DOCSLIB.ORG

Pharmacology Review with Action List

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Pharmacology Review with Action List Review of Year Y2 Medical Pharmacology Essentials (PHAR 216) • Course occurs in the fall term of Year 2. • Course Director – Sarah J. Freemantle, PhD (co-director) David Nierenberg, MD • Course has 33 curricular hours (plus the Final Exam and Narrative Assessment evaluation events) • Course was last reviewed in April 2012. The formal review is missing, however, and annual summary letters from Dr Nierenberg are substituted for this purpose. Action Plan from Prior Review From David Nierenberg's letter dated Oct 30, 2012: Overall, well organized with excellent scores and logical organization. Suggestions - Provide written notes in addition to lecture PPT Involve all students in each small group conference, not just the students presenting the cases. Have other lecturers use the “pharm card” system to help students focus on the most important information they need to know. From David Nierenberg's letter dated Oct 28, 2013: New method of student survey through Oasis, however, the overall evaluation was “good to very good”, with the overall evaluation of 3.71. The students really loved the “clinical correlations” and the use of the Pharm cards. Suggestions - Provide written notes in addition to the PPT files, which most but not all lecturers do. Get all students involved with the small groups, not just the student presenters. Also, prepare “model” answers to the cases discussed. Having all lecturers use the Pharm card system, in order to help students know the most important information about each drug. Old Course Objectives (Ilios) Course Objectives (CO) Links (GO) Sessions (CO) 1 Explain the basic concepts of drug-receptor interactions and second messenger systems how MS2,MS1 40 dose response curves can be used to define safe dosing practice. 2 Demonstrate the ability to assess pharmacodynamic and pharmacokinetic parameters using MS2,MS1 23 commonly prescribed drugs as examples. 3 Solve common pharmacokinetic calculations including loading doses and maintenance doses MS2,MS1 11 using knowledge of volume, distribution and clearance. 4 Formulate different regimens for special patient groups (e.g. pregnant women, patients with MS2,MS1, 11 compromised immune/kidney/liver function etc.) MS5,CC13,PH2 5 Recognize and anticipate common drug-drug interactions including those interactions that can MS2,MS1,CC6,CC 16 be predicted from genetic testing of metabolizing enzymes e.g. P450 isozyme testing, 10,CC1,P7,PPLD3 6 Recognize and anticipate common drug interactions with OTC medications, herbal or MS2,MS1,CC6,CC 7 nutritional supplements and specific food groups. 10,CC1,P7,PPLD3 7 Discriminate between pharmacological substances, based on generic drug name, MS2,MS1,CC6,CC 67 pharmacological classification (using class representative compounds), mechanism of action, major clinical indications and most clinically relevant adverse effects. 10,P1,P6 8 Distinguish treatments, which may become the standard of care on the horizon based on MS2,MS1,MS5,PP 2 their proximity to FDA approval e.g. Qnexa for weight loss. LD1,MS4,CC14,EI M2,PH4 GO = New Geisel Objectives Old Course Objectives (continued) Course Objectives (CO) Links (GO) Sessions (CO) 9 Recognize signs of common drug overdose, and propose how to initiate therapy where appropriate MS1,MS2,CC13, 0 when the causal agent is known or unknown. PH2 10 Integrate their knowledge from years 1 and 2 of anatomy, biochemistry, genetics, microbiology, MS1,MS2 49 physiology, and pathophysiology with the actions of drugs at all levels from the receptor to the cell, organ, circulatory systems and whole-body levels. 