Showing posts with label Pharmacology. Show all posts
Showing posts with label Pharmacology. Show all posts

28 June 2013

Institutional Animal Care and Use Committee Guidelines




Institutional Animal Care and Use Committee Guidelines of University of Minnesota

Hope this information will be useful to all researchers who deal with laboratory animals and members of Institutional Ethical Committee.


ANIMAL USE GUIDELINES & EXPECTATIONS
Guidance from Professional Organizations

Federal and University Regulations
U of M Board of Regents Policies
Occupational and Environmental Health & Safety Links
Office of Laboratory Animal Welfare (OLAW)
U.S. Department of Agriculture (USDA)
Other Policies


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18 July 2012

Drug Approval



Core Concepts in Pharmacology Drug Regulation and Approval
http://www.mac.edu/

Quantitative “Learning” Approaches Influence Drug Approval
Hao Zhu, Ph.D.
http://www.ncsu.edu

Human Subjects in Research
Helen Tamer
http://open.umich.edu

FDA - Introduction to Drug Regulation
Edward P. Richards
http://biotech.law.lsu.edu

Drug Development - A view on the process from the idea to the registered pharmaceutical
Dr. Matthias Kreuter
http://www.aucegypt.edu

Evolution of a New Medication
http://cstl-cla.semo.edu

Drug Disposal Labeling to Improve Safety - FDA Update on Drug Disposal Labeling Activities
James R. Hunter, R.Ph., MPH
http://www.benzos.une.edu

The Drug Approval Process
http://www.kishwaukeecollege.edu

The Role of the DMF in the FDA Approval Process
John B. Dubeck
http://www.dmfworkshop.msu.edu/

Direct-to-Consumer Advertising: Dangerous Game of Pitching Products to Parents
Lynne Wells Graziano
http://www.pitt.edu

The Food and Drug Administration: then and now
Satish R Raj MD
http://www.mc.vanderbilt.edu

Working With Pharma Sponsors In Research
Becky Hubbell
https://www2.kumc.edu

From Bench to Bedside : Getting New Drugs Approved by the FDA
Getting a New Drug Approved : The Procedure
http://www.library.health.ufl.edu

Biopharmaceutical Development & Regulation
Ron Guido
http://www.columbia.edu/

Ethics
http://www.wou.edu

Single Patient Use of Investigational Drugs - A Tutorial for UH Physicians and Staff
http://www.hawaii.edu

Evaluation & Categorization of Drugs
Frank F. Vincenzi
https://courses.washington.edu

94 Published articles on Drug Approval

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23 June 2012

Phosphodiesterase inhibitors Lecture notes and 119 Scholarly Published articles free access



Drugs for Heart Failure
Drugs for Heart Failure.ppt

G-Protein membrane receptors
G-Protein membrane receptors.ppt

Viagra
Otega Edukuye
Viagra.ppt

Congestive Heart Failure
Chris Hague, PhD
Congestive Heart Failure.ppt

Positive Inotropic Agents
Pharmacology-Positive-PositiveInotropicAgentsfixed.ppt

The G Protein Pathway in Neuroscience
Henry Lester
The G Protein Pathway in Neuroscience.ppt

Dalteparin Pharmacodynamics/Mechanism of Action
Akash Bhakta
Dalteparin Pharmacodynamics/Mechanism of Action.ppt

Drugs for Heart Failure
Drugs for Heart Failure.ppt

Vision
vision.ppt

What is Heart Failure?
What is Heart Failure.ppt

Hemodynamic Disorders: Hemostasis Thrombogenesis: Platelet, Endothelial And Clotting Factor Interactions
Arthur S. Schneider, M.D
schneider-thrombosis_1112.ppt

Viagra and the Neonate
Robert E. Lyle, M.D.
Viagra and the Neonate.ppt

Antihypertensives, Diuretics, Anticoagulants and Dyslipidemics
Linda Self
Antihypertensives, Diuretics, Anticoagulants and Dyslipidemics.ppt

Medical Complications of Substance Abuse
Phil Green MD, Vishal Madaan, MD
Medical Complications of Substance Abuse.ppt

Drug Targets: Receptors
Drug Targets: Receptors.ppt

Pharmacologic Management of Acute Circulatory Failure: Vasoactive Medications
Suanne Daves, MD
Pharmacologic Management of Acute Circulatory Failure.ppt

