1. Pharmacology
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A variety of topics involved with pharmacology, including neuropharmacology, renal
pharmacology, human metabolism, intracellular metabolism, and intracellular regulation.
Pharmacology (from Greek φάρμακον, pharmakon, "poison" in classic Greek; "drug" in modern
Greek; and -λογία, -logia "study of", "knowledge of") is the branch of medicine and biology
concerned with the study of drug action,[1] where a drug can be broadly defined as any man-
made, natural, or endogenous (within the cell) molecule which exerts a biochemical and/or
physiological effect on the cell, tissue, organ, or organism. More specifically, it is the study of
the interactions that occur between a living organism and chemicals that affect normal or
abnormal biochemical function. If substances have medicinal properties, they are considered
pharmaceuticals. The field encompasses drug composition and properties, interactions,
toxicology, therapy, and medical applications and antipathogenic capabilities. The two main
areas of pharmacology are pharmacodynamics and pharmacokinetics. The former studies the
effects of the drugs on biological systems, and the latter the effects of biological systems on the
drugs. In broad terms, pharmacodynamics discusses the chemicals with biological receptors, and
pharmacokinetics discusses the absorption, distribution, metabolism, and excretion of chemicals
from the biological systems. Pharmacology is not synonymous with pharmacy and the two terms
are frequently confused. Pharmacology, a biomedical science, deals with how drugs interact
within biological systems to affect function. It is the study of drugs, of the reactions of the body
and drug on each other, the sources of drugs, their nature, and their properties. In contrast,
pharmacy, a health services profession, is concerned with application of the principles learned
from pharmacology in its clinical settings; whether it be in a dispensing or clinical care role. In
either field, the primary contrast between the two are their distinctions between direct-patient
care, for pharmacy practice, and the science-oriented research field, driven by pharmacology.
Dioscorides' De Materia Medica is often said to be the oldest and most valuable work in the
history of pharmacology.[2] The origins of clinical pharmacology date back to the Middle Ages in
Avicenna's The Canon of Medicine, Peter of Spain's Commentary on Isaac, and John of St
Amand's Commentary on the Antedotary of Nicholas.[3] Clinical pharmacology owes much of its
foundation to the work of William Withering.[4] Pharmacology as a scientific discipline did not

2. further advance until the mid-19th century amid the great biomedical resurgence of that period.[5]
Before the second half of the nineteenth century, the remarkable potency and specificity of the
actions of drugs such as morphine, quinine and digitalis were explained vaguely and with
reference to extraordinary chemical powers and affinities to certain organs or tissues.[6] The first
pharmacology department was set up by Rudolf Buchheim in 1847, in recognition of the need to
understand how therapeutic drugs and poisons produced their effects.[5]
Early pharmacologists focused on natural substances, mainly plant extracts. Pharmacology
developed in the 19th century as a biomedical science that applied the principles of scientific
experimentation to therapeutic contexts.[7]
Divisions
Clinical pharmacology
The basic science of pharmacology, with added focus on the application of pharmacological
principles and methods in the real world
Neuropharmacology
Effects of medication on nervous system functioning.
Psychopharmacology
Effects of medication on the brain; observing changed behaviors of the body and read the effect
of drugs on the human brain.
Pharmacogenetics
Clinical testing of genetic variation that gives rise to differing response to drugs.
Pharmacogenomics
Application of genomic technologies to new drug discovery and further characterization of older
drugs.
Pharmacoepidemiology
Study of effects of drugs in large numbers of people.
Toxicology

3. Study of harmful or toxic effects of drugs.
Theoretical pharmacology
Study of metrics in pharmacology.
Posology
How medicines are dosed. It also depends upon various factors like age, climate, weight, sex,
and so on.
Pharmacognosy
A branch of pharmacology dealing especially with the composition, use, and development of
medicinal substances of biological origin and especially medicinal substances obtained from
plants.
Behavioral pharmacology
Behavioral pharmacology, also referred to as psychopharmacology, is an interdisciplinary field
which studies behavioral effects of psychoactive drugs. It incorporates approaches and
techniques from neuropharmacology, animal behavior and behavioral neuroscience, and is
interested in the behavioral and neurobiological mechanisms of action of psychoactive drugs.
Another goal of behavioral pharmacology is to develop animal behavioral models to screen
chemical compounds with therapeutic potentials. People in this field (called behavioral
pharmacologists) typically use small animals (e.g. rodents) to study psychotherapeutic drugs
such as antipsychotics, antidepressants and anxiolytics, and drugs of abuse such as nicotine,
cocaine, methamphetamine, etc.
Environmental pharmacology
Environmental pharmacology is a new discipline.[8] Focus is being given to understand gene–
environment interaction, drug-environment interaction and toxin-environment interaction. There
is a close collaboration between environmental science and medicine in addressing these issues,
as healthcare itself can be a cause of environmental damage or remediation. Human health and
ecology is intimately related. Demand for more pharmaceutical products may place the public at
risk through the destruction of species. The entry of chemicals and drugs into the aquatic
ecosystem is a more serious concern today. In addition, the production of some illegal drugs
pollutes drinking water supply by releasing carcinogens.[9] More and more biodegradability of
drugs are needed.
Scientific background
The study of chemicals requires intimate knowledge of the biological system affected. With the
knowledge of cell biology and biochemistry increasing, the field of pharmacology has also

