General pharmacology and pharmocokineticsSwapnil Singh
Basic pharmacology and Pharmacokinetics principles and concepts covering routes of drug administration, absorption phenomena, metabolism and excretion from the body.
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.
Pharmacokinetics is the study of the movement of drug molecules in the body. It includes absorption, distribution, metabolism, and excretion of drugs. Pharmacokinetics is the study of what happens to drugs once they enter the body (the movement of the drugs into, within, and out of the body). For a drug to produce its specific response, it should be present in adequate concentrations at the site of action. This depends on various factors apart from the dose.
Four pharmacokinetic properties determine the onset, intensity, and the duration of drug action (Figure 1.6.1):
• Absorption: First, absorption from the site of administration permits entry of the drug (either directly or indirectly) into plasma.
• Distribution: Second, the drug may then reversibly leave the bloodstream and distribute it into the interstitial and intracellular fluids.
• Metabolism: Third, the drug may be biotransformed by metabolism by the liver or other tissues.
• Elimination: Finally, the drug and its metabolites are eliminated from the body in urine, bile, or feces.
In short, pharmacokinetics means what the body does to the drug.
General pharmacology and pharmocokineticsSwapnil Singh
Basic pharmacology and Pharmacokinetics principles and concepts covering routes of drug administration, absorption phenomena, metabolism and excretion from the body.
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.
Pharmacokinetics is the study of the movement of drug molecules in the body. It includes absorption, distribution, metabolism, and excretion of drugs. Pharmacokinetics is the study of what happens to drugs once they enter the body (the movement of the drugs into, within, and out of the body). For a drug to produce its specific response, it should be present in adequate concentrations at the site of action. This depends on various factors apart from the dose.
Four pharmacokinetic properties determine the onset, intensity, and the duration of drug action (Figure 1.6.1):
• Absorption: First, absorption from the site of administration permits entry of the drug (either directly or indirectly) into plasma.
• Distribution: Second, the drug may then reversibly leave the bloodstream and distribute it into the interstitial and intracellular fluids.
• Metabolism: Third, the drug may be biotransformed by metabolism by the liver or other tissues.
• Elimination: Finally, the drug and its metabolites are eliminated from the body in urine, bile, or feces.
In short, pharmacokinetics means what the body does to the drug.
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“ Bioavailability-
means the rate and extent to which the active ingredient or active moiety is absorbed from a drug product and becomes available at the site of action."
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“ Bioavailability-
means the rate and extent to which the active ingredient or active moiety is absorbed from a drug product and becomes available at the site of action."
Ace Your NAPLEX Exam: Master Kinetics, DDI, and Pharmacogenomics in Lecture 2!Jackson Wang
https://youtu.be/C1Rb4BFugzo
Attention all NAPLEX students! Are you ready to take your studying to the next level? In this video, we dive deep into the world of Kinetics, DDI, and Pharmacogenomics. With other pharmacy students that seeks to inspire, this lecture provides insight on how to approach your NAPLEX studies with a fresh perspective. But, we want to know, what's been your biggest challenge so far while memorizing this vital information? Leave your thoughts below and let's engage in a discussion that will motivate us all. Remember, don't just study harder, study smarter. Join the conversation and elevate your NAPLEX studying game.
https://youtu.be/C1Rb4BFugzo
ADME is the abbreviation for Absorption, Distribution, Metabolism and Excretion. ADME studies are designed to investigate how a chemical (e.g. a drug compound) is processed by a living organism. Toxicology tests are often a part of this process, yielding the acronym ADMET.
Objectives for this present are to define:
terminology
explain principles of drug action
describe pharmacokinetic functions
principles of pharmacodynamics
identify adverse drug reactions
Pharmacokinetics of Drug_Pharmacology Course_Muhammad Kamal Hossain.pptxMuhammad Kamal Hossain
Pharmacokinetics is defined as the kinetics of drug absorption, distribution, metabolism and excretion (ADME) and their relationship with the pharmacological, therapeutic or toxicological response in man and animals.
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.