Heart Failure and Antidysrhythmics
Linda Self
Heart_Failure_and_Antidysrhythmics.ppt

Drug Classes Cardiovascular Agents
Drug Classes Cardiovascular Agents.ppt

Review of Anticoagulants, Thrombolytics and Anti-platelet Drugs
Review of Anticoagulants, Thrombolytics and Anti-platelet Drugs.ppt

Pharmacology Review of Everything
Pharmacology Review of Everything.ppt

Xanomeline M1/M4 agonist
Xanomeline M1/M4 agonist.ppt

119 Scholarly Published articles free access

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15 May 2012

World's Scariest Drug - Scopolamine



World's Scariest Drug
Read Here
and Here and Here

Scopolamine
Julia Bedell, Laci Click, Meredith Barr
Scopolamine.ppt

Indirect cholinergic agonists
Indirect cholinergic agonists.ppt

Cholinergic Agonism and Antagonism Module
MARCELO G. BONINI
Cholinergic Agonism and Antagonism.ppt

Psychoactive and Poisonous Plants
psychoactiveplants_spring11.ppt

Anesthesia for Trauma
Christopher DeSantis, MD
Anesthesia_for_Trauma_1_.ppt

Belladonna leaves
Belladonna.ppt

Muscarinic Antagonists
Neil M. Nathanson
Muscarinic Antagonists.ppt

Cholinergics & anticholinesterases
Cholinergics & anticholinesterases.ppt

Cholinergic System
Cholinergic System.ppt

Gastrointestinal Agents
Gastrointestinal Agents.ppt
200 free full text articles on Scopolamine

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30 April 2012

Proton pump inhibitors 200 scholarly articles free access



Proton Pump Inhibitors
Andres Marin, MD
Protonpump.ppt

Gastrointestinal Drugs
Karen Ruffin RN, MSN Ed.
GastrointestinalDrugs.ppt

Pediatric Laproscopic Nissen Fundoplication
Lindsey Bendure
Fundoplication.ppt

Acid-Controlling Agents
Acid-Controlling Agents.ppt

Gastric Acid Modifiers
Frank F. Vincenzi
Gastric Acid Modifiers.ppt

Gastrointestinal Drugs
Patrick T. Ronaldson, Ph.D.
GastrointestingDrugs.ppt

Gastric Secretion and Function
Gastricsecretion.ppt

Swallowing Difficulty & Pain
Tim Farrell, MD, Tom Egan, MD
Swallowing Difficulty & Pain.ppt

Drugs that Affect the Gastrointestinal System
Pharmacology/GIDrugs.ppt

Proton pump inhibitors
Proton pump inhibitors.ppt

Gastrointestinal Agents
Gastrointestinal Agents.ppt

Gastro Reflux
Debbie Tinus
Gastro Reflux.ppt

Drugs for Peptic Ulcer Disease
Gastro Reflux.ppt

Gastrointestinal Pharmacology
Gastrointestinal Pharmacology.ppt

Pathophysiology of GERD
Vicki Orzel RN/BSN
Pathophysiology of GERD.ppt

Gastroesophageal Reflux Disease (GERD)
Fantry_GERD_September7_2nd.ppt

Chronic Cough -Evaluation and Treatment
Bill Mariencheck
Chronic Cough Treatment.ppt

Pharmacology in Rehabilitation Gastrointestinal Drugs
Mary Worthington, Pharm.D.
Gastrointestinal Drugs.ppt
200 scholarly published articles free access

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27 April 2012

Norepinephrine Ppt and 100 free full text articles



Monoamine Neurotransmitters
Monoamines.ppt

Norepinephrine and the Role of REM Sleep in Brain Maturation
Erin JohnsonNorepinephrine.ppt

Autonomic Nervous System - ANS AnatomyANS Anatomy.ppt

Autonomic Nervous SystemANS Anatomy.ppt

Antidepressants
Samaiya Mushtaq
Antidepressants.ppt

Psychotherapeutic Drugs
Gerianne R. Bliss, M.D., Chuck Hensley, R. Ph.
Psychotherapeutic Drugs.ppt

Epinephrine (EPI) and Norepinephrine (NE)Epinephrine (EPI) and Norepinephrine (NE).ppt

Autonomic Nervous SystemAutonomic Nervous System.ppt

Adrenergic and anti-adrenergic drugs
Linda Self
Adrenergic_and_anti-adrenergic_drugs.ppt

