
organophosphorus poisoning.
6. In
7. In
parkinsonism.
8. In motionsickness.
9. In myocardial
infarction.
Belladonna Poisoning
9.Acute Atropine Poisoning/Acute
overdosing of atropine
The poisoning with atropine is caused due to
during treatment or ingestion of
leaves or seeds of belladonna.
Signs and Symptoms

1. DrynesS of mouth
2. Mydriasis
3. Blurring of vision and

photophobia
4. Urinary retention
5. Hyperpyrexia
6. Restlessness
7. Slurring of speech
8. Intense thirst
9. Difficulty in swallowing
10. Mania and delirium
Treatments
by mouth, to remove the poison gastric
1.
If the poisoning is
lavage is advised. photophobia.
room is given to the patient to relieve
2.Dark management of urinary
retention.
Catheterisation is advised for

98
To treat hyperpyrexia ice cold
sponging is advised.
4.
Artificial respiration is advised.
5. diazepam is given.
6. To treat delirium and restlessness,
7. Good nursing care is essential.
8. Alkaloidal inactivators such as universal antidotes are given
before and after gastric lavage.
9. Physostigmine (14 mg) is given intravenously as it rapid
blocks the central effects of atropine.
Questions
Define cholinergics and classify with examples. (S. 96, 02,

1.
09; W. 05, 07)
2. Give the signs, symptonms and treatments of organophosphorus
poisoning. (S. 08)
3. What is myasthenia gravis? Suggest drugs used in myasthenia
gravis. (W. 04)
4. Define anticholinergics and classify parasympatholytic drugs
with examples. (S. 97)
5. Mention the symptoms and treatment of atropine poisoning.
(S. 03, 05, 09; W. 96, 02)
6. Describe drug treatment of glaucoma. (S. 98)
7. Write a note on antispasmodics (S. 98)
8. Write a note on mydriatics. (W. 98)
9. Write a note on atropine substitutes. (S. 00)
10. Give pharmacological actions and uses of atropine. (S. 03)
11. Define and classify adrenergics with examples. (S. 99; W. 96,
98, 06)
12. What is meant by a Dale's vasomotor reversal'? (S.
00, 04,
05, 06, 09; W. 02)
13. Discuss the mechanism of action and therapeutic uses
of
adrenaline. (S. 01; W. 03)
14. Give therapeutic uses and adverse
effects of ephedrine.
(W. 02)
15. Define sympatholytics/antiadrenergics.
Classify with examples.
(S. 08)
16. Write a note on B-adrenergic blockers.
(S. 00, 01, 02, 04; W.
00, 01, 02, 05)

CHAPTER 22
Neuromuscular Blockers/
Skeletal Muscle Relaxants
Definition
The drugs that block transmission of nerve impulses at the skeletal

aeuromuscular junction and cause skeletal muscle relaxation are
called neuromuscular blocking agents.
Classification
1. Nondepolarising blockers, e.g. d-tubocurarine, gallamine.
2. Depolarising blockers, e.g. succinylcholine, decamethonium.
3. Dual action blockers, e.g. benzoquinonium.
Questions
relaxants with
1. Classify neuromuscular blockers/skeletal muscle
examples. (S. 98, 00, 03; W. 98, 99)

CHAPTER 23
Mydriatics and Miotics
1 Mydriatics
The drugs which produce dilation of pupils are called mydriatics
e8. adrenaline, ephedrine, cocaine, atropine, homatropine.
Mechanism
When mydriatics are instilled in eye, it causes relaxation of circular
muscle fibres and causes tightening of radial muscles fibres. This
causes flattening of lens known as mydriasis.
Because of mydriasis, the focal length is also increased which fixes
the sight for far vision, i.e. person can see the objects which are
long distance but fails to see the near objects. This is known as
at
cycloplegia.
Therapeutic Applications of Mydriatics

1. To produce mydriasis.
2. For ophthalmological examinations.
2 Miotics
The drugs which produce constriction of pupils are called miotics,
e.g. acetylcholine, pilocarpine, carbachol, physostigmine.
Mechanism
When miotics are instilled in eye, it causes contraction of circular
muscle fibres and relaxation of radial muscle fibres.
This causes marked reduction in size of pupil which is referred as
miosis. Because of miosis, focal length of pupil is also reduced. Thus
100

Mydriatics and Miotics 101
he things which are near but fails to observe the

see the
erson can
Pers at This is known as paralysis of accommodation.
Pc
thingsat
long
long distance.
Therapeutic Applications of Miotics
1. To treat glaucoma.
. To break adhesion between
iris and lens.
To control mydriasis and cycloplegia produced by atropine.
3.
Glaucoma and its Treatment

3 disease in which intraocular pressure is
Glaucoma is an ocular
nerve producing visual loss.
increased and causes damage to optic
The damage to optic
nerve and visual loss is probably due to
ischaemia (deficient blood supply to
any part of the body) and may
pressure on nerve. Glaucoma is a major cause of
he due to direct
age.
blindness in persons over 40 years of
There are two major types:
i. Open angle glaucoma
ii. Narrow angle glaucoma.
Drugs used in Glaucoma

physostigmine.
1.Miotics: Pilocarpine, carbachol,
pilocarpine mixture.
2. Adrenergic agents: Adrenaline and
3. p-adrenergic blockers: Timolol.
Acetazolamide.
4. Carbonic anhydrase inhibitor:
5. Osmotic agents: Mannitol.
Questions
1. Write a note on mydriatics. (W. 98)
glaucoma.
2. What is glaucoma? Describe drug treatment of
S. 98)

CHAPTER 24
Cardiovascular Agents
1 Definition
The drugs which are used in the treatment

of various cardio-
vascular disorders are called CVS
agents.
2 Classification of Cardiovascular
Agents
a. Cardiotonics, e.g. digoxin,
oubain, strophanthin.
b. Antiarrhythmics, e.g. quinidine,
procainamide
c. Antianginals, e.g. ethylnitrite,
glyceryl trinitrite,
d. Antihypertensives, e.g. clonidine, amylnitrite
e. Lipid lowering agents,
reserpine, methyldopa.
e.g. clofibrate, nicotinic
acid.
3 Cardiotonics
The drugs which increase
the activity of heart
are called cardiotonics.
Digitalis
Mechanism of action: The Ca** is essential
contractility. Digitalis inhibits sodium-potassiumfor myocardial
entry of Na* into the pump and Ises
cell. This extracellular
the intracellular K*. Na* exchanges
for
Due to exchange
intracellular Ca** concentration between Na and
Tses. Digitalis K", the
stores in the cells also Tses the Ca
and due to Ca**,
Tses myocardial
contractility.
Intracellular
fluid
Extracellular
fluid
Na
K
Ca
-Cardiac muscle
102

Cardiovascular Agents
103
.Pharmacological actions of digitalis
1. Myocardial contractility:
Digitalis increases
systolic contraction of the the force of
heart muscles.
2. Heart rate: Digitalis produces decrease
vagus stimulation. in heart rate by
3. Conduction velocity: Digitalis
velocity.
increases conduction
4. Automaticity: Digitalis increases
the automaticity of
ventricular muscles.
5. BP: Digitalis increases the mean
arterial pressure.
6. Refractory period: Digitalis
prolongs the functional
refractory period of AV node.
7. Digitalis and calcium: Calcium ions
increase the force of
contraction of heart. Excessive Cat* ion concentration
leads
to cardiac arrest in systole. Digitalis acts synergistically
with calcium. Hence digitalis toxicity can be enhanced by
calcium.
Adverse effects of digitalis
1. GIT toxicity: Anorexia, vomiting, diarrhoea.
2. Cardiac toxicity: Cardiac arrhythmia, ventricular tachycar-
dia, ventricular fibrillation.
3. Hypokalemia (Jse K* level in blood)
4. Neurological toxicity: Headache, visual disturbances like
appearance of dancing and flickering dots and disturbance
of colour vision.
5. Miscellaneous toxicity: Skin rash, digitalis can cross
placental barrier and may lead to premature delivery.
Preparation and dose: Digoxin tablets IP
Dose: 0.25 mg once or twice daily.
Trade name: Lanoxin.
Therapeutic uses (Indications): Digitalis is indicated in:

1. Congestive heart failure
2. Left ventricular failure
3. Atrial fibrillation
4. Atrial flutter.

4 Antlarrhythmic Agents
Definition
The drugs which are used to prevent cardiac
arrhythmia are
antiarrhythmic agents. called
Classification
1. Drugs that depress myocardium:
Quinidine, procainamide
2. Calcium channel blockers: Verapamil,
nifedipine.
3. Digitalis.
4. Sympatholytics: Propranolol.
5 Quinidine
It is an alkaloid obtained from
cinchona bark.
Pharmacological actions
1. Automaticity: Quinidine
depresses the automaticity.
2. Excitability: Quinidine
depresses excitability
tissue. of cardiac
3. Refractory period:
Quinidine prolongs
4. Conduction velocity: the refractory period.
Quinidine decreases
velocity in all cardiac tissues. conduction
5. AV conduction:
Quinidine depresses the myocardial
contractility.
Adverse effects
1. Cardiac
toxicity: Bradycardia,
ventricular fibrillation. conduction block,
2. Embolic phenomenon:
Formation of emboli
into the circulation. or thrombus
3. Hypotension:
Quinidine produces
doses. hypotension in larger
Preparation: Quinidine
Dose: 200 to sulphate tablet
400 mg every or capsule IP.
6 hrs.
Therapeutic uses
(Indications):
following conditions: Quinidine is indicated
in the
1. Atrial fibrillation
2. Atrial flutter
3. Ventricular fibrillation
4. Ventricular flutter

Cardiovascular Agents 105
Antianginal Agents
6
Definition
whic are used in the treatment
drugswhich of angina pectoris are
The
agents.
called antianginal
.Classification
1. Organic nitrates
a. Short acting: Glyceryl trinitrate
b. Long acting: Isosorbide dinitrate, isosorbide trinitrate,
pentaerythritol tetranitrate.
2. Calcium channel blockers: Verapamil, nifedipine.
3. B-blockers: Propranolol, labetalol
4. Miscellaneous: Papaverine, oxyphendrine.
Write a note on calcium channel blockers.

The drugs which block the calcium entry into the myocardium are
called calcium channel blockers.
Calcium is necessary for the excitation and contraction in both
skeletal and smooth muscle. The contractility of skeletal, cardiac and
vascular muscle is highly dependant on the extracellular calcium
concentration.
The calcium channel blockers act by interfering with calcium entry
into the myocardium and thus decreasing the availability of
intracellular Ca**. Due to this, there is a decrease in myocardial
contractility.
Calcium channel blockers are useful in angina pectoris because of
following reasons:
i. Decrease inmyocardial contractility
i. Decrease in oxygen consumption
1. Decrease preload to neart
. Increase inin coronary blood flow due to dilation of coronary
blood vessels.
Preparations
1.Verapamil tablet IP.
Dose: 240 to 480 mg/day orally.
Trade name: Cardilox
2. Nifedipine tablet IP.
Dose: 10 mg 8 hourly
Tradename: Calciguard.