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.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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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2. Pharmacology
• It is the study of the interactions
that occur between a living organism
and chemicals that affect normal or
abnormal biochemical function.
• It is mainly concerned with safety
and efficacy of a drug.
3. Pharmacology
This field includes drug :
• Composition
• Properties
• Synthesis
• Medical Applications
• Antipathogenic capabilities
5. Importance of Pharmacokinetics and Pharmacodynamics
• Individualize patient drug therapy
• Monitor medications with a narrow therapeutic index
• Decrease the risk of adverse effects while maximizing
pharmacologic response of medications
7. Pharmacokinetics
• Study of drug movement in, through and out of the
body.
• It includes the following processes : (ADME)
Absorption Distribution Metabolism Excretion
8. Absorption
• The process by which drug proceeds from the site of
administration to the blood stream within the body.
• Orally administered solid drugs should break down into particles
of the active drug the released drug then dissolve in the aqueous
GI contents.
11. First Pass Metabolism
• A fraction of a drug is lost during the process of absorption generally
related to the liver and gut wall and its concentration is greatly
reduced before it reaches the systemic circulation.
• It leads to decreased bioavailability of a drug.
• Maximum in orally administered drugs.
12. Bioavailability
• First fundamental parameter of Pharmacokinetics.
• Rate and extent of absorption of a drug from a dosage form.
• Determined by concentration-time curve of the drug in blood or its
excretion in urine.
PLASMACONCENTRATION
TIME
C
Therapeutic success of a rapidly
and completely absorbed drug.
Therapeutic failure of a
slowly absorbed drug
Therapeutic Concentration
13. Bioavailability
• Fraction of administered dose of a drug that reaches the
systemic circulation in the unchanged form.
• IV injected drug : 100 % bioavailability
• Orally ingested drug : reduced bioavailability because :
Drug may be incompletely absorbed
The absorbed drug may undergo first pass metabolism
• SC or IM injection MAY have reduced bioavailability due to local
binding of the drug.
14. Distribution
• Process by which drug leaves the site of administration and
distributed throughout the tissues of the body.
• Factors affecting volume of drug distribution :
Lipid:water partition coefficient of the drug
pKa value of the drug
Degree of plasma protein binding
Affinity for different tissues
Fat:Lean body mass ratio
Diseases like CHF, Uraemia, Cirrhosis
15. Distribution
APPARENT VOLUME OF DISTRIBUTION ( V )
• Second fundamental parameter of Pharmacokinetics.
• Volume of distribution is the volume of plasma that would be
necessary to account for the total amount of drug in the
patient's body, if that drug were present throughout the body at
the same concentration as found in the plasma.
V = Dose administered IV
Plasma concentration
16. Metabolism (Biotransformation)
• Chemiacal alteration of the drug in the body.
• converts non-polar (lipid soluble) compounds polar so they are not
reabsorbed in the renal tubules and are excreted.
• Hydrophilic drugs eg. Gentamycin are not biotransformed and are excreted
unchanged.
• PRIMARY SITES :
Kidney Intestine Lung Plasma
19. Metabolism (Biotransformation)
NON SYNTHETIC REACTIONS
OXIDATION
• carried out by
monooxygenases in
the liver
• involve cytoP450
haemoprotein, NADPH,
cytoP450 reductase and
molecular O2
• eg. Paracetamol
REDUCTION
• converse of oxidation
• cytochrome P450
works in opposite
direction
• eg. Chloramphenicol
HYDROLYSIS
• cleavage of drug
molecule by taking up
a molecule of water
• Ester + H2O esterase
Acid + Alcohol
20. Metabolism (Biotransformation)
SYNTHETIC REACTIONS
• conjugation of the drug or its phase 1 metabolite with an
endogenous substrate to form a polar highly ionized organic acid
which is easily excreted in urine or bile.
Glucuronide
conjugation
Acetylation Methylation
Sulfate
conjugation
Glycine
conjugation
Glutathione
conjugation
21. Excretion
• Passage out of systemically absorbed drug in :
• Through the kidneyUrine
• Derived from bileFaeces
• Eliminated by lungsExhaled Air
• Important in respect to suckling infantsMilk
22. Kinetics of Elimination
• Drug Elimination = Metabolic Inactivation + Excretion
• CLEARANCE (CL) :
Third fundamental parameter of Pharmacokinetics.
Volume of plasma from which the drug is completely removed in unit
time.
CL = Rate of Elimination
Plasma Concentration
23. Kinetics of Elimination
FIRST ORDER (EXPONENTIAL) KINETICS
• Rate of elimination is directly proportional to drug concentration
• CL remains constant
• t½ is constant
ZERO ORDER (LINEAR) KINETICS
• Rate of elimination is constant irrespective of drug concentration
• CL decreases with increase in concentration
• t½ increases with dose
24. Kinetics of Elimination
PLASMA HALF-LIFE (t½)
• Time taken for the plasma concentration of a drug to be reduced to
half of its original value.
t½ = ln2 = log 2 or (0.693)
k Elimination Rate Constant
ELIMINATION RATE CONSTANT (k) :
• Fraction of the total amount of the drug in the body which is
removed per unit time.
k = CL t½ = 0.693 × V
V CL
25. Kinetics of Elimination
1 half life = 50% drug is eliminated
2 half lives = 75% (50 + 25)
3 half lives = 87.5% (50 + 25 + 12.5)
4 half lives = 93.75% (50 + 25 + 12.5 + 6.25)
So 4-5 half lives are needed for nearly complete drug elimination.
27. Kinetics of Elimination
Repeated Drug Administration
• when a drug is repeated at relatively short intervals, it accumulates in the body until
elimination and input become balanced and a steady-state plasma (Cpss) is attained.
Cpss = Dose rate
CL
• Dose rate and Cpss are in linear relation only in case of drugs that follow first order
kinetics.
Plateau Principle
• when constant dose is repeated before 4 half lives, it would achieve higher peak
concentration, because some remnants of the previous dose will be present in the body.
• After almost 4-5 half lives, increasing rate of elimination balances the amount
administered over the dose interval. Subsequently, plasma concentration plateaus and
fluctuates about an average steady-state level.
30. Pharmacodynamics
Mechanism of Drug action
1. Physical or chemical properties :
• Physical mass
• adsorptive property
• osmotic activity
• neutralization of gastric HCl
• oxidising property
31. Pharmacodynamics
2. Enzymes
• Drugs can either increase or decrease the rate of enzymatically mediated
reactions.
• Stimulation of an enzyme increases its affinity for the substrate so that
rate constant kM of the reaction is lowered.
• Induction of an enzyme ( synthesis of more protein) also increases enzyme
activity. kM does not change.
• Inhibition of enzymes.
a) Non specific inhibition
b) Specific inhibition
32. Pharmacodynamics
3. Carriers
• Drugs produce their action by interacting with the carrier protein to
inhibit the ongoing physiological transport of the metabolite.
• eg. Furosemide inhibits the Na-K-2Cl cotransporter in the ascending limb
of loop of Henle.
4. Ion channels
• Drugs affect ion channels either through specific receptors (ligand gated,
G-protein operated) or by directly binding to the channel and affecting
ion movement through it.
• Certain drugs modulate opening and closing of the channel. eg.
Sulfonylurea hypoglycaemics inhibit pancreatic ATP-sensitive k+ channels.
33. Pharmacodynamics
5. Receptors
• Drugs act through specific receptor (macromolecule or binding site that
serves to recognize and initiate the response to a signal molecule or drug)
which regulate critical functions like enzyme activity, permeability,
structural features, template function.
• Agonist activates receptor to produce effect similar to the physiological
signal molecule.
• Inverse agonist - activates receptor to produce opposite effect.
• Antagonist - prevents the action of the agonist.
• Partial Agonist - activates receptor to produce sub-maximal effect but
antagonizes the action of a full agonist.
34. Pharmacodynamics
Receptor occupation theory
• Propounded by Clark in 1937.
• Intensity of response is proportional to the fraction of receptors occupied by a
drug.
• Drug exert an all or none action on each receptor.
• A drug and its receptor have Lock and Key relationship.
• Affinity : ability of the drug to combine with the receptor.
• Intrinsic activity (Efficacy) : ability of the drug to activate the receptor.
35. Pharmacodynamics
The Two-State Receptor Model
l Equilibrium
ll Response
lll No Response
lv Partial Response
v Opposite Response
Ra Ri
RaA + Ra Ri
RaB + Ra RiB + Ri
RaC + Ra Ri +RiC
Ra Ri +RiD
36. Pharmacodynamics
Action-Effect Sequence
• Drug Action is the initial combination of the drug with its receptor resulting
in a confirmational change in the receptor (AGONIST) or prevention of
confirmational change through exclusion of the agonist (ANTAGONIST).
• Drug Effect is the ultimate change in biological function brought about as a
consequence of drug action.
Dose-Response Relationship
• Intensity of response increases with increase in dose.
• Dose-Response curve is a hyperbola because Drug-Receptor interaction
obeys Law of mass action.
E = Emax × [D]
KD + [D]
37. Pharmacodynamics
• E = observed effect at a dose [D] of the drug
• Emax = maximal response
• KD = dissociation constant of drug-receptor
complex = dose of drug at which half
maximum response is produced
• If dose is plotted on log scale, the curve
becomes sigmoid and a linear relationship is
seen between log of dose and the response
in the intermediate zone (30-70%
response)
Dose
Response
Dose
Log Dose
38. Pharmacodynamics
Drug Potency and Efficacy
• Drug potency is the amount of drug
needed to produce certain response.
• Drug efficacy is the maximum response
achievable from a drug.
• Upper limit of DRC is the index of
efficacy.
• Steep DRC means moderate increase in
dose leads to marked increase in response.
• Flat DRC means little increase in response
over a wide dose range.
• Drug B is less potent but equally
efficacious as A.
• Drug D is more potent than A, B and C
but less efficacious than A and B, and
D
C
A B
Log Dose
Response
39. Pharmacodynamics
A B
Log Dose
Response
Drug Selectivity
• Extent of separation of DRCs of a drug for different
effects is a measure of selectivity.
Therapeutic Index
• Gap between the therapeutic effect DRC and adverse
effect DRC
• Also known as Safety Margin
Therapeutic Index = Median Lethal Dose = LD 50
Median Effective Dose ED50
Therapeutic Effect
Adverse Effect
Minimal
therapeutic
effect
Maximum
acceptable
adverse
effect
Therapeutic Range
40. Pharmacodynamics
Combined effect of drugs :
• given simultaneously or in quick succession
Synergism Antagonism
Additive
Drug A + B = Drug A + Drug B
PhysiologicalPhysical Chemical
Supra-Additive
Drug A + B > Drug A + Drug B
Receptor
Non
Competitive
Competitive
41. Pharmacodynamics
Competitive (Equilibrium Type) Non-Competitive
• Antagonist binds with same receptor as agonist • Binds with different receptor
• Antagonist chemically resemble agonist • Does not resemble
• Parallel rightward shift of agonist DRC • Flattening of agonist DRC
• Surmountable antagonism • Unsurmountable antagonism
• Antagonist reduces potency of agonist • Antagonist reduces efficacy of agonist
• Response depends on both agonist and antagonist • Depends only on antagonist
• eg. ACh-Atropine • Diazepam-Bicuculline
42. Pharmacodynamics
Drug Dosage
• Dose is the amount of drug needed to produce a certain degree of response
in a patient.
• It depends on the potency and pharmacokinetics of the drug.
Types of dose
• Standard dose : Same dose is appropriate for most patients. eg OCP
• Regulated dose : Dosage is accurately adjusted by repeated measurement of
the affected physiological parameter. eg Anti-hypertensives
• Target Level dose : An emperical dose aimed at attaining the target level is
given in the beginning and adjustments are made later by actual monitoring
of plasma concentrations. eg Anti-epileptics
• Titrated dose : Optimal dose is arrived at by titrating it with an acceptable
level of adverse effect.