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PHARMACODYNAMICS
• In Greek

Pharmacon = Drug
Dynamics = Action/Power
It covers all the aspects relating to
“What a drug does to the body”
Mechanism of action
• Action: How and Where the
effect is produced is called as
Action.
• Effect: The type of response
producing by drug.
Site of Drug Action
• Where:

1. Extra cellular
2. Cellular
3. Intracellular
Types of Drug Action
EFFECT (Type of responses):-

1.Stimulation
2.Inhibition/Depression
3.Replacement
4.Irritation
5.Cytotoxic
Mechanism of Action of Drugs
• Drug act either by receptor or by non
receptor or by targeting specific genetic
changes.
Majority of drugs acts by (HOW)

Receptor mediated

Non receptor mediated
Receptor Mediated action
• Drug produce their effect through interacting
with some chemical compartment of living
organism c/s Receptor.
• Receptors are macromolecules
• Most are proteins
• Present either on the cell surface, cytoplasm or
in the nucleus
Ligand binding
domain

Transduction of
signal into response

Receptor Functions : Two essential functions
• 1. Recognization of specific ligand molecule
(Ligand binding domain)
• 2. Transduction of signal into response (Effector
domain)
Drug(D) +Receptor®

Drug receptor complex

Response

Drug receptor interaction:1. Selectivity:- Degree of complimentary co relation
between drug and receptor.
Ex:- Adrenaline Selectivity for α, ß Receptor

2. Affinity:- Ability of drug to get bound to the
receptor.
3. Intrinsic activity (IA) or Efficacy:- Ability of drug
to produce a pharmacological response after
making the drug receptor complex.
Drug classification
(on the basis of affinity & efficacy)
Response

No response
• Partial agonist :These drug have full affinity to
receptor but with low intrinsic activity (IA=0 to 1).
• These are only partly as effective as agonist

(Affinity is lesser when comparison to agonist)

Ex: Pindolol, Pentazocine
• Inverse agonist: These have full affinity
towards the receptor but intrinsic activity is
zero to -1 i.e., produces effect is just
opposite to that of agonist.

Ex:- ß-Carboline is inverse agonist for
Benzodiazepines receptors.
Receptor families
Four types of receptors families
1. Ligand-gated ion channels (inotropic
receptors)
2.G-protien coupled receptor (Metabotropic
receptors)
3. Enzymatic receptors (tyrosinekinase)
4.Receptor regulating gene expression
(transcription factors/ Steroid )
Characteristics of receptor families
Ligand
gated

G-protein
coupled

Enzymatic Nuclear

Location

Membrane

Membrane

Membrane

Intracellular

Effector

Ion channel

Ion Channel
or enzyme

Enzyme

Gene

coupling Direct

G-protein

Direct

Via DNA

Example Nicotinic

Muscarinic Insulin

Steroid ,
hormone
Signal transduction mechanism
• Ion gated receptors:- Localized on cell
membrane and coupled directly to an ion
Io
channel.
n
Blocker
Agonist
Receptor

Receptor
Na+2
Hyper polarization or
depolarization

Permeation of
ion is blocked

No cellular effect
Cellular effect
• Ex: Nicotinic cholinergic receptor
G-protein coupled receptors
• Membrane bound, which are coupled to
effector system through GTP binding
proteins called as G-proteins

Bound to inner
face of plasma
membrane (2nd
messenger)
Varieties of G-protein
G-protein

Gs

Receptor for

Gi1,2,3

ß adrenegic,
H,5HT,Glucagon
α2 adrenergic, Ach,

Gq

Ach

Go

Neurotransmitters
in brain

Signaling pathway/
Effector
AC— cAMP
AC— cAMP,
Open K+
Phospholipase-C,
IP3’cytoplasmic Ca+2
Not yet clear
G-protein effector systems
• 1.Adenylase cyclase : cAMP system
• 2.Phospholipase –C: Inositol phosphate system
• 3. Ion channels
cAMP system
Phospholipase-C system
Ion channel regulation
• G-protein coupled receptors can control
the functioning of ion channel by don't
involving any second messenger
• Ex:- In cardiac muscle
Enzymatic receptors
• These receptor are directly linked tyrosine
kinase.
• Receptor binding domain present in extra
cellular site.
• Produce conformational changes in intra
cellular
Ex:- Insulin receptors
Enzymatic receptors
Extra cellular receptor
binding domain

Intra cellular
changes
Receptor regulating gene expression

(transcription factors)
Increase RNA
polymerase activity

Unfolds the receptor and
expose normally
masked DNA binding
site
Receptor regulation theory

• Receptors are in dynamic state.

• The affinity of the response to drugs is not fixed.
It alters according to situation.
• Receptor down regulation:
Prolonged use of agonist
Receptor number and sensitivity
Drug effect
Ex: Chronic use of salbutamol down regulates ß2 adrenergic receptors.
• Receptor up regulation:
Prolonged use of antagonist
Receptor number and sensitivity
Drug effect
• Ex:- propranolol is stopped after prolong
use, produce withdrawal symptoms. Rise
BP, induce of angina.
Agonist: Both the high affinity as well as
intrinsic activity (IA=1)
These drug trigger the maximal biological response or
mimic effect of the endogenous substance.

