ACTION AND USES OF MEDICINE

AUM 221

SCHOOL OF PHARMACY TECHNICIAN

DEPARTMENT OF CERTIFIED PHARMACY TECHNICIAN

COLLEGE OF HEALTH TECHNOLOGY NINGI

LECTURE NOTE

BY

IBRAHIM MUHAMMAD(B. Pharm PGDE, MPSN)

 DRUG NOMENCLATURE

A drug generally has three categories of names

(a) Chemical name It describes the substance chemically, e.g. 1-
(Isopropylamino)-3-(1-naphthyloxy) propan-2-ol for
propranolol.
(b) Non-proprietary name It is the name accepted by a competent
scientific body/authority, e.g. the United States Adopted Name
(USAN) by the USAN council. Similarly, there is the British
Approved name (BAN) of a drug. The nonproprietary names
of newer drugs are kept uniform by an agreement to use the
Recommended International Nonproprietary Name (rINN) in
all member countries of the WHO.
• Until the drug is included in a pharmacopoeia, the nonproprietary
name may also be called the approved name. After its appearance
in the official publication, it becomes the official name.

• In common parlance, the term generic name is used in place of

nonproprietary name. Etymologically this is incorrect: ‘generic’
should be applied to the chemical or pharmacological group (or
genus) of the compound, e.g. phenothiazines, tricyclic
antidepressants, aminoglycoside antibiotics, etc. However, this
misnomer is widely accepted and used even in official parlance.
(c) Proprietary (Brand) name It is the name assigned by the
manufacturer(s) and is his property or trade mark. One drug may
have multiple proprietary names, e.g. ALTOL, ATCARDIL,
ATECOR, ATEN, BETACARD, LONOL, TENOLOL,
TENORMIN for atenolol from different manufacturers.
 ESSENTIAL MEDICINES (DRUGS)
CONCEPT