Exploring the Pathophysiology of Major Unipolar Depression
Trisha L. OlsonPathophysiology of Major Unipolar Depression .ppt

Psychopharmacology in Psychiatry
Heidi Combs, MD, Shamim Nejad, MD
Psychopharmacology.ppt
100 free full text articles

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03 March 2012

Respiratory pharmacology Ppt




Respiratory Care Technology
AlliedHealth-RT-RespiratoryCareCareer.ppt

Respiratory  Therapy
RespiratoryCareInfo08.ppt

Respiratory Pharmacology
Dr. Daniel Weinreich
PulmonaryPharmacol.ppt

Pharmacology of Respiratory Drugs
Dr. Lal. C. Garg
Respiratory_Drugs.ppt

Respiratory Pharmacology ‘ Tis the Season for Sneezin’ and Wheezin’
Respiratory Pharmacology.ppt

Respiratory  Pharmacology
Dan Farrell
Calculations.ppt

Pharmacology  of Nicotine
Colleen Miller, Lesley-Ann Giddings
Pharmacology  of Nicotine .ppt

Inhaled Anesthetics And Gases
Harry Singh, MD
Inhaled Anesthetics And Gases .ppt

Pharmacokinetics  of Local Anesthetics
Pharmacokinetics  of Local Anesthetics.ppt

Drugs for  Respiratory Disorders
Gerianne  R. Bliss, M.D., Chuck Hensley  R.Ph.
Drugs for  Respiratory Disorders.ppt

Sedative-Hypnotics Benzodiazepines
Megan  Trimble
Sedative-Hypnotics Benzodiazepines.ppt

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24 February 2012

Free access to Pharmacological Reports



Pharmacological Reports until 2004 known as Polish Journal of Pharmacology.

Scope of the journal. The Pharmacological Reports, formerly Polish Journal of Pharmacology, publishes papers concerning all aspects of pharmacology, dealing with the drug action at the cellular and molecular level, and papers on relationship between molecular structure and biological activity. The language of all publications is English.

Free full text access from 2001 onwards.  From 1998 to 2000 abstracts only available

http://www.if-pan.krakow.pl/pjp/index.html

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23 February 2012

Aldosterone receptor Ppts and Published papers



Selective Aldosterone receptor Antagonist SARA
by John  A. Heit, MD
http://www.surgeongeneral.gov/topics/deepvein/workshop/presentations/heit_practice-patient.ppt

Drugs for Hypertension
http://www.mac.edu/faculty/christinestaake/Nursing%20311/Web%20Drugs%20for%20Hypertension%20Chapter%2023.ppt

Antihypertensives Approaches to  Hypertension Treatment
http://www.patheyman.com/sites/default/files/nursing/notes/06-CV2-BloodPressure-2.ppt

Evolution of  Steroid Receptor Gene Families
https://mywebspace.wisc.edu/carollee/web/Lee/611%202009%20ReadingWEB/11.EvolutionHormoneRecept2011.ppt

Got  Aldosterone? Aldosterone  Synthesis
http://medicine.med.nyu.edu/nephrology/files/med_nephrology/attachments/Got_Aldosterone.ppt

Aldosterone  and MR Activation Revisited   
by Philip  J. Klemmer, MD
http://www.med.unc.edu/medicine/web/8.28.07%20Aldosterone%20Klemmer.ppt

Adrenal Steroids:  A Review
http://www.calstatela.edu/faculty/mchen/439Lectures/439EnAdrenals14.ppt

Publications

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19 January 2012

Drug Discovery Process Ppts



Drug Discovery Process
http://faculty.mc3.edu/lrehfuss/bit120/drug.ppt

An iterative  algorithm for metabolic network-based drug  target identification
by Padmavati Sridhar,  Tamer Kahveci, Sanjay Ranka
http://www.cise.ufl.edu/~tamer/papers/psb2007.ppt

Mining metabolic  networks for optimal drug target identification
http://www.cise.ufl.edu/~cap5510fa10/08-CAP5510-Fall10.ppt

Structural  Bioinformatics in Drug  Discovery
by Melissa  Passino
http://www.sdsc.edu/pb/edu/pharm202/03/passino.ppt

Drug Discovery:  Proteomics, Genomics
by Philip  E. Bourne, Professor  of Pharmacology UCSD
http://www.sdsc.edu/pb/edu/spps273/spps273.ppt