11 Access and evaluate different levels of biomedical literature relevant to the treatment of disease MS1,MS5 3 through experts, Internet sources, books, and other databases 12 Discuss the principals of evidence based medicine and be familiar with the current resources MS1,MS5 1 available online and through the biomedical library 13 Discuss procedures relevant to disease diagnosis and alternatives to medical therapy (e.g., MS1,MS2,MS5,C 4 percutaneous coronary intervention, arrhythmia ablation, implantable defibulator) C8,CS6,CS1,PH1 14 Discuss how to serve patients interest when evaluating brand name vs. generic drugs, and CC13,PH2,P2,PP 6 pharmaceutical advertising to patients and clinicians. LD1,PH3,CC7,EI M2,PH1,EIM5,EI M3,P5 15 Explain what is required to write a complete, unambiguous, and legal prescription and also what is MS2,CC13,PH2, 0 required to insure the patient is fully counseled about medications, their drug history is comprehensively evaluated and they have printed drug information. P2,PPLD1,PH3,C C7,EIM2,PH1 Old Course Objectives (continued) Course Objectives (CO) Links (GO) Sessions (CO) 16 Recognize signs of drug/alcohol abuse and describe potential treatment strategies. CC13,PH2,P5,PH 0 5 17 Communicate effectively with fellow students and faculty. CC8,CS6,CS1 4 18 Demonstrate team skills by participating effectively in team exercises. CC1,P7 3 19 Take responsibility for his- or her-own medical education. PPLD1 16 20 Search efficiently for and obtain recent, high quality, relevant medical information and scientific MS1,MS4 4 literature to solve problems. 21 Read critically, evaluate, and assess medical information and scientific literature about important MS1,MS4 3 neurological topics and questions. 22 Practice clinical reasoning skills in the context of a simulated patient scenario. CC6,CC7 6 23 Demonstrate skills necessary for assisting patients to understand treatment options and the need for CC12,CS4,CS7 4 care. 24 To help colleagues by contributing constructive suggestions during peer review PPLD3, 3 25 To meet professional responsibilities fully, including being punctual, present, and engaged, and being P7 6 reliable in commitment to tasks. Updated Course Objectives Geisel Competenc How # Course Objectives (CO) Sessions y Assessed Describe an overview of drug pharmacokinetic properties (e.g. absorption, distribution, metabolism, and excretion) that apply 1to all therapeutic agents 1, 3, 4, 5, 6, 8, 24 MS Exam Describe how drugs interact with receptors, cells, tissues, and organs to produce their desired and unintended 2pharamcodynamic effects 1, 5, 8 MS Exam Calculate a loading dose, maintenance dose, and half-life of a drug, using previously validated measurement of drug bioavailability, clearance, and volume of distribution 3 1,3,4,7,28 MS Exam Explain the basic concepts of drug-receptor interactions)e.g. agonists, antagonists, partial agonists, ED50, potency) 5,6 4 MS Exam Describe how drug-receptor binding can lead to a cascade of intracellular changes through second messenger systems and 5,6 beyond (e.g. cyclic AMP, cyclic GMP, etc.) 5 MS Exam Describe in detail the most common pathways in man for drug metabolism, and their pharmacogenetic importance and 8, 24 implications (e.g. ultraslow or ultrafast metabolizers) 6 MS Exam Describe the purpose, neuroanatomy, neutrotransmitters, and phsiological effects of the two branches of the autonomic 9 nervous system (sympathetic, parasympathetic) 7 MS Exam Describe in detail the most common drugs used clinically as agonists and antagonists at the various adrenergic receptors (e.g. 10, 11 beta-receptor agonists and antagonists, alpha-receptor agonists and antagonists) 8 MS Exam Describe in detail the most common drugs used clinically as agonists and antagonists at the various cholinergic receptors (e.g. 12, 13 muscarinic-receptor agonists and antagonists, nicotinic-receptor agonists and antagonists) 9 MS Exam Describe the most common adverse drug reactions for drugs