Causes of non linearity in pharmacokinetics pdf
•
51 likes•8,108 views
It includes the basic concept of linear and non-linear pharmacokinetics and the causes of non linearity in pharmacokinetics.
Report
Share
Report
Share
Download to read offline
Recommended
Causes of Non linear pharmacokinetics
Nonlinear pharmacokinetics can occur when the rate processes of drug absorption, distribution, metabolism, or excretion become dependent on dose size due to saturation of carrier proteins or enzymes. Some specific causes of nonlinearity include saturation of transporters during drug absorption, saturation of plasma protein binding sites or tissue binding sites during distribution, capacity-limited drug metabolism by enzyme saturation, and saturation of active tubular secretion or reabsorption processes during excretion. The Michaelis-Menten equation can describe the kinetics of these saturable, capacity-limited processes.
Non linear pharmacokinetics
The document discusses nonlinear pharmacokinetics and chronopharmacokinetics. Nonlinear pharmacokinetics occurs when the body's absorption, distribution, metabolism, or excretion of a drug becomes saturated at higher doses. This can cause the rate of drug elimination to decrease. Examples of processes that can become saturated include drug metabolism and renal excretion. Circadian rhythms can also impact drug pharmacokinetics by influencing absorption, distribution, metabolism, and excretion over 24-hour periods. Accounting for these temporal changes can improve drug therapy for circadian phase-dependent diseases.
Non linear kinetics
This document discusses linear and nonlinear pharmacokinetics. [1] Linear pharmacokinetics follow first-order kinetics where the rate of drug absorption, distribution, metabolism and excretion is proportional to dose. [2] Nonlinear pharmacokinetics occur when these processes become saturated at high doses due to limited enzyme or transporter capacity. [3] Michaelis-Menten kinetics are often used to model nonlinear processes and estimate parameters like Vmax and Km.
Pharmacokinetic models
This document discusses various approaches used to model pharmacokinetics. It describes compartment models, physiological models, and distributed parameter models that can be used to mathematically describe drug absorption, distribution, metabolism and excretion over time. It also discusses model-independent or non-compartmental analysis, which does not require assumptions about specific compartment models. Compartment models include mammillary and catenary models. Physiological models group tissues into compartments based on similar perfusion properties. Distributed parameter models account for variations in organ blood flow and drug diffusion.
Methods for Measurement of bioavailability
Which are the Methods for Measurement of bioavailability?- Pharmacokinetic method- Plasma level time studies, Urinary excretion studies.
Pharmacodynamic method: Acute pharmacologic response, Therapeutic response.
Non compartment model
The document discusses the non-compartmental pharmacokinetic model, which does not assume a specific number of compartments and instead assumes first-order elimination. It is a simple approach used to calculate parameters like half-life, clearance, and volume of distribution without complex compartmental assumptions. Key parameters like area under the curve (AUC) and mean residence time can be estimated using this model from concentration-time data using trapezoidal integration without assuming an underlying multi-compartment structure. While simple, this model provides essential exposure parameters needed to understand drug behavior without more complex compartmental modeling.
Pharmacokinetic models
PHARMACOKINETIC MODELS
Drug movement within the body is a complex process. The major objective is therefore to develop a generalized and simple approach to describe, analyse and interpret the data obtained during in vivo drug disposition studies.
The two major approaches in the quantitative study of various kinetic processes of drug disposition in the body are
Model approach, and
Model-independent approach (also called as non-compartmental analysis).
Bioavailability and bioequivalence
This document discusses bioavailability and bioequivalence concepts including definitions, objectives of bioavailability studies, types of bioavailability studies, and methods of measuring bioavailability. It also covers bioequivalence experimental study designs including completely randomized, randomized block, repeated measures, and Latin square designs. In vitro dissolution studies and developing in vitro-in vivo correlations to help assess bioavailability without human studies are also summarized.
Recommended
Causes of Non linear pharmacokinetics
Nonlinear pharmacokinetics can occur when the rate processes of drug absorption, distribution, metabolism, or excretion become dependent on dose size due to saturation of carrier proteins or enzymes. Some specific causes of nonlinearity include saturation of transporters during drug absorption, saturation of plasma protein binding sites or tissue binding sites during distribution, capacity-limited drug metabolism by enzyme saturation, and saturation of active tubular secretion or reabsorption processes during excretion. The Michaelis-Menten equation can describe the kinetics of these saturable, capacity-limited processes.
Non linear pharmacokinetics
The document discusses nonlinear pharmacokinetics and chronopharmacokinetics. Nonlinear pharmacokinetics occurs when the body's absorption, distribution, metabolism, or excretion of a drug becomes saturated at higher doses. This can cause the rate of drug elimination to decrease. Examples of processes that can become saturated include drug metabolism and renal excretion. Circadian rhythms can also impact drug pharmacokinetics by influencing absorption, distribution, metabolism, and excretion over 24-hour periods. Accounting for these temporal changes can improve drug therapy for circadian phase-dependent diseases.
Non linear kinetics
This document discusses linear and nonlinear pharmacokinetics. [1] Linear pharmacokinetics follow first-order kinetics where the rate of drug absorption, distribution, metabolism and excretion is proportional to dose. [2] Nonlinear pharmacokinetics occur when these processes become saturated at high doses due to limited enzyme or transporter capacity. [3] Michaelis-Menten kinetics are often used to model nonlinear processes and estimate parameters like Vmax and Km.
Pharmacokinetic models
This document discusses various approaches used to model pharmacokinetics. It describes compartment models, physiological models, and distributed parameter models that can be used to mathematically describe drug absorption, distribution, metabolism and excretion over time. It also discusses model-independent or non-compartmental analysis, which does not require assumptions about specific compartment models. Compartment models include mammillary and catenary models. Physiological models group tissues into compartments based on similar perfusion properties. Distributed parameter models account for variations in organ blood flow and drug diffusion.
Methods for Measurement of bioavailability
Which are the Methods for Measurement of bioavailability?- Pharmacokinetic method- Plasma level time studies, Urinary excretion studies.
Pharmacodynamic method: Acute pharmacologic response, Therapeutic response.