Fragment- Based Drug Design
Yemane Mengistu, Michigan State University
http://www2.chemistry.msu.edu/courses/cem958/FS07_SS08%5CYemaneMengistu.ppt

LC-MS in Drug Discovery 
by Timothy V. Olah, Ph.D. 
http://web.uconn.edu/rusling/Olah.ppt

Antimicrobial  Drug Discovery Through  Bacteriophage Genomics
by Manoj  kumar
http://www.pitt.edu/~super7/30011-31001/30231.ppt

Chemical Structure Representation and Search Systems
by John Barnard
http://www.indiana.edu/~cheminfo/C571/c571_Barnard7.ppt

Analysis of  High-Throughput Screening Data
http://www.indiana.edu/~cheminfo/C371/371HTS.ppt

Insilico  drug designing
by Dinesh Gupta
http://sta.uwi.edu/fsa/dms/icgeb/documents/28-01-10InsilicoDrugDesigningDGL7.ppt

Active Learning Strategies for Drug Screening
http://genomics10.bu.edu/megonw/al_2.ppt

dentification  of Drug Metabolites via Mass Spectrometry
by Besnik  Bajrami
http://web.uconn.edu/rusling/besnik.ppt

Small Molecule  Based Drug Design: SAR/Lead Compound Identification
overheads/drug_discovery_1.ppt

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29 March 2010

Placebo Control: What is it? Why do we use it? Is it ethical?



Placebo Control: What is it? Why do we use it? Is it ethical?
By:Tom Talbot, MD MPH
Vanderbilt School of Medicine

Placebo
* Placebo = “I shall please”
* Pharmocologically inert substances used to satisfy patients that something being done for them (“please the patient”)
* “Any therapeutic procedure (or that component of any therapeutic procedure) which is given deliberately to have an effect, or unknowingly has an effect on a patient, symptom, syndrome, or disease, but which is objectively without specific activity for the condition being treated. The therapeutic procedure may be given with or without the conscious knowledge that the procedure is a placebo, may be an active (non-inert) or inactive (inert) procedure, and includes, therefore, all medical procedures no matter how specific – oral and parenteral medications, topical preparations, inhalants, and mechanical, surgical, and psycho-therapeutic procedures. The placebo must be differentiated from the placebo effect which may or may not occur and which may be favorable or unfavorable. The placebo effect is defined as the changes produced by placebos. The placebo is also used to describe an adequate control in research.” -- Shapiro

Placebo: Why Use it?
* Need to control for therapeutic aspects of prescribing a medication or procedure not directly due to the medication or procedure itself
* i.e. . . . The Placebo Effect

Placebo: History
* First placebo-controlled trial:
o Sanocrysin vs. distilled water to treat TB
o 1931
The Story of Kebrozion
* Pt. with lymphosarcoma
* Patient given Kebrozion
* “The tumor masses had melted like snowballs on a hot stove, and in only a few days, they were half their original size!”
* 2 months later – Kebrozion outed
* Pt given a “new form” of Kebrozion
* Water injections
* Tumors resolved remission
* 2 months later: AMA – “This stuff’s worthless”
* Pt. returns in extremis and dies

Kebrozion, Pt 2
Issues
* Does use of placebo remove access to effective standard of care?
* Is a trial that does not use placebo arm scientifically rigorous?
* Does use of a placebo sacrifice ethics and an individual patient’s welfare?

Placebo-Control: PROS
* Need placebo control to insure validity
Placebo-Control: PROS
* Need placebo control to insure validity
* Argue that no drug should be approved for patient use if it is not clearly superior to placebo or no treatment
* Scientifically invalid research is itself unethical
* Harm and discomfort nonexistent or small in some cases

Placebo-Control: PROS
* Places patients at less risk of harm due to need for smaller numbers for placebo-controlled trials
o Greater power with smaller numbers than noninferiority trial
o Many more exposed to drug in non- placebo trial
* FDA:
o Placebo controls required for disorders of moderate severity and pain
o Beta-blocker not approved for angina (even though it was shown to be as efficacious as proven tx) due to lack of placebo comparison
* Unethical to withhold effective treatment
* Places demands of science ahead of right and well-being of patients
* Your study question has to change:
o Is the new drug better than proven effective therapy?

