Dr. V. S.

PAWAR

BASICS OF

MEDICAL
PHARMACOLOGY
 Dedicated to
My Mother
Mrs. Urmila Pawar.

Basics
of
MEDICAL
PHARMACOLOGY
AUTHOR
DR.V.S.PAWAR
(MD)
 Basics
of
MEDICAL PHARMACOLOGY
AUTHOR
DR.V.S.PAWAR
(MD)
Email-drvspawar175@gmail.com

PUBLISHED BY
DR.V.S.PAWAR
Nagpur, Maharashtra-440034.
INDIA

1st EDITION
2023

All Rights Reserved

This book or any part there of must not be reproduced in any form
without the written permission of the author, DR. V.S.PAWAR.
Copyright © DR. DR. V.S.PAWAR

ISBN
978-93-5812-881-9
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 CONTENTS
1. General Pharmacology …………………………………………………………..………………………..…...1
▪ Pharmacodynamics.
▪ Pharmacokinetics.
▪ Drug Nomenclature.
▪ Routes of Drug Administration.
▪ Bioavailability.
▪ Absorption.
▪ BBB.
▪ Biotransformation.
▪ Excretion.
▪ Principal of drug action.
▪ Mechanism of drug action.
▪ Drug effect.
▪ Drug doses.
▪ Anaphylactic reaction.
2. NSAIDs ………………………………………………………………………….............................................9
3. Drugs for Migrain & Gout ………………………...……………………………………………..…………15
4. Drugs for Rheumatoid Arthritis …………………………………………………………………..………….19
5. Histamines & Anti-histamines …………………………...…………………………………….…………….21
6. Corticosteroids ……………………….……………………………………………………….……………...25
7. Drugs for Thyroid Disorder ……………………………….....…………………………………....................31
8. Drugs for DM ………………………………………………………………………………….…...………...33
9. Drugs for Respiratory system
▪ Drugs for Cough …………………..………………………………………………………..…….………....39
▪ Drugs for Bronchial Asthma ………………………………………………………………..…….………...40
10. GIT Drugs
▪ Drugs for Peptic ulcer & GERD ………………………………………...…………………………….…....45
▪ Anti-emetics drugs ………………….………………………………………………………………….…....49
▪ Drugs for Constipation ……………………………………………………………………………….……...53
▪ Drugs for Diarrhoea …………………………………..……………………………………………….…….56
▪ Drugs for IBD …………….………………………………………………………………………..………..57
11. Adrenergic drugs …………………………..……………………………………………….………….….…59
12. Adrenergic blocking drugs
▪ Alpha-Adrenergic blocking drugs ……………………………………...…….……………..…….………....61
▪ Beta-Adrenergic blocking drugs …………………….………………………………………………….…...62
▪ α + β Adrenergic blocking drugs ………………………..…….…………………………………….………64
13. CVS Drugs
▪ ACE Inhibitor ………………….....………………………………………………………….....…………..65
▪ ARB …………………………..……..…………………………………………………………..………..…66
▪ Nitrates ………………………………………………………………...……………………….…................67
▪ CCB …………………………………………………..………………………………………..………...….69
▪ Potassium Channel opener …………………………………………...……………………….……….….....71
14. Anti-cholinergic drugs ……………………………………………………………………….….…….……..73
15. Diuretics ……………………………….…………………………………………………….……….……...75
16. Haematinics
▪ Haematinics ………………………………………………………….……………………….…………….79
▪ Folic Acid …………………………………………………………………………………….……………..80
▪ Anti-coagulant (Heparin)………………..……...…………………………………………………….……...80
▪ Fibrinolytics ………………………………….……………………………………………………….…..…81
▪ Anti-fibrinolytics drugs……………………………...……………………...……………………………......81
▪ Anti-Platelets Drugs ………………………………….…………………………………………………...…82
17. Anti-tubercular Drugs……………………………..……………………………….………….……………...85
18. Anti-fungal Drugs ……………………..……………………………………………………………………..87
19. Anti-Viral Drugs
▪ Anti-Retroviral Drugs ………………………...….……………………………………………….................91
▪ Anti-Herpes Drugs …………………….……...….……………………………………………….................93
▪ Anti-Hepatitis Drugs ………………………...….………………………………………………...................94
20. Anti-Amoebic Drugs ..……………………………………………..………………………………................96
21. Anti-Helminthic Drugs ……………………………………………………………………………................97
22. Anti-Malarial Drugs ……………………………………………………………………………....................99
23. Anti-biotics
▪ Sulfonamides ……………………………………………………………………………………………....103
▪ Cotrimoxazole …………………………………………….……………………………………………….103
▪ Quinolones ………………………………………………………………………………………...............104
▪ Macrolides ……………………………...………………………………………………………….............105
▪ Penicillins…………………...………………………………...…………………………………………….106
▪ Beta Lactamase Inhibitors …………………………….……………………………………………............107
▪ Cephalosporins ………………………..……………………………………………………….…………...108
▪ Monobactum ……………………………………..…………………………………………….…………..111
▪ Tetracyclines …………………………………………………….…………………………….……...........111
▪ Chloramphenicol………....………………….………………………………………………….…………..112
▪ Aminoglycoside ………....………………….……………………...………...………………….…………..113
▪ Clindamycin ………....……………….…….…………………………………………………..…………..114
▪ Glycopeptides ………....………………….………………………………………...………….…………..114
▪ Oxazolidinone-Linezolid ………....………………….…………………...………...………….…………..115
▪ Topical Antibiotics ………....………………….………………………………………...………….……..115
24. Drugs for Acne ……………………………………………….………………………….………………...116
25. Sedatives & Hypnotics …………………………………………………………………………….……....118
26. Anti-epileptics drugs ………………………………………………………………………………………..120
27. Muscle Relaxant ……………………………………….………………………………………………...…125
28. Drugs for Scabies ……………………………………………………..………………………….……...…129
29. Drugs for Parkinson Disease …………………………………………………………….………………….131
30. Hypolipidaemic Drugs ……………………………………………………………………………………...133
31. Opioid Analgesic …………………………………………………………………………………………...135
32. Hormonal Drugs ………………………………………………………………….………………………...138
 SECTION 1. GENERAL PHARMACOLOGY 1

SECTION 1.
GENERAL PHARMACOLOGY
proprietary names, e.g. DYNAPER, DICKA,
INTRODUCTION DICLO PLUS for DICLOFENAC from
PHARMACODYNAMICS different manufacturers.
▪ What the drug does to the body.
▪ This includes physiological and biochemical
effects of drugs and their mechanism of
action at organ system/ subcellular
/macromolecular levels.
▪ E.g.- Adrenaline- interaction with
adrenoceptors- increased intracellular cyclic
3',5' AMP-cardiac stimulation, hepatic
glycogenolysis and hyperglycaemia, etc. Generic Chemical Brand Name
Name Name
PHARMACOKINETICS Paracetamol Aceto Amino Dolo, Fepanil,
▪ What the body does to the drug. Phenol Crocin
▪ This refers to movement of the drug in and Aspirin Acetyl Ecosprin,
alteration of the drug by the body; includes salicylic acid Disprin.
absorption, distribution, binding/ localization Metformin 1-1 dimethyl Glyciphage
/storage, biotransformation and excretion of biguanide
the drug,
▪ E.g. Paracetamol is rapidly and almost
ROUTES OF DRUG ADMINISTRATION
completely absorbed orally & attaining peak
blood levels at 30-60 min; 25% bound to
plasma proteins, widely and almost
uniformly distributed in the body.

DRUG NOMENCLATURE
A drug generally has three categories of names:
1. CHEMICAL NAME
▪ It describes the substance chemically, e.g. 1-
(lsopropylamino)-3-(1naphthyloxy) propan-
2-ol for propranolol.
▪ This is not suitable for use in prescribing.
2. NON-PROPRIETARY NAME
▪ It is the name accepted by a competent
scientific body or authority.
▪ The term generic name is used in place of
nonproprietary name.
3. PROPRIETARY (BRAND) NAME
▪ It is the name assigned by the
manufacturer(s) and is his property or trade
mark.
▪ It is the name assigned by the
manufacturer(s) and is his property or trade
mark. One drug may have multiple
LOCAL ROUTES
▪ These routes can only be used for localized
lesions at accessible sites and for drugs
whose systemic absorption from these sites is
minimal or absent.
▪ High concentrations are attained at the
desired site without exposing the rest of the
body.
▪ Systemic side effects are absent or minimal.
▪ E.g. Glyceryl trinitrate (GTN) applied on the
skin as ointment or transdermal patch.
1. TOPICAL
▪ This refers to external application of the drug
to the surface for localized action.

BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR

 SECTION 1. GENERAL PHARMACOLOGY 2

▪ It is more convenient. 4) The medicament need not be sterile and so is

▪ Drugs can be efficiently delivered to the cheaper.
localized lesions on skin, oropharyngeal/ 5) Both solid dosage forms (powders, tablets,
nasal mucosa, eyes, ear canal, anal canal or capsules, spansules,) and liquid dosage forms
vagina in the form of lotion, ointment, cream, (elixirs, syrups, emulsions, mixtures) can be
powder, paints, drops, spray, given orally.
lozengens,Ssuppositories. LIMITATIONS OF ORAL ROUTE
1) Action of drugs is slower and thus not
2. DEEPER TISSUES suitable for emergencies.
▪ Certain deep areas can be approached by 2) Unpalatable drugs are difficult to administer.
using a syringe and needle, but the drug 3) May cause nausea and vomiting.
should be such that systemic absorption is 4) Cannot be used for uncooperative/
slow, e.g. intra-articular injection unconscious/ vomiting patient.
(hydrocortisone acetate), infiltration around a 5) Absorption of drugs may be variable; certain
nerve or intrathecal injection (lidocaine), drugs are not absorbed orally (streptomycin).
retrobulbar injection (hydrocortisone Others are destroyed by digestive juices
acetate). (PenicillinG, Insulin) or in liver (GTN,
testosterone).

a.Intra articular injection
Retrobulbar injection
2. SUBLINGUAL (S.L.)
▪ The tablet containing the drug is placed
under the tongue or crushed in the mouth and
spread over the buccal mucosa.
▪ Only lipid soluble and non-irritating drugs
b. Injection around nerve
can be so administered.
▪ Absorption is relatively rapid-action can be
produced in minutes.
▪ The chief advantage is that liver is bypassed
and drugs with high first pass metabolism
can be absorbed directly into systemic
circulation.
▪ Drugs given sublingually are-GTN.

3. ARTERIAL SUPPLY
▪ Close intra-arterial injection is used for
contrast media in angiography; anticancer
drugs can be infused in femoral or brachial
artery to localise the effect for limb
malignancies.
SYSTEMIC ROUTES
This routes help in absorption of drug into the
blood stream and distributed all over, including
the site of action, through circulation.
3. RECTAL
▪ Certain irritant and unpleasant drugs can be
put into rectum as suppositories or retention
enema for systemic effect.
▪ This route can also be used when the patient
is having recurrent vomiting or is
unconscious.
▪ It is inconvenient and embarrassing;
absorption is slower, irregular and often
unpredictable.
▪ Drug absorbed into external haemorrhoidal
veins (about 50%) bypasses liver.

