Dosage Regimens II Arthur G. Roberts. Question Can a drug have a low therapeutic index and a broad therapeutic window? No therapeutic index= [drug] min,toxicity.

Slides:

Advertisements

Similar presentations

Anticonvulsants David G. Standaert, MD, PhD Massachusetts General Hospital Harvard Medical School.

Advertisements

First, zero, pseudo-zero order elimination Clearance

Mechanism of action of Antiepileptic Drugs

III. Drug Metabolism  The aim of drug metabolism is to convert lipid soluble (non polar) drugs to polar metabolites easily excreted in urine.  The liver.

Therapeutic Drug Monitoring (TDM)

Introduction:  The preparation of parenteral admixture usually involves the addition of one or more drugs to large volume solutions such as intravenous.

LECTURE 9: INTEGRATION OF SYNAPTIC INPUTS (Ionotropic Receptors) REQUIRED READING: Kandel text, Chapter 12 At neuromuscular synapse, single axonal action.

Novel Treatment of Excitotoxicity: Targeted Disruption of Intracellular Signalling From Glutamate Receptors.

Nerve physiology.

Ion Channels. Cell membrane Voltage-gated Ion Channels voltage-gated because they open and close depending on the electrical potential across the membrane.

Inhibitory and Excitatory Signals

ANTICONVULSANT DRUGS Edward D. French, Ph.D. Department of Pharmacology University of Arizona College of Medicine.

Pharmacokinetics Questions

ProCalc Nsg 231 Calculating IV Drug Dose based on Weight Example 1 Your patient’s current weight is 22 lbs. Dopamine is to be infused at 10 mcg/kg/minute.

Multiple IV Dosing Pharmacokinetic Research, Bioequivalence Studies,

Mitzi Payne, MD Pediatric Neurology Hoops Family Children’s Hospital at Cabell Huntington Hospital Marshall University Department of Neuroscience.

CNS depressants CNS depressants

6.1 Examples of small-molecule and peptide neurotransmitters. (Part 1)

Epilepsy Lecture Neuro Course 4th year. Objectives – To Review: What the term epilepsy means Basic mechanisms of epilepsy How seizures and epilepsies.

Chapter 16 Sedatives and Hypnotics  Graded dose-dependent depression of central nervous system function is a charicteristic of sedative-hypnotics.  Classification.

Anticonvulsive Effects of Sodium Phenobarbital. Experimental purpose  To master the anticonvulsive effects of sodium phenobarbital and the elementary.

PHARMACOKINETICS 1. Fate of drugs in the body 1.1 absorption

Non-linear Pharmacokinetics Arthur G. Roberts. Linear Pharmacokinetics AUC dose K Cl dose [Drug] plasma time ln[Drug] plasma time Increasing Dose.

ANTIEPILEPTICS Dr: Samah Gaafar Hassan.  a periodic recurrence of seizures with or without convulsions.  A convulsion implies violent, involuntary contraction(s)

Drugs in the Body (1) Recurrence Relations A patient is given an initial dose of 50mg of a drug. Each hour the patient is given a 20mg tablet of the.

PLASMA HALF LIFE ( t 1/2 ).  Minimum Effective Concentration (MEC): The plasma drug concentration below which a patient’s response is too small for clinical.

Multiple Dosing: Intermittent or multiple dose regimen

 all drugs not in gaseous state need to use fluid routes of excretion ◦ fluid routes include -sweat, tears, saliva, mucous, urine, bile, human milk ◦

Synaptic Transmission / Central Synapses II Tom O’Dell Department of Physiology C8-161 (NPI), x64654.

1 Single-dose kinetics Plasma [Drug] curve Upon administration [drug] plasma reaches a max Then begins to decline as the Drug is eliminated Cp max = max.

CLINICAL PHARMACOKINETICS OF LIDOCAINE

Clinical Pharmacokinetics of Carbamazepine

Sober Neuron Cl - Na + or K + GABA A receptor (Ligand-gated Ion Channel) GABA Glutamate (Glu) Action.

1. Fate of drugs in the body 1.1 absorption 1.2 distribution - volume of distribution 1.3 elimination - clearance 2. The half-life and its uses 3. Repeated.

BIOPHARMACEUTICS.

Principles of pharmacokinetics Prof. Kršiak Department of Pharmacology, Third Faculty of Medicine, Charles University in Prague Cycle II, Subject: General.

Clinical Pharmacokinetics of Phenobarbital

Prof. Dr. Henny Lucida, Apt

Some problems. Problem #1 A typical mammalian cell has, in mEq/liter [K + ] in = 140; [K + ] out = 5 [Na + ] in = 15; [Na + ] out = 145 [Cl - ] in = 4;

Neurological Disorders Lesson 3.2 How do our neurons communicate with each other? Chemical Signal Electrical Signal.

Clinical Pharmacokinetics of Procainamide Dr. Muslim Suardi Faculty of Pharmacy University of Andalas 2013.

Clarifications of Lecture #36- Drug Interactions I

Neural Mechanisms of Learning & Memory Lesson 24.

Clinical Pharmacokinetic Equations and Calculations

Dr. Laila M. Matalqah Ph.D. Pharmacology PHARMACOLOGY OF CNS part 2 General Pharmacology M212.

DEFINITIONS T1/2 & Tmax Cmax AUC 1st order kinetics

Sedatives, Hypnotics & Anxiolytics. BARBITURATES Derivatives of Barbituric Acid Barbituric acid itself has no sedative effect No more used as sedative.

Tetraodotoxin (fish) Saxitoxin (dinoflagellate-red tide) -blocks sodium channels -75 deaths/year in Japan X more potent than cocaine -little bit.

1 Back to Biochemistry… diffusion (passive, through PLBL) facilitative diffusion (passive, through channels) channels come in several flavors: ligand-gated.

Do Now Complete Part 1 on your worksheets with a partner. A problem for you to solve: – Given that you know the axon sends signals electrically, and that.

Pharmacokinetic Questions

The term epilepsy refers to a group of disorders characterized by excessive excitability of neurons within the CNS. This abnormal activity can produce.

ALLIE PUNKE PHARMCOKINETICS. PHENYTOIN THE BASICS What is the volume of distribution: Regular floor patient: L/kg Critically ill patient: 0.8.

Date of download: 6/25/2016 Copyright © 2016 American Medical Association. All rights reserved. From: Therapeutic Restoration of Spinal Inhibition via.

MULTIPLE DOSAGE REGIMEN

Anxiolytic , Sedative and Hypnotic Drugs

THERAPEUTIC WINDOW Lecture #19. Therapeutic Effectiveness ineffective effective minor ADR major ADR Therapeutic Effectiveness = Effective Therapy –

Metabolite Kinetics I Arthur G. Roberts. DrugMetabolite Renal Excretion Metabolite of a Metabolite Biliary Excretion keke Options keke keke keke Other.

Unit IV Lesson III, Activity I

Pharmacokinetics Tutoring

Anticonvulsants: Valproic acid

Neuronal Networks So far: the building blocks of neurons/networks

Pharmcokinetics Allie punke.

Pharmacogenetics and Pharmacoepidemiology “PHCY 480”

Postsynaptic currents and potentials

Volume 32, Issue 3, Pages (November 2001)

Drug Metabolism.

A representation of the central spinal and peripheral changes that accompany neuropathy. A representation of the central spinal and peripheral changes.

Presentation transcript:

Dosage Regimens II Arthur G. Roberts

Question Can a drug have a low therapeutic index and a broad therapeutic window? No therapeutic index= [drug] min,toxicity /[drug] min,effectiveness f(Effectiveness) [drug] Toxicity Therapeutic Window

Multiple-Dose Regimens Arthur G. Roberts

Dosing Frequency

drug p

Dosing Frequency N

t dose,N

Dosing Frequency drug p, max

Dosing Frequency drug p, min

Dosing Frequency drug ss, max

Dosing Frequency drug ss, min

Dosing Frequency f lost1 Only during the initial dose

Accumulation Index

Phenobarbital Neuron Cl - Na + or K + GABA A receptor (Ligand-gated Ion Channel) GABA Glutamate (Glu) Glutamate receptor (Ligand-gated Ion Channel) KCC2 (K+/Cl- symporter) (a.k.a. SLC12A5) Na + Voltage-Gated Ion Transporter Na + GABA K + and Cl - X Action potential used for seizures

Phenobarbital Cl (Normalized)=0.035 L/(hr*kg) no active metabolites V d (Normalized)=0.5L/kg dose IV = 30 mg = drug p0 dosing interval = 4 hours number of doses = 4 weight=70 kg Cl,Vd,k,t 1/2,f lost1,drug p,max,drug p,min drug ss,max,drug ss,min,AI induces CYP2C9 (effects?)