Placebo-Control: CONS
* Patients are owed medical care for ailments when they present to healthcare providers
* Not truly testing therapy against “no treatment” placebo effect
Rothman KJ et al NEJM 1994;331:394 Enserink M Science 2000;490:418-9
* Declaration of Helsinki:
o “Every patient -- including those of a control group, if any -- should be assured of the best proven diagnostic and therapeutic method.”
o 2000 Revision: Placebos may be used only when there are no other therapies available for comparison with a test procedure
* “Concedes to individual investigators and to IRBs the right to determine how much discomfort or temporary disability patients should endure for the purpose of research”
Clinician/Physician Clinical Researcher
Ethical?
* Subjects: Cancer patients
* Intervention: Odansetron vs. placebo
* Indication: Post-chemotherapy emesis and nausea
* ? Proven effective therapy for nausea
* Subjects: Men with hair loss
* Intervention: Compound X vs. placebo
* Indication: Prevent hair loss
* ? Lack of sequelae from placebo use
* Subjects: Pts. with depression
* Intervention: Compound X vs. placebo
* Indication: Reduction in depressive sx.
* ? Places placebo pts. at risk for severe sequelae of depression

Ethical Balance
* Valid research vs. Undue harm
Validity Minimize Risk
Ethical Balance Validity
Minimize Risk
* Valid research vs. Undue harm
Placebo-Control and Procedures/Surgery
“A Controlled Trial of Arthroscopic Surgery for Osteoarthritis of the Knee”
* Randomized, PLACEBO-controlled trial
* Endpoint: Pain in study knee
* Placebo:
o Did not receive general anesthesia
o Knee prepped, draped
o Three 1cm incisions made
o Knee manipulated as if arthroscopy performed
o No instruments entered the incisions
Placebo-Control and Procedures/Surgery
* Informed Consent:
o Explained study thoroughly
o Subjects had to write the following:
+ “On entering this study, I realize that I may receive only placebo surgery. I further realize that this means that I will not have surgery on my knee joint. This placebo surgery will not benefit my knee arthritis.”
o 44% declined
So . . . What do you think? Is this ethical?
Placebo-Control and Procedures/Surgery
* Placebo is not necessarily without risk
* Placebo surgery “violates an essential standard for research: the requirement to minimize the risk of harm to subjects.”
* Again – is there harm in performing an unvalidated procedure?
* Does the risk exceed that of other research procedures from which the subject does not receive benefit?
o Bronchoscopy in healthy adults
o Placement of P-A catheter in non-critically- ill subjects
o Muscle biopsy in healthy adults
* Must be informed
* Must be told that misleading tactics may be used
* Must not be misled about the chances of receiving the sham procedure
* Must be debriefed after study complete and unblinded
* Arthroscopy Study Results:
o No difference in pain scores
o The surgery itself had been causing undue risk (and cost – $3.25 billion/year)
o Without the placebo-controlled study, this would never had been discovered

Cultural Issues and Placebo-Control
* What about when conducting research in other countries?
* “Standard of care” is different due to:
o Access to meds
o Access to healthcare
o Basic infrastructure issues
o Cultural beliefs
* Prevention of fetal-maternal transmission of HIV
* Population: African women
* Intervention: Short course AZT vs. placebo
* Problem: AZT shown effective (longer course)
* Critics: Withheld effective, morbidity-reducing treatment
* Supporters: “Standard of care” in the country was no meds – no money or availability

Cultural Issues and Placebo-Control – Ethical?
* Generally felt that the cultural “standard of care” for studies in developing countries should be that of the investigator’s host country

THE USE OF PLACEBO
Placebo Acceptable If . . .
* Use of placebo does not impair health or cause “severe” discomfort
* Existing therapies only partly effective or have very serious side effects
* Low frequency of condition – would prevent enrollment for a larger trial
* Participants at risk of harm from nonresponse are excluded
* Placebo period is a limited to minimum required
* Careful monitoring is insured
* Explicit withdrawal criteria for AE
* Informed consent explicit as to why placebo should be used
* Improved survival or prevention of irreversible morbidity does not exist for any therapy
Questions

Placebo Control: What is it? Why do we use it? Is it ethical?.ppt

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14 March 2010

Genetically (devoid of RNA) Virus Particles as Drug Delivery Agent



Genetically (devoid of RNA) Virus Particles as Drug Delivery Agent




Scientists at John Innes Centre in Norwich, UK managed to create Cowpea mosaic virus particles that are missing their genetic material (devoid of RNA), turning them into drug ferrying containers that may prove useful against cancer and other localized diseases.