8 Antihypertensives
The drugs which reduce elevated blood pressure to normallevel
levat
called antihypertensives. are
.Classification
1. Centrally acting, e.g. clonidine, d-methyldopa.
2. Catecholamine depleter, e.g. reserpine
3. Adrenergic receptor blockers, e.g. propranolol,
metoprolat
4. Adrenergic neuron blocker, e.g. guanethidine.
5. Ganglionic blockers, e.g. mecamylamine.
6. Diuretics, e.g. chlorthiazide, frusemide.
7. Calcium channel blockers, e.g. verapamil.
8. Vasodialators, e.g. hydrallazine.
9 Drugs used in Arteriosclerosis (Lipid

Lowering Agents)
(Antihyperipidaemic Agents)
.Hyperlipidaemia: It means an increased
blood level of
triglycerides.
Arteriosclerosis: It means hardening
of blood vessels due to
hyperlipidaemia. In this case, there
is a deposition of
material in the inner walls of arteries. lipid
This may lead to coronary
thrombosis and myocardial infarction.
.Lipid lowering agents: The drugs which lower
the blood are known as lipid lowering lipid level in
agents, e.g. clofibrate,
nicotinic acid.
.Clofibrate: It is useful in long-term
treatment of hyperlipid-
aemias.
It inhibits cholesterol synthesis.
Dose: 2 gm daily in 4 divided
doses.
Trade name: Atromid-S
.Nicotinic acid
Dose: 1.5 gm to 8 gm/day
Trade name: Niacin.
Questions
1. Define cardiac glycosides.
How does digitalis act in
Mention adverse effects of digitalis. CCF
(S. 05, 07; W. 04, 07)

Cardiovascular Agents 107
(S. 99, 06)

2. Explain the mechanism of action of digitalis.
the drug 'digexin' give the following information: (S. 99,06)
3. For
i. Main therapeutic uses
ii. Major undesirable effects
antiarrhythmic agents and classify them with examples.
4. Define
(S. 99; W. 96, 00, 02, 05)
pharmacological actions of quinidine. (S. 02; W. 08)
5. Discuss
is angina pectoris? Classify antianginal drugs with
6. What
examples. (S. 97; W. 07)
pectoris. (S. 03)
7. Write the treatment of angina
classify antihypertensive agents according to site
8. Define and
01; W. 03, 05, 08)
of action. (S. 96, 00, atherosclerosis. (W. 03)
9. Describe drugs used in clofibrate.
pharmacological actions and uses of
10. Write down
(W. 04)

||CHAPTER 25||
DiuretiCS
1 Definition
The drugs which increase formation and excretion of
urine are
called diuretics.
Classification
1. Weak diuretics
a. Osmotic diuretics, e.g.
mannitol, urea.
b. Carbonic anhydrase inhibitor,
e.g. acetazolamide
2. Moderately potent diuretics,
e.g. chlorthiazide, hydro-
chlorthiazides (thiazides).
3. Very potenthigh ceiling/loop
diuretics, e.g. organic
Mercaptomerin, mersalyl, mercurials:
frusemide, ethacrynic
4. Potassium sparing acid.
diuretics, e.g. spironolactone,
triameterene. amiloride,
5. Xanthine diuretics,
e.g. caffeine, theophylline.
6. Acid forming salt,
e.g. ammonium
chloride.
2 Indications of Diuretic
Uses) Therapy (Therapeutic/Clinical
Diuretics are indicated in
1. In edema the following conditions:
2. In hypertension
3. In congestive
heart failure
4. In chronic renal
failure
5. In glaucoma
6. In diabetes insipidus
7. In salicylate and barbiturate
poisoning
108

Diuretics 109
cerebraledema
8.In pregnancy.
9. In edema of
Antidiuretics
3 The drugs
which prevent the process of formation of urine aree
led antidiuretics. For example, antidiuretic hormone (ADH)
callea
(vasopressin)
Orhers: Chlorpropamide, clofibrate, carbamazepine.
Acetazolamide
4
Acetazolamide is a sulphonamide with a limited use as a diuretic.
Mechanism of Action
enzyme carbonic anhydrase is present in the renal cortex,
gastric
The
mucosa and pancreas, CNS, RBCs, etc.
This enzyme catalyses the following reaction:
CO,+ H0 > H,CO, (carbonic acid)
This enzyme plays important role in the tubular
reabsorption of
sodium and bicarbonate by providing carbonic
acid which makes H*
ions available for exchange with sodium.
HCO3 =H+HCO,
Acetazolamide inhibits this enzyme by noncompetitive mechanism
so that hydrogen ion is not available for sodium
exchange leading to
excretion of sodium along with water, 1.e. diuresis.
5 Organic Mercurial Diuretics

Organic mercurial compounds act as diuretics, e.g. mersalyl,
mercaptomerin.
Mechanism of Action
mercurials act directly at various sites in the nephron. They

nic
nhibit the intracellular enzyme and thus depress the reabsorption of
Na' and C
causing diuresis.
The internal release
of divalent mercury ion (Hg*) is responsible
or causing diuretic
action.
mercurial ion (Hg") has affinity for sulphidryl group of
hbs
tubular enzymes.

The mercurial ions react with sulphidry

group of enzyme
yme
responsible for tubular reabsorption of Na
As sulphidryl group from the enzyme
1S made inactive,
th
reabsorption of Na* decreases and thus causes diuresis.
Questions
1. Define and classify diuretics with suitable examples. (S. 00
07; W. 98, 04)
2. Explain the therapeutic uses/clinical uses of diuretics. (S. 99
05, 06, 08; W. 07)
3. Give the contraindications of diuretics. (W. 99)
4. What are diuretics? Describe carbonic anhydrase inhibitor
(S. 07; W. 04)
5. Discuss the mechanism of action of acetazolamide. (W. 01)
6. Mention therapeutic uses of thiazide diuretics. (S. O0; W. 98)

CHAPTER 26||
Chemotherapy
Definition
1. Chemotherapy: Chemotherapy is defined as use of chemical

compounds in the treatment of infectious disease so as to
destroy microorganisms without damaging host tissue.
2. Chemotherapeutic agents: The agents which destroy or
inhibit the growth of microorganisms without damaging host
tissue, are known as chemotherapeutic agents.
3. Chemotherapeutic index: It is the ratio of maximum tolerated
dose of a dug to its minimum curative dose.
tolerated dose
Chemotherapeutic index =maximum
minimum curative dose
4. Bacteriocidals: The agents which kill or destroy the micro-
organisms are called bacteriocidal agents.
5. Bacteriostatics: The agents which stop or prevent growth of
microorganisms are called bacteriostatics.
A Sulphonamides
1. Definition
The antimicrobial compounds containing sulphonamide group

-SO,NH) are called sulphonamides.
Classification
1. For systemic use:
a. Short àcting suphonamides, e.g. sulphadiazine, sulpha
cetamide, sulphadimidine.
b. Intermediate acting sulphonamides, e.g. sulphamethoxa-
zole.
111

c. Long acting sulphonamides, e.g. sulphamethoy

Pyridazine.
y-
2. For GIT infection, e.g. sulphaguanidine, succinyl sulnho
pha-
thiazole, sulphasalazine, pthalyl sulphathiazole.
2. Mechanism of Action of Sulphonamides

i. Sulphonamide has structural similarity to p-aminobenzoic
acid (PABA).
i. Hence it competes with PABA in bacterial metabolism.
ii. Folic acid derived from PABA is important in bacterial
metabolism.
iv. Sulphonamide inhibits the enzyme folic acid synthetase
which is useful for conversion of PABA into folic acid.
v. This causes folic acid deficiency resulting in injury to the
bacterial cell.
vi. Such injured cells can be phagocytosed easily.d
PABA
Sulphonamides Folic acid synthetase enzyme
Folic acid
Dihydrofolic acid
Tetrahydrofolic acid
Bacterial metabolism
roi1ot1
3. Adverse Effects (Toxic Effects) of
Sulphonamides
i. Intolerance: Skin rash, toxic
hepatitis, toxic nephritis, acute
haemolytic anemia.
ii. Urinary toxicity: Renal irritation,
obstruction in urine flow,
haematuria, albiminuria, crystalluria.
ii. Haemopoietic system: Aplastic anemia, agranulocytosis,
intravascular hemolysis.

Chemotherapy 113
TherapeuticUses of Sulphonamides
4. 7
In urinary tract infections
ii. In acute bacillary dysentery
GIT infection
ii. In influenza
iv. In
v. In meningitis
vi. In meningococcal meningitis
conjunctivitis
vii. In
rheumatoid arthritis.
vii. In
B Antibiotics
1.
Definition
microorga-
Antibiotics are the chemical substances produced by
s
nisms having the property of inhibiting
the growth or destroying the
microorganisms in high dilution.
.Classification
e.g.
1. Antibiotics mainly
effective against gram +ve bacteria,
erythromycin.
penicillins, ampicillin, bacitracin,
mainly effective against gram-ve bacteria, e.g.
2. Antibiotics cycloserine.
streptomycin, gentamicin, -ve
effective against both gram +ve and gram
3. Antibiotics e.g.
rickettsiae and chlamydia species,
bacteria and also amoxycillin, cephalospor-
tetracyclines,
chloramphenicol,
are
spectrum of activity antibiotics
ins. According
to
grouped as follows: The antibiotics
which
spectrum antibiotics:
a. Narrow bacteria or
effective either on gram +ve
are selectively
certain fungi or yeast are called
gram-ve bacteria or e.g. benzyl
penicillin,
antibiotics,
narrow spectrum
erythromycin, vancomycin. antibiotics which are
antibiotics: The
b. Broad spectrum pathogens, not only gram
number of
effective on a large also affect the intracel-
bacteria but chlamydia
+ve and gram -ve viruses and rickettsiae,
lular organisms
like antibiotics, e.g. tetra-
broad spectrum
species, are called streptomycin, amoxycillin.
chloramphenicol,
cyclines,
2. Penicillins
Penicillin was discovered in 1929 by Alexander Fleming in i

England. It is extracted from the mould Penicillium notatumand
Penicillum chrysogenum.
.Classification
1. Natural penicillins, e-g. benzyl penicilin, phenoxymethyl
penicillin.
2. Penicillinase resistant penicillins, e.g. cloxacillins, OXa.
cillin, methicillin.
3. Broad spectrum penicillins, e.g. ampicillin, amoxycillin.
4. Penicillins active against pseudomonas, e.g. carbencillin,
Mechanism of action of penicillins: Penicillin is bactericidal
in action. It is effective mainly against multiplying organisms.
Penicillins act by interfering with synthesis of bacterial cell
wall. This makes the cell membrane of the organism possible to
damage by solutes in the surrounding medium.
As the cell wall synthesis occurs during the growth phase,
the antibiotic is most effective against actively multiplying orga-
nisms. The cell walls of gram -ve bacilli are chemically more
complex. These cell walls contain B-lactamases in small amounts
that are enough to inactivate penicillin.
Adverse effects of penicillins
i. Intolerance: It involves anaphylactic shock, idiosyncrasy
and allergic reactiors.
ii. Superinfection.
ii. Hyperkalemia: On administration of potassium salts of
penicillins.
iv. Hypertension, palpitation, auditory
and visual disturbance,
headache.
v. Renal complications like
haematuria, albuminuria.
vi. Thrombocytopenia, drug fever,
eosinophillia, asthma, skin
rash.
.Test for detection of penicillin allergy
A small quantity of penicillin
solution containing 10,000
units/ml is injected intradermally.
If a central wheal due to local edema occurs
after 15 minutes
it is considered as a positive reaction for
penicillin allergy.

Chemotherapy 115
Therapeutic uses of penicillin
:To treat pneumococcal infections
ii, To treat streptococcal infections
treat stapnyiococcal infections
ii. To
iv. To treat meningococcal infections
V. To treat syphillis and gonorthoea
vi. To treat actinomycosis
vii. 1o reat anthraxX
vii. To treat diphtheria, tetanus
ix. To treat rheumatic fever
x. To treat agranulocytosis.
Aminoglycoside Antibiotics
3.
Aminoglycoside antibiotics are the amino sugars with glycosidic
inkage
They are highly effective against gram -ve
bacteria, e.g.
steptomycin, gentamicin, kanamycin, tobramycin, neomycin.
Write a note on "streptomycin'".
It is obtained from Streptomyces griseus.
Mechanism of action of streptomycin
- The ribosomes prepare enzymes under the directions from
messengers RNA (mRNA).
- Streptomycin combines with bacterial ribosomes and inter-
feres with mRNA ribosome combination and destroys the
bacterial cell.
- According to another hypothesis streptomycin induces the
ribosomes to manufacture peptide chains with wrong amino
acids which ultimately destroy the bacterial cell.
Adverse effects
1. Ototoxicity: Streptomycin causes damage to 8th cranial
nerve (auditory nerve). Thus causes deafness.
2. Nephrotoxicity: Renal irritation, albuminuria.
3. Superinfection:
Development of secondary infection during
the course of primary infection.
4. Intolerance: Skin rash, eosinophillia, dermatitis, pericardi-
tis.
.Oraly it may cause nausea, vomiting.

