Abbrevations-1 (Part1 - 11 Files Merged) (2 Files Merged)

ABBREVIATIONS
DR. GUNESH KUMAR

Abbreviations
Abbreviation Meaning
◼ ac before meal
◼ ad upto
◼ Aq aqua
◼ bid twice a day
◼ BP british pharmacopia
◼ cap capsule
◼ gtt drops
◼ hs at night
◼ IM intramuscular
◼ IV intravenous
◼ od once a day
◼ PO by mouth
◼ pc after meal
◼ PR per rectum
◼ qid four times a day
◼ R you take
◼ stat at once
◼ SC subcutaneous
◼ sos if needed
◼ sus suspension
◼ tab tablets
◼ tid three times a day
◼ usp united states
pharmacopia
House Hold Measurements
◼ 1 tea spoon full = 5 ml

◼ 1 dessert spoon full = 10 ml
◼ 1 table spoon full = 15 ml
◼ 1 cup of tea = 120 ml
◼ 1 glass of water = 250 ml
◼ 1 pint = 500 ml
AMINOGLYCOSIDES
DR. GUNESH KUMAR
AMINOGLYCOSIDES ARE A GROUP OF
BACTERICIDAL ANTIBIOTICS ORIGINALLY
OBTAINED FROM VARIOUS STREPTOMYCES
SPECIES AND SHARING CHEMICAL,
ANTIMICROBIAL, PHARMACOLOGIC, AND
TOXIC CHARACTERISTICS.
General properties of
Aminoglycosides
PHYSICAL AND CHEMICAL
PROPERTIES
•WATER-SOLUBLE
•MORE ACTIVE AT ALKALINE THAN AT
ACID PH
PHARMACOKINETICS
• AMINOGLYCOSIDES ARE ABSORBED VERY POORLY FROM THE
INTACT GI TRACT; VIRTUALLY THE ENTIRE ORAL DOSE IS
EXCRETED IN FECES AFTER ORAL ADMINISTRATION.
• THE DRUGS MAY BE ABSORBED IF ULCERATION IS PRESENT.

• AFTER INTRAMUSCULAR INJECTION, AMINOGLYCOSIDES ARE
WELL ABSORBED, GIVING PEAK CONCENTRATIONS IN BLOOD
WITHIN 30-90 MINUTES.
PHARMACOKINETICS
• DISTRIBUTION:
• FREELY INTO THE VASCULAR SPACE
• INTERSTITIAL SPACES OF MOST TISSUES
• EXCRETED BY THE KIDNEYS
• HALF-LIFE: 1.5 TO 3.5 HOURS
PROTEIN SYNTHESIS
MECHANISM OF ACTION
•BACTERICIDAL
•INHIBIT PROTEIN SYNTHESIS
•BIND TO BACTERIAL 30S
RIBOSOMAL SUBUNIT
1. Blocks initiation of protein
synthesis
2. Cause misreading of mRNA
template
3. Cause premature termination
of translocation
RESISTANCE OF AMINOGLYCOSIDES
AMINOGLYCOSIDES RESISTANCE
• DECREASED PERMEATION OF AMINOGLYCOSIDES

• LOW AFFINITY FOR BACTERIAL RIBOSOME
• DRUG INACTIVATION BY MICROBIAL ENZYMES
TOXICITY
• DEPENDENT ON TOTAL AMOUNT OF DRUG AND

DURATION OF THERAPY
• NEPHROTOXICITY
• MOST OFTEN REVERSIBLE
• ACCUMULATION OF DRUG IN PROXIMAL
TUBULAR CELLS
• REDUCED EXCRETION OF DRUG = INCREASED
RISK OF OTOTOXICITY
•OTOTOXICITY
• LARGELY IRREVERSIBLE IF NOT CAUGHT
EARLY
• DESTRUCTION OF VESTIBULAR AND
COCHLEAR SENSORY CELLS
• HIGH-PITCHED TINNITUS IS OFTEN 1ST
SYMPTOM
• AMIKACICIN, KANAMYCIN & NETILMYCIN
CAUSE COCHLEAR NERVE DAMAGE(TINNITUS,
HEARING LOSS)
• GENTACIN, STREPTOMYCIN & TOBRAMYCIN
CAUSE VESTIBULAR NERVE DAMAGE
(VERTIGO, ATAXIA, DIZZINESS)
AMINOGLYCOSIDE IN PREGNANCY
✓THERE ARE LIMITED DATA ON THE TRANS
PLACENTAL PASSAGE OF AMINOGLYCOSIDES.
✓ONLY GENTAMICIN IS LISTED IN CATEGORY C.

✓THE OTHER AGENTS (E.G., TOBRAMYCIN,
AMIKACIN, NETILMICIN, STREPTOMYCIN,
KANAMYCIN) ARE CATEGORY D BECAUSE EIGHTH
CRANIAL NERVE DAMAGE HAS BEEN REPORTED IN
CHILDREN WHOSE MOTHERS RECEIVED
STREPTOMYCIN AS LONG-TERM THERAPY FOR
TUBERCULOSIS.
Q#1: Which of the following protein synthesis
inhibitors besides the streptogramins are
bactericidal?
A. AMINOGLYCOSIDES
B. CHLORAMPHENICOL
C. CLINDAMYCIN
D. MACROLYDES
E. PENICILLINS
Q#2: Bactericidal action of aminoglycoside
antibiotic is most likely due to;
A. ALTERATION OF BACTERIAL CELL MEMBRANE

B. DAMAGE TO BACTERIAL DNA
C. DAMAGE TO BACTERIAL CELL WALL
D. INHIBITION OF BACTERIAL OXIDATIVE METABOLISM
E. INHIBITION OF PROTEIN SYNTHESIS
Q#3: Which of the following is the reason why
aminoglycosides are not effective against
anaerobic bacteria?
A. ANAEROBES HAVE NO BINDING SITES FOR THESE DRUG

B. ANAEROBES SYNTHESIZE PROTEINS DIFFERENTLY
C. THEY ARE ACTIVELY EFFLUXES FROM ANAEROBES
D. THEY ARE IMMEDIATELY INACTIVATED BY ANAEROBES
E. THEY FAIL TO ENTER INTO ANAEROBES
Q#4: A PATIENT IS TAKING A LOOP
DIURETIC FOR A CERTAIN
CARDIOVASCULAR DISEASE. WHICH OF
THE DRUG WILL MOST LIKELY BE
AVOIDED DUE TO FEAR OF INCREASED
OTOTOXICITY?
A. AMPICILLIN
B. CEFOTAXIME
C. CIPROFLOXACIN
D. GENTAMYCIN
E. TETRACYCLINE
Q#5: WHICH OF THE FOLLOWING
AMINOGLYCOSIDE IS USED ORALLY TO
PREVENT HEPATIC ENCEPHALOPATHY IN
PATIENTS OF LIVER CIRRHOSIS?
A. AMIKACIN
B. KANAMYCIN
C. NEOMYCIN
D. TOBRAMYCIN
Thanks !
BIOAVAILABILITY AND
HALF LIFE
DR. GUNESH KUMAR

BIOAVAILABILITY
Bioavailability is rate and extent to

which a drug reaches to the systemic
concentration in an unchanged form.
Factors That Affect The
Bioavailability Of The Drug
1. Route Of Administration
2.Solubility Of Drug.
3. First Pass Hepatic Effect
 When a drug is absorbed from the GIT after

oral administration, it enters the portal
circulation before entering the systemic
circulation. If the drug is rapidly metabolized
in the liver or gut wall during this initial
passage, the amount of unchanged drug
entering the circulation is decreased. It is
known as first pass hepatic effect.
4. Chemical Stability.
5. Nature Of Drug Formulation.
Bioequivalent:
If two similar drugs have the same

bioavailability, they are called
bioequivalent.
Therapeutic Equivalent
If two similar drugs perform the same

effect, have same efficacy and toxicity,
then they are called Therapeutically
Equivalent.
Half life
 The time required for the amount of

drug in the body to fall by 50% of its
initial concentration.
t1/2 = 0.693 x Vd
CL
unit – time.
Half Life Determines:
 The duration of action after a single dose.
 The time required to reach steady state.
 The dosing frequency.
Steady State Concentration
 In pharmacokinetics, the condition in which

the average total amount of drug in the body
does not change over multiple dosing cycles.
 i.e the condition in which the rate of drug
elimination equals the rate of administration.
BCQS TEST
Q#01: Oral bioavailability of a drug is
DIRECTLY related to its: ( means more the
factor, more the bioavailability).
A. Degree of ionization in GIT
B. 1st pass metabolism
C. Hardness of tablet
D. Lipid solubility
E. Particle size
Q#02: Which of the following factor
affect bioavailability?
A. Half life
B. Chelation with drugs or foods in the
intestine
C. Kidney excretion
D. Plasma protein binding
Q#03: Half life means the time taken for
the initial ---------- of a drug to reduce
by one half.
A. Absorbed amount
B. Administered dose
C. Plasma concentration
D. Urinary concentration
Q#04: Half life is dependent on all the
following factors EXCEPT?.
A. Bioavailability
B. Plasma protein binding
C. Rate of metabolism
D. Rate of tubular filtration & secretion
DRUG
BIOTRANSFORMATION
Dr. GUNESH KUMAR
WHAT IS BIOTRANSFORMATION
Biotransformation Of Drug
Series of chemical alterations of a drug that
occur within body by enzymatic activity are
called biotransformation
OR
Biotransformation is Enzymatic modification
of the drug occurring within human body.
Sites Of Biotransformation
Liver is the principal organ of drug biotransformation.
Other tissues that display
considerable activity include:
GIT
Lungs
Skin
Kidney
Brain
PHASES OF BIOTRANSFORMATION
PHASE – I REACTIONS:
• Phase – I reactions usually convert the parent
drug to a more polar metabolite by
introducing or unmasking a functional group
(-OH, -NH2).
Cytochrome P450 System
 Phase I reactions involves enzyme family known as Cytochrome P450
System.
 They are found in liver.
Phase - I Reactions
 Oxidation:
 Oxidation, P450 Dependent.
 eg: Codeine.
 Oxidation, P450 Independent.
 eg: Ethanol
 Reduction:
 eg: Chloramphenicol, Dantroline.
 Hydrolysis:
 eg: Aspirin, Lidocaine.
INDUCERS:
Drugs which induces the activity of Cytochrome P450
Enzymes are called as INDUCERS.
They results in:
▪ Increase biotransformation of drugs.
▪ Leads to decrease in plasma concentration of the drug.
Examples:
➢ Phenobarbbitone.
➢ Rifampin,
➢ Carbamazepine.
INDUCERS:
➢Phenobarbitoal,
carbamazepine.
CYP1AC === Acetamenophen,
Barbiturates, phenytoin.
CYP3A4 === Erythromycin,
Antiarrhythmic drugs.
INHIBITORS:
 Some drugs inhibits the Cytochrome P450 Enzymes.
 They are called as INHIBITORS.
Examples:
➢ Omeprazole,
➢ Ketoconazole,
➢ Erythromycin
INHIBITORS
➢Amiodarone, cimetidine.
CYP2D6 === Betablockers, opioids.
➢Erythromycin
CYP 3A4 === Ca channel blockers, Antiarrhythmic drugs.
PHASE – II REACTIONS
These reactions are also called as Conjugation Reactions.
• Phase –II Reactions increase water solubility by conjugation of
the drug molecule with a polar groups such as glucoronate,
acetate or sulfate.
• Parent drugs OR their Phase- I metabolites that contain suitable

chemical groups often undergo coupling or conjugation
reactions with an endogenous substance to yield conjugates.
 Conjugates are polar molecules or water soluble groups
that are readily excreted out and mostly inactive.
 Conjugate formation involves high energy intermediates
and specific transfer enzymes.
 Such enzymes (Transferases) may be located in
microsomes or in cytosol.
 Uridine
5’- diphosphate (UDP) glucoronosyl transferases
UGTs are the most dominant enzymes.
 Some natural substances in the
body are also metabolized by
conjugation reactions. E.g. Billirubin,
Estrogen, Adrenal Steroid.
Primary Enzymes Involved In Phase-II
Reactions
✓ Glocoronosyl transferase.
✓ Sulfotransferase.
✓ Glutathione - S – transferase,
✓ Acetyl transferase.
EXAMPLES OF PHASE – II REACTIONS
 Glucoronidation: Acetaminophen. Diazepam.
 Acetylation: Clonazepam, isonizid.
 Glutathione: Ethacrynic Acid.
 Glycine: Nicotinic Acid, Salicylic Acid.
 Sulfation: Methyldopa.
 Methylation: Dopamine, Epinephrine.
Glucoronide Conjugation
 Itis the most common metabolic reaction of
phase -II Biotransformation.
 This reaction primarily occurs in the liver
metabolites are excreted into bile & then into
small intestine.
 These reactions are catalyzed by enzyme glucronyl
transferase .
 Activity of the enzyme is very low in new born infant.
 Drug chloramphenicol (antibiotic) in new born infant

deficient in glucoronyl transferase result in
accumulation of free drug in blood & tissues and
cause toxicity i.e. grey baby syndrome.
GRAY BABY SYNDROME
ACETYLATION
 This reaction is catalyzed by enzyme N.acetyl
transferase & the co-factor is acetyl co-A.
 They are present in the cytosol of liver, kidney, lungs &
intestine.
 Some persons are rapid acetylators & have high
N.acetyl transferase activity & they show rapid
metabolism & decreased pharmacologic action of
drug.
Some persons
are slow
acetylators &
have low
enzyme
activity & they
show drug
toxicity.
FIRST PASS EFFECT
1
DRUG DISTRIBUTION
2/26/2021
DR. GUNESH KUMAR
MBBS,MPHIL
Pharmacokinetics 2
2/26/2021
The study of how the drug is:
- Absorbed
-Distributed
- Metabolized
- Excreted
Pharmacokinetics: 3
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Absorption
Distribution
Metabolism
Excretion
Transcellular
Fluid & brain 4
2/26/2021
Plasma Interstitial Intracellular fluid
fluid
1.5 L
Heparin
3L
Gentamicin
15 L
Ethanol
42 L
Fluid compartments in the body

Volume of distribution
5
Definition:
2/26/2021
The Apparent volume of distribution is defined as the volume of
fluid required to contain the total amount of drug in the body at
the same concentration
as that present in the plasma.
Dose
Vd = C
Volume of Distribution 6
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confined to plasma distributed in
body tissue
Example:
Volume of distribution
Dose administered = 7
500 mg
2/26/2021
Plasma concn.= 50 mg / liter
Vd = 500 / 50 = 10 liters
Significance
A low Vd indicates that most
of the drug is in the vascular
compartment
(e.g. bound to plasma proteins)
Volume of distribution (Vd) = Dose administered
Concentration 8
Example:Dose administered =
2/26/2021
500 mg
Plasma concn. = 2 mg / litre
Vd = 500 / 2 = 250 litres
Significance
A high Vd indicates that
most of the drug is in the
extra vascular compartment
Apparent Volume of Distribution (Vd)
9
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Amt of Drug (dose)
Vd =
Concentration
Small Vd Large Vd
Low tissue binding
Drug tightly bound
APPARENT DISTRIBUTON 10
VOLUME OF SOME DRUGS
2/26/2021
DISTRIBUTION
DRUG
VOLUME Vd (L)
Heparin 5
Aspirin 11
Gentamicin 18
Amoxycillin 28
Atenolol 77
Distribution volume cont. 11
2/26/2021
DISTRIBUTION
DRUG
Diazepam 140 VOLUME VD (L)
Pethidine 280
Digoxin 420
Nortryptyline 1000
Chloroquine 13000
Plasma proteins and binding 12
2/26/2021
α1
glycoprotein
Albumin Globulin
4g/100ml 40 - 100mg/100ml Very little

(weak acids
neutral drugs)
(weak bases) e.g. Prednisolone
eg. Diazepam, e.g. Lidocaine,
Phenytoin, Propranolol
Dysopyramide
CLINICAL IMPORTANCE OF: 13
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❑ Estimating Vd of each drug
❑ Plasma protein binding
❑ Tissue distribution (binding)

Important physiological barriers 14
affecting distribution of each drug
2/26/2021
✓Blood-Brain barrier &
Blood-CSF barrier
✓Placental barrier
15
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Placental transfer of drugs 16
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(a) Placental blood flow
(b) lipid solubility

- sulphonamides, barbiturates, anticonvulsants,
narcotic analgesics, steroids, etc.
(c) Molecular size of drug

Placental transfer of drugs 17
2/26/2021
(a) Placental blood flow
(b) Lipid solubility
(c) Molecular size of drug

MATERNAL-FETAL DISTRIBUTION 18
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Mother Fetus
Polar drug
Non-polar drug Non-polar drug
Polar metabolite Polar metabolite

Drug Reservoir (storage)
19
Other than plasma protein

(Tissue binding)
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BONES: Tetracyclines,
heavy metals
TEETH: Tetracyclines,
heavy metals
BRAIN: Chlorpromazine
RETINA, Chloroquine
CORNEA:
Drug Reservoir continued: 20
 HEART,
KIDNEY : Digoxin, Digitoxin
2/26/2021
 LIVER:
 THYROID GLAND:
Chloroquin,Digoxin
 FAT:
 SKIN, HAIR:
Iodine
 COLLAGN TISSUE
Diazepam, verapamil
Arsenic
Ca, Mg
21
Tetracycline
2/26/2021
staining
of teeth
People don’t always believe what you say…. 22
2/26/2021
But they will always believe what you do.
DRUG EXCRETION
Dr. GUNESH KUMAR

WHAT IS DRUG EXCRETION
DRUG EXCRETION
The process by which drugs or metabolites are
irreversibly transferred from internal to external
environment through renal or non renal route.

TYPES OF EXCRETION
A. RENAL EXCRETION
B. NON RENAL EXCRETION

1. Biliary excretion.
2. Pulmonary excretion.
3. Salivary excretion.
4. Skin / Dermal excretion.
5. Gastrointestinal excretion.
4
RENAL EXCRETION
❖Glomerular filtration
❖Tubular secretion
❖Tubular re-absorption
GLOMERULAR FILTRATION
GLOMERULAR FILTRATION RATE:

a) It Is non selective , unidirectional
process.
a) Out of 25% of cardiac out put or
1.2 liters of blood/min that goes to b) Ionized or unionized drugs are
the kidney via renal artery only filtered, except those that are
10% or 120 to 130ml/min is bound to plasma proteins.
filtered through glomeruli. c) Driving force for GF is
b) The rate being called as hydrostatic pressure of blood
glomerular filtration rate. flowing in capillaries.

PASSIVE TUBULAR REABSORPTION
▪Most substances are reabsorbed across renal tubular

cells if unionized and lipid soluble.
▪It occurs after the glomerular filtration of drugs.

▪It takes place all along the renal tubules.
▪Reabsorption results in increase in the half life of the

drug.
11
ACTIVE TUBULAR SECRETION
▪ This mainly occurs in proximal tubule.
▪ It is carrier mediated process which requires energy for transportation of
compounds against concentration gradient.
▪ Two secretion mechanisms are identified.
a) System for secretion of organic acids/anions e.g. Penicillin,
salicylates
b) System for organic base /cations e.g. morphine, mecamylamine
▪ These active secretory systems are important in drug excretion because
charged anions and cations are often strongly bound to plasma proteins
and therefore are not readily available for excretion by filtration.
▪ Active secretory systems can rapidly and efficiently remove many protein-
bound drugs from the blood and transport them into tubular fluid.
FACTORS AFFECTING RENAL EXCRETION
➢Urine pH
➢Blood flow to the kidney
➢Biological factor (age, species)
➢Disease state
14
NON-RENAL ROUTE OF DRUG EXCRETION
Biliary Excretion
Pulmonary Excretion
Salivary Excretion
Skin/dermal Excretion
Gastrointestinal Excretion
BILIARY EXCRETION
▪ Compounds excreted by this route are sodium, potassium,
glucose, bilirubin, Glucuronide, sucrose, Inulin, muco-proteins
e.t.c.
▪ Greater the polarity better the excretion.

▪ The metabolites are more excreted in bile than parent drugs
due to increased polarity.
GASTROINTESTINAL EXCRETION
▪ Water soluble and ionized form of weakly acidic

and basic drugs are excreted in GIT.
▪ Drugs excreted in GIT are reabsorbed into

systemic circulation & undergo recycling.
PULMONARY EXCRETION
➢ Gaseous and volatile substances such as general

anesthetics (Halothane) are absorbed through lungs by
simple diffusion.
➢ Intact gaseous drugs are excreted but not metabolites.

Alcohol which has high solubility in blood and tissues are
excreted slowly by lungs.
CLEARANCE
Defined as the hypothetical volume of body fluids containing
drug from which the drug is removed/ cleared completely in a
specific period of time. Expressed in ml/min.
Clearance = Rate of elimination ÷ plasma conc.
• First Order Kinetics

• Zero Order Kinetics
ROUTES OF DRUG ADMINISTRATION
DR. GUNESH KUMAR

MBBS,MPHIL
Routes of Drug Administration
(Medication Administration Routes)
No single method of drug
administration is ideal for all drugs
in all circumstances
Important
Info
The route of administration (ROA), that is

chosen may have a profound effect upon
the speed and efficiency with which the
drug acts
Important
Info
The ROA is determined by the physical

characteristics of the drug, the speed which
the drug is absorbed and/ or released, as
well as the need to bypass hepatic
metabolism and achieve high conc. at
particular sites.
General Steps in Administering Medication
 The possible routes of drug entry
into the body may be divided into
two classes:
⚫Enteral
⚫Parenteral
Routes Of Administration
Routes Of Drug
Administration
Parenteral Enteral
Injection Topical Respiratory Rectal Oral S/L

Swallowing Placed under the
tongue
Absorption through the

rectum
1. ORAL ROUTE DRUG ADMINISTRATION
Any medication taken by mouth and

swallowed into the GI tract.
Oral Drug Forms
 Capsules  Elixirs
 Tablets  Emulsions
 Pills  Lozenges
 Enteric coated/time  Suspensions
release capsules and  Syrups
tablets
ADVANTAGES OF ORAL ROUTE
 Commonest
 Can be self- administered NO EXPERTIZE
REQUIRED
 Pain free, easy to take
 Compared to most other parenteral
routes, cheaper
 Safe, does not break the skin.
 No any sterilization required.
DIS-ADVANTAGES OF ORAL ROUTE
 Inappropriate in patients with nausea and
vomiting.
 Drug may have unpleasant taste.
 May cause irritation of gastro intestinal tract.
 Drug may discolor teeth.
 Drug can be aspirated by ill client.
 Sometimes inefficient - only part of the drug

may be absorbed
DIS-ADVANTAGES OF ORAL ROUTE
First-pass effect - drugs absorbed orally

are initially transported to the liver via the
portal vein
Destruction of drugs by gastric acid and
digestive juices
Effect too slow for emergencies
Unable to use in unconscious patient.
Intravenous
Administration
Oral
Administration
Metabolism Liver
Intestines
2. SUB-LINGUAL ROUTE DRUG
ADMINISTRATION
A drug placed under the tongue, where it

dissolved and diffuse into the capillary network.
ADVANTAGES OF SUB-LINGUAL
ROUTE
 Drug may administered for local effect.

 Drug rapidly absorbed into blood stream.
 More potent than oral.
 Avoid first-pass effect
DIS-ADVANTAGES OF SUB-LINGUAL
ROUTE
Inconvenient
Irritation to oral mucosa
Unpleasant taste of some drugs
Large doses can not be given
3. RECTAL ROUTE DRUG
ADMINISTRATION
A drug placed INSIDE the rectum through the

anus.
ADVANTAGES OF RECTAL ROUTE
1. Unconscious patients and children
2. Prevented from destruction of intestinal enzymes

and low pH of stomach
3. If patient is nauseous or having vomiting
4. Good for drugs affecting the bowel such as

laxatives
DIS-ADVANTAGES OF RECTAL
ROUTE
• Irritating drugs are contraindicated
• Absorption is imperfect
• Rectal inflammation on repeated administration

BCQS PRACTICE
Q#01: A patient is being administered a drug that
offers the most first pass metabolism. Through
which route is the drug most likely being
administered?
A. Inhalation
B. Intramuscular
C. Oral
D. Rectal
E. Sublingual
Q#02: Which of the following is an
enteral route of administration that
minimizes passage through the
liver?
A. Subcutaneous
B. Topical
C. Oral
D. Rectal
E. Transdermal
Q#03: Advantages of sublingual
route include all of the following
except?
A. Allows lower doses to be used.
B. It avoids first pass hepatic metabolism.
C. It has rapid onset of action.
D. Its usefulness is limited to treat local
conditions.
E. Spitting out the tablet can terminate its
action
Q#04: Dis-advantages of oral route
include all of the following except?
A. Irritation of gastro intestinal tract.
B. 1st pass effect.
C. Unable to use in unconscious patient.
D. Destruction of drugs by gastric acid and
digestive juices not possible.
Q#05: A rectal suppository is used to
treat a fever. This would represent what
type of drug delivery?
A. Parenteral and local

B. Parenteral and systemic
C. Enteral and local
D. Enteral and systemic
Q#06:The feature of the
sublingual route include;
A. Pretty fast absorption

B. A drug is exposed to gastric secretion
C. A drug is exposed more prominent
liver metabolism
D. A drug can be administrated in a
variety of doses
PHARMACOLOGY
• The word “PHARMACOLOGY” is derived from the Greek word

“Pharmakon”(medicine or Drug), and “Logos”(study).
• The science which deals with the study of actions of drugs on

living system.
2
WHAT IS DRUG
• A drug is a chemical which is given to people in order
to treat or prevent an illness or disease.
PHARMACOKINETICS
It derived from the Greek word ‘kinesis’( a movement ).

➢ It deals with the route of administration, time course of
drug absorption, distribution , metabolism and elimination
of drug.
➢It is simply defined as “What the body does to the drug”
5
DRUG NAMES
THIS WAS FIRST STEP
JOURNY BEGINS NOW
MACROLIDES
DR. GUNESH KUMAR
INTRODUCTION TO MACROLIDES
 The chemical structure of macrolides is characterized by a
large lactone ring containing from 12 to 16 atoms to which
are attached, via glycosidic bonds, one or more sugars.
 Macrolides are one of the most commonly used families of

antibiotics. Currently available macrolides are erythromycin
and the newer agents clarithromycin, azithromycin,
roxithromycin, dirithromycin, and telithromycin.
CLASSIFICATION OF MACROLIDES
 Based on the number of carbon atoms in the lactone
ring, the macrolides are classified into:
1. 14-membered ring agents: Clarithromycin,

Erythromycin, Dirithromycin, Flurithromycin
2. 15-membered ring agents (Azalides):
Azithromycin
3. 16-membered ring agents: Josamycin,
Spiramycin
PHARMACOKINETICS
 Available in both oral and parenteral forms.
 Macrolide antibiotics are basic compounds, poorly soluble in
water, which are mostly absorbed in the alkaline intestinal
environment.
 They are acid unstable, but the newer semi synthetic
derivatives (i.e. roxithromycin and azithromycin) are
characterized by increased stability under acidic conditions.
 Macrolides are highly liposoluble and consequently penetrate
well into tissue, especially bronchial secretions, prostatic
tissue, middle ear exudates and bone tissues.
 Macrolides undergo extensive biotransformation in the liver.
 Under normal conditions, the major route of elimination is

the liver. Renal elimination also takes place but it contributes
to total clearance only to a small degree.
 The degree of modification of macrolide pharmacokinetics by

renal insufficiency or hepatic disease is usually not
considered clinically relevant, and no recommendation for
dose modification is necessary in these patients.
And Upper Airway ANAEROBES
ADVERSE EFFECTS
 Macrolides are considered to be one of the safest anti-
infective groups in clinical use, with severe adverse
reactions being rare.
 Gastrointestinal reactions represent the most frequent
disturbance.
 Serious side effects including allergic reaction and
cholestatic hepatitis are generally associated with the
use of erythromycin only.
 All macrolides are associated with QTc interval
prolongation with risk apparently greater with
erythromycin and clarithromycin than with
azithromycin.
DRUG INTERACTIONS
 Macrolide antibiotics can
interact adversely with
commonly used drugs,
usually by altering
metabolism due to
complex formation and
inhibition of cytochrome
P-450 IIIA4 (CYP3A4) in
the liver and enterocytes.
THANK YOU
(Medication Administration Routes)
DR. GUNESH KUMAR

MBBS, M.PHIL
CLASSIFICATION
LOCAL
SYSTEMIC •Skin topical
•Intranasal
•Ocular drops
Enteral Parenteral Mucosal-throat,
vagina, mouth, ear
Oral Inhalational
Transdermal
Sublingual injectable
Rectal Transdermal
Intravenous
Intramuscular
Subcutaneous
Intra-arterial
Intra-articular
Intrathecal
Intradermal
PARENTERAL ROA
INTRODUCTION
• The term parenteral comes from Greek words
– par, meaning outside
– enteron, meaning the intestine
• This route of administration bypasses the alimentary canal

PARENTERAL INJECTABLE ROUTES
Intradermal (I.D.) (into skin)
Subcutaneous (S.C.) (into subcutaneous tissue)
Intramuscular (I.M.) (into skeletal muscle)
Intravenous (I.V.) (into veins)
Intra-arterial (I.A.) (into arteries)
Intrathecal (I.T.) (cerebrospinal fluids )
Intraperitoneal (I.P.) (peritoneal cavity)
Intra - articular (Synovial fluids)

Kinds of Injectable Drug Containers
• Glass ampules
• Single and multi dose vials
• Prefilled syringes
• Intravenous medication fluids

Intradermal Injection
Intradermal Injections
• Given into capillary-rich layer just below epidermis for

– diagnostic tests
– immunizations
Subcutaneous Injections
▪ Medications administered below the
skin into the subcutaneous fat
– outside of the upper arm
– top of the thigh
– lower portion of each side of the

abdomen
▪ Often have a longer onset of action
and a longer duration of action

– compared with IM or IV injection
Subcutaneous Injections
• Medications administered by
this route include:
– epinephrine (or adrenaline)
• for emergency asthmatic
attacks or allergic reactions
– insulin
– sumatriptan or Imitrex
• for migraines
– many vaccines
Advantages & Disadvantages
Advantages
• Can be given by the owner
• Vasoconstrictor can be added to prolong effect at site of interest
Disadvantages
• Variability
• dehydration, cold, stress, DECREASE blood flow
• heat INCREASES blood flow

INTRAMUSCULAR ROUT
Intramuscular Injection Sites
• Deltoid
• Dorsal gluteal
• Vastus lateralis
• Rectus femoris
Intramuscular Injections
Used to administer
• Antibiotics
• Vitamins
• Iron
• vaccines
Absorption of drug by IM route is
unpredictable
• Not recommended for patients who are
unconscious or in a shock like state
Advantages & Disadvantages
Disadvantages:
Advantages:
• Absorption dependent on
• Simple and accessible blood flow.
• No indwelling medical • Slower absorption than
intravenous, i.e. not good
devices required, for immediate analgesia.
• Required for certain types • Painful.
of drugs, e.g. • Limited volume.
• Nerve damage, if incorrectly
immunoglobulins, vaccines
performed (often confusion
over meaning of upper,
outer quadrant).
INTRA VENOUS ROUT
Advantages Of IV Route
The IV route is the fastest method for delivering systemic drugs
• preferred administration in an emergency situation
It can provide fluids, electrolytes, and nutrition
• patients who cannot take food or have serious problems with
the GI tract
It provides higher concentration of drug to bloodstream or

tissues
• advantageous in serious bacterial infection
INHALATIONAL ROUT
Disadvantages of the IV Route
▪ Traumatic injury from the insertion of needle
• Potential for introducing:
o Toxic agents
o Microbes
o Pyrogens
• Impossible to retrieve if adverse reaction occurs
• IV injections and infusions are introduced directly into
the bloodstream
o Must be free of air bubbles and particulate matter
o Introduction of air or particles might cause embolism,
blockage in a vessel, or severe painful reaction at the
injection site
The intra respiratory route of administration is the application
of drug through inhalation into the lungs.
• lungs are designed for exchange of gases from tissues into
bloodstream
• usual dose form is an aerosol
• Used for gaseous and volatile agents and aerosols.
Inhaled Medications
• Metered-dose inhalers
(MDI) provide medication
with compressed gas
• Nebulizers create a mist
when a stream of air flows
over a liquid
• commonly utilized for
young children or elderly
patients with asthma or
lung disease
Topical Routes of Administration
• Is the application of a drug directly to the surface
of the skin
• Includes administration of drugs to any mucous
membrane
– eye – vagina
– nose – urethra
– ears
Topical Dose Forms
Dose forms for topical
administration include:
• Eye or ear:
• Skin:
– solutions
– creams
– ointments – suspensions
– lotions – ointments
– gels • Nose and lungs:
– transdermal patches
– sprays and powders
Vagina
– tablets
– creams
– ointments
– suppositories
Advantages of the Topical Route
➢ Local therapeutic effects
➢ Not well absorbed into the deeper layers of the skin or

mucous membrane
➢ lower risk of side effects
➢ Transdermal route offers steady level of drug in the

system
Topical Routes of Administration
Absolute Bioavailability: results about
different routes
Concentrations
I.V
I.M
S.C
Oral
Time
Review
Which of the following routes of medication
administration has the fastest effect?
A. Oral
B. Intravenous
C. Subcutaneous
D. Intramuscular
The nurse is giving a medication that has a high first-pass effect.
The physician has changed the route from IV to PO. The nurse
expects the oral dose to be:
A. Higher because of the first-pass effect.
B. Lower because of the first-pass effect.
C. The same as the IV dose.
D. Unchanged.
. A patient is complaining of severe pain and has orders
for morphine sulfate. The nurse knows that the route
that would give the slowest pain relief would be which
route?
A. IV
B. IM
C. SC
D. PO
No single method of drug
administration is ideal for all
drugs in all circumstances
PENICILLINS
DR. GUNESH KUMAR
MBBS,M.PHIL
PENICILLINS
• ALL PENICILLINS ARE DERIVATIVES OF 6-AMINOPENICILLANIC ACID
AND CONTAINS A BETA-LACTAM RING STRUCTURE THAT IS ESSENTIAL
FOR ANTIBACTERIAL ACTIVITY.
BACTERIAL CELL WALL
CELL WALL IS RIGID OUTER LAYER THAT IS NOT FOUND IN
ANIMAL CELLS,
IT COMPLETELY SURROUNDS THE CYTOPLASMIC
MEMBRANE,
PREVENTING CELL LYSIS FROM HIGH OSMOTIC PRESSURE,
MAINTAIN THE SHAPE OF THE CELL.
MECHANISM OF ACTION
PENICILLINS INHIBIT CELL WALL SYNTHESIS BY THE
FOLLOWING STEPS:
1. BINDING OF PENICILLIN TO THE SPECIFIC ENZYMES
(PENICILLIN BINDING PROTEINS, PBPS).
2. INHIBITION OF TRANSPEPTIDATION REACTION THAT
CROSS-LINKS THE LINEAR PEPTIDOGLYCAN CHAIN
CONSTITUENTS OF CELL WALL .
3. ACTIVATION OF AUTOLYTIC ENZYMES THAT CAUSE
LESIONS IN THE BACTERIAL CELL WALL.
PHARMACOKINETICS
1. ADMINISTRATION:
• METHICILLIN, TICARCILLIN, PIPRACILLIN,
AND THE COMBINATIONS OF :
AMPICILLIN WITH SULBACTAM,
TICARCILLIN WITH CLAVULANIC AND
PIPRACILLIN WITH TAZOBACTAM USED I/V,
I/M.
• PENICILLIN-V AND AMOXICILLIN COMBINED
WITH CLAVULANIC ACID ARE ONLY AVAILABLE
AS ORAL PREPARATION.
• PROCAINE PENICILLIN G AND BENZATHINE PENICILLIN G
ARE ADMINISTERED I/M.
• THEY ARE SLOWLY ABSORBED INTO THE CIRCULATION
OVER A LONG PERIOD.
2. ABSORPTION:-
• MOST OF THE PENICILLINS ARE INCOMPLETELY ABSORBED
(ORALLY). THEY REACH THE INTESTINE IN SUFFICIENT
AMOUNT TO EFFECT THE COMPOSITION OF THE INTESTINAL
FLORA.
3. METABOLISM:- IS INSUFFICIENT.
4. DISTRIBUTION:-THROUGH OUT THE BODY IS GOOD.

• ALL PENICILLIN CROSS THE PLACENTAL BARRIER, BUT NON
TERATOGENIC.
• PENETRATION INTO BONE OR CEREBROSPINAL FLUID IS
INSUFFICIENT FOR THERAPY, UNLESS THESE SITES ARE
INFLAMMED.
5. EXCRETION:-
THE PRIMARY ROUTE OF EXCRETION IS THROUGH KIDNEYS.
• PROBENECID INHIBIT THE SECRETION OF PENICILLIN.
• NAFCILLIN IS PRIMARILY ELIMINATED THROUGH BILIARY
ROUTE.
ADVERSE REACTIONS
1. ALLERGIC OR HYPERSENSITIVITY REACTIONS:
• 3-10% OF THE GENERAL POPULATION ARE ALLERGIC TO PENICILLIN.
• ONCE AN INDIVIDUAL IS ALLERGIC TO ONE PENICILLIN, HE OR SHE IS

MOST LIKELY ALLERGIC TO ALL OF THE PENICILLINS.
• THOSE ALLERGIC TO PENICILLIN ALSO HAVE A HIGHER INCIDENCE OF

ALLERGY TO THE CEPHALOSPORIN ANTIBIOTICS.
• THE MOST SERIOUS ALLERGIC REACTION CAN CAUSE SKIN RASH,

ITCHING, DIFFICULTY IN BREATHING, JOINT SWELLING, SHOCK, AND
UNCONSCIOUSNESS. (ANAPHYLACTIC SHOCK)
2. GIT DISTRUBANCES: DIARRHEA,
NAUSEA, VOMITING. (AMPICILLIN).
3. METHICILLIN CAUSES INTERSTITIAL NEPHRITIS.
4. NAFICILLIN CAUSES NEUTROPENIA.
5. OXACCILLIN CAUSES HEPATITIS.
6. AMPICILLIN HAS BEEN ASSOCIATED WITH
PSEUDOMEMBRANOUS COLITIS.
RESISTANCE TO PENICILLIN
RESISTANCE
RESISTANCE TO PENICLLINS AND OTHER BETA-
LACTAM ANTIBIOTICS IS DUE TO:
1. INACTIVATION OF ANTIBIOTICS BY BETA
LACTAMASES.
2. MODIFICATION OF TARGET PBPS.
3. IMPAIRED PENETRATION OF DRUG TO
TARGET PBPS.
4. EFFLUX THROUGH PUMP
CEPHALOSPORINS
CEPHALOSPORINS ARE BETA-LACTAM

ANTIBIOTICS.
THEY ARE DERIVATIVES OF 7-AMINOCEPHALOSPORANIC

ACID AND CONTAIN BETA-LACTAM RING IN THEIR
STRUCTURE.
CLOSELY RELATED STRUCTURALLY AND FUNCTIONALLY

TO THE PENICILLINS.
MORE STABLE THAN PENICILLINS, TO
BACTERIAL BETA-LACTAMASES .
HAVE BROADER SPECTRUM OF ACTIVITY.
THEY KILL THE BACTERIA OR PREVENT

THEIR GROWTH.
MECHANISM OF
ACTION:
 CEPHALOSPORINS LIKE ALL Β-LACTAM ANTIBIOTICS,
INTERFERE WITH BACTERIAL CELL WALL SYNTHESIS
( TRANSPEPTIDATION OR CROSS-LINKAGE ).
 ONLY EFFECTIVE AGAINST RAPIDLY GROWING

ORGANISMS THAT SYNTHESIZE A PEPTIDOGLYCAN CELL
WALL.
PHARMACOKINETICS
• METABOLISM,
• EXCRETION,
• CEFOPERAZONE AND CEFTRIAXONE.
• FIRST & SECOND GENERATION.
CLASSIFICATION
 FIRST GENERATION CEPHALOSPORINS,
(MORE EFFECTIVE AGAINST GRAM POSITIVE BACTERIA)

 SECOND GENERATION CEPHALOSPORINS,
(MORE EFFECTIVE AGAINST GRAM NEGATIVE AND LESS AGAINST GRAM POSITIVE
BACTERIA)
 THIRD GENERATION CEPHALOSPORINS,
(NO ACTIVITY AGAINST GRAM POSITIVE BACTERIA)

 FOURTH GENERATION CEPHALOSPORINS
(NO ACTIVITY AGAINST GRAM POSITIVE, EFFECTIVE AGAINST GRAM NEGATIVE

ONLY).
FIRST GENERATION
ORAL
• CEPHALEXIN,
• CEFRADINE
• CEFADROXIL
PARENTERAL
• CEFAZOLIN
INDICATIONS
• GRAM POSITIVE ORGANISMS,
• KLEBSIELLA,
• PROTEUS
• E COLI.
URINARY TRACT INFECTIONS,
CELLULITIS, SOFT TISSUE ABSCESS,
CEFAZOLIN IS DRUG OF CHOICE FOR
SURGICAL PROPHYLAXIS.
SECOND GENERATION
• PARENTERAL
• CEFAMANDOLE,
• CEFOXITIN
• ORAL
• CEFACLOR,
• CEFUROXIME
• CEFPROZIL
• LORACARBEF
INDICATIONS
H. INFLUENZA, MORAXELLA CATARRHALIS
USED IN INFECTIONS OF SINUSITIS, OTITIS
MEDIA, LOWER RESPIRATORY INFECTION,
PNEUMONIA.
USED IN PERITONITIS, DIVERTICULITIS & PID.
CEFURAXIME IS USED TO TREAT COMMUNITY
ACQUIRED PNEUMONIA.
THIRD GENERATION
• PARENTERAL
• CEFTRIAXONE,
• CEFOTAXIME,
• CEFTAZIDIME,
• CEFOPERAZONE
• ORAL
• CEFIXIME, CEFDINIR, CEFTIBUTEN, CEFPODOXIME
INDICATIONS
• SERIOUS INFECTION CAUSED BY GRAM
NEGATIVE.
• HOSPITAL-ACQUIRED INFECTIONS.
• MENINGITIS.
FORTH GENERATION
• CEFEPIME
INDICATIONS
• CEFIPIME HAS GOOD ACTIVITY AGAINST P. AERUGINOSA,

ENTEROBACTEREAE, S. AUREUS, S. PNEUMONIAE
• IT IS HIGHLY ACTIVE AGAINST HAEMOPHILUS & NEISSERIA. SP
• IT PENETRATES WELL INTO CSF.
• IT IS ALSO USEFUL IN TREATMENT OF ENTEROBACTER INFECTION
PHARMACOKINETICS
• AFTER ABSORPTION WELL DISTRIBUTED IN BODY

COMPARTMENTS, HAVING GOOD PENETRATION IN SOFT
TISSUES, MUSCLES, BONES AND JOINTS. THESE DRUGS
CAN ALSO CROSS PLACENTA AND ENTER FETAL
CIRCULATION.
• CEPHALOSPORINS ARE SAFER IN PREGNANCY. ALSO
ATTAIN HIGH CONCENTRATION IN AQUEOUS HUMOR.
ALSO HAVE HIGH CONCENTRATION IN VARIOUS
PERITONEAL, PERICARDIAL AND SYNOVIAL FLUIDS.
• MOST OF THESE DRUGS ARE EXCRETED UNCHANGED IN
URINE BY TUBULAR FILTRATION AND SECRETION.
• CEFTRIAXONE, CEFAMANDOLE AND CEFOPAROZONE
ARE EXCRETED IN FECES (BILE) THUS ARE SAFER IN
PATIENTS SUFFERING FROM RENAL FAILURE.
• SOME OF THESE DRUGS CROSS BBB, EFFECTIVE IN
MENINGITIS. DRUGS WHICH CROSS BBB INCLUDE:
• CEFOTAXIME
• CEFTRIAXONE
ADVERSE REACTIONS
ALLERGIC REACTIONS, IDENTICAL TO THOSE OF

PENICILLINS, INCLUDING ANAPHYLAXIS, FEVER,
SKIN RASHES, GRANULOCYTOPENIA AND
HAEMOLYTIC ANEMIA.
LOCAL IRRITATION AFTER I/M INJECTION.
THROMBOPHLEBITIS AFTER I/V INJECTION.
NEPHROTOXICITY,
BLEEDING DISORDERS:
HYPOPROTHROMBINAEMIA
(CEFOMANADOLE, CEFOPERAZONE).
THEY INTERFERE WITH PLATELET CAUSES
SEVERE BLEEDING.
RESISTANCE MECHANISMS
RESISTANCE TO CEPHALOSPORINS AND OTHER Β-
LACTAMS IS DUE TO ONE OF THE FOUR GENERAL
MECHANISMS:
1. INACTIVATION OF ANTIBIOTIC BY Β – LACTAMASE.
2. MODIFICATION OF TARGET PBP.
3. IMPAIRED PENETRATION OF DRUG TO TARGET PBP.
4. PRESENCE OF AN EFFLUX PUMP.
PHARMACODYNAMICS-1
DR. GUNESH KUMAR
DRUG
DRUG ADDITION
• When two drugs are combined and the
response is equal to the combined
response of the individual drugs is called
drug addition.
• Means 1 + 1 = 2
DRUG SYNERGISIM
• When two drugs are combined and the response
is MORE than the individual drugs is called drug
synergism.
• Means 1 + 1 > 2
DRUG POTENTIATION
• When two drugs are combined, one drug has no
effect but enhance the effect of other drug is
called drug potentiation.
• Means 0 + 1 = 2
IDIOSYNCRASY
Ada call kar

PLACEBO DRUG
1. ION CHANNELS
1. ION CHANNELS
1. Acetylcholine
2. Serotonin
3. GABA
4. Glutamate
2. TYROSINE KINASE LINKED RECEPTORS
2. TYROSINE KINASE LINKED RECEPTORS
1. INSULIN
2. EPIDERMAL GRPWTH FACTOR
3. PLATELET DERIVED GROWTH FACTOR
4. TRANSFORMING GROWTH FACTOR-BETA
CYTOKINE RECEPTORS
CYTOKINE RECEPTORS
1. GROWTH HORMONE
2. ERYTHROPOIETIN
3. INTERFERONS
3. G PROTEIN RECEPTORS
4. INTRACELLULAR RECEPTORS
4. INTRACELLULAR RECEPTORS
1. STEROIDS
2. THYROID HORMONES
3. VITAMIN D
Prescription Writing
A Prescription is the written order by a physician

or Surgeon to Pharmacist or dispenser to
prepare or dispense a specific treatment usually
medication for a specific disease.
27 February 2021 LUMHS, JAMSHORO 1

ELEMENTS OF THE SYSTEM
The major elements of a prescription order

are eight (8).
01
The identity of the prescriber (Name, professional
degree, reg. no:, address and telephone number)

02
Date- when the prescription order is written.
03
Name: Age and address of the Pt.
Name is for identification
Age is important for calculation of dose
Address for follow up of the Pt.

04
A
Diagnosis shown by small
Symbol Rx is an abbreviation for recipe or take

B thou (address to the pharmacist/ to the Pt).
05
Elements 5th is the body of the prescription that
specify the medication, the strength, dosage, route
of administration & duration of therapy.

06
Direction to the pharmacist regarding the strength,
duration of the prescribed drug. It should be in
medical terms.
07
Directions to the patient, contain instruction
regarding the amount of drug to be taken, time and
frequency of the dose and route of administration

08
Signature: The prescription order is completed by
the signature of the prescriber & its stamp.

Model of Prescription
Common form of out patient Prescription
Dr. John B. Doe MD (1)

West city CA 94999
(234) 555 – 6789
For (3) Date (2)

Address
:-
Rx (4)
Drug name strength quantity (5)
Direction to the Pharmacist (6)
Direction to the patient (7)
Signature (8)
Quinolones and Fluoroquinolones
Introduction and Classification
Essential Metabolite
Quinolones And Fluoroquinolones
o The quinolones (Qs) and fluoroquinolones (FQs) are a family
of broad-spectrum synthetic antimicrobial agents.
o The parent of the group is nalidixic acid, which was introduced

in 1962.
o The fluoroquinolones have a fluoro group attached the central

ring system.
o Qs and FQs are bactericidal drugs.
o FQs enter into the host cells and therefore are active against
intracellular pathogens such as Legionella spp., Mycoplasma
spp. and Chlamydia spp.
Classification
GENERATIONS DRUGS INCLUDED
1st generation Nalidixic acid

Cinoxacin (removed from clinical use)
2nd generation Ciprofloxacin

Enoxacin
Norfloxacin
Ofloxacin
3rd generation Levofloxacin

Grepafloxacin
Sparfloxacin
4th generation Moxifloxacin

Trovafloxacin
MECHANISM OF ACTION
• Quinolones block bacterial DNA synthesis by inhibiting
bacterial topoisomerase II (DNA gyrase) and
topoisomerase IV.
• Inhibition of DNA gyrase prevents the relaxation of
positively supercoiled DNA that is required for normal
transcription and replication.
• Inhibition of topoisomerase IV interferes with separation
of replicated chromosomal DNA into the respective
daughter cells during cell division.
Mechanism of action
Mechanism of action
Gram-negative bacteria Gram-positive bacteria
• primary target is DNA • primary target is

gyrase. topoisomerase IV.
Example Antibacterial Spectrum
Nalidixic acid Gram-negative bacteria: E. coli, Proteus spp,

Klebsiella spp, Shigells spp.
Have no activity against P.aeruginosa
Ciprofloxacin Gram-negative including P.aeruginosa
Gram-positive: only Staphylococcus spp.
Have no activity against Streptococcus
pneumonia.
Atypical bacteria: Legionella spp.
Levofloxacin Gram-negative
Gram-positive. Improved activity against
Streptococcus pneumonia
Atypical bacteria. Improved activity against
Mycoplasma spp., Chlamydia spp.
Moxifloxacin Gram-negative
Gram-positive including Streptococcus pneumonia
Antianaerobic activity
Nalidixic Acid
• Well absorbed from GIT.

• Partly metabolized in liver.
• Poor tissue penetration and low plasma levels.
Cannot be used for the treatment of systemic infections.
 Excreted in urine. High urine concentration.
 Norflxacin is effectives against gram –ve and gram +ve
organisms in treating complicated and uncomplicated
urinary tract infections and prostitis.
• Bacterial gastrointeritis caused by E. coli, Proteus spp,
Klebsiella spp, Shigella spp.
Ciprofloxacin
• The most potent of the
fluoroquinolones for P.
aeruginosa.
• Long post-antibiotic effect.
• Well absorbed from GIT.
• Administration: orally, IV.
• Excreted in urine.
• Potent CYP450 inhibitor

Levofloxacin
• An isomer of Ofloxacin and
has largely replaced it
clinically.
• Very well absorbed from
GIT.
• Administration: orally, iv.
• Excreted unchanged
• Long post-antibiotic effects.
• Long-acting (single daily
dose)
Moxifloxacin
• Long-acting (single daily dose).
• Long post-antibiotic effect.
• Mostly used for the treatment respiratory tract infections
(pneumonia, COPD exacerbation).
• Used for the treatment severe bacterial infections including
sepsis, peritonitis.
• The most potent fluoroquinolones against M. tuberculosis.
• Poor activity against P.aeruginosa.
ADVERSE DRUG REACTIONS
Adverse Effects
Abnormalities of bone
and cartilage formation.
(Cause cartilage damage in
weight bearing joints in
animal studies)
Qs and FQs are contraindicated

in children under 18 and
pregnant women!!!
Adverse Effects
• Photosensitivity
(photodermatitis)
Avoid sun and U.V. radiation

exposure during therapy!!!
Adverse Effects
• Tendonitis/tendon rupture
• CNS: confusion, insomnia,

fatigue, depression,
somnolence, seizures.
• CVS: QT-prolongation.
DRUG INTERACTIONS
DRUG INTERACTIONS
• Ciprofloxacin is a potent CYP450

inhibitor. Increases plasma levels
and toxic effects of anticoagulants,
digoxin, theophylline
CONTRAINDICATIONS
Contraindications
Fluoroquinolones are
contraindicated in patients
with known hypersensitivity
reactions with any member
of fluoroquinolones class of
antimicrobial agents.
Contraindications
• Fluoroquinolones generally should not be

administered to patients younger than 18
years of age.
• Fluoroquinolones should not be
administerd to pregnant or lactating
women.
• Should not be given to arrythmic patient.
TETRACYCLINE AND
CHLORAMPHENICOL
DR.GUNESH KUMAR
TETRACYCLINE
• Tetracyclines are crystalline amphoteric

substances of low solubility.
CLASSIFICATION
• SHORT ACTING (half life: 6 - 8 Hours):
1. Chlortetracycline
2. Tetracycline
3. Oxytetracycline
• INTERMEDIATE ACTING (half life: 12 hours):
1. Demeclocycline
2. Methacycline
• LONG ACTING (half life: 16-18 hours):
1. Doxycycline
2. Minocycline
ANTIMICROBIAL ACTIVITY
• Tetracyclines are broad spectrum,

bacteriostatic antibiotics that inhibit protein
synthesis.
• They are active against many Gram +ve and
Gram –ve bacteria, including Anaerobes,
rickettsiae, Chlamydia, mycoplsmas and
against some protozoa (eg: Amebas).
MECHANISM OF ACTION
• Tetracyclines enter microorganisms in part

by passive diffusion and in part by an
energy-dependent process of active
transport.
• Once inside the cell, tetracyclines bind to
the 30s Subunit of the bacterial ribosome.
RESISTANCE
RESISTANCE
• Three mechanism of resistance to Tetracyclines
have been described:
1. Impaired influx or increased efflux by an
active transport protein pump.
2. Ribosome protection due to production of
proteins that interfere with Tetracycline
binding to the ribosome.
3. Enzymatic inactivation.
PHARMACOKINETICS
• Tetracycline mainly differ in their absorption after

oral administration.
• Chlortetracycline 30%
• Tetracycline 60%
• Oxytetracycline
• Demclocycline
• And methacycline 70%
• Doxycycline and minoxycycline 95 – 100%
• Absorption occurs mainly in the upper small
intestine and is impaired by food.
• Tetracycline are 40-80% bound by plasma
proteins.
• Tetracycline are distributed widely to tissues and
body fluids except for CSF.
• Minoxycycline reaches in very high conc: in tears
and salive which makes it useful for eradication
of the meningococcal carrier state.
• Tetracycline cross the placenta to reach the
fetus and are also excreted in milk.
• As a result of chelation with Calcium,
tetracycline are bound to, and damage growing
bones and teeth.
• Carbamazepine, phenytoin, barbiturates and
chronic alcohol ingestion may shorten the half
life of doxycycline 50% by induction of hepatic
enzymes that metabolize the drug.
• Tetracycline are mainly excreted in bile and
urine.
CLINICAL USES
• Tetracycline is the drug of choice in infections
with mycoplasma pneumoniae, chlamydiae,
rickettsia and some spirochetes.
• They are used in combination regimens to treat
gastric and duodenal ulcer disease caused by H-
pylori.
• In combination with an aminoglycoside,
tetracycline is used in plague, tularemia and
brucellosis.
ADVERSE EFFECTS
• GIT Adverse effects:
• Nausea,
• Vomiting,
• Diarrhea,
• Pruritus,
• Oral and vaginal candidiasis,
• Enterocolitis with shock and death.
•BONY STRUCTURES AND TEETH:
Tetracyclines can be deposited in teeth and bone
of fetus and may cause fluorescence,
discoloration, enamel dysplasia, deformity and
growth inhibition of bone, because of these
changes, tetracyclines are avoided in pregnancy.
Similar changes can occur if drug is given for long
periods to children under 8 years of age.
Liver toxicity,
Renal toxicity,
Local tissue toxicity,
Photosensitization,
Vestibular reactions.
CHLORAMPHENICOL
• Chloramphenicol has a simple and distinctive
structure.
• It is effective orally as well as parenterally and

is widely distributed, readily crossing the
placental and blood brain barriers.
• Most of the drug is inactivated by a Hepatic
Glucoronosyltransferase.
• Chloramphenicol has a wide spectrum of

antimicrobial activity and is usually
bacteriostatic.
• Some strains of Heamophilas influenzae,
nisseria meningitidia and bacteroides are
highly susceptible and for these organisms
chloramphenicol may be bacteriocidal.
MECHANISM OF ACTION
CLINICAL USES
• It is a back up drug for severe infections
caused by salmonella species and for the
treatment of pneumococcal and
meningococcal meningitis in beta-lactam-
sensitive persons.
• It is also used against rickettsiae and
anaerobic infections.
• The drug is mostly used as topical
antimicrobial agent.
ADVERSE EFFECTS
1. GIT DISTURBANCES
2. BONE MARROW TOXICITY
3. GRAY BABY SYNDROME
4. DRUG INTERACTIONS
•BCQS PRACTICE
Q#1 Which of the following tetracycline is
almost completely absorbed when given
orally as well as long acting?
A. Chlortetracycline
B. Demeclocycline
C. Doxycycline
D. Tetracycline
E. oxytetracycline
Q#2: Which of the following should not be
given during pregnancy for they get bound
to calcium & thus they may cause inhibition
of fetal growth?
A. Aminoglycosides
B. Cephalosporins’
C. Macrolides
D. Penicillins
E. Tetracyclines
Q#3: Which of the following best
explain the interaction between
tetracycline & dairy products?
A. Decreased bacterial permeability to drug

B. Decreased drug binding to bact: ribosome
C. Decreased drug bioavailability
D. Increased drug elimination
E. Increase drug toxicity
Q#4: which of the following
tetracycline can be used for
eradication of the meningococcal
carrier state?
A. Demeclocycline
B. Doxycycline
C. Minocycline
D. Tetracycline
E. Oxytetracycline
Q#5: Which antibiotic is commonly
associated with Gray Baby Syndrome?
A. Chloramphenicol
B. Ceftriaxone
C. Gentamycin
D. Tetracycline
E. Neomycin
TETRACYCLINE AND
CHLORAMPHENICOL
DR.GUNESH KUMAR
TETRACYCLINE

CLASSIFICATION
2. Tetracycline
3. Oxytetracycline
1. Demeclocycline
2. Methacycline
1. Doxycycline
2. Minocycline

synthesis.
MECHANISM OF ACTION

transport.
RESISTANCE
RESISTANCE
PHARMACOKINETICS

• Oxytetracycline
• Demclocycline
proteins.
bones and teeth.
urine.
CLINICAL USES
pylori.
brucellosis.
ADVERSE EFFECTS
• Nausea,
• Vomiting,
• Diarrhea,
• Pruritus,
Liver toxicity,
Renal toxicity,
Photosensitization,
CHLORAMPHENICOL
structure.


bacteriostatic.
MECHANISM OF ACTION
CLINICAL USES
sensitive persons.
ADVERSE EFFECTS
1. GIT DISTURBANCES
•BCQS PRACTICE
B. Demeclocycline
C. Doxycycline
D. Tetracycline
E. oxytetracycline
of fetal growth?
A. Aminoglycosides
C. Macrolides
D. Penicillins
E. Tetracyclines

carrier state?
A. Demeclocycline
B. Doxycycline
C. Minocycline
D. Tetracycline
E. Oxytetracycline
A. Chloramphenicol
B. Ceftriaxone
C. Gentamycin
D. Tetracycline
E. Neomycin
TETRACYCLINE AND
CHLORAMPHENICOL
DR.GUNESH KUMAR
TETRACYCLINE

CLASSIFICATION
2. Tetracycline
3. Oxytetracycline
1. Demeclocycline
2. Methacycline
1. Doxycycline
2. Minocycline

synthesis.
MECHANISM OF ACTION

transport.
RESISTANCE
RESISTANCE
PHARMACOKINETICS

• Oxytetracycline
• Demclocycline
proteins.
bones and teeth.
urine.
CLINICAL USES
pylori.
brucellosis.
ADVERSE EFFECTS
• Nausea,
• Vomiting,
• Diarrhea,
• Pruritus,
Liver toxicity,
Renal toxicity,
Photosensitization,
CHLORAMPHENICOL
structure.


bacteriostatic.
MECHANISM OF ACTION
CLINICAL USES
sensitive persons.
ADVERSE EFFECTS
1. GIT DISTURBANCES
•BCQS PRACTICE
B. Demeclocycline
C. Doxycycline
D. Tetracycline
E. oxytetracycline
of fetal growth?
A. Aminoglycosides
C. Macrolides
D. Penicillins
E. Tetracyclines

carrier state?
A. Demeclocycline
B. Doxycycline
C. Minocycline
D. Tetracycline
E. Oxytetracycline
A. Chloramphenicol
B. Ceftriaxone
C. Gentamycin
D. Tetracycline
E. Neomycin
Folic Acid Synthesis Inhibitors
Essential Metabolite
Inhibited by Dihydropteroat
e synthase
SULFONAMIDES
Folic Acid
Synthesis in
Bacteria
Classification:
A. Sulfonamides: c. Topical.
a. Oral absorbable : • Sulfacetamide,
 Short acting • Mafenidic acid,
e.g. sulfisoxazole • silver sulfadiazine.
 Intermediate
e.g. sulfadiazine & B. Diaminopyrimidines:
sulfamethxazole a. Trimethoprim
 Long acting b. Pyrimethamine
e.g. sulfadoxine
b. Oral non-absorbable
e.g. sulfasalazine
Sulfonamides
Gram-negative
Wheel of
Neissseria sppBugs H. influenzae
E. Coli
(coliforms)
Bacteroides spp
Anaerobic
P. aeruginosa
Clostridium spp
S. aureus
Enterococcus spp Streptococcus spp
Gram-positive
Mechanism Of Action of
Sulfonamides
More Specific: Pteridine + PABA
Dihydropteroate
Sulfonamides
Synthetase
Dihydropteroic Acid
Pharmacokinetics of Sulfonamides
All sulfonamides EXCEPT specially designed for their local action in
the bowel (Sulfasalazine) are rapidly absorbed from G.I Tract.
70% to 100% dose is absorbed
Peak plasma levels – 2 – 6 hrs .
 Elimination:
Kidneys – unchanged + metabolic products i.e. good clearance

depends upon renal functions. In acid urine older drugs may
precipitate and form crystals – cause urinary retention.
Therapeutic uses
• Urinary tract infections
• Upper respiratory tract infections
• Nocardiosis
• Sulfasalazine in IBD.
• Sulfacetamide in bacterial conjunctivitis & trachoma
• Silver sulfadiazine for prevention of infection of burn

wounds .
Adverse effects
• Hypersensitivity reactions
• Crystalluria, hematuria, renal obstruction.
• Allergic nephritis
• Haemolytic anaemia, aplastic anaemia,

thrombocytopenia.
• Kernicterus in new born

Diaminopyrimidines
• Trimethoprim
• Pyremethamine
Spectrum:
• Same as that of sulfonamides – but 20 to 100 times more
potent.
Mechanism Of Action of
trimethoprim
Pteridine + PABA
Blocked By
Sulfonamides
Dihydropteroic Acid
glutamate
Dihydrofolic acid
NADPH
Blocked By
NADP
Trimethoprim
Tetrahydrofolic Acid
The Combinations
Sulfamethoxazole + Trimethoprim = Co-
Trimoxazole
The combination is SYNERGISTIC and
the drug becomes Bactericidal.

Mechanism Of Action of Co-
Trimoxazole
Pteridine + PABA
Blocked By
Sulfamethoxazole
Dihydropteroic Acid
glutamate
Dihydrofolic acid
NADPH
Blocked By
NADP
Trimethoprim
Tetrahydrofolic Acid
Synergism
Antibacterial Spectrum of Co-trimoxazole
• Chlamydia diphtheria • Pseudomonas pseudomallei
• N. Meningitidis
• Serratia
• S. Pneumoniae Staphylococcus aureus
• Alcalgenes
• Staphylococcus epidermidis
• Klebsiella species
• S. pyogenes
• E.Coli
• Brucella abortus
• Proteus mirabilis • Pasturella haemolytica
• Proteus morganii • Yersinia pseudotuberculosis

• Proteus rettgeri
• Yersinia enterocolitica
• Enterobacter species
• Nocardia asteriodes
• Salmonella
• Shigella
ADVANTAGES
• Expanded number of organisms inhibited.
• Bactericidal .
• Decreased resistance.
• Decreased toxicity.
Therapeutic uses of Co-Trimoxazole
• Urinary Tract Infections:
• Bacterial Respiratory tract infections:
• Gastrointestinal infections
• Infections by Pneumocystis carinii (an opportunistic infection in
patients with AIDS)

ANTI-TUBERCLOSIS DRUGS
DR. GUNESH KUMAR
LECTURER
DEPARTMENT OF PHARMACOLOGY
WHAT IS TUBERCLOSIS?
 An infectious bacterial disease characterized by the

growth of nodules (tubercles) in the tissues, especially the
lungs.
PATIENT HISTORY
TREATMENT
ANTI –TUBERULOSIS
DRUGS
ISONIAZID
(Isonicotinylhydrazide) (INH)
 Structurally similar to vitamin B6

( pyridoxine).
ANTI-TUBERCLOSIS DRUGS-II
DR. GUNESH KUMAR
LECTURER
DEPARTMENT OF PHARMACOLOGY
ISONIAZID
(Isonicotinylhydrazide) (INH)
 Structurally similar to vitamin B6

( pyridoxine).
RIFAMPIN
 Itis a semisynthetic derivative of rifamycin B
obtained from Streptomyces mediterranei.
 Rifampin is bactericidal to M.tuberculosis and

many other gram positive and gram negative
bacteria like Staph. aureus,E.coli.,
H.influenzae etc.
ADVERSE EFFECTS
PYRAZINAMIDE
ETHAMBUTOL
 Ethambutol (EMB, E) is a medication primarily used
to treat tuberculosis.
 It is usually given in combination with other
tuberculosis medications, such as isoniazid,
rifampicin and pyrazinamide.
 It may also be used to treat Mycobacterium avium
complex, and Mycobacterium kansasii.
STREPTOMYCIN
 Streptomycin is the first aminoglycoside antibiotic
which was isolated from the actinomycetes bacteria
STREPTOMYCES GRISEUS and several related soil
microorganisms.
 Streptomycin was first discovered in 1943 by SELMAN
ABRAHAM WAKESMAN and received a Nobel prize in
1952.
 It was introduced primarily for the treatment of
tuberculosis.
 It is an aminoglycoside.
SITE DURATION OF
TREATMENT
Lymphnode 6 months
Bone & joints 6-9 mpnths
Pleura 6 months
Pericardits 6 months
CNS 12 months
Q: 01 All are following are the first line anti
tubercular drugs except?
 A. RIFAMPIN
 B. RIFABUTIN
 C. INH
 D. PYRAZINAMIDE
 E. ETHAMBUTOL
Q: 02 Which of the following drug is given
against neuropathy developing due to INH?
 A. THIAMINE
 B. NIACIN
 C. PYRIDOXIN
 D. ASCORBIC ACID
Q: 03 Which of the following drug inhibit
mycolic acid synthesis?
 A. ETHAMBUTOL
 B. INH
 C. PYRAZINAMIDE
 D. RIFAMPIN
Q: 04 Which of the following ATT drug
cause red green color blindness?
 A. ETHAMBULTO
 B. STREPTOMYCIN
 C. PYRAZINAMIDE
 D. INH

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ABBREVIATIONS

DR. GUNESH KUMAR

◼ 1 tea spoon full = 5 ml

• THE DRUGS MAY BE ABSORBED IF ULCERATION IS PRESENT.

• DECREASED PERMEATION OF AMINOGLYCOSIDES

• DEPENDENT ON TOTAL AMOUNT OF DRUG AND

✓ONLY GENTAMICIN IS LISTED IN CATEGORY C.

A. ALTERATION OF BACTERIAL CELL MEMBRANE

A. ANAEROBES HAVE NO BINDING SITES FOR THESE DRUG

DR. GUNESH KUMAR

Bioavailability is rate and extent to

 When a drug is absorbed from the GIT after

If two similar drugs have the same

If two similar drugs perform the same

 The time required for the amount of

 In pharmacokinetics, the condition in which

• Parent drugs OR their Phase- I metabolites that contain suitable

 Activity of the enzyme is very low in new born infant.

 Drug chloramphenicol (antibiotic) in new born infant

Fluid compartments in the body

VOLUME OF SOME DRUGS

4g/100ml 40 - 100mg/100ml Very little

❑ Plasma protein binding

❑ Tissue distribution (binding)

affecting distribution of each drug

(b) lipid solubility

(c) Molecular size of drug

(b) Lipid solubility

(c) Molecular size of drug

Non-polar drug Non-polar drug

Polar metabolite Polar metabolite

Other than plasma protein

Dr. GUNESH KUMAR

irreversibly transferred from internal to external

environment through renal or non renal route.

B. NON RENAL EXCRETION

GLOMERULAR FILTRATION RATE:

10% or 120 to 130ml/min is bound to plasma proteins.

filtered through glomeruli. c) Driving force for GF is

b) The rate being called as hydrostatic pressure of blood

glomerular filtration rate. flowing in capillaries.

▪Most substances are reabsorbed across renal tubular

▪It occurs after the glomerular filtration of drugs.

▪Reabsorption results in increase in the half life of the

▪ Greater the polarity better the excretion.

▪ Water soluble and ionized form of weakly acidic

▪ Drugs excreted in GIT are reabsorbed into

➢ Gaseous and volatile substances such as general

➢ Intact gaseous drugs are excreted but not metabolites.

• First Order Kinetics

DR. GUNESH KUMAR

The route of administration (ROA), that is

The ROA is determined by the physical

Injection Topical Respiratory Rectal Oral S/L

Absorption through the

Any medication taken by mouth and

 Drug may have unpleasant taste.

 May cause irritation of gastro intestinal tract.

 Drug may discolor teeth.

 Drug can be aspirated by ill client.

 Sometimes inefficient - only part of the drug

First-pass effect - drugs absorbed orally