The document discusses different types of interactions that can occur when two or more drugs are taken together. It describes additive or summation effects when the effects of the drugs combine in an additive fashion. It also explains drug synergism, where the combined effect is greater than the sum of the individual drug effects. Additionally, it covers drug antagonism, where the combined effect is less than additive due to one drug opposing or decreasing the effects of another drug. The types of antagonism discussed include competitive, non-competitive, chemical, physiological, and physical antagonism.
A brief presentation on the factors affecting bioavailability of drugs along with a quick overview on what is bioequivalence, clinical equivalence, therapeutic equivalence, chemical equivalence and pharmaceutical equivalence.
A brief presentation on the factors affecting bioavailability of drugs along with a quick overview on what is bioequivalence, clinical equivalence, therapeutic equivalence, chemical equivalence and pharmaceutical equivalence.
Drug Antagonism
The effect of one drug blocked (or inhibited) due to another drug is said to be antagonism. In other word, an interaction between two or more drugs that have opposite effects on the body. Drug antagonism may block or reduce effectiveness of one or more of the drugs.
e.g., atropine blocks the action of acetylcholine
Types of antagonism
1. Pharmacological antagonism: Competitive and Non-Competitive
2. Physiological antagonism
3. Chemical antagonism
Competitive Antagonism
If both the agonist and the antagonist compete for the same receptor in a reversible manner, they are said to be “competitive.” The antagonist drug interacts with the receptor and blocks it. Therefore it does not produce pharmacological action. The extent of antagonism depends on number of receptors occupied by the both drugs (agonist and antagonist), their affinity for receptors and their concentration. The increase in concentration of either one of these drugs can displace the other from receptor binding sites. Drugs interact with their receptors by weak bonds i.e. ionic bond or Hydrogen bond or Vander wal force. Hence duration of action of drug is short. Both agonist and antagonist have chemical resemblance (structural similarity).
Receptor types, mechanism, receptor pharmacology, drug receptor interactions, theories of receptor pharmacology, spare receptors and new concepts like biased agonism
DRUG INTERACTIONS (MECHANISMS OF DRUG-DRUG INTERACTIONS)N Anusha
A Drug interaction is an interaction between a drug and some other substance, such as another drug or a certain type of food, which leads to interaction that could manifest as an increase or decrease in the effectiveness or an adverse reaction or a totally new side effect that is not seen with either drug alone that can be severe enough to alter the clinical outcome.
Every time a drug is administered with any other prescription medicine, OTC products, herbs or even food we expose ourselves to the risk of a potentially dangerous interaction.
Drug Antagonism
The effect of one drug blocked (or inhibited) due to another drug is said to be antagonism. In other word, an interaction between two or more drugs that have opposite effects on the body. Drug antagonism may block or reduce effectiveness of one or more of the drugs.
e.g., atropine blocks the action of acetylcholine
Types of antagonism
1. Pharmacological antagonism: Competitive and Non-Competitive
2. Physiological antagonism
3. Chemical antagonism
Competitive Antagonism
If both the agonist and the antagonist compete for the same receptor in a reversible manner, they are said to be “competitive.” The antagonist drug interacts with the receptor and blocks it. Therefore it does not produce pharmacological action. The extent of antagonism depends on number of receptors occupied by the both drugs (agonist and antagonist), their affinity for receptors and their concentration. The increase in concentration of either one of these drugs can displace the other from receptor binding sites. Drugs interact with their receptors by weak bonds i.e. ionic bond or Hydrogen bond or Vander wal force. Hence duration of action of drug is short. Both agonist and antagonist have chemical resemblance (structural similarity).
Receptor types, mechanism, receptor pharmacology, drug receptor interactions, theories of receptor pharmacology, spare receptors and new concepts like biased agonism
DRUG INTERACTIONS (MECHANISMS OF DRUG-DRUG INTERACTIONS)N Anusha
A Drug interaction is an interaction between a drug and some other substance, such as another drug or a certain type of food, which leads to interaction that could manifest as an increase or decrease in the effectiveness or an adverse reaction or a totally new side effect that is not seen with either drug alone that can be severe enough to alter the clinical outcome.
Every time a drug is administered with any other prescription medicine, OTC products, herbs or even food we expose ourselves to the risk of a potentially dangerous interaction.
THIS PPT INCLUDE PHARMACODYNAMICS AND THIS PPT IS VERY USEFUL FOR (MBBS,BDS ) STUDENTS ,POSTGRADUATE STUDENT (MD,MDS,Phd) STUDENTS TO UNDERSTAND PHARMACODYNAMICS.
At the end of this e-learning session you are able to…
Discuss about agonist and antagonist.
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bind to receptors and produce a response-
effects of various types
2. Antagonists
bind to receptors without producing a response and by occupying the receptors they prevent action of agonists.