• The WHO has defined Essential Medicines (drugs) as “those

that satisfy the priority healthcare needs of the population.
They are selected with due regard to public health relevance,
evidence on efficacy and safety, and comparative cost
effectiveness. Essential medicines are intended to be available
within the context of functioning health systems at all times
and in adequate amounts, in appropriate dosage forms, with
assured quality and adequate information, and at a price the
individual and the community can afford.
• The WHO has laid down criteria to guide selection of an essential
medicine.
(a) Adequate data on its efficacy and safety should be available
from clinical studies.
(b) It should be available in a form in which quality, including
bioavailability, and stability on storage can be assured.
(c) Its choice should depend upon pattern of prevalent diseases;
availability of facilities and trained personnel; financial resources;
genetic, demographic and environmental factors.
(d) In case of two or more similar medicines, choice should be made
on the basis of their relative efficacy, safety, quality, price and
availability. Cost-benefit ratio should be a major consideration.
(e) Choice may also be influenced by comparative pharmacokinetic
properties and local facilities for manufacture and storage.
(f) Most essential medicines should be single compounds. Fixed
ratio combination products should be included only when dosage of
each ingredient meets the requirements of a defined population
group, and when the combination has a proven advantage in
therapeutic effect, safety, adherence or in decreasing the emergence
of drug resistance.
(g) Selection of essential medicines should be a continuous process
which should take into account the changing priorities for public
health action, epidemiological conditions as well as availability of
better medicines/formulations and progress in pharmacological
knowledge.
(h) Recently, it has been emphasized to select essential medicines
based on rationally developed treatment guidelines.
 ROUTES OF DRUG ADMINISTRATION
• Most drugs can be administered by a variety of routes. The choice of
appropriate route in a given situation depends both on drug as well as
patient related factors. Mostly common sense considerations, feasibility
and convenience dictate the route to be used.
Routes can be broadly divided into those for
(a) Local action and (b) Systemic action.
Factors governing choice of route
1. Physical and chemical properties of the drug (solid/liquid/gas; solubility,
stability, pH, irritancy).
2. Site of desired action—localized and approachable or generalized and not
approachable.
3. Rate and extent of absorption of the drug from different routes.
4. Effect of digestive juices and first pass metabolism on the drug.
5. Rapidity with which the response is desired (routine treatment or
emergency).
6. Accuracy of dosage required (i.v. and inhalational can provide fine tuning).
7. Condition of the patient (unconscious, vomiting).
 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. Thus, high concentrations are attained at the
desired site without exposing the rest of the body. Systemic side
effects or toxicity are consequently absent or minimal.
• The local routes are:
1. Topical
This refers to external application of the drug to the surface for
localized action. It is often more convenient as well as encouraging
to the patient. Drugs can be efficiently delivered to the localized
lesions on skin, oropharyngeal/nasal mucosa, eyes, ear canal, anal
canal or vagina in the form of lotion, ointment, cream, powder,
rinse, paints, drops, spray, lozengens, suppositories or pesseries.
2. Deeper tissues
Certain deep areas can be approached by using a syringe and
needle, but the drug should be in such a form that systemic
absorption is slow, e.g. intra-articular injection (hydrocortisone
acetate in knee joint), infiltration around a nerve or intrathecal
injection (lidocaine), retrobulbar injection (hydrocortisone acetate
behind the eyeball).
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
The drug administered through systemic routes is intended to
be absorbed into the blood stream and distributed all over,
including the site of action, through circulation.
1. Oral
Oral ingestion is the oldest and commonest mode of drug
administration. It is safer, more convenient, does not need assistance,
noninvasive, often painless, the medicament need not be sterile and so
is cheaper. Both solid dosage forms (powders, Tablet, capsules etc.)
and liquid dosage forms (elixirs, syrups, emulsions, mixtures) can be
given orally.
Limitations of oral route of administration
• Action of drugs is slower and thus not suitable for emergencies.
• Unpalatable drugs (chloramphenicol) are difficult to administer;
drug may be filled in capsules to circumvent this.
• May cause nausea and vomiting (emetine).
• Cannot be used for uncooperative/unconscious/vomiting patient.
• Absorption of drugs may be variable and erratic; certain drugs are
not absorbed (streptomycin).
• Others are destroyed by digestive juices (penicillin G, insulin) or in
liver (GTN, testosterone, lidocaine).
2. Sublingual (s.l.) or buccal
The tablet or pellet 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 can be so administered. Absorption is
relatively rapid—action can be produced in minutes. Though it is
somewhat inconvenient, one can spit the drug after the desired effect has
been obtained. 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, buprenorphine,
desamino-oxytocin.
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.
However, it is rather inconvenient and embarrassing; absorption is slower,
irregular and often unpredictable, though diazepam solution and
paracetamol suppository are rapidly and dependably absorbed from the
rectum in children. Drug absorbed into external haemorrhoidal veins
(about 50%) bypasses liver, but not that absorbed into internal
4. Cutaneous
Highly lipid soluble drugs can be applied over the skin for slow and
prolonged absorption. The liver is also bypassed. The drug can be
incorporated in an ointment and applied over specified area of skin.
Absorption of the drug can be enhanced by rubbing the preparation,
by using an oily base and by an occlusive dressing.
Transdermal therapeutic systems (TTS)
These are devices in the form of adhesive patches of various shapes
and sizes (5–20 cm2) which deliver the contained drug at a constant
rate into systemic circulation via the stratum corneum. Usually chest,
abdomen, upper arm, lower back, buttock or mastoid region are
utilized. Transdermal patches of GTN, fentanyl, nicotine and estradiol
are available.
they provide smooth plasma concentrations of the drug without
fluctuations; minimize interindividual variations (drug is subjected
to little first pass metabolism) and side effects. They are also more
convenient, many patients prefer transdermal patches to oral tablets
of the same drug; patient compliance is better. Local irritation and
erythema occurs in some, but is generally mild; can be minimized
by changing the site of application each time by rotation.
Discontinuation has been necessary in 2–7% cases.
5. Inhalation
Volatile liquids and gases are given by inhalation for systemic
action, e.g. general anaesthetics. Absorption takes place from the
vast surface of alveoli—action is very rapid. When administration
is discontinued the drug diffuses back and is rapidly eliminated in
expired air. Thus, controlled administration is possible with
moment to moment adjustment. Irritant vapours (ether) cause
inflammation of respiratory tract and increase secretion.
6. Nasal
The mucous membrane of the nose can readily absorb many drugs;
digestive juices and liver are bypassed. However, only certain drugs
like GnRH agonists and desmopressin applied as a spray or
nebulized solution have been used by this route. This route is being
tried for some other peptide drugs like insulin, as well as to bypass
the blood brain barrier.
7. Parenteral
(Par—beyond, enteral—intestinal)
Conventionally, parenteral refers to administration by injection
which takes the drug directly into the tissue fluid or blood without
having to cross the enteral mucosa. The limitations of oral
administration are circumvented.
 7. Parenteral

• Drug action is faster and surer (valuable in emergencies).