1. ORAL 4. CUTANEOUS
ADVANTAGES OF ORAL ROUTES ▪ Highly lipid soluble drugs can be applied
1) It is safer & more convenient. over the skin for slow and prolonged
2) Does not need assistance. absorption in form of ointment.
3) Noninvasive & painless. ▪ The liver is also bypassed.
BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR
 SECTION 2. NSAIDS
SECTION 2.
NON STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDs)
INTRODUCTION
▪ All drugs grouped in this class have
analgesic, antipyretic and antiinflammatory
actions in different measures.
▪ They do not depress CNS, do not produce
physical dependence, have no abuse liability.
▪ They are also called nonnarcotic, nonopioid
or aspirin like analgesics.
▪ They act primarily on peripheral pain
mechanisms, but also in the CNS to raise
pain threshold.
CLASSIFICATION
A. Nonselective COX inhibitors (traditional
NSAIDs)
1. Salicylates: Aspirin.
2. Propionic acid derivatives:
▪ Ibuprofen,Naproxen,Ketoprofen,Flurbiprofe.
3. Fenamate: Mephenamic acid.
4. Enolic acid derivatives:
▪ Piroxicam, Tenoxicam.
5. Acetic acid derivatives:
▪ Ketorolac, Indomethacin, Nabumetone.
6. Pyrazolone derivatives:
▪ Phenylbutazone, Oxyphenbutazone.
B. Preferential COX-2 inhibitors
▪ Nimesulide,Diclofenac,Aceclofenac,
Meloxiam, Etodolac.
C. Selective COX-2 inhibitors
▪ Celecoxib, Etoricoxib, Parecoxib.
D. Analgesic-antipyretics with poor
antiinflammatory action
▪ Paracetamol (Acetaminophen).
PHARMACOLOGICAL ACTION OF NSAIDS
BASICS OF MEDICAL PHARMACOLOGY
9
1. Antipyresis
▪ NSAIDs reduce body temperature in fever.
▪ Fever during infection and tissue injury is
produced through the generation of pyrogens
including ILs, TNFα, interferons which
induce PGE2 production in hypothalamus—
raise its temperature set point.
▪ NSAIDs block the action of pyrogens.
2. Antiinflammatory
▪ NSAIDs cause inhibition of COX-2 mediated
enhanced PG synthesis at the site of injury.
3. Dysmenorrhoea
▪ Intermittent ischaemia of the myometrium is
probably responsible for menstrual cramps.
▪ NSAIDs reduce uterine PG levels—afford
excellent relief.
4. Antiplatelet aggregatory
▪ NSAIDs, mainly Aspirin inhibit synthesis of
TXA2.
5. Ductus arteriosus (DA) closure
▪ During foetal circulation ductus arteriosus is
kept patent by local elaboration of PGE2 by
COX-2.
▪ At birth level of PGE2 decreses and the
ductus closes.
▪ If level of PGE2 is not reduced at birth then
DA may remain patent resulting in PDA.
▪ In such situation, small doses of
indomethacin or aspirin bring about closure
of DA in majority of cases within a few
hours by inhibiting PG production.
▪ NSAIDs should be avoided near term as it
may promote premature closure of ductus in
some cases and increase the risk of post-
partum haemorrhage.
6. Gastric mucosal damage
▪ All NSAIDs produce gastric pain, mucosal
erosion/ulceration and blood loss.
▪ Inhibition of COX-1 mediated synthesis of
gastroprotective PGs (PGE2, PGI2) is clearly
involved.
▪ Deficiency of PGs reduces mucus and
HCO3¯ secrection and increases acid
secretion and may promote mucosal
ischaemia. Thus, NSAIDs are ulcerogenic.
DR.V.S.PAWAR
 SECTION 3. DRUGS FOR MIGRAINE & GOUT
SECTION 3.
DRUGS FOR MIGRAINE & GOUT
DRUGS FOR MIGRAINE
Migraine is characterized by pulsating headache,
usually restricted to one side and is often
associated with nausea, vomiting, sensitivity to
light and sound, flashes of light, vertigo, loose
motions and other symptoms.
MILD MIGRAINE
▪ Less than one attack per month of throbbing
but tolerable headache lasting upto 8 hours
which does not incapacitate the individual.
1. Simple analgesics like Paracetamol (0.5– 1
g).
2. Nonsteroidal antiinflammatory drugs
(NSAIDs) and their combinations Ibuprofen
(400–800 mg 8 hourly), Naproxen (500 mg
followed by 250 mg 8 hourly), Diclofenac
(50 mg 8 hourly), Mephenamic acid (500
mg 8 hourly), either alone or combined with
paracetamol/codeine/ diazepam or another
sedative/diphenhydramine or another
antihistaminic/caffeine.
3. Antiemetics
Metoclopramide (10 mg oral/i.m.).
Domperidone (10–20 mg oral) and
Prochlorperazine (10–25 mg oral/i.m.).
MODERATE MIGRAINE
▪ Throbbing headache is more intense, lasts for
6–24 hours, nausea/vomiting and other
features are more prominent and the patient
is functionally impaired.
▪ One or more attacks occur per month.
▪ Stronger NSAIDs or their combinations
mentioned above are beneficial in many
cases.
▪ The remaining are treated with a specific
antimigraine drug, i.e. a triptan or an ergot
preparation.
▪ Antiemetics are almost regularly needed.
SEVERE MIGRAINE
▪ 2–3 or more attacks per month of severe
throbbing headache lasting 12–48 hours,
accompanied by vertigo, vomiting and other
symptoms.
BASICS OF MEDICAL PHARMACOLOGY
15
▪ The individual is grossly incapacitated
during the attack.
▪ Analgesics/NSAIDs and their combinations
usually do not afford adequate relief—
specific drugs have to be prescribed along
with antiemetics.
▪ Prophylactic regimens lasting 6 months or
more are recommended.
ERGOTAMINE
▪ It is the most effective ergot alkaloid for
migraine.
▪ Given early in attack, relief is often dramatic.
▪ Oral/sublingual route is preferred.
▪ 1 mg is given at half hour intervals till relief
is obtained or a total of 6 mg is given.
▪ Parenteral administration is more hazardous.
▪ Ergotamine acts by constricting the dilated
cranial vessels and/or by specific constriction
of carotid A-V shunt channels.
▪ Ergotamine and DHE have also been shown
to reduce neurogenic inflammation and
leakage of plasma in duramater.
DIHYDROERGOTAMINE (DHE)
▪ It is nearly as effective as ergotamine and
preferred for parenteral administration.
▪ Because of frequent side effects, especially
nausea and vomiting, and availability of
triptans, ergot preparations are rarely used
now.
▪ Caffeine 100 mg taken with ergotamine
enhances its absorption from oral routes and
adds to the cranial vasoconstricting action.
VASOGRAIN: Ergotamine 1 mg, caffeine 100
mg, paracetamol 250 mg, prochlorperazine 2.5
mg tab.
SELECTIVE 5-HT1D/1B AGONISTS (TRIPTANS)
▪ This drugs are selectively activate 5-
HT1D/1B receptors, and are called ‘triptans’.
▪ Currently, they are the first line drugs for
patients who fail to respond to analgesics.
SUMATRIPTAN
▪ Sumatriptan is as effective and better
tolerated than ergotamine.
DR.V.S.PAWAR
 SECTION 4. DRUGS FOR RHEUMATOID ARTHRITIS
SECTION 4.
DRUGS FOR RHEUMATOID ARTHRITIS
▪ NSAIDs are the first line drugs and afford
symptomatic relief in pain, swelling,
morning stiffness, immobility, but do not
arrest the disease process.
▪ DMARDs are drugs which suppress the
rheumatoid process, bring about a remission
and retard disease progression.
CLASSIFICATION
Disease modifying antirheumatic drugs
(DMARDs)
1. Immunosuppressants:
a. Methotrexate,
b. Azathioprine,
c. Cyclosporine
2. Sulfasalazine
3. Chloroquine or Hydroxychloroquine
4. Leflunomide.
5. TNFα inhibitors:
a. Etanercept,
b. Infliximab,
c. Adalimumab
6. IL-1 antagonist: Anakinra
7. Corticosteroids: Prednisolone and others
METHOTREXATE (MTX)
▪ This has prominent immunosuppressant and
antiinflammatory property.
▪ It inhibit cytokine production, chemotaxis
and cell-mediated immune reaction.
▪ Onset of symptom relief is relatively rapid
(4–6 weeks), therefore preferred for initial
treatment.
▪ Mtx is now the DMARD of first choice and
the standard treatment for most patients,
including cases of juvenile RA.
▪ Oral bioavailability of Mtx may be affected
by food.
▪ Its excretion is hindered in renal disease: not
recommended for such patients.
▪ Oral ulceration and g.i. upset are the major
side effects of low dose Mtx regimen.
▪ Incidence of chest infection is increased.
BASICS OF MEDICAL PHARMACOLOGY
19
▪ Mtx is contraindicated in pregnancy, breast-
feeding, liver disease, active infection,
leucopenia and peptic ulcer.
Dose-oral low-dose (7.5–15 mg) weekly
FOLOTRAX 2.5,5,10 mg tab.
AZATHIOPRINE
▪ It is a potent suppressant of cell-mediated
Immunity.
▪ It also suppresses inflammation.
▪ However, it is less commonly used.
▪ It is not combined with Mtx.
Dose: 50–150 mg/day; AZORAN 50 mg tab.
SULFASALAZINE
▪ Exerts anti-inflammatory activity in the
bowel and is useful in ulcerative colitis.
▪ It also suppress the disease in significant
number of RA patients.
▪ The mechanism of action is not known.
▪ Generation of cytokine by inflammatory cells
may be suppressed.
▪ Neutropenia/thrombocytopenia occurs in
about 10% patients and hepatitis is possible.
Dose: 1–3 g/day in 2–3 divided doses.
SALAZOPYRIN, SAZO-EN 0.5 g tab.
CHLOROQUINE AND
HYDROXYCHLOROQUINE
▪ These are antimalarial drugs found to induce
remission in upto 50% patients of RA, but
take 3–6 months.
▪ Their mechanism of action is not known,
however, they have been found to reduce
monocyte IL–I, consequently inhibiting B
lymphocytes.
▪ Adverse effects are rashes, graying of hair,
irritable bowel syndrome, myopathy and
neuropathy.
▪ HCQ are use in milder nonerosive disease or
they are combined with Mtx/sulfasalazine.
Dose: Hydroxychloroquine 400 mg/day for
4–6 weeks, followed by 200 mg/day for
maintenance. HCQS 200 mg tab
DR.V.S.PAWAR
 SECTION 4. DRUGS FOR RHEUMATOID ARTHRITIS 19
NOTES

BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR

 SECTION 5. HISTAMINES & ANTI-HISTAMINES 21

SECTION 5.
HISTAMINES & ANTI-HISTAMINES
HISTAMINES 2. Allergic phenomena
▪ Histamine is causative in urticaria,
PHARMACOLOGICAL ACTIONS angioedema, bronchoconstriction and
anaphylactic shock.
1. Blood vessels ▪ The H1 antagonists are effective in
▪ Histamine causes dilatation of smaller blood controlling these manifestations, except
vessels. asthma in which leukotrienes (LTs) and PAF
▪ Rapid i.v. injection causes fall in BP. appear to be more important.
▪ Dilatation of cranial vessels causes pulsatile 3. As transmitter
headache. ▪ Histamine is believed to be the afferent
▪ Larger arteries and veins are constricted by transmitter which initiates the sensation of
histamine: mediated by H1 receptor on itch and pain at sensory nerve endings.
vascular smooth muscle. ▪ Nonmast cell histamine occurs in brain,
▪ Histamine also increases capillary especially hypothalamus and midbrain. It is
permeability → exudation of plasma. involved in maintaining wakefulness; H1
▪ Injected intradermally, it cause the triple anti-histaminics owe their sedative action to
response consisting of: blockade of this function.
1) Red spot: due to intense capillary dilatation. 4. Inflammation
2) Wheal: due to exudation of fluid from ▪ Histamine is a mediator of vasodilatation and
capillaries and venules. other changes during inflammation.
3) Flare: i.e. redness in the surrounding area
due to arteriolar dilatation. BETAHISTINE
2. Heart ▪ It is H1 selective histamine analogue, which
▪ In isolated heart, especially of guinea pig— is used to control vertigo in patients of
rate as well as force of contraction is Meniéré’s disease: possibly acts by causing
increased. vasodilatation in the internal ear.
3. Visceral smooth muscle ▪ It is contraindicated in asthmatics and ulcer
▪ Histamine causes bronchoconstriction. patients.
4. Glands VERTIN 8, 16 mg tab.1 tab. TDS.
▪ Histamine increases gastric secretion.
▪ This is a direct action exerted on parietal H1 ANTAGONISTS
cells through H2 receptors. These drugs competitively antagonize actions of
1. Sensory nerve endings histamine at the H1 receptors.
▪ After IV Injection Histamine produce HIGHLY SEDATIVE-1st GENERATION
itching. Drug Dose M/N
Dimenhydrinate 25–50 mg oral Tab.
2. Autonomic ganglia and adrenal medulla VERTENASE.
▪ These are stimulated and release of Adr Promethazine 25–50 mg oral, PHENERGAN
occurs, which cause a secondary rise in BP. I.M. 10, 25 mg tab.,
7. CNS 5 mg/ml elixir,
25 mg/ml inj
▪ Histamine does not penetrate blood brain
Hydroxyzine 25–50 mg oral, ATARAX 10,
barrier—no central effects.
I.M. 25 mg tab, 10
mg/5 ml syr, 6
PATHOPHYSIOLOGICAL ROLES mg/ml drops.
1. Gastric secretion Diphenhydramine 25–50 mg oral BENADRYL
▪ Histamine increases secretion of HCl in the 25, 50 mg cap,
stomach. syp.

BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR

 SECTION 6. CORTICOSTEROIDS
SECTION 6.
CORTICOSTEROIDS
Actions of corticoids are divided into:
Glucocorticoid
Effects on carbohydrate, protein and fat
metabolism.
Mineralocorticoid
Effects on Na+, K+ and fluid balance.
MINERALOCORTICOID ACTIONS
▪ They increase Na+ reabsorption in the distal
convoluted tubule in kidney.
▪ They increase in K+ and H+ excretion.
GLUCOCORTICOID ACTIONS
1. CARBOHYDRATE AND PROTEIN METABOLISM
▪ They promote glycogen deposition in liver.
▪ They inhibit glucose utilization by peripheral
tissues.
▪ They increase glucose release from liver
results in hyperglycaemia.
▪ They also cause protein breakdown and
amino acid mobilization from peripheral
tissues. This is responsible for side effects
like muscle wasting, lympholysis, loss of
osteoid from bone and thinning of skin.
2. FAT METABOLISM
▪ They promote lipolysis.
▪ Subcutaneous tissue over extremities loses
fat which is deposited over face, neck and
shoulder producing ‘moon face’, ‘fish
mouth’ and ‘buffalo hump’.
3. CALCIUM METABOLISM
▪ Glucocorticoids inhibit intestinal absorption
and enhance renal excretion of Ca2+.
▪ Loss of osteoid (decreased formation and
increased resorption) indirectly results in loss
of Ca2+ from bone.
4. WATER EXCRETION
▪ In adrenal insufficiency, the capacity to
excrete a water load is markedly reduced—
such patients are prone to water intoxication
from i.v. infusions.
▪ Glucocorticoids also enhance secretory
activity of renal tubules.
BASICS OF MEDICAL PHARMACOLOGY
25
5. CVS
▪ They cause cutaneous vasoconstriction.
▪ They have a permissive role for the pressor
action of Adr and angiotensin. They also play
a permissive role in development of
hypertension-should be used cautiously in
hypertensives.
6. SKELETAL MUSCLES
▪ Optimum level of corticosteroids is needed
for normal muscular activity.
▪ Weakness occurs in both hypo- and
hypercorticism, but the causes are different.
▪ Hypocorticism: diminished work capacity
and weakness are primarily due to
hypodynamic circulation.
▪ Hypercorticism: excess mineralocorticoid
action→ hypokalaemia → weakness; Excess
glucocorticoid action → muscle wasting and
myopathy → weakness.
7. CNS
▪ Mild euphoria.
8. STOMACH
▪ They increases secretion of gastric acid and
pepsin - may aggravate peptic ulcer.
9. LYMPHOID TISSUE AND BLOOD CELLS
▪ Glucocorticoids enhance the rate of
destruction of lymphoid cells. However, a
marked lytic response is shown by malignant
lymphatic cells. This is the basis of their use
in lymphomas.
▪ Glucocorticoids increase the number of
RBCs, platelets and neutrophils in
circulation.
▪ They decrease lymphocytes, eosinophils and
basophils.
10. INFLAMMATORY RESPONSES
▪ Inflammatory response is suppressed by
glucocorticoids. They covers all components
and stages of inflammation.
▪ This includes attenuation of- increased
capillary permeability, local exudation,
cellular infiltration, phagocytic activity and
DR.V.S.PAWAR
 SECTION 7. DRUGS FOR THYROID DISORDER 31