Similar to Combined effects of Drugs, Pharmacology (20)
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- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
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- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
NVBDCP.pptx Nation vector borne disease control program
Combined effects of Drugs, Pharmacology
1. COMBINED EFFECTS OF DRUGS
By:
Dr. Dhruva Kumar Sharma
Department of Pharmacology
Moderator:
Dr. Supratim Datta
Associate Professor
Department of Pharmacology
SMIMS
3. EFFECT OF COMBINATION OF DRUGS
Combinations of two/ more drugs, simultaneously or
in quick succession
1. No interference with each other’s effects.
2. May oppose each other’s actions (antagonism)
3. May produce similar actions on the same organ
(synergism)
6. Drug Synergism:
This is facilitation of the effects of one drug
by another when given together
Types:
a. Additive (summation)
b. Supra-additive (Potentiation)
7. Summation /Addition
Effect of drugs A + B = Effect of drug A + Effect of drug B
• Final effect is same as the algebraic sum of the
magnitude of individuals drugs
• Side effects do not add up
Examples of Summation: Different MOA
Aspirin : (-) PG synthesis analgesia +
Codeine : Opioid agonist analgesia +
Examples of Addition: Same MOA
Ibuprofen: (-) PG synth analgesia +
Paracetamol: (-) PG synth analgesia+
Analgesia
++
Analgesia
++
8. Other Additive Drug Combinations
Drug
Combination
Effect
Amlodipine +
Atenolol
Antihypertensive
Glibenclamide +
Metformin
Hypoglycemic
9. Supraadditive ( Potentiation)
Effect of drug A + B > Effect of drug A + Effect of drug B
When two drugs are given together the final effect is much
more than the simple algebraic sum of the magnitude of
individuals drugs.
Examples:
Sulphamethoxazole & Trimethoprim--- sequential blockade
of two steps in synthesis of folic acid in micro-organisms.
12. Other supraadditive drug
combinations
DRUG PAIR BASIS OF POTENTIATION
Ach + Physostigmine Inhibition of break
down
Adrenaline + Cocaine Inhibition of neuronal
uptake
Tyramine + MAO
inhibitors
Increasing
releaseable CAT
store
14. Drug Antagonism
Definition:
Combined effect of two drugs is less than the sum of
the effects of the individual drugs
Effect of drugs A + B < Effect of drug
A + Effect of drug B
One drug decreases / opposes / reverses / counters
the effect of other drug by different mechanisms
15. Types:
a. Pharmacological Antagonism :
i. Competitive (Reversible)
ii. Non-competitive (Irreversible)
b. Chemical Antagonism
c. Physiological Antagonism
d. Physical antagonism
27. 28
LDRC shift to R
B
R
D
D
D
D
D
Reversible-Competitive
Conc dependant Dynamic Equilibrium
28. Competitive (Reversible) Antagonism /Competitive
(Equilibrium ) Antagonism
1. Same receptor by forming Weak bonds
2. Maximal response depends on concentration of
both agonist and antagonist
3. The effect of antagonist can be overcome by
increasing the concentration of agonist. The same
maximal response can be attained by increasing
dose of agonist---It is “surmountable antagonism”.
4. Parallel rightward shift of DRC
31. Examples: Atropine and Acetylcholine at Muscarinic -R
Naloxone and Morphine at opioid-R
Propranolol and NE at β2 - R
%Response
50
ED 50 ED 50 ED 50
32. Irreversibly Competitive or Non
Equilibrium Competitive Antagonism:
1.Have affinity for the same receptor sites and
bind in an irreversible manner by covalent
bond
2.Effects cannot be overcome even by
increasing the concentration of the agonist
(unsurmountable)
3.LDR curves of agonist (in presence of
antagonist) would show reduced efficacy but
unaltered potency
36. • DOA of irreversible antagonist is longer
• Equilibrium between Antagonist - Agonist
cannot be established even after increasing
the dose of agonist hence the term “Non-
equilibrium competitive antagonism”
• E.g. Dibenamine and NE at α1 adrenoceptors
37. Pseudo-reversible Antagonism:
• Lesser degree of receptor occupancy by the
antagonist & availability of spare receptors
• Increasing conc. of agonist- shift LDR to right
• Increasing conc. of antagonist- reduction in
maximal response.
• Hence the term “Pseudo-reversible
Antagonism”
42. 43
Non Competitive Antagonism
• Via Allosteric Modulation
• Receptor-Effector pathway
modulation
(Down-stream regulation)
NO Competition
for Agonist site
44. i. Binds to site other than the agonist site
ii. Prevent the receptor activation by the
agonist
E.g.
• Flumazenil by binding to BZD site
antagonises the effects of BZD by
preventing the binding of GABA to GABAA
receptor
• Bicuculline and BZD
Antagonism through Allosteric
receptor site binding:
47. Receptor-Effector pathway modulation
(Down-stream regulation)
48
AT1-R
NE
Ag II
Prazosin
Comp. Ant
Losartan
Comp. Ant
IP3,
DAG
α1-R
Ca2+
channel Activation
Free Ca2+
entry
Ca2+
Channel blocker
(eg., Nifedipine,
non-competitive antagonist
Vasoconstriction
48. Effects on log DRC
• There is downward shift .The slope is reduced
and maximum response is diminished
• The parallelism is not maintained
• No shift of curve on dose axis
49. 50
• Competitive Antagonism
(equilibrium or reversible)
Action of agonist is blocked if
conc. of antagonist is
Antagonism can be overcome
by conc. of agonist
Agonist can produce max.
response in higher conc.
Competitive antagonist shifts
LDRC of agonist to right
ED50 of agonist in presence
of antagonist, e.g., Ach &
atropine; Adr & Prop.;
Morphine & Naloxone
• Non-competitive
(non-surmountable
Antagonist)
Antagonist binds to another
site of receptor
LDRC is flattened + max.
response is
e.g. Diazepam and bicuculline
50. Chemical Antagonism
A type of antagonism where a drug counters the effect
of another by simple chemical reaction / neutralization
(not binding to the receptor)
1. Protamine sulphate & Heparin
2. Calcium sodium edetate form insoluble complexes
with arsenic / lead
3. Neutralization of gastric acid by antacids like
Aluminium hydroxide, Magnesium hydroxide,
Sodium bicarbonate
51. Physiological Antagonism
Definition:
A type of antagonism in which one drug opposes
/ reverses the effect of another drug by binding
to a different receptor and producing opposite
physiological effects
Examples:
1. Histamine and adrenaline on bronchial
muscles and BP
2. Glucagon and insulin on blood sugar level
52. Physical antagonism
• Based on the physical property of drugs e.g.
Charcoal adsorbs alkaloids and can prevent
their absorption- used in alkaloidal poisonings
53
53. REFERENCES
• Goodman Gilman - The Pharmacological Basis of
Therapeutics, 12th
Edition
• Katzung – Basic & Clinical Pharmacology,
12th
Edition
• Sharma – Priciples of Pharmacology,
2nd
Edition
• K.D Tripathi – Essentials of Medical
Pharmacology, 7th
edition
• R.S Satoskar – Pharmacology and
Pharmacotherapeutics, 18th
Edition
• www.google .com
Respected prof dr Kc swain sir, Assoc. Prof. Dr supratim sir Assoc prof dr Chandrakala mam, other faculties deb sir, sunil sir , my senior PGs and my dear colleague .I am here to present a seminar on combined effects of drug action and this seminar has been moderated by Assoc. Prof dr supratim
When 2 or more
Interaction may take place at pharmacokinetic or pharmacodynamic level
Synergism: sharma-AB&gt;A+B, Additive and summation diff entity,doesnot talk about potentition/supraadditive
Tripathi says synergism as facilitation of the effects of one drug by another when given together, and classifies synergism as additive and supraadditive
Pg. 496 sharma opioid Recptors mu and delta, inhbn of ad. cy.—dec camp—dec cell excitablity, activation of K channels-hyperpolarisation,decrease ca conductance
???additive/???summative
NO & Halothane: 373 tripathi
Amlo-268 sharma
Gli+Met=kdt 274,fig 19.6
Pharmacodynamic beneficial combinatoin
Other eg. Beta blocker and frusemide
Competitive antagonists added to an agonist will also shift the curve to the right, as a higher conc of agonist will be needed to overcome the antagonist and produce the maximum tissue response. An irreversible antagonist will bind permanently, so a maximum response will never be able to be reached.
Non competitive Antagonism
Antagonist binds strongly to different receptor site
in an irreversible or nearly irreversible fashion
Two types:
Non competitive antagonism through Interference in the Down-stream Events of Receptor Activation:
Same pattern of log dose response curve as that of irreversible competitive antagonism
The effect of antagonist can not be overcome by increasing the concentration of agonist.
Maximal response can not be achieved by increasing the conc. of agonist --unsurmountable antagonism
Bzd enhance binding of gaba to GABAa (increase frequency rather than duration of binding of gaba to gaba A)
Note: bicuculline is a competitive antagonist of binding of GABA to its receptor site hence antagonises the action of BZD non-competitively- another eg. of non comp antagonism at BZD Receptor
Protamine- strong positively charged & Heparin- strong negatively charged protein
Protamine sulphate is Antidote in Heparin overdosage
Essential point about physiological antagonism is- effects produced by the two drugs counteract each other, but each drug in unhindered in its ability to elicit its own response