presented in the course, as well as the most common drug-drug 1, 5, 6, 8, 10, 11, 12, interactions (e.g. tremor from albuterol, sedation from clonidine) 13, 15, 16, 17, 20, 21, 22, 26, 27, 29 10 Updated Course Objectives Explain how foods, herbal products, nutritional supplements, and over-the-counter drugs can cause clinically 8, 17 important interactions with commonly used therapeutic drugs 11 MS, CC Exam Describe how each class of therapeutic drugs is named in a common fashion, and also how generic and branded drugs 1 have different types of testing prior to approval, naming, and pricing strategies 12 MS, CC Exam Describe the basic and clinical pharmacology of the most common drugs used to treat hypertension and coronary 15, 16, 22 artery disease (e.g. angina, MI, etc.) 13 MS, CC Exam Describe the basic anc clinical pharmacology of the most common drugs used to treat hyperlipidemia and cardiac 21, 26 arrhythmias 14 MS, CC Exam Describe the basic and clinical pharmacology of the most common drugs used to treat congestive heart failure 27, 29 15 MS, CC Exam Describe the most common drugs used to treat respiratory conditions such as asthma, reactive airways disease, 20, 25 chronic obstructive pulmonary disease, and cough 16 MS, CC Exam While discussing clinical cases in small groups, demonstrate the ability to reason from symptoms and signs to a 14, 18, 23 diagnosis, and from a diagnosis to recommendations for treatment of that condition, including the ability to access and evaluate different current reliable sources of biomedical information 17 CC, Conf While discussing clinical cases in small groups, demonstrate the ability to communicate clearly and effectively with 14, 18, 23 students and faculty, and to participate effectively as a team member 18 CS,CT Conf By completing all assignments on time, and coming to each conference on time and well prepared, demonstrate the 14, 18, 23 ability to behave professionally, and to take responsibility for your own
Load more

Recommended publications
  • Selective Mtorc2 Inhibitor Therapeutically Blocks Breast Cancer Cell Growth and Survival
    Author Manuscript Published OnlineFirst on January 22, 2018; DOI: 10.1158/0008-5472.CAN-17-2388 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Selective mTORC2 inhibitor therapeutically blocks breast cancer cell growth and survival Thomas A. Werfel1, 3, Shan Wang2, Meredith A. Jackson1, Taylor E. Kavanaugh1, Meghan Morrison Joly3, Linus H. Lee1, Donna J. Hicks3, Violeta Sanchez4, Paula Gonzalez Ericsson4, Kameron V. Kilchrist1, Somtochukwu C. Dimobi1, Samantha M. Sarett1, Dana Brantley-Sieders2, Rebecca S. Cook1,3,4* and Craig L. Duvall1* 1Department of Biomedical Engineering, Vanderbilt University, Nashville, TN 37232 USA 2Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232.USA 3Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN 37232 USA 4Breast Cancer Research Program, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN 37232 USA Running Title: A selective mTORC2 inhibitor blocks breast cancer growth Key Words: Breast Cancer, mTOR, Rictor, RNA interference, Nanomedicine *To whom correspondence should be addressed: Craig L. Duvall, PhD Vanderbilt University School of Engineering Department of Biomedical Engineering Nashville, TN 37232 Phone: (615) 322-3598 Fax: (615) 343-7919 Email: [email protected] Rebecca S. Cook, PhD Vanderbilt University Medical Center Department of Cancer Biology Nashville, TN 37232 Phone: (615) 936-3813 Fax: (615) 936-3811 Email: [email protected] Funding. This work was supported by Specialized Program of Research Excellence (SPORE) grant NIH P50 CA098131 (VICC), Cancer Center Support grant NIH P30 CA68485 (VICC), NIH F31 CA195989-01 (MMW), NIH R01 EB019409, DOD CDMRP OR130302, NSF GFRP 1445197, and CTSA UL1TR000445 from the National Center for Advancing Translational Sciences.