SECTION 7.
DRUGS FOR THYROID DISORDER
DRUGS FOR HYPOTHYROIDISM μg i.v. followed by 100 μg i.v. OD till oral
therapy can be instituted.
L-THYROXINE 5. Nontoxic goiter
PHARMACOKINETICS AND INTERACTIONS 6. Papillary carcinoma of thyroid
▪ Oral bioavailability of l-thyroxine is ~ 75%,
but severe hypothyroidism can reduce oral DRUGS FOR HYPERTHYROIDISM
absorption.
▪ It should be administered in empty stomach
to avoid interference by food. CLASSIFICATION
▪ Sucralfate, iron, calcium and proton pump 1. Inhibit hormone synthesis (Antithyroid
inhibitors reduce l-thyroxine absorption. drugs)
▪ Dose-75 to 150 μg (1.7 μg/kg/day). a) Propylthiouracil,
▪ The recommended starting dose in the b) Methimazole,
elderly is 25 -50μg /day, which is then c) Carbimazole.
2. Inhibit iodide trapping (Ionic inhibitors)
increased by 12.5 to 25 μg at monthly
a) Thiocyanates (–SCN),
intervals. b) Perchlorates (–ClO4),
▪ Increase in dose is mostly needed during c) Nitrates (–NO3).
pregnancy. 3. Inhibit hormone release
▪ ELTROXIN 25 μg, 50 μg, 100 μg tabs, a) Iodine,
THYRONORM 12.5 μg, 25 μg, 50 μg, 62.5 b) Iodides of Na and K,
μg, 75 μg, 88 μg, 100 μg, 112 μg, 125 μg, c) Organic iodide.
137 μg, 150 μg tabs, THYROX 25 μg, 50 μg, 4. Destroy thyroid tissue
75 μg, 100 μg tabs. Radioactive iodine (131I, 125I, 123I).
ANTITHYROID DRUGS
Antithyroid drugs bind to the thyroid peroxidase
USES
and prevent oxidation of iodide/ iodotyrosyl
1. Cretinism
residues, thereby;
▪ Treatment with thyroxine should be started
a) Inhibit iodination of tyrosine residues in
as early as possible. Response is dramatic:
thyroglobulin
physical growth and development are
b) Inhibit coupling of iodotyrosine residues to
restored and further mental retardation is
form T3 and T4.
prevented.
2. Adult hypothyroidism (Myxoedema)
PHARMACOKINETICS
▪ Start with a low dose-50 μg of l-thyroxine
▪ All antithyroid drugs are quickly absorbed
daily and increase every 2–3 weeks to an
orally, widely distributed in the body, enter
optimum of 100–200 μg/day (adjusted by
milk and cross placenta; are metabolized in
clinical response and serum TSH levels).
liver and excreted in urine primarily as
▪ Further dose adjustments are made at 4–6
metabolites.
week intervals needed for reaching steady-
▪ Carbimazole acts largely by getting
state.
converted to methimazole in the body and is
3. Subclinical hypothyroidism
longer acting than propythiouracil.
4. Myxoedema coma
▪ It is an emergency; characterized by
ADVERSE EFFECTS
progressive mental deterioration due to acute
▪ Hypothyroidism and goiter can occur due to
hypothyroidism: carries significant mortality.
overtreatment, but is reversible on stopping
Drug of choice is l-thyroxine (T4) 200–500
the drug

BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR

 SECTION 8. DRUGS FOR DM 33

SECTION 8.
DRUGS FOR DM
INSULIN TYPES OF INSULIN PREPARATIONS
ACTIONS OF INSULIN REGULAR (SOLUBLE) INSULIN
▪ It is generally injected ½-1 hour before a
1. Insulin facilitates glucose transport across meal.
cell membrane.
2. The first step in intracellular utilization of ISOPHANE (NEUTRAL PROTAMINE HAGEDORN
glucose is its phosphorylation to form OR NPH) INSULIN
glucose- 6-phosphate. This is enhanced by ▪ It is mostly combined with regular insulin
insulin. (70:30 or 50:50) and injected s.c. twice daily
3. Insulin facilitates glycogen synthesis from before breakfast and before dinner.
glucose in liver, muscle and fat.
4. It also inhibits glycogen degrading enzyme HUMAN INSULINS
→ decreased glycogenolysis in liver. 1) HUMAN ACTRAPID: Human regular
5. Insulin inhibits gluconeogenesis. insulin; 40 U/ ml, 100 U/ml, WOSULIN-R
6. Insulin inhibits lipolysis. 40 U/ml inj vial and 100 U/ml pen injector
7. Insulin facilitates AA entry and their cartridge.
synthesis into proteins, as well as inhibits 2) HUMAN MONOTRAD, HUMINSULIN-L:
protein breakdown in muscle. Human lente insulin; 40 U/ml, 100 U/ml.
3) HUMINSULIN-N: Human isophane insulin
FATE OF INSULIN 40 U/ml. WOSULIN-N 40 U/ml inj. vial and
▪ It is a peptide; gets degraded in the g.i.t. if 100 U/ml pen injector cartridge.
given orally. 4) HUMINSULIN 30/70, HUMAN
▪ Injected insulin or that released from MIXTARD: Human soluble insulin (30%)
pancreas is metabolized primarily in liver and isophane insulin (70%), 40 U/ml. and
and to a smaller extent in kidney and 100 U/ml vials. WOSULIN 30/70: 40 U/ml
muscles. The plasma t½ is 5–9 min. vial and 100 U/ml cartridge.
5) ACTRAPHANE HM PENFIL: Human
CLASSIFICATION OF INSULIN soluble insulin 30% + isophane insulin 70%
RAPID ACTING 100 U/ml pen injector.
Insulin Onset(hr) Peak(hr) Duration(hr 6) WOSULIN 50/50: Human soluble insulin
Insulin lispro 0.2–0.3 1–1.5 3–5 50% + isophane insulin 50% 40 U/ml inj;
Insulin aspart 0.2–0.3 1–1.5 3–5 HUMINSULIN 50:50, HUMAN MIXTARD
Insulin glulisine 0.2–0.4 1–2 3–5 50/50 40 U/ml vial, 100 U/ml cartridge.
INSULIN ANALOGUES
SHORT ACTING ▪ It produce by recombinant DNA technology.
Insulin Onset(hr) Peak (hr) Duration (hr) Insulin lispro
Regular 0.5–1 2–3 6–8 1. It needs to be injected immediately before or
(soluble) insulin
even after the meal.
2. It can be used on 2–3 daily meal time. It
INTERMEDIATE ACTING
Insulin Onset (hr) Peak(hr) Duration (hr)
show greater reduction in HbA1c compared
Insulin zinc 1–2 8–10 20–24 to regular insulin.
suspension or HUMALOG 100 U/ml, 3 ml cartridge, 10 ml
Lente vial.
Neutral protamine 1–2 8–10 20–24
hagedorn (NPH) or
Insulin aspart
isophane insulin NOVOLOG, NOVORAPID 100 U/ml inj;
Insulin glulisine -Properties and advantages are
similar to insulin lispro.

BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR

 SECTION 9. RESPIRATORY SYSTEM DRUGS 39

SECTION 9.
RESPIRATORY SYSTEM DRUGS
DRUGS FOR COUGH MUCOLYTICS
BROMHEXINE
1. Pharyngeal demulcents ▪ A derivative of the alkaloid vasicine obtained
Lozenges, linctuses containing syrup, glycerine. from Adhatoda vasica (Vasaka), is a potent
2. Expectorants (Mucokinetics) mucolytic and mucokinetic, capable of
a) Bronchial secretion enhancers: inducing thin copious bronchial secretion.
1. Sodium or Potassium citrate, ▪ It depolymerises mucopolysaccharides
2. Potassium iodide, directly as well as by liberating lysosomal
3. Guaiphenesin enzymes—network of fibres in tenacious
4. Vasaka, sputum is broken.
5. Ammonium chloride. ▪ Side effects are rhinorrhoea and lacrimation,
b) Mucolytics: nausea, gastric irritation, hypersensitivity.
1. Bromhexine, Dose: Adults- 8 mg TDS, children 1–5 years-
2. Ambroxol, 4 mg BD, 5–10 years-4 mg TDS.
3. Acetyl cysteine, BROMHEXINE 8 mg tablet.
4. Carbocisteine
3. Antitussives (Cough centre suppressants) AMBROXOL
a) Opioids: ▪ A metabolite of bromhexine having similar
1. Codeine, mucolytic action, uses and side effects.
2. Pholcodeine. Dose: 15–30 mg TDS.
b) Nonopioids: AMBROLITE, AMBRODIL, 30 mg tab, 30
1. Noscapine, mg/5 ml liquid, 7.5 mg/ml drops.
2. Dextromethorpan.
c) Antihistamines: ACETYLCYSTEINE
1. Chlorpheniramine, ▪ It opens disulfide bonds in mucoproteins
2. Diphenhydramine and Promethazine. present in sputum—makes it less viscid, but
4.Bronchodilators: Salbutamol, Terbutalin. has to be administered directly into the
respiratory tract.
DEMULCENTS AND EXPECTORANTS ▪ MUCOMIX 200 mg/ml inj in 1,2,5 ml amps;
▪ Pharyngeal demulcents sooth the throat and injectable solution may be nebulized/instilled
reduce afferent impulses from the through trachiostomy tube.
inflamed/irritated pharyngeal mucosa, thus
provide symptomatic relief in dry cough CARBOCISTEINE
arising from throat. ▪ It liquefies viscid sputum in the same way as
▪ Expectorants (Mucokinetics) are drugs acetylcysteine and is administered orally
believed to increase bronchial secretion or (250–750 mg TDS).
reduce its viscosity, facilitating its removal ▪ It may break gastric mucosal barrier; is
by coughing. contraindicated in peptic ulcer patients.
▪ Sodium and potassium citrate are considered ▪ Side effects -gastric discomfort and rashes.
to increase bronchial secretion by salt action. ▪ MUCODYNE 375 mg cap, 250 mg/5 ml syr.
▪ Guaiphenesin, vasaka are plant products ▪ It is available in combination with
which are supposed to enhance bronchial amoxicillin or cephalexin for treatment of
secretion and mucociliary function. bronchitis, bronchiectasis, sinusitis, etc.
▪ Steam inhalation and proper hydration may
be more helpful in clearing airway mucus.

BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR

 SECTION 10. GIT DRUGS 45

SECTION 10.
GIT DRUGS
DRUGS FOR PEPTIC ULCER AND GERD 2. Gastric secretion
H2 blockers reduce gastric secretion. The
basal nocturnal acid secretion is suppressed
more completely.
3. The H2 blockers have antiulcerogenic effect.
4. Gastric ulceration due to stress and drugs
(NSAIDs, cholinergic, histaminergic) is
prevented.

PHARMACOKINETICS
▪ Cimetidine is adequately absorbed orally.
▪ Bioavailability is 60–80% due to first pass
hepatic metabolism.
▪ Absorption is not interfered by presence of
C.Ase.—Carbonic anhydrase; Hist.—Histamine; ACh.—Acetylcholine; CCK2—Gastrin cholecystokinin receptor; food in stomach.
▪ It crosses placenta and reaches milk, but
M.—Muscarinic receptor; N—Nicotinic receptor; H2—Histamine H2 receptor; EP3—Prostaglandin receptor; ENS—
Enteric nervous system; ECL cell—Enterochromaffin-like cell; GRP—Gastrin releasing peptide; + Stimulation; –
Inhibition. Ref-KDT Pharmacology.

1. Reduction of gastric acid secretion penetration in brain is poor.

a) H2 antihistamines: Cimetidine, Ranitidine, ▪ Excretion - in urine and bile.
Famotidine, Roxatidine
b) Proton pump inhibitors: Omeprazole, ADVERSE EFFECTS
Esomeprazole, Lansoprazole, Pantoprazole, ▪ Headache, dizziness, bowel upset, dry
Rabeprazole, Dexrabeprazole mouth, rashes.
c) Prostaglandin analogue: Misoprostol ▪ Cimetidine (but not other H2 blockers) has
2. Neutralization of gastric acid (Antacids) antiandrogenic action, increases plasma
a) Systemic: Sodium bicarbonate, Sod. Citrate prolactin and inhibits degradation of estradiol
b) Nonsystemic: Magnesium hydroxide, Mag. by liver.
trisilicate, Aluminium hydroxide gel, ▪ High doses given for long periods have
Magaldrate, Calcium carbonate produced gynaecomastia, loss of libido,
3. Ulcer protectives: Sucralfate, Colloidal impotence and temporary decrease in sperm
bismuth subcitrate (CBS) count.
4. Anti-H. pylori drugs: Amoxicillin, ▪ Transient elevation of plasma
Clarithromycin, Metronidazole, Tinidazole, aminotransferases; but hepatotoxicity is rare.
Tetracycline.
DOSE
H2 ANTAGONISTS For ulcer healing—400 mg BD or 800 mg at bed
▪ H2 Antagonists are highly effective drugs for time orally; maintenance—400 mg at bed time.
acid-peptic disease, but have been surpassed For stress ulcer—50 mg/hr i.v. infusion.
by proton pump inhibitors (PPIs). CIMETIDINE 200 mg, 400 mg, 800 mg tabs,
200 mg/2 ml inj.
CIMETIDINE
Cimetidine was the first H2 blocker to be RANITIDINE
introduced clinically. ▪ About 5 times more potent than cimetidine.
▪ No antiandrogenic action, does not increase
PHARMACOLOGICAL ACTIONS prolactin secretion or spare estradiol from
1. H2 blockade - Cimetidine and all other H2 hepatic metabolism—no effect on male
antagonists block histamine-induced gastric sexual function or gynaecomastia.
secretion.
BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR
 SECTION 10. GIT DRUGS 46
HP-KIT, HELIBACT: Omeprazole 20 mg 2 cap +
Amoxicillin 750 mg 2 tab + Tinidazole 500 mg 2 tab.
LANSI KIT: Lansoprazole 30 mg 1 cap + Amoxicillin 750
mg 1 tab + Tinidazole 500 mg 1 tab (one kit twice a day)
PYLOKIT, HELIGO: Lansoprazole 30 mg 2 cap +
Clarithromycin 250 mg 2 cap + Tinidazole 500 mg 2 tab.
LANPRO AC: Lansoprazole 30 mg 2 cap + Clarithromycin
250 mg 2 tab + Amoxicillin 750 mg 2 tab.
ANTIEMETIC DRUGS

These are drugs used to prevent or suppress

vomiting.

Ref-KDT Pharmacology.

ANTICHOLINERGICS
HYOSCINE
▪ It is the most effective drug for motion
sickness.
▪ It interference with the transmission of
vestibular input to the vomiting centers. This
acts to inhibit the vomiting impulse normally
CLASSIFICATION OF ANTIEMETICS DRUGS activated by motion sickness
▪ It has a brief duration of action; produces
sedation, dry mouth and other anticholinergic
side effects; suitable only for short brisk
journies.
Dose: 0.2–0.4 mg oral, i.m. Tab. KWELLS

DICYCLOMINE
▪ It has been used for prophylaxis of motion
sickness and for morning sickness.
Dose: 10–20 mg oral.

BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR

 SECTION 11. ADRENERGIC DRUGS
SECTION 11.
ADRENERGIC DRUGS
▪ These are drugs with actions similar to that
of Adr or of sympathetic stimulation.
▪ Direct sympathomimetics- They act directly
as agonists on α and/or β adrenoceptors.
▪ Indirect sympathomimetics- They act on
adrenergic neurone to release NA, which
then acts on the adrenoceptors.
▪ Mixed action sympathomimetics - They act
directly as well as indirectly.
PHARMACOLOGICAL ACTIONS
1. Heart
▪ Adr increases heart rate, Force of cardiac
contraction, cardiac output and oxygen
consumption of the heart.
▪ Adr increases conduction velocity of heart.
▪ When BP rises markedly, reflex bradycardia
occurs due to stimulation of vagus— this is
the usual response seen when NA is injected
i.v.
2. Blood vessels
▪ Both vasoconstriction (α) and vasodilatation
(β2) can occur depending on the drug, its
dose.
▪ Constriction occure mainly in cutaneous,
mucous membrane and renal beds.
▪ Dilatation occure mainly in skeletal muscles,
liver and coronaries.
3. BP
▪ Adr causes rise in systolic but fall in
diastolic BP when given by slow i.v. infusion
or s.c. injection.
▪ NA causes rise in systolic, diastolic and
mean BP.
▪ Isoprenaline causes rise in systolic but
marked fall in diastolic BP (β1—cardiac
stimulation, β2— vasodilatation).
BASICS OF MEDICAL PHARMACOLOGY
59
4. Respiration
▪ Adr and isoprenaline causes
bronchodilatation.
5. CNS
▪ Restlessness, apprehension and tremor may
occur.
6. Metabolic
▪ Adr causes glycogenolysis →
hyperglycaemia; lipolysis → rise in plasma
free fatty acid (FFA).
PREPARATIONS
1. Adrenaline (Epinephrine)
▪ For systemic action, 0.2–0.5 mg s.c., i.m.,
action lasts ½ to 2 hrs. ADRENALINE 1
mg/ml inj.
▪ As local vasoconstrictor, 1 in 200,000 to 1
in 100,000 added to lidocaine; in
XYLOCAINE with ADRENALINE inj.
2. Noradrenaline (Norepinephrine)
▪ 2–4 μg/min i.v. infusion.
▪ Action starts declining within 5 min of
discontinuing infusion.
▪ NORAD, VASCUE, NORDRIN 2 mg
(base)/2 ml amp.
3. Isoprenaline (Isoproterenol)
▪ 20 mg sublingual, 1–2 mg i.m., 5–10 μg/min
i.v. infusion;
▪ Action lasts 1–3 hrs.
▪ ISOPRIN, ISOSOL 4 mg/2 ml inj,
NEOEPININE 20 mg sublingual tablets.
ADVERSE EFFECTS AND CONTRAINDICATIONS
▪ Transient restlessness, headache, palpitation,
anxiety, tremor and pallor may occur after
s.c./ i.m. injection of Adr.
▪ Marked rise in BP leading to cerebral
haemorrhage, ventricular tachycardia/
fibrillation, angina, myocardial infarction are
the hazards of large doses or i.v. injection of
Adr.
▪ Adr is contraindicated in hypertensive,
hyperthyroid and angina patients.
DOPAMINE (DA)
▪ It is a dopaminergic (D1 and D2) as well as
adrenergic α and β1 (but not β2) agonist.
DR.V.S.PAWAR
 SECTION 11. ADRENERGIC DRUGS 59
spray
Oxymetazoline 0.025– NASIVION,
0.05% SINAREST
topical in 0.025%
nose (pediatric),
0.05% nasal
drops.

Naphazoline 0.1% PRIVINE 0.1%

topical in nasal drops.
nose
▪ Regular use of these agents for long periods
should be avoided because mucosal ciliary
function is impaired: atrophic rhinitis and
anosmia can occur due to persistent
Drug Dose M/N vasoconstriction.
Xylometazoline 0.05–0.1% OTRIVIN
topical in 0.05%
nose (pediatric), 0.1%
(adult) nasal
drops and nasal

BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR

 SECTION 12. ADRENERGIC BLOCKING DRUGS
SECTION 12.
ADRENERGIC BLOCKING DRUGS
ALPHA- ADRENERGIC BLOCKING DRUGS
GENERAL EFFECTS OF α BLOCKERS
1. Blockade of vasoconstrictor α1 (also α2)
receptors reduces peripheral resistance and
causes pooling of blood in capacitance
vessels → venous return and cardiac output
are reduced → fall in BP.
2. Reflex tachycardia occurs due to fall in
mean arterial pressure.
3. Intestinal motility is increased.
4. Hypotension produced by α blockers can
reduce renal blood flow → g.f.r. is reduced
→ Na+ retention and expansion of blood
volume.
5. Tone of smooth muscle in bladder trigone,
sphincter and prostate is reduced by blockade
of α1 receptors → urine flow in patients with
benign hypertrophy of prostate (BHP) is
improved.
PRAZOSIN
▪ It block all subtypes of α1 receptor.
▪ Postural hypotension can occurs, which may
cause dizziness and fainting as ‘first dose
effect’. This can be minimized by starting
with a low dose and taking it at bedtime.
Subsequently tolerance develops to this side
effect.
▪ Prazosin is effective orally (bioavailability
~60%), metabolized in liver and excreted
primarily in bile.
▪ It used as an antihypertensive.
BASICS OF MEDICAL PHARMACOLOGY
61
▪ Other uses are—Raynaud’s disease and
benign hypertrophy of prostate (BHP).
Dose- Start with 0.5–1 mg at bedtime; usual
dose 1–4 mg BD or TDS.
MINIPRESS XL: 2.5 mg and 5 mg tablets; 1
tab OD. PRAZOPRES 0.5, 1.0 and 2.0 mg
tabs.
TERAZOSIN
▪ Similar to prazosin; with higher
bioavailability (90%) and a single daily dose
lowers BP over 24 hrs.
▪ It used in BPH which may retard the
progression of prostatic hypertrophy.
Dose: 2–10 mg OD. HYTRIN 1, 2, 5 mg tab.
DOXAZOSIN
▪ Similar to terazosin.
▪ It is used in hypertension and BPH.
Dose: 1 mg OD initially, increase upto 8 mg
BD; DOXAPRESS 1, 2, 4 mg tabs.
ALFUZOSIN
▪ It used for symptomatic treatment of BPH.
Dose: 2.5 mg BD-QID or 10 mg as extended
release (ER) tablet. ALFOO 10 mg ER tab.
TAMSULOSIN
▪ It is uroselective α 1A blocker and is
effective in improving BPH symptoms,
because α1A subtype predominate in the
bladder base and prostate.
▪ It is not used as an antihypertensive.
Dose- 0.2, 0.4 mg OD
URIMAX, DYNAPRES 0.2, 0.4 mg cap.
USES OF α BLOCKERS
1. Hypertension.
2. Benign hypertrophy of prostate (BHP)
▪ Two classes of drugs are available:
a) α1 adrenergic blockers (prazosin like):
decrease tone of prostatic/bladder neck
muscles.
b) 5-α reductase inhibitor (finasteride): arrest
growth/reduce size of prostate.
DR.V.S.PAWAR
 SECTION 13. CARDIOVASCULAR DRUGS 65

SECTION 13.
CARDIOVASCULAR DRUGS
▪ They form effective combinations with
diuretics and CCBs.
▪ They are preferentially used in diabetic
hypertensive patients, for cardioprotection
post-myocardial infarction and in
hypertension with heart failure.
▪ These are also known to reduce proteinuria
especially in diabetics.
▪ ACE inhibitors retard diabetic nephropathy,
reduce attendant proteinuria, and are
renoprotective.

PHARMACOKINETICS
ANGIOTENSIN CONVERTING ENZYME ▪ About 70% of orally administered captopril
INHIBITORS (ACE-INHIBITOR) is absorbed. Presence of food in stomach
Drug Dose M/N reduces bioavailability of Captopril.
Captopril 25–75 mg/day T.Captopril 12.5,25 mg. ▪ Penetration in brain is poor.
Enalapril 5–40 mg/day T.Envas 2.5,5,5 mg. ▪ It is partly metabolized and partly excreted in
Lisinopril 5–40 mg/day T. Listril 5, 10 mg. urine.
Fosinopril 10–40 mg/day T. Fovas 10, 20 mg.
Quinapril 2.5–10 mg/day T.Accupril10,20,40mg. ADVERSE EFFECTS
Ramipril 1.25-10mg/day T. Ramipres 2.5, 5 mg
1. Cough due to increase bradykinin in airway.
Imidapril 5-10 mg/day T. Tanatril 5, 10 mg.
2. Angioedema.
Trandolapril 2-4 mg/day T. Zetpril 1, 2 mg.
3. Proteinuria.
Benazepril 20-40mg/day T. Benace 10mg.
4. Taste change.
5. Orthostatic hypotension.
▪ ACE-inhibitor block the conversion of
6. Pregnancy related problem (Foetopathic):
angiotensin I to angiotensin II. Therefore,
foetal growth retardation, hypoplasia of
these lower arteriolar resistance.
organs and foetal death may occur.
7. Renal failure: is precipitated by ACE
inhibitors in patients with bilateral renal
artery stenosis due to dilatation of efferent
arterioles and fall in glomerular filtration
pressure. ACE inhibitors are contraindicated
in such patients.
▪ ACE-inhibitor preferentially relax the renal 8. Increase Potassium excess (Hyperkalemia).
efferent arterioles, thereby reduce 9. Leucopenia
intraglomerular pressure, and may cause a 10. Headache, dizziness, nausea and bowel
rise in serum creatinine. They should be upset.
avoided when serum creatinine is >3 mg%. 11. Urticaria & rash.

INTERACTIONS
▪ Diuretics synergise with the hypotensive
action of ACE inhibitors by depleting Na+
levels.
▪ Indomethacin (and other NSAIDs) attenuate
the hypotensive action by retaining salt and

BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR

 SECTION 13. CARDIOVASCULAR DRUGS 65

NOTES

BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR

 SECTION 14. ANTI-CHOLINERGIC DRUGS 73

SECTION 14.
ANTI-CHOLINERGIC DRUGS
This drugs block the actions of Ach on
autonomic effectors and in the CNS exerted
through muscarinic receptors.
▪ About 50% of atropine is metabolized in
liver and rest is excreted unchanged in urine.
▪ It has a t½ of 3–4 hours.
▪ Atropine sulfate: 0.6–2 mg i.m., i.v.
(children 10 μg/kg), 1–2% topically in eye.
ATROPINE SULPHATE: 0.6 mg/ml inj.,
1% eye drop/ointment; ATROSULPH 1%
eye drop, 5% eye oint.
▪ Hyoscine hydrobromide: 0.3–0.5 mg oral,
i.m.; also as transdermal patch.

ATROPINE SUBSTITUTES

1. HYOSCINE BUTYL BROMIDE

▪ Less potent and longer acting than atropine;
PHARMACOLOGICAL ACTIONS ▪ Used for esophageal and gastrointestinal
(ATROPINE AS PROTOTYPE) spastic conditions.
1. CVS Dose: 20–40 mg oral, i.m., s.c., i.v.
▪ Atropine cause tachycardia. BUSCOGAST 10 mg tab., 20 mg/ml amp.
▪ It raise BP.
2. CNS 2. IPRATROPIUM BROMIDE
▪ It stimulate CNS. ▪ It acts selectively on bronchial muscle.
▪ Atropine stimulates many medullary centres ▪ It is more suitable for regular prophylactic
—vagal, respiratory, vasomotor. use for B. Asthma. Action lasts 4–6 hours.
▪ It depresses vestibular excitation and has ▪ Ipratropium is more effective in COPD than
antimotion sickness property. in bronchial asthma.
3. Eye Dose: 40–80 μg by inhalation IPRAVENT
Topical instillation of atropine causes 20 μg and 40 μg/puff metered dose inhaler, 2
mydriasis. puffs 3–4 times daily; 250 μg/ml respirator
4. Smooth muscles soln., 0.4–2 ml nebulized in conjunction with
▪ Visceral smooth muscles are relaxed by a β2 agonist 2–4 times daily.
atropine.
▪ Tone and amplitude of contractions of 3. TIOTROPIUM BROMIDE
stomach and intestine are reduced. ▪ It produce long lasting bronchodilatation.
5. Glands
▪ Atropine decreases sweat, salivary, 4. CLIDINIUM
tracheobronchial and lacrimal secretion. ▪ This antisecretory, antispasmodic has been
▪ Skin and eyes become dry, talking and used in combination with benzodiazepines
swallowing may be difficult. for nervous dyspepsia, gastritis, irritable
bowel syndrome, colic, peptic ulcer, etc.
PHARMACOKINETICS Dose: ARWIN 2.5 mg tab with
▪ Atropine and hyoscine are rapidly absorbed chlordiazepoxide 5 mg.
from g.i.t.
▪ Applied to eyes they freely penetrate cornea.
BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR
 SECTION 15. DIURETICS 75