Gastric irritation and vomiting are not provoked. Parenteral
routes can be employed even in unconscious, uncooperative or
vomiting patient. There are no chances of interference by food
or digestive juices. Liver is bypassed.
• Disadvantages of parenteral routes are—the preparation has to
be sterilized and is costlier, the technique is invasive and
painful, assistance of another person is mostly needed (though
self injection is possible, e.g. insulin by diabetics), there are
chances of local tissue injury and, in general, parenteral route
is more risky than oral.
The important parenteral routes are:

(i) Subcutaneous (s.c.)

The drug is deposited in the loose subcutaneous tissue which is
richly supplied by nerves (irritant drugs cannot be injected) but is
less vascular (absorption is slower than intramuscular). Only small
volumes can be injected s.c. Self-injection is possible because deep
penetration is not needed. This route should be avoided in shock
patients who are vasoconstricted absorption will be delayed.
Repository (depot) preparations that are aqueous suspensions can
be injected for prolonged action.
(ii) Intramuscular (i.m.)
The drug is injected in one of the large skeletal muscles—deltoid,
triceps, gluteus maximus, rectus femoris, etc. Muscle is less richly
supplied with sensory nerves (mild irritants can be injected) and is
more vascular (absorption of drugs in aqueous solution is faster). It
is less painful, but self injection is often impracticable because deep
penetration is needed. Depot preparations (oily solutions, aqueous
suspensions) can be injected by this route. Intramuscular injections
should be avoided in anticoagulant treated patients, because it can
produce local haematoma.
(iii) Intradermal injection
The drug is injected into the skin raising a bleb (e.g. BCG vaccine,
sensitivity testing) or scarring/multiple puncture of the epidermis
through a drop of the drug is done. This route is employed for
specific purposes only.
 (iv) Intravenous (i.v.)
The drug is injected as a bolus (Greek: bolos–lump) or infused
slowly over hours in one of the superficial veins. The drug reaches
directly into the blood stream and effects are produced immediately
(great value in emergency). The intima of veins is insensitive and
drug gets diluted with blood, therefore, even highly irritant drugs
can be injected i.v., but hazards are—thrombophlebitis of the
injected vein and necrosis of adjoining tissues if extravasation
occurs. These complications can be minimized by diluting the drug
or injecting it into a running i.v. line.
• One big advantage with this route is—in case response is accurately
measurable (e.g. BP) and the drug short acting (e.g. sodium
nitroprusside), titration of the dose with the response is possible.
• However, this is the most risky route—vital organs like heart, brain,
etc. get exposed to high concentrations of the drug.
 FACTORS MODIFYING DRUG ACTION

• Variation in response to the same dose of a drug between

different patients and even in the same patient on different
occasions is a rule rather than exception.
• One or more of the following categories of differences among
individuals are responsible for the variations in drug response:
(1) Individuals differ in pharmacokinetic handling of drugs:
attain varying plasma/target site concentration of the drug.
This is more marked for drugs disposed by metabolism (e.g.
propranolol) than for drugs excreted unchanged (e.g. atenolol).
(2) Variations in number or state of receptors, coupling
proteins or other components of response effectuation
 (3) Variations in neurogenic/hormonal tone or concentrations of
specific constituents, e.g. atropine tachycardia depends on vagal
tone, propranolol bradycardia depends on sympathetic tone,
captopril hypotension depends on body Na status.
• The factors modify drug action either:
(a) Quantitatively The plasma concentration and/or the action of
the drug is increased or decreased. Most of the factors introduce
this type of change and can be dealt with by adjustment of drug
dosage.
(b) Qualitatively The type of response is altered, e.g. drug allergy
or idiosyncrasy. This is less common but often precludes further
use of that drug in the affected patient.
 1. Body size: It influences the concentration of the drug attained at
the site of action. The average adult dose refers to individuals of
medium built. For exceptionally obese or lean individuals and for
children dose may be calculated on body weight (BW) basis:
Individual dose = BW(kg) × average adult dose
70

