Pharmacokinetics refers to what the body does to drugs, including absorption, distribution, metabolism and excretion. It describes the movement and fate of drugs in the body over time. Pharmacodynamics describes how drugs act on the body including their effects, mechanisms of action, and relationships between dose and effect. The major mechanisms of drug action involve interactions with receptors, enzymes, ion channels and transporters. Drugs produce their intended and side effects by altering the normal functioning of these biomolecules.
This is the material for the 2nd week meeting on Food and Drugs Interaction for Nutrition students. This topic will cover the drug metabolism, looking at the pharmacokinetics and pharmacodynamics of drugs.
This is the material for the 2nd week meeting on Food and Drugs Interaction for Nutrition students. This topic will cover the drug metabolism, looking at the pharmacokinetics and pharmacodynamics of drugs.
Pharmacokinetics (PK) is the study of how the body interacts with administered substances for the entire duration of exposure (medications for the sake of this article). This is closely related to but distinctly different from pharmacodynamics, which examines the drug’s effect on the body more closely. The four main parameters generally examined by this field include absorption, distribution, metabolism, and excretion (ADME). Wielding an understanding of these processes allows practitioners the flexibility to prescribe and administer medications that will provide the greatest benefit at the lowest risk and allow them to make adjustments as necessary, given the varied physiology and lifestyles of patients.
When a provider prescribes medication, it is with the ultimate goal of a therapeutic outcome while minimizing adverse reactions. A thorough understanding of pharmacokinetics is essential in building treatment plans involving medications. Pharmacokinetics, as a field, attempts to summarize the movement of drugs throughout the body and the actions of the body on the drug. By using the above terms, theories, and equations, practitioners can better estimate the locations and concentrations of a drug in different areas of the body.
The appropriate concentration needed to obtain the desired effect and the amount needed for a higher chance of adverse reactions is determined through laboratory testing. Using the equations given above, a clinician can easily estimate safe medication dosing over a period of time and how long it will take for a medication to leave a patient’s system. These are, however, statistically-based estimations, influenced by differences in the drug dosage form and patient pathophysiology. This is why a deep understanding of these concepts is essential in medical practice so that improvisation is possible when the clinical situation requires it.
General pharmacology Diploma in pharmacy second year YogeshShelake
The General pharmacology ,Toxicology & Pharmacotherapeutics
To Undastanding the general pharmacology & Definitions of PHARMACODYNAMECIS ,PHARMACOKINITICS (Absorbation,Distribution,Metabolism,Excreation )Pharmacology ,Toxicology ,Pharmacotherapeutic ,
Advantages of Routs of Administration & Their Disadvantages
Factors affecting of absorpation ,excreation of drug,factor modifing deug action
- Routes of administration
- First pass metabolism, bioavailablilty, drug distribution,
- Drug interactions with proteins, Drug metabolism, elimination, Half-life
Objectives for this present are to define:
terminology
explain principles of drug action
describe pharmacokinetic functions
principles of pharmacodynamics
identify adverse drug reactions
Pharmacokinetics (PK) is the study of how the body interacts with administered substances for the entire duration of exposure (medications for the sake of this article). This is closely related to but distinctly different from pharmacodynamics, which examines the drug’s effect on the body more closely. The four main parameters generally examined by this field include absorption, distribution, metabolism, and excretion (ADME). Wielding an understanding of these processes allows practitioners the flexibility to prescribe and administer medications that will provide the greatest benefit at the lowest risk and allow them to make adjustments as necessary, given the varied physiology and lifestyles of patients.
When a provider prescribes medication, it is with the ultimate goal of a therapeutic outcome while minimizing adverse reactions. A thorough understanding of pharmacokinetics is essential in building treatment plans involving medications. Pharmacokinetics, as a field, attempts to summarize the movement of drugs throughout the body and the actions of the body on the drug. By using the above terms, theories, and equations, practitioners can better estimate the locations and concentrations of a drug in different areas of the body.
The appropriate concentration needed to obtain the desired effect and the amount needed for a higher chance of adverse reactions is determined through laboratory testing. Using the equations given above, a clinician can easily estimate safe medication dosing over a period of time and how long it will take for a medication to leave a patient’s system. These are, however, statistically-based estimations, influenced by differences in the drug dosage form and patient pathophysiology. This is why a deep understanding of these concepts is essential in medical practice so that improvisation is possible when the clinical situation requires it.