SECTION 15.
DIURETICS
Diuretics (natriuretics) are drugs which cause a 2. BUMETANIDE
net loss of Na+ and water in urine. ▪ It is similar to furosemide in all respects, but
is 40 times more potent.
HIGH CEILING (LOOP) DIURETIC ▪ It induces very rapid diuresis and is highly
1. FUROSEMIDE (FRUSEMIDE) effective in pulmonary edema.
Mechanism of action ▪ Bumetanide may act in some cases not
responding to furosemide, and may be
tolerated by patients allergic to furosemide.
▪ Oral bioavailability is 80–100%.
▪ Bumetanide is partly metabolized and partly
excreted unchanged in urine.
▪ Plasma t½ ~60 min.
▪ It is preferred for oral use in severe CHF.
Dose: 1–5 mg oral OD in the morning, 2–4
mg i.m./i.v., (max. 15 mg/day in renal
failure). BUMET, 1 mg tab., 0.25 mg/ml inj.
▪ The major site of action is the thick AscLH
(therefore called loop diuretics).
3. TORASEMIDE (TORSEMIDE)
▪ Furosemide inhibits Na+-K+-2Cl¯
▪ Similar to furosemide, but 3 times more
cotransport.
potent.
▪ Loop diuretics bind to a chloride channel
▪ Oral absorption is more rapid and more
receptor site in the ascending limb of the
complete. The t½ (3.5 hours) and duration of
loop of Henle, inhibiting the reabsorption of
action (4–8 hours) are longer.
filtered sodium and chloride.
▪ Torasemide has been used in edema and in
▪ It also inhibits water reabsorption by the
hypertension.
collecting ducts.
Dose: 2.5–5 mg OD in hypertension; 5–20
▪ It is active even in patients with relatively
mg/day in edema; upto 100 mg BD in renal
severe renal failure.
failure. DYTOR 5, 10, 20, 100 mg tabs, 10
▪ The onset of action is prompt (I.V. 2–5 min.,
mg/2 ml inj
I.M.10–20 min., oral 20–40 min.) and
duration of action is short (3–6 hours).
USE OF HIGH CEILING DIURETICS
▪ Furosemide increases Ca2+ excretion
1. Edema:
(contrast thiazides which reduce it) as well as
▪ Diuretics are used in cardiac, hepatic or renal
Mg2+excretion.
oedema.
▪ It tends to raise blood uric acid level.
▪ They preferred in CHF for rapid mobilization
Pharmacokinetics
of edema fluid.
▪ Furosemide is rapidly absorbed orally but
2. Acute pulmonary edema (acute LVF):
bioavailability is about 60%.
Intravenous administration of furosemide
▪ It mainly excreted by glomerular filtration as
produces prompt relief.
well as tubular secretion.
3. Cerebral edema:
▪ Plasma t½ averages 1–2 hour.
Though osmotic diuretics are primarily used
Dose:
to lower intracranial pressure by withdrawing
20–80 mg once daily in the morning.
water, furosemide may be combined to
In renal insufficiency, upto 200 mg 6 hourly
improve efficacy.
has been given by i.m./i.v. route.
4. Hypertension:
In pulmonary edema 40–80 mg i.v.
High ceiling diuretics are indicated in
LASIX 40 mg tab., 20 mg/2 ml inj. LASIX
hypertension only in the presence of renal
HIGH DOSE 500 mg tab, 250 mg/25 ml inj.
BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR
 SECTION 16. HAEMATINICS, HEPARIN, FIBRINOLYTIC & ANTI-PLATELETS DRUGS
SECTION 16.
HAEMATINICS, HEPARIN, FIBRINOLYTICS & ANTI-PLATELETS DRUGS
HAEMATINICS
These are substances required for the formation
of blood, and are used for treatment of anaemias
ORAL IRON
▪ It is a preferred route of iron administration.
▪ The elemental iron content should be taken
into consideration.
▪ Some oral preparations are:
Ferrous sulfate, Ferrous gluconate, Ferrous
fumarate,Colloidal ferric hydroxide,Carbonyl
iron, Ferrous succinate, Iron choline citrate,
Iron calcium complex, Ferric ammonium
citrate.
▪ Absorption is much better when iron
preparations are taken in empty stomach.
However, side effects are also more.
Dose: 180-200 mg elemental iron (infants
and children 3–5 mg/kg).
Prophylactic dose is 30 mg iron daily.
Tab./Syp OROFER XT, FERIARK XT, Cap.
AUTRIN.
ADVERSE EFFECTS OF ORAL IRON
Epigastric pain, heartburn, nausea, vomiting,
bloating, staining of teeth, metallic taste,
colic, Constipation is more common than
diarrhoea.
PARENTERAL IRON
INDICATION
a. Oral iron is not tolerated: bowel upset is too
much.
b. Failure to absorb oral iron: malabsorption;
inflammatory bowel disease.
c. In presence of severe deficiency with chronic
bleeding.
Iron requirement (mg) = 4.4 × body weight
(kg) × Hb deficit (g/dl)
ADVERSE EFFECTS
Local: Pain at site of i.m. injection, pigmentation
of skin, sterile abscess.
Systemic : Fever, headache, joint pains, flushing,
palpitation, chest pain, dyspnoea, lymph node
enlargement.
BASICS OF MEDICAL PHARMACOLOGY
79
IRON-DEXTRAN
▪ Iron dextran can be injected 2 ml daily, or on
alternate days, or 5 ml each side on the same
day.
▪ Intravenous: After a test dose of 0.5 ml iron
dextran injected i.v. over 5–10 min, 2 ml can
be injected per day taking 10 min for the
injection.
▪ Alternatively, the total calculated dose is
diluted in 500 ml of glucose/saline solution
and infused i.v. over 6–8 hours under
constant observation.
▪ Injection should be terminated if the patient
complains of giddiness, paresthesias or
tightness in the chest.
FERRIC CARBOXYMALTOSE
▪ It is the latest formulation of iron
▪ It is administered either as daily 100 mg i.v.
injection, or upto 1000 mg is diluted with
100 ml saline (not glucose solution) and
infused i.v. taking 15 min or more.
USES
Iron deficiency anaemia
▪ Iron should be normally administered orally;
parenteral therapy is to be reserved for
special circumstances.
▪ A rise in Hb level by 0.5–1 g/dl per week is
an optimum response to iron therapy
▪ However, therapy should be continued till
normal Hb level is attained (generally takes
1–3 months).
DR.V.S.PAWAR
 SECTION 17. ANTI-TUBERCULAR DRUGS 85

SECTION 17.
ANTI-TUBERCULAR DRUGS
2. These are due to interference with production
of the active coenzyme pyridoxal phosphate
from pyridoxine.
3. Pyridoxine given prophylactically (10
mg/day) prevents the neurotoxicity.
4. Hepatitis, a major adverse effect of INH.
5. Other side effects are lethargy, rashes, fever,
acne and arthralgia.
ISONEX 100, 300 mg tabs.

RIFAMPIN (RIFAMPICIN, R)
▪ Rifampin is bactericidal to M. tuberculosis
and many other gram-positive and gram-
negative bacteria like Staph. aureus, N.
meningitidis, H. influenzae, E. coli,
Klebsiella, Pseudomonas, Proteus.
▪ Against TB bacilli, it is as efficacious as
INH.
▪ The bactericidal action covers all TB bacilli,
but acts best on slowly or intermittently
FIRST LINE ANTI-TB DRUGS dividing ones.
▪ Both extra- and intracellular organisms are
ISONIAZID (ISONICOTINIC ACID HYDRAZIDE, H)
affected.
▪ Isoniazid is an essential component of all
Mechanism of action
antitubercular regimens.
Rifampin inhibits DNA dependent RNA
▪ It is primarily tuberculocidal.
polymerase of mycobacterium.
▪ Fast multiplying organisms are rapidly killed,
Pharmacokinetics
but quiescent ones are only inhibited.
1. It is well absorbed orally, (bioavailability is ~
▪ It acts on extracellular as well as on
70%), but food decreases absorption;
intracellular TB (bacilli present within
rifampin is to be taken in empty stomach.
macrophages).
2. It penetrates intracellularly, enters tubercular
Mechanism of action
cavities and placenta.
It inhibits of synthesis of mycolic acids
3. It is metabolized in liver and excreted mainly
which are unique fatty acid components of
in bile, some in urine also.
mycobacterial cell wall.
Adverse effects
Pharmacokinetics
1. Similar to INH.
1. INH is completely absorbed orally and
2. Hepatitis and Jaundice.
penetrates all body tissues, tubercular
3. Cutaneous syndrome: flushing, pruritus +
cavities, placenta and meninges.
rash, redness and watering of eyes.
2. It is extensively metabolized in liver and
4. Flu syndrome: with chills, fever, headache,
excreted in urine.
malaise and bone pain.
Adverse effects
5. Abdominal syndrome: nausea, vomiting,
1. Peripheral neuritis and a variety of
abdominal cramps with or without diarrhoea.
neurological manifestations (paresthesias,
6. Urine and secretions may become orange-
numbness, mental disturbances.
red— but this is harmless.

BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR

 SECTION 18. ANTI-FUNGAL DRUGS 87

SECTION 18.
ANTI FUNGAL DRUGS
FUNGAL INFECTIONS ANTIFUNGAL DRUGS

CLASSIFICATION
1. Antibiotics
▪ Amphotericin B (AMB), Nystatin, Hamycin
▪ Griseofulvin
2. Azoles
A. Imidazoles
▪ Topical: Clotrimazole, Econazole,
TINEA CAPITIS TINEA CORPORIS
Miconazole, Oxiconazole
▪ Systemic: Ketoconazole
B. Triazoles:
▪ Fluconazole, (systemic)
▪ Itraconazole,
▪ Voriconazole,
▪ Posaconazole
3. Allylamine Terbinafine
TINEA PEDIS
4. Other topical agents
▪ Tolnaftate, Undecylenic acid, Benzoic acid,
Quiniodochlor, Ciclopirox olamine,
Butenafine, Sod. thiosulfate.

AMPHOTERICIN B (AMB)
▪ It is obtained from Streptomyces nodosus.
▪ AMB is active against—Candida albicans,
Histoplasma capsulatum, Cryptococcus
TINEA UNGUIUM TINEA BARBAE
neoformans, Blastomyces dermatitidis,
Rhodotorula, Aspergillus, Sporothrix, etc.
▪ Concentrations of AMB attained in infected
skin are low and ineffective.
▪ It is fungicidal at high and static at low
concentrations.
Pharmacokinetics
▪ AMB is not absorbed orally; it can be given
orally for intestinal candidiasis without
PITYRIASIS ROSEA PITYRIASIS ALBA systemic toxicity.
▪ Penetration in CSF is poor.
▪ About 60% of AMB is metabolized in the
liver. Excretion occurs slowly both in urine
and bile.
Dose
▪ Amphotericin B can be administered orally
(50–100 mg QID) for intestinal
moniliasis;also topically for vaginitis,
otomycosis, etc.: FUNGIZONE OTIC 3%
P. VERSICOLOUR CANDIDIASIS ear drops. FUNGIZONE INTRAVENOUS,
MYCOL 50 mg vial.

BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR

 SECTION 19. ANTI-VIRAL DRUGS 91

SECTION 19.
ANTI VIRAL DRUGS
ANTI-RETROVIRUS DRUGS ▪ AZT also reduces neurological
manifestations of AIDS and new Kaposi’s
▪ These are drugs active against human lesions do not appear.
immunodeficiency virus (HIV) which is a ▪ Mortality among AIDS patients is reduced.
retrovirus. ▪ However, beneficial effects are limited from
▪ They do not cure the infection but they are a few months to a couple of years after which
useful in prolonging and improving the progressively non-responsiveness develops.
quality of life and postponing complications
of AIDS or AIDS related complex (ARC). DIDANOSINE (DDI)
▪ It is a purine nucleoside analogue which
NUCLEOSIDE REVERSE TRANSCRIPTASE inhibits HIV reverse transcriptase and
INHIBITORS (NRTIS) terminates proviral DNA.
ZIDOVUDINE ▪ Its use has declined due to higher toxicity
▪ It is a thymidine analogue. than other NRTIs.
▪ It inhibits viral reverse transcriptase. Side effects
▪ Zidovudine prevents infection of new cells ▪ Peripheral neuropathy.
by HIV, but has no effect on proviral DNA ▪ Diarrhoea, abdominal pain, dry mouth and
that has already integrated into the host nausea.
chromosome. Dose: 400 mg/day (for > 60 kg BW), 250
▪ The oral absorption of AZT is rapid, but mg/day (< 50 kg BW) 1 hour before or 2
bioavailability is ~65%. hour after meals. DDRETRO 250 mg, 400
▪ It crosses placenta and is found in milk. mg tabs.
Dose
Adults 300 mg BD; Children 180 mg/m2 STAVUDINE (D4T)
(max 200 mg) 6–8 hourly. ▪ Similar to AZT.
RETROVIR, ZIDOVIR 100 mg cap, 300 mg ▪ It should also not be combined with
tab, 50 mg/5 ml syr didanosine, because both cause peripheral
neuropathy.
Adverse effects Side effects
▪ Anaemia, neutropenia. ▪ Frequent peripheral neuropathy,
▪ Nausea, anorexia, abdominal pain, headache, lipodystrophy, lactic acidosis.
insomnia and myalgia are common at the Dose: 30 mg BD. STAVIR 30, 40 mg caps.
start of therapy, but diminish later.
▪ Myopathy, pigmentation of nails, lactic LAMIVUDINE (3TC)
acidosis, hepatomegaly, convulsions and ▪ It inhibits HIV reverse transcriptase as well
encephalopathy. as HBV DNA polymerase.
Use ▪ Its incorporation into DNA results in chain
▪ Zidovudine is used in HIV infected patients termination.
only in combination with at least 2 other ▪ Oral bioavailability is high and plasma t½
ARV drugs. longer (6–8 hours).
▪ HIV-RNA titer is reduced to undetectable ▪ It is mainly excreted unchanged in urine.
levels and CD4 count increases ▪ Lamivudine is used in combination with
progressively. other anti-HIV drugs.
▪ Immune status is improved and opportunistic ▪ It is an first line drug for AIDS and chronic
infections become less common. hepatitis B.
▪ There is a sense of well-being and patients ▪ HBV viraemia recure after 1–4 years due to
gain weight. emergence of resistant mutants.

BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR

 SECTION 20. ANTI-AMOEBIC DRUGS
SECTION 20.
ANTI-AMOEBIC DRUGS
These are drugs useful in infection caused by the
anaerobic protozoa Entamoeba histolytica.
METRONIDAZOLE
▪ It is active against Giardia lamblia,
Entamoeba histolytica as well as many
anaerobic bacteria. Metronidazole does not
affect aerobic bacteria.
Pharmacokinetics
▪ Metronidazole is almost completely absorbed
from the small intestines. Plasma t½ is 8 hrs.
▪ Metabolism occurs in liver and excreated by
Kidney.
Adverse effects
▪ Anorexia, nausea, metallic taste and
abdominal cramps.
▪ Headache, glossitis, dryness of mouth,
Thrombophlebitis and dizziness.
▪ Peripheral neuropathy and CNS effects on
prolonged administration.
Contraindications
▪ Neurological disease.
▪ First trimester of pregnancy.
Dose: 400mg TDS x 7days. children 30–50
mg/kg/day. FLAGYL, METROGYL 200,
400 mg tab, 200 mg/5 ml susp; 500 mg/100
ml i.v. infusion; METROGYL GEL: 1% gel
for vaginal/topical use.
Uses
1. Amoebiasis.
2. For dysentery and liver abscess.
3. In severe cases of amoebic dysentery or liver
abscess 500 mg may be infused i.v. slowly
every 6–8 hours.
4. Giardiasis.
5. Trichomonas vaginitis.
6. Anaerobic bacterial infections
7. Helicobacter pylori gastritis/peptic ulcer:
combined with amoxicillin/clarithromycin
and a proton pump inhibitor in triple drug 2
week regimens.
TINIDAZOLE
▪ It is similar to metronidazole. Duration of
action is longer.
▪ It appears to be better tolerated; the incidence
of side effects is lower.
BASICS OF MEDICAL PHARMACOLOGY
96
Doses & Uses:
1. Intestinal amoebiasis: 2 g OD for 3 days
(children 30–50 mg/kg/day) or 0.6 g BD for
5–10 days.
2. Amoebic liver abscess: The 2 g daily dose
for 3–6 days.
3. Trichomoniasis and giardiasis: 2 g single
dose or 0.6 g OD for 7 days.
4. Anaerobic infections: 2 g followed by 0.5 g
BD for 5 days.
5. H. pylori: 500 mg BD for 2 weeks in triple
combination. TINIBA 300, 500, 1000 mg
tabs; 800 mg/400 ml i.v. infusion.
SECNIDAZOLE
▪ It is similar to metronidazole.
▪ Side effect -similar to metronidazole.
Dose:
1. 2 g single dose (children 30 mg/kg) for mild
intestinal amoebiasis, giardiasis, trichomonas
vaginitis.
2. For acute amoebic dysentery 0.5 g TDS for 5
days is recommended. SECNIL 0.5, 1.0 g
tabs.
ORNIDAZOLE
▪ It has activity similar to metronidazole, but it
is slowly metabolized.
▪ Dose – Similar to tinidazole.
▪ Side effect -similar to tinidazole.
ORNIDA 500 mg tab, 125 mg/5 ml susp
Tab.O2, NORFLOX OZ
DR.V.S.PAWAR
 SECTION 21. ANTI-HELMINTHIC DRUGS
SECTION 21.
ANTI-HELMINTHIC DRUGS
Anthelmintics are drugs that either kill
(vermicide) or expel (vermifuge) infesting
helminths.
MEBENDAZOLE
▪ It effective in roundworm, hook worm,
Enterobius and Trichuris infestations.
▪ It is also used in hydatid cysts in the liver.
▪ It blocks glucose uptake in the parasite and
depletes its glycogen stores.
Pharmacokinetics
▪ Absorption of mebendazole from intestines is
minimal; excreted in the urine/faeces.
Adverse effects
▪ Diarrhoea, nausea and abdominal pain.
▪ Incidents of expulsion of Ascaris from mouth
or nose have occurred, probably due to
starvation of the parasite and their slow
death.
▪ Allergic reactions, loss of hair and
granulocytopenia with high doses.
▪ It is contraindicated in pregnancy.
Uses and administration
▪ For Roundworm, Hookworm, Whipworm:
For >2 years of age-100 mg twice a day for 3
days. For 1–2 yr age- 50 mg twice a day for 3
days. MEBEX, WORMIN 100 mg chewable
tab and 100 mg/5 ml suspension.
▪ For Hydatid disease: 200–400 mg BD or
TDS for 3–4 weeks.
ALBENDAZOLE
▪ Single dose treatment has produced cure
rates in ascariasis, hookworm and
enterobiasis.
Mechanism of action
▪ Similar to that of mebendazole.
Pharmacokinetics
▪ It absorbed orally.
▪ It is enhanced when the drug is taken with
fatty meal.
▪ It excreted in urine.
Side effects
▪ Gastrointestinal side effects, dizziness.
▪ On prolonged use it caused headache, fever,
alopecia, jaundice and neutropenia.
▪ Use in pregnant women is contraindicated.
BASICS OF MEDICAL PHARMACOLOGY
97
ZENTEL, BANDY 400 mg tab, 200 mg/5 ml
suspension.
Uses
▪ Ascaris, hookworm, Enterobius and
Trichuris: a single dose of 400 mg (for
adults and children above 2 yrs, 200 mg for
1–2 yr age).
▪ Tapeworms and strongyloidosis: 400 mg
daily for 3 consecutive days.
▪ Neurocysticercosis: Usually 8–15 days
course of 400 mg BD (15 mg/kg/day) is
employed.
▪ Hydatid disease: 400 mg BD for 4 weeks,
repeat after 2 weeks (if required), up to 3
courses.
▪ Filariasis: A single dose of Albendazole
combination with either diethylcarbamazine
(DEC) or ivermectin given yearly has been
used in mass programmes to suppress
microfilaraemia and disease transmission.
PYRANTEL PAMOATE
▪ Effective against Ascaris, Enterobius and
Ancylostoma.
▪ Only 10–15% of an oral dose of pyrantel
pamoate is absorbed.
▪ It metabolized and excreted in urine.
Adverse effects
G.I. symptoms, headache and dizziness is
reported.
Use and administration
For Ascaris, Ancylostoma and Enterobius: a
single dose of 10 mg/kg is recommended.
NEMOCID, 250 mg tab, 50 mg/ml suspension.
PIPERAZINE
▪ It is a second choice drug to
albendazole/mebendazole.
▪ It is partly metabolized in liver and excreted
in urine.
Side effects
▪ Nausea, vomiting, abdominal discomfort and
urticaria.
▪ Dizziness and excitement occur at high
doses; toxic doses produce convulsions;
death is due to respiratory failure.
DR.V.S.PAWAR
 SECTION 22. ANTI-MALARIAL DRUGS
SECTION 22.
ANTI-MALARIAL DRUGS
▪ Malaria is caused by protozoa of the genus
Plasmodium.
▪ The malarial parasite is transmitted by the
mosquito vector of the Anopheles family.
CHLOROQUINE
▪ It is a rapidly acting erythrocytic
schizontocide against all species of
plasmodia.
▪ Most of plasmodium has acquired significant
resistance to CQ.
Mechanism of action
▪ Plasmodia derive nutrition by digesting
haemoglobin in their acidic vacuoles.
▪ By accumulating in the acidic vecuoles of the
parasite, it raises the vacuolar pH and thereby
interferes with degradation of haemoglobin
by parasitic lysosomes.
▪ It inhibits DNA and RNA biosynthesis and
produces rapid degradation of ribosomes and
dissimilation of ribosomal RNA.
▪ Inhibition of protein synthesis is also
observed, evidently as a secondary effect.
BASICS OF MEDICAL PHARMACOLOGY
99
Pharmacokinetics
▪ It is well absorbed orally.
▪ Its accumulation in retina is responsible for
the ocular toxicity seen with prolonged use.
▪ Chloroquine is partly metabolized by liver
and slowly excreted in urine.
Adverse effects
▪ Nausea, vomiting, anorexia, uncontrollable
itching, epigastric pain, uneasiness, difficulty
in accommodation and headache.
▪ Prolonged use of high doses (as needed for
rheumatoid arthritis) may cause loss of vision
due to retinal damage.
▪ Corneal deposits may also occur and affect
vision, but are reversible on discontinuation.
▪ Loss of hearing, rashes, photoallergy, mental
disturbances, myopathy and graying of hair
can occur on long-term use.
Dose:
Chloroquine 600 mg (10 mg/kg) followed by
300 mg (5 mg/kg) after 8 hours and then for
next 2 days (total 25 mg/kg over 3 days).
LARIAGO 250 mg tab, 500 mg forte tab,
100 mg (base) per 10 ml oral susp.
AMODIAQUINE (AQ)
▪ Similar to CQ in properties.
Dose: 10-12 mg of base/kg body wt OD for 3
days.
AMODIA 200 mg tab.
MEFLOQUINE
Mechanism of action
▪ Like CQ it accumulates in infected RBCs
binds to haeme and this complex may be
damaging the parasite membranes.
Pharmacokinetics
▪ Oral absorption of MQ is good.
▪ Metabolism occurs in liver and it is primarily
secreted in bile.
Adverse effects & Contraindications
▪ MQ is bitter in taste.
▪ Dizziness, nausea, vomiting, diarrhoea,
abdominal pain, sinus bradycardia.
DR.V.S.PAWAR
 SECTION 22. ANTI-MALARIAL DRUGS 99

▪
TREATMENT OF SEVERE MALARIA

BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR

 SECTION 23. ANTIBIOTICS 103

SECTION 23.
ANTIBIOTICS
SULFONAMIDES ▪ It produces burning sensation and severe pain
▪ Sulfonamides are primarily bacteriostatic on topical application.
against many gram-positive and gram- SULFAMYLON 1% cream for surface
application.
negative bacteria.
▪ Currently it used in combination with ADVERSE EFFECTS
trimethoprim (as cotrimoxazole) or ▪ Nausea, vomiting and epigastric pain.
pyrimethamine (for malaria). ▪ Hypersensitivity reactions and hepatitis.
▪ Haemolysis can occur in G-6-PD deficient
MECHANISM OF ACTION individuals with high doses of sulfonamides.
Sulfonamides inhibit bacterial folate synthase →
FA is not formed and a number of essential USES
metabolic reactions suffer. ▪ Combined with trimethoprim (as
1. SULFADIAZINE cotrimoxazole) sulfamethoxazole is used for
Dose: 0.5 g QID to 2 g TDS; many bacterial infections.
SULFADIAZINE 0.5 g tab. ▪ Malaria- In combination with pyrimethamine.
▪ Ocular sulfacetamide sod. (10–30%)-
2. SULFAMETHOXAZOLE trachoma/inclusion conjunctivitis,
Dose: 1 g BD for 2 days, then 0.5 g BD. ▪ Topical silver sulfadiazine or mafenide -
GANTANOL 0.5 g tab. preventing infection on burn surfaces.

3. SULFACETAMIDE SOD. COTRIMOXAZOLE

It is used topically for ocular infections. The fixed dose combination of trimethoprim and
LOCULA 10%, 20%, 30% eye drops, 6% sulfamethoxazole is called cotrimoxazole.
eye oint.
MECHANISM OF ACTION
4. SILVER SULFADIAZINE
▪ Used topically as 1% cream. It slowly
releases silver ions which appear to be
largely responsible for the antimicrobial
action.
▪ It is considered to be one of the most
effective drugs for preventing infection of
burnt surfaces and chronic ulcers and is
well tolerated.
SILVIRIN 1% cream, ARGENEX 1% cream.
▪ Local side effects: burning sensation on
application and itch. ADVERSE EFFECTS
1. Nausea, vomiting, stomatitis, headache and
5. MAFENIDE rashes.
▪ It is used only topically—inhibits a variety of 2. Folate deficiency.
gram- positive and gram-negative bacteria. 3. Avoided during pregnancy.
▪ Used for burn dressing to prevent infection,
4. Patients with renal disease may develop
but not to treat already infected cases.
uremia.
BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR
 SECTION 23. ANTIBIOTICS 103
FIRST GENERATION CEPHALOSPORINS

Drug Dose M/N

CEPHALEXIN 0.25–1 g 6–8 SPORIDEX,
hourly (children ALCEPHIN,
25–100 CEPHAXIN 250,
mg/kg/day). 500 mg cap
CEFADROXIL 0.5–1 g BD CEFADROX 0.5
g cap, 125 mg/5
ml syr and 250
mg kid tab

CEFAZOLIN 0.5 g 8 hourly ORIZOLIN 0.25

(mild cases), 1 g 6 g, 0.5 g, 1 g per
hourly (severe vial inj.
cases), children
25–50 mg/kg/day
i.m. or i.v

Drug Dose M/N

CEFUROXIME 0.75–1.5 g i.m. FUROXIL 250
or i.v. 8 hourly, mg and 750
children 30– mg/vial inj
100 mg/kg/day
CEFUROXIME 250–500 mg CEFTUM, 125,
AXETIL BD 250, 500 mg
tab and 125
mg/5 ml susp.

CEFACLOR 0.25–1.0 g 8 KEFLOR 250

hourly mg cap, 125
and 250 mg tab,
125 mg/5 ml
dry syr,
CEFPROZIL 250–500 mg ORPROZIL
BD, (child 20 250, 500 mg
mg/kg/day) tab

Drugs Dose M/N

Oxytetracycline 250-500 mg OID TERRAMYCIN
250, 500 mg cap,
50 mg/ml in 10 ml
vials inj; 3% skin
oint, 1% eye/ear
oint.
Tetracycline 250-500 mg OID ACHROMYCIN,
250, 500 mg cap.
3% skin oint, 1%
eye/ear drops.

Demeclocycline 300mg BD LEDERMYCIN

150, 300 mg
cap/tab
Doxycycline 200 mg initially, DOXY, 100 mg
then 100–200 mg cap
OD
Minocycline 200 mg initially, CYANOMYCIN,
then 100–200 mg CNN 50, 100 mg
OD caps

BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR

 SECTION 24. DRUGS FOR ACNE
SECTION 24.
DRUGS FOR ACNE
▪ Under androgenic stimulation the sebaceous
follicles of face and neck produce excess of
sebum and get colonized by bacteria and
yeast (Propionibacterium acnes, Staph.
epidermidis, Pityrosporum ovale).
▪ Bacterial lipases produce fatty acids which
irritate the follicular ducts causing retention
of secretions and hyperkeratosis—
‘comedones’ are formed which may rupture
into the dermis causing inflammation and
pustulation.
TOPICAL THERAPY
1. BENZOYL PEROXIDE
▪ It is one of the most effective and widely
used drugs in acne.
▪ It gradually liberates oxygen (in the presence
of water) which kills bacteria, especially
anaerobic. It is highly effective against P.
acnes.
▪ It has keratolytic and comedolytic properties.
Adverse effect
▪ Burning and stinging sensation is often felt
initially, localized erythema may occur.
▪ Most patients gradually develop tolerance to
these actions; if not, use should be
discontinued.
▪ Avoid contact with eyes, lips, mucous
membranes.
▪ Excessive dryness of skin, marked scaling,
erythema, edema and contact sensitization.
It is used as 5–10% cream, gel or lotion. start
with 15 min once daily.
PERSOL 2.5% and 5% gel; in PERSOL
FORTE 10% cream.
2. RETINOIC ACID
▪ It is a potent comedolytic.
BASICS OF MEDICAL PHARMACOLOGY
116
▪ It is highly efficacious in acne, but response
is delayed (may take 6–10 weeks).
Adverse effects
▪ Feeling of warmth, stinging, excessive
redness, edema and crusting.
▪ Teratogenic risk with topical retinoic acid is
minor because of low blood levels produced;
but it should be avoided during pregnancy.
▪ Tretinoin has the potential to irritate the skin;
start with the lower concentration applied
once daily.
Used as a 0.025–0.05% gel or cream, it can
be alternated with benzoyl peroxide (one in
the morning the other at night), but both
should not be applied together because
benzoyl peroxide accelerates degradation of
tretinoin.
RETINO-A 0.025% and 0.05% cream.
3. ADAPALENE
▪ It is a newer synthetic tretinoin like drug.
▪ It also exerts anti-inflammatory action;
comedone formation is suppressed.
It remains stable in the presence of benzoyl
peroxide; can be combined with it.
ADAFERIN, ADAPEN, ADAPLE,
ACLENE 0.1% gel; apply once daily at bed
time.
4. TOPICAL ANTIBIOTICS
▪ Clindamycin, erythromycin and tetracyclines
are less effective against P. acnes than
benzoyl peroxide.
▪ They do not irritate skin.
Erythromycin: ACNEDERM 2% lotion and
oint; ERYTOP 3% lotion and cream.
Clindamycin: CLINDAC-A, CLINCIN 1%
gel.
Nadifloxacin: NADIBACT, NADOXIN 1%
cream for topical application.
5. AZELAIC ACID
▪ It is a natural product from Pityrosporum
ovale that has been developed for topical
treatment of acne.
▪ Used as 10%, 20% cream.
▪ It has also benefited melasma
DR.V.S.PAWAR
 SECTION 25. SEDATIVES & HYPNOTICS
SECTION 25.
SEDATIVES & HYPNOTICS
BENZODIAZEPINES (BZDs)
▪ They exert anxiolytic, hypnotic, muscle
relaxant and anticonvulsant effects.
▪ With chronic administration relief of anxiety
is maintained, but drowsiness wanes off due
to development of tolerance.
SITE AND MECHANISM OF ACTION
▪ Benzodiazepines act preferentially on
midbrain ascending reticular formation
(which maintains wakefulness) and on
limbic system (thought and mental
functions).
▪ Muscle relaxation is produced by a primary
medullary site of action and ataxia is due to
action on cerebellum.
▪ BZDs act by enhancing
presynaptic/postsynaptic inhibition through a
specific BZD receptor which is an integral
part of the GABAA receptor–Cl¯ channel
complex.
▪ Benzodiazepines are metabolized in liver and
are excreted in urine.
▪ BZDs cross placenta and are secreted in
milk.
CHLORDIAZEPOXIDE
▪ It was the first BZD to be used clinically.
▪ Oral absorption is slow.
▪ It used in chronic anxiety.
▪ Its anticonvulsant action is weak.
Dose: 25–100 mg; LIBRIUM 10, 25 mg tabs
FLURAZEPAM
▪ It used for frequent nocturnal awakenings.
Dose:15-30 mg/day. FLURAZ 15 mg cap.
DIAZEPAM
▪ It is used as anxiolytic, hypnotic, muscle
relaxant, anaesthetic and for emergency
control of seizures.
BASICS OF MEDICAL PHARMACOLOGY
118
Dose: 5–30 mg VALIUM, CALMPOSE 5,
10 mg tab, 2 mg/5 ml Syr. 10 mg/2 ml inj.
NITRAZEPAM
▪ Similar to diazepam.
▪ It used for frequent nocturnal awakenings.
Dose: 5-20mg/day. NITRAVET 5 mg tab, 5,
10 mg cap.
ALPRAZOLAM
▪ It used for anxiety disorder.
Dose: 0.25–1.0 mg TDS; upto 6 mg/day in
panic disorder; ALPRAX 0.25, 0.5, 1.0 mg
tabs., 0.5, 1.0, 1.5 mg SR tabs; RESTYL
0.25, 0.5, 1.0 mg tabs.
OXAZEPAM
▪ It used for short lasting anxiety states.
Dose: 30–60 mg in 2–3 divided portions;
SEREPAX 15, 30 mg tab.
LORAZEPAM
▪ Has slow oral absorption.
▪ Being less lipid-soluble than diazepam, its
rate of entry in brain is slower.
▪ It has been preferred for short lasting anxiety
states, panic, OCD and tension syndromes, as
well as for psychosomatic diseases and for
i.v. use in status epilepticus.
Dose: 1–6 mg LARPOSE 1, 2 mg tab.
ADVERSE EFFECTS
▪ Dizziness, vertigo, ataxia, disorientation,
amnesia, impairment of psychomotor skills
(should not drive).
▪ Weakness, blurring of vision, dry mouth and
urinary incontinence.
▪ Irritability and sweating may occur in an
occasional patient.
▪ Tolerance to the sedative effects develops
gradually.
▪ Withdrawal syndrome - Anxiety, insomnia,
restlessness, loss of appetite, bad dreams.
INTERACTIONS
▪ BZDs synergise with alcohol and other CNS
depressants leading to excessive impairment.
DR.V.S.PAWAR
 SECTION 26. ANTI-EPILEPTIC DRUGS 120

SECTION 26.
ANTI-EPILEPTIC DRUGS
PHENOBARBITONE ▪ Phenytoin is metabolized in liver.
▪ Phenobarbitone was the first efficacious
antiepileptic.
Mechanism of action
▪ It enhances GABA effects by prolonging
opening of the chloride channel.

▪ It raises seizure threshold as well as limits

spread and suppresses seizures.
▪ Phenobarbitone has slow oral absorption, it
metabolized in liver as well as excreted
unchanged by kidney.
Side effects
▪ Sedation.
▪ Long term administration (as needed in
epilepsy) may produce—behavioral
abnormalities, diminution of intelligence,
impairment of learning and memory, mental
confusion in older people.
▪ On prolonged use: Rashes, megaloblastic
anaemia and osteomalacia.
Uses
▪ Generalized tonic-clonic (GTC), simple Adverse effects
partial (SP) and complex partial (CP) 1. Gum hypertrophy: Commonest, more in
seizures in a younger patients.
Status epilepticus: 2. Hirsutism.
▪ Phenobarbitone sod. may be injected i.m. or 3. Hypersensitivity reactions:
i.v. but response is slow to develop. rashes, lymphadenopathy; neutropenia is rare
▪ It is not effective in absence seizures. but requires discontinuation of therapy.
Dose: 60 mg 1–3 times a day in adults; in 4. Megaloblastic anaemia: Phenytoin decreases
children (3–5 mg/ kg/day); GARDENAL 30, folate absorption and increases its excretion.
60 mg tabs, 20 mg/5 ml syr; 5. Osteomalacia: Phenytoin interferes with
PHENOBARBITONE SODIUM 200 mg/ml inj.
metabolic activation of vit D and with
calcium absorption/metabolism.
PHENYTOIN 6. It can inhibit insulin release and cause
▪ Phenytoin is not a CNS depressant; some hyperglycaemia.
sedation occurs at therapeutic doses. 7. Used during pregnancy, phenytoin can
▪ It limits spread of seizure activity.
produce cleft palate, lip, microcephaly).
Pharmacokinetics
8. At high doses- Cerebellar and vestibular
▪ Absorption of phenytoin by oral route is
manifestations: ataxia, vertigo, diplopia,
slow, mainly because of its poor aqueous
nystagmus are the most characteristic
solubility.
features.
BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR
 SECTION 27. MUSCLE RELAXANT
SECTION 27.
MUSCLE RELAXANT
CENTRALLY ACTING MUSCLE RELAXANTS
▪ They reduce skeletal muscle tone without
altering consciousness.
▪ They selectively depress spinal and
supraspinal polysynaptic reflexes involved in
the regulation of muscle tone.
▪ Polysynaptic pathways in the ascending
reticular formation which are involved in the
maintenance of wakefullness are also
depressed. All centrally acting muscle
relaxants do have some sedative property.
CARISOPRODOL
▪ It is sedative with weak analgesic, antipyretic
and anticholinergic properties.
▪ It is used in musculoskeletal disorders
associated with muscle spasm.
CARISOMA 350 mg tab; one tab. TDS-QID.
CHLORZOXAZONE
▪ It has a longer duration of action and is better
tolerated orally.
FLEXON-MR 250 mg + ibuprofen 400 mg +
paracetamol 325 mg tab. MOBIZOX 500 mg
+ diclofenac 50 mg + paracetamol 500 mg
tab; 1–2 tab TDS.
CHLORMEZANONE
▪ It has antianxiety and hypnotic actions.
DOLOBAK 100 mg + paracetamol 450 mg
tab, 1–2 tab TDS.
METHOCARBAMOL
▪ It is less sedative and longer acting.
▪ Orally it has been used in reflex muscle
spasms and chronic neurological diseases.
▪ It can be injected i.v. for orthopedic
procedures and tetanus.
ROBINAX 0.5 g tab, 1 TDS: 100 mg/ml inj.
for i.v. or i.m. use. ROBIFLAM 750 mg +
ibuprofen 200 mg tab.
DIAZEPAM
▪ It act in the brain on specific receptors
enhancing GABAergic transmission.
▪ It produce sedation.
▪ It is particularly valuable in spinal injuries
and tetanus.
BASICS OF MEDICAL PHARMACOLOGY
125
Dose: 5 mg TDS orally, 10–40 mg i.v. (in
tetanus).
BACLOFEN
▪ It reduces the release of excitatory
neurotransmitters in the pre-synaptic neurons
and stimulates inhibitory neuronal signals in
the post-synaptic neurons with resultant
relief of spasticity.
▪ The primary site of action of baclofen is
considered to be in the spinal cord where it
depresses both polysynaptic and
monosynaptic reflexes.
▪ It is less sedative than diazepam.
▪ Spasticity in many neurological disorders
like multiple sclerosis, amyotropic lateral
sclerosis (ALS), spinal injuries and flexor
spasms is reduced.
▪ It is relatively ineffective in stroke, cerebral
palsy, rheumatic and traumatic muscle
spasms and parkinsonism.
▪ Side effects- drowsiness, mental confusion,
weakness and ataxia; serum transaminases
may rise. Sudden withdrawal after chronic
use may cause hallucinations, tachycardia
and seizures.
Dose: 10 mg BD to 25 mg TDS.
LIOFEN 10 mg, 25 mg tab.
THIOCOLCHICOSIDE
▪ It act as a GABA mimetic.
▪ Combined with NSAIDs, it is being used for
painful muscle spasms, such as torticolis,
sprains, backache, etc.
Side effects
Gastric upset and photosensitivity reactions
Dose: 4 mg TDS-QID; NUCOXIA-MR:
Thiocolchicoside 4 mg + etoricoxib 60 mg
tabs.
TIZANIDINE
▪ It is a central α2 adrenergic agonist—inhibits
release of excitatory amino acids in the
spinal interneurones.
▪ It may facilitate the inhibitory transmitter
glycine.
DR.V.S.PAWAR
 SECTION 28. DRUGS FOR SCABIES
SECTION 28.
DRUGS FOR SCABIES
1. PERMETHRIN
▪ It is most effective drug for both scabies and
lice.
▪ It causes neurological paralysis in insects.
▪ After application, permethrin persists on the
skin for days; systemic absorption is
minimal.
▪ Nearly 100% cure rates have been obtained
in scabies and pediculosis.
▪ Single application is needed in most cases.
▪ Few patients may experience mild and
transient burning, itching, tingling, erythema
or rash.
For scabies: PERMITE 5% cream; apply all
over the body except face and head; wash
after 8–12 hours. SCABERID 5% cream, 1%
soap; SCABPER 5% lotion.
For head lice: PERLICE 1% cream rinse,
ELICE 5% lotion, SCALTIX 1% lotion;
massage about 30 g into the scalp, wash off
after 10 min.
Permethrin is now the 1st choice drug for
scabies and pediculosis.
2. LINDANE (GAMMA BENZENE
HEXACHLORIDE, BHC)
▪ Lindane is highly effective in treating
headlice and scabies by single treatment.
However, efficacy is lower than permethrin.
▪ Both lice and mites can develop resistance to
lindane.
▪ Combining it with benzyl benzoate precludes
resistance and improves cure rate to nearly
100%.
GAB 1% lotion, ointment; GAMADERM
1% lotion; GAMASCAB 1% lotion, cream;
BENZO 1% lotion, 1% soap.
▪ For pediculosis: apply to scalp and hair
(taking care not to enter eyes), leave for 12–
24 hr and then wash off. If lice are still
present, repeat treatment after 1 week. For
scabies: the lotion/cream is rubbed over the
body (below neck) and a scrub bath taken
12–24 hr later. Single treatment suffices in
most patients; can be repeated after a week.
▪ Disadvantages: It can be absorbed through
the skin and produce systemic toxicity like
BASICS OF MEDICAL PHARMACOLOGY
131
CNS stimulation, vertigo, convulsions
(especially in children) and cardiac
arrhythmias.
▪ It should be avoided in infants, young
children and during pregnancy.
3. BENZYL BENZOATE
▪ The emulsion is applied all over except face
and neck after a cleansing bath.
▪ A second coat is applied next day which is
washed after 24 hours.
▪ Benzyl benzoate is minimally absorbed
through the skin; systemic toxicity is low, but
neurological symptoms have occurred in
children—contraindicated in them.
▪ Skin irritation is common, especially in
children. Contact dermatitis is possible.
DERMIN 25% lotion. SCABINDON 25%
oint with DDT 1% and benzocaine 2%
▪ For pediculosis, it can be applied to the
scalp, taking care not to enter eyes, and is
washed off after 24 hours.
▪ Benzyl benzoate is 2nd choice drug for
scabies.
4. CROTAMITON
▪ It is an effective scabicide, pediculocide and
antipruritic, but has produced lower cure
rates in scabies.
▪ It is less prone to cause skin irritation and has
low systemic toxicity—may be preferred for
children.
▪ It is applied twice at 24 hr interval and
washed off day after that. CROTON 10%
cream, lotion.
5. IVERMECTIN
▪ It is highly effective in scabies and
pediculosis.
▪ It is the only orally administered drug used
for ectoparasitosis.
▪ A single 0.2 mg/kg (12 mg in adults) dose
has cured upto 91–100% patients of scabies.
▪ Most cases of head/ body lice have been
successfully treated.
▪ It should be avoided in children < 5 yr,
pregnant and lactating women.
DR.V.S.PAWAR
 SECTION 29. DRUGS FOR PARKINSON DISEASE
SECTION 29.
DRUGS FOR PARKINSON DISEASE
Parkinsonism was characterized as a DA
deficiency state and levodopa was used to make
good this deficiency, because DA itself does not
cross the blood-brain barrier.
DRUGS FOR PD
a) Dopamine precursor : Levodopa (l-dopa)
b) Peripheral decarboxylase inhibitors:
Carbidopa, Benserazide.
c) Dopaminergic agonists: Bromocriptine,
Ropinirole, Pramipexole
d) MAO-B inhibitor: Selegiline, Rasagiline
e) COMT inhibitors: Entacapone, Tolcapone
f) Glutamate (NMDA receptor) antagonist
(Dopamine facilitator): Amantadine.
LEVODOPA
▪ More than 95% of an oral dose is
decarboxylated into DA in the peripheral
tissues.
▪ This DA acts on heart, blood vessels, other
peripheral organs and on CTZ.
▪ About 1–2% of administered levodopa
crosses to the brain & converted to DA
Actions of Levodopa
▪ It produced symptomatic improvement.
▪ It resolve hypokinesia, rigidity and tremors.
▪ Therapeutic benefit is nearly complete in
early disease, but declines as the disease
advances.
Adverse effects
1. Nausea and vomiting
2. Postural hypotension -patients experience
dizziness, fainting attacks.
3. Cardiac arrhythmias
4. Exacerbation of angina
After prolonged therapy
1. Abnormal movements (dyskinesias).
2. Behavioural effects: Range from mild
anxiety to severe depression, hallucinations,
mental confusion or frank psychosis.
3. Fluctuation in motor performance: After 2–
5 years of therapy, the level of control of
parkinsonian symptomatology starts showing
fluctuation. (‘on-off’ effect).
BASICS OF MEDICAL PHARMACOLOGY
133
▪ Cautious use of levodopa is needed in the
elderly; patients with ischaemic heart
disease; cerebrovascular, psychiatric, hepatic
and renal disease; peptic ulcer.
Dose: Start with 0.25 g BD after meals,
gradually increase till adequate response is
obtained. Usual dose is 2–3 g/day.
LEVOPA 0.5 g tab.
PERIPHERAL DECARBOXYLASE INHIBITORS
▪ Carbidopa and benserazide are extracerebral
decarboxylase inhibitors; they do not
penetrate blood-brain barrier and do not
inhibit conversion of levodopa to DA in the
brain.
Benefits of the combination with Levodopa
1. The plasma t½ of levodopa is prolonged and
its dose is reduced to approximately 1/4th.
2. Systemic concentration of DA is reduced,
nausea and vomiting are not prominent
3. Cardiac complications are minimized
4. ‘On-off’ effect is minimized since cerebral
DA levels are more sustained.
5. Degree of improvement may be higher.
Currently, levodopa is practically always
used along with a decarboxylase inhibitor
SYNDOPA-110, 10 mg (Carbidopa) + 100
mg (Levodopa) tab.
BENSPAR: Benserazide 25 mg + levodopa
100 mg cap
DOPAMINERGIC AGONISTS
▪ The DA agonists can act on striatal DA
receptors even in advanced patients who
have largely lost the capacity to synthesize,
store and release DA from levodopa.
1. BROMOCRIPTINE
▪ It produced improvement within ½–1 hr of
an oral dose of bromocriptine and lasts for 6–
10 hours.
Side effects:
▪ Vomiting, hallucinations, hypotension, nasal
stuffiness, conjunctival injection.
▪ First dose hypotension in some patients.
DR.V.S.PAWAR
 SECTION 30. HYPOLIPIDAEMIC DRUGS 133

SECTION 30.
Hypolipidaemic Drugs
These drugs lower the levels of lipids and ▪ It exert antiatherosclerotic action by
lipoproteins in blood. They have potential to improving endothelial function due to
prevent cardiovascular disease by retarding the increased NO production and reduction in
accelerated atherosclerosis in hyperlipidaemic LDL oxidation.
individuals. ▪ They are the first choice drugs for
dyslipidaemia in diabetics.
HMG-COA REDUCTASE INHIBITORS
(STATINS) BILE ACID SEQUESTRANTS (Not used now)
Drugs Daily Dose M/N Mechanism of action: ↓ bile acid absorption, ↑
Lovastatin 10–80 mg TAB. LOVACARD hepatic conversion of CH to bile acids, ↑ LDL
Simvastatin 5–40 mg TAB. SIMVOTIN receptors on hepatocytes.
Atorvastatin 10–80 mg TAB. ATORVA
Drugs Daily Dose M/N
Rosuvastatin 5–20 mg TAB. ROSUVAS
Cholestyramine 4–16 g TAB. CHOLTRAN
▪ Mechanism of action: They competitively Colestipol 5–30 g TAB. COLESTID
inhibit conversion of 3-Hydroxy-3-methyl
glutaryl coenzyme A (HMG-CoA) to LIPOPROTEIN-LIPASE ACTIVATORS
mevalonate (rate limiting step in CH (FIBRATES)
synthesis) by the enzyme HMG-CoA Drugs Daily Dose M/N
reductase. Gemfibrozil 1200 mg CAP.LOPID 300,600
▪ All statins produce peak LDL-CH lowering Bezafibrate 600 mg TAB. BEZALIP
after 1–2 weeks therapy. Fenofibrate 200 mg TAB. FINOBRATE 200
▪ Because HMG-CoA reductase activity is
maximum at midnight, all statins are ▪ The fibrates activate lipoprotein lipase which
administered at bed time to obtain maximum is a key enzyme in the degradation of VLDL
effectiveness. resulting in lowering of circulating TGs.
▪ Fibrates decrease hepatic TG synthesis.
ADVERSE EFFECTS ▪ It also reduce circulating free fatty acids.
▪ All statins are well tolerated.
▪ Gastrointestinal complaints and headache are GEMFIBROZIL
usually mild. ▪ It lowers plasma TG level by enhancing
▪ Rise in serum transaminase can occur. breakdown and suppressing hepatic synthesis
Monitoring of liver function is of TGs.
recommended. Pharmacokinetics
▪ Muscle aches are the commonest (10%) side ▪ Gemfibrozil is completely absorbed orally,
effect. Rise in CPK levels occurs metabolized in liver and excreted in urine.
infrequently. Adverse effects
▪ Myopathy is the only serious reaction, but is ▪ Epigastric distress, loose motions.
rare (< 1 per 1000). ▪ Skin rashes, body ache, eosinophilia,
▪ Few fatalities due to rhabdomyolysis are on impotence, headache and blurred vision.
record. ▪ Myopathy is uncommon.Gemfibrozil + statin
▪ Statins should be avoided in pregnancy. increases risk of myopathy.
▪ It is contraindicated during pregnancy.
USE Use
▪ Statins are the first choice drugs for primary ▪ In a dose of 600 mg BD taken before meals,
hyperlipidaemias with raised LDL and total gemfibrozil is a first line drug for patients
CH levels, with or without raised TG levels, with markedly raised TG levels.
as well as for secondary (diabetes, nephrotic ▪ Fibrates may also be used to supplement
syndrome) hypercholesterolaemia. statins.

BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR

 SECTION 31. OPIOID ANALGESICS
SECTION 31.
OPIOID ANALGESICS
MORPHINE
PHARMACOLOGICAL ACTIONS
1. CNS
a) Morphine act by interacting with the μ opioid
receptor.
b) Morphine is a strong analgesic.
c) Pain arising from stimulation of peripheral
pain receptors is relieved better than neuritic
pain (such as trigeminal neuralgia).
d) It acts in the substantia gelatinosa of dorsal
horn to inhibit release of excitatory
transmitters (e.g. substance P) from primary
afferents carrying pain impulses.
e) Morphine also produce sedation. Higher
doses progressively induce sleep and then
coma.
f) Morphine has a calming effect.
g) Morphine depresses respiratory centre in a
dose dependent manner. Analgesic dose in an
otherwise healthy individual produces no
cognizable respiratory depression, but it may
be marked in the presence of other sedatives,
cardiopulmonary/liver/kidney disease, etc.
Death in morphine poisoning is due to
respiratory failure.
h) It depress cough centre.
i) It depress vasomotor centre at higher doses
and contributes to the fall in BP.
j) Morphine stimulates CTZ which cause
nausea and vomiting.
k) Larger doses depress vomiting centre
directly.
l) It stimulate vagal centre → bradycardia is the
usual response to morphine.
m) It may cause muscular rigidity and
immobility especially on i.v. injection.
2. Neuro-endocrine
▪ It reduce hypothalamic activation.
▪ Hypothalamic influence on pituitary is
reduced. As a result FSH, LH, ACTH levels
are lowered, while prolactin and GH levels
are raised. The sex hormone and cortisol
levels are lowered.
▪ Morphine can release ADH and reduce urine
volume.
3. CVS
BASICS OF MEDICAL PHARMACOLOGY
135
▪ Morphine causes vasodilatation.
▪ Postural hypotension and fainting do occur
due to venodilatation.
▪ Morphine has little direct effect on heart rate
generally decreases due to stimulation of
vagal centre, but may increase reflexly if the
BP falls.
▪ Cardiac work is consistently reduced due to
decrease in peripheral resistance.
▪ Intracranial tension tends to rise as a
consequence of CO2 retention leading to
cerebral vasodilatation.
4. GIT
▪ The enteric plexus neurones and g.i. mucosa
are rich in opioid receptors.
▪ Morphine reduce g.i. motility which produce
constipation.
5. Biliary tract
Morphine causes spasm of sphincter of Oddi
→ intra-biliary pressure is increased → may
cause biliary colic.
6. Urinary bladder
Tone of both detrusor and sphincter muscle
is increased → urinary urgency and difficulty
in micturition.
7. Bronchi
In asthmatics morphine cause
bronchoconstriction due to release of
histamine.
8. ANS
Morphine causes mild hyperglycaemia due to
central sympathetic stimulation.
PHARMACOKINETICS
▪ Oral bioavailability is 1/6th to 1/4th of
parenterally administered drug. Only a small
fraction enters brain slowly.
▪ Morphine freely crosses placenta and can
affect the foetus more than the mother.
▪ It is primarily metabolized in liver by
glucuronide conjugation.
▪ Plasma t½ of morphine averages 2–3 hours.
▪ Effect of a parenteral dose lasts 4–6 hours.
SIDE EFFECTS
1. Sedation, mental clouding, lethargy.
2. Vomiting and constipation.
DR.V.S.PAWAR
 SECTION 32. HORMONAL DRUGS 138

SECTION 32.
HORMONAL DRUGS
ESTROGENS 2. Fusion of epiphyses and reduction of adult
Synthetic estrogens stature when given to children.
1. Steroidal: 3. In postmenopausal women, estrogens can
Ethinylestradiol, Mestranol, Tibolone. increase the risk of irregular bleeding and
2. Nonsteroidal : endometrial carcinoma.
Diethylstilbestrol (stilbestrol) Hexestrol, 4. Estrogens can accelerate the growth of
Dienestrol existing breast cancer.
5. Long-term estrogen therapy doubles the
MECHANISM OF ACTION incidence of gallstones.
▪ Estrogens bind to specific nuclear receptors 6. Migraine, epilepsy and endometriosis may be
in target cells and produce effects by worsened by estrogens.
regulating protein synthesis. 7. Stilbestrol given to pregnant women,
▪ Estrogen receptors (ERs) have been especially during first trimester (as test of
demonstrated in female sex organs, breast, pregnancy or otherwise)—increased the
pituitary, liver, bone, blood vessels, heart, incidence of vaginal and cervical carcinoma
CNS and in certain hormone responsive in the female offspring in childhood or early
breast carcinoma cells. adulthood.

PHARMACOKINETICS USES
▪ Synthetic Estrogens are well absorbed orally 1. Hormone replacement therapy (HRT):
and transdermally. ▪ Conjugated estrogens are used at 0.625
▪ Estradiol esters injected i.m. are slowly mg/day dose (equivalent to ethinylestradiol
absorbed and exert prolonged action. 10 μg) either cyclically (3 weeks treatment 1
week gap) or continuously, but there is a
DOSE trend now to use lower doses (0.3–0.45
Oestrogen Dose mg/day).
Estradiol 2.5–10 mg ▪ A progestin (medroxy progesterone
benzoate/cypionate/enanthate/valarate i.m acetate/norethisterone 2.5 mg daily) is added
Conjugated estrogens 0.625–1.25 for the last 10–12 days each month.
mg/day oral 2. Senile vaginitis
Ethinylestradiol 0.02–0.2 mg/ ▪ Estrogens change vaginal cytology to the
day oral
premenopausal pattern and are effective in
Mestranol 0.1–0.2
preventing as well as treating atrophic
mg/day oral
Estriol succinate 1–2 mg/day vaginitis that occurs in elderly women.
oral 3. Delayed puberty in girls.
Fosfestrol tetrasodium 120–240
mg/day oral ANTIESTROGENS
or 300 mg CLOMIPHENE CITRATE
1–3 times a ▪ It induces Gn secretion in women by
week i.v. blocking estrogenic feedback inhibition of
Dienestrol 0.01% pituitary.
topically in ▪ The amount of LH/FSH released at each
vagina secretory pulse is increased.
▪ In response, the ovaries enlarge and
ADVERSE EFFECTS ovulation occurs if the ovaries are responsive
1. Suppression of libido, gynaecomastia and to Gn.
feminization when given to males.

BASICS OF MEDICAL PHARMACOLOGY DR.V.S.PAWAR

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