Unit 2 General Pharmacology (As per PCI syllabus)

Presented by: Prof.Mirza Anwar Baig
Anjuman-I-Islam's Kalsekar Technical Campus
School of Pharmacy,New Pavel,Navi Mumbai,Maharashtra
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• Introduction to physiological receptors
• Structural and functional families of receptors
• Mechanisms of drug action:
-Drug receptor interaction
-Dose response curve (DRC)
-Drug antagonism
Compiled by: Prof.Mirza Anwar Baig

 Explain the pharmacological basis of drug action.
 Define the scientific terms mentioned in this section.
 Identify type of antagonism
 Rearrange the drugs in ascending or descending order for their
efficacy and potency.

Actions of a drug on the body.
Influence of drug concentrations on the
magnitude of the response.
Drugs exert their effects, both
beneficial and harmful, by interacting
with receptors (macromolecules)
present on the cell surface or within the
cell.
The drug–receptor complex initiates
alterations in biochemical and/or
molecular activity of a cell by a process
called signal transduction

 Drugs act as signals, and their receptors act as signal detectors.
 “Agonist” refers to a naturally occurring small molecule or a
drug that binds to a site on a receptor protein and activates it.
 “Second messenger” or effector molecules are part of the
cascade of events that translates agonist binding into a cellular
response.

1. Cells have many different types of receptors, each of which is specific for
a particular agonist and produces a unique response.
2. Cardiac cell membranes, for example, contain β receptors that bind and
respond to epinephrine or norepinephrine, as well as muscarinic receptors
specific for acetylcholine.
3. The magnitude of the response is proportional to the number of drug–
receptor complexes.
4. Most receptors are named for the type of agonist that interacts best with it.
For example,the receptor for histamine is called a histamine receptor.
5. it is important to know that not all drugs exert their effects by interacting
with a receptor.
6. Antacids, for instance, chemically neutralize excess gas-tric acid, thereby
reducing the symptoms of “heartburn.”

 Inactive (R) and active (R*) states ,are in reversible equilibrium, usually
favoring the inactive state.
 Aagonists causes the equilibrium to shift from R to R* to produce a
biologic effect.
 Antagonists but do not increase the fraction of R* and may stabilize the
receptor in R state.
 Partial agonists cause equilibrium shift from R to R*, fraction of R* is
less than that caused by an agonist (but still more than that caused by an
antagonist).
 Magnitude of biological effect α fraction of R*.
 Agonists, antagonists, and partial agonists are examples of ligands, or
molecules that bind to the activation site on the receptor.

Receptor is a biologic molecule to which a drug binds and produces a
measurable response.
Receptor may be Enzymes, nucleic acids, and structural proteins
Protein is the richest sources of therapeutically relevant pharmacologic receptors
Four Receptor Families:
1) ligand-gated ion channels,
2) G protein–coupled receptors,
3) enzyme-linked receptors,
4) intracellular receptors.
Hydrophilic ligands interact with receptors that are found on the cell surface.
Hydrophobic ligands enter cells through the lipid bilayers of the cell membrane to
interact with receptors found inside cells

 Contains the ligand-binding site regulates the shape of the pore
through which ions can flow across cell membranes.
 Agonist opens the channel briefly for a few milliseconds.
 Depending on the ion conducted through these channels, these
receptors medi-ate diverse functions

 For example, stimulation of the nicotinic receptor by
acetylcholine results in sodium influx and potassium outflux
(action potential in a neuron or contraction in skeletal muscle).
 Agonist stimulation of the γ-aminobutyric acid (GABA)
receptor increases chloride influx and hyperpolarization of
neurons.
 Local anesthetics bind to the voltage-gated sodium channel,
inhibiting sodium influx and decreasing neuronal conduction.

 Receptor contains the ligand-binding area, and the intracellular
domain interacts (when activated) with a G protein or effector
molecule.
 There are many kinds of G proteins (for example, Gs , Gi , and Gq
), but they all are composed of three protein subunits.
 The α subunit binds guanosine triphosphate (GTP).
 β and γ subunits anchor the G protein in the cell membrane.

 Binding of an agonist to the receptor increases GTP binding to
the α subunit, causing dissociation of the α-GTP complex from
the β γ complex.
 These two complexes can then interact with other cellular
effectors, usually an enzyme, a protein,or an ion channel, that
are responsible for further actions within the cell. These
responses usually last several seconds to minutes.