General pharmacology Diploma in pharmacy second year YogeshShelake
The General pharmacology ,Toxicology & Pharmacotherapeutics
To Undastanding the general pharmacology & Definitions of PHARMACODYNAMECIS ,PHARMACOKINITICS (Absorbation,Distribution,Metabolism,Excreation )Pharmacology ,Toxicology ,Pharmacotherapeutic ,
Advantages of Routs of Administration & Their Disadvantages
Factors affecting of absorpation ,excreation of drug,factor modifing deug action
- Routes of administration
- First pass metabolism, bioavailablilty, drug distribution,
- Drug interactions with proteins, Drug metabolism, elimination, Half-life
Objectives for this present are to define:
terminology
explain principles of drug action
describe pharmacokinetic functions
principles of pharmacodynamics
identify adverse drug reactions
This presentation provides a basic understanding of Rational use of medicines, it's significance, hazards of irrational drug used, factors contributing to irrational drug use, etc.
This presentation provide the basics of nutrition and nutritional supplements, the classification, sources, therapeutic uses, deficiency symptoms and toxicity.
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.
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.
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.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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.
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
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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.
2. 2
PK refers to what body does to drug(s) when administered
It describes time course of drugs in the body
In other words, it is the kinetics (movement) of drugs in the body
3. Significance of PK
Optimize drug formulation during development
Determine dosage regimen
Determine dosing frequency
Monitor plasma level of drug with narrow TI
(digoxin, theophylline)
Reduced noxious effects
3
4. Drug Absorption
Passage of drugs from site of
administration into the
blood/lymphatic system
Many barriers (membranes) are
encountered
Sites include stomach, small and
large intestines, alveolar surface,
skin
Sites of drug absorption
Oral cavity
Sublingual
Stomach
Small intestine
Large intestine
Alveolar surface
Skin
4
5. 5
Mechanisms of Drug Transport
Mechanism Description
Passive diffusion Movement freely down the concentration gradient.
Use by most drugs
Filtration Movement through pores on membrane
Usually by small-water soluble molecules e.g. urea
Active transport Movement against concentration gradient and usually
requires energy (ATP) and carriers, saturability, selectivity and
competitive inhibition e.g. amino acids, levodopa, methyldopa
Facilitated diffusion Movement down concentration gradient requires carrier
(transporters) but no extra ATP is required
Ion pair transport Movement aided by pairing with ions
7. FACTORS AFFECTING DRUG
ABSORPTION
• Local pH
• Concentration
• Vascularity of the absorbing surface
• Surface area
• Gut motility
• Food/Other drugs
• Disintegration time
• Dissolution time
8. 8
Local pH
• Most drugs are weak electrolytes (acid or bases).
• When they dissociate or ionized, the ion being insoluble in
lipid cannot cross the cell membrane by lipid diffusion.
• The dissociation or ionization depends upon the pH of the
medium.
• Polar or ionized molecules cannot cross the cell membrane
because they are not lipid-soluble.
• Nonpolar or unionized and nonelectrolytes (uncharged)
molecules have excellent lipid solubility and can cross the cell
membrane by diffusion.
9. 9
Concentration
• Passive diffusion depends on concentration
gradient; drug given as concentrated solution is
absorbed faster than from dilute solution.
Vascularity of the absorbing surface
• Blood circulation removes the drug from the site
of absorption and maintains the concentration
gradient across the absorbing surface.
• Increased blood flow hastens drug absorption.
10. 10
Surface area
• Larger is the surface area, faster is the
absorption.
Gut motility
• Diarrhoea drives out the GIT content rapidly,
thus may reduce drug absorption.
11. 11
Food/Other drugs
• Presence of food dilutes the drug and retards
absorption.
• Certain drugs form poorly absorbed
complexes with food constituents, e.g.
tetracyclines with calcium present in milk;
moreover food delays gastric emptying.
• Thus, most drugs are absorbed better if taken
in empty stomach.
• There are some exceptions, e.g. fatty food
greatly enhances lumefantrine absorption.
12. 12
Disintegration time
• It means the time taken for a tablet to
disintegrate, i.e. breakdown in the GIT
completely.
• Longer the disintegration time delayed is the
absorption.
Dissolution time
• This is the time taken for entering the tablet into
the solution within the GIT after it has been
disintegrated.
13. Drug Distribution
• Once in the bloodstream, a drug is distributed throughout the body
• Distribution of drugs begins when it enters blood (i.e. absorbed) and is
completed when the drug has reached all the possible sites where it can
go.
• Most of the drug is in areas remote from the site of action (of interest),
such as
– Plasma binding sites
– Muscle tissue
– Adipose tissue (fat)
– Liver
– Kidneys
13
14. Factors Affecting Drug Distribution
• Plasma protein binding
• The rate of blood flow to the various organs
• Binding with cellular proteins
• Concentration in fatty tissue
14
15. Drug Metabolism
• Drugs, which are the chemical substances, must be
removed from the body after its effect on living organism.