Ex:- Methacholine is a cholinomimetic drug which
mimics the effect of Ach on cholinergic receptors.
Types of agonism
• Summation :- Two drugs eliciting same
response, but with different mechanism and their
combined effect is equal to their summation.
(1+1=2)
Aspirin

Codiene

PG

Opiods receptor

Analgesic+

Analgesic+

++
Types of agonism
• Additive: combined effect of two drugs acting by
same mechanism
Aspirin
PG

PG

Analgesic+

Analgesic+

++
• Synergism (Supra additive):-

(1+1=3)

The combined effect of two drug effect is
higher than either individual effect.
Ex:1.Sulfamethaxazole+ Trimethoprim
2. Levodopa + Carbidopa.
Types of antagonism
Antagonism: Effect of two drugs is less than sum
of the effects of the individual drugs.

1. Chemical antagonism
Ex: -heparin(-ve) protamine +ve, Chelating agents

1. Physiological /Functional antagonism
2. Pharmacokinetic antagonism
3. Pharmacological antagonism
I. Competitive ( Reversible)
II. Non competitive (Irreversible)
Pharmacokinetic antagonism
• One drug affects the absorption,
metabolism or excretion of other drug and
reduce their effect.

Ex:-Warfarin in presence of phenobarbitone,
warfarin metabolism is increased, it effect
is reduced.
Pharmacological antagonism
• Pharmacodynamic antagonism between two
drugs acting at same receptors.
• Two important mechanism according to which
these antagonists

»1.Reversible(Competitive)
»2.Irreversible(Non)
Reversible antagonism
(Competitive antagonism)
• These inhibition is commonly observed
with antagonists that bind reversibly to the
same receptor site as that of an agonist.

• These type inhibition can be overcome
increasing the concentration of agonist
• Ex:- Atropine is a competitive antagonist of
Ach.
Irreversible Antagonism
• It occurs when the antagonist dissociates
very slow or not at all from the receptors
result that no change when the agonist
applied.
• Antagonist effect cannot be overcome
even after increasing the concentration of
agonist
Non receptor mediated action
• All drugs action are not mediated by receptors.
Some of drugs may act through chemical action
or physical action or other modes.
»Chemical action
»Physical action (Astringents, sucralfate)
»False incorporation (PABA)
»Being protoplasmic action (antiseptics)
»Formation of antibody (Vaccines)
»Targeting specific genetic changes.
Dose
• It is the required amount of drug in
weight, volumes, moles or IU to provide a
desired effect.
• In clinical it is called as Therapeutic dose
• In experimental purpose it is called as effective
dose.

• The therapeutic dose varies from person to
person
Single dose:
1.Piperazine (4-5g) is sufficient to eradicate round
worm.
2.Single IM dose of 250mg of ceftriaxone to treat
gonorrhoea.
Daily dose:
It is the quantity of a drug to be administered in
24hr, all at once or equally divided dose.
1.10mg of cetrizine (all at once) is sufficient to
relive allergic reactions.
2.Erythromycin is 1g per day to be given in 4
equally divided dose (i.e., 250mg every 6 hr)
• Total dose: It is the maximum quantity of the
drug that is needed the complete course of the
therapy.
Ex:- procaine penicillin early syphilis is 6 million unit 
given as 0.6 million units per day for 10days.

Loading dose:- It is the large dose of drug to be
given initially to provide the effective plasma
concentration rapidly. The drugs having high Vd
of distribution.
Chloroquine in Malaria – 600 mg Stat
300mg after 8 hours
300 mg after 2 days.
Maintenance dose:- Loading dose normally
followed by maintenance dose.
• Needed to maintain the steady state
plasma concentration attained after giving
the loading dose.
Therapeutic index:
• Margin of safety
• Depend upon factor of dose producing
desirable effect  dose eliciting toxic
effect.
Therapeutic index

LD 50
ED 50

• TI should be more than one
Therapeutic window:
Optimal therapeutic range of plasma
concentrations at which most o the patients
experience the desired effect.
Therapeutic range Therapeutic window

Sub
optimal

optimal
Toxic
•
•
•
•
•
•

Cyclosporine – 100-400ng/ml
Carbamazapine- 4-10µg/ml
Digoxin- 0.8-2ng/ml
Lithium- 0.8-1.4 mEq/L
Phenotoin – 10-20µg/ml
Qunindine- 2-6µg/ml
• Tolerance: Increased amount of drug
required to produce initial pharmacological
response.
• Usually seen with alcohol, morphine,
barbiturates, CNS active drugs
• Reverse tolerance:- Same amount drug
produces inc pharmacological response.
• Cocaine, amphetamine  rats- inc. motor
activity
Types of tolerances
• Innate tolerance: Genetically lack of
sensitivity to a drug.
Ex:
• Rabbits tolerate to atropine large doses
• Chinese Castor oil
• Negros  Mydriatic action of sympathomimetics
• Eskimos high fatty diets
• Acquired tolerances:
• Occurs due to repeated use of drug
– Pharmacokinetic tolerances
– Pharmacodynamic tolerance
– Acute tolerance

Pharmacokinetic tolerances:- Repetitive
administration causes decrease their
absorption or inc. its own metabolism
Ex: Alcohol  dec. absorption
Barbiturates Inc. own metabolism
• Pharmacodynamic tolerance
• Down regulation of receptors

• Impairment in signal transduction
• Ex: Morphine, caffeine, nicotine.