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24 February 2010

Drug Induced Dementia: Proceed with Caution



Drug Induced Dementia: Proceed with Caution
By:David M. Angaran, MS, FASHP, FCCP
Clinical Professor University Florida College of Pharmacy
Angaran Associates, LTD

Presentation Objectives
* Explain how and when this may happen.
* Present examples of drug caused conditions and symptoms that worsen dementia.
* Provide drug examples that can worsen dementia
* Describe how to reduce the chance of this happening.

Dementia
* Mental condition which represents a deterioration from previous function in at least three of the following functions:
* Language, understand what you are seeing, memory/reasoning and emotion
* Includes:
o Alzheimer’s, Mild Cognitive Impairment, Lewy Body, and Vascular

But First a Reminder
“The SUNNY side”
Medications can be vital to a better life for the caregiver and patient

Drugs make Dementia Worse:
How?
* Direct acting on the brain
o Delirium Dizziness
o Agitation Hallucinations
o Memory Loss Depression
* Indirect acting on the body
o Constipation Blood sugar
o Urinary retention Dehydration

How often does this happen?
* No ONE really knows
* Patients with mental changes
o 10-30% thought to be drug induced.
* Adverse drug effects emergency room visits for >65 yr. (Gurwitz JH et al. JAMA 2003;289:1107-1116)
o Dementia related
+ Neuropsychiatry 5%
+ Falls, dizzy, 8.5%
* If it happens to you or a loved one it is 100%.

Who is at greatest risk?
* Already demented or brain injury
* Frail elderly, the older the more susceptible.
* Has other disease states
* Taking more drugs
* Taking drugs unknown to physician or pharmacist
o Prescription (another Dr, another Pharmacy)
o Over the counter (OTC) eg. Sleep meds.
o Herbal

When can it happen?
* When a new drug is started.
o >65 yr. Go low and slow
* When the dose is changed.
* When another drug is added, stopped, or changed
* When a drug is stopped
o Treated condition can get worse
o Withdrawal side affects eg. Valium, antidepressants

What Can YOU Do To Help?
“Talk with your Dr. and RPh”
* Must know every drug the person is taking.
o OTC: Benadryl
o Herbal: St. Johns Wart
o Home remedy
o Nutritional supplements eg. Ephedrine
o Alcohol
* Must know HOW the drugs are being taken.
o How much
o How often
o How regular
o How long

What Can you Do to Help?
“Be Informed”
* Keep a Drug log. Name, Use, Directions.
* Do NOT stop, start or change drug regimen without consulting your Dr. or RPh.
* Know what trouble looks like and what to do.
o Side effects
o What action to take
* Ensure the drugs are taken as prescribed.
o What to do if you miss a dose.
* Ask for a “Medication Review” at regular intervals.

Drugs that MAY worsen Dementia
* Anti Cholinergic Alternative
o Elavil- antidepressant Paxil
o Benadry-allergy Claritin
o Demerol-pain Percocet
o Mellaril-antipsychotic Risperdal
* Anti anxiety
o Valium Xanax
* The list goes on and on……….

Nursing Home Do NOT use list
Pentazocine (Talwin): Confusion, hallucinations, dizziness, lightheadedness, euphoria, and sedation
Long-acting benzodiazepines(Librium): Sedation, drowsiness, ataxia, fatigue, confusion, weakness, dizziness, vertigo, syncope, psychological changes
Amitriptyline(Elavil) Anticholinergic and sedating properties, which can result in confusion, delirium, or hallucinations
Doxepin(Sinequan):Anticholinergic and sedating properties, which can result in confusion, delirium, or hallucinations
Meprobamate(Equanil): Highly addictive and sedating, which can result in drowsiness and ataxia
Lisi DM. Medscape Pharmacotherapy 2000;2 www.medscape.com adapted
Digoxin(Lanoxin): Toxic signs include headache, fatigue, malaise, drowsiness, and depression
Methyldopa(Aldomet) May exacerbate depression
Chlorpropamide(Diabenese) Hypoglycemia, which can result in altered mental state (confusion, amnesia, coma)
GI antispasmodics(Bentyl) Highly anticholinergic properties, which can result in confusion, delirium, or hallucinations
Barbiturates(Seconal) Highly addictive and sedative, resulting in drowsiness, lethargy, depression, severe CNS depression
Muscle relaxants(Robaxin): Anticholinergic properties, which can result in sedation, weakness, confusion, delirium, or hallucinations
Antihistamines(Chlortrimeton): Anticholinergic properties, which can result in confusion, delirium, or hallucinations
Reserpine: Depression, sedation
Diphenhydramine(Bendaryl) Highly anticholinergic, which can result in confusion, delirium, or hallucinations
Indomethacin(Indocin) Headache, dizziness, vertigo, somnolence, depression, fatigue
Disopyramide(Norpace): Strongly anticholinergic properties, which can result in confusion, delirium, and hallucinations
* What is IN that over the counter (OTC)?
o DON’T trust the name: Excedrin/Excedrin PM
o Unfamiliar contents: Ask and let them know why you are asking.
o Cautions on the labels are NOT enough.
+ Heavy machinery and driving cautions
+ Sedation and excitement