4. changed substantially. It has become possible, through molecular analysis of receptors, to design
chemicals that act on specific cellular signaling or metabolic pathways by affecting sites directly
on cell-surface receptors (which modulate and mediate cellular signaling pathways controlling
cellular function).
A chemical has, from the pharmacological point-of-view, various properties. Pharmacokinetics
describes the effect of the body on the chemical (e.g. half-life and volume of distribution), and
pharmacodynamics describes the chemical's effect on the body (desired or toxic).
When describing the pharmacokinetic properties of a chemical, pharmacologists are often
interested in LADME:
Liberation - disintegration (for solid oral forms {breaking down into smaller particles}),
dispersal and dissolution
Absorption - How is the medication absorbed (through the skin, the intestine, the oral
mucosa)?
Distribution - How does it spread through the organism?
Metabolism - Is the medication converted chemically inside the body, and into which
substances. Are these active? Could they be toxic?
Excretion - How is the medication eliminated (through the bile, urine, breath, skin)?
Medication is said to have a narrow or wide therapeutic index or therapeutic window. This
describes the ratio of desired effect to toxic effect. A compound with a narrow therapeutic index
(close to one) exerts its desired effect at a dose close to its toxic dose. A compound with a wide
therapeutic index (greater than five) exerts its desired effect at a dose substantially below its
toxic dose. Those with a narrow margin are more difficult to dose and administer, and may
require therapeutic drug monitoring (examples are warfarin, some antiepileptics, aminoglycoside
antibiotics). Most anti-cancer drugs have a narrow therapeutic margin: toxic side-effects are
almost always encountered at doses used to kill tumors.
Medicine development and safety testing
Development of medication is a vital concern to medicine, but also has strong economical and
political implications. To protect the consumer and prevent abuse, many governments regulate
the manufacture, sale, and administration of medication. In the United States, the main body that
regulates pharmaceuticals is the Food and Drug Administration and they enforce standards set by
the United States Pharmacopoeia. In the European Union, the main body that regulates
pharmaceuticals is the EMEA and they enforce standards set by the European Pharmacopoeia.
The metabolic stability and the reactivity of a library of candidate drug compounds have to be
assessed for drug metabolism and toxicological studies. Many methods have been proposed for
quantitative predictions in drug metabolism; one example of a recent computational method is
SPORCalc.[10] If the chemical structure of a medicinal compound is altered slightly, this could
slightly or dramatically alter the medicinal properties of the compound depending on the level of
alteration as it relates to the structural composition of the substrate or receptor site on which it
exerts its medicinal effect, a concept referred to as the structural activity relationship (SAR). This

5. means that when a useful activity has been identified, chemists will make many similar
compounds called analogues, in an attempt to maximize the desired medicinal effect(s) of the
compound. This development phase can take anywhere from a few years to a decade or more and
is very expensive.[11]
These new analogues need to be developed. It needs to be determined how safe the medicine is
for human consumption, its stability in the human body and the best form for delivery to the
desired organ system, like tablet or aerosol. After extensive testing, which can take up to 6 years,
the new medicine is ready for marketing and selling.[11]
As a result of the long time required to develop analogues and test a new medicine and the fact
that of every 5000 potential new medicines typically only one will ever reach the open market,
this is an expensive way of doing things, costing millions of dollars. To recoup this outlay
pharmaceutical companies may do a number of things:[11]
Carefully research the demand for their potential new product before spending an outlay
of company funds.[11]
Obtain a patent on the new medicine preventing other companies from producing that
medicine for a certain allocation of time.[11]
Education
The study of pharmacology is offered in many universities worldwide in programs that differ
from pharmacy programs. Students of pharmacology are trained as biomedical researchers,
studying the effects of substances in order to better understand the mechanisms which might lead
to new drug discoveries, for example, or studying biological systems for the purpose of re-
defining drug mechanisms or discovering new mechanisms against which novel therapies can be
directed (or new pathways for the sake of a more complete picture of its biochemistry). In
addition, students of pharmacology must have detailed working knowledge of those areas in
which biological or chemical therapeutics play a role. These may include (but are not limited to):
biochemistry, molecular biology, genetics, chemical biology, physiology, chemistry,
neuroscience, and microbiology. Whereas a pharmacy student will eventually work in a
pharmacy dispensing medications or some other position focused on the patient, a
pharmacologist will typically work within a laboratory setting.
Pharmacological Glossary
Definitions of commonly used pharmacological terms

6. Term Description
A drug that binds to and activates a receptor. Can be full, partial or
inverse. A full agonist has high efficacy, producing a full response while
occupying a relatively low proportion of receptors. A partial agonist has
lower efficacy than a full agonist. It produces sub-maximal activation
Agonist
even when occupying the total receptor population, therefore cannot
produce the maximal response, irrespective of the concentration applied.
An inverse agonist produces an effect opposite to that of an agonist, yet
binds to the same receptor binding-site as an agonist.
A drug that binds to a receptor at a site distinct from the active site.
Induces a conformational change in the receptor, which alters the affinity
Allosteric Modulator of the receptor for the endogenous ligand. Positive allosteric modulators
increase the affinity, whilst negative allosteric modulators decrease the
affinity.
A drug that attenuates the effect of an agonist. Can be competitive or
non-competitive, each of which can be reversible or irreversible. A
competitive antagonist binds to the same site as the agonist but does not
activate it, thus blocks the agonist’s action. A non-competitive antagonist
Antagonist binds to an allosteric (non-agonist) site on the receptor to prevent
activation of the receptor. A reversible antagonist binds non-covalently to
the receptor, therefore can be “washed out”. An irreversible antagonist
binds covalently to the receptor and cannot be displaced by either
competing ligands or washing.
The maximum amount of drug or radioligand, usually expressed as
picomoles (pM) per mg protein, which can bind specifically to the
Bmax
receptors in a membrane preparation. Can be used to measure the
density of the receptor site in a particular preparation.
Used to determine the Ki value from an IC50 value measured in a
competition radioligand binding assay:
Cheng-Prusoff Equation
Where [L] is the concentration of free radioligand, and Kd is the
dissociation constant of the radioligand for the receptor.
Competitive Antagonist See Antagonist

7. A reduction in response to an agonist while it is continuously present at
Desensitization the receptor, or progressive decrease in response upon repeated
exposure to an agonist.
The molar concentration of an agonist that produces 50% of the
EC50
maximum possible response for that agonist.
In vitro or in vivo dose of drug that produces 50% of its maximum
ED50
response or effect.
Describes the way that agonists vary in the response they produce when
they occupy the same number of receptors. High efficacy agonists
produce their maximal response while occupying a relatively low
Efficacy
proportion of the total receptor population. Lower efficacy agonists do
not activate receptors to the same degree and may not be able to
produce the maximal response (see Agonist, Partial).
Ex vivo Taking place outside a living organism.
Half-life (t½) is an important pharmacokinetic measurement. The
metabolic half-life of a drug in vivo is the time taken for its concentration
in plasma to decline to half its original level. Half-life refers to the
Half-life duration of action of a drug and depends upon how quickly the drug is
eliminated from the plasma. The clearance and distribution of a drug
from the plasma are therefore important parameters for the
determination of its half-life.
i.a. Intra-arterial route of drug administration (see Useful Abbreviations).
In a functional assay, the molar concentration of an agonist or antagonist
which produces 50% of its maximum possible inhibition. In a radioligand
IC50
binding assay, the molar concentration of competing ligand which
reduces the specific binding of a radioligand by 50%.
i.c. Intracerebral route of drug administration (see Useful Abbreviations).
Intracerebroventricular route of drug administration (see Useful
i.c.v.
Abbreviations).
In vitro or in vivo dose of a drug that causes 50% of the maximum
ID50
possible inhibition for that drug.