    [Show full text]
  • Angiotensin-Converting Enzyme (ACE) Inhibitors Single Entity Agents
    Therapeutic Class Overview Angiotensin-Converting Enzyme (ACE) Inhibitors Single Entity Agents Therapeutic Class Overview/Summary: The renin-angiotensin-aldosterone system (RAAS) is the most important component in the homeostatic regulation of blood pressure.1,2 Excessive activity of the RAAS may lead to hypertension and disorders of fluid and electrolyte imbalance.3 Renin catalyzes the conversion of angiotensinogen to angiotensin I. Angiotensin I is then cleaved to angiotensin II by angiotensin- converting enzyme (ACE). Angiotensin II may also be generated through other pathways (angiotensin I convertase).1 Angiotensin II can increase blood pressure by direct vasoconstriction and through actions on the brain and autonomic nervous system.1,3 In addition, angiotensin II stimulates aldosterone synthesis from the adrenal cortex, leading to sodium and water reabsorption. Angiotensin II exerts other detrimental cardiovascular effects including ventricular hypertrophy, remodeling and myocyte apoptosis.1,2 The ACE inhibitors block the conversion of angiotensin I to angiotensin II, and also inhibit the breakdown of bradykinin, a potent vasodilator.4 Evidence-based guidelines recognize the important role that ACE inhibitors play in the treatment of hypertension and other cardiovascular and renal diseases. With the exception of Epaned® (enalapril solution) and Qbrelis® (lisinopril solution), all of the ACE inhibitors are available generically. Table 1. Current Medications Available in Therapeutic Class5-19 Generic Food and Drug Administration
    [Show full text]
  • Introduction to Hospital and Health-System Pharmacy Practice 59 Tients with a Specific Disease State Or for Activities Related to Self Governance Diagnosis
    Part II: Managing Medication Use CHAPTER 4 Medication Management Kathy A. Chase ■■ ■■■ Key Terms and Definitions Learning Objectives ■■ Closed formulary: A list of medica- After completing this chapter, readers tions (formulary) which limits access should be able to: of a practitioner to some medications. 1. Describe the purpose of a formulary A closed formulary may limit drugs to system in managing medication use in specific physicians, patient care areas, or institutions. disease states via formulary restrictions. 2. Discuss the organization and role of the ■■ Drug formulary: A formulary is a pharmacy and therapeutics committee. continually updated list of medications 3. Explain how formulary management and related information, representing works. the clinical judgment of pharmacists, 4. List the principles of a sound formulary physicians, and other experts in the system. diagnosis and/or treatment of disease 5. Define key terms in formulary manage- and promotion of health. ment. ■■ Drug monograph: A written, unbi- ased evaluation of a specific medica- tion. This document includes the drug name, therapeutic class, pharmacology, indications for use, summary of clinical trials, pharmacokinetics/dynamics, ad- verse effects, drug interactions, dosage regimens, and cost. ■■ Drug therapy guidelines: A document describing the indications, dosage regi- mens, duration of therapy, mode(s) of administration, monitoring parameters and special considerations for use of a specific medication or medication class. ■■ Drug use evaluation (DUE): A process used to assess the appropriate- ness of drug therapy by engaging in the evaluation of data on drug use in a given health care environment against predetermined criteria and standards. ◆■ Diagnosis-related DUE: A drug use evaluation completed on pa- INTRODUCTION TO HOSPITAL AND HEALTH-SYSTEM PHARMACY PRACTICE 59 tients with a specific disease state or for activities related to self governance diagnosis.