• Acute tolerance: Tachyphylaxis Acute
development of tolerance after a rapid and
repeated administration of a drug in shorter
intervals
• Ex; Ephedrine, tyramine
• Ex: Monday disease.
• Nitroglycerine – Monday , Tuesday
workers get headache, after they get
tolerances.
• After holiday (Sunday) they get again
headache .
• Cross tolerances: Cross tolerance among
drugs belonging to same category.
• MORPHINHEROIN NARCOTIC
FACTORS MODIFYING THE
EFFECTS OF DRUGS


Individuals differ both in the degree and the
character of the response that a drug may elicit



Variation in response to the same dose of a drug
between different patients and even in the same
patient on different occasions.


Differences among individuals are responsible for

the variations in drug response:


Individuals differ in pharmacokinetic handling of drugs



Variation in number or state of receptors, coupling
proteins or other components of response



Variation in neurogenic/ hormonal tone or
concentrations of specific constituents


These factors modify drug action either:
a)

Quantitatively


The plasma concentration and / or the drug action is
increased or decreased

b)

Qualitatively


The type of response is altered, eg: drug allergy and
idiosyncrasy

1.

The various factors are:
Body weight/size:


It influences the concentration of drug attained at the
site of action



The average adult dose refers to individuals of
medium built
•

For exceptionally obese or lean individuals and for children
dose may be calculated on body weight basis

Individual dose

Individual dose



BW (kg)
x Average adult dose
70

BSA (m2)
x Average adult dose
1.7

BSA=BW(Kg)0.425 x Height(cm)0.725 x 0.007184
2.

Age:

Infants and Children:


The dose of drug for children often calculated from the adult
dose

Age
Child dose
x adult dose .........( Young' s formula)
Age 12

Child dose

Age
x adult dose......
...(Dilling' s formula)
20


However, infants and children are have important
physiological differences



Higher proportion of water



Lower plasma protein levels




More available drug

Immature liver/kidneys


Liver often metabolizes more slowly



Kidneys may excrete more slowly
Elders:


In elderly, renal function progressively declines (intact

nephron loss) and drug doses have to be reduced


Chronic disease states



Decreased plasma protein binding



Slower metabolism



Slower excretion



Dietary deficiencies



Use of multiple medications



Lack of compliance
3.

Sex:



Females have smaller body size, and so require
doses of drugs on the lower side of the dose
range



They should not be given uterine stimulants
during menstruation, quinine during pregnancy

and sedatives during lactation
4.

Pregnancy:



Profound physiological changes which may affect
drug responses:


GI motility reduced –delayed absorption of orally
administered drugs



Plasma and ECF volume expands



Albumin level falls



Renal blood flow increases markedly



Hepatic microsomal enzyme induction
5.

Food:



Delays gastric emptying, delays absorption (ampicillin)



Calcium in milk –interferes with absorption of
tetracyclines and iron by chelation



Protein malnutrition


Loss of BW



Reduced hepatic metabolizing capacity



Hypoproteinemia
6.

Species and race:



Rabbits resistant to atropine



Rat & mice are resistant to digitalis



In humans: blacks require higher Mongols require
lower concentrations of atropine and ephedrine to
dilate their pupil
7.

Route of drug administration:



I.V route dose smaller than oral route



Magnesium sulfate:


Orally –purgative



Parenterally –sedative



Locally –reduces inflammation
8.

Biorhythm: (Chronopharmacolgy)



Hypnotics –taken at night



Corticosteroid –taken at a single morning dose

9.

Psychological state:



Efficacy of drugs can be effected by patients
beliefs, attitudes and expectations



Particularly applicable to centrally acting drugs



In some patients inert drugs (placebo) may

produce beneficial effects equivalent to the drug,
and may induce sleep in insomnia
10.

Presence of diseases/pathological states:



Drug may aggravate underlying pathology



Hepatic disease may slow drug metabolism



Renal disease may slow drug elimination



Acid/base abnormalities may change drug absorption
or elimination



Severe shock with vasoconstriction delays absorption
of drugs from s.c. or i.m



Drug metabolism in:


Hyperthyroidism –enhanced



Hypothyroidism -diminished
11.

Cumulation:



Any drug will cumulate in the body if rate of

administration is more than the rate of elimination


Eg: digitalis, heavy metals etc.
12.

Genetic factors:



Lack of specific enzymes



Lower metabolic rate


Acetylation



Plasma cholinesterase (Atypical pseudo cholinesterase)



G-6PD



Glucuronide conjugation
13.

Tolerance:



It means requirement of a higher dose of the drug
to produce an effect, which is ordinarily produced

by normal therapeutic dose of the drug


Drug tolerance may be:


Natural



Acquired



Cross tolerance



Tachyphylaxis (ephedrine, tyramine, nicotine)



Drug resistance
14.