.Therapeutic uses: Streptomycin is used in the treatment

of
Tuberculosis
1.
2. Plague
3. Urinary tract infection
4. Meningitis due to H.
influenzae
5. Bacteremia
6. Endocarditis
7. Respiratory tract infection
8. Gonorrhoea
9. Brucellosis.
mg intramuscu.
Preparation: Streptomycin injection U.-z00 IsCu-
larly per day.
4. Macrolide Antibiotics
Macroides: Macrolides consist of a large latone ring to which

sugars are attached, e.g. erythromycin, oleandomycin, spiramycin
lincomycin, roxithromycin.
Erythromycin: It is a macrolide antibiotic.
Mechanism of action: It inhibits protein synthesis at 50S
ribosomal level.
Adverse effects
Allergic reactions such as fever, eosinophillia, skin eruptions
1.
2. Obstructive jaundice
3. Epigastric distress
4. Nausea, vomiting
5. Hepatitis.
Therapeutic uses
1. In
respiratory tract infections (whooping cough)
2. Sinusitis
3. Alternative to penicillin hypersensitive
patients.
.Preparation: Erythromycin tablet 250-500 mg orally.
Trade name: Althrocin.
5. Tetracyclines
Tetracyclines are broad spectrum antibiotics and are naphthalene

derivative.
Mechanism of action
Tetracyclines act by inhibiting
u
-
certain enzyme system ofthe

bacterial cell.

hemotherapy 117
also suppress the synthesis of proteins in the micro-

They also
-
organisms.
Tetracyclines form complexes with certain cations like
calcium and magnesium which are essential for the functional
activity of various enzyme systems and ribosomes.
Thus, tetracycines are Dacteriostatic in action.
In higher concentrations or parenteral administration
tetracyclines may exert a bactericidal effect.
tetracyclines
Adverse effects of
1, On oral administration,
it causes nausea, vomiting,
epigastric distress, looSe stools.
2, Intolerance:
Pigmentation of teeth, a brown black colouration
dyscrasis.
of teeth and nails, skin rash, dermatitis, blood
3. Superinfection: Suppress of
normal intestinal flora with
resultant superinfection after prolonged tetracycline
therapy
4. Livertoxicity: Pancreatitis, fatty generation of liver, jaundice.
5. Toxicity on bones and teeth (defective bones and teeth)
Tetracycline chelates with calcium and, therefore,
teeth.
deposited in the areas of calcification in bones and
Administration of tetracycline to pregnant women may
the infant,
lead to yellow staining of the teeth of
teeth
defective formation of enamel and hypoplasia of
may also Occur.
may
Pigmentation of teeth and increased risk of caries
short-term therapy
occur in children receiving a long or
tetracyclines should be avoided
of tetracyclines. Hence
in infants and in children
up to the age of 12 years.
are
Tetracyclines administered during pregnancy.
a linear grôwt
n nodeposited in foetal bones and may reduce
damage to the bbnes
of the foetus. However to prevent
tetracyclines should be
and teeth in the growing foetus,
pregnancy.
avoided after fourth month of
and
Tetracyclines are also deposited in the nails
fluorescence of nail may be demonstrated after
prolonged tetracycine therapy.
Preparation: Tetracycline HCl capsule.
Dose: I to 3 gm daily in divided doses.
SE.
Trade name: Tetracyn, Resteclin, Terramycin

Therapeutic uses of tetracyclines

1. In rickettsieal infection
2. In plague
3. In cholera
4. In chlamydia infection
5. In bacillary infection
toit6. In urinary tract infection
7. In veneral diseasesS
8. In pneumonia
9. In respiratory tract infections.
i197bA
6. Chloramphenicol
Chloramphenicol is a broad spectrum antibiotic originally de-
rived from Streptomyces venezuelae.
Mechanism of action: It inhibits protein synthesis at 50S
ribosomal level. Thus acts as a bacteriostatic.
Adverse etfects
1. Intolerance: Skin rash,
dermatitis, haemorrhages.
2. Bone marrow toxicity
i. Bone marrow depression
ii. Thrombocytopenia
is. Agranulocytosis
iv. Aplastic anemia
v. Cyanosis
Vi. Gray baby
syndrome
3. Superinfection
4. Nausea, vomiting, diarrhoea
5. Headache, mental confusion,
peripheral neuritis, delirium.
Preparation
1. Chloramphenicol capsule
1.5 to 3 gm daily chloromycetin
in divided doses.
2. Chloramphenicol palmitate
(suspension) 125 mg/ml for
paediatric use 50 mg/kg/day.
.Therapeuticuses: Chloramphenicol
is used to treat:
i. Typhoid and paratyphoid
11.
fever
Meningitis
ii. Urinary tract infection
iv. Infection of eye
and ear
ineg1
v. In plague

Chemotherapy 119
vi. Ricketsiae infection

vii. Chlamydia infection
.vii. Intracranial bacterial infection.
Write a note on "gray baby syndrome".
It is a dangerous complication of chloramphenicol therapy.
It is observed in infants and neonates.
It develops when the dose of chloramphenicol is allowed to
exceed 100 mg/kg body weight/day.
The clinical manifestations appear within 2 to 9 days following
chloramphenicol.
first dose of
The initial signs and symptoms are:
i. Vomiting
ii. Letharg
ii. Anorex1a
iv. Abdominal distension
v.Irregular respiration
vi. Shock
After 24 hrs, the condition changes and produces:
i. Hypothermia
ii. Peripheral vascular collapse
11. Gray cyanosis
iv. Shock and finally death.
The factors responsible for this
type of complication by chloram-
phenicol are:
i. In neonates and intants, the liver
enzymes are not fully developed
glucuronic acid conjugation.
to metabolize the drug by
ii. Immaturity of the renal tubules
in the infant leads to disturbance
hence it accumulates in the
in excretion of chloramphenicol
body and produces toxicity.
C Urinary Antiseptics tract infec-

The drugs which are used in the treatment of urinary
tion are called urinary antiseptics.
bladder
drugs have localised action in the kidney, urinary
HSe
and ureters. So they are called urinary antiseptics.
i. Nalidixic acid
ii. Methenamine
ii. Nitrofurantoin

iv. Furazolidine
v. Oxalinic acid
vi. Ciprofloxacin
D Antitubercular Agents
FTuberculosis is a diseascaused by an organism Mycobacterium
tuberculosis.
1. Antitubercular Agents
The drugs which are used in the treatment of tuberculosis are called
antitubercular drugs.
Classification
1. Standard drugs/primary drugs/first line drugs, e.g. isoniazid
(INH), rifampicin (R), ethambutol (E), streptomycin (S),
Pyrazinamide (Z), p-amino salicylic acid (PAS), Thiaceta-
Zone.
2. Reserve drugs/secondary drugs/second line drugs, e.g.
kanamycin (K), capreomycin (A), cycloserine (C).
2. Isoniazid (lso-nicotinic Acid Hydrazide) (NH)

It is most effective and cheapest antitubercular agent.
Mechanism of action: Isoniazid inhibits the enzymes essential
for synthesis of mycobacterial cell walls.
Isoniazid inhibits phospholipid synthesis and damages the
membrane of tubercle bacilli. Intracellular and extracellular
chelation of divalent cations essential for bacterial metabolism
is another possible mechanism of action.
INH suppresses the formation of DNA
and RNA and also
inhibits various oxidative mechanisms.
Adverse effects of isoniazid
1. Peripheral neuritis,
hepatotoxicity, anaemia
2. Convulsions, loss of memory,
loss of self-control.
Preparation of antitubercular drugs
1. Isoniazid tablet IP 200 to 300 mg daily Isokin,
in a single dose Isonex
2. Rifampicin tablet IP 10 mg/kg
dailyt Rifamycin

Chemotherapy
121
Ethambutol tablet IP 25 mg/kg for
3. 8 to 12 weeks
E-tibi,
Mycobutol
ACycloserine tablet BP 0.5 to 2 gm daily
cyclorine
in divided doses
Therapeutic uses
1, In the treatment of tuberculosis
2. In the treátment of meningitis.
EAntileprotic Agents
Definition
1.
Leprosy is caused by an organism Mycobacterium leprae.

Antileprotic agents: The drugs which are used in the treatment
of leprosy are called antileprotic agents.
Classification of antileprotics
1. Sulphones, e.g. dapsone (DDS), solapsone.
2. Phenazine derivative, e.g. clofazimine
rifampicin, ethionamide
3. Antitubercular drugs, e.g.
e.g. sulphadoxine.
4. Long-acting sulphonamides,
2. Dapsone
sulphone. It is a drug of choice in leprosy.
a diaminodiphenyl
Itis bacteriostatic as well as
Mechanism of action: Dapsone is a derived from PABA is
bacteriocidal in activity. Folic acid
Dapsone inhibits the enzyme
important in bacterial metabolism.
involved in the synthesis of folic
folic acid synthetase, which is
a antibacterial agent.
acid from PABA and acts as
PABA
enzyme
Folic acid synthetase
Dapsone ************
Folic acid
Precursor
Folinic acid
Nucleotidese

Adverse effects of dapsone

. Anorexia, nausea and vomiting
2. Allergic reactions: Dermatitis, drug fever
3. Haematuria, methaemoglobinemia, liver damage
Preparations of antileprotic drugs
1.Dapsone tablet IP 100 mg daily Novaphane
.
2. Clofazimine tablet 100 to 300 mg daily Lamprene
3. Rifampicin tablet 600 mg orally Rifadin
once a day 12A
FAntimalarials
Malaria
It is caused by parasitic protozoa of the genus Plasmodium which
includes four types:
Plasmodium vivax
Plasmodium falciparum
Plasmodium ovale
Plasmodium malariae
1. Antimalarials
The drugs which are used in the

treatment of malaria are called
antimalarials.
Classification
1. Cinchona alkaloids, e.g.
quinine
2. 4-aminoquinolines, e.g.
chloroquine, amodiaquine
3. 8-aminoquinolines, e.g.
primaquine
4. Acridine, e.g. mepacrine
5. Biguanides, e.g. proguanil
6. Diamino pyrimidines,
e.g. pyrimethamine.
7. Quinoline methanol,
e.g. mefloquine
8. Miscellaneous, e.g.
sulphonamides, tetracyclines
2. Quinine
It is an alkaloid obtained
from
cinchona bark.
Mechanism of action: Quinine
useful as a suppressive. is schizonticidal and,
therefore

Chemotherapy 123
Ouinine has been termed as a general protoplasmic
deoresses the vanety ot enzymatic processes poison.
w depr and reduces ciliary
It
tivity and inhibits phagocytosis and growth of fibroblasts.
activity
Adverse effects
1.Cinchonism
2. Black water fever
3. Nephrotoxicity
4. Ringing in ears
5. Blumng of vision
6. Nausea, vomiting
7. Disturbances of colour vision
8. Acute renal damage
9. Ventricular arrhythmia
10. Deafness.
. Therapeutic uses
pi. In malaria e
ii. In cramps
Preparation: Quinine hydrochloride tablets IP
Dose: 300 to 600 mg daly
Trade name: Vigo-tablet, Fluo-foe.
3. Chloroquine
It is a dng of choice in malaria.

Chloroquine is superior to quinine and mepacrine.
Mechanism of action: Chloroquine acts by inhibiting the
incorporation of phosphate into RNA and DNA of plasmodia.
Adverse reaction
1. Skin rash, dermatitis, photosensitivity
2. Retinopathy Ahore AeoneoinA
3. Muscular degeneration
4. Hypotension by IV use of chloroquine
Uses of chloroquine
1. In malaria
2. Hepatic amoebiasis
3. Giardiasis
4. Taeniasis nop org out

5. Rheumatoid arthritis loilteun/
6. To control lepra reactions
Scanned With camscanner

Preparation: Chloroquine phosphate tablet P.