• Otherwise, there would be a persistent effects on the body
which may not be desired.
• Our body gets ride of this persistent effect by changing
the drug molecules.
• This kind of chemical change of drugs that occur in living
body is known as biotransformation or drug metabolism.
15
16. Phases of Drug Metabolism
Phase I (non-synthetic)
• Phase I reactions convert lipophilic drugs into more
polar molecules by introducing or unmasking a
polar functional group, such as –OH or –NH2.
• Phase I reactions usually involve reduction,
oxidation, or hydrolysis.
• Phase I metabolism may increase, decrease, or have
no effect on pharmacologic activity.
16
17. 17
Phase II (synthetic)
• This phase consists of conjugation reactions.
• If the metabolite from phase I metabolism is
sufficiently polar, it can be excreted by the
kidneys.
• However, many phase I metabolites are still too
lipophilic to be excreted.
• A subsequent conjugation reaction with an
endogenous substrate, such as glucuronic acid,
sulphuric acid, acetic acid, or an amino acid,
results in polar, usually more water-soluble
compounds that are often therapeutically inactive.
18. Phase II reactions include;
• Glucuronidation
• Acetylation
• Methylation
• Sulfation
Enzymes (mainly in the cytosol)
• Glucuronosyl transferase (UGTs) – also in endoplasmic
reticulum
• N- acetyltransferase (NAT)
• Sulfotransferase (SULTs)
• Methyltransferase (MTs)
• Glutathione-S-transferase (GST)
• Dehydrogenases (alcohol metabolism)
19. 19
NOTE:
All these reactions are to make the drug from
lipid-soluble to more water-soluble or nonpolar
to polar compound or unionized to ionized.
20. Factors affecting drug metabolism
i. Individual metabolic rates
ii. Genetic variation (e.g. NAT, CYP2D6)
iii. Diet e.g. Grapefruit juice
iv. Social habit such as smoking and alcohol consumption
v. Age
vi. Drugs (ketoconazole vs PI)
vii. Disease
21. 21
• Biotransformation of drugs may lead to the following.
Inactivation
• Most drugs and their active metabolites are rendered inactive
or less active, e.g. ibuprofen, paracetamol, lidocaine,
chloramphenicol, propranolol.
Active metabolite from an active drug
• Many drugs have been found to be partially converted to one
or more active metabolite; the effects observed are the
sumtotal of that due to the parent drug and its active
metabolite(s) e.g. diazepam
22. 22
Activation of inactive drug
• Few drugs are inactive as such and need
conversion in the body to one or more active
metabolites.
• Such a drug is called a prodrug.
• The prodrug may offer advantages over the active
form in being more stable, having better
bioavailability or other desirable pharmacokinetic
properties or less side effects and toxicity.
• Some prodrugs are activated selectively at the site
of action.
23. Drug Excretion
• Process by which drugs and/or metabolites are
irreversibly transferred from internal to external
environs
• Most drugs are excreted in urine either as unchanged
drugs and/or drug metabolites
• Primarily in the kidneys but also takes place in lungs,
biliary system, GIT & skin
23
24. Types of Excretion
• Renal Excretion: via the kidney
• Non-renal Excretion: other routes outside kidney
Biliary excretion
Pulmonary excretion
Salivary excretion
Mammary excretion
Dermal excretion
24
25. Renal Excretion
Via the kidneys
Primary route of drug
excretion
Nephron, the
fundamental unit
26. 3 principal processes are
involved:
(i) Glomerular filtration
(ii) Tubular secretion
(iii) Tubular reabsorption
27. Excretion in Urine
Water Soluble Lipid Soluble
LIVER
KIDNEY
Lipid soluble drugs
are reabsorbed!!!
Back diffusion is dependent
on pH of tubular fluid & lipid
solubility of drug
Secretion of
organic
acids and
bases
Filtration
in Glomerulus
28. Biliary Excretion
Drug secretion via bile into gall bladder
Examples: cardiac glycosides, heavy metals
Secretion usually by diffusion, carrier mediated
active transport
Fate
Excrete in faeces
Enter enterohepatic circulation
29. Pulmonary Excretion
Via lungs
Simple diffusion
Volatile compounds
Depends on rate of pulmonary blood flow, rate of
respiration and gas solubility in blood
Examples: halothane, NO, ethanol, chloroform,
ethane etc.
30. Salivary Excretion
pH of saliva: 5.8 – 8.4
Unionized lipid soluble drugs
Mainly by passive diffusion
Evident by bitter taste and mouth dryness
(basic drug)
E.g. caffeine, theophylline, phenytoin
31. Mammary Excretion
pH of milk: 6.4 – 7.6
Milk rich in fats and proteins
Unionized lipid soluble drugs
Mainly by passive diffusion
May have implication on breast feeding infants
E.g. caffeine, theophylline, phenytoin
33. • Pharmacodynamics is the study of drug effects.
