Pharmacodynamics covers how drugs act on the body. Drugs can act through receptor-mediated or non-receptor mediated mechanisms. Receptor-mediated actions involve drug binding to receptors, which then trigger signal transduction pathways. There are various types of receptors including ion channels, G-protein coupled receptors, and nuclear receptors. Drug effects are determined by factors like affinity, efficacy, and intrinsic activity. Individual drug responses can be modified by pharmacokinetic and pharmacodynamic factors such as age, weight, disease states, genetic differences, and drug interactions.
For More Medicine Free PPT - http://playnever.blogspot.com/
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A power point presentation on Pharmacodynamics (what drug does to the body) suitable for undergraduate medical students beginning to study Pharmacology
For More Medicine Free PPT - http://playnever.blogspot.com/
For Health benefits and medicine videos Subscribe youtube channel - https://www.youtube.com/playlist?list=PLKg-H-sMh9G01zEg4YpndngXODW2bq92w
A power point presentation on Pharmacodynamics (what drug does to the body) suitable for undergraduate medical students beginning to study Pharmacology
Pharmacokinetics - drug absorption, drug distribution, drug metabolism, drug ...http://neigrihms.gov.in/
A power point presentation on general aspects of Pharmacokinetics suitable for undergraduate medical students beginning to study Pharmacology. Also suitable for Post Graduate students of Pharmacology and Pharmaceutical Sciences.
Pharmacology is the branch of pharmaceutical sciences which is concerned with the study of drug or medication action, where a drug can be broadly defined as any man-made, natural, or endogenous molecule which exerts a biochemical or physiological effect on the cell, tissue, organ, or organism
The slides describe concept of distribution, Volume of distribution, factors affecting volume of distribution and the barriers to distribution. Blood brain barrier and placental barrier.
Pharmacokinetics - drug absorption, drug distribution, drug metabolism, drug ...http://neigrihms.gov.in/
A power point presentation on general aspects of Pharmacokinetics suitable for undergraduate medical students beginning to study Pharmacology. Also suitable for Post Graduate students of Pharmacology and Pharmaceutical Sciences.
Pharmacology is the branch of pharmaceutical sciences which is concerned with the study of drug or medication action, where a drug can be broadly defined as any man-made, natural, or endogenous molecule which exerts a biochemical or physiological effect on the cell, tissue, organ, or organism
The slides describe concept of distribution, Volume of distribution, factors affecting volume of distribution and the barriers to distribution. Blood brain barrier and placental barrier.
It will provide you a complete journey through the routes of drug administration, with all the basics covered I hope this presentation will make your fundamentals crystal clear.
In pharmacology, the term mechanism of action (MOA) refers to the specific biochemical interaction through which a drug substance produces its pharmacological effect. A mechanism of action usually includes mention of the specific molecular targets to which the drug binds, such as an enzyme or receptor.
Principles and mechanisms of drug action. Receptor theories and classification of receptors, regulation of receptors. drug
receptors interactions signal transduction mechanisms, G protein–coupled receptors, ion channel receptor, transmembrane enzyme linked receptors,
transmembrane receptor and receptors that regulate
transcription factors, dose response relationship, therapeutic index, combined effects of drugs and factors modifying drug action.
Pharmacodynamics, mechanism of drug actionAsma Aslam
complete information on receptors and their mechanism of actions... briefly discussed about pharmacodynamics and up regulation and desensitization of receptors,
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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. Receptor Functions : Two essential functions
• 1. Recognization of specific ligand molecule
(Ligand binding domain)
• 2. Transduction of signal into response (Effector
domain)
Ligand binding
domain
Transduction of
signal into response
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.
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.
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
channel.
Receptor
Agonist
Hyper polarization or
depolarization
Receptor
Blocker
Permeation of
ion is blocked
Cellular effect
No cellular effect
Io
n
Na+2
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 Receptor for Signaling pathway/
Effector
Gs ß adrenegic,
H,5HT,Glucagon
AC— cAMP
Gi1,2,3 α2 adrenergic, Ach, AC— cAMP,
Open K+
Gq Ach Phospholipase-C,
IP3’cytoplasmic Ca+2
Go Neurotransmitters
in brain
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. • 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
26. Receptor regulating gene expression
(transcription factors)
Unfolds the receptor and
expose normally
masked DNA binding
site
Increase RNA
polymerase activity
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.
• TI should be more than one
50
50
ED
LD
indexcTherapeuti
44. Toxic
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
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.
• MORPHINHEROIN 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. One or more of the following categories of
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. The various factors are:
1. 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
BSA=BW(Kg)0.425 x Height(cm)0.725 x 0.007184
doseadultAveragex
70
(kg)BW
doseIndividual
doseadultAveragex
1.7
(m2)BSA
doseIndividual
57. 2. Age:
Infants and Children:
The dose of drug for children often calculated from the adult
dose
formula)sYoung'.........(doseadultx
12Age
Age
doseChild
formula)sg'...(Dillindose......adultx
20
Age
doseChild
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.
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. E Cam E*
Gq PLC PIP2
DAG
S
Agonist
HydrolysisActivation
IP3
PKC
ATP ADP
Product
Ca+2Cam
Water soluble
release
Response
Phospholipase-C system
Hydrolysis
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 heart
muscle and blood vessels.
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. or
FC of heart muscle
Lipolysis Glycogen Glycogen breakdown
synthesis to glucose
G protein
+ -
Effector
AC
cAMP ATP
Protein kinase Active
Ca+2 release
Phosphorylation
Gs/Gi
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
Rabbit liver contain atropinase enzyme , which destroys fasterChinese cook their food in castor oil