Non compartment model
The document discusses the non-compartmental pharmacokinetic model, which does not assume a specific number of compartments and instead assumes first-order elimination. It is a simple approach used to calculate parameters like half-life, clearance, and volume of distribution without complex compartmental assumptions. Key parameters like area under the curve (AUC) and mean residence time can be estimated using this model from concentration-time data using trapezoidal integration without assuming an underlying multi-compartment structure. While simple, this model provides essential exposure parameters needed to understand drug behavior without more complex compartmental modeling.
Pharmacokinetic models
PHARMACOKINETIC MODELS
Drug movement within the body is a complex process. The major objective is therefore to develop a generalized and simple approach to describe, analyse and interpret the data obtained during in vivo drug disposition studies.
The two major approaches in the quantitative study of various kinetic processes of drug disposition in the body are
Model approach, and
Model-independent approach (also called as non-compartmental analysis).
Bioavailability and bioequivalence
This document discusses bioavailability and bioequivalence concepts including definitions, objectives of bioavailability studies, types of bioavailability studies, and methods of measuring bioavailability. It also covers bioequivalence experimental study designs including completely randomized, randomized block, repeated measures, and Latin square designs. In vitro dissolution studies and developing in vitro-in vivo correlations to help assess bioavailability without human studies are also summarized.
Multicompartment Models
This document discusses multicompartment models, including two-compartment models. A two-compartment model classifies body tissues into a central compartment (blood, highly perfused tissues) and peripheral compartment (poorly perfused tissues). Depending on the compartment of drug elimination, two-compartment models can describe intravenous bolus administration, intravenous infusion, or extravascular administration. Compartment models are useful for characterizing drug behavior in patients and optimizing dosage regimens.
Mechanism of drug absorption in git
1. Drug absorption involves the movement of unchanged drug molecules from the site of administration into systemic circulation. It occurs primarily through the gastrointestinal (GI) tract and is influenced by factors like solubility, permeability, and transport mechanisms.
2. There are three main mechanisms of drug transport across the GI tract - transcellular, paracellular, and vesicular. Transcellular transport occurs across cells and includes passive diffusion, active transport, and carrier-mediated transport. Paracellular transport is between cell junctions. Vesicular transport involves endocytosis within cells.
3. The most common mechanism is passive diffusion, which does not require energy. Other mechanisms like active transport and carrier-mediated transport use
one compartment model ppt
The document discusses compartment modeling and one compartment open models. It describes how the body can be represented as a single well-mixed compartment and outlines the assumptions of compartmental models. It then covers one compartment open models for intravenous bolus administration, intravenous infusion, and extravascular administration. For intravenous bolus administration, the elimination phase can be characterized by parameters like elimination rate constant, half-life, and clearance. Intravenous infusion allows for constant rate input into the compartment. Extravascular administration models absorption as either zero-order or first-order kinetics.
ONE COMPARTMENT OPEN MODEL I.V BOLUS (Contact me: dr.m.bharathkumar@gmail.com)
ONE COMPARTMENT OPEN MODEL I.V BOLUS (Contact me: dr.m.bharathkumar@gmail.com)DR. METI.BHARATH KUMAR
The document appears to be a scanned receipt from a grocery store listing various food and household items purchased totaling $123.45. It includes the store name, date, time of purchase, payment method (credit card), and signature of the cashier. The receipt provides details of the transaction including item names, quantities, and individual prices.Methods of enhancing Dissolution and bioavailability of poorly soluble drugs
Bioavailability refers to the amount of drug that reaches systemic circulation after administration. It is reduced when drugs are administered orally rather than intravenously due to incomplete absorption and first-pass metabolism. The document discusses several methods for enhancing bioavailability of orally administered drugs with poor solubility or permeability. These include micronization, use of surfactants, salt forms, altering pH, polymorphism, complexation, molecular encapsulation, and forming solid solutions, eutectic mixtures or solid dispersions to improve solubility and dissolution rate.
Non linear pharmacokinetics and different volumes of distribution
This document discusses linear and nonlinear pharmacokinetics. Linear pharmacokinetics follow first-order kinetics and nonlinear pharmacokinetics follow Michaelis-Menten kinetics. Nonlinearity can occur due to saturation of drug absorption, distribution, metabolism or excretion processes. The Michaelis-Menten equation can describe nonlinear kinetics and data plots of drug concentration versus time can indicate nonlinear behavior.
Measurements of bioavailability
This document discusses measurements of bioavailability. It defines bioavailability and bioequivalence. There are two main methods to measure bioavailability - pharmacokinetic and pharmacodynamic. Pharmacokinetic methods include plasma level time studies and urinary excretion studies which measure parameters like Cmax, Tmax, and AUC from plasma data or urinary excretion rate and amount excreted from urine data. Pharmacodynamic methods include measuring acute pharmacological responses or therapeutic responses but have disadvantages like variable individual responses.
Bioequivalence studies
The document discusses bioequivalence, which refers to two drug products having the same rate and extent of absorption. There are two types of bioequivalence testing: in vivo, which involves human subjects; and in vitro, which involves dissolution testing. In vivo testing is generally required for immediate-release oral drugs that are systemically absorbed, have a narrow therapeutic index, or have complicated absorption properties. In vitro dissolution testing may suffice in some cases, such as when only the drug strength differs between products or when an acceptable in vitro-in vivo correlation exists.
MULTI COMPARTMENT MODELS (Contact me: dr.m.bharathkumar@gmail.com)
This document appears to be a scanned receipt from a grocery store listing various food and household items purchased totaling $123.45. The receipt details 11 separate items bought including milk, eggs, bread, toilet paper and more. It provides the item names, quantities, and individual prices for each item along with the subtotal, tax amount, and total cost of the purchase.
Nonlinear Pharmacokinetics
Nonlinear pharmacokinetics occurs when the body's processing of a drug is saturated at higher doses, causing kinetics parameters like clearance and half-life to change with dose. Michaelis-Menten kinetics are commonly used to model nonlinear metabolism, where the metabolic rate approaches a maximum (Vmax) at high concentrations. Parameters like Vmax and KM can be estimated from steady-state dosing and concentration data by linearizing the Michaelis-Menten equation. Drugs like phenytoin exhibit nonlinear kinetics due to capacity-limited hepatic metabolism.
Measurement of bioavailability
Bioavailability is defined as the rate and extent of absorption of a drug from its dosage form and the amount available at the site of action. It depends on pharmaceutical, patient, and route of administration factors. The objectives of bioavailability studies are to develop new formulations, determine the influence of excipients and other drugs, and control drug product quality. Bioavailability can be assessed using pharmacokinetic methods like plasma concentration-time profiles from single and multiple dose studies, and urinary excretion studies. Key parameters analyzed are Cmax, Tmax, and AUC which indicate rate and extent of absorption. Pharmacodynamic methods like acute pharmacological response and therapeutic response studies can also be used when pharmacokinetic methods are not suitable. In
Biopharmaceutics: Mechanisms of Drug Absorption
Biopharmaceutics is the study of factors influencing drug absorption, distribution, metabolism and excretion (ADME). There are three main mechanisms of drug absorption in the body: 1) transcellular/intracellular transport across epithelial cells, 2) paracellular/intercellular transport between epithelial cells, and 3) vesicular or corpuscular transport through endocytosis. Transcellular transport can occur passively through diffusion, pores or ion pairs, or actively through carriers or pumps. Paracellular transport is between tight cell junctions or through temporary openings. Vesicular transport involves pinocytosis or phagocytosis of substances into cells.
WAGNER NELSON METHOD (Contact me: dr.m.bharathkumar@gmail.com)
This document appears to be 3 scanned pages from a mobile device application called CamScanner. The pages are blank except for a watermark indicating they were scanned with CamScanner. In summary, the document provides no substantive information due to being 3 blank scanned pages from a mobile scanning application.
In-Vivo In-Vitro Correlation
This document discusses in vitro-in vivo correlations (IVIVCs). It defines IVIVC as a predictive mathematical model relating an in vitro property (e.g. dissolution rate) to an in vivo response (e.g. absorption rate). The document outlines the significance of IVIVCs in reducing bioequivalence studies and supporting biowaivers. It describes different levels of IVIVC (A, B, C) and parameters that can be correlated (dissolution rate to absorption rate; percent dissolved to percent absorbed). The document provides examples of IVIVC case studies and concludes that current regulatory guidelines only apply to oral dosage forms, while further research is needed to develop IVIVCs for other drug products.
Bioavailability & Bioequivalence Studies
This presentation summarizes key concepts regarding bioavailability and bioequivalence studies. It defines bioavailability as a measure of the rate and amount of drug reaching systemic circulation following administration of a dosage form. Absolute bioavailability compares intravenous and oral administration, while relative bioavailability compares oral formulations. The objectives of these studies are outlined. Methods of measuring bioavailability through pharmacokinetic methods like plasma level time studies and urinary excretion studies are described. Bioequivalence ensures two dosage forms reach systemic circulation at the same rate and extent. Study designs for in vivo and in vitro bioequivalence experiments are discussed, including completely randomized, randomized block, repeated measures, cross-over, and Latin square designs.
Two compartment open model sulekhappt.x.1
This document describes the two compartment open model for drug distribution and elimination. It discusses:
- How the body is divided into a central compartment (blood, highly perfused tissues) and peripheral compartment (poorly perfused tissues)
- How drugs distribute between compartments according to first-order rate constants K12 and K21, and are eliminated from the central compartment at a rate of KE
- Equations that describe drug concentrations in each compartment over time after intravenous or oral administration
- Methods for determining pharmacokinetic parameters like absorption rate constant Ka, distribution and elimination rate constants, and compartment volumes from drug concentration-time data.
Methods of Assessing Bioavailability
1. Measurement of Bioavailability:
Direct and indirect methods may be used to assess drug bioavailability. The in-vivo bioavailability of a drug product is demonstrated by the rate and extent of drug absorption, as determined by comparison of measured parameters, e.g., concentration of the active drug ingredient in the blood, cumulative urinary excretion rates, or pharmacological effects.
For drug products that are not intended to be absorbed into the bloodstream, bioavailability may be assessed by measurements intended to reflect the rate and extent to which the active ingredient or active moiety becomes available at the site of action.
The design of the bioavailability study depends on the objectives of the study, the ability to analyze the drug (and metabolites) in biological fluids, the pharmacodynamics of the drug substance, the route of drug administration, and the nature of the drug product.
Pharmacokinetic and/or pharmacodynamic parameters as well as clinical observations and in-vitro studies may be used to determine drug bioavailability from a drug product.
1.1. Pharmacokinetic methods:
These are very widely used and based upon the assumption that the pharmacokinetic profile reflects the therapeutic effectiveness of a drug. Thus these are indirect methods. The two major pharmacokinetic methods are:
The major pharmacokinetic methods are:
Plasma / blood level time profile.
o Time for peak plasma (blood) concentration (t max)
o Peak plasma drug concentration (Cmax)
o Area under the plasma drug concentration–time curve (AUC)
Urinary excretion studies.
o Cumulative amount of drug excreted in the urine (Du)
o Rate of drug excretion in the urine (dDu/dt)
o Time for maximum urinary excretion (t)
C. Other biological fluids
1.2. Pharmacodynamic methods:
IT involves direct measurement of drug effect on a (patho) physiological process as a function of time. Disadvantages of it may be high variability, difficult to measure, limited choices, less reliable, more subjective, drug response influenced by several physiological & environmental factors.
They involve determination of bioavailability from:
Acute pharmacological response.
Therapeutic response.
1.3. In-vitro dissolution studies
Closed compartment apparatus
Open compartment apparatus
Dialysis systems.
1.4. Clinical observations
Well-controlled clinical trials
Methods of enhancing bioavailability of drugs
This document discusses various approaches to enhancing the bioavailability of drugs, including enhancing drug solubility, permeability, stability, and gastrointestinal retention. It describes how bioavailability can be improved by increasing a drug's dissolution rate through methods like micronization, nanosuspensions, and use of surfactants. Permeability can be enhanced using lipid technologies, ion pairing, or penetration enhancers. Stability can be improved with enteric coatings or complexation. Gastrointestinal retention time can be lengthened to boost absorption.
IVIVC
It is defined as “the predictive mathematical model that describes the relationship between in vitro property (such as rate & extent of dissolution) of a dosage form and in vivo response (such as plasma drug concentration or amount of drug absorbed)”.
Absorption of drugs from non per os extravascular administration
Non-oral routes of drug administration provide advantages over oral routes by bypassing the gastrointestinal tract and avoiding first-pass metabolism. Common non-oral routes discussed include buccal/sublingual, rectal, topical, intramuscular, subcutaneous, pulmonary, intranasal, intraocular, and vaginal administration. Absorption through these routes occurs primarily via passive diffusion, carrier-mediated transport, or pore transport depending on the drug properties and administration site. Non-oral routes allow for rapid drug absorption, higher bioavailability compared to oral routes, and targeted delivery for local or systemic effects.
Non linear pharmacokinetics
pharmacokinetics is the important topic in both pharmacology and pharmaceutics in degree and masters level . the thorough knowledge in the fiels of pharmacokinetics will helps to choose the proper medicine to treat a particular disesse
BPharma-6Sem-Biopharmaceutics & Pharmacokinetics.pdf
Michaelis-Menten kinetics is commonly used to describe non-linear pharmacokinetics when drug metabolism or elimination involves saturable enzyme systems. Non-linearity occurs when the capacity of the enzyme is exceeded, leading to saturation. This document discusses various causes and examples of non-linear pharmacokinetics, including saturation of absorption, distribution, metabolism and excretion processes. It also describes the two-compartment open model and how drug concentrations change in each compartment over time following intravenous bolus dosing.
More Related Content
What's hot
Multicompartment Models
This document discusses multicompartment models, including two-compartment models. A two-compartment model classifies body tissues into a central compartment (blood, highly perfused tissues) and peripheral compartment (poorly perfused tissues). Depending on the compartment of drug elimination, two-compartment models can describe intravenous bolus administration, intravenous infusion, or extravascular administration. Compartment models are useful for characterizing drug behavior in patients and optimizing dosage regimens.
Mechanism of drug absorption in git
1. Drug absorption involves the movement of unchanged drug molecules from the site of administration into systemic circulation. It occurs primarily through the gastrointestinal (GI) tract and is influenced by factors like solubility, permeability, and transport mechanisms.
2. There are three main mechanisms of drug transport across the GI tract - transcellular, paracellular, and vesicular. Transcellular transport occurs across cells and includes passive diffusion, active transport, and carrier-mediated transport. Paracellular transport is between cell junctions. Vesicular transport involves endocytosis within cells.
3. The most common mechanism is passive diffusion, which does not require energy. Other mechanisms like active transport and carrier-mediated transport use
one compartment model ppt
The document discusses compartment modeling and one compartment open models. It describes how the body can be represented as a single well-mixed compartment and outlines the assumptions of compartmental models. It then covers one compartment open models for intravenous bolus administration, intravenous infusion, and extravascular administration. For intravenous bolus administration, the elimination phase can be characterized by parameters like elimination rate constant, half-life, and clearance. Intravenous infusion allows for constant rate input into the compartment. Extravascular administration models absorption as either zero-order or first-order kinetics.
ONE COMPARTMENT OPEN MODEL I.V BOLUS (Contact me: dr.m.bharathkumar@gmail.com)
ONE COMPARTMENT OPEN MODEL I.V BOLUS (Contact me: dr.m.bharathkumar@gmail.com)DR. METI.BHARATH KUMAR
The document appears to be a scanned receipt from a grocery store listing various food and household items purchased totaling $123.45. It includes the store name, date, time of purchase, payment method (credit card), and signature of the cashier. The receipt provides details of the transaction including item names, quantities, and individual prices.Methods of enhancing Dissolution and bioavailability of poorly soluble drugs
Bioavailability refers to the amount of drug that reaches systemic circulation after administration. It is reduced when drugs are administered orally rather than intravenously due to incomplete absorption and first-pass metabolism. The document discusses several methods for enhancing bioavailability of orally administered drugs with poor solubility or permeability. These include micronization, use of surfactants, salt forms, altering pH, polymorphism, complexation, molecular encapsulation, and forming solid solutions, eutectic mixtures or solid dispersions to improve solubility and dissolution rate.
Non linear pharmacokinetics and different volumes of distribution
This document discusses linear and nonlinear pharmacokinetics. Linear pharmacokinetics follow first-order kinetics and nonlinear pharmacokinetics follow Michaelis-Menten kinetics. Nonlinearity can occur due to saturation of drug absorption, distribution, metabolism or excretion processes. The Michaelis-Menten equation can describe nonlinear kinetics and data plots of drug concentration versus time can indicate nonlinear behavior.
Measurements of bioavailability
This document discusses measurements of bioavailability. It defines bioavailability and bioequivalence. There are two main methods to measure bioavailability - pharmacokinetic and pharmacodynamic. Pharmacokinetic methods include plasma level time studies and urinary excretion studies which measure parameters like Cmax, Tmax, and AUC from plasma data or urinary excretion rate and amount excreted from urine data. Pharmacodynamic methods include measuring acute pharmacological responses or therapeutic responses but have disadvantages like variable individual responses.
Bioequivalence studies
The document discusses bioequivalence, which refers to two drug products having the same rate and extent of absorption. There are two types of bioequivalence testing: in vivo, which involves human subjects; and in vitro, which involves dissolution testing. In vivo testing is generally required for immediate-release oral drugs that are systemically absorbed, have a narrow therapeutic index, or have complicated absorption properties. In vitro dissolution testing may suffice in some cases, such as when only the drug strength differs between products or when an acceptable in vitro-in vivo correlation exists.
MULTI COMPARTMENT MODELS (Contact me: dr.m.bharathkumar@gmail.com)
This document appears to be a scanned receipt from a grocery store listing various food and household items purchased totaling $123.45. The receipt details 11 separate items bought including milk, eggs, bread, toilet paper and more. It provides the item names, quantities, and individual prices for each item along with the subtotal, tax amount, and total cost of the purchase.
Nonlinear Pharmacokinetics
Nonlinear pharmacokinetics occurs when the body's processing of a drug is saturated at higher doses, causing kinetics parameters like clearance and half-life to change with dose. Michaelis-Menten kinetics are commonly used to model nonlinear metabolism, where the metabolic rate approaches a maximum (Vmax) at high concentrations. Parameters like Vmax and KM can be estimated from steady-state dosing and concentration data by linearizing the Michaelis-Menten equation. Drugs like phenytoin exhibit nonlinear kinetics due to capacity-limited hepatic metabolism.
Measurement of bioavailability
Bioavailability is defined as the rate and extent of absorption of a drug from its dosage form and the amount available at the site of action. It depends on pharmaceutical, patient, and route of administration factors. The objectives of bioavailability studies are to develop new formulations, determine the influence of excipients and other drugs, and control drug product quality. Bioavailability can be assessed using pharmacokinetic methods like plasma concentration-time profiles from single and multiple dose studies, and urinary excretion studies. Key parameters analyzed are Cmax, Tmax, and AUC which indicate rate and extent of absorption. Pharmacodynamic methods like acute pharmacological response and therapeutic response studies can also be used when pharmacokinetic methods are not suitable. In
Biopharmaceutics: Mechanisms of Drug Absorption
Biopharmaceutics is the study of factors influencing drug absorption, distribution, metabolism and excretion (ADME). There are three main mechanisms of drug absorption in the body: 1) transcellular/intracellular transport across epithelial cells, 2) paracellular/intercellular transport between epithelial cells, and 3) vesicular or corpuscular transport through endocytosis. Transcellular transport can occur passively through diffusion, pores or ion pairs, or actively through carriers or pumps. Paracellular transport is between tight cell junctions or through temporary openings. Vesicular transport involves pinocytosis or phagocytosis of substances into cells.
WAGNER NELSON METHOD (Contact me: dr.m.bharathkumar@gmail.com)
This document appears to be 3 scanned pages from a mobile device application called CamScanner. The pages are blank except for a watermark indicating they were scanned with CamScanner. In summary, the document provides no substantive information due to being 3 blank scanned pages from a mobile scanning application.
In-Vivo In-Vitro Correlation
This document discusses in vitro-in vivo correlations (IVIVCs). It defines IVIVC as a predictive mathematical model relating an in vitro property (e.g. dissolution rate) to an in vivo response (e.g. absorption rate). The document outlines the significance of IVIVCs in reducing bioequivalence studies and supporting biowaivers. It describes different levels of IVIVC (A, B, C) and parameters that can be correlated (dissolution rate to absorption rate; percent dissolved to percent absorbed). The document provides examples of IVIVC case studies and concludes that current regulatory guidelines only apply to oral dosage forms, while further research is needed to develop IVIVCs for other drug products.
Bioavailability & Bioequivalence Studies
This presentation summarizes key concepts regarding bioavailability and bioequivalence studies. It defines bioavailability as a measure of the rate and amount of drug reaching systemic circulation following administration of a dosage form. Absolute bioavailability compares intravenous and oral administration, while relative bioavailability compares oral formulations. The objectives of these studies are outlined. Methods of measuring bioavailability through pharmacokinetic methods like plasma level time studies and urinary excretion studies are described. Bioequivalence ensures two dosage forms reach systemic circulation at the same rate and extent. Study designs for in vivo and in vitro bioequivalence experiments are discussed, including completely randomized, randomized block, repeated measures, cross-over, and Latin square designs.
Two compartment open model sulekhappt.x.1
This document describes the two compartment open model for drug distribution and elimination. It discusses:
- How the body is divided into a central compartment (blood, highly perfused tissues) and peripheral compartment (poorly perfused tissues)
- How drugs distribute between compartments according to first-order rate constants K12 and K21, and are eliminated from the central compartment at a rate of KE
- Equations that describe drug concentrations in each compartment over time after intravenous or oral administration
- Methods for determining pharmacokinetic parameters like absorption rate constant Ka, distribution and elimination rate constants, and compartment volumes from drug concentration-time data.
Methods of Assessing Bioavailability
1. Measurement of Bioavailability:
Direct and indirect methods may be used to assess drug bioavailability. The in-vivo bioavailability of a drug product is demonstrated by the rate and extent of drug absorption, as determined by comparison of measured parameters, e.g., concentration of the active drug ingredient in the blood, cumulative urinary excretion rates, or pharmacological effects.
For drug products that are not intended to be absorbed into the bloodstream, bioavailability may be assessed by measurements intended to reflect the rate and extent to which the active ingredient or active moiety becomes available at the site of action.
The design of the bioavailability study depends on the objectives of the study, the ability to analyze the drug (and metabolites) in biological fluids, the pharmacodynamics of the drug substance, the route of drug administration, and the nature of the drug product.
Pharmacokinetic and/or pharmacodynamic parameters as well as clinical observations and in-vitro studies may be used to determine drug bioavailability from a drug product.
1.1. Pharmacokinetic methods:
These are very widely used and based upon the assumption that the pharmacokinetic profile reflects the therapeutic effectiveness of a drug. Thus these are indirect methods. The two major pharmacokinetic methods are:
The major pharmacokinetic methods are:
Plasma / blood level time profile.
o Time for peak plasma (blood) concentration (t max)
o Peak plasma drug concentration (Cmax)
o Area under the plasma drug concentration–time curve (AUC)
Urinary excretion studies.
o Cumulative amount of drug excreted in the urine (Du)
o Rate of drug excretion in the urine (dDu/dt)
o Time for maximum urinary excretion (t)
C. Other biological fluids
1.2. Pharmacodynamic methods:
IT involves direct measurement of drug effect on a (patho) physiological process as a function of time. Disadvantages of it may be high variability, difficult to measure, limited choices, less reliable, more subjective, drug response influenced by several physiological & environmental factors.
They involve determination of bioavailability from:
Acute pharmacological response.
Therapeutic response.
1.3. In-vitro dissolution studies
Closed compartment apparatus
Open compartment apparatus
Dialysis systems.
1.4. Clinical observations
Well-controlled clinical trials
Methods of enhancing bioavailability of drugs
This document discusses various approaches to enhancing the bioavailability of drugs, including enhancing drug solubility, permeability, stability, and gastrointestinal retention. It describes how bioavailability can be improved by increasing a drug's dissolution rate through methods like micronization, nanosuspensions, and use of surfactants. Permeability can be enhanced using lipid technologies, ion pairing, or penetration enhancers. Stability can be improved with enteric coatings or complexation. Gastrointestinal retention time can be lengthened to boost absorption.
IVIVC
It is defined as “the predictive mathematical model that describes the relationship between in vitro property (such as rate & extent of dissolution) of a dosage form and in vivo response (such as plasma drug concentration or amount of drug absorbed)”.
Absorption of drugs from non per os extravascular administration
Non-oral routes of drug administration provide advantages over oral routes by bypassing the gastrointestinal tract and avoiding first-pass metabolism. Common non-oral routes discussed include buccal/sublingual, rectal, topical, intramuscular, subcutaneous, pulmonary, intranasal, intraocular, and vaginal administration. Absorption through these routes occurs primarily via passive diffusion, carrier-mediated transport, or pore transport depending on the drug properties and administration site. Non-oral routes allow for rapid drug absorption, higher bioavailability compared to oral routes, and targeted delivery for local or systemic effects.
What's hot (20)
ONE COMPARTMENT OPEN MODEL I.V BOLUS (Contact me: dr.m.bharathkumar@gmail.com)
ONE COMPARTMENT OPEN MODEL I.V BOLUS (Contact me: dr.m.bharathkumar@gmail.com)
Methods of enhancing Dissolution and bioavailability of poorly soluble drugs
Methods of enhancing Dissolution and bioavailability of poorly soluble drugs
Non linear pharmacokinetics and different volumes of distribution
Non linear pharmacokinetics and different volumes of distribution
MULTI COMPARTMENT MODELS (Contact me: dr.m.bharathkumar@gmail.com)
MULTI COMPARTMENT MODELS (Contact me: dr.m.bharathkumar@gmail.com)
WAGNER NELSON METHOD (Contact me: dr.m.bharathkumar@gmail.com)
WAGNER NELSON METHOD (Contact me: dr.m.bharathkumar@gmail.com)
Absorption of drugs from non per os extravascular administration
Absorption of drugs from non per os extravascular administration
Similar to Causes of non linearity in pharmacokinetics pdf
Non linear pharmacokinetics
pharmacokinetics is the important topic in both pharmacology and pharmaceutics in degree and masters level . the thorough knowledge in the fiels of pharmacokinetics will helps to choose the proper medicine to treat a particular disesse
BPharma-6Sem-Biopharmaceutics & Pharmacokinetics.pdf
Michaelis-Menten kinetics is commonly used to describe non-linear pharmacokinetics when drug metabolism or elimination involves saturable enzyme systems. Non-linearity occurs when the capacity of the enzyme is exceeded, leading to saturation. This document discusses various causes and examples of non-linear pharmacokinetics, including saturation of absorption, distribution, metabolism and excretion processes. It also describes the two-compartment open model and how drug concentrations change in each compartment over time following intravenous bolus dosing.
non linear pharmakokinetic causes of nonlinearity
This document discusses nonlinear pharmacokinetics, which occurs when the rate processes of drug absorption, distribution, metabolism, or excretion are dependent on carrier proteins or enzymes that have a limited capacity and can become saturated at high drug concentrations. This results in pharmacokinetic parameters like clearance and half-life varying with dose. Nonlinearity can be detected by determining parameters like bioavailability, elimination half-life, and clearance at different doses. It is commonly caused by saturation of absorption, distribution, metabolic or excretory pathways. Some examples of drugs that exhibit nonlinear kinetics due to different mechanisms like saturation of plasma protein binding or metabolic enzymes are provided.
A PPT on Non-linear Pharmacokinetics
This document discusses non-linear pharmacokinetics and pharmacodynamics. It begins by defining basic kinetic parameters like absorption and elimination rate constants, volume of distribution, and bioavailability fraction. It then explores possible causes of non-linearity, including saturation of absorption, distribution, metabolism and excretion processes. Non-linear binding due to saturation of plasma protein binding sites is also covered. The document concludes by giving an example of non-linear pharmacological responses with phenytoin, where capacity-limited metabolism leads to fluctuating clearance and half-life with changing plasma concentrations.
Non Linear Pharmacokinetics
Non-linear pharmacokinetics occurs when the rate of absorption, distribution, metabolism, or excretion of a drug depends on the dose administered. This can be due to saturation of enzymes involved in drug metabolism or transporters involved in absorption and excretion. According to the Michaelis-Menten equation, the rate of drug clearance will approach a maximum theoretical rate (Vmax) as the drug concentration increases, leading to non-linear kinetics. In linear kinetics, pharmacokinetic parameters are constant regardless of dose, while in non-linear kinetics they are dose-dependent.
Biopharmaceutics
This document discusses linear and nonlinear pharmacokinetics. It defines linear pharmacokinetics as processes where drug parameters are proportional to dose. Nonlinear pharmacokinetics occurs when absorption, distribution, or metabolism pathways become saturated at high doses. Michaelis-Menten kinetics are used to model saturation effects. Methods for determining the Michaelis-Menten constants Km and Vmax using steady state drug concentrations include Lineweaver-Burk plots, direct linear plots, and graphical methods. Common drugs exhibiting nonlinear behavior and their causes are also outlined.
non linear.pptx
This document discusses linear and non-linear pharmacokinetics. Linear pharmacokinetics follow first-order kinetics where the rate of drug elimination is directly proportional to drug concentration. With non-linear kinetics, the rate of elimination appears zero-order at higher concentrations as a constant amount is eliminated per unit time. Non-linear kinetics occur when absorption, distribution, metabolism or excretion processes become saturated at higher doses. This can be detected by determining how pharmacokinetic parameters change with different doses. Causes of non-linearity include saturation of transporters, binding proteins, metabolic enzymes and renal reabsorption/secretion mechanisms.
Nonlinear pharmacokinetics.pptx1[1]
This document discusses linear and nonlinear pharmacokinetics. Linear pharmacokinetics follow first-order kinetics and the concentration of a drug is proportional to the administered dose. Nonlinear pharmacokinetics occur when absorption, distribution, metabolism or excretion processes become saturated, leading to dose-dependent changes in pharmacokinetic parameters. Nonlinearity can be detected by examining steady state plasma concentrations and pharmacokinetic parameters at different doses. Causes of nonlinearity include saturation of drug transporters, plasma protein binding sites, metabolic enzymes, and renal excretion mechanisms.
Inhibition and induction of drug metabolism
The document discusses inhibition and induction of drug metabolism. Induction increases enzyme activity and intracellular enzyme concentration, while inhibition decreases enzyme activity. The cytochrome P450 system, specifically CYP3A4, metabolizes many drugs and its inhibition or induction can cause drug-drug interactions. Factors like genetic polymorphisms, disease, age, and gender can also affect biotransformation. Drug interactions are an important consideration in polypharmacy and when monitoring drug levels.
Drug interactions by amna samin
The document discusses drug interactions, defining it as when the pharmacological activity of one drug is altered by the concomitant use of another drug. It describes the main types of interactions as pharmacokinetic, involving effects on absorption, distribution, metabolism and excretion, and pharmacodynamic, involving effects on pharmacological activity. The key mechanisms of pharmacokinetic interactions are induction or inhibition of drug-metabolizing enzymes and displacement from plasma protein binding. Food and herbs can also cause interactions.
NONLINEAR PHARMACOKINETICS
ONE CAN UNDERSTAND THE DIFFERENCE BETWEEN LINEARITY AND NONLINEARITY IN PHARMACOKINETICS, CAUSES AND DERIVATION OF MICHAELIS MENTEN KINETICS
Drug metabolism
1. Drug metabolism is the process by which the body breaks down or alters drugs through specialized enzyme systems. It aims to make drugs more polar, water soluble, and less lipid soluble to promote excretion.
2. Drug metabolism occurs through two phases - phase 1 involves changes like oxidation, reduction, or hydrolysis. Phase 2 involves conjugating the drug or its metabolites to endogenous substances.
3. Factors that influence drug metabolism include age, diet, genetic variation, health, nutrition, gender, protein binding, species differences, substrate competition, and enzyme induction or inhibition. Cytochrome P450 and conjugating enzymes are involved in the metabolic processes.
Pharmacokinetics variations in Disease States.
The biggest issue in PK/PD and drug therapy is variability in
response. Variability factors that affect pharmacokinetics and pharmacodynamics influence clinical trials and dose regimen designs.
EFFECT OF HEPATIC DISEASE ON PHARMACOKINETICS.pptx
The document discusses the effect of hepatic (liver) disease on drug pharmacokinetics. Hepatic diseases can alter how drugs are metabolized, distributed, and eliminated from the body. This can lead to drug accumulation, changes in active metabolites formed, and altered protein binding. Several factors are relevant when considering drug dosing in patients with hepatic impairment, including changes in enzyme activity and blood flow. Tests are used to assess liver function and severity of disease, but do not fully capture changes to drug metabolism. Drugs may require dose adjustments in patients with hepatic impairment depending on the fraction of the drug metabolized by the liver.
Introduction to pharmacokinetics and pharmacodynamics principles
This presentation will give u overall basic information regarding pharmacokinetics and pharmacodynamics...
Pk2
This document discusses clinical pharmacokinetics and pharmacodynamics. It defines pharmacokinetics as how the body affects a drug through absorption, distribution, metabolism and elimination. Factors like age can impact these processes in pediatric patients. It also discusses pharmacodynamics, how drugs act on the body, and how pharmacokinetics and pharmacodynamics together can help individualize drug therapy and decrease adverse effects.
Drug metabolism affected by diseases
Thyroid disease and renal disease can influence drug metabolism in several ways. Thyroid dysfunction can cause changes in drug metabolism ranging from profound to moderate or negligible, depending on the drug. Renal impairment requires dosage reductions for drugs that are primarily cleared renally. Liver diseases like cirrhosis, jaundice, alcoholic liver disease, viral hepatitis, and hepatoma can also impact drug metabolism through various mechanisms such as decreasing drug clearance or inhibiting metabolic enzyme pathways. The effects are complex and unpredictable, varying with the type and severity of the disease.
Pharmakokinetics & pharmakodynamics of chemotherapy drugs
This presentation includes important factors to be considered prior to deciding anti cancer drugs and dosage
Pharmacokinetic_absorption_and_distribut.pptx
This document discusses pharmacokinetics concepts related to drug absorption and distribution. It defines pharmacokinetics as what the body does to drugs and pharmacodynamics as what drugs do to the body. It describes factors that influence drug absorption like pharmaceutical form, gastrointestinal contents, and concurrent medications. It also explains distribution is determined by vascularization, lipid solubility, and protein binding. Drugs must cross membranes to reach systemic circulation unless administered intravenously.
Similar to Causes of non linearity in pharmacokinetics pdf (20)
BPharma-6Sem-Biopharmaceutics & Pharmacokinetics.pdf
BPharma-6Sem-Biopharmaceutics & Pharmacokinetics.pdf
EFFECT OF HEPATIC DISEASE ON PHARMACOKINETICS.pptx
EFFECT OF HEPATIC DISEASE ON PHARMACOKINETICS.pptx
Introduction to pharmacokinetics and pharmacodynamics principles
Introduction to pharmacokinetics and pharmacodynamics principles
Pharmakokinetics & pharmakodynamics of chemotherapy drugs
Pharmakokinetics & pharmakodynamics of chemotherapy drugs
Recently uploaded
Journal Article Review on Rasamanikya
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.
Osteoporosis - Definition , Evaluation and Management .pdf
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Hemodialysis: Chapter 4, Dialysate Circuit - Dr.Gawad
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler Community Health Nursing A Canadian Perspective, 5th Edition TEST BANK by Stamler Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Study Guide Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Studocu Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Course Hero Community Health Nursing A Canadian Perspective, 5th Edition Answers Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Course hero Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Studocu Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Study Guide Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Ebook Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Questions Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Studocu Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Stuvia
REGULATION FOR COMBINATION PRODUCTS AND MEDICAL DEVICES.pptx
It includes regulation of combination products and medical devices. FDA and industry liaisons.
Histopathology of Rheumatoid Arthritis: Visual treat
Histopathology of Rheumatoid Arthritis: Visual treat
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...
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).
Top-Vitamin-Supplement-Brands-in-India List
Swisschem Dermacare provides the Top 10 Vitamin Supplement Brands in India. To know more about us give us call at our official number
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptx
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.share - Lions, tigers, AI and health misinformation, oh my!.pptx
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
vonoprazan A novel drug for GERD presentation
Vonoprazan, a new potassium acid channel blocker used in the conditions of GERD and gastric ulcer, duodenal ulcer ....
Identifying Major Symptoms of Slip Disc.
Our backs are like superheroes, holding us up and helping us move around. But sometimes, even superheroes can get hurt. That’s where slip discs come in.
Cell Therapy Expansion and Challenges in Autoimmune Disease
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Integrating Ayurveda into Parkinson’s Management: A Holistic Approach
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Adhd Medication Shortage Uk - trinexpharmacy.com
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
Recently uploaded (20)
Osteoporosis - Definition , Evaluation and Management .pdf
Osteoporosis - Definition , Evaluation and Management .pdf
Hemodialysis: Chapter 4, Dialysate Circuit - Dr.Gawad
Hemodialysis: Chapter 4, Dialysate Circuit - Dr.Gawad
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...
REGULATION FOR COMBINATION PRODUCTS AND MEDICAL DEVICES.pptx
REGULATION FOR COMBINATION PRODUCTS AND MEDICAL DEVICES.pptx
Vestibulocochlear Nerve by Dr. Rabia Inam Gandapore.pptx
Vestibulocochlear Nerve by Dr. Rabia Inam Gandapore.pptx
Histopathology of Rheumatoid Arthritis: Visual treat
Histopathology of Rheumatoid Arthritis: Visual treat
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptx
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptx
share - Lions, tigers, AI and health misinformation, oh my!.pptx
share - Lions, tigers, AI and health misinformation, oh my!.pptx
Cell Therapy Expansion and Challenges in Autoimmune Disease
Cell Therapy Expansion and Challenges in Autoimmune Disease
Integrating Ayurveda into Parkinson’s Management: A Holistic Approach
Integrating Ayurveda into Parkinson’s Management: A Holistic Approach
Tests for analysis of different pharmaceutical.pptx
Tests for analysis of different pharmaceutical.pptx
Causes of non linearity in pharmacokinetics pdf
- 1. Causes of non-linearity in Pharmacokinetics Presented by: Niva Rani Gogoi M.Pharm 2nd sem Roll no: 05
- 2. What is Linear Pharmacokinetics ? The change in the amount of drug in the body or the change in its plasma concentration is proportional to its dose. In such situation the rate processes follow first order or linear kinetics. Pharmacokinetic parameters of a drug remains unaffected. Dose-independent pharmacokinetics Increased or chronic medication → deviation from linear pharmacokinetics
- 3. What is Non-linear Pharmacokinetics ? The rate process of drug’s ADME are dependent upon carrier or enzymes that are: In such cases, an essentially first-order kinetics transforms into a mixture of first-order and zero-order rate processes. Pharmacokinetics of such drugs are said to be dose-dependent. Enzymes or Carriers Substrate specific Definite capacities Susceptible to saturation
- 4. Detection of non-linearity Determination of steady state plasma concentration at different doses: If, Css ∝ Xo (linear) Determination of some important pharmacokinetic parameters :F, t1/2 , Cl. Any change in these parameters is indicative to non- linearity.
- 5. What are the DIFFERENCES? Linear Pharmacokinetics Dose independent Follows first-order rate kinetics Non-linear Pharmacokinetics Dose dependent Follows mixture of first and zero-order rate kinetics
- 6. When dose ∝ Css : linear pharmacokinetics When Css changes in a disproportionate fashion after altering the dose: non-linear pharmacokinetics.
- 7. Why non-linearity occurs ? A. Drug Absorption Three sources 1. When absorption is solubility or dissolution rate-limited. Eg: Griseofulvin 2. When absorption involves carrier - mediated transport system. Eg: Ascorbic acid 3. When presystemic gut wall / hepatic metabolism attains saturation. Eg: Propranolol. Parameters affected F, Ka , Cmax and AUC.
- 8. Other causes 4. Changes in gastric emptying 5. Changes in gastric blood flow 6. Changes in physiological factors
- 9. B. Drug Distribution 1. Saturation of binding sites on plasma proteins. Eg: Phenylbutazone. 2. Saturation of tissue binding sites. Eg: Thiopental In both the cases there is an increase in free plasma drug concentration. Increase in Vd only in (1) Clearance with high ER get increased due to saturation of binding sites.
- 10. C. Drug Metabolism Two imp causes: 1. Capacity - limited metabolism due to enzyme and/or cofactor saturation. Eg: Phenytoin 2. Enzyme induction - decrease in peak plasma concentration. Eg: Carbamazepine. Other causes: 3. Saturation of binding sites 4. Inhibitory effect of the metabolite and enzyme 5. Pathological conditions 6. Changes in hepatic blood flow
- 11. Most clinical importance: small dose administered cause large variation in Css Major source of large intersubject variability
- 12. D. Excretion Two active processes which are saturable: 1. Active tubular secretion. Eg: Penicillin G 2. Active tubular reabsorption. Eg: Water soluble vitamins & Glucose. Saturation of carrier systems - decrease in renal clearance in both the cases. Other causes 3. Forced diuresis 4. Changes in urine pH 5. Nephrotoxicity 6. Saturation of binding sites.
- 13. Examples of drugs Causes Examples GI absorption: Saturable transport in gut wall Saturable GI decomposition Intestinal metabolism Riboflavin, Gabapentin Penicillin G, Omeprazole Propranolol, Salicylamide Distribution: Saturable plasma protein binding Tissue binding Phenylbutazone, Lidocaine Imipramine Metabolism: Saturable metabolism Enzyme induction Metabolite inhibition Phenytion, Salicylic acid Carbamazepine Diazepam Renal elimination: Active secretion Tubular reabsorption Change in urine pH Para- aminohippuric acid Ascorbic acid, Riboflavin Salicylic acid, Dextroamphetamine
- 14. Thank you !!