• It starts with describing what the drugs do, and goes on to
explain how they do it.
• Thus, it attempts to elucidate the complete action-effect
sequence and the dose-effect relationship.
• It provides fundamental insights into biochemical and
physiological regulation.
• Modification of the action of one drug by another drug is
also an aspect of pharmacodynamics.
33
34. PRINCIPLES OF DRUG ACTION
• Drugs (except those gene based) do not impart new
functions to any system, organ or cell; they only alter the
pace of ongoing activity.
• However, this alone can have profound medicinal as well
as toxicological impact. The basic types of drug action
can be broadly classed as:
• Stimulation: It refers to selective enhancement of the
level of activity of specialized cells, e.g. adrenaline
stimulates heart.
34
35. PRINCIPLES OF DRUG ACTION...
• Depression: It means selective diminution of activity of
specialized cells, e.g. barbiturates depress CNS, quinidine
depresses heart, omeprazole depresses gastric acid
secretion.
• Replacement: This refers to the use of natural
metabolites, hormones or their congeners in deficiency
states, e.g. insulin in diabetes mellitus, iron in anaemia.
• Cytotoxic action: Selective cytotoxic action on invading
parasites or cancer cells, attenuating them without
significantly affecting the host cells is utilized for
cure/palliation of infections and neoplasms.
35
36. MECHANISM OF DRUG ACTIONS
• Majority of drugs produce their effects by interacting with a
discrete target biomolecule, which usually is a protein.
• Such mechanism confers selectivity of action to the drug.
• Functional proteins that are targets of drug action can be
grouped into four major categories, viz.
o Receptors
o Enzymes
o Ion channels and
o Transporters.
36
37. RECEPTORS
• Receptors are macromolecules that serves to recognize the
signal molecule/drug and initiate the response to it, but
itself has no other function.
• May be cell surface or nuclear receptors
• The concept of drugs acting on receptors (receptive
substance) generally is credited to John Langley (1878)
• The word receptor was introduced in 1909 by Paul Ehrlich
• They are usually protein in nature, specific and have affinity
• Receptors serve two essential functions, viz, recognition of
the specific ligand molecule and transduction of the signal
into a response.
37
38. Drug – Receptor Interactions
• The following terms are used in describing drug-receptor interaction:
• Agonist: An agent which activates a receptor to produce an effect similar to that of
the physiological signal molecule.
• Partial agonist: An agent which activates a receptor to produce submaximal effect
but antagonizes the action of a full agonist.
• Inverse agonist: An agent which activates a receptor to produce an effect in the
opposite direction to that of the agonist.
• Antagonist: An agent which prevents the action of an agonist on a receptor or the
subsequent response, but does not have any effect of its own.
38
39. Drug – Receptor Interactions...
Characteristics
Chemical bond: ionic, hydrogen, Van der Waals, and covalent.
Saturable
Competitive
Specific and Selective
Structure-activity relationships
Transduction mechanisms
39
Receptor activities
42. Enzymes
• Common drug target, next to receptors
• Enzymes are involve in biosynthesis
• Some drugs bind to enzymes and inhibit their
activities.
• Loss of product due to the inhibition mediates the
effects of the drug
• Few drugs also activate enzymes
Nitroglycerin (Guanylyl cyclase)
Pralidoxime (cholinesterase)
42
45. Ion Channels
• Proteins which act as ion selective channels participate in
transmembrane signalling and regulate intracellular ionic composition.
• Thus, certain drugs modulate opening and closing of the channels.
• This makes them a common target of drug action.
45
46. Examples
Channel Drug
Ca channel blocker Verapamil
Amlodipine
Diltiazem
Na channel blocker Lidocaine
Amiodarone
K Channel activator Minoxidil
Cl channel activator alprazolam
46
47. Transporters
• Several substrates are translocated across membranes by binding to
specific transporters (carriers) which either facilitate diffusion in the
direction of the concentration gradient or pump the metabolite/ion
against the concentration gradient using metabolic.
• Many drugs produce their action by directly interacting with the solute
carrier (SLC) class of transporter proteins to inhibit the ongoing
physiological transport of the metabolite/ion.
47
49. Unconventional Mechanisms
• Being nutrients e.g. vitamins and minerals
• Being antigens e.g. vaccines
• Being Enzymes e.g. streptokinase for thrombolysis
• Reacting chemically with small molecules e.g. antacids
• Disruption of structural proteins e.g. vinca alkaloids for cancer,
colchicine for gout
49