A common effector, activated by Gs and inhibited by Gi , is adenylyl
cyclase, which produces the second messenger cyclic adenosine
monophosphate (cAMP).
Gq activates phospholipase C, generating two other second
messengers: inositol 1,4,5-trisphosphate (IP 3 ) and diacylglycerol
(DAG).
DAG and cAMP activate different protein kinases within the cell,
leading to a myriad of physiological effects.
IP 3 regulates intracellular free calcium concentrations, as
well as some protein kinases.

 This family of receptors consists of a protein that may differ form
dimers or multisubunit complexes.
 When activated, these receptors undergo conformational changes
resulting in increased cytosolic enzyme activity, depending on their
structure and function.
 This response lasts on the order of minutes to hours.
 Examples:
Epidermal growth factor, platelet-derived growth factor, atrial
natriuretic peptide, insulin, and others) possess tyrosine kinase
activity as part of their structure.
 The activated receptor phosphorylates tyrosine residues on itself
and then other specific proteins.

 Phosphorylation can substantially modify the structure of the
target protein, thereby acting as a molecular switch.
 For example, when the peptide hormone insulin binds to two
of its receptor subunits, their intrinsic tyrosine kinase activity
causes autophosphorylation of the receptor itself.
 In turn, the phosphorylated receptor phosphorylates other
peptides or proteins that subsequently activate other important
cellular signals.
 This cascade of activations results in a multiplication of the
initial signal, much like that with G protein–coupled receptors.

a) It is entirely intracellular, and, therefore, the ligand must diffuse into the cell.
b) The ligand must have sufficient lipid solubility.
c) The primary targets are transcription factors in the cell nucleus.
d) Binding of the ligand with its receptor generally activates the receptor via
dissociation from a variety of binding proteins.
e) The activated ligand–receptor complex then translocates to the nucleus, where it
often dimerizes before binding to transcription factors that regulate gene expression.
f) The activation or inactivation of these factors causes the transcription of DNA into
RNA and translation of RNA into an array of proteins.
g) The time course is on the order of hours to days.
h) For example, steroid hormones exert their action on target cells via intracellular
receptors.
i) Other targets of intracellular ligands are structural proteins, enzymes, RNA,and
ribosomes.

 For example, tubulin is the target of antineo-plastic
agents such as paclitaxel.
 The enzyme dihydrofolate reductase is the target of
antimicrobials such as trimethoprim.
 50S subunit of the bac-terial ribosome is the target of
macrolide antibiotics such as erythromycin.

Signal transduction has two important features: 1) the ability to amplify
small signals and 2) mechanisms to protect the cell from excessive
stimulation.
1.Signal amplification: Spare receptors
A characteristic of G protein–linked and enzyme-linked receptor.
It is the ability to amplify signal intensity and duration.
Example, The binding of albuterol, may only exist for a few milliseconds,
but the subsequent activated G proteins may last for hundreds of
milliseconds.
Systems that exhibit this behavior are said to have spare receptors.
A certain number of receptors are “spare.”
Spare receptors are receptors that exist in excess of those required to
produce a full effect
TISSUES WITH A HIGH PROPORTION OF SPARE RECEPTORS WILL
RESPOND TO AGONISTS AT LOWER CONCENTRATIONS.

2. Desensitization, up & down-regulation of receptors:
Tachyphylaxis (repeated adminsteration of agonist or
antagonist)
Refractory receptors (receptors in recovery phase)
3. Up-regulation of receptors: repeated exposure of a receptor to
an antagonist may result in up-regulation of receptors, in
which receptor reserves are inserted into the membrane,
increasing the total number of receptors available

 Graded dose–response relations
1. Potency: amount of drug

 Biologic response is based on the concentration of the agonist
and the fraction of activated receptors.
 The intrinsic activity of a drug determines its ability to fully or
partially activate the receptors.
 Drugs may be categorized according to their intrinsic activity
and resulting Emax values.
A. Full agonists
B. Partial agonists
C. Inverse agonists
D. Antagonists

 Antagonists bind to a receptor with high affinity but possess
zero intrinsic activity.
 An antagonist has no effect in the absence of an agonist but
can decrease the effect of an agonist when present.
 Antagonism may occur either by blocking the drug’s ability to
bind to the receptor or by blocking its ability to activate the
receptor.
1. Competitive antagonists:
2. Irreversible antagonists:
3. Allosteric antagonists:
4. Functional antagonism:

Competitive
antagonists
Irreversible
antagonists
Allosteric antagonists Functional antagonism
Antagonist and
the agonist bind
to the same site
on the receptor in
a reversible
manner
Irreversible
antagonists bind
covalently to the active
site of the receptor,
thereby reducing the
number of receptors
available to the agonist
Antagonist binds to a
site (“allosteric site”)
other than the agonist-
binding site and
prevents the receptor
from
being activated by the
agonist.
An antagonist may act at
a completely
separate receptor,
initiating effects that are
functionally opposite
those of the agonist
Inhibition can be
overcome by
increasing the
concentration of
agonist relative
to antagonist.
The effect of
irreversible antagonists
cannot be overcome by
adding more agonist
The effect of
irreversible
antagonists cannot be
overcome by adding
more agonist
Inhibition can be
overcome by increasing
the concentration of
agonist relative to
antagonist.

Competitive
antagonists
Irreversible
antagonists
Allosteric
antagonists
Functional
antagonism
Shift the agonist
DRC to the right
(increased EC50 )
without affecting
E max
It causes a
downward shift of
the Emax , with no
shift of EC50
values (unless spare
receptors are
present)
Causes a
downward shift of
the Emax , with no
change in the EC50
value of an agonist.
Shift the agonist
DRC to the right
(increased EC50 )
without affecting
E max
Reduce agonist
potency (increase
EC50)
It reduce agonist
efficacy (decrease E
max )
It reduce agonist
efficacy (decrease E
max )
Reduce agonist
potency (increase
EC50)
Terazosin competes
norepinephrine at
α1 -adrenoceptors,
reducing blood
pressure.
Binding of
picrotoxin to
interior site of
GABA controlled
chloride channel
Histamine
causes broncho-
constriction
Epinephrine causes
muscles to relax.

 It is a dose–response relationship in between the dose of the drug
and the proportion of a population that responds to it. ED50 values
are used instead of EC50

 Measure of a drug’s safety
 Larger value indicates a wide margin between doses that are
effective and doses that are toxic.
Formula:
For Human TI = TD50 / ED50
For Animal TI = LD50 / ED50
 ED50 (median effective dose): is the dose that produce
therapeutic effect in 50% of the population.
 TD50/LD50 (median toxic/lethal dose): is the dose that is
toxic/lethal to 50% of the population.

 It may exhibit synergism or antagonism.
 May take place at pharmacokinetic level or at pharmacodynamic
level.
SYNERGISM
 (Greek: Syn—together; ergon—work)
 Refers to the interaction between two or more “drugs" when the
combined effect is greater than if you added the “drugs" on their
own
 (a type of "when is one plus one is greater than two" effect).

(a) Additive Effect:
effect of drugs A + B = effect of drug A + effect of drug B
Examples:
 Combination is better tolerated than higher dose of one
component.

(b) Supraadditive (potentiation):
 The effect of combination is greater than the individual effects of the
components:
effect of drug A + B > effect of drug A + effect of drug B
 This is always the case when one component given alone produces no
effect, but enhances the effect of the other (potentiation).

Fig. 4.17: Log dose-response curves of a drug ‘A’
depicting additive synergism (in purple) and potentiation (Supra-additive
synergism) in blue.
A: An agonist drug.
B: Another agonist in a fixed submaximal dose producing 40% response.
C: A potentiating drug which itself has no agonistic activity

 Adverse effect is ‘any undesirable or unintended consequence of drug
administration’(trivial, serious or even fatal).
 For the purposes of detecting and quantifying only those adverse effects the
term adverse drug reaction (ADR) has been defined.
 ADR is ‘any noxious change which is suspected to be due to a drug, occurs
at doses normally used in man.
 Requires treatment or decrease in dose or indicates caution in the future use
of the same drug’.
 This definition excludes trivial or expected side effects and poisonings
or overdose.

 May develop promptly or only after prolonged medication or even after
stoppage of the drug.
 Not rare; an incidence of 10–25% has been documented in different clinical
settings.
 Common with multiple drug therapy and in the elderly.
 The magnitude of risk has to be considered along with the magnitude of
expected therapeutic benefit in deciding whether to use or not to use
a particular drug in a given patient.
 Examples: even risk of bone marrow depression may be justified in
treating cancer, while mild drowsiness caused by an antihistaminic in
treating common cold may be unacceptable

 Side Effects
It is an undesired effect that occurs when the medication is administered regardless
of the dose.
 Unlike adverse events, side effects are mostly foreseen by the physician and the
patient is told to be aware of the effects that could happen while on the therapy.
 Side effects differ from adverse events and later resolve on their own with time after
taking the medication for several weeks.
 Some medications are even utilized due to their side effects, one example being
mirtazapine used in anorexic patients due to the medications potential to cause
weight gain.
 Side effects are tracked and investigated extensively during clinical trials before
entering the market.

1. Predictable (Type A or Augmented) reactions (mechanism based adverse
reactions):
• Based on the pharmacological properties of the drug.
• Qualitatively normal response to the drug;
• Include side effects, toxic effects and consequences of drug withdrawal.
• More common, dose related and mostly preventable and reversible.
2. Unpredictable (Type B or Bizarre) reactions:
• These are based on peculiarities of the patient and not on drug’s known
actions; include allergy and idiosyncrasy.
• They are less common, often non-dose related, generally more serious and
require withdrawal of the drug.
• Some of these reactions can be predicted and prevented if their genetic
basis is known and suitable test to characterize the individual’s phenotype
is performed.

Pharmacovigilance:
‘Science and activities relating to the detection, assessment,
understanding and prevention of adverse effects or any other
drug
related problems.’
Useful in educating doctors about ADRs and in the official
regulation of drug use.
Its main purpose is to reduce the risk of drug-related harm to the
Patient
Activities in Pharmacovigilance ?????

can be minimized but not altogether eliminated by observing the following
practices:
1. Avoid all inappropriate use of drugs in the context of patient’s clinical
condition.
2. Use appropriate dose, route and frequency of drug administration based on
patient’s specific variables.
3. Elicit and take into consideration previous history of drug reactions.
4. Elicit history of allergic diseases and exercise caution (drug allergy is more
common in patients with allergic diseases).
5. Rule out possibility of drug interactions when more than one drug is
prescribed.
6. Adopt correct drug administration technique (e.g. intravenous injection of
vancomycin must be slow).
7. Carry out appropriate laboratory monitoring (e.g. prothrombin time with
warfarin, serum drug levels with lithium).

1. Side effects
2. Secondary effects
3. Toxic effects
4. Intolerance
5. Idiosyncrasy
6. Drug allergy
7. Photosensitivity
8. Drug dependence
9. Drug withdrawal reactions
10. Teratogenicity
11. Mutagenicity and Carcinogenicity
12. Drug induced diseases

 Unwanted
 Often unavoidable pharmacodynamic effects
 Not serious,
 Predictable
 Reduction in dose, usually ameliorates the symptoms
Examples
Atropine (preanaesthetic medication) for its antisecretory action. produces
dryness of mouth
Glyceryl trinitrate (angina pectoris) by dilating peripheral vasculature
produces postural hypotension and throbbing headache.

 Indirect consequences of a primary action of the drug
Example:
Suppression of bacterial flora by tetracyclines paves the way
for superinfections
Corticosteroids weaken host defence mechanisms so that
latent tuberculosis gets activated.

 Result of excessive pharmacological action
 Due to overdosage or prolonged use.
 Overdosage may be absolute (accidental,homicidal, suicidal) or
relative (i.e. usual dose of gentamicin in presence of renal failure).
 The manifestations are predictable and dose related.
Examples:
High dose of atropine causing delirium (functional alteration)
 Hepatic necrosis from paracetamol overdosage.(drug induced
tissue damage)

 Characteristic toxic effects of a drug in an individual at therapeutic
doses.
 Converse of tolerance
 Indicates a low threshold of the individual to the action of a drug.
Examples:
A single dose of triflupromazine induces muscular dystonias in some
individuals,specially children.
Only few doses of carbamazepine may cause ataxia in some people.
One tablet of chloroquine may cause vomiting and abdominal pain in an
occasional patient.

Genetically determined abnormal reactivity to
a chemical.
The drug interacts with some unique feature of the individual, not found in
majority of subjects.
Restricted to individuals with a particular genotype.
Examples:
Barbiturates cause excitement and mental confusion in some individuals.
Quinine/quinidine cause cramps, diarrhoea,purpura, asthma and vascular
collapse in some patients.
Chloramphenicol produces nondose-related serious aplastic anaemia in rare
individuals.