Mental status has suddenly gotten worse;what will your Dr. Do?
* Drug related questions:
o Could it be caused by a drug?
o What are ALL the drugs the patient is taking?
o Has any drug been started, stopped, or changed?
o How are they TAKING these drugs?
* Actions that may take place.
o Medication review
o Stop, substitute, increase/decrease dose

Getting Help
* Your Pharmacist
o Consultants for nursing homes and assisted living homes.
o Drug needs at ONE pharmacy
+ Complete drug profile
+ Get to know you and your situation
+ Rx medication information sheet NOT written for people suffering from dementia
* Web sites
o www.medscape.com Medscape
o www.intelihealth.com Harvard Medical School

REMEMBER
* Medications can be VERY beneficial for you and your loved one.
* Keep all your healthcare providers informed about what and how drugs are used.
* Keep a record of all the drugs.
* Know what “trouble” looks like and what to do about it.

Drug Induced Dementia: Proceed with Caution.ppt

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06 February 2010

Drugs for Viral Infections



Drugs for Viral Infections

Virus vs. Bacteria

* Compare and contrast structural components of bacteria and viruses
* Describe a viron.
* Identify indications for viral infection pharmacotherapy.

Challenges of Anti-Viral Therapy
* Rapid mutation
* Intracellular nature of virus
* Drugs have narrow spectrum of activity

HIV vs. AIDS
* Discuss the difference between a virus and a retrovirus.
* Differentiate between HIV infection and AIDS.
* Describe the replication of HIV.

Pharmacotherpy for HIV-AIDS
* Identify the therapeutic goals of therapy.
* Classifications:
o Nucleoside reverse transcriptase inhibitors (NRTI)
o Nonnucleoside reverse transcriptase inhibitors (NNRTI)
o Protease Inhibitors
o Neucleotide reverse transcriptase inhibitor (NtRTI)
o Fusion (entry) inhibitor

HIV-AIDS Pharmacotherapy
* Compare and contrast the mechanism of action of:
o Reverse transcriptase inhibitors
o Protease inhibitors
o Fusion inhibitors
* Identify reasons treatment failures occur.

Antiretrovirals: NCs
* Drug is not a cure
* Prior to RX: assess for sx of HIV, opportunistic infection, use of herbals
* Monitor viral load
* Verify ordered combination drugs
* Common side effects:
o Fatigue, headache, GI disturbances
* Other side effects dependent upon specific drug

Antiretrovirals: NCs

* Most contraindicated: pregnancy, lactation
* Side effects can influence ADLs
* NRTIs: cautiously: pancreatitis, PVD, neuropathy, kidney or liver disorders, cardiac disease, alcohol abuse
* NNRTIs: judiciously use in liver impairment, CNS disease
* PIs: potential risks if sensitive to sulfonamides, liver disorders, renal insufficiency

Antiretrovirals: NCs

* Variations in administration instructions:
o NRTIs: empty stomach, water only, no fruit juice
o Nevirapine (Viramune) and saquinavir (Invirase) – take with food to decrease GI upset
o Contact HCP before taking any OTC med or supplement

Antiretrovirals: Client Teaching

* NRTIs: report fever, skin rash, abd pain, n/v, numbness or burning of hands/feet
* NNRTIs: report fever, chills, rash, blistering or reddening of the skin, muscle or joint pain
* PIs: report rash, abd pain, headache, insