pharmacokinetics of injectable anesthetics / dental implant courses by India...Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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Pharmacokinetic concepts and principles in humans in order to design individualized dosage regimens which optimize the therapeutic response of a medication while minimizing the chance of an adverse drug reaction.
A slide set covering important pharmacokinetic principles, including drug elimination kinetics, drug clearance, dosing, effective and maximum tolerated concentration and the therapeutic ratio. Provided by Professor John A Peters, University of Dundee.
pharmacokinetics of injectable anesthetics / dental implant courses by India...Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Pharmacokinetic concepts and principles in humans in order to design individualized dosage regimens which optimize the therapeutic response of a medication while minimizing the chance of an adverse drug reaction.
A slide set covering important pharmacokinetic principles, including drug elimination kinetics, drug clearance, dosing, effective and maximum tolerated concentration and the therapeutic ratio. Provided by Professor John A Peters, University of Dundee.
This presentation is about the process by which prolonged therapeutic activity of drug is achieved and it's importance. By this presentation you will learn about dosage regimen, steady state concentration, principle of superposition, drug accumulation, repetitive intravenous injections etc. By this you will also learn how to adjust the dose to the patient.
KINETICS OF MULTIPLE DOSING under the Unit Multicompartment Models According to New PCI syllabus 2017 by Ms. Preeti Patil-Vibhute, Assistant Professor, Sarojini College of Pharmacy, Kolhapur.
The presentation concisely describes the different pharmacokinetic parameters and basics of compartment modelling. It will help undergraduate students to understand the basic concepts of Biopharmaceutics.
The One compartment open model treats the body as one homogeneous volume in which blending is quick and where info and yield are from this one volume. The one-compartment open model is the least difficult approach to depict the procedure of medication appropriation and end in the body and this model accept that the medication can enter or leave the body and the whole body acts like a solitary, uniform compartment. The least complex pharmacokinetic model that portrays medicate manner in the body is the IV bolus model where the medication is infused at the same time into a container which is the human body or compartment and where the medication circulates/equilibrates momentarily and quickly all through the compartment. Again the easiest course of medication organization from a demonstrating point of view is a quick intravenous infusion (IV bolus). Medication end from the compartment likewise starts to happen following the IV bolus infusion.
Pharmacokinetics of IV infusion, one-compartment open modelAsuprita Patel
OCOM is the simplest model that represents the body as a single homogeneous system. Rapid i.v. injection is unsuitable when the drug has potential to precipitate toxicity or when maintenance of a stable concentration or amount of drug in the body is desired.
In such situation, the drug is administered at a constant rate by i.v. infusion.
This presentation is about the process by which prolonged therapeutic activity of drug is achieved and it's importance. By this presentation you will learn about dosage regimen, steady state concentration, principle of superposition, drug accumulation, repetitive intravenous injections etc. By this you will also learn how to adjust the dose to the patient.
KINETICS OF MULTIPLE DOSING under the Unit Multicompartment Models According to New PCI syllabus 2017 by Ms. Preeti Patil-Vibhute, Assistant Professor, Sarojini College of Pharmacy, Kolhapur.
The presentation concisely describes the different pharmacokinetic parameters and basics of compartment modelling. It will help undergraduate students to understand the basic concepts of Biopharmaceutics.
The One compartment open model treats the body as one homogeneous volume in which blending is quick and where info and yield are from this one volume. The one-compartment open model is the least difficult approach to depict the procedure of medication appropriation and end in the body and this model accept that the medication can enter or leave the body and the whole body acts like a solitary, uniform compartment. The least complex pharmacokinetic model that portrays medicate manner in the body is the IV bolus model where the medication is infused at the same time into a container which is the human body or compartment and where the medication circulates/equilibrates momentarily and quickly all through the compartment. Again the easiest course of medication organization from a demonstrating point of view is a quick intravenous infusion (IV bolus). Medication end from the compartment likewise starts to happen following the IV bolus infusion.
Pharmacokinetics of IV infusion, one-compartment open modelAsuprita Patel
OCOM is the simplest model that represents the body as a single homogeneous system. Rapid i.v. injection is unsuitable when the drug has potential to precipitate toxicity or when maintenance of a stable concentration or amount of drug in the body is desired.
In such situation, the drug is administered at a constant rate by i.v. infusion.
Drug Distribution & Factors Affecting DistributionVijay Kevlani
To have the full content of slide, kindly download it and convert it to ppt form.
Drug distribution is the process by which a drug reversibly leaves the bloodstream and enters the interstitium (extracellular fluid) and/or the cells of the tissues.
clinical pharmacokinetics half-life first-order elimination zero order elimination steady-state conc applied aspect of steady-state applied aspect of half-life advantage and disadvantage
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
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
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Best Ayurvedic medicine for Gas and IndigestionSwastikAyurveda
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
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.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
4. Constant rate infusion
If a drug is administered intravenously in a constant
rate, the concentration rises from zero, rapidly at first,
then more slowly
until a steady state level
is reached.
At steady state , the
rate of input of drug to
the body is equal to
the rate of elimination
of drug.
5. Continued…
At steady state, administration rate=elimination rate
elimination rate=Cssx clearance
clearance=
𝐸𝑙𝑖𝑚𝑖𝑛𝑎𝑡𝑖𝑜𝑛 𝑟𝑎𝑡𝑒
𝐶𝑠𝑠
Clearance : The clearance is defined as the volume of fluid from which
the drug is totally eliminated in a given period of time.
For therapeutic drug, knowing the clearance in an individual patient
enables the physician to adjust the maintenance dose to achieve
a desired target steady state concentration.
Since, required administration rate = desired Css x clearance
Elimination half-life: The time taken for plasma concentration to reach
half of the initial concentration is half-life ( t1/2 ). This decline is
exponential.
6. Continued…..
Loading dose: It is the maximum amount of dose of drug given to subject
to maintain steady state plasma concentration with a follow up of lowest
maintenance dose.
Maintenance dose: It is the dose of a drug just to replace the drug that
has been eliminated from the body during the dosing interval, so as to
maintain steady state
level.
7. Single bolus dose
Immediately following a bolus dose D, the plasma concentration rises to
a peak (Cp) which is theoretically equal to D/Vd and then declines
exponentially.
Plasma drug conc. Cp=
The volume of distribution is the amount of fluid in which the total drug is
distributed. The Vd defines the relationship between the mass of a bolus
dose of a drug and the plasma concentration that results.
It is not necessarily the real volume of a body compartment , since it may
be greater or lower than the volume of the whole body.
At the lower end, Vd is limited by the plasma volume (approximately 3 L in
an adult).
𝑇𝑜𝑡𝑎𝑙 𝑎𝑚𝑜𝑢𝑛𝑡 𝑜𝑓 𝑑𝑟𝑢𝑔 𝑖𝑛 𝑡ℎ𝑒 𝑏𝑜𝑑𝑦(𝐷)
𝑉𝑜𝑙𝑢𝑚𝑒 𝑜𝑓 𝑑𝑖𝑠𝑡𝑟𝑖𝑏𝑢𝑡𝑖𝑜𝑛(𝑉𝑑)
8. Continued….
This is the smallest volume in which a drug could distribute following
intravenous injection, but there is no theoretical upper limit on Vd, with
very large values occurring when very little of the injected dose remains in
the plasma, most being taken up into fat or bound to tissues.
Example: Suppose, a 300 mg drug is injected intravenously into a human.
Now that distribution within the body occurs instantenously and before
elimination of drug the serum is sampled and concentration of drug
measured in the plasma is 0.1 mg/mL.
The Vd= D/Cp =300/0.1= 3 L .
So, the drug has distributed in 3 L, and we would say that this is the apparent
volume of distribution.
But, if the measured plasma concentration was 0.01 mg/mL, we would say
that the apparent volume of distribution would be 30 L, and if the measured
concentration was 0.001 mg/mL, the apparent volume of distribution would
be 300 L.
9. Continued….
Importance of Vd: Vd identifies the peak plasma concentration
expected following a bolus dose. It is useful to know Vd when
considering dialysis as a means of accelerating drug elimination
in poisoned patients.
Drugs with a large Vd (e.g. many tricyclic antidepressants) are
not removed efficiently by haemodialysis because only a small
fraction of the total drug in the body is present in plasma.
Since, highly lipid-soluble compounds that are able to penetrate
cells and fatty tissues have a larger Vd than more polar
water-soluble compounds.
10. Repeated(multiple) dosing
If repeated doses are administered at dosing intervals much greater than
the drug’s elimination half-life, then the drug is accumulated in a little
amount in the body.
11. Continued….
But a steady state concentration is often needed to produce a consistent
effect throughout the dose interval. The following figure shows the
plasma concentration–time curve when a bolus is administered
repeatedly at an interval less than t1/2. The mean concentration rises
toward
steady
state
level.
12. Continued…..
If a drug is administered once every half-life, the peak plasma
concentration (Cmax) will be double the trough concentration (Cmin). In
practice, this amount of variation is tolerable in many therapeutic
situations, so a dosing interval approximately equal to the half-life is often
acceptable.
But several drugs have active metabolites that are eliminated more slowly
than the parent drug. This is the case with several of the benzodiazepines
which have active metabolites with half-lives of many days. Consequently,
adverse effects (e.g. confusion) may appear only when the steady state is
approached after several weeks of treatment. Such effect resolve when
the drug is stopped.
13. DEVIATIONS FROM THE ONE-COMPARTMENT MODEL WITH
FIRST-ORDER ELIMINATION (TWO-COMPARTMENT MODEL)
The one compartment model assumes that the drug can enter or leave the
body and the body acts like a single, uniform compartment. The drug is
distributed instantaneously and homogenously throughout the
compartment. Drug elimination also occurs from the compartment
immediately after injection.
In reality the body is more complex than a single compartment.
Here comes the two compartment model. The two compartment model
treats the body as a central compartment and a peripheral compartment.
These compartments have no precise anatomical meaning, although the
central compartment is assumed to consist of blood (from which samples
are taken for analysis) and the extracellular spaces of some well-perfused
tissues. The peripheral compartment consists of less well-perfused tissues
into which drug permeates more slowly.
14. Continued….
This figure shows plasma concentration -time curve following an
intravenous bolus dose of a drug that fits two compartment
model .
The initial rapid fall is
called the α phase, and mainly
reflect the distribution from
central compartment to the
pheripheral compartment.
The second, slower phase
reflects the drug elimination.
It is called the β phase.
15. NON-LINEAR (‘DOSE-DEPENDENT’)
PHARMACOKINETICS
Although many drugs are eliminated at a rate that is approximately
proportional to their concentration (‘first-order’ kinetics), there are
several therapeutically important exceptions.
Consider a drug that is eliminated by conversion to an inactive metabolite
by an enzyme. At high concentrations, the enzyme becomes saturated.
The drug concentration and reaction velocity are related by the Michaelis–
Menten equation. At low concentrations, the rate is linearly related to
concentration, whereas at saturating concentrations the rate is
independent of concentration (‘zero-order’ kinetics).
The same applies when a drug is eliminated by a saturable transport
process.
In clinical practice, drugs that exhibit non-linear kinetics are the exception
rather than the rule. This is because most drugs are used therapeutically
at doses that give rise to concentrations that are well below the Michaelis
constant (Km), and so operate on the lower, approximately linear, part of
the Michaelis–Menten curve relating elimination velocity to plasma
concentration.
17. CONTINUED….
Drugs that show non-linear kinetics in the therapeutic range
include heparin, phenytoin and ethanol. Some drugs(e.g.
barbiturates) show non-linearity in the part of the toxic range
that is encountered clinically.
Implications of non-linear pharmacokinetics include:
1. The decline in concentration vs. time following a bolus
dose of such a drug is not exponential.Instead, elimination
begins slowly and accelerates as plasma concentration falls.
18. Continued….
2. The time required to eliminate 50% of a dose increases with
increasing dose, so half-life is not constant.
3. A modest increase in dose of such a drug disproportionately increases
the amount of drug in the body once the drug elimination process is
saturated.This is very important clinically when using plasma
concentrations of, for example, phenytoin as a guide to dosing.
19. Case study
A young man develops idiopathic epilepsy and treatment is started
with phenytoin, 200 mg daily, given as a single dose last thing at night.
After a week, the patient’s serum phenytoin concentration is 25
μmol/L. (Therapeutic range is 40–80 μmol/L.) The dose is increased to
300 mg/day. One week later he is complaining of unsteadiness, there
is nystagmus and the serum concentration is 125 μmol/L. The dose is
reduced to 250 mg/day. The patient’s symptoms slowly improve and
the serum phenytoin concentration falls to 60 μmol/L (within the
therapeutic range).