 Immunologically mediated reaction producing stereotype
symptoms
 unrelated to the pharmacodynamic profile of the drug.
 Occur even with much smaller doses
 Have a different time course of onset and duration.
 Target organs: skin, airways, blood
vessels, blood and gastrointestinal tract

Drug induced sensitization of the skin to UV radiation.
The reactions are of two types:
(a) Phototoxic:
Drug or its metabolite accumulates in the skin, absorbs light
and undergoes a photochemical reaction followed by a
photobiological reaction resulting in local tissue damage
(sunburn-like), i.e. erythema, edema, blistering.

(b) Photoallergic:
 Drug or its metabolite induces a cell mediated immune
response.
 On exposure to light of longer wave lengths (320–400 nm,
UV) produces a papular or eczematous contact dermatitis.

 Drugs capable of altering mood and feelings.
 Patient used it to derive euphoria, recreation, withdrawal from reality,
social adjustment, etc.
 Patient takes drugs for personal satisfaction rather than other basic needs,
often in the face of known risks to health.
Terminologies used to simplify it…..
• Psychological dependence
• Physical dependence

 Individual believes that optimal state of wellbeing
is achieved only through the actions of the drug.
 The subject feels emotionally distressed if the drug is not taken.
 May vary from desire to craving

 Altered physiological state
 Produced by repeated administration of a drug
 Continued presence of the drug to maintain physiological equilibrium.
 Discontinuation of the drug results in a characteristic withdrawal syndrome.
Drugs producing physical dependence are—
 Depressants drugs: opioids, barbiturates and alcohol and benzodiazepines.
 Stimulant drugs: e.g. amphetamines, cocaine produce little or no physical
dependence.

• Result of sudden interruption of therapy with certain other drugs
• Mostly in the form of worsening of the clinical condition for which the
drug was being used, e.g.:
(i) Acute adrenal insufficiency may be precipitated by abrupt cessation of
corticosteroid therapy
ii) Severe hypertension, restlessness and sympathetic overactivity may
occur shortly after discontinuing clonidine.
(iii) Worsening of angina pectoris, precipitation of myocardial infarction
may result from stoppage of β blockers.

 It refers to the capacity of a drug to cause foetal abnormalities when
administered to the pregnant mother.
 The placenta does not constitute a strict barrier, and any drug can cross it to
a greater or lesser extent.
11. Mutagenicity and Carcinogenicity
 Capacity of a drug to cause genetic defects and cancer respectively.
 Examples are—anticancer drugs, radioisotopes, estrogens, tobacco.
 Generally, drugs which show mutagenic or carcinogenic potential are not
approved for marketing/are withdrawn, unless they are useful in life-
threatening conditions

 Iatrogenic (physician induced) diseases.
 Functional disturbances (disease) caused by drugs which persist even after
the offending drug has been withdrawn and largely eliminated.
Examples:
• Peptic ulcer by salicylates and corticosteroids.
• Parkinsonism by phenothiazines and other antipsychotics.
• Hepatitis by isoniazid.
• .

 Modification of response to one drug by another when they are administered
simultaneously or in quick succession.
 Mostly quantitative and rarely qualitative.
 Many medical conditions are treated with a combination of drugs.
Examples:
 Antibiotic with an analgesic to treat a painful infective condition.
 Antitubercular drugs are combined to prevent drug resistance;
 Mixed aerobic-anaerobic bacterial infections are treated with a combination
of antimicrobials.

 Broadly divided into pharmacokinetic and pharmacodynamic interactions.
 Few interactions take place even outside the body .
Pharmacokinetic interactions
 Alter the concentration of the object drug at its site of action (and consequently
the intensity of response)
Absorption:
Absorption of an orally administered drug can be affected by other
concurrently ingested drugs.
Examples:
 Mostly due to formation of insoluble and poorly absorbed complexes in
the gut lumen, (eg; tetracyclines and calcium/iron salts, antacids or sucralfate.)
 Phenytoin absorption is decreased by sucralfate due to binding in the g.i.
lumen.

Distribution:
o Displacement of one drug from its binding sites on plasma proteins by
another drug.
o Displacing drug should bind to the same sites on the plasma proteins
with higher affinity.
o Displacement of bound drug will initially raise the concentration of the free
and active form of the drug in plasma that may result in toxicity.
Example:
Quinidine + digoxin = digoxin toxicity ????
1. Quninidine reduces the binding of digoxin to tissue proteins.
2. Affect its renal and biliary clearance by inhibting the efflux transporter P-
glycoprotein,
3. Resulting in nearly doubling of digoxin blood levels and toxicity.

 Certain drugs reduce or enhance the rate of metabolism of other drugs.
 Affect the bioavailability and the plasma half-life of the drug.
 May be due to competition for the same CYP450 isoenzyme or cofactor.
Examples:
 Macrolide antibiotics, azole antifungals, chloramphenicol, omeprazole,
SSRIs, HIV-protease inhibitors, cimetidine, ciprofloxacin and metronidazole
are some important inhibitors of metabolism of multiple drugs.
 Lidocaine metabolism is dependent on hepatic blood flow, propranolol
reducing blood flow to the liver hence t½ of lidocain increases.

Mostly important in case of drugs actively
secreted by tubular transport mechanisms.
Examples:
 Probenecid inhibits tubular secretion of
penicillins and cephalosporins and prolongs
their plasma t½.
 Aspirin blocks the uricosuric action of
probenecid and decreases tubular secretion
of methotrexate.
 Change in the pH of urine can also affect
excretion of weakly acidic or weakly basic
drugs.

 Derive from modification of the action of one drug at the
target site by another drug, independent of a change in its
concentration.
 Result in…..
1. an enhanced response (synergism),
2. an attenuated response (antagonism)
3. an abnormal response.

 Measurement of potency of a drug or unknown mediator from the
magnitude of the biological effect that it produces.
 Involves comparison of the unknown preparation with a standard.
 Estimates that are not based on comparison with standards are liable to
vary from laboratory to laboratory.
 Comparisons are best made on the basis of dose–response curves.
 The biological response may be quantal (the proportion of tests in which a
given all-or-nothing effect is produced) or graded.
 Approaches to measure drug response range through molecular and
chemical techniques, in vitro and in vivo animal studies and clinical studies

Studies involving human subjects range from
 Experimental pharmacodynamic or
 Experimental pharmacokinetic investigations
 Formal clinical trials.

 Special type of bioassay done to compare the clinical efficacy of a new drug or
procedure with that of a known drug or procedure.
 Aim is a straight comparison of unknown (A) with standard (B) at a single dose
level.
 The result may be: ‘B better than A’, ‘B worse than A’, or ‘No difference
detected’.
 Efficacy, not potency, is compared.
 To avoid bias, clinical trials should be:
– controlled (comparison of A with B, rather than study of A alone)
– randomised (assignment of subjects to A or B on a random basis)
– double-blind (neither subject nor assessor knows whether A or B is being
used).

 Require approval by an independent ethical committee.
 Require very careful planning and execution, and are inevitably expensive.
 Clinical outcome measures may comprise:
– physiological measures (e.g. blood pressure, liver function tests)
– subjective assessments (e.g. pain relief, mood)
– long-term outcome (e.g. survival or freedom from recurrence)
– overall ‘quality of life’measures
– ‘quality-adjusted life years’(QALYs), which combine survival with
quality of life.
 Meta-analysis is a statistical technique used to pool the data from several
independent trials.

1. Rang H. P., Dale M. M., Ritter J. M., Flower R. J., Rang and Dale‘s
Pharmacology,.Churchil Livingstone Elsevier
2. Katzung B. G., Masters S. B., Trevor A. J., Basic and clinical pharmacology, Tata
Mc Graw-Hill
3. Goodman and Gilman‘s, The Pharmacological Basis of Therapeutics
4. Marry Anne K. K., Lloyd Yee Y., Brian K. A., Robbin L.C., Joseph G. B., Wayne A.
K.,Bradley R.W., Applied Therapeutics, The Clinical use of Drugs, The Point
Lippincott Williams & Wilkins
5. Mycek M.J, Gelnet S.B and Perper M.M. Lippincott‘s Illustrated Reviews-
Pharmacology
6. K.D.Tripathi. Essentials of Medical Pharmacology, JAYPEE Brothers Medical
Publishers (P) Ltd, New Delhi.
Presented by: Prof.Mirza Anwar Baig 75

76

Unit 2 General Pharmacology (As per PCI syllabus)

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