Dose: gm followed by 0.5 gm after 6 hrs.
1
Trade name: Resochin, Nivaquin, M-quin.
G Antifungal Agents
Fungal infections
1. Candidiasis
2. Blastomycosis
3. Cryptococcosis
4. Dermatophytic infections of skin, hair, nails.
.Antifungal agents: The drugs which are used in the treatment
of fungal infections are called antifungal agents.
Classification
1.Topical antifungal agents: Nystatin, tolnaftate,
hamycin
2. Systemic antifungal agents: Griseofulvin, amphotericin-B
3. Official fatty acid: Undecylenic
acid.
HAntiviral Agents
The drugs which are used in the treatment
of viral infections are
called antiviral agents.
Classification
1.Drugs interfering with nucleic
acid synthesis, e.g. idoxu-
ridine, ribavirin, acyclovir.
2. Thiosemicarbazones,
e.g. methisazone
3. Natural subs., e.g.
interferon
4. Miscellaneous, e.g.
amantidine.
Anticancer/Antitumor/Antineoplastic/Antimalignan
Cytotoxic Agents
The drugs which are
used in the treatment
anticancer agents.
Classification
of cancer are
aalled
1. Alkylating agents,
e.g.
phamide, melphalan, chlorambucil, busulphan, cycio s-
2. Antimetabolites, nitrogen mustards.
e.g. methotrexate,
rouracil. mercaptopurine,
fluo
sgel iog
Chemotherapy
3. Antibiotics, e.g. mitomycin-C, 1
4. Hormones, e.g. androgens, actinomycin-D.
teroids. estrogens, progestins,
corticos-
5. Radioactive isotopes, e.g. radioiodine,
6. Enzyme, e.g. L-asparginase. radio gold.
7. Vinca alkaloids, e.g. vinblastin,
8. Miscellaneous, vincristin
e.8. cisplatin, procarbazine.
JAntiamoebic Agents
1. Amoebiasis
It is an infectious disease caused
by protozoa Entamoeba
histolytica.
Antiamoebic agents: The drugs which are used in
the treatment
of amoebiasis are called antiamoebic agents.
Classification
1. Tissue amoebicides-e.g.
emetine, dehydroemetin,
chloroquine, metronidazole, tinidazole.
2. Luminal amoebicides-e.g. iodohydroxyquin, diloxanide
furoate, paramomycin, tetracyclines.
2. Metronidazole
It drug of choice in most forms of amoebiasis.
is the
On oral administration, it is completely absorbed from small
intestine.
Adverse effects
1. Metallic taste in mouth
2. Nausea, vomiting, headache
3. Abdominal pains
4. Stomatitis
5. Neurotoxicity
6. Allergic reactions-urticaria,
pruritus.
Therapeutic uses
.In amoebiasis
2. In trichomoniasis
3. In giardiasis
4. In ulcerative stomatitis
. In trichomonal vaginitis

Preparations of antiamoebic agents

1. Metronidazole tablet IP 600 to 800 mg thrice dait.
2. Tinidazole tablet 600 mg twice daily ily
3. Diloxanide furoate tablet 500 mg every 8 hrs
4. Emetine HCI tablet 60-200 mg daily
KAnthelmintics
The drugs which are used in the treatment of worm infestationsa.
called anthelmintics, e.g. mebendazole, albendazole, are
thiabendazol
Pyrante/pamoate, niclosamide, piperazine, DEC. ole,
.Vermicidal or wormicidal: The drugs which kill
or destrov th
worms are called vermicidal or wormicidal
agents.
.Vermifuge or wormifuge: The drugs which
act on the worme
in such a way that they can be easily
expelled out, are known as
vermifuges.
Requirements of an ideal anthelmintic
1. t should have a broad
spectrum action.
2. It should achieve a high percentage
of cure with a single
dose.
3. The purgation before and following
the anthelmintic should
not be necessary.
4.
5.
It should not get absorbed.
It should be palatable and cheap.
rott
6. It should be free from toxic effects.
Questions
A Sulphonamide
1. Write a note on
co-trimoxazole. (S. 96,
2. Explain the mechanism 09; W. 05)
of action of sulpha drugs
sulphonamides. (S. 01, 03, 04, 07;
W. 99, 00, 05, 06, 07)
3. Give the mechanism
of action of 'co-trimoxazole. (\W.O1)
B Antibiotics
1. Define and classify antibiotics
giving examples. (S. 98)
2. Define antibiotics and classify
penicillins with examples
(S. 96)

Chemotherapy 127
3. ive the mode of action of penicillin and mention

therapeutic uses of it. (W. 96, 07) any four
,Wite mechanism of action and adverse

effects of penicillin.
(S. 05)
5. Write
Wh a note on use of penicillin in syphilis. (W.
01)
6. Explain whi
which antibiotic causes the grey baby syndrome in
newborn but not in adults.
7 What are broad spectrum antibiotics? Describe toxic effects
and therapeutic uses of tetracyclines. (W. 98, 06)
g What are macrolide antibiotics? Give the antibacterial activity
and clinical use of erythromycin. (S. 97; W. 03)
9.What are amino glycosides? Mention the toxicity of amino
glycoside antibiotics. (W. 96)
10. Give the mode of action and therapeutic uses of chlorampheni-
col. (S. 97)
c 1.
Urinary Antiseptics
Write a note on urinary antiseptics. (S. 97)
D Antitubercular Agents
1. Define tuberculosis. Classify antitubercular drugs with
examples. (W. 06)
2. Mention four drugs used in the treatment of tuberculosis along
with doses and route of administration. (S. 98)
E Antileprotic Agents
antileprotics. (S. 99)
1. Write a note on
F Antimalarials
example. Mention uses
.Define and classify antimalarials with
of chloroquine. (W. 98, 04, 05)
side effects. (W. 96)
2. Name two antimalarial drugs with their
GAntifungal Agents
. Write a note on antifungal agents.
(S. 96; W. 96)

H Antiviral Agents
1. Discuss antiviral agents. (W. 05)
Anticancer Drugs
1. Define and classify cytotoxic/anticancer agents with examples
(S. 96, 02, 04, 06, 09; w. 96, 98, 99, 00, 03, 05, 07)
2. What is antimetabolite? Mention three examples of metabolites
used in cancer. (W. 96)
JAntiamoebic Agents
1. What is amoebiasis? Classify antiamoebic drugs.
KAnthelmintics
1. Define anthelmintics. Mention two drugs for roundworm
infestation along with dose and route of administration.
(S. 96)
2. Describe the drugs used in the treatment of roundworm
infestation along with their doses and route of administration.
(S. 98)
3. Describe the drugs used in the treatment of threadworm
infestation, along with their doses and route of administration.
(W. 98)

CHAPTER 27
.
Oxytocics/Echbolics
Oxytocics/Echbolics
promote
F The drugs which stimulate the contraction of uterus and
the expulsion of its contents
are called oxytocics or echbolics. For
example:
ergotamine.
1. Ergot alkaloids such as ergotoxin,
2. Bromocryptine.
3. Oxytocin or pitocin.

CHAPTER 28
Hormone and
Hormonal Antagonists
Write a note on oral contraceptives.
Oral contraceptives are the pharmacological agents when admin-.

istered extenally, prevent conception (pregnancy).
These preparations are commonly known as "oral pill" and are used
for effective fertility control in women.
Types of Oral Contraceptives

1. Combination pill: Oestrogen, progesterone
2. Sequential pill: Sequential estrogen, progesterone
3. Mini pil: Continuous low dose progesterone.
Mechanism of Action of Oral Contraceptives

The combination of estrogen and progestin produces their
contraceptive effect by following mechanism.
1. Inhibits pituitary function thus inhibits FSH and LH which
results in inhibition of ovulation.
2. The combination produces changes in cervical
mucus in uterus
endometrium, changes in secretions in fallopian tubes. Due to
all these changes, decreases possibility of conception and
implantation.
Side Effects of Oral Contraceptives

1. Nausea, vomiting, headache, lethargy, anorexia.
2. Oedema, weight gain, mental depression, amenorrhoea.
3. Bleeding irregularities, breast cancer, myocardial infarctio
130

Hormone and Hormonal Antagonists
131
Therapeutic Uses
contraceptive
1. As an oral
treat menstrual irregularities.
2. To
Preparations
1Ethinyl estradiol (0.05 mg) + norgestrel (0.5 mg)
Trade name: Ovral.
(O.05 mg) + nor-ethisterone acetate (1 mg)
9. Ethinylestradiol
Trade name: Miniovral ED.
Questions
(S. 02, 03, 04, 09; W. 96,
1. Write a note on oral contraceptives.
02, 05, 06)
account of oral contraceptives. What are the undesir-
2. Give an
(S. 98)
able effects of these preparations.
mechanism of action of oral contraceptives. (W. 01)
3. Explain

CHAPTER 29
Antiseptics and Disinfectants
Antiseptics
Antiseptics are the agents that destroy or prevent the growth of
microorganisms when applied to living tissues.
Disinfectants
The disinfectants are the agents that kill vegetative bacteria but
not necessarily spores when used on an inanimate object.
Classification of Antiseptics and Disinfectants

1.Phenols and related compounds, e.g. phenol, cresol, chlorocresol
2. Alcohols and related compounds, e.g.
ethyl alcohol, isopropyl
alcohol.
3. Aldehydes, e.g. formaldehyde.
4. Carboxylic acids, e.g. benzoic acid, salicylic acid, boric acid.
5. Halophors, e.g. iodoform, povidone-iodine.
6. Heavy metal compounds, e.g. thiomersal, silver protein.
7. Dyes, e.g. proflavin, brilliant green, crystal violet.
8. Quaternary ammonium compounds, e.g. cetrimide,
benzalko
nium chloride.
9. Oxidising agents, e.g. H,O, and KMNO4.
10. Miscellaneous, e.g. nitrofurantoin, nitrofurazone.
2 Properties of an ldeal Antiseptic Agent

1.It should have wide spectrum of antibacterial activity.
2. It should not give iritation.
3. It should have high penetrability.
132

Antiseptics and Disinfectants
133
A Tt should have low toxicity.
have an activit in presence of pus and necrotic tissue.
5. It should
Tt should not interefere with normal healing process.
7. It should be cheap and easily available.
It should be noncorrosive and should not affect surgical
instrument.
9. It should produce
rapid action.
3 Propeties of an ldeal Disinfectant

1. It should have wide spectrum of antibacterial action.
2. It should not give iritation.
3. It should have high permeability
4. It should have low toxicity.
5. It should have activity in presence of pus and necrotic tissue.
6. It should not interfere with normal healing process.
7. It should be cheap and easily available.
8. It should be noncorrosive and should not affect surgical
instrument.
and films
9. It should have an ability to penetrate surface cavity
of organic matter.
It should have an ability to maintain lethal
concentration of
10.
be obtained in
the agent so that a cidal (killing) effect can
faecal
presence of organic matters such as blood, soil and
matter.
disinfectant
|4 Explain four examples of antiseptics and
agents.
1. Boric acid: It is a weak bacteriostatic agent.
Dose: 1 to 5% topically
Uses: 1. In eye ointment
2. In eye lotion
3. In eardrops
4. In throat paints
2. Benzoic acid: It is a bacteriostatic.
Dose: 0.1o, 3%
Uses: 1. As a preservative in foods
and drinks.