• It has been argued that body surface area (BSA) provides a more
accurate basis for dose calculation, because total body water,
extracellular fluid volume and metabolic activity are better
paralleled by BSA.
Individual dose = BSA (m2) × average adult dose
1.7
• The BSA of an individual can be calculated from Dubois formula:
BSA (m2) =BW (kg)0.425 × Height (cm)0.725 × 0.007184
 2. Age: The dose of a drug for children is often calculated from the
adult dose
Child dose = Age × adult dose ... (Young’s formula)
Age12
Child dose = Age × adult dose ... (Dilling’s formula)
20

• However, infants and children are not small adults. They have
important physiological differences from adults. The newborn has
low g.f.r. and tubular transport is immature. As such, the t½ of
drugs excreted by glomerular filtration (gentamicin) and tubular
secretion (penicillin) is prolonged by 3 to 5 times. Glomerular
filtration reaches adult rates by 5 month of age and tubular
• Similarly, hepatic drug metabolizing system is inadequate in
newborns —chloramphenicol can produce gray baby syndrome.
Blood-brain barrier is more permeable—drugs attain higher
concentration in the CNS (accumulation of unconjugated bilirubin
causes kernicterus). Drug absorption may also be altered in infants
because of lower gastric acidity and slower intestinal transit.
Transdermal absorption however, is faster because their skin is thin
and more permeable. Rectal absorption is fast and more predictable
in infants and young children.
• Elderly In the elderly, renal function progressively declines (intact
nephron loss) so that g.f.r. is ~ 75% at 50 years and ~ 50% at 75
years age compared to young adults.
• There is also a reduction in the hepatic microsomal drug
metabolizing activity and liver blood flow: oral bioavailability of
drugs with high hepatic extraction is generally increased, but the
overall effects
 3. Sex: Females have smaller body size and require doses that are
on the lower side of the range. Subjective effects of drugs may
differ in females because of their mental makeup.
• A number of antihypertensives (clonidine, methyldopa, β-blockers,
diuretics) have potential to interfere with sexual function in males
but not in females.
4. Species and race: Among human beings some racial
differences have been observed, e.g. blacks require higher and
mongols require lower concentrations of atropine and ephedrine to
dilate their pupil. β-blockers are less effective as antihypertensive
in Afro-Caribbeans.
5. Genetics: The dose of a drug to produce the same effect may
vary by 4–6 fold among different individuals. All key determinants
of drug response, viz. transporters, metabolizing enzymes, ion
channels, receptors with their couplers and effectors are controlled
genetically.
6. Route of administration: Route of administration governs the
speed and intensity of drug response. Parenteral administration is
often resorted to for more rapid, more pronounced and more
predictable drug action.
7. Environmental factors and time of administration
8. Psychological factor: Efficacy of a drug can be affected by
patient’s beliefs, attitudes and expectations.
9. Pathological states Not only drugs modify disease processes,
several diseases can influence drug disposition and drug action
[Link] drugs: Drugs can modify the response to each other by
pharmacokinetic or pharmacodynamic interaction between them.

11. Cumulation Any drug will cumulate in the body if rate of

administration is more than the rate of elimination. However,
slowly eliminated drugs are particularly liable to cause cumulative
toxicity, e.g. prolonged use of chloroquine causes retinal damage.
 12. Tolerance: It refers to the requirement of higher dose of a drug
to produce a given response. Loss of therapeutic efficacy (e.g. of
sulfonylureas in type 2 diabetes, or of β2 agonists in bronchial
asthma), which is a form of tolerance, is often called
‘refractoriness’. Tolerance is a widely occurring adaptive biological
phenomenon. Drug tolerance may be:
• Natural The species/individual is inherently less sensitive to the
drug, e.g. rabbits are tolerant to atropine; black races are tolerant to
mydriatics.
• Acquired This occurs by repeated use of a drug in an individual
who was initially responsive. Body is capable of developing
tolerance to most drugs, but the phenomenon is very easily
recognized in the case of CNS depressants.
 GASTROINTESTINAL DRUGS

