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The scope of pharmacy practice includes more traditional roles such as compounding and
dispensing medications, and it also includes more modern services related to health care,
including clinical services, reviewing medications for safety and efficacy, and providing drug
information. Pharmacists, therefore, are the experts on drug therapy and are the primary health
professionals who optimize medication use to provide patients with positive health outcomes.
The word pharmacy is derived from its root word pharma which was a term used since the 15th
17th centuries. n addition to pharma responsi!ilities, the pharma offered general medical advice
and a range of services that are now performed solely !y other specialist practitioners, such as
surgery and midwifery. The pharma "as it was referred to# often operated through a retail shop
which, in addition to ingredients for medicines, sold to!acco and patient medicines. The pharmas
also used many other her!s.
n its investigation of her!al and chemical ingredients, the wor$ of the pharma may !e regarded
as a precursor of the modern sciences of chemistry and pharmacology, prior to the formulation of
the scientific method.
%n esta!lishment in which pharmacy "in the first sense# is practiced is called a pharmacy,
chemists or drug store.
The etymological roots are& pharmakon "'ree$#, (drug)* and vigilare "+atin#, (to $eep awa$e or
alert, to $eep watch.*
Pharmacy is the health profession that lin$s the health sciences with the chemical sciences and it
is charged with ensuring the safe and effective use of pharmaceutical drugs. The word derives
from the 'ree$ word "pharmakon#, meaning ,drug, or ,medicine
Pharmacogenomics is the !ranch of pharmacology which deals with the influence of genetic
variation on drug response in patients !y correlating gene expression or single-nucleotide
polymorphisms with a drug.s efficacy or toxicity.
Pharmacogenomics is the whole genome application of pharmaco genetics, which examines the
single gene interactions with drugs.
Pharmacogenomics is !eing used all critical illnesses li$e cancer, cardio vascular disorders, /0,
tu!erculosis, asthma, and dia!etes.
Pharmacodynamics is the study of the physiological effects of drugs on the !ody or on
microorganisms or parasites within or on the !ody and the mechanisms of drug action and the
relationship !etween drug concentration and effect.
Pharmacovigilance "a!!reviated PV or PhV# is the pharmacological science relating to the
detection, assessment, understanding and prevention of adverse effects, particularly long term
and short term side effects of medicines with a view to&
identifying new information a!out hazards associated with medicines
preventing harm to patients.
Pharmacognosy is the study of medicines derived from natural sources.
The American Society of Pharmacognosy defines pharmacognosy as ,the study of the physical,
chemical, !iochemical and !iological properties of drugs, drug su!stances or potential drugs or
drug su!stances of natural origin as well as the search for new drugs from natural sources.
The terms pharmacogenomics and pharmacogenetics tend to !e used interchangea!ly.
Pharmacokinetics, sometimes a!!reviated as PK, "derived from %ncient 'ree$ pharmakon
,drug, and kinetikos ,to do with motion,)# is a !ranch of pharmacology dedicated to the
determination of the fate of su!stances administered externally to a living organism.
Pharmacokinetics is the study of the fate of a pharmaceutical product "drug# when administered
to a living organism. The word is derived from the term "pharmacon", meaning drug or the
science of preparing and dispensing medicines, and "kinetics", meaning motion.
The study of the action of a drug in living cells or organisms can include the rate of a!sorption,
which organs it migrates to, whether or not it is meta!olized or simply excreted2eliminated. This
is the main focus of Phase clinical trials, which use healthy volunteer test su!3ects to study the
pharmaco$inetics of a new drug. These studies also evaluate the conse4uences of ingestion,
in3ection, a!sorption or other modes of exposure to the drug, since some pharmaceuticals can
interfere with normal meta!olic processes, through various modes of action that include inducing
or inhi!iting !iochemical reactions, competing with enzymes for active sites, or !inding to 56%
to initiate or prevent transcription.
Pharmaco$inetics is often studied in con3unction with pharmacodynamics. Pharmaco$inetics
includes the study of the mechanisms of a!sorption and distri!ution of an administered drug, the
rate at which a drug action !egins and the duration of the effect, the chemical changes of the
su!stance in the !ody "e.g. !y enzymes# and the effects and routes of excretion of the meta!olites
of the drug.
Pharmacokinetics is the study of what the !ody does to a drug.
Pharmacodynamics is the study of what a drug does to the !ody.
%ll pharmaco$inetic process involves transport of the drug across !iological mem!ranes. 5rugs
are transported across the mem!ranes !y&
Passive diffusion and filtration.
7pecialized transport.
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The drug diffuses across the mem!rane in the direction of its concentration gradient, the
mem!rane playing no active role in the process. +ipid solu!le drugs acts through this process.
t is passage of drugs through a4ueous pores in the mem!rane or through paracellar spaces. +ipid
insolu!le drugs ta$es place through this action.
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This can !e carrier mediated or !y pinocytosis.
Carrier mediated: the drug com!ines with a carrier present in the mem!rane and the complex
then translocates from one face of the mem!rane to another. The carriers for polar molecules
appear to form a hydropho!ic coating over the hydrophilic groups and thus facilitate passage
through the mem!rane. This is of two types&
%ctive transport
9acilitated diffusion.
%ctive transport& movement occurs against the concentration gradient, needs energy and is
inhi!ited !y meta!olic poisons. t results in selective accumulation of the su!stance on one side
of the mem!rane. 8g& levodopa.
9acilitated diffusion& this proceeds more rapidly than simple diffusion and translocates even non
diffusi!le su!strates, !ut along their concentration gradient, therefore, does not need energy.
Pinocytosis: it is the process of transport across the cell in particulate form !y formation of
%!sorption is the movement of drug from its site of administration into the circulation. 8xcept
when given through 0 the drug has to cross !iological mem!ranes. 9actors affecting a!sorption
A"#eo#s sol#$ility: drugs given in solid form must dissolve in the a4ueous !iophase !efore they
are a!sor!ed. ;!viously a drug given as watery solution is a!sor!ed faster than from dilute
Concentration: passive transport depends on concentration gradient. 5rug given a concentrated
solution is a!sor!ed faster than the diluted solution.
Area o% a$sor$ing s#r%ace: larger it is faster the a!sorption.
Vasc#larity o% the a$sor$ing s#r%ace: !lood circulation removes the drug from the site of
a!sorption and maintains the concentration gradient across the mem!rane. ncreased !lood flow
hastens drug a!sorption.
Ro#te o% administration: this affects drug a!sorption, !ecause each route has its own
;=%+& the effective !arrier to orally administered drugs is the epithelial lining of the
gastrointestinal tract, which is lipoidal. %cidic drugs eg& salicylates are predominantly unionized
in the acid gastric 3uice and are a!sor!ed from stomach, while !asic drugs eg& morphine are
largely ionized and are a!sor!ed only on reaching the duodenum. /owever even for acidic drugs
a!sorption from stomach is slower, !ecause the mucosa is thic$ covered with mucus and the
surface area is small. Thus faster gastric emptying accelerates drug a!sorption in general.
7:@>:T%68;:7 %65 6T=%A:7>:+%=& @y these routes the drug is deposited directly in
the vicinity to the capillaries. +ipid solu!le drugs pass readily across the whole surface of the
capillary endothelium. >apillary highly porous do not o!struct a!sorption of even large lipid
insolu!le molecules or ions. 0ery large molecules are a!sor!ed through lymphatics. Thus many
drugs not a!sor!ed orally are a!sor!ed parenterally.
T;P>%+ 7T87& "7B6, >;=68% A:>;:7 A8A@=%687#&
7ystemic a!sorption after topical application depends primarily on lipid solu!ility of the drugs.
/owever only few drugs significantly penetrate intact s$in.
8g& corticosteroids applied over extensive areas can produce systemic effects and pituitary
adrenal suppression. >ornea is permea!le to lipid solu!le, unionized !ut not to highly ionized
Aucous mem!ranes of mouth, rectum, and vagina a!sor! lipophilic drugs.
Pharmaco$inetics is divided into several areas including the extent and rate of a!sorption,
distri!ution, meta!olism and excretion. This is commonly referred to as the %5A8 scheme.
/owever recent understanding a!out the drug-!ody interactions !rought a!out the inclusion of
new term Liberation. 6ow Pharmaco$inetics can !e !etter descri!ed as )A&'(.
+i!eration - the process of release of drug from the formulation.
%!sorption - the process of a su!stance entering the !lood circulation.
5istri!ution - the dispersion or dissemination of su!stances throughout the fluids and
tissues of the !ody.
Aeta!olism - the irreversi!le transformation of parent compounds into daughter
8xcretion - the elimination of the su!stances from the !ody. n rare cases, some drugs
irreversi!ly accumulate in !ody tissue.
Pharmaco$inetics descri!es how the !ody affects a specific drug after administration.
Pharmaco$inetic properties of drugs may !e affected !y elements such as the site of
administration and the dose of administered drug. These may affect the a!sorption rate.
The following are the most commonly measured pharmaco$inetic parameters&
Varia$le &escription
A$$reviation+s, -orm#la
loading dose "+5#, or steady
state 2maintenance dose
1DDD mg
0olume of
The apparent volume in
which a drug is distri!uted
immediately after it has !een
in3ected intravenously and
e4uili!rated !etween plasma
and the surrounding tissues.
15 +
initial or steady-state
concentration of drug in
?D.D mg2+
The time re4uired for the
concentration of the drug to
reach half of its original
1? hr
rate constant
The rate at which drugs are
removed from the !ody.
D.D5 2hr
rate of infusion re4uired to
!alance elimination
5D mg2hr
%rea under the
The integral of the plasma
drug concentration ">p# after
it is administered.
The volume of plasma
cleared of the drug per unit
1.15 +2hr
The fraction of drug that is
The pea$ plasma
concentration of a drug after
oral administration.
?D.D mg2+
>min The lowest "trough#
concentration that a drug
reaches !efore the next dose
1.D mg2+ direct
is administered.
Pharmaco$inetic analysis is performed !y non compartmental "model independent# or
compartmental methods. 6oncompartmental methods estimate the exposure to a drug !y
estimating the area under the curve of a concentration-time graph. >ompartmental methods
estimate the concentration-time graph using $inetic models.
Pop#lation pharmacokinetics
Population pharmacokinetics is the study of the sources and correlates of varia!ility in drug
concentrations among individuals who are the target patient population receiving clinically
relevant doses of a drug of interest. >ertain patient demographic, pathophysiological, and
therapeutical features, such as !ody weight, excretory and meta!olic functions, and the presence
of other therapies, can regularly alter dose-concentration relationships. 9or example, steady-state
concentrations of drugs eliminated mostly !y the $idney are usually greater in patients suffering
from renal failure than they are in patients with normal renal function receiving the same drug
Population pharmaco$inetics see$s to identify the measura!le pathophysiologic factors that cause
changes in the dose-concentration relationship and the extent of these changes so that, if such
changes are associated with clinically significant shifts in the therapeutic index, dosage can !e
appropriately modified.
7oftware pac$ages used in population pharmaco$inetics modeling include 6;6A8A.
=outes of 5rug %dministration&
1. ntravenous
1. ;ral
<. @uccal
?. 7u!lingual
5. =ectal
C. ntramuscular
7. Transdermal
F. 7u!cutaneous
G. nhalational
1D. Topical
;f all of these routes most li$ely to !e as$ed a!out the transdermal, as it is fashiona!le.
;therwise, most other !asic pharmacology 4uestions tend to concern the pharmacology of
intravenous agents) that is what is discussed !elow.
9irst ;rder Binetics&
% constant fraction of the drug in the !ody is eliminated per unit time. The rate of elimination is
proportional to the amount of drug in the !ody. The ma3ority of drugs are eliminated in this way.

The Vol#me o% &istri$#tion +Vd, is the amount of drug in the !ody divided !y the concentration
in the !lood. 5rugs that are highly lipid solu!le, such as digoxin, have a very high volume of
distri!ution "5DD litres#. 5rugs which are lipid insolu!le, such as neuromuscular !loc$ers, remain
in the !lood, and have a low 0d.
The Clearance +Cl, of a drug is the volume of plasma from which the drug is completely
removed per unit time. The amount eliminated is proportional to the concentration of the drug in
the !lood.
The fraction of the drug in the !ody eliminated per unit time is determined !y the elimination
constant +kel,.
=ate of elimination H clearance x concentration in the !lood.
8limination half life "t121#& the time taken for plasma concentration to reduce by 50%. A%ter .
hal% lives/ elimination is 0.1 complete.
t can !e shown that the $el H the log of 1 divided !y the t121 H D.CG<2t121.
+i$ewise, >l H $el x 0d, so, >l H D.CG<0d2t121.
%nd t121 H D.CG< x 0d 2 cl
The rate of elimination is the clearance times and the concentration in the plasma
=oe H >l x >p
9raction of the total drug removed per unit time H >l20d.
f the volume of distri!ution is increased, then the $el will decrease, the t121 will increase, !ut the
clearance won.t change.
8xample& Iou have a 1Dml container of orange s4uash. Iou put this into a litre "GGDml# of water.
The 0d of the orange s4uash is 1DDDml. f, each minute, you empty 1Dml of the orange li4uid
into the 1Dml container, discard this, and replace it with 1Dml of water. The clearance is 1D ml per
minute. The elimination half life is& 7D minutes . The $el is >l20d H 1D21DDD H D.D1.
f the volume of the container is increased to 1DDDml, then the clearance remains the same, !ut
the 0d, and conse4uently the t121, increases "to 1?D minutes#.
Jhat is descri!ed a!ove is a single compartment model, what would occur if the !loodstream
was the only compartment in the !ody "or if the 0d H the !lood volume#. @ut the human !ody is
more complex than this& there are many compartments& muscle, fat, !rain tissue etc. n order to
descri!e this, we use multicompartment models.
Aulticompartment Aodels&
Jhy does a patient wa$e up after 5 minutes after an in3ection of thiopentone when we $now that
it ta$es several hours to eliminate this drug from the !odyK Jhat happens is that, initially the
drug is all in the !lood and this !lood goes to ,vessel rich, organs) principally the !rain. %fter a
few minutes the drug starts to venture off into other tissues "fat, muscle etc# it redistri$#tes, the
concentration in the !rain decreases and the patient wa$es upL The drug thus redistri!utes into
other compartments.
f you were to represent this phenomenon graphically, you would follow a picture of rapid fall in
!lood concentration, a plateau, and then a slower gradual fall. The first part is the rapid
redistri!ution phase, the alpha phase, the plateau is the e4uili!rium phase "where !lood
concentration H tissue concentration#, and the slower phase, the !eta phase, is the elimination
phase where !lood and tissue concentrations fall in tandem. This is a simple two compartment

%n couple of interesting pieces of information can !e derived from the log concentration versus
time graph. f you extrapolate !ac$ the elimination line to the y axis, then you get to a point
called the >PD - a theoretical point representing the concentration that would have existed at the
start if the dose had !een instantly distri!uted "dose20d#. 9rom this new straight line you can
figure out how long it ta$es for the concentration to drop !y 5DM& the elimination half life.
+i$ewise, a similar procedure can !e performed on the phase& the redistri!ution half life.
This is the fraction of the administered dose that reaches the systemic circulation. @ioavaila!ility
is 1DDM for intravenous in3ection. t varies for other routes depending on incomplete a!sorption,
first pass hepatic meta!olism etc. Thus one plots plasma concentration against time, and the
!ioavaila!ility is the area under the curve.
Nero ;rder 8limination
Jhen a patient had ethyl alcohol !efore midnight he will fail a !reath analyzer test at F am the
following morning. Jhat happens is that the meta!olic pathways responsi!le for alcohol
meta!olism are rapidly saturated and that clearance is determined !y how fast these pathways can
wor$. The meta!olic pathways wor$ to their limit. This is $nown as zero order $inetics& a
constant amount of drug is eliminated per unit time. This form of $inetics occurs with several
important drugs at high dosage concentrations& phenytoin, salicylates, theophylline, and
thiopentone "at very large doses#. @ecause high dose this is very slow to clear, we no longer use it
in infusion for status epileptic us
5osage regimens
The strategy for treating patients with drugs is to give sufficient amounts that the re4uired
therapeutic effect arises, !ut not a toxic dose.
The maintenance dose is e4ual to the rate of elimination at steady state " steady state, rate of
elimination H rate of administration#&
&osing rate 2 clearance * desired plasma concentration.
5rugs will accumulate within the !ody if the drug has not !een fully eliminated !efore the next
dose. 7teady state concentration is thus arrived at after four half lives.
The loading dose 2 the vol#me o% distri$#tion * the desired concentration +i.e. the
concentration at steady state,.
/epatic 5rug >learance
Aany drugs are extensively meta!olized !y the liver. The rate of elimination depends on 1# The
liver.s inherent a!ility to meta!olize the drug, 1# the amount of drug presented to the liver for
meta!olism. This is important !ecause drugs administered orally are delivered from the gut to the
portal vein to the liver& the liver go!!les up a varying chun$ of the administered drug "pre-
systemic elimination# and less is availa!le to the !ody for therapeutic effect. This is why you
have to give a higher dose of morphine, for example, orally, than intravenously.
/epatic drug clearance "i.e. the amount of each drug go!!led up !y the liver# depends on&
3, The ntrinsic clearance +Cl int,.
4, 5epatic $lood %lo6.
These two factors are independent of one another, and their com!ined effect is the proportion of
drug go!!led up& the extraction ratio.
9or drugs that have a low intrinsic clearance, this effect can !e increased !y giving a second
agent that !oosts the effect of the liver.s enzyme system) these are enzyme inducers. 8xamples of
such drugs are antiepileptic "car!amazepine O phenytoin#, rifampicin, alcohol and spironolactone
Palso !ar!ituratesQ. 8nzyme inhi!itors have the opposite effect& examples are flagyl, allopurinol,
cimetidine, and erythromycin.
+i$ewise, if the !lood flow increases, the liver has less chance to go!!le up the drug, and the
extraction ratio falls. This is particularly the case, as you would expect, of the intrinsic clearance
is low.
5rug distri!ution
;nce a drug has gained access to the !lood stream, it gets distri!uted to other tissues that initially
had no drug, concentration gradient !eing in the direction of plasma to tissues.
%pparent volume of distri!ution "0#)
0H dose administered i.v
Plasma concentration.
Redistri$#tion& highly lipid solu!le drugs given iv or !y inhalation initially get distri!uted to
organs with high !lood flow eg. @rain, heart, $idney etc. later, less vascular !ut more !ul$y
tissues "muscle, fat# ta$e up the drug- plasma concentration falls and the drug is withdrawn from
these sites.
Penetration into $rain and CS-: the capillary endothelial cells in !rain have tight 3unctions and
lac$ large intercellular pores. 9urther an investment of neural tissue covers the capillaries.
Together they constitute so called !lood !rain !arrier. % similar !lood >79 !arrier is located in
the choroid plexus. @oth these !arriers are lipoidal and limit the entry of entry of non lipid
solu!le drugs. 8g& streptomycin, neostigmine. ;nly lipid solu!le drugs are therefore are a!le to
penetrate and have action on the central nervous system.
Passage across placenta: placental mem!ranes are lipoidal and allow free passage of lipophilic
drugs, while restricting hydrophilic drugs. The placental efflux P-glycoprotein also serves to limit
fetal exposure to maternally administered drugs.
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5rugs may also accumulate in specific organs or get !ound to specific tissue constituents.
organ &r#g
7$eletal muscle, heart 5igoxin,emetine "to muscle proteins#
liver >hloro4uine, digoxin.
$idney >hloro4uine, digoxin.
thyroid odine
!rain soniazid, chlorpromazine.
retina >hloro4uine
iris %tropine, ephedrine.
@one and teeth Tetracyclines, heavy metals.
%dipose tissue Thiopentone, ether.
Jhen a drug is introduced into the !ody, where it ends up depends on a num!er of factors&
1# !lood flow, tissues with the highest !lood flow receive the drug first,
1# protein !inding, drugs stuc$ to plasma proteins are crippled, they can only go where the
proteins go
<# lipid solu!ility and the degree of ionization, this descri!es the a!ility of drugs to enter tissues
"highly lipid solu!le 2 unionized drugs can !asically go anywhere#.
Protein Binding
Aost drugs !ind to proteins, either al!umin or alpha-1 acid glycoprotein "%%'#, to a greater or
lesser extent. 5rugs prefer to !e free, it is in this state that they can travel throughout the !ody, in
and out of tissues and have their !iological effect. The downside of this is that they are easy prey
for meta!olizing enzymes.
The amount of al!umin does not appear to !e hugely relevant. n disease states such as sepsis, the
serum al!umin drops drastically, !ut the free drug concentration does not appear to increase.
&egree o% ioni7ation
This is really important with regard to local anesthetics. The essential fact to $now is that highly
ionized drugs cannot cross lipid mem!ranes "!asically they can.t go anywhere# and unionized
drugs can cross freely. Aorphine is highly ionized, fentanyl is the opposite. >onse4uently the
latter has a faster onset of action. The degree of ionization depends on the pBa of the drug and
the p/ of the local environment. The pBa is the p/ at which the drug is 5DM ionized. Aost drugs
are either wea$ acids or wea$ !ases. %cids are most highly ionized at a high p/ "i.e. in an
al$aline environment#. @ases are most highly ionized in an acidic environment "low p/#. 9or a
wea$ acid, the more acidic the environment, the less ionized the drug, and the more easily it
crosses lipid mem!ranes. f you ta$e this acid, at pBa it is 5DM ionized, if you add 1 p/ points to
this "more al$aline#, it !ecomes GDM ionized, if you reduce the p/ "more acidic# !y two units, it
!ecomes 1DM ionized. Jea$ !ases have the opposite effect.
+ocal anesthetics are wea$ !ases& the closer the pBa of the local anesthetic to the local tissue p/,
the more unionized the drug is. That is why lignocaine "pBa 7.7# has a faster onset of action than
!upivicaine "pBa F.<#. f the local tissues are al$alinized "e.g. !y adding !icar!onate to the local
anesthetic#, then the tissue p/ is !rought closer to the pBa, and the onset of action is hastened.
The primary site for drug meta!olism is liver) others are $idney, intestine, lungs and plasma. @io
transformation of drugs may lead to the following&
nactivation: most drugs and their active meta!olites are rendered inactive or less active. 8g&
Active meta$olite %rom an active dr#g: many drugs have !een found to !e partially converted
to one or more active meta!olite. The effects o!served are the sum total of that due to the parent
drug and its active meta!olites.
Activation o% inactive dr#g: few drugs are inactive as such and need conversion in the !ody to
one or more active meta!olites. 7uch a drug is called a pro dr#g.
Bio trans%ormation reactions can $e classi%ied into:
6on synthetic 2phase reactions- meta!olite may !e active or inactive.
7ynthetic2con3ugation2phase reactions-meta!olite is mostly inactive.
6on synthetic reactions&
O*idation: this reaction involves addition of oxygen 2 negatively charged radical or removal of
hydrogen2positively charged radical. ;xidations are the most important drug meta!olizing
8x&paracetamol, phenothiazines.
Red#ction: this reaction is the converse of oxidation and involves cytochrome P-?5D enzymes
wor$ing in the opposite direction. 8x& halothane.
5ydrolysis: this is cleavage of drug molecule !y ta$ing up a molecule of water. t occurs in liver,
intestines, plasma and other tissues.
Cycli7ation: this is formation of ring structure from a straight chain compound. 8g& proguanil.
&ecycli7ation: this is opening up of ring structure of the cyclic drug molecule ex& !ar!iturates.
7I6T/8T> =8%>T;67&
These involve the con3ugation of the drug or its phase meta!olite with an endogenous su!strate,
generally derived from car!ohydrate or amino acid, to form a polar highly ionized organic acid
which is easily excreted in the urine or !ile.
8l#c#ronide con9#gation& compounds with a hydroxyl or car!oxylic group are easily
con3ugated with a glucuronic acid which is derived from glucose. 8x& Aorphine.
Acetylation& compounds having amino or hydrazine residues are con3ugated with the help of
acetyl coenzyme. 8x& sulphonamides.
'ethylation& the amines and phenols can !e methylated 8x& adrenaline
S#lphate con9#gation& the phenolic compounds and steroids are suphated !y the supho$inases.
8x& chloramphenicol.
8lycine con9#gation& salicylates and other drugs having car!oxylic acid group are con3ugated
with glycine, !ut this is not a ma3or pathway of meta!olism.
Ri$o n#cleoside or n#cleotide synthesis& it is important for the activation of many purine and
pyrimidine antimeta!olites used in cancer chemotherapy.
8xcretion is the passage out of systematically a!sor!ed drug. 5rugs and their meta!olites are
excreted in
8xhaled air
;rine: it is the most important channel of excretion of most drugs.
Renal e*cretion: the $idney is responsi!le for all water solu!le su!stances. The amount of drug
or its meta!olites ultimately present in urine is the sum total of glomerular filtration, tu!ular re
a!sorption and tu!ular secretion.
8lomer#lar %iltration& 'lomerular capillaries have pores larger than usual) all protein !ound
drug "whether lipid solu!le or insolu!le# presented to the glomerulus is filtered. Thus it depends
on the plasma protein !inding and renal !lood flow.
T#$#lar re a$sorption: this depends upon the lipid solu!ility and the ionization of the drug at
the existing urinary P/. +ipid solu!le drugs filtered at the glomerulus diffuse !ac$ in the tu!ules
!ecause GGM of glomerular filtrate is re a!sor!ed, !ut lipid insolu!le and highly ionized drugs are
una!le to do so. Thus rate of excretion of drug such as amino glycoside anti!iotics parallels
T#$#lar secretion: this is the active transfer of organic acids and !ases !y two separate non
specific mechanisms which operate in the proximal tu!ules.
;rganic acid transport& penicillin, salicylates.
;rganic !ase transport& thiazides, cimetidine.
@oth transport process are !i directional i.e they can transport their su!strates from !lood to
tu!ular fluid and vice versa.
-aeces: apart from una!sor!ed fraction, most of the drug present in faeces is derived from !ile.
+iver actively transports into !ile organic acids "especially glucoranides#, organic !ases and
steroids !y separate non specific active transport mechanisms. =elatively larger molecules are
eliminated in the !ile most of the drug including that released !y decon3ugation of glucoranides
!y !acteria in the intestine is rea!sor!ed.
8x& erythromycin, ampicillin.
>ertain drugs excreted directly in the colon. 8g& purgatives.
(*haled air: gases and volatile li4uids are eliminated !y lungs, irrespective of their lipid
solu!ility. %lveolar transfer of the gas2vapour depends on its partial pressure in the !lood.
Saliva and s6eat: these are of minor importance for drug excretion. +ithium, heavy metals and
rifampicin are excreted through these secretions.
'ilk: the excretion of drug is not important for the mother, !ut the suc$ling infant inadvertently
receives the drug. Aost drugs enter !reast mil$ !y passive diffusion. +ipid solu!le and less
protein !ound drugs cross !etter.
8x& morphine, monteleu$ast, theophylline.
t is sometimes advantageous to modify a drug in such a way that it acts for a longer period. @y
doing so,
9re4uency of administration is reduced.
mproved patient compliance.
+arge fluctuations in plasma concentration.
5rug effect could !e maintained overnight without distur!ing sleep.
@y prolonging a!sorption from site of administration&
;ral& !y administering sustained release ta!lets.
Parenteral& su!cutaneous and intramuscular in3ections in insolu!le form "ex& lente insulin# or as
oily solution "depot progestin# and inclusion of vasoconstrictor with the drug "adrenaline with
local anesthetics#.
Transdermal& the drugs impregnated in adhesive patches, strips or as ointment applied on the s$in
ex& nitroglycerine.
@y retarding rate of meta!olism& small chemical modification mar$edly affects the rate of
meta!olism without affecting the !iological action. 8x & addition of ethinyl group to estradiol
ma$es it longer acting and suita!le for use as oral contraceptive.
@y retarding renal excretion& the tu!ular secretion of drug !eing an active process can !e
suppressed !y a competing su!stance ex& pro!enecid prolongs the action of penicillin and
8R%AP+8 9;= %A+;5P68&
%mlodipine is a dihydropyridine calcium antagonist drug with distinctive pharmaco$inetic
characteristics which appear to !e attri!uta!le to a high degree of ionisation. 9ollowing oral
administration, !ioavaila!ility is CD to C5M and plasma concentrations rise gradually to pea$ C to
Fh after administration. %mlodipine is extensively meta!olised in the liver "!ut there is no
significant presystemic or first-pass meta!olism# and is slowly cleared with a terminal
elimination half-life of ?D to 5Dh. 0olume of distri!ution is large "11 +2$g# and there is a high
degree of protein !inding "GFM#. There is some evidence that age, severe hepatic impairment and
severe renal impairment influence the pharmaco$inetic profile leading to higher plasma
concentrations and longer half-lives. There is no evidence of pharmaco$inetic drug interactions.
%mlodipine shows linear dose-related pharmaco$inetic characteristics and, at steady-state, there
are relatively small fluctuations in plasma concentrations across a dosage interval. Thus, although
structurally related to other dihydropyridine derivatives, amlodipine displays significantly
different pharmaco$inetic characteristics and is suita!le for administration in a single daily dose.
=;+8 ;9 6:=78&
1.right drug
<.right dose
?.right time
5. =ight route
5 %dditional =ights
1. right assessment
1. right documentation
<. clientSs right to education
?. right evaluation
5. clientSs right to refuse
A. Right Client
!#rse m#st do:
verify client chec$ 5 !racelet O room num!er
have client state his name
distinguish !etween 1 clientSs with same last names
B. Right &r#g
>omponents of a drug order& O time the order is written
1.drug name "genericpreferred#
<.drug dosage
?.fre4uency O duration of administration
5.any special instructions for withholding or ad3usting dosage.
C.physician or other health care providerSs signature or name.
7.signature of licensed practitioner.
!#rse m#st do:
T chec$ medication order is complete O legi!le.
T $now general purpose or action, dosage O route of drug
T compare drug card with drug la!el three times.
1. at time of contact with drug !ottle2 container
1. !efore pouring drug
<. after pouring drug
? >ategories of 5rug ;rders&
7tanding ;rder 2 =outine ;rder
ongoing order
may have special instructions to !ase administration
include P=6 orders
ex. digoxin D.1 mg P; 4.d., maintain !lood level at D.5 1.D ng2ml
1.;ne-time "single# order
given only once, at a specific time
ex. >efixime 1mg A at 7 %A on 11-1-D5
<. P=6 order
given at clientSs re4uest O nurseSs 3udgement for need O safety
ex Aefenamic %cid 5DDmg 4 ?h P=6 for pain
?. 7T%T order
given once, immediately
ex. Aorphine 1mg 0 7T%T

C. Right &ose
!#rse m#st do:
>alculate and chec$ drug dose accurately.
>hec$ P5=, drug pac$age insert or drug hand!oo$ for recommended range of
specific drugs.
&. Right Time
!#rse m#st do:
%dminister drugs at specified times.
%dminister drugs that are affected !y foods, !efore meals.
%dminister drugs that can irritate stomach, with food.
5rug administration may !e ad3usted to fit schedule of clientSs lifestyle, O
activities. O diagnostic procedures.
>hec$ expiration date.
%nti!iotics should !e administered at even intervals.
(. Right Ro#te
!#rse m#st do&
assess a!ility to swallow !efore giving oral meds.
5o not crush or mix meds in other su!stances !efore consultation with
physician or pharmacist
:se aseptic techni4ue when administering drugs.
%dminister drug at appropriate sites.
7tay with client until oral drugs have !een swallowed.
-. Right Assessment
'et !aseline data !efore administration.
%ssess the colour of the urine, sweat etc.
>hec$ !lood urea , creatinine level for nephrotoxic drugs.
nvestigate for liver function if the drug is acting through liver.
>hec$ for any adverse reactions.
8. Right &oc#mentation
mmediately record appropriate information
T 6ame, dose, route,time O date, nurseSs initial or signature
>lientSs response&
T narcotics
T analgesics
T antiemetics
T sedatives
unexpected reactions to medications.
:se correct a!!reviations O sym!ols.
5. Right to (d#cation
>lient teaching &
T therapeuticpurpose
T side-effects
T diet restrictions or re4uirements
T s$ill of administration
T la!oratory monitoring
Principle of nformed >onsent
. Right (val#ation
clientSs response to medications.
extent of side-effects or any adverse reactions.
<. Right to Re%#se
!#rse m#st do:
determine, when possi!le, reason for refusal.
explain ris$ for refusing medications O reinforce the reason for medication.
=efusal should !e documented immediately.
/ead nurse or health care provider should !e informed when omission pose
Aos!ySs 5ictionery ;f Aedicine 6ursing %nd /ealth Professions, Philadelphia,1
8dition, 8lsevier /elath 7ciences.
>ovey Tr, +ee 8d, /enion Ud, %nnals ;f >hemistry,1GGC,11
8d, Aos!y Pu!lications,
7heiner +!, =osen!erg, @ "1G77#,Pharmaco Binetic Parameters,5
Aiichael 8, Jinter @asic >linical Pharmaco$inetics,"1DD?#,?
8d,+ippincott Jilliams
%nd Jil$ins,Pp&1-11.
@ennett Pn, @rown A3,>linical Pharmacology,G
8d "1DD<#, 8lsevier >hurchill +iving
7tone P&?5.
Aarshall 7halfer,Pharmacology "1DD5# 11
8d, Ac 'raw /ill >ompanies,6orth
=ang O 5ales, Pharmacology,"1DDF#, C
8d, 8lsevier >hurchill +iving 7tone P&GF-117.
7haronr >ole,+a!us 5iane A,6ursing Pharmacology,1
8dition, +ippincott Jilliams %nd
Ailo 'i!aldi,5onald Perrier,Pharmaco$inetics,"1DDC#,1
8d, Aarcel 5e$$erinc 6ew
7ingi Iatira3,Pharmacology >lassification, %nd =ationales,1DDC,1
8d,Uaypee Aedical
Pu!lishers,6ew 5elhi,Pp&<.
'upta +c,Busum 'upta,Aanual ;f Pharmacy,?
8d, "1DD?#,+ordson Pu!lishers,6ew
Tripati B 5 8ssentials ;f Aedical Pharmacology, "1DD<#,5
8d, Uaypee Aedical @rothers
Pu!lications +imited, 6ew 5elhi,Pp&11-<1.