    [Show full text]
  • Utilization and Program Costs of Statins for Wisconsin Medicaid
    To: Prescribing Physicians, Pharmacies From: Wisconsin Medicaid, Division of Health Care Financing January 2004 Utilization and Program Costs of Statins for Wisconsin Medicaid PRIOR AUTHORIZATION GUIDELINES (atorvastatin), Zocor (simvastatin), Pravachol (pravastatin), Crestor (rosuvastatin), Lescol (fluvastatin), and Lescol XL In order to encourage the use of generic lovastatin, the Wis- (fluvastatin XL). Products that contain an HMG-CoA reductase consin Medicaid program began requiring prior authorization inhibitor combined with another ingredient (e.g. Advicor) were for brand name HMG-CoA reductase inhibitors on April 15, not included in this analysis. 2003. Prior authorization was made available through the STAT-PA system. Only recipients new to statin drugs are re- The generic form of lovastatin is significantly less expen- quired to try lovastatin first. The criteria for determining prior sive to the Medicaid program than brand name products. authorization includes: Average cost to the Wisconsin Medicaid Program for generic 1 · Any recipient currently on an effective brand name statin lovastatin 40 mg is $1.20 per tablet and for a brand name will be granted PA to continue on that statin drug. HMG-CoA reductase inhibitors (including the brand name · Any recipient who requires >35% reduction in low-density forms of lovastatin) range from $1.65 to $4.18 per equipotent dosage2 (table 1). lipoprotein (LDL) cholesterol will be granted PA to start on the brand name statin drugs. Table I · Any recipient who has impaired renal function will be Cost Per Tablet for Wisconsin Medicaid granted PA to start on the brand name statin drugs. · Any recipient who is at high risk for drug interactions will be granted PA to start on the brand name statin drugs.
    [Show full text]
  • S1 Table. List of Medications Analyzed in Present Study Drug
    S1 Table. List of medications analyzed in present study Drug class Drugs Propofol, ketamine, etomidate, Barbiturate (1) (thiopental) Benzodiazepines (28) (midazolam, lorazepam, clonazepam, diazepam, chlordiazepoxide, oxazepam, potassium Sedatives clorazepate, bromazepam, clobazam, alprazolam, pinazepam, (32 drugs) nordazepam, fludiazepam, ethyl loflazepate, etizolam, clotiazepam, tofisopam, flurazepam, flunitrazepam, estazolam, triazolam, lormetazepam, temazepam, brotizolam, quazepam, loprazolam, zopiclone, zolpidem) Fentanyl, alfentanil, sufentanil, remifentanil, morphine, Opioid analgesics hydromorphone, nicomorphine, oxycodone, tramadol, (10 drugs) pethidine Acetaminophen, Non-steroidal anti-inflammatory drugs (36) (celecoxib, polmacoxib, etoricoxib, nimesulide, aceclofenac, acemetacin, amfenac, cinnoxicam, dexibuprofen, diclofenac, emorfazone, Non-opioid analgesics etodolac, fenoprofen, flufenamic acid, flurbiprofen, ibuprofen, (44 drugs) ketoprofen, ketorolac, lornoxicam, loxoprofen, mefenamiate, meloxicam, nabumetone, naproxen, oxaprozin, piroxicam, pranoprofen, proglumetacin, sulindac, talniflumate, tenoxicam, tiaprofenic acid, zaltoprofen, morniflumate, pelubiprofen, indomethacin), Anticonvulsants (7) (gabapentin, pregabalin, lamotrigine, levetiracetam, carbamazepine, valproic acid, lacosamide) Vecuronium, rocuronium bromide, cisatracurium, atracurium, Neuromuscular hexafluronium, pipecuronium bromide, doxacurium chloride, blocking agents fazadinium bromide, mivacurium chloride, (12 drugs) pancuronium, gallamine, succinylcholine
    [Show full text]
  • Angiotensin-Converting Enzyme (ACE) Inhibitors
    Angiotensin-Converting Enzyme (ACE) Inhibitors Summary Blood pressure reduction is similar for the ACE inhibitors class, with no clinically meaningful differences between agents. Side effects are infrequent with ACE inhibitors, and are usually mild in severity; the most commonly occurring include cough and hypotension. Captopril and lisinopril do not require hepatic conversion to active metabolites and may be preferred in patients with severe hepatic impairment. Captopril differs from other oral ACE inhibitors in its rapid onset and shorter duration of action, which requires it to be given 2-3 times per day; enalaprilat, an injectable ACE inhibitor also has a rapid onset and shorter duration of action. Pharmacology Angiotensin Converting Enzyme Inhibitors (ACE inhibitors) block the conversion of angiotensin I to angiotensin II through competitive inhibition of the angiotensin converting enzyme. Angiotensin is formed via the renin-angiotensin-aldosterone system (RAAS), an enzymatic cascade that leads to the proteolytic cleavage of angiotensin I by ACEs to angiotensin II. RAAS impacts cardiovascular, renal and adrenal functions via the regulation of systemic blood pressure and electrolyte and fluid balance. Reduction in plasma levels of angiotensin II, a potent vasoconstrictor and negative feedback mediator for renin activity, by ACE inhibitors leads to increased plasma renin activity and decreased blood pressure, vasopressin secretion, sympathetic activation and cell growth. Decreases in plasma angiotensin II levels also results in a reduction in aldosterone secretion, with a subsequent decrease in sodium and water retention.[51035][51036][50907][51037][24005] ACE is found in both the plasma and tissue, but the concentration appears to be greater in tissue (primarily vascular endothelial cells, but also present in other organs including the heart).