PEPTIC ULCER:
Peptic ulcer occurs in that part of the gastrointestinal tract (g.i.t.)
which is exposed to gastric acid and pepsin, i.e. the stomach and
duodenum. The etiology of peptic ulcer is not clearly known. It
results probably due to an imbalance between the aggressive (acid,
pepsin, bile and H. pylori) and the defensive (gastric mucus and
bicarbonate secretion, prostaglandins, nitric oxide, high mucosal
blood flow, innate resistance of the mucosal cells) factors. A variety
of psychosomatic, humoral and vascular derangements have been
implicated and the importance of Helicobacter pylori infection as a
contributor to ulcer formation and recurrence has been recognized.
Regulation of gastric acid secretion
• Figure 46.1: Secretion of HCl by gastric parietal cell and its
regulation
[Link].—Carbonic anhydrase; Hist.—Histamine; ACh.—
Acetylcholine; CCK2—Gastrin cholecystokinin receptor; 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.
• Approaches for the treatment of peptic ulcer are:
1. Reduction of gastric acid secretion
(a) H2 antihistamines: Cimetidine,
Ranitidine, Famotidine, Roxatidine
(b) Proton pump inhibitors: Omeprazole, Esomeprazole,
Lansoprazole, Pantoprazole, Rabeprazole, Dexrabeprazole
(c) Anticholinergic drugs: Pirenzepine, Propantheline, Oxyphenonium
(d) Prostaglandin analogue: Misoprostol
2. Neutralization of gastric acid (Antacids)
(a) Systemic: Sodium bicarbonate, Sod. citrate
(b) Nonsystemic: Magnesium hydroxide, Mag. trisilicate, Aluminium
hydroxide gel, Magaldrate, Calcium carbonate
3. Ulcer protectives: Sucralfate, Colloidal bismuth subcitrate (CBS)
4. Anti-H. pylori drugs: Amoxicillin, Clarithromycin, Metronidazole,
Tinidazole, Tetracycline
 Anti Spasmodic
1. Anticholinergics
• Hyoscine
• Dicyclomine
Anti Diarrhoeal
• Diarrhoea is defined by WHO as 3 or more loose or watery stools in
a 24 hour period. In pathological terms, it occurs due to passage of
excess water in faeces. This may be due to:
• Decreased electrolyte and water absorption.
• Increased secretion by intestinal mucosa.
• Increased luminal osmotic load.
• Inflammation of mucosa and exudation into lumen.

1. REHYDRATION
2. Zinc in pediatric diarrhoea
• Drugs used in diarrhoeas may be categorised into:
1. Specific antimicrobial drugs
2. Probiotics:Lactobacillus sp., Bifidobacterium, Streptococcus
faecalis, Enterococcus sp. and the yeast Saccharomyces boulardii,
etc.
3. Drugs for inflammaory bowel disease (IBD):
5-Amino salicylic acid (5-ASA) compounds
• Corticosteroids
• Immunosuppressants
• TNFα inhibitors
4. Nonspecific antidiarrhoeal drugs:
A. Absorbants and adsorbants
B. Antisecretory drugs
C. Antimotility drugs:Diphenoxylate, Loperamide.
DRUGS FOR COUGH
1. Pharyngeal demulcents Lozenges, cough drops, linctuses
containing syrup, glycerine, liquorice.
2. Expectorants (Mucokinetics)
(a) Bronchial secretion enhancers: Sodium or Potassium citrate,
Potassium iodide, Guaiphenesin (Glyceryl guaiacolate), balsum of
Tolu, Vasaka, Ammonium chloride.
(b) Mucolytics: Bromhexine, Ambroxol, Acetylcysteine, Carbocisteine
3. Antitussives (Cough centre suppressants)
(a) Opioids: Codeine, Ethylmorphine, Pholcodeine.
(b) Nonopioids: Noscapine, Dextromethorphan, Chlophedianol.
(c) Antihistamines: Chlorpheniramine, Diphenhydramine,
Promethazine.
(d) Peripherally acting: Prenoxdiazine.
4. Adjuvant antitussives
Bronchodilators: Salbutamol, Terbutalin.
• Corticosteroids
A. Systemic: Hydrocortisone, Prednisolone and others.
B. Inhalational: Beclomethasone dipropionate, Budesonide, Fluticasone propionate,
Flunisolide, Ciclesonide.
• Antifungal
1. Antibiotics
A. Polyenes: Amphotericin B (AMB), Nystatin, Hamycin
B. Echinocandins:Caspofungin, Micafungin, Anidulafungin
C. Heterocyclic benzofuran: Griseofulvin
2. Antimetabolite Flucytosine (5-FC)
3. Azoles
A. Imidazoles
Topical: Clotrimazole, Econazole, Miconazole, Oxiconazole
Systemic: Ketoconazole
B. Triazoles:
(systemic) : Fluconazole, Itraconazole, Voriconazole, Posaconazole
4. Allylamine Terbinafine
5. Other topical agents Tolnaftate, Undecylenic acid, Benzoic acid, Quiniodochlor,
Ciclopirox olamine, Butenafine, Sod. thiosulfate.
• Antivirals
1. Anti-Herpes virus
Idoxuridine, Trifluridine, Acyclovir, Valacyclovir, Famciclovir, Ganciclovir,
Valganciclovir, Cidofovir, Foscarnet, Fomivirsen
2. Anti-Influenza virus
Amantadine, Rimantadine, Oseltamivir, Zanamivir
3. Anti-Hepatitis virus/Nonselective antiviral
Drugs Primarily for hepatitis B: Lamivudine, Adefovir dipivoxil, Tenofovir
Primarily for hepatitis C: Ribavirin, Interferon α
4. Anti-Retrovirus
(a) Nucleoside reverse transcriptase inhibitors (NRTIs): Zidovudine (AZT),
Didanosine, Stavudine, Lamivudine, Abacavir, Emtricitabine, Tenofovir (Nt RTI)
(b) Nonnucleoside reverse transcriptase inhibitors (NNRTIs): Nevirapine,
Efavirenz, Delavirdine
(c) Protease inhibitors: Ritonavir, Atazanavir, Indinavir, Nelfinavir, Saquinavir,
Amprenavir, Lopinavir
(d) Entry (Fusion) inhibitor: Enfuvirtide
(e) CCR5 receptor inhibitor: Maraviroc
(f) Integrase inhibitor: Raltegravir
• Classification of Antibiotics
• Based on Chemical Structures
– Sulfonamides - Sulfamethoxazole, sulfadiazine
– Penicillin - Penicillin G (Benzylpenicillin), Penicillin
V, Ampicillin, amoxicillin, nafcillin
– Cephalosporins - cefalotin, cefazolin, cefamandole,
cefuroxime, cefotaxime, ceftriaxone.
– Aminoglycosides - streptomycin, neomycin,
kanamycin, gentamycin, tobramycin
– Chloramphenicol - chloramphenicol, tiamphenicol
– Tetracyclines - chlortetracycline, oxytetracycline,
doxycycline, minocycline HCl
– Macrolides - erythromycin, roxithromycin, spiramycin,
azithromycin
– Polyenes - amphotericin B, nystatin
– Lincomycins - lincomycin, clindamycin
– Polymixins - Polymyxin B, Polymyxin E
– Sulfone - dafsone
– Quinolones - nalidixic acid, norfloxacin, ciprofloxacin,
ofloxacin
– Other groups - vancomycin, cycloxerine, bacitracin,
metronidazole
 Antimalarial Drugs
• CLASSIFICATION
1. 4-Aminoquinolines: Chloroquine (CQ), Amodiaquine (AQ),
Piperaquine
2. Quinoline-methanol Mefloquine
3. Cinchona alkaloid Quinine, Quinidine
4. Biguanide Proguanil (Chloroguanide)
5. Diaminopyrimidine Pyrimethamine
6. 8-Aminoquinoline: Primaquine, Tafenoquine
7. Sulfonamides and sulfone: Sulfadoxine, Sulfamethopyrazine,
Dapsone
8. Antibiotics Tetracycline, Doxycycline, Clindamycin
9. Sesquiterpine lactones: Artesunate, Artemether, Arteether,
Arterolane
10. Amino alcohols Halofantrine Lumefantrine
11. Naphthyridine Pyronaridine
12. Naphthoquinone Atovaquone