Other drugs:

By interactions in many ways
Pharmacodynamics
Drug classification

(on the basis of affinity & efficacy)

Agonist: Both the high affinity as well as
intrinsic activity (IA=1)
These drug trigger the maximal biological response or
mimic effect of the endogenous substance.

Ex:- Methacholine is a cholinomimetic drug which
mimics the effect of Ach on cholinergic receptors.
• Antagonist:- Which have only the affinity
no intrinsic activity (IA=0). IA=0 so no
pharmacological activity.
• Rather these drug bind to the receptor
and produce receptor blockade.
• Atropine blocks the effects of Ach on the
cholinergic muscarinic receptors.
cAMP system
Some drugs, hormones or neurotransmitters
produce their effect by increasing or
decreasing the activity of adenylate cyclase
and thus raising or lower cAMP with in the
cell.
Stimulation
• Some of drug act by increasing the activity
of specialized cells.
Ex: Catecholamines stimulate the heart and
Heart rate, Force of contraction
Inhibition
• Some drug act by decreasing the activity of
specialized cells.
Ex: Alcohol, Barbiturates, General anesthetic
these drug depress the CNS system.
Atropine inhibits Ach action.
Replacement
• When there is a deficiency of endogenous
substances, they can replaced by drugs.
Ex: Insulin in Diabetes mellitus
Throxine in cretinism and myxedema
Irritation
• Certain drugs on topical application cause
irritation of the skin and adjacent tissues.
• These drugs are using for counter irritant.
Ex: Eucalyptus oil, methyl salicylates (Used
in sprains, joint pain, myalgia.
Cytotoxic
• Treatment of infectious disease/cancer
with drugs that are selectively toxic for
infecting organism/cancer cells

Ex: Anticancer drugs
All Antibiotics
Phospholipase-C system
Activation

Hydrolysis

Agonist
Gq

PIP2

PLC

Hydrolysis

DAG

Water soluble
release

PKC

IP3
ATP
S

Cam

E

ADP
Product

Ca+2

Cam E*
Response

PLC= Phospholipase-C
PIP2 =Phosphotiydl inositol 4,5 di phosphate
IP3 =Inositol tri phosphate DAG = Diacylglycerol
E= Ezyme
PKC = Phosphokinase -C
Extra cellular site of action
1.Antacids neutralizing gastric acidity.
2.Chelating agents forming complexes
with heavy metals.
3.MgSo4 acting as purgative by
retaining the fluid inside the lumen of
intestine.
Cellular Site of Action
1.Ach on Nicotinic receptors of motor end
plate, leading to contraction of skeletal
muscle.
2.Effect of sympathomimetics on
muscle and blood vessels.

heart
Intracellular site of action
-Folic acid synthesis inhibitors.
Folic acid which is intracellular component
essential for synthesis of proteins.

Trimethoprim and sulfa drug interfere with
synthesis.
Gs/Gi
G protein

Effector

or

AC

+

cAMP

ATP
Phosphorylation

Ca+2 release

Protein kinase Active

FC of heart muscle

Lipolysis

Glycogen
synthesis

Glycogen breakdown
to glucose
Physical action
• Absorption: Kaolin absorbs bacterilal toxin
and thus acts as antidiarrhoeal agent.
• Protectives:- Various dusting powders.
• Antagonist:- Which have only the affinity
no intrinsic activity (IA=0). IA=0 so no
pharmacological activity.
• Rather these drug bind to the receptor
and produce receptor blockade.
• Atropine blocks the effects of Ach on the
cholinergic muscarinic receptors.
Physical Action
• Osmosis:- MgSo4 acts as a purgative by
exerting osmatic effect within lumen of the
intestine.
• Astringents:- They precipitate the surface
proteins and protect the mucosa Ex: tannic
acid in gum patients
• Demulcent:- These drugs coat the
inflamed mucus membrane and provide
soothing effect. Ex: Menthol
False incorporation
• Bacteria synthesis folic acid from PABA
(Para Amino Benzoic Acid), for growth
sand development.

• Sulfa drugs resemble PABA, therefore
falsely enter into the synthesis process of
PABA, cause nonfunctional production
and no utility for bacterial growth.
Protoplasmic poison
• Germicides and antiseptics like phenol
and formaldehyde act as non specifically
as protoplasmic poison causing the death
of bacteria
Through formation of antibodies
• Vaccines produce their effect by inducing
the formation of antibodies and thus
stimulate the defense mechanism of the
body
• Ex:- Vaccines against small pox and
cholera
Targeting specific genetic changes.
• Anti cancer drugs that specifically target
genetic changes.
• Inhibitors of specific tyrosine kinase that
that block the activity of oncogenic
kinases.
Physiological antagonism
• Two antagonists, acting at different sites,
counter balance each other by producing
opp. effect on same physiological system.

• Histamine –Vasodilatation
• Nor epinephrine – Vasoconstriction
Chemical action
1.Ion Exchanges:-Anticoagulant effect of
heparin(-ve charge) antagonized by
protamine (+ve charged) protein.