    [Show full text]
  • Calcium Channel Blockers
    Calcium Channel Blockers Summary In general, calcium channel blockers (CCBs) are used most often for the management of hypertension and angina. There are 2 classes of CCBs: the dihydropyridines (DHPs), which have greater selectivity for vascular smooth muscle cells than for cardiac myocytes, and the non-DHPs, which have greater selectivity for cardiac myocytes and are used for cardiac arrhythmias. The DHPs cause peripheral edema, headaches, and postural hypotension most commonly, all of which are due to the peripheral vasodilatory effects of the drugs in this class of CCBs. The non-DHPs are negative inotropes and chronotropes; they can cause bradycardia and depress AV node conduction, increasing the risk of heart failure exacerbation, bradycardia, and AV block. Clevidipine is a DHP calcium channel blocker administered via continuous IV infusion and used for rapid blood pressure reductions. All CCBs are substrates of CYP3A4, but both diltiazem and verapamil are also inhibitors of 3A4 and have an increased risk of drug interactions. Verapamil also inhibits CYP2C9, CYP2C19, and CYP1A2. Pharmacology CCBs selectively inhibit the voltage-gated L-type calcium channels on cardiac myocytes, vascular smooth muscle cells, and cells within the sinoatrial (SA) and atrioventricular (AV) nodes, preventing influx of extracellular calcium. CCBs act by either deforming the channels, inhibiting ion-control gating mechanisms, and/or interfering with the release of calcium from the major cellular calcium store, the endoplasmic reticulum. Calcium influx via these channels serves for excitation-contraction coupling and electrical discharge in the heart and vasculature. A decrease in intracellular calcium will result in inhibition of the contractile process of the myocardial smooth muscle cells, resulting in dilation of the coronary and peripheral arterial vasculature.
    [Show full text]
  • Drug Class Review on Targeted Immune Modulators
    Drug Class Review on Targeted Immune Modulators Final Report December 2005 The purpose of this report is to make available information regarding the comparative effectiveness and safety profiles of different drugs within pharmaceutical classes. Reports are not usage guidelines, nor should they be read as an endorsement of, or recommendation for, any particular drug, use or approach. Oregon Health & Science University does not recommend or endorse any guideline or recommendation developed by users of these reports. Gerald Gartlehner, MD, MPH Richard A. Hansen, PhD Patricia Thieda, MA Beth Jonas, MD Kathleen N. Lohr, PhD Tim Carey, MD, MPH Produced by RTI-UNC Evidence-based Practice Center Cecil G. Sheps Center for Health Services Research University of North Carolina at Chapel Hill 725 Airport Road, CB# 7590 Chapel Hill, NC 27599-7590 Tim Carey, MD, MPH, Director Oregon Evidence-based Practice Center Mark Helfand, MD, MPH, Director Copyright © 2005 by Oregon Health & Science University Portland, Oregon 97201. All rights reserved Final Report Drug Effectiveness Review Project TABLE OF CONTENTS List of Abbreviations ............................................................................................................................... 4 Introduction............................................................................................................................................... 6 Scope and Key Questions ............................................................................................................. 12 Methods
    [Show full text]
  • Annrheumdis-2019-216655.Full.Pdf
    Recommendation Ann Rheum Dis: first published as 10.1136/annrheumdis-2019-216655 on 22 January 2020. Downloaded from EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease- modifying antirheumatic drugs: 2019 update Josef S Smolen ,1 Robert B M Landewé,2,3 Johannes W J Bijlsma,4 Gerd R Burmester,5 Maxime Dougados,6 Andreas Kerschbaumer ,1 Iain B McInnes,7 Alexandre Sepriano ,8 Ronald F van Vollenhoven,9 Maarten de Wit ,10 Daniel Aletaha,1 Martin Aringer ,11 John Askling,12 Alejandro Balsa,13 Maarten Boers,14 Alfons A den Broeder,15 Maya H Buch ,16 Frank Buttgereit,5 Roberto Caporali,17 Mario Humberto Cardiel,18 Diederik De Cock,19 Catalin Codreanu,20 Maurizio Cutolo ,21 Christopher John Edwards,22 Yvonne van Eijk- Hustings ,23 Paul Emery ,24 Axel Finckh,25 Laure Gossec ,26 Jacques-Eric Gottenberg,27 Merete Lund Hetland,28 Tom W J Huizinga ,29 Marios Koloumas,30,31 Zhanguo Li,32 Xavier Mariette,33 Ulf Müller- Ladner,34 Eduardo F Mysler,35 Jose A P da Silva ,36 Gyula Poór,37 Janet E Pope ,38 Andrea Rubbert- Roth ,39 Adeline Ruyssen- Witrand,40 Kenneth G Saag,41 Anja Strangfeld,42 Tsutomu Takeuchi,43 Marieke Voshaar,44 René Westhovens,19 Désirée van der Heijde 29 Handling editor Dimitrios T ABStract fails, any other bDMARD (from another or the same Boumpas Objectives To provide an update of the European class) or tsDMARD is recommended. On sustained For numbered affiliations see League Against Rheumatism (EULAR) rheumatoid remission, DMARDs may be tapered, but not be stopped.
    [Show full text]
  • Introduction to Pharmacodynamics Reza Karimi 6
    CHAPTER Introduction to Pharmacodynamics Reza Karimi 6 1. Understand the physiology behind the gastrointestinal tract and the route of oral drug administration and VES physiological influences on pharmacodynamics. I 2. Understand the dynamics and functions of the major signal transduction systems and their different biomedi- cal and biological responses in regard to receptor–ligand interactions. 3. Learn about the dynamics and mathematical expressions behind receptor–ligand interactions. OBJECT 4. Understand dose–response relationships and factors that affect a pharmacological response. 5. Learn about agonistic, antagonistic, and partial agonistic binding of drugs to receptors. 6. Learn about different concepts such as addition, synergism, and potentiation that lead to an enhancement effect of drugs. 7. List a few regulatory mechanisms for receptors. 8. Implement a series of Learning Bridge assignments at your experiential sites to bridge your didactic learning with your experiential experiences. 1. cAMP: cyclic adenosine 3' ,5''-monophosphate; a second messenger that plays an important role in signal NS transduction. IO T 2. cGMP: cyclic guanosine 3' ,5''monophosphate; a second messenger that plays an important role in signal I N transduction. I 3. Dose–response relationship: when an endogenous or exogenous ligand binds to a receptor and produces a EF D pharmacological effect. The effect can approach a maximum value (also called Emax) in which a further increase in the ligand concentration does not produce any higher response. 4. Efficacy: the ability of a drug to produce a pharmacological response when it interacts with its receptor. 5. First-pass metabolism: a type of metabolism in which drugs that are absorbed by the gastrointestinal tract go through the portal vein to the liver and are metabolized there before they are distributed to the general ERMS AND AND ERMS circulation.
    [Show full text]
  • Disease-Modifying Antirheumatic Drug Initiation Among Patients Newly Diagnosed with Rheumatoid Arthritis
    ORIGINAL RESEARCH Disease-Modifying Antirheumatic Drug Initiation Among Patients Newly Diagnosed With Rheumatoid Arthritis Machaon Bonafede, PhD, MPH; Barbara H. Johnson, MBA; Neel Shah, PhD, BPharm; David J. Harrison, PhD; Derek Tang, PhD, BSPharm; and Bradley S. Stolshek, PharmD heumatoid arthritis (RA) is a systemic autoimmune disease characterized by inflammation of the joints and ABSTRACT R surrounding tissues. This inflammation leads to destruc- tion of cartilage and bone in affected joints, which can result in OBJECTIVES: To determine the rate of timely disease- 1 modifying antirheumatic drug (DMARD) initiation in substantial pain and disability. Bone erosion has been shown patients newly diagnosed with rheumatoid arthritis (RA), to occur as early as 4 months after observation of the first joint as recommended per a quality measure endorsed by the symptoms.2 Patients with RA suffer significant impairments in work National Quality Forum. performance, productivity, and overall quality of life.3 Effective STUDY DESIGN: Retrospective analysis of claims data from treatment of RA symptoms with disease-modifying antirheumatic the Truven Health MarketScan commercial and Medicare claims databases. drugs (DMARDs) has been shown to increase productivity at work and in the home and to improve health-related quality of life.4,5 METHODS: Patients newly diagnosed with RA were identified in the claims databases. Outcomes included rate Early diagnosis and treatment of RA is important to limit progres- of nonbiologic or biologic DMARD initiation within 12 months sion of the disease and improve clinical outcomes.6 With treatment, of diagnosis; initiation by year (2009-2012), US state, and patients with early disease are more likely to achieve optimal prescription drug plan; and time to initiation.
    [Show full text]
  • Pharmacology of Diabetes Medications
    Pharmacology of Diabetes Medications Krista Dominguez-Salazar PharmD, PhC Associate Professor of Clinical Pharmacy University of New Mexico College of Pharmacy Estimates of Diabetes and Its Burden on the US CDC National Diabetes Statistics Report, 2014 • 9.3% (29.1 million) of the US Population have diabetes. • Treatment of DM in people > 18 years old: • 14% use insulin only • 14.7% use both insulin and oral medication • 56.9% use oral medication only • 14.4% Neither insulin nor oral medication • 282,000 ER visits had hypoglycemia as the first diagnosis and DM as other. • 175,000 ER visits with hyperglycemia crisis (DKA or HHS) as the first diagnosis. https://www.cdc.gov/diabetes/pubs/statsreport14/national-diabetes-report-web.pdf Estimates of Diabetes and Its Burden on the US CDC National Diabetes Statistics Report, 2014 • 71% had BP > 140/90 mmHg or used Rx medications for treating HBP. • 65% had LDL > 100 mg/dL. • Hospitalization rates for MI were 1.8 times higher and stroke, 1.5 times higher. • 4.2 million had diabetic retinopathy. • 44% of kidney failure patients had DM listed as the primary cause. • 60% of non-traumatic lower-limb amputations occurred in people with diagnosed diabetes. https://www.cdc.gov/diabetes/pubs/statsreport14/national-diabetes-report-web.pdf Standards of Medical Care in Diabetes - 2017 1. Promoting Health and Reducing Disparities in Populations 2. Classification and Diagnosis of Diabetes 3. Comprehensive Medical Evaluation and Assessment of Comorbidities 4. Lifestyle Management 5. Prevention or Delay of Type 2 Diabetes 6. Glycemic Targets 7. Obesity Management for the Treatment of Type 2 Diabetes 8.
    [Show full text]