• PERIPHERALLY ACTING MUSCLE RELAXANTS
I. Neuromuscular blocking agents
A. Nondepolarizing (Competitive) blockers
1. Long acting: d-Tubocurarine, Pancuronium, Doxacurium,
Pipecuronium
2. Intermediate acting: Vecuronium, Atracurium, Cisatracurium,
Rocuronium, Rapacuronium
3. Short acting: Mivacurium
B. Depolarizing blockers: Succinylcholine (SCh.,
Suxamethonium), Decamethonium (C-10)
II. Directly acting agents
Dantrolene sodium, Quinine
Note: 1. Decamethonium is not used clinically.
2. Aminoglycoside, tetracycline, polypeptide antibiotics interfere
with neuromuscular transmission at high doses, but are not
employed as muscle relaxants.
• ANTISEPTICS AND DISINFECTANTS
The terms antiseptic and disinfectant connote an agent which
inhibits or kills microbes on contact. Conventionally, agents used
on living surfaces (skin, mouth) are called antiseptics while those
used for inanimate objects (instruments, privies, water supply) are
called disinfectants. There is considerable overlap and many agents
are used in either way. A practical distinction between the two on
the basis of a growth inhibiting versus direct lethal action is futile
because these are often concentration dependent actions. The term
Germicide covers both category of drugs. There, however, is
difference between ‘disinfection’ and ‘sterilization’. While
sterilization means complete killing of all forms of
microorganisms, disinfection refers to reduction in the number of
viable pathogenic microbes to a level that they do not pose a risk to
individuals with normal host defence. The terms ‘sanitization’ and
‘decontamination’ also have similar connotation. Thus, in ordinary
usage, disinfectants do not eliminate all microbes.
• A good antiseptic/disinfectant should be:
(i) Chemically stable.
(ii) Cheap.
(iii) Nonstaining with agreeable colour and odour.
(iv) Cidal and not merely static, destroying spores as well.
(v) Active against all pathogens—bacteria, fungi, viruses, protozoa.
(vi) Require brief time of exposure.
(vii) Able to spread through organic films and enter folds and crevices.
(viii) Active even in the presence of blood, pus, exudates and excreta.
• A disinfectant in addition should not corrode or rust instruments and be
easily washable.
An antiseptic in addition should be:
• Rapid in action and exert sustained protection.
• Nonirritating to tissues, should not delay healing.
• Nonabsorbable, produce minimum toxicity if absorbed.
• Nonsensitizing (no allergy).
• Compatible with soaps and other detergents.
• CLASSIFICATION
1. Phenol derivatives: Phenol, Cresol, Hexylresorcinol, Chloroxylenol,
Hexachlorophene.
2. Oxidizing agents: Pot. permangnate, Hydrogen peroxide, Benzoyl peroxide.
3. Halogens: Iodine, Iodophores, Chlorine, Chlorophores.
4. Biguanide: Chlorhexidine.
5. Quaternary ammonium (Cationic): Cetrimide, Benzalkonium chloride,
Dequalinium chloride.
6. Soaps: of Sod. and Pot.
7. Alcohols: Ethanol, Isopropanol.
8. Aldehydes: Formaldehyde, Glutaraldehyde.
9. Acids: Boric acid, Acetic acid.
10. Metallic salts: Silver nitrate, Silver sulfadiazine, Mild silver protein, Zinc
sulfate, Calamine, Zinc oxide.
11. Dyes: Gentian violet, Acriflavine, Proflavine.
12. Furan derivative: Nitrofurazone.
• All drugs grouped in this class have analgesic, antipyretic and
antiinflammatory actions in different measures. In contrast to
morphine they do not depress CNS, do not produce physical
dependence, have no abuse liability and are weaker analgesics
(except for inflammatory pain). They are also called nonnarcotic,
nonopioid or aspirinlike analgesics. They act primarily on
peripheral pain mechanisms, but also in the CNS to raise pain
threshold. They are more commonly employed and many are over-
the-counter drugs.
• The antipyretic-analgesics are chemically diverse, but most are organic acids.
CLASSIFICATION
A. Nonselective COX inhibitors (traditional NSAIDs)
1. Salicylates: Aspirin.
2. Propionic acid derivatives: Ibuprofen, Naproxen, Ketoprofen, Flurbiprofen.
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,
Meloxicam, Etodolac.
C. Selective COX-2 inhibitors Celecoxib, Etoricoxib, Parecoxib.
D. Analgesic-antipyretics with poor antiinflammatory action
1. Paraaminophenol derivative: Paracetamol (Acetaminophen).
2. Pyrazolone derivatives: Metamizol (Dipyrone), Propiphenazone.
3. Benzoxazocine derivative: Nefopam.