2.Neutralization:- Excessive gastric acid is
neutralized by antacids.
3. Chelation:-These are trap the heavy
metals. Ex:-EDTA, BAL.

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Pharmacodynamics

  • 2. • In Greek Pharmacon = Drug Dynamics = Action/Power It covers all the aspects relating to “What a drug does to the body” Mechanism of action
  • 3. • Action: How and Where the effect is produced is called as Action. • Effect: The type of response producing by drug.
  • 4. Site of Drug Action • Where: 1. Extra cellular 2. Cellular 3. Intracellular
  • 5. Types of Drug Action EFFECT (Type of responses):- 1.Stimulation 2.Inhibition/Depression 3.Replacement 4.Irritation 5.Cytotoxic
  • 6. Mechanism of Action of Drugs • Drug act either by receptor or by non receptor or by targeting specific genetic changes. Majority of drugs acts by (HOW) Receptor mediated Non receptor mediated
  • 7. Receptor Mediated action • Drug produce their effect through interacting with some chemical compartment of living organism c/s Receptor. • Receptors are macromolecules • Most are proteins • Present either on the cell surface, cytoplasm or in the nucleus
  • 8. Ligand binding domain Transduction of signal into response Receptor Functions : Two essential functions • 1. Recognization of specific ligand molecule (Ligand binding domain) • 2. Transduction of signal into response (Effector domain)
  • 9. Drug(D) +Receptor® Drug receptor complex Response Drug receptor interaction:1. Selectivity:- Degree of complimentary co relation between drug and receptor. Ex:- Adrenaline Selectivity for α, ß Receptor 2. Affinity:- Ability of drug to get bound to the receptor. 3. Intrinsic activity (IA) or Efficacy:- Ability of drug to produce a pharmacological response after making the drug receptor complex.
  • 10. Drug classification (on the basis of affinity & efficacy)
  • 12. • Partial agonist :These drug have full affinity to receptor but with low intrinsic activity (IA=0 to 1). • These are only partly as effective as agonist (Affinity is lesser when comparison to agonist) Ex: Pindolol, Pentazocine
  • 13. • Inverse agonist: These have full affinity towards the receptor but intrinsic activity is zero to -1 i.e., produces effect is just opposite to that of agonist. Ex:- ß-Carboline is inverse agonist for Benzodiazepines receptors.
  • 14. Receptor families Four types of receptors families 1. Ligand-gated ion channels (inotropic receptors) 2.G-protien coupled receptor (Metabotropic receptors) 3. Enzymatic receptors (tyrosinekinase) 4.Receptor regulating gene expression (transcription factors/ Steroid )
  • 15. Characteristics of receptor families Ligand gated G-protein coupled Enzymatic Nuclear Location Membrane Membrane Membrane Intracellular Effector Ion channel Ion Channel or enzyme Enzyme Gene coupling Direct G-protein Direct Via DNA Example Nicotinic Muscarinic Insulin Steroid , hormone
  • 16. Signal transduction mechanism • Ion gated receptors:- Localized on cell membrane and coupled directly to an ion Io channel. n Blocker Agonist Receptor Receptor Na+2 Hyper polarization or depolarization Permeation of ion is blocked No cellular effect Cellular effect
  • 17. • Ex: Nicotinic cholinergic receptor
  • 18. G-protein coupled receptors • Membrane bound, which are coupled to effector system through GTP binding proteins called as G-proteins Bound to inner face of plasma membrane (2nd messenger)
  • 19. Varieties of G-protein G-protein Gs Receptor for Gi1,2,3 ß adrenegic, H,5HT,Glucagon α2 adrenergic, Ach, Gq Ach Go Neurotransmitters in brain Signaling pathway/ Effector AC— cAMP AC— cAMP, Open K+ Phospholipase-C, IP3’cytoplasmic Ca+2 Not yet clear
  • 20. G-protein effector systems • 1.Adenylase cyclase : cAMP system • 2.Phospholipase –C: Inositol phosphate system • 3. Ion channels
  • 23. Ion channel regulation • G-protein coupled receptors can control the functioning of ion channel by don't involving any second messenger • Ex:- In cardiac muscle
  • 24. Enzymatic receptors • These receptor are directly linked tyrosine kinase. • Receptor binding domain present in extra cellular site. • Produce conformational changes in intra cellular Ex:- Insulin receptors
  • 25. Enzymatic receptors Extra cellular receptor binding domain Intra cellular changes
  • 26. Receptor regulating gene expression (transcription factors) Increase RNA polymerase activity Unfolds the receptor and expose normally masked DNA binding site
  • 27. Receptor regulation theory • Receptors are in dynamic state. • The affinity of the response to drugs is not fixed. It alters according to situation. • Receptor down regulation: Prolonged use of agonist Receptor number and sensitivity Drug effect Ex: Chronic use of salbutamol down regulates ß2 adrenergic receptors.
  • 28. • Receptor up regulation: Prolonged use of antagonist Receptor number and sensitivity Drug effect • Ex:- propranolol is stopped after prolong use, produce withdrawal symptoms. Rise BP, induce of angina.
  • 29. Agonist: Both the high affinity as well as intrinsic activity (IA=1) These drug trigger the maximal biological response or mimic effect of the endogenous substance. Ex:- Methacholine is a cholinomimetic drug which mimics the effect of Ach on cholinergic receptors.
  • 30. Types of agonism • Summation :- Two drugs eliciting same response, but with different mechanism and their combined effect is equal to their summation. (1+1=2) Aspirin Codiene PG Opiods receptor Analgesic+ Analgesic+ ++
  • 31. Types of agonism • Additive: combined effect of two drugs acting by same mechanism Aspirin PG PG Analgesic+ Analgesic+ ++
  • 32. • Synergism (Supra additive):- (1+1=3) The combined effect of two drug effect is higher than either individual effect. Ex:1.Sulfamethaxazole+ Trimethoprim 2. Levodopa + Carbidopa.
  • 33. Types of antagonism Antagonism: Effect of two drugs is less than sum of the effects of the individual drugs. 1. Chemical antagonism Ex: -heparin(-ve) protamine +ve, Chelating agents 1. Physiological /Functional antagonism 2. Pharmacokinetic antagonism 3. Pharmacological antagonism I. Competitive ( Reversible) II. Non competitive (Irreversible)
  • 34. Pharmacokinetic antagonism • One drug affects the absorption, metabolism or excretion of other drug and reduce their effect. Ex:-Warfarin in presence of phenobarbitone, warfarin metabolism is increased, it effect is reduced.
  • 35. Pharmacological antagonism • Pharmacodynamic antagonism between two drugs acting at same receptors. • Two important mechanism according to which these antagonists »1.Reversible(Competitive) »2.Irreversible(Non)
  • 36. Reversible antagonism (Competitive antagonism) • These inhibition is commonly observed with antagonists that bind reversibly to the same receptor site as that of an agonist. • These type inhibition can be overcome increasing the concentration of agonist • Ex:- Atropine is a competitive antagonist of Ach.
  • 37. Irreversible Antagonism • It occurs when the antagonist dissociates very slow or not at all from the receptors result that no change when the agonist applied. • Antagonist effect cannot be overcome even after increasing the concentration of agonist
  • 38. Non receptor mediated action • All drugs action are not mediated by receptors. Some of drugs may act through chemical action or physical action or other modes. »Chemical action »Physical action (Astringents, sucralfate) »False incorporation (PABA) »Being protoplasmic action (antiseptics) »Formation of antibody (Vaccines) »Targeting specific genetic changes.
  • 39. Dose • It is the required amount of drug in weight, volumes, moles or IU to provide a desired effect. • In clinical it is called as Therapeutic dose • In experimental purpose it is called as effective dose. • The therapeutic dose varies from person to person
  • 40. Single dose: 1.Piperazine (4-5g) is sufficient to eradicate round worm. 2.Single IM dose of 250mg of ceftriaxone to treat gonorrhoea. Daily dose: It is the quantity of a drug to be administered in 24hr, all at once or equally divided dose. 1.10mg of cetrizine (all at once) is sufficient to relive allergic reactions. 2.Erythromycin is 1g per day to be given in 4 equally divided dose (i.e., 250mg every 6 hr)
  • 41. • Total dose: It is the maximum quantity of the drug that is needed the complete course of the therapy. Ex:- procaine penicillin early syphilis is 6 million unit  given as 0.6 million units per day for 10days. Loading dose:- It is the large dose of drug to be given initially to provide the effective plasma concentration rapidly. The drugs having high Vd of distribution. Chloroquine in Malaria – 600 mg Stat 300mg after 8 hours 300 mg after 2 days.
  • 42. Maintenance dose:- Loading dose normally followed by maintenance dose. • Needed to maintain the steady state plasma concentration attained after giving the loading dose.
  • 43. Therapeutic index: • Margin of safety • Depend upon factor of dose producing desirable effect  dose eliciting toxic effect. Therapeutic index LD 50 ED 50 • TI should be more than one
  • 44. Therapeutic window: Optimal therapeutic range of plasma concentrations at which most o the patients experience the desired effect. Therapeutic range Therapeutic window Sub optimal optimal Toxic
  • 45. • • • • • • Cyclosporine – 100-400ng/ml Carbamazapine- 4-10µg/ml Digoxin- 0.8-2ng/ml Lithium- 0.8-1.4 mEq/L Phenotoin – 10-20µg/ml Qunindine- 2-6µg/ml
  • 46. • Tolerance: Increased amount of drug required to produce initial pharmacological response. • Usually seen with alcohol, morphine, barbiturates, CNS active drugs • Reverse tolerance:- Same amount drug produces inc pharmacological response. • Cocaine, amphetamine  rats- inc. motor activity
  • 47. Types of tolerances • Innate tolerance: Genetically lack of sensitivity to a drug. Ex: • Rabbits tolerate to atropine large doses • Chinese Castor oil • Negros  Mydriatic action of sympathomimetics • Eskimos high fatty diets
  • 48. • Acquired tolerances: • Occurs due to repeated use of drug – Pharmacokinetic tolerances – Pharmacodynamic tolerance – Acute tolerance Pharmacokinetic tolerances:- Repetitive administration causes decrease their absorption or inc. its own metabolism Ex: Alcohol  dec. absorption Barbiturates Inc. own metabolism
  • 49. • Pharmacodynamic tolerance • Down regulation of receptors • Impairment in signal transduction • Ex: Morphine, caffeine, nicotine. • Acute tolerance: Tachyphylaxis Acute development of tolerance after a rapid and repeated administration of a drug in shorter intervals • Ex; Ephedrine, tyramine
  • 50. • Ex: Monday disease. • Nitroglycerine – Monday , Tuesday workers get headache, after they get tolerances. • After holiday (Sunday) they get again headache . • Cross tolerances: Cross tolerance among drugs belonging to same category. • MORPHINHEROIN NARCOTIC
  • 52.  Individuals differ both in the degree and the character of the response that a drug may elicit  Variation in response to the same dose of a drug between different patients and even in the same patient on different occasions.
  • 53.  Differences among individuals are responsible for the variations in drug response:  Individuals differ in pharmacokinetic handling of drugs  Variation in number or state of receptors, coupling proteins or other components of response  Variation in neurogenic/ hormonal tone or concentrations of specific constituents
  • 54.  These factors modify drug action either: a) Quantitatively  The plasma concentration and / or the drug action is increased or decreased b) Qualitatively  The type of response is altered, eg: drug allergy and idiosyncrasy
  • 55.  1. The various factors are: Body weight/size:  It influences the concentration of drug attained at the site of action  The average adult dose refers to individuals of medium built
  • 56. • For exceptionally obese or lean individuals and for children dose may be calculated on body weight basis Individual dose Individual dose  BW (kg) x Average adult dose 70 BSA (m2) x Average adult dose 1.7 BSA=BW(Kg)0.425 x Height(cm)0.725 x 0.007184
  • 57. 2. Age: Infants and Children:  The dose of drug for children often calculated from the adult dose Age Child dose x adult dose .........( Young' s formula) Age 12 Child dose Age x adult dose...... ...(Dilling' s formula) 20
  • 58.  However, infants and children are have important physiological differences  Higher proportion of water  Lower plasma protein levels   More available drug Immature liver/kidneys  Liver often metabolizes more slowly  Kidneys may excrete more slowly
  • 59. Elders:  In elderly, renal function progressively declines (intact nephron loss) and drug doses have to be reduced  Chronic disease states  Decreased plasma protein binding  Slower metabolism  Slower excretion  Dietary deficiencies  Use of multiple medications  Lack of compliance
  • 60. 3. Sex:  Females have smaller body size, and so require doses of drugs on the lower side of the dose range  They should not be given uterine stimulants during menstruation, quinine during pregnancy and sedatives during lactation
  • 61. 4. Pregnancy:  Profound physiological changes which may affect drug responses:  GI motility reduced –delayed absorption of orally administered drugs  Plasma and ECF volume expands  Albumin level falls  Renal blood flow increases markedly  Hepatic microsomal enzyme induction
  • 62. 5. Food:  Delays gastric emptying, delays absorption (ampicillin)  Calcium in milk –interferes with absorption of tetracyclines and iron by chelation  Protein malnutrition  Loss of BW  Reduced hepatic metabolizing capacity  Hypoproteinemia
  • 63. 6. Species and race:  Rabbits resistant to atropine  Rat & mice are resistant to digitalis  In humans: blacks require higher Mongols require lower concentrations of atropine and ephedrine to dilate their pupil
  • 64. 7. Route of drug administration:  I.V route dose smaller than oral route  Magnesium sulfate:  Orally –purgative  Parenterally –sedative  Locally –reduces inflammation
  • 65. 8. Biorhythm: (Chronopharmacolgy)  Hypnotics –taken at night  Corticosteroid –taken at a single morning dose 9. Psychological state:  Efficacy of drugs can be effected by patients beliefs, attitudes and expectations  Particularly applicable to centrally acting drugs  In some patients inert drugs (placebo) may produce beneficial effects equivalent to the drug, and may induce sleep in insomnia
  • 66. 10. Presence of diseases/pathological states:  Drug may aggravate underlying pathology  Hepatic disease may slow drug metabolism  Renal disease may slow drug elimination  Acid/base abnormalities may change drug absorption or elimination  Severe shock with vasoconstriction delays absorption of drugs from s.c. or i.m  Drug metabolism in:  Hyperthyroidism –enhanced  Hypothyroidism -diminished
  • 67. 11. Cumulation:  Any drug will cumulate in the body if rate of administration is more than the rate of elimination  Eg: digitalis, heavy metals etc.
  • 68. 12. Genetic factors:  Lack of specific enzymes  Lower metabolic rate  Acetylation  Plasma cholinesterase (Atypical pseudo cholinesterase)  G-6PD  Glucuronide conjugation
  • 69. 13. Tolerance:  It means requirement of a higher dose of the drug to produce an effect, which is ordinarily produced by normal therapeutic dose of the drug  Drug tolerance may be:  Natural  Acquired  Cross tolerance  Tachyphylaxis (ephedrine, tyramine, nicotine)  Drug resistance
  • 72. Drug classification (on the basis of affinity & efficacy) Agonist: Both the high affinity as well as intrinsic activity (IA=1) These drug trigger the maximal biological response or mimic effect of the endogenous substance. Ex:- Methacholine is a cholinomimetic drug which mimics the effect of Ach on cholinergic receptors.
  • 73. • Antagonist:- Which have only the affinity no intrinsic activity (IA=0). IA=0 so no pharmacological activity. • Rather these drug bind to the receptor and produce receptor blockade. • Atropine blocks the effects of Ach on the cholinergic muscarinic receptors.
  • 74. cAMP system Some drugs, hormones or neurotransmitters produce their effect by increasing or decreasing the activity of adenylate cyclase and thus raising or lower cAMP with in the cell.
  • 75. Stimulation • Some of drug act by increasing the activity of specialized cells. Ex: Catecholamines stimulate the heart and Heart rate, Force of contraction
  • 76. Inhibition • Some drug act by decreasing the activity of specialized cells. Ex: Alcohol, Barbiturates, General anesthetic these drug depress the CNS system. Atropine inhibits Ach action.
  • 77. Replacement • When there is a deficiency of endogenous substances, they can replaced by drugs. Ex: Insulin in Diabetes mellitus Throxine in cretinism and myxedema
  • 78. Irritation • Certain drugs on topical application cause irritation of the skin and adjacent tissues. • These drugs are using for counter irritant. Ex: Eucalyptus oil, methyl salicylates (Used in sprains, joint pain, myalgia.
  • 79. Cytotoxic • Treatment of infectious disease/cancer with drugs that are selectively toxic for infecting organism/cancer cells Ex: Anticancer drugs All Antibiotics
  • 80. Phospholipase-C system Activation Hydrolysis Agonist Gq PIP2 PLC Hydrolysis DAG Water soluble release PKC IP3 ATP S Cam E ADP Product Ca+2 Cam E* Response PLC= Phospholipase-C PIP2 =Phosphotiydl inositol 4,5 di phosphate IP3 =Inositol tri phosphate DAG = Diacylglycerol E= Ezyme PKC = Phosphokinase -C
  • 81. Extra cellular site of action 1.Antacids neutralizing gastric acidity. 2.Chelating agents forming complexes with heavy metals. 3.MgSo4 acting as purgative by retaining the fluid inside the lumen of intestine.
  • 82. Cellular Site of Action 1.Ach on Nicotinic receptors of motor end plate, leading to contraction of skeletal muscle. 2.Effect of sympathomimetics on muscle and blood vessels. heart
  • 83. Intracellular site of action -Folic acid synthesis inhibitors. Folic acid which is intracellular component essential for synthesis of proteins. Trimethoprim and sulfa drug interfere with synthesis.
  • 84. Gs/Gi G protein Effector or AC + cAMP ATP Phosphorylation Ca+2 release Protein kinase Active FC of heart muscle Lipolysis Glycogen synthesis Glycogen breakdown to glucose
  • 85. Physical action • Absorption: Kaolin absorbs bacterilal toxin and thus acts as antidiarrhoeal agent. • Protectives:- Various dusting powders.
  • 86. • Antagonist:- Which have only the affinity no intrinsic activity (IA=0). IA=0 so no pharmacological activity. • Rather these drug bind to the receptor and produce receptor blockade. • Atropine blocks the effects of Ach on the cholinergic muscarinic receptors.
  • 87. Physical Action • Osmosis:- MgSo4 acts as a purgative by exerting osmatic effect within lumen of the intestine. • Astringents:- They precipitate the surface proteins and protect the mucosa Ex: tannic acid in gum patients • Demulcent:- These drugs coat the inflamed mucus membrane and provide soothing effect. Ex: Menthol
  • 88. False incorporation • Bacteria synthesis folic acid from PABA (Para Amino Benzoic Acid), for growth sand development. • Sulfa drugs resemble PABA, therefore falsely enter into the synthesis process of PABA, cause nonfunctional production and no utility for bacterial growth.
  • 89. Protoplasmic poison • Germicides and antiseptics like phenol and formaldehyde act as non specifically as protoplasmic poison causing the death of bacteria
  • 90. Through formation of antibodies • Vaccines produce their effect by inducing the formation of antibodies and thus stimulate the defense mechanism of the body • Ex:- Vaccines against small pox and cholera
  • 91. Targeting specific genetic changes. • Anti cancer drugs that specifically target genetic changes. • Inhibitors of specific tyrosine kinase that that block the activity of oncogenic kinases.
  • 92. Physiological antagonism • Two antagonists, acting at different sites, counter balance each other by producing opp. effect on same physiological system. • Histamine –Vasodilatation • Nor epinephrine – Vasoconstriction
  • 93. Chemical action 1.Ion Exchanges:-Anticoagulant effect of heparin(-ve charge) antagonized by protamine (+ve charged) protein. 2.Neutralization:- Excessive gastric acid is neutralized by antacids. 3. Chelation:-These are trap the heavy metals. Ex:-EDTA, BAL.

Editor's Notes

  1. Rabbit  liver contain atropinase enzyme , which destroys fasterChinese cook their food in castor oil