8. i.d. Intradermal route of drug administration (see Useful Abbreviations).
i.g. Intragastric route of administration (see Useful Abbreviations).
i.m. Intramuscular route of drug administration (see Useful Abbreviations).
Inverse Agonist See Agonist
Taking place in a test-tube, culture dish or elsewhere outside a living
In vitro
organism.
In vivo Taking place in a living organism.
i.p. Intraperitoneal route of drug administration (see Useful Abbreviations).
Irreversible Antagonist See Antagonist
i.t. Intrathecal route of drug administration (see Useful Abbreviations).
i.v. Intravenous route of drug administration (see Useful Abbreviations).
The equilibrium dissociation constant for a competitive antagonist: the
KB molar concentration that would occupy 50% of the receptors at
equilibrium.
The dissociation constant for a radiolabeled drug determined by
Kd saturation analysis. It is the molar concentration of radioligand which, at
equilibrium, occupies 50% of the receptors.
The inhibition constant for a ligand, which denotes the affinity of the
ligand for a receptor. Measured using a radioligand competition binding
Ki assay, it is the molar concentration of the competing ligand that would
occupy 50% of the receptors if no radioligand was present. It is calculated
from the IC50 value using the Cheng-Prusoff equation.
Negative Allosteric Modulator See Allosteric Modulator
Neutral Antagonist See Silent Antagonist
The proportion of radioligand that is not displaced by other competitive
Non-Specific Binding ligands specific for the receptor. It can be binding to other receptors or
proteins, partitioning into lipids or other things.

9. Measure of the potency of an antagonist. It is the negative logarithm of
pA2 the molar concentration of an antagonist that would produce a 2-fold
shift in the concentration response curve for an agonist.
pD2 The negative logarithm of the EC50 or IC50 value.
pEC50 The negative logarithm of the EC50 value.
pIC50 The negative logarithm of the IC50 value.
pKB The negative logarithm of the KB value.
pKd The negative logarithm of the Kd value.
pKi The negative logarithm of the Ki value.
p.o. Oral (by mouth) route of drug administration (see Useful Abbreviations).
Positive Allosteric Modulator See Allosteric Modulator
Potency A measure of the concentrations of a drug at which it is effective.
s.c. Subcutaneous route of drug administration (see Useful Abbreviations).
The proportion of radioligand that can be displaced by competitive
Specific Binding
ligands specific for the receptor.
A drug that attenuates the effects of agonists or inverse agonists,
producing a functional reduction in signal transduction. Effects only
Silent Antagonist
ligand-dependent receptor activation and displays no intrinsic activity
itself. Also known as a neutral antagonist.
In the periphery of the body (not in the central nervous system – see
Systemic
Useful Abbreviations).
t½ Biological half-life; (see Half-life).
Latin Abbreviations
Abbreviation Meaning Latin
ad.lib. freely as wanted ad libitum

10. aq. water Aqua
b.i.d. twice a day bis in die
cap. capsule capula
c with bar on top with Cum
div. divide divide
eq.pts. equal parts equalis partis
gtt. a drop Gutta
h. hour Hora
no. number numero
O. pint octarius
p.r.n. as occasion requires pro re nata
q.s. a sufficient quantity quantum sufficiat
q4h every 4 hours quaque 4 hora
q6h every 6 hours quaque 6 hora
q1d every day quaque 1 die
q1w every week
q.i.d. four times a day quater in die
s.i.d. once a day semel in die

11. Sig., S. write on the label Signa
stat. immediately statim
tab. a tablet tabella
t.i.d. three times a day ter in die
Weights and measures used in prescribing and toxicology
The Metric System
Weight
1 picogram (pg) 10-12 gram
1000 picograms 1 nanogram (ng) or 10-9 gram
1000 nanograms 1 microgram (ug) or 10-6 gram
1000 micrograms 1 milligram (mg) or 10-3 gram
1000 milligrams 1 gram (g)
1000 grams 1 kilogram (kg)
Volume
1000 milliliters (ml) 1 liter (L)
Be able to interconvert all of these values
Prefixes for volumes correspond to those for weight.
IMPORTANT: Know that 1 part per million (ppm) is a frequently used term in toxicology and drug
residue discussions. For example, the following are 1 ppm:
1 mg / kg, 1 mcg/g. An analogy is "Percent" that represents 1 part per hundred, i.e., 1 g/100 g = 1%
w/w. The expression "w/w" indicates that the amount of both substances is on a weight basis. It is

12. assumed that ppm is w/w unless otherwise specified.
The Apothecaries' System
Weight
20 grains (gr) 1 scruple ( )
3 scruples 1 dram( ) = 60 grains
8 drams 1 ounce ( ) = 480 grains
Volume
60 minims (m) 1 fluid dram ( )
8 fluid drams 1 fluid ounce ( )
16 fluid ounces 1 pint (O.)
Know eqivalents in bold faced typed
Conversion Equivalents
Approximate Exact
1 milligram 1/60 grain 1/65 grain
1 gram 15 grains 15.432 grains
1 kilogram 2.2 pounds* 2.2 pounds*
1 milliliter 15 minims 16.23 minims

13. 1 liter 1 quart 1.06 quarts or 33.8 fluid ounces
1 grain 60 milligrams 65 milligrams
1 dram 4 grams 3.88 grams
1 ounce 30 grams 31.1 grams
1 pound* 450 grams 454 grams
1 minim 0.06 milliliter 0.062 milliliter
1 fluid dram 4 milliliters 3.7 milliliters
1 fluid ounce 30 milliliters 29.57 milliliters
1 pint 500 milliliters 473 milliliters
1 quart 1000 milliters 946 milliliters
1 drop 1 minim
1 teaspoonful 5 milliliters
1 dessertspoonful 8 milliliters
1 tablespoonful 15 milliliters
Know equivalents in bold faced type.
Note: Where possible, use suitable units rather than decimal fractions, e.g., 10 mg not 0.010 g. When a
decimal fraction is used the decimal point must be preceded by a zero, e.g., 0.5 not .5.
* = avoirdupois pound (the one used in the USA!)
Conversion factors for obtaining approximate equivalents
To convert To Multiply by

14. gr/lb mg/lb 60
gr/lb mg/kg 143
mg/lb gr/lb 0.015
mg/lb mg/kg 2.2
mg/kg gr/lb 0.007
mg/kg mg/lb 0.45
Know conversions in bold typeface
Pharmaceutical Abbreviations | Abbreviations in product information leaflets and literature
Acronyms | G
Sources of Drugs
August 7, 2011 9:45 am
Many drugs were discovered long ago by trial and error. Some were good and are still used
today like the opium from the poppy tree, digitalis from the foxglove plant, etc. Discovery of
medicinal plants was largely by chance and when tribal people looked for food they
discovered various roots, leaves, and barks. The people ate, and, by trial and error, they
learned about healing effects of these plants. They also learned about toxic effects. Today,
there is a synthetic version of drugs to conserve their sources, for resource effectiveness,
better dosage and control. We would learn about these sources of drugs in this lesson.
Sources of Drugs
1. Primitive Medicine; Folklore, witchcraft, dreams, trances etc. Also from observing the
reaction of some animals to particular herbs. Through primitive medicine quinine was
discovered from Africa; used for malaria and limejuice for Ascorbic acid/Vitamin C and
this is used for scurvy and gum bleeding.
2. Plants; Roots, bark, sap, leaves, flowers, seeds were sources for drugs e.g. Reserpine
from Rauwolfia Vomitora, Digitalis from foxglove, opium from the poppy plant.
3. Animal sources; gave us hormones for replacement in times of deficiencies e.g. Insulin
from the pancreases of pigs and cattle, Liver extracts for anemia etc
4. Minerals; including acids, bases and salts like potassium chloride
5. Natural; OCCURRING SUBSTANCES like proteins

15. 6. Happy Chance; Discovery is by chance not by any premeditated effort.
7. Synthesis of Substances; from natural products in the laboratory.
Currently most drugs are synthetics produced in the laboratories with few from natural
extractions.
Drugs are obtained from six major sources:
1. Plant sources
2. Animal sources
3. Mineral/ Earth sources
4. Microbiological sources
5. Semi synthetic sources/ Synthetic sources
6. Recombinant DNA technology
1. Plant Sources:
Plant source is the oldest source of drugs. Most of the drugs in ancient times were derived from
plants. Almost all parts of the plants are used i.e. leaves, stem, bark, fruits and roots.
Leaves:
a. The leaves of Digitalis Purpurea are the source of Digitoxin and Digoxin, which are cardiac
glycosides.
b. Leaves of Eucalyptus give oil of Eucalyptus, which is important component of cough syrup.
c. Tobacco leaves give nicotine.
d. Atropa belladonna gives atropine.
Flowers:
1. Poppy papaver somniferum gives morphine (opoid)
2. Vinca rosea gives vincristine and vinblastine
3. Rose gives rose water used as tonic.
Photo of Papaver somniferum by Evelyn Simak

16. Fruits:
1. Senna pod gives anthracine, which is a purgative (used in constipation)
2. Calabar beans give physostigmine, which is cholinomimetic agent.
Seeds:
1. Seeds of Nux Vomica give strychnine, which is a CNS stimulant.
2. Castor oil seeds give castor oil.
3. Calabar beans give Physostigmine, which is a cholinomimetic drug.
Roots:
1. Ipecacuanha root gives Emetine, used to induce vomiting as in accidental poisoning. It also has
amoebicidal properties.
2. Rauwolfia serpentina gives reserpine, a hypotensive agent.
3. Reserpine was used for hypertension treatment.
Bark:
1. Cinchona bark gives quinine and quinidine, which are antimalarial drugs. Quinidine also has
antiarrythmic properties.
2. Atropa belladonna gives atropine, which is anticholinergic.
3. Hyoscyamus Niger gives Hyosine, which is also anticholinergic.
Stem:
Chondrodendron tomentosum gives tuboqurarine, which is skeletal muscle relaxant used in
general anesthesia.
2. Animal Sources:
1. Pancreas is a source of Insulin, used in treatment of Diabetes.
2. Urine of pregnant women gives human chorionic gonadotropin (hCG) used for the treatment of
infertility.
3. Sheep thyroid is a source of thyroxin, used in hypertension.
4. Cod liver is used as a source of vitamin A and D.
5. Anterior pituitary is a source of pituitary gonadotropins, used in treatment of infertility.
6. Blood of animals is used in preparation of vaccines.
7. Stomach tissue contains pepsin and trypsin, which are digestive juices used in treatment of
peptic diseases in the past. Nowadays better drugs have replaced them.
3. Mineral Sources:
i. Metallic and Non metallic sources:
1. Iron is used in treatment of iron deficiency anemia.

17. 2. Mercurial salts are used in Syphilis.
3. Zinc is used as zinc supplement. Zinc oxide paste is used in wounds and in eczema.
4. Iodine is antiseptic. Iodine supplements are also used.
5. Gold salts are used in the treatment of rheumatoid arthritis.
ii. Miscellaneous Sources:
1. Fluorine has antiseptic properties.
2. Borax has antiseptic properties as well.
3. Selenium as selenium sulphide is used in anti dandruff shampoos.
4. Petroleum is used in preparation of liquid paraffin.
4. Synthetic/ Semi synthetic Sources:
i. Synthetic Sources:
When the nucleus of the drug from natural source as well as its chemical structure is altered, we
call it synthetic.
Examples include Emetine Bismuth Iodide
ii. Semi Synthetic Source:
When the nucleus of drug obtained from natural source is retained but the chemical structure is
altered, we call it semi-synthetic.
Examples include Apomorphine, Diacetyl morphine, Ethinyl Estradiol, Homatropine, Ampicillin
and Methyl testosterone.
Most of the drugs used nowadays (such as antianxiety drugs, anti convulsants) are synthetic
forms.
5. Microbiological Sources:
1. Penicillium notatum is a fungus which gives penicillin.
2. Actinobacteria give Streptomycin.
3. Aminoglycosides such as gentamicin and tobramycin are obtained from streptomycis and
micromonosporas.
6. Recombinant DNA technology:
Recombinant DNA technology involves cleavage of DNA by enzyme restriction endonucleases.
The desired gene is coupled to rapidly replicating DNA (viral, bacterial or plasmid). The new
genetic combination is inserted into the bacterial cultures which allow production of vast amount
of genetic material.

18. Advantages:
1. Huge amounts of drugs can be produced.
2. Drug can be obtained in pure form.
3. It is less antigenic.
Disadvantages:
1. Well equipped lab is required.
2. Highly trained staff is required.
3. It is a complex and complicated technique.
Relevant Terms in Drug Intake, Absorption, Metabolism
and Elimination
Bioavailability; This is the proportion of administered drug, which reaches the
circulation. Drugs given IV have high bioavailability whilst those given orally have to
pass through the portal circulation so have lower bioavailability.
Absorption; For the oral route this denotes how drugs pass through the stomach walls,
intestines before entering the systemic circulation through the portal vein.The other
routes of IV, IM, Subcutaneous, Sublingual, Inhalation, Rectal etc. get absorbed cells
membranes and tissues.
First-Pass; Drugs absorbed from the G.I. tract pass through the portal vein before the
general circulation. They are metabolized and some get removed leaving only a
proportion. Removal of the drug as passes through the liver is known as the first-pass.
Drugs with high first-pass are inactive when swallowed e.g. glycerol dinitrate. They need
to be given by other routes like IM, Sublingual or IV.
Distribution; Movement of drugs from the blood to the tissues and cells
Elimination or Excretion; Movement of the drug and its metabolites out of the body
Metabolism; This is the process of breaking down the drugs by the liver and elimination
of the foreign and undesirable compounds from the body
Drug effects; this is the action of the drug which could be:
1. Efficacy; which is the drugs ability to produce a desired chemical change in the body
2. Tolerance refers to when the effects get lessened than desired due to abuse and the
dosage must be increased.
3. Adverse or side effects are undesired. They are unpleasant and/or harmful.
4. Local effect is when drug does not get into the blood stream. The action is at the site of
application.
5. Systemic is when effect is throughout the body because the drug is absorbed into the
bloodstream and distributed.
Classification

19. Medications can be classified in various ways,[3] such as by chemical properties, mode or route
of administration, biological system affected, or therapeutic effects. An elaborate and widely
used classification system is the Anatomical Therapeutic Chemical Classification System (ATC
system). The World Health Organization keeps a list of essential medicines.
A sampling of classes of medicine includes:
1. Antipyretics: reducing fever (pyrexia/pyresis)
2. Analgesics: reducing pain (painkillers)
3. Antimalarial drugs: treating malaria
4. Antibiotics: inhibiting germ growth
5. Antiseptics: prevention of germ growth near burns, cuts and wounds
Types of medications (type of pharmacotherapy)
For the gastrointestinal tract (digestive system)
Upper digestive tract: antacids, reflux suppressants, antiflatulents, antidopaminergics, proton
pump inhibitors (PPIs), H2-receptor antagonists, cytoprotectants, prostaglandin analogues
Lower digestive tract: laxatives, antispasmodics, antidiarrhoeals, bile acid sequestrants, opioid
For the cardiovascular system
General: β-receptor blockers ("beta blockers"), calcium channel blockers, diuretics, cardiac
glycosides, antiarrhythmics, nitrate, antianginals, vasoconstrictors, vasodilators, peripheral
activators
Affecting blood pressure (antihypertensive drugs): ACE inhibitors, angiotensin receptor blockers,
α blockers, calcium channel blockers
Coagulation: anticoagulants, heparin, antiplatelet drugs, fibrinolytics, anti-hemophilic factors,
haemostatic drugs
Atherosclerosis/cholesterol inhibitors: hypolipidaemic agents, statins.
For the central nervous system
See also: Psychiatric medication and Psychoactive drug
Drugs affecting the central nervous system include: hypnotics, anaesthetics, antipsychotics,
antidepressants (including tricyclic antidepressants, monoamine oxidase inhibitors, lithium salts,
and selective serotonin reuptake inhibitors (SSRIs)), antiemetics, anticonvulsants/antiepileptics,
anxiolytics, barbiturates, movement disorder (e.g., Parkinson's disease) drugs, stimulants
(including amphetamines), benzodiazepines, cyclopyrrolones, dopamine antagonists,
antihistamines, cholinergics, anticholinergics, emetics, cannabinoids, and 5-HT (serotonin)
antagonists.
For pain and consciousness (analgesic drugs)

20. See also: Analgesic
The main classes of painkillers are NSAIDs, opioids and various orphans such as paracetamol.
For musculo-skeletal disorders
The main categories of drugs for musculoskeletal disorders are: NSAIDs (including COX-2
selective inhibitors), muscle relaxants, neuromuscular drugs, and anticholinesterases.
For the eye
General: adrenergic neurone blocker, astringent, ocular lubricant
Diagnostic: topical anesthetics, sympathomimetics, parasympatholytics, mydriatics, cycloplegics
Anti-bacterial: antibiotics, topical antibiotics, sulfa drugs, aminoglycosides, fluoroquinolones
Antiviral drug
Anti-fungal: imidazoles, polyenes
Anti-inflammatory: NSAIDs, corticosteroids
Anti-allergy: mast cell inhibitors
Anti-glaucoma: adrenergic agonists, beta-blockers, carbonic anhydrase
inhibitors/hyperosmotics, cholinergics, miotics, parasympathomimetics, prostaglandin
agonists/prostaglandin inhibitors. nitroglycerin
For the ear, nose and oropharynx
sympathomimetics, antihistamines, anticholinergics, NSAIDs, steroids, antiseptics, local
anesthetics, antifungals, cerumenolyti
For the respiratory system
bronchodilators, NSAIDs, anti-allergics, antitussives, mucolytics, decongestants
corticosteroids, Beta2-adrenergic agonists, anticholinergics, steroids
For endocrine problems
androgens, antiandrogens, gonadotropin, corticosteroids, human growth hormone, insulin,
antidiabetics (sulfonylureas, biguanides/metformin, thiazolidinediones, insulin), thyroid
hormones, antithyroid drugs, calcitonin, diphosponate, vasopressin analogues
For the reproductive system or urinary system
antifungal, alkalising agents, quinolones, antibiotics, cholinergics, anticholinergics,
anticholinesterases, antispasmodics, 5-alpha reductase inhibitor, selective alpha-1 blockers,
sildenafils, fertility medications
For contraception

21. Hormonal contraception
Ormeloxifene
Spermicide
For obstetrics and gynecology
NSAIDs, anticholinergics, haemostatic drugs, antifibrinolytics, Hormone Replacement Therapy
(HRT), bone regulators, beta-receptor agonists, follicle stimulating hormone, luteinising
hormone, LHRH
gamolenic acid, gonadotropin release inhibitor, progestogen, dopamine agonists, oestrogen,
prostaglandins, gonadorelin, clomiphene, tamoxifen, Diethylstilbestrol
For the skin
emollients, anti-pruritics, antifungals, disinfectants, scabicides, pediculicides, tar products,
vitamin A derivatives, vitamin D analogues, keratolytics, abrasives, systemic antibiotics, topical
antibiotics, hormones, desloughing agents, exudate absorbents, fibrinolytics, proteolytics,
sunscreens, antiperspirants, corticosteroids
For infections and infestations
antibiotics, antifungals, antileprotics, antituberculous drugs, antimalarials, anthelmintics,
amoebicides, antivirals, antiprotozoals
For the immune system
vaccines, immunoglobulins, immunosuppressants, interferons, monoclonal antibodies
For allergic disorders
anti-allergics, antihistamines, NSAIDs
For nutrition
tonics, electrolytes and mineral preparations (including iron preparations and magnesium
preparations), Parental nutritional supplements, vitamins, anti-obesity drugs, anabolic drugs,
haematopoietic drugs, food product drugs
For neoplastic disorders
cytotoxic drugs, therapeutic antibodies, sex hormones, aromatase inhibitors, somatostatin
inhibitors, recombinant interleukins, G-CSF, erythropoietin
For diagnostics

22. contrast media
For euthanasia
See also: Barbiturate#Other non-therapeutical us
Drug action
From Wikipedia, the free encyclopedia
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This article does not cite any references or sources. Please help improve this article by adding
citations to reliable sources. Unsourced material may be challenged and removed. (August
2009)
The action of drugs on the human body is called pharmacodynamics, and what the body does
with the drug is called pharmacokinetics. The drugs that enter the human tend to stimulate
certain receptors, ion channels, act on enzymes or transporter proteins. As a result, they cause the
human body to react in a specific way.
There are two different types of drugs:
Agonists - they stimulate and activate the receptors
Antagonists - they stop the agonists from stimulating the receptors
Once the receptors are activated, they either trigger a particular response directly on the body, or
they trigger the release of hormones and/or other endogenous drugs in the body to stimulate a
particular response.
Contents
1 Short Note on Receptors
o 1.1 Ionic Bonds
o 1.2 Hydrogen bonds
2 How shape of Drug Molecules affect drug action
o 2.1 Potency
o 2.2 The specificity of drugs
o 2.3 Affinity
3 References
4 External links

23. Short Note on Receptors
The drugs interact at receptors by bonding at specific binding sites. Most receptors are made up
of proteins, the drugs can therefore interact with the amino acids to change the conformation of
the receptor proteins.
These interactions are very basic, just like that of other chemical bondings:
Ionic Bonds
Mainly occur through attractions between opposite charges. For example, between protonated
amino (on salbutamol) or quaternary ammonium (e.g. acetylcholine), and the dissociated
carboxylic acid group. Similarly, the dissociated carboxylic acid group on the drug can bind with
amino groups on the receptor.
This type of bonds are very strong, and varies with so it could act over large distances.
Cation-π interactions can also be classified as ionic bonding. This occurs when a cation, e.g.
acetylcholine, interacts with the negative π bonds on an aromatic group of the receptor.
Ion-dipole and dipole-dipole bonds have similar interactions, but are more complicated and are
weaker than ionic bonds.
Hydrogen bonds
Refer to the attraction between Hydrogen atoms and polar functional groups e.g. The Hydroxyl (-
OH) group. Only act over short distances, and are dependent on the correct alignment between
functional groups.
Of course, drugs not only just act on receptors. They also act on ion channels, enzymes and cell
transporter proteins.
Receptors are located on all cells in the body. The same receptor can be located on different
organ, and even on different types of tissues. There are also different subtypes of receptor which
ellicit different effects in response to the same agonist, e.g.
There are two types of Histamine receptor; H1 and H2, activation of H1 subtype causes
contraction of smooth muscle whereas activation of the H2 receptors stimulates gastric secretion.
It is this phenomenon that gives rise to drug specificity.
How shape of Drug Molecules affect drug action

24. When talking about the shape of molecules, the scientists are mainly concerned with the 3D
conformation of drug molecules. There are many isomers of a particular drug, and each one will
have their own effects. This effect is not only what the drug activates, but also changes the
potency of each drug.
Potency
Potency is a measure of how much a drug is required in order to produce a particular effect.
Therefore, only a small dosage of a high potency drug is required to induce a large response. The
other terms used to measure the ability of a drug to trigger a response are:
Intrinsic Activity which defines:
o Agonists as having Intrinsic Activity = 1
o Antagonists as having Intrinsic Activity = 0
o and, Partial Agonist as having Intrinsic Activity between 0 and 1
Intrinsic Efficacy also measures the different activated state of receptors, and the ability for a
drug to cause maximum response without having to bind to all the receptors.
The specificity of drugs
Drug companies invest significant effort in designing drugs that interact specifically with
particular receptors[citation needed], since non-specific drugs can cause more side effects.
An example is the endogenous drug acetylcholine (ACh). ACh is used by the parasympathetic
nervous system to activate muscarinic receptors and by the neuromuscular system to activate
nicotinic receptors. However, the compounds muscarine and nicotine can each preferentially
interact one of the two receptor types, allowing them to activate only one of the two systems
where ACh itself would activate both.
Affinity
The specificity of drugs cannot be talked about without mentioning the affinity of the drugs. The
affinity is a measure of how tightly a drug binds to the receptor. If the drug does not bind well,
then the action of the drug will be shorter and the chance of binding will also be less. This can be
measured numerically by using the dissociation constant KD. The value of KD is the same as the
concentration of drug when 50% of receptors are occupied.
The equation can be expressed as KD =
But the value of KD is also affected by the conformation, bonding and size of the drug and the
receptor. The higher the KD the lower the affinity of the drug.
References