134 Pharmacology and Toxicoloy
2. Antifungal in treatment of ringworm infectiom

nfection
skin. o
3. Hydrogen peroxide
Uses: 1. For cleaning wounds
2. As a mouthwash and deodorant.
3. In dental practice to remove stain from
teeth.
4. Cetrimide
Uses: 1. For disinfection and cleansing
of wounds.
2. Preoperative preparation of skin.
3. Sterilization of surgical instruments.
Questions
1. Define and classify antiseptics
and disinfectants with examples.
(S. 98; W. 05, 06)
2. Define antiseptics and
disinfectants and mention the
characteristics of ideal antiseptics. (S.
97)
3. Define antiseptics and disinfectants.
Give ideal properties
antiseptics and disinfectants. (S. of
02)

CHAPTER 30
Principles of
Drug Interactions
Definition
1 interaction may be defined as an alteration of the effects
Drug of
one drug by prior or concurrent administration of another drug.
classification of Drug Interactions
Drug interactions
A. Pharmacokinetic B. Pharmacodynamic C. Miscellaneous drug

drug interactions drug interactions interactions
Causing electrolyte
a. Affecting
absorption of drug
-a. Synergism disturbances
-b. Affecting Lb. Antagonism Food drug

interactions
distribution of drug
With additives in
c. Affecting
formulation
metabolism of drug
-d. Affecting
excretion of drug
2 Give significancelimportance of drug interactions.

.To get an important therapeutic effect.
1o provide greater margin of safety.
lo get a more appropriate onset or duration of action.
4. To lower toxicity
of drugs.
.lo enhance or increase the potency of
drug.
gniy improved therapy is possible by use of drug interactions.
135

7. To modify effects of drug by prior administration, e,g. pre.

anaesthetic medication.
3 Give advantages and disadvantages of drug interactions
FAdvantages
1. It produces an important therapeutic effect.
2. It provides a greater margin of safety
3. It provides a prolonged drug action.
4. It provides lower toxicity of drugs.
5. It may increase the potency ot drugs.
Disadvantages
1. Sometimes drug interaction may produce adverse reaction.
2. Certain drugs may reduce therapeutic activity of another drug.
3. Some drugs may produce food-drug interactions.
4. Some drug interactions may pròduce allergic complications.
4 What are the reasons/causes of drug interactions?

1. Administration of two or more drugs simultaneously: In
common practice, more drugs are prescribed at a time which
may be one of the main causes of drug interaction.
2. Patient may refer many doctors/multiprescription practice:
Sometimes patient is not satisfied by one doctor and may refer
other doctors without informing about the previous
consultation with the first doctor. This may result in taking
the drugs which may interact with each other.
3. Concurrent use of prescribed and nonprescribed
drugs: Patient
may take the drugs like aspirin, paracetamol which are available
without prescription. If such patients take other drugs
prescribed by physician then drug interaction may ocur and
may be detrimental to the patient.
4. Patient's noncompliance: Sometimes patient does not comply
with instructions given by physician, e.g. patient may take toOu
which is being prohibited.
5. Availability of potent drugs: Potent drugs may interact wi
other drugs and thus may produce dangerous complications

Principles of Drug Interactions 137
is the role of pharmacist

to avoid drug interactions?
What
counselling to aware the patients
1, Pharmacist should do patient
about drug
interactions.
should providé vital information about the drugs
Pharmacist
drug selection and administration.
9.
to patients regarding
drug history
Pharmacists working in hospitals should maintain
3.
patient.
and medical record of the
can educate the public for safe and effective use
4. Pharmacist well as by
medications through verbal communications as
of
use ot computers.
written materials and
Questions
drug interaction? Explain with suitable
1. What is meant by
examples. (S. 00, 04) drug interactions.
disadvantages of
2. Give advantages and
(S. 98; W. 99) Explain the significance of
drug-
interactions?
3. What are drug
interactions. (S. 01)

CHAPTER 31 t an
Miscellaneous
A Reasons
1. Why is chloroform not safe/good general anaesthetic
agent?
OR Why is chloroform not used as general
anaesthetic in clinical
practice? (S. 97, 09; W. 00, 01)
Because
i. Chloroform may produce toxic effects on heart, liver
and kidney,
ii. It produces hepatotoxicity, cardiotoxicity, cirhosis
of liver.
ii. It also precipitates "delayed chloroform poisoning" and 'post-
anaesthetic toxemia".
iv. It also produces hypotension, cardiac arrest and arrhythmia.
Hence because of its less margin of safety, it is not used in clinical
practice
2. Why is ether a safe anaesthetic agent?
Because:
i. Ether produces smooth effects during
induction of anaesthesia.
ii. Ether has sweet, fruity odour.
ii. Recovery of anaesthesia is fast, smooth.
iv. Possibility of nausea,
vomiting is les.
v. It does not produce bronchospasm
and laryngospasm.
vi. lt is also used to reduce labour pains.
Hence ether is a safe anaesthetic.
3. Why are halothane and cyclopropane
costly anaestheticS
Because
i. Halothane and cyclopropane
are poor analgesics and pou
muscle relaxants. Hence require preanaesthetic
which adds to the cost of therapy.
medicaio
138

Miscellaneous 139
iministration
Adminis of halothane and cyclopropane needs special
ii. apparatus,
lothane and cyclopropane are costly anaesthetics, i.e.
halot
Hence
expensive
stored in amber-coloured bottles? (W. 02)
Whyis ether
4.
Because:
liquid with pungent odour.
Ether is a colourless volatile
i. to air or moisture or light, may form ether
Ether when exposed irritant.
ii.
peroxides which are very
amber-coloured bottles
this ether is marketed in
avoid paper.
covered with black
preanaesthetic
Why are
atropine (anticholinergics) used in
medication? (S. 02; W. 01, 04)

5.
Because: may cause nasal irritation and

anaesthetics
i.Some volatile and salivary secretions which interfere with
increase nasal
anaesthesia.
antisecretory agent thus it blocks all secretions
is
i. Atropine anaesthesia.
which interefere with
used with ether when ether is used as an
6. Why is
atropine
general anaesthetic?
(S. 05)
Because: respiratory, lacrimal,

vapours are imitant, which imitate
Ether
salivary secretions. well as
normal repiration as
. These secretions interefere with
with anaesthetic process. and
antisecretory agent, it blocks all secretions
11. Atropine is an
increases anaesthetic process.
injections of local anaesthetics?
Why is adrenaline added to with procaine to produce local
ny adrenaline is given along
naesthesia ? (S. 99, 00, 02, 04, 00)
Because
local anaesthetic from site of
Adrenaline limits absorption of
injection. anaesthetics.
systemic toxicity of local
drenaline prevents action of local anaesthetics.
Adrenaline prolongs duration of

8. While treating the patient of epllepsy, the dose of drug shos

bereduced slowly? OR During the treatment of epilepsyd
should be discontinued or withdrawn gradually, why?
antiepileptics should be withdrawn abruptly?
why2
Why w
Because:
i.If antiepileptic drugs are discontinued suddenly,individualma
suffer from rebound epileptic attack, which may be severemay
previous one.
than
ii. The antiepileptic drugs show wthdrawal symptoms
such as
delusions and hallucinations.
ii. All antiepileptic drugs are quite sedative in nature.
Hence to reduce above side effects, the dose
of drug is reduced
slowly.
9. Why is phenobarbitone
used in epilepsy?
Because phenobarbitone inhibits the spread
discharge in the brain and exerts an of convulsive
antiepileptic effect. Due to this
property it is used in epilepsy.
10. Why is chlorpromazine called

"largactil"? (S. 07; W. 00,
03, 07,08) 02,
Because chlorpromazine shows a large
number of pharmaco-
logical actions as follows:
iIt causes sedation.
i. In psychotic patients causes tranquillizing
effect.
ii. It has an antiemetic effect.
iv. It causes hypothermia
by acting on hypothalamus.
v. It promotes lactation
in women and blocks
vi. It has weak antihistaminic ovulation.
activity.
vii. In normal individuals,
it causes emotional quietening
Due to all these actions,
chlorpromazine is called largactil.
11. Why is chlorpromazine
not effective in the vomiting of motio
sickness? (S. 02, 04)
Because:
i. Motion sickness means vomiting induced
be due to repetitive and during travelling.
rhythmic changes in the spre or
direction of travel.

Miscellaneous
141
Motion sickne
sickness is caused by stimulation
ii. of vestibular nucleus
not by CTZ.
butChlorpromazine is antiemetic drug,
ii. induced and it prevents the vomiting
induced due to stimulation of CTZ
only.
Thus
Thus chlorpromazine is not erfective in motion
sickness.
why is aspirin taken after meals/salicylates
are advised on
stomach? Why Is
full SOdium bicarbonate or alkali
given with
salicylates ? (S. 03, 08)
Because:
i If aspirin is administered before meals, it causes gastric
irrita-
tion, gastritis, nausea, vomiting, ulcers.
i Tf aspirin is advised after meals, it gets mixed with food and
there is no direct contact of drug with walls of stomach, thus
avoids GIT iritation.
Thus to avoid these gastric complications, aspirin it taken after
meals.
13. Why is aluminium hydroxide combined with magnesium

oxide? OR Why are antacids given in combination? (S. 01, 03,
06, 08; W. 96, 00)
Because:
Aluminium hydroxide and magnesium oxide are nonsystemic
i.
antacids.
i. Constipation is the only major adverse effect.
il. To overcome this ide effect, they are combned.
14. aspirin not used/strictly contraindicated in patients
Why is
with peptic ulcer? (S. 00, 07, 09; W. 96, 02)
component of gastric
1. Aspirin precipitates theH*glycoprotein
mucosa and allows free ion to attack (stick) to the mucosa
and causes gastric irritation.
1. Aspirin decreases prostaglandin synthesis and may cause
increase in ulceration.
1. As aspirin itself causes gastric irritation, gastritis, gastric ulcer,
15 contraindicated in peptic ulcer patients.
Why is salicylate therapy always supported with vitamin K?

i. Salicylate administration causes GIT bleeding and ulcers.

ii. Vitamin K favours coagulation, i.e. increases

clotting
prevents GIT bleeding. Hence vitamin K is supplimentedand
with
salicylates.
16. Why is nitrous oxide called "laughing gas"?
Because nitrous oxide when administered along with air,

prodices
a stage of excitement, delirium and also produces amnesia.
It shou
laughing expressions. Hence called laughing gas.
17. Why is sodium bicarbonate given in barbiturate

poisoningo
i. Sodium bicarbonate is an alkaline and barbiturates are the
derivatives of barbituric acid.
ii. In barbiturate poisoning, unionized
barbiturate is reabsorbed
into the body and increases toxicity.
ii. Sodium bicarbonate increases alkalinisation urine
of and there
is an ionisation of barbiturates.
iv. Ionised barbiturates are
not reabsorbed by tubules and increases
its excretion.
v. Sodium bicarbonate increases
the excretion of barbiturates and
hence it is used in barbiturate poisoning.
18. Why is sodium bicarbonate

given with aspirin in salicylate
poisoning?
i. If aspirin is given alone, it sticks
to the gastric mucosa dueto
unionized nature and causes
gastric irritation.
ii. Sodium bicarbonate increases
the ionization of salicylates and
forms water soluble sodium
salicylates.
ii. Hence administration of sodium
bicarbonate increases the rate
of excretion of aspirin and
thus used as antidote in salicylate
poisoning.
19. Why are bitters given

half an hour before meals?
i. Bitters are the substances
with bitter taste, stimulate thetaste
buds and increase the saliva,
gastric juice and improve
ii. The bitters increase the appeic
motility of stomach.
ii. As the bitters stimulate the appetite,
they are given halfan hou
before meals.

Miscellaneous 143
is is insulin not given orally? (S. 97, 02, 04, 05, 07, 09;
Why
20
W.01)
Tnsulin, when given orally, is destroyed by an enzyme
Insulin,
i. sulinase, especially in the liver, kidney and pancreas.
biological half-life is comparatively very short, and only
Its
ame about 40 minutes. Hence it is ineffective orally
Why is irenaline inactive orally? (W. 00)

21.
On oral
administration, adrenaline is rapidly inactivated in GIT
ei
by catechol orthomethyl transferase (COMT) and mono-amino
Oxidase (MAO) enzymes.
Also adrenaline is excreted immediately when given
orally.
Hence adrenaline is not administered orally.
not given/used clinically? Or Why the

2.Why is acetylcholine acetylcholine
action of acetylcholine is very short lived? Or Why
has a short
duration of action? (S. 00, 02, 05; W. 96, 98, 99)
compound and is not effective
Fi.It is a quaternary ammonium
orally.
hygroscopic in nature.
i. Acetylcholine is
hydrolysed into acetic acid and choline.
ii. It is rapidly
iv. On parenteral
administration, it is rapidly destroyed by true
and pseudocholine esterases.
v. Due to these effects it has
very short duration of action.
intravenously?
23. Why is adrenaline never administered
blood
Adrenaline has direct action on peripheral, skeletal
i.
vessels and heart.
ii. If adrenaline is administered intravenously
it may increase
sudden blood levels which is to be toxic.
arrhythmia
11. It may also produce palpitation, severe hypetension,
in larger doses.
Hence, adrenaline is never administered intravenously.
4 Why is adrenaline/salbutamol used in bronchial asthma?

(W.01)
In bronchial asthma, there is a bronchoconstriction and

1. abnormal breathing.

ii. Adrenaline is a bronchodilator and immediately prod uces

mue
dilation of bronchi and relaxation of bronchial smoothmuscles
and improves breathing.
ii. Adrenaline inhibits mucosal secretions.
Hence adrenaline is used in bronchial asthma.
25. Why is nalorphine used in morphine poisoning? (S. 08)

i. Nalorphine is antagonist of morphine.
ii. Thus it blocks the undesirable effects produced in morphins
poisoning and thus is used in it.
26. Why. are potassium salts given with thiazide diuretics

(S. 01)
i. Thiazides may produce an excessive loss of potassium from m

the body and may produce hypokalemia.
ii. To corect this potassium loss by thiazides, potassium salts are
administered along with it.
27. Why is ammonium chloride given with mercurial diuretics?

i. Mercurial diuretics may produce an excessive loss of chlorides
and may produce hypochloremia.
ii. To correct this chloride loss by mercurial diuretics, ammonium
chloride is given along with it.
28. Why is tincture of opium used in diarrhoea? (S. 96, 03;

W. 00)
i. Because morphine is a main alkaloid of opium.

ii. Morphine reduces peristalsis and motility of the gut.
ii. Morphine increases reabsorption of water from the intestineE
and prevents the evacuation of watery stools.
iv. Hence due to constipating effect, morphine is used in diarrhoea.
29. Why is tincture of belladonna (atropine) used in diarrhoea?

i. Tincture of belladonna contains atropine which causes decreas
in tone and motility (peristalsis) and produces constipation.
ii. In diarrhoea condition, there is an increased motility and
evacuation of watery stools.

Miscellaneous 145
s atropine reduces motility of GIT,

As atropine it is a good treatment for
i.diarrhoea.
is1s the patient on digitalis therapy given a potassium
90. Why
supplement? (S. 09; W. 02)
Digitalis is a cardiotonic drug

drug.
i. During the action ot digitalis there is a loss of potassium and it
ii.
produces hypokalemia.
To prevent this loss of K° by digitalis, potassium salts are
supplemented with digitalis therapy.
1.Why is morphine not given in head injury? OR Why is

morphine strictuy contraindicated in brain injury/head injury?
(S. 07)
Fi. Morphine is a narcotic analgesic.

ii. Morphine has mixed actions on CNS. Some areas are depressed
while other are stimulated.
ii. Morphine, if administered in head injury, may produce an
increase in the cerebrospinal fluid pressure, and stimulate spinal
cord and produce respiratory depression.
iv, Miosis and mental clouding produced by morphine may
interfere with diagnosis. Hence morphine is not given in head
injury.
32. Why does morphine cause addiction? (S. 08)
i. Morphine is a narcotic analgesic.

11. Morphine relieves severe types of pains associated with burns,
fractures, tremors, cancer, etc.

11. Morphine when consumed in the absence of pain or disease,
produces euphoria. Due to euphoria, person continues the drug

and produces tolerance, dependance and addiction.
Why is digitalis called "cardiotonic"? (S. 07; W. 01, 08)
1. Digitalis directly acts on myocardium and increases rapidity

force of systolic contraction of the myocardium of the heart.
. and
Digitalis produces complete ventricular emptying.

ener
i. The digitalized heart can do same work with less energyor
more work with same energy expenditure.
Hence digitalis is called "cardiotonic".
34. Why is water called "physiologicallnatural diuretie

(S. 03, 06)
i. Water when given in excess, can act as a physiological diures:.
etic,
ii. When large quantity of water is administered, it inhibits
action of ADH. This prevents reabsorption of water into the
body.
t
111. Thus increases urine output, i.e. diuresis.
iv. Water helps to increase clearance of substances like urea, dio

metabolites. Hence water is called physiological diuretic.
35. Why are vitamin B12 injections given for the treatment ot
pernicious anemia? (S. 02, 04, 09; W. 01)
i. In pernicious anemia, there is a lack of "intrinsic factor" which
is responsible for absorption of vitamin B12 from the intestine
ii. Hence administration of vitamin Bj2 removes the deficiency
of this factor.
36. Why is toxicity of digitalis increased by chlorthiazide?

(S. 97; W. 00)
i. Hypokalemia (loss of K*) is a complication of digitalis.
ii. Chlorthiazide also produces loss of potassium during prolonged
use.
ii. If such CHF patient is kept on prolonged chlorthiazide therapy
it may further increase potassium loss.
iv. Hence if chlorthiazide like diuretics are administered with
digitalis, it naturally increases hypokalemic toxicity.
37. Why is probencid used in the treatment of gout?

i. In gout, there is an increased deposition of uric acid in the
joint.
i. Probencid is a uricosuric agent, i.e. it increases excretion f
uric acid.
and
ii. Probencid blocks the tubular reabsorption of uric acid
increases its excretion and thus decreases level of uric acu
the body.

Miscellaneous 147
drenalineis used in the treatment of epistaxis (nose

38 why? OR Why are packs soaked in adrenaline
5. ing), why?
bleeding),
preferred in dental
practice after tooth extraction. (W. 06)
Adrenaline
Adt is a peripheral vasoconstrictor.
i
ii. When
adrenaline is used as haemostatic agent, it produces
vasoconstriction which stops bleeding.
39. Why
is adren
enaline found in the emergency kit of the
physiclan? (S. 97, 00, 02, 09; W. 05, 08)
Adrenaline is the life-saving drug in various clinical conditions like:
i. Anaphylactic shock
ii. Cardiac
shock
Bronchial asthma
i.
iv. Haemostatic to stop nasal and dental bleeding
v. Adrenaline is added to local anaesthetics.
Hence adrenaline is always Iound in emergency kit of the physician.
40. Why is atropine used in peptic ulcer?

i. Hypersecretion of HCI 1s one of the causes of peptic ulcer.
ii. In peptic ulcer,there is a hypersecretion of gastric juice.
and thus blocks all exocrine
ii. Atropine is an antisecretory agent
secretions.
iv. Hence atropine assists
ulcer-healing process.
constipation? (S. 00;

41. Why does morphine cause/produce
W.08)
gut.
Morphine reduces peristaltic movements the
of
i. food in intestine and
ii. Due to this there is a delay in passage of
reabsorbed from the intestinal
thus large amount of water is
contents.
1. Hence intestinal contents
become hard and do not evacuate
easily. Hence morphine produces
constipation.
myasthenia
y Is edrophonium used in the diagnosis of
gravis?
paralysis
1. Edrophonium stimulates the skeletal muscle even after
ofmotor nerve. intravenously, has very short
Earophonium when administered
duration of action.

43.Why is neostigmine used in the treatment of myastho

nenla
gravis? (W. 05)
i Neostigmine acts on nicotinic receptors of skeletal muscle
esand
.
improves muscle power in myasthenic patients.
ii. In a single dose neostigmine produces marked strii king
improvement in muscle power in myasthenic patients, Hen Hence
neostigmine is used in the treatment of myasthenia gravis
44. Why is atropine given with neostigmine in treatment of

myasthenia gravis? (S. 97; W. 03)
i. Myasthenia gravis is a disease characterised by skeletal muscle
weakness.
ii. Skeletal muscle contains nicotinic receptors.
ii. Neostigmine is a cholinergic agent thus it shows muscarinicas
well as nicotinic actions.
iv. Atropine blocks only muscarinic actions and allows to produce
only nicotinic actions which are useful in treatment
myasthenia gravis.
of
45. Why is morphine not used in acute or severe abdominal pains
before diagnosis is made? (W. 00)
i. Morphine is a potent narcotic analgesic, it relieves abdominal
pains temporarily.
ii. Morphine interferes with abdominal diagnosis by masking true
pain and creates a false sense of security.
46. Why is a morphine addict given a methadone substitution

therapy in hospitals?
i. Morphine is a narcotic analgesic and methadone is a substitute
of morphine.
ii. Methadone has less addiction property than morphine.
ii. The withdrawal symptoms produced by methadone are m
slowly and less intense than that of morphine.
iv. Methadone is effective orally, its analgesic potency is equa
that of morphine.
v. The hypnotic effect produced by
methadone is less intense
morphine.

Miscellaneous
149
Why is morphine strictly contraindicated
47.
A1 or Carrying women, i.e.
people, or car
in children or
pregnancy/labour condition. old
Morphin if administered in children,
si. and depth of respiration.
may decrease the
rate
In people,
ii. In old people, morphine develops bronchospasm and asthma.
n In carrying women, morphine can cross the placental
and may depress the foetal respiration. barrier
why are
48. Why
diur
are diuretics combined with antihypertensives?
(S.96, 08)
Excess plasma Na", Ca" levels and plasma level in circulation
causes hypertension.
ii. Diuretics help to eliminate the excess Ca*, Na* in the form of
their salt and help to decrease blood pressure, i.e. antihyper-
tensive action. Thus, due to combination of antihypertensive
action increases.
49. Why does acetazolamide enhance (increase) the action of

mecamylamine?
is an antihyper-
F i. Acetazolamine is diuretic and mecamylamine
tensive.
ii. Excess of plasma Na*, Ca** levels and plasma level
in
circulation causes hypertension.
sodium and water which
ii. Acetazolamide increases excretion of
ultimately reduces BP.
iv. Thus acetazolamide increases the
antihypertensive action of
mecamylamine.
W. 02, 07)
50. Why is dextran given by IV drip? (S. 05;
Dextran is a plasma expander.
i. be absorbed slowly.
11.It takes about a week for dextran to
When it is administered parenterally, it remains in bloodstream
1.
volume by exerting an osmotic
and increases circulatory fluid
pressure.
. d0 to maintain blood volume dextran is given by IV drip.
MAO
forbidden in patients with
Why is eating of cheese
inhibitor therapy (S. 96, 04, 08; W. 00, 01, 03,
05, 07)
contain tyramine.
Cheese, butter, chocolate, bananas

ii. Tyramine is metabolised in the liver by mono-amino oxidace

se
enzyme.
ii. If MAO inhibitors are given, they inhibit the MAO enzyme
and thus tyramine is accumulated in the body.
iv. Increased level of tyramine causes hypertensive crises. There
fore, eating of cheese is forbidden while on MAO inhibitor
therapy.
52. Why is levodopa always given in combination with

carbidopa? (S. 06; w. 03, 08)
i. Levodopa is a precursor of dopamine.
ii. Levodopa can cross the blood brain barier but dopamine cannot
cross the blood brain barrier.
ii. Levodopa DOPA decarboxylase dopamine.
iv. The enzyme DOPA decarboxylase is also present in the blood
plasma which converts absorbed L-dopa to dopamine.
V. Thus larger dose of L-dopa is required to increase clinically
effective level of dopamine in the brain, which results in
toxicity.
vi. Carbidopa does not cross the blood brain barrier but it inhibits
peripherally dopa decarboxylase.
vii. Carbidopa prevents the conversion of levodopa out
of the CNS
peripherally.
Therefore, levodopa is always given in combination with carbidopa.
53. Why is male fern not combined with castor oil?

i. When castor oil is taken orally, it gets hydrolysed
by intestinal
lipase to glycerol and ricinoleic acid.
ii. Ricinoleic acid is active cathartic
which stimulates small
intestine and induces rapid peristalsis. Fluid motions are
produced within 2-3 hrs.
As male ferm is saline purgative, it is not combined
with castor ol.
54. Why therapeutic index' indicates
safety of a drug? OR A
drug with larger therapeutic index is more
safe one with
smaller therapeutic index. OR "Why the drugs than
having lesser
therapeutic index should be administered
Therapeutic
cautiously?" (S.
index indicates the relative margin of safety
o
drug. of

Miscellaneous 151
therratio between median

utic index is the
TherapeuticC lethal dose and median
effective dose
Therapeutic index =LD
ED
0
median lethal dose (toxic)
here, LDs0=
Whe
EDs0 median effective dose
Therapeutic ingindex gives an estimate of separation between the
oc nroducing a therapeutic effect and doses producing toxic effects.
This is called margin of safety of the drug.
Larger the therapeutic index, greater is the safety of drug. For
therapeutic application, therapeutic index must be more than 1. Thus
the drugs having lower margin of safety should be used carefully as
the ratio between toxic and effective dose is very small.
or more are almost sure tobe
Drugs with a therapeutic index of 10
safe.
55. Why does atropine produce photophobia? OR How does

08)
atropine produce photophobia? (W. 00, 03, 07,
Because: paralysis of
When atropine is instilled into the eye, causes
it
i.
ciliary muscles of eye.
the lens. The increase in
ii. This causes increase in focal length of
size of pupil is called mydriasis.
are paralySed, the person cannot
ii. As the ciliary muscles of eye object or in response to
constrict the pupil for viewing near
bright light.
is termed as cycloplegia.
iv. This paralysis of accommodation
fails to constrict the pupil in
Because of cycloplegia individual
'photophobia'.
response to bright light, this is termed as
REASONS ON CHEMOTHERAPY
sulphamethoxazole combined with trimethoprim?

Why is
.97,00, 02, 08; W. 04, 08)
1. PABA is essential for bacteria
for their growth.
synergistically by blocking the formation
two agents act
hese
of folic acid and its utilisation. The combination is called co-
trimoxazole (5:1).

Toxicology
152 Pharmacology and
Sulphamethoxazole inhibits the conversion of PABA into
ii. enzyme dihydrofolic acid
dihydrofolic acid by inhibiting the lic
synthetase.
iv. Trimethoprim inhibits conversion of dihydrofolic acid int
tetrahydrofolic acid by inhibiting the enzyme dihydrofolic aci
acid
reductase.
v. THF acid is necessary in purine and DNA synthesis.
vi. The combination of sulphonamides reduces adverse effects of
each other.
PABA
Dihydrofolic acid
Inhibited by sulphamethoxazole
synthetase
Dihydrofolic acid
Dihydrofolic acid
************ Inhibited by trimethoprim
reductase
Tetrahydrofolic acid
Purine (DNA) synthesis
2. Why are sulpha drugs not

effectivelineffective in
00, 03, 05; W. 96, 99, 02,
03, 04, 05, 08)
pus? (S. 98,
i. PABA is required for synthesis
of folic acid.
ii. Due to structural similarity
inhibitor of PABA.
of sulphonamide it is a competitive
i. Since pus contains large

therapeutic doses amount of PABA, sulphonamides
are not effective. in
iv. If the larger
doses of sulphonamides
PABA, it results are
into renal complicationsused to compete w
haematuria and such as crystallunas
renal damage.
v. To avoid these
renal complications
in large doses sulphonamides are not useu
and hence they
pus. are ineffective presenece of in

Miscellaneous 153
Uhy
Why is large amount of fluid and alkali given
with sulpha
3.
3.
drug
OR Patient on sulpha
therapy is advised to drink more
drwhy
ater, why?? OR Why is simultaneous antacid
therapy given to
patient on sulpha drugs? (S. 96, 06; W. 06)
Sulphonamides cause renal complications
Sulphonamides
i. such as renal imita-
tion, obstruction in urine flow, crystalluria, albuminuria,
haematuria, oliguria and anuria.
i. To avoid renal complications and to increase excretion of sulpha
drugs large amount of fluid is given.
ii, Antacids are alkaline drugs, thus alkalinisation of urine
increases excretion of sulphonamides.
4. Why is penicillin a life-saving as well as life-threatening drug?

(S. 01; W. 03, 08)
i. Penicillin is used in different types of life-threatening diseases

like:
a. Syphilis
b.Gonorrhoea
c. Diphtheria
d.Meningitis
i. If penicillin is administered in therapeutic doses without
checking its allergy, it may produce anaphylactic shock.
Hence penicilin is life-saving as well as life-threatening drug.
5. Why isprobencid given along with penicillin? OR How can

excretion of penicillin-G be reduced? OR Probencid is sometimes
given as an adjuvent in penicillin therapy, why? (S. 03, 04;
W.96, 04)
Fi. Penicillin is widelydistributed in the body after absorption.

ii. After parenteral administration, excretion of penicillin is very
fast thus declines plasma penicillin levels.
ii. Probencid inhibits the renal tubular secretion of penicillin and
tnus increases or prolongs the blood level of penicillin.
iv. Thus for
prolonging the blood levels of penicillin probencid is
administered along with penicillin.
6. Why
does penicillin kill many bacteria but spare host cells?
Penicillin is effective mainly against multiplying organisms.

ii. It interferes with synthesis of bacterial cell wall mucopeptid

of gram-poSitive coccl.
ii. This makes the cell membrane of the organism susceptibleto
damage by solute in surrounding medium.
iv. A cell wall synthesis occurs during the growth phase. Thus, it
acts as bactericidal.
v. It does not interfere with the tissue cell wall synthesis in human
beings.
vi. Thus, it is nontoxic even in higher doses. Thus, it spares host
cells.
7. Why should tetracyclines be avoided/contraindicated in

children or pregnant women or labour women/carrying women?
(S. 96,03, 04, 07,08; W. 99, 00, 01, 07)
i. Tetracyclines form complexes with ions like Cat*, Mg*, Al
etc.
ii. This makes deficiency of these ions in the body.
ii. These ions are required for the growth of bones and teeth
formation.
iv. Tetracycline by forming complexes with Cat*, Mg* and Al
may retard the growth of child or foetus in pregnant women.
Hence, it is contraindicated.
8. Why
are tetracy cl ines avoided to be given with milk or antacid?
(S. 97, 00)
i. Antacids contain Ca", Mg*", AI** ions and milk contains Ca*
ions.
ii. Tetracyclines if administered with milk or antacid, form
insoluble complexes with these ions.
11. Due to formation of complexes, absorption of tetracycline is
poor, inadequate thus reduces pharmacological action of
tetracycline.
Hence tetracyclines are avoided to be given with milk or antacids.
9. Why are tetracyclines called broad spectrum antibiotics?

i. The tetracyclines are effective against large number 0
pathogens not only gram-positive and gram-negative bactena
but also affect the intracellular organisms like viruses,
rickettsiae, chlamydia, actinomyces.

Miscellaneous 155
tetracyclines havea wide spectrum of activity they

Thus, as
iii.are called broad spectrum antibiotics.
frequent blood count" necessary during prolonged

Why is
10. of chloramphenicol? (S. 96, 00, 04; W. 96)
thera
Chloramphenic causes toxic effects such as bone marrow
i depression, granulocytosis and aplastic anemia, cyanosis,
etc.
: infantsitit causes circulatory collapse due to cumulative
In infants
In
i. effect.
In in accumulates and may produce gray baby
infants in
iii.
syndrome.
depression there may be a decrease in
iy Due to bone marTow
peripheral blood smears should be
count of RBC. Hence
chloramphenicol therapy.
checked at least twice a week during
chloramphenicols not to be repeated for longer

11,Why should
time? (W. 01, 02)
such as bone marrow
Chloramphenicol causes toxic effects
Fi. depression, agranulocytosis, aplastic anemia and cyanosis,
thrombocytopenia, etc.
should not be
these side effects chloramphenicols
ii. To prevent
repeated for longer time.
(S. 06)
not be given in infants?
chloramphenicol
12. Why should
effects such as bone
Chloramphenicols have major toxicagranulocytosis, etc.
i. marrow depression, aplastic
anemia,
collapse.
infants and cause circulatory
1. It may
accumulate in gray baby
gray in colour hence called
ne baby appears
syndrome. infants is due to immaturity
chloramphenicol toxicity in
1. The impairment in excretion of
causes
Or the renal tubules,
in the body.
chloramphenicol and thus deposits
supplemented with
therapy
hay is chloramphenicol (W. 07)
dematinic or iron preparations? causes bone
chloramphenicol also
T i. The therapeutic dose of
depression and inhibits erythropoiesis,
dTOW
Scanned with camscanner

ii. This results in aplastic anemia, 1.e. decrease in

haemoglobin.
RBC
ii. To overcome this side effect and to promote erythropoie.
haematinics like iron preparations are supplemented sis,
with
chloramphenicol therapy.
14. Why are anthelmintics administered with purgatives? 0p
Use of purgatives is essential with piperazine, why?
i. Anthelmintics are either vermicidal or vermifuge in action,
ii. Thus after killing or paralysing these worms by anthelmintic
agent these should be expelled out from the intestine.
ii. Hence purgatives are advised as a supportive treatment with
anthelmintic. Thus combination acts synergistically.
15. In tuberculosis treatment the drugs are always given in

combination or synergistically, why? (S. 00, 01, 04, 05; W. 05)
Tuberculosis is a long-term disease.
It requires a treatment for about months and years.
.The microorganisms of tuberculosis develop more resistant
against single drug therapy.
Hence combination of drug is used in tuberculosis treatment.
i. To avoid resistance.
ii. To avoid viability, multiplication of bacilli
during treatment.
ii. To achieve synergistic effect.
iv. To reduce the adverse effects of combined
drugs.
v. After combination the dose and
drug is reduced. yi
16. Why is iodohydroxyquin useful in intestinal
amoebiasis while
chloroquine is useful in hepatic amoebiasis?
Because:
i. Iodohydroxyquin is not absorbed
into the blood circulation, so
it will remain in the intestine and
cure amoebiasis in intestin
ii. While chloroquine is absorbed
into the blood and weu
concentrated in the liver.
Hence it is more effective in hepatic amoebiasis.
B Antidotes used in Poisoning

1.
Casesw
Morpine poisoning: Naloxone, nalorphine.
o be
194d3
(opium poisoning)

Miscellaneous 157
Atropine poisonin
poisoning (belladonna poisoning): Physostigmine.
2.
Orcanophosphorus poisoning: Atropine, pralidoxime.
Nicotine poisoning: Clonidine, haloperidol.
4.
Strychnine poison Diazepam, barbiturates.
5.
Digitalis poisoning: Potassium chloride.
6.
1,
Alcohol poisoning: Disulfiram.
8. Salicylate poisoning: Sodium bicarbonate.
8.
a Barbiturate poisoning: Sodium thiosulphate, sodium nitrite.
10 Cyanide poisoning: Sodium thiosulphate, sodium nitrite.
11. Insecticide poisoning: Atropine.
12. Carbon monoxide poisoning: Oxygen.
13. Bromide poisoning: Sodium chloride.
14. Mercury, gold, arsenic poisoning: Dimercaprol (BAL).
15. Lead, copper, manganese poisoning: Calcium disodium edetate.
16. Copper, mercury: Penicillamine.
17. Iron poisoning: Desferrioxamine.
c Inhibitors and Blockers

F1. a-blockers: Ergotamine, phentolamine, tolazoline, phenoxy-
benzamine.
2. B-blockers: Propranolol, labetalol, atenolol, metoprolol.
3. Adrenergic neuron blockers: Guanethidine, reserpine.
4. Neuromuscular blockers: Gallamine, succinylcholine, d-tubo

Curarine.
5. Ganglionic blockers: Mecamylamine, hexamethonium.
6. Calcium channel blockers: Verapamil, nifedipine.
7. MAO inhibitors: Isocarboxazid, phenelzine, pargyline.
8. Cholinesterase inhibitors: Physostigmine, neostigmine, pyri-
dostigmine.
9. Carbonic anhydrase inhibitor: Acetazolamide, methazolamide.
10. ACE inhibitor (angiotensin converting enzyme inhibitor)
Captopril, enalapril.
1. Na, K ATPase inhibitor: Digitalis (digoxin).
12. Prostaglandin synthesis inhibitor: Aspirin.
DMajor Adverse/Toxic Effects

1. Gray baby syndrome: Chloramphenicol.
2. Ototoxicity: Streptomycin.

3. Discolouration of teeth: Tetracycline

4. Allergy (anaphylaxis): Penicillin
5. Triple response: Histamine
6. Constipation: Morphine, atropine
7. Black water fever: Quinine
8. Retinopathy: Chloroquine
9. Metallic taste in mouth: Metronidazole
10. Dryness of mouth: Atropine
11. Methaemoglobinemia: Dapsone
12. Liver toxicity: Chloroform
13. Photophobia: Atropine
14. Peripheral neuritis: Isoniazid
15. Drug automatism: Phenobarbitone
16. Urinary retention: Atropine, morphine
17. Cyanosis: Chloramphenicol
18. Suicidal tendencies: Diazepam, morphine
19. Palpitation: Adrenaline, ephedrine
20. Cinchonism: Quinine
21. Pin-point pupil: Morphine
22. Haematuria: Dapsone
23. Bone marrow depression: Chloramphenicol
24. Hypokalemia: Chlorthiazide, digitalis
25. Parkinsonism: Chlorpromazine, methyldopa
26. Anorexia: Amphetamine, carbamazepine
27. Parasthesia: Physostigmine, neostigmine
28. Cholestatic jaundice: Imipramine
29. Difficulty in micturition: Atropine
30. Nephrotoxicity: Cephalosporins
31. Aplastic anemia: Chloramphenicol
32. Obstruction in urine flow: Sulphonamides
33. Cardiac arrest: Acetylcholine
34. Damage to vestibulocochlear nerve (auditory/8th crania
deafness): Streptomycin.
35. Difficulty in swallowing: Atropine
36. Agranulocytosis: Chloramphenicol
37. Pin-point pupil: Morphine
38. Blurring of vision: Chloroquine
39. Postural hypotension: Methyldopa
40. Obstructive jaundice: Erythromycin eg

Miscellaneous 159
41. Blood dyscrasia: Paracetamol

42. Heart burn: Aspirin
43. Haemorrhage: Warfarin
44. Peptic ulceration: Aspirin
45. Euphoria: Morphine, heroin
46. Diplopia: Atropine, primidone
47. Mental clouding: Morphine, lignocaine
48.
Cycloplegia/dysphagia: Atropine
49. Tremors: Adrenaline, ephedrine
Thrombocytopenia: Quinidine
50.
Methyldopa
51. Rebound hypertension:
52.
Hyperkalemia: Spironolactone
53. Alopecia: Heparin
54. Hypoglycemia: Insulin
bicarbonate
55. Rebound acidity: Sodium sulphadimidine
56. Stevens-Johnson syndrome: Sulphadiazine,
57. Crystalluria: Sulphonamides
58. Presbiopia: Insulin
59. Glossitis: Penicillin-G
ampicillin
60. Colitis: Amoxycillin,
61. Eosinophillia: Erythromycin
Tetracycline
62. Hypoplasia of gums:
Mention the drugs of choice

E ranitidine
1. Peptic ulcer: Cimetidine,
2. Status epilepticus: Diazepam
3. Myasthenia gravis: Neostigmine
4. Status asthmaticus:
Hydrocortisone
5. Parkinsonism: Levodopa, carbidopa
6. Bronchial asthma: Adrenaline
7. Grand-mal-epilepsy: Phenytoin
Constipation: Castor oil, senna
9. Diarrhoea: Loperamide, atropine
10. Glaucoma: Pilocarpine
l1. Motion sickness: Promethazine
12. Angina pectoris: Glyceryl trinitrate
5, Thyrotoxicosis: Carbimazole, methimazole

14. Gout: Colchicine, probencid

15. Rheumatism: Indonmethacin, aspirin

16. Obesity: Amphetamine
17. Cycloplegia: Pilocarpine
18. Schizophrenia: Chlorpromazine
19. Depression: Imipramine
20. Heart block: Adrenaline, isoprenaline
21. CCF/CHF: Digitalis
22. Migraine: Aspirin
23. Diabetes mellitus: Insulin
24. Tonsilitis: Co-trimoxazole
25. Stokes adams syndrome: Adrenaline
26. Narcolepsy: Ephedrine, amphetamine
27. Insomnia: Diazepam, phenobarbitone
28. Raynauds disease: Tolazoline
29. Oedema: Frusemide, mannitol
30. Paralytic ileus: Carbachol, bethanechol
31. Dropsy: Frusemide
32. Hypertension: Clonidine, methyldopa
33. Anxiety: Diazepam, nitrazepam
34. Eosinophillia: Iron, Vitamin Bj2
35. Pellagra: Nikethamide
36. Spondylitis: Phenyl butazone
37. Psychosis: Chlorpromazine
38. Haemorrhage: Thrombin, menadione
39. Bradycardia: Isoprenaline
40. Tachycardia: Propranolol, digoxin
41. Thrombosis: Heparin
42. Diabetes insipidus: Vasopressin
43. Hyperthyroidism: Propylthiouracil
44. Whooping cough: Ephedrine
45. Amoebiasis: Metronidazole
46. Helminthiasis: Piperazine
47. Candidiasis: Nystatin, griseofulvin
48. Ascariasis: Piperazine, tetramisole
49. Oxyguriasis: Pyrental pamoate
50. Giardiasis: Metronidazole
51. Onchomycosis: Griseofulvin, nystatin
52. Blastomycosis: Amphotericin
53. Trichomoniasis: Metronidazole nioitg) c

Miscellaneous 161
54. Plague: Tetracycline

55. Typhoid and paratyphoid: Chloramphenicol
56.
Meningitis: Benzyl penicillin
57. Tuberculosis: Isoniazid, ethambutol
LeproSy: Dapsone,
solapsone
58.
59. Malaria: Quinine, chloroquine
Albendazole
60.
Hookworm infestation:
chlorambucil
Malignancy: Busulphan,
61. Chloramphenicol
Trachoma:
62.
Gonorrhoea: Penicillin-G
63. Streptomycin
64. Urinary tract infection:
Penicillin-GG
65.
Rheumatic fever:
66.
Embolism: Heparin
paracetamol
67. Lumbago, sciatica: Aspirin,
68. Mania: Imipramine Propranolol
Pheochromocytoma:
69. nicotinic acid.
Arteriosclerosis: Clofibrate,
70.
contraindicated in the following
Name one drug each
conditions.
Glaucoma:Atropine testosterone
1. enlargement: Propranolol,
2. Prostate
Aspirin, reserpine
3. Peptic ulcer: Phenobarbitone, alcohol
Cirhosis of liver:
4.
renal function: Sulpha drugs
5. Impairment of
6.
Hypertension: Adrenaline Quinidine
failure:
7. Congestive cardiacAcetylcholine, carbachol
8. Bronchial asthma: Quinidine
Stokes-Adams syndrome:
9. Atropine, morphine
10. Intestinal obstruction:
Morphine (brain injury)
11. Head injury: nikethamide
12. Insomnia: Bemegride,Methyldopa, guanethidine
Pheochromocytoma:
13. kanamycin.
14. Myasthenia gravis: Streptomycin,

CES Confdent Pharmacy Serles

for Second Year Diploma in Phamacy
Second Edition |
Tme second edition ofthe now popular and successtul book includes Board
Ouestion Papers 2010 to 2014.1he book is wriffen, presented and publisheed
to meet the tequirements of students of diploma in pharmacy (D Pharm) in
acCordance with the new revised syllabus under ER 1991 of Pharmacy
ounci ofrindia. Wrnten in a lucid and Simple language, aftempts to
demystity and simplify the basic concepts for the students ofitpharmacy for
proper understanding of the subject and to get a sure success in
the state
boardexaminations.
The salientfeatures otthe presentbook are:
Topics described in easy language
To the polntanswers and
Showsthe way to aftemptboardexaminations in the simplest way
The series, Comprising six books
diplomastudents,is aptly named aseach
for the first year and second year
CBS Confident Pharmacy Series
volumeis designed to inspire self-confidence in the reader. as each
This book, as well as the entire
serles, will be useful not only to both the
students and the teachers of diploma in pharmacy, but also the candidates
desiring to attempt competitive examinations for job
pharmacY profession such as hospital pharmacist (PHC, Civilopportunities in
Hospital, etc.).
V.N. Raje is curently Principal, Gourishankar Education Society's
(GES) College of Pharmacy (D Pham), Limb, satara,
Maharashtra.
He has over 22 years of experience in teaching to
pharmacy level students. He has excellent track
diploma in
record in various
academic institutes of high repute and is actively engaged in teaching,L
administration and service to the profession. He has contributed
programmes by counselling and guiding through radio programmes to social awareness
the students regarding the career opportunities in pharmacy and motivating
profession. He has put in
extensive effort in compiling this series comprising 12 titles, 6
second year each for first year and
diplomain pharmacy students.
CBS SRN
CBS Publishers &

4819/X1, Prahlad Street, 24 Ansari Road, Distributors Pvt Ltd
Daryaganj. New Delhl110 002, India
E-moil: delhi@cbspd.com, cbspubs@oirtelmail
in; Wcbsite: www.cbspd.com
New Delhi | Bengaluru |
Chennai | Kochi | Mumbai | Pune
Hyderabad | Kolkata | Nagpur Patna | Vijayawada
I
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CBS Confident Pharmacy SerieS

for Second Year Diploma in Pharmacy

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First Year D Pharm

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Pharmacology and Toxicology

1. Introduction to Pharmacology, Scope of Pharmacology.

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g. Antacids, Physiological role of histamine and serotonin, His-

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Preface to the Second Edition ..

11. Parkinsonism and Antiparkinsonism Agents ... ************e***59

12. Heavy Metal Poisoning. .61

17. Histamine and Antihistaminics... .77

21. Drugs Acting on ANS

24. Cardiovascular Agents... 102

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Board Question Papers.

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Introduction and Routes of

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analeptics. For example, caffeine, theophylline, nikethamide

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20. Diuretics: The drugs which increase rate of formation and

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cosis are called antithyroid drugs. For

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42. Lipid lowering agents: The drugs which reduce excessive

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55. Antibiotics: These are the chemical substances produced by

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b. As per Nature of Drugs

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ROUTES OF ADMINISTRATION OF DRUGS

1 Classification/Types of Routes of Drug Administration

Routes of Administration of Drug

Oral route Sublingual route Parenteral route

Injections Inhalations Local application

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possibilities of adverse reactions.

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Intravenous Route route)

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9 Local Route/Local Application/Topical Route

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1.Enumerate/enlist/give/classify various routes of administration

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8. Give the examples of drugs administered by inhalation and

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The absorption of drug through membrane occurs by following

b. Active Transport Process

Active transport process

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In this process, cell forms a cavity lIke pseudopodium and particlee

3 Discuss factors affecting (influencing) the absorption

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4 Distribution of Drug in the Body

11. Parkinsonism and Antiparkinsonism Agents ... **********e*59