25. External links
BASIC PHARMACOLOGY
How Do Drugs Work?
What Are Receptors?
Basic Pharmacokinetics
Correlating Blood Levels with Effects of Impairment
How Do Drugs Work?
Did you ever wonder how aspirin knows to go to your head when you have a headache and to
your elbow when you have "Tennis Elbow"? Or how one or two small aspirins containing only
325-650 mg of active drug can relieve a headache or ease the inflammation of a strained muscle
or tendon in a 195 lb. athlete?
The answer to the first question is that drugs are distributed throughout the body by the blood
and other fluids of distribution (see distribution below). Once they arrive at the proper site of
action, they act by binding to receptors, usually located on the outer membrane of cells, or on
enzymes located within the cell.
What Are Receptors?
Receptors are like biological "light switches" which turn on and off when stimulated by a drug
which binds to the receptor and activates it. For example, narcotic pain relievers like morphine
bind to receptors in the brain that sense pain and decrease the intensity of that perception. Non-
narcotic pain relievers like aspirin, Motrin (ibuprofen) or Tylenol (acetaminophen) bind to an
enzyme located in cells outside of the brain close to where the pain is localized (e.g., hand, foot,
low back, but not in the brain) and decrease the formation of biologically-active substances

26. known as prostaglandins, which cause pain and inflammation. These "peripherally-acting" (act
outside of the central nervous system (CNS)) analgesics may also decrease the sensitivity of the
local pain nerves causing fewer pain impulses to be sensed and transmitted to the brain for
appreciation.
In some instances, a drug's site of action or "receptor" may actually be something which resides
within the body, but is not anatomically a part of the body. For example, when you take an
antacid like Tums or Rolaids, the site of action is the acid in the stomach which is chemically
neutralized. However, if you take an over-the-counter (OTC) medication which inhibits stomach
acid production instead of just neutralizing it (e.g., Tagamet (cimetidine) or Pepsid-AC
(famotidine)), these compounds bind to and inhibit recptors in the stomach wall responsible for
producing acid.
Another example of drugs which bind to a receptor that is not part of your body are antibiotics.
Antibiotics bind to portions of a bacterium that is living in your body and making you sick. Most
antibiotics inhibit an enzyme inside the bacteria which causes the bacteria to either stop
reproducing or to die from inhibition of a vital biochemical process.
In many instances, the enzyme in the bacteria does not exist in humans, or the human form of the
enzyme does not bind the inhibiting drug to the same extent that the bacterial enzyme does, thus
providing what pharmacologists call a "Selective Toxicity". Selective toxicity means that the
drug is far more toxic to the sensitive bacteria than it is to humans thus providing sick patients
with a benefit that far outweighs any risks of direct toxicity. Of course, this does not mean that
certain patients won't be allergic to certain drugs.
Penicillin is a good example to discuss. Although penicillin inhibits an enzyme found in sensitive
bacteria which helps to "build" part of the cell wall around the outside of the bacteria, and this
enzymatic process does not occur in human cells, some patients develop an allergy to penicillin
(and related cepahlosporin) antibiotics. This allergy is different from a direct toxicity and
demonstrates that certain people's immune system become "sensitized" to some foreign drug
molecules (xenobiotics) which are not generally found in the body.
As medical science has learned more about how drugs act, pharmacologists have discovered that
the body is full of different types of receptors which respond to many different types of drugs.
Some receptors are very selective and specific, while others lack such specificity and respond to
several different types of drug molecules.
To date, receptors have been identified for the following common drugs, or neurotransmitters*
found in the body: narcotics (morphine), benzodiazepines (Valium, Xanax), acetylcholine*
(nicotinic and muscarinic cholinergic receptors), dopamine*, serotonin* (5-hydroxytryptamine;
5-HT), epinephrine (adrenalin) and norepinephrine* (a and b adrenergic receptors), and many
others.
Neurotransmitters* are chemicals released from the end of one neuron (nerve cell) which diffuse
across the space between neurons called the synaptic cleft and stimulate an adjacent neuron to
signal the transmission of information.

27. The rest of this section is designed to explain the complicated journey of a drug through the
body, which pharmacologists call pharmacokinetics.
Basic Pharmacokinetics
Pharmacokinetics is the branch of pharmacology which deals with determining the movement
(kinetics) of drugs into and out of the body. Experimentally, this is done by administering the
drug to a group of volunteer subjects or patients and obtaining blood and urine specimens for
subsequent quantitative (how much) analysis. When the results of these analyses are plotted on
graph paper with blood levels or urinary excretion on the verticle axis and time on the horizontal
axis, a blood level-time or urinary excretion pattern is obtained.
These graphs can be used to calculate the rates of appearance and elimination of the drug in the
bloodstream, the rates of formation of the compounds into which the drugs are transformed in the
liver (metabolized), and finally the rates of elimination or excretion of the metabolites.
There are four scientific or pharmacokinetic processes to which every drug is subject in the
body:
1. ABSORPTION
2. DISTRIBUTION
3. METABOLISM
4. EXCRETION
These four processes occur contemporaneously until (1) all of the drug is absorbed from the GI
tract, the muscle or subcutaneous tissue site into which it was injected, and there is no more
absorption phase, and (2) all of the drug has been metabolized, and there is no more "parent"
drug and it is no longer detectable in the blood.
Figure 1 depicts the four contemporaneous pharmacokinetic processes. Figure 2 depicts the
blood level-time profile of a single oral and intravenous (IV) dose of a drug. Figure 3, shows the
accumulation pattern of a drug given orally once per half-life for six half-lives, at which time
steady-state or equilibrium (the amount of drug entering the body equals the amount being
excreted) is achieved.
Absorption

28. Absorption is the process by which a drug is made available to the fluids of distribution of the
body (e.g., blood, plasma, serum, aqueous humor, lymph, etc.).
In the fasting state, most orally-administered drugs reach a maximum or "peak" blood
concentration within 1-2 hours. Intravenous (IV) administration is the most rapid route of
administration, with intra-nasal, smoking (inhalation), sublingual (under the tongue), intra-
muscular (IM), subcutaneous (e.g., under the skin, SC or SQ), and percutaneous (through the
skin) being the next most rapid.
The RATE of absorption of orally-administered drugs and the subsequent appearance of the
drug in the blood is dependent on the following factors:
1. The rates of disintegration and dissolution of the pill or capsule in the stomach or
gastrointestinal (GI) tract,
2. The solubility of the drug in stomach or intestinal fluids (the more soluble, the faster),
3. The molecular charge on the drug molecule (charged substances are soluble, but don't pass
through lipid (fat) soluble biologic membranes well),
4. Aqueous (water) solubility vs. lipid (fat) solubility. Water-soluble drugs are soluble but don't pass
through lipid-soluble biologic membranes well,
5. The presence or absence of food in the stomach (food delays the absorption of some drugs and
enhances the absorption of others),
6. The presence of any concomitant medication(s) that can interfere with gastrointestinal (GI)
motility, e.g., Reglan increases GI motility, Aluminum antacids slow, drugs like atropine or
scopolamine used for ulcers or "queasy stomachs" slow GI motility keeping some drugs in the
stomach slowing absorption, while drugs like Tagamet, Zantac and Prilosec (Pepcid-AC) decrease
gastric acid production increasing the rate of gastric emptying and increasing the rate of
absorption of some drugs.
Distribution
Once a drug has been absorbed from the stomach and/or intestines (GI Tract) into the blood, it
is circulated to some degree to all areas of the body to which there is blood flow. This is the
process of distribution. Organs with high blood flow e.g., brain, heart, liver, etc. are the first to
accumulate drugs, while connective tissue and lesser perfused organs are the last.
Many drugs are bound to plasma proteins such as albumin. Since only drugs which are not bound
are free to exert a pharmacologic effect, the ratio of "free" to "bound" drug is important in
determining the onset and duration of action of drugs. Highly bound drugs are distributed less
extensively throughout the body and are slower to act. By virtue of their high binding to plasma
proteins, they also stay in the body for longer periods of time because the binding sites act as a
sort of "reservoir" for the drug, releasing drug molecules slowly.

29. Metabolism
Drugs in the blood and tissues must be inactivated and excreted from the body. This process is
initiated by altering the chemical structure of the drug in such a way as to promote its excretion.
The transformation of the drug molecule into a chemically related substance that is more easily
excreted from the body is called metabolism, biotransformation or detoxification.
In the case of ethanol, the alcohol molecule is metabolized in the liver by the enzyme alcohol
dehydrogenase, to acetaldehyde which causes dilatation of the blood vessels and, after
accumulation, is responsible for the subsequent hangover which ensues. The acetaldehyde is
subsequently metabolized by the enzyme aldehyde dehydrogenase to acetate, a substance very
similar to acetic acid or vinegar.
Therapeutic agents like antibiotics and drugs used for the treatment of high blood pressure,
epilepsy (e.g., phenobarbital, Dilantin), pain (e.g., morphine, codeine), anxiety (e.g., Valium,
Xanax) are also metabolized to chemically-related compounds called metabolites, which are then
excreted in the urine.
REMEMBER: Urine drug screens usually determine metabolites in urine, not the original
"parent" drug which was ingested or taken. For example, if cocaine is snorted, smoked or
injected, a urine drug screen will most often detect the cocaine metabolite benzoylecgonine in
the urine, not cocaine itself. The same analogy applies to other drugs of abuse like: heroin,
morphine, amphetamines, PCP (Angel Dust), barbiturates, marijuana, etc.
Excretion
Excretion is the process by which a drug is eliminated from the body.
Drugs can be excreted by various organs including the kidney and lungs, and found in many
biological fluids like: bile, sweat, hair, breast milk, or tears. However, the most common fluid in
which to look for drugs is the urine.
In order to determine the rate of excretion of any drug from blood, one must first be certain that
all the drug in the subject's GI tract has been absorbed. If not, calculation of a rate of excretion
would be confounded be the ongoing absorption of more drug. Once all the drug has been
absorbed, this is called the post-absorbtive, or distributive stage. At this time, serial (multiple)

30. blood level determinations should show a decline with time. The slope of the log concentration-
time graph is called the half-life (T1/2) and is indicative of the drug's half-life, or rate of
excretion. The half-life represents the amount of time required to eliminate half of the drug from
the body.
Figure 4 shows a typical plot of the log of the drug's blood concentration on the verticle axis vs.
time on the horizontal axis. The log of the blood concentration is used to convert the curved
portions of the graph shown in Figure 2 to a straight line.
Generally, it takes six half-lives to rid the body of 98% of a drug and 10 half-lives to completely
eliminate the drug from the body. Using these mathematical relatonships allows pharmacologists
to determine how often a therapeutic drug should be administered to a patient or toxicologists to
determine a time interval within which one would test positive for drugs of abuse. Table I shows
the approximate time intervals individuals will test positive in blood and urine for common drugs
of abuse.
Correlating Drug or Ethanol Blood Levels and Positive Urine Tests
With Effects of Impairment
A statutory level for the presumption of DWI is just that, an arbitrary standard. Any BAC level,
whether 0.10% or 0.08%, speaks only to a legal standard, and not a scientific (physiological)
standard.
The same analogy applies for intoxicating drugs or drugs with an ability to impair an individual's
mental or physical capacity. In order for an individual to be presumed under the influence of an
intoxicating or mind-altering drug, it is necessary to establish that there was a significant or
pharmacologic concentration of the drug present in the individual's bloodstream, and that the
individual was not sufficiently tolerant to the effects of the drug such as to mitigate any
intoxicating effect(s). For example, an individual who had been taking a drug known to cause
sedating or intoxicating effects to which the subject could become tolerant, could not be
presumed to be too impaired to drive while taking the medication if the subject had been taking
the drug long enough to permit the development of tolerance to the sedating or intoxicating
properties of that drug.
Some examples would include benzodiazepines like Valium or Xanax, tricyclic antidepressant
drugs like Elavil or Tofranil, anti-epileptic drugs like barbiturates and Dilantin which induce
their own metabolism and are excreted more rapidly after they have been taken for several
weeks, or narcotics like codeine, which are well-known to produce tolerance. In situations like

31. these, it is important to obtain the testimony of other individuals such as co-worders or family
members who can corroborate the lack of observable impairment in the subject following drug
ingestion.
If an individual is accustomed to having 2-3 (or more) alcoholic drinks per day, with dinner or
while watching TV after work, it is quite likely that they will have developed some tolerance to
the intoxicating properties of alcohol and might not show signs of intoxication even at BACs
over 0.10%. On the other hand, an individual who drinks infrequently would have developed no
tolerance and might show signs of intoxication at BACs below the statutory level.
CONTACT INFORMATION
David M. Benjamin, Ph.D.
77 Florence Street
Suite 107
Chestnut Hill, MA 02467
Telephone: 617-969-1393
Fax: 617-969-4285
send e-mail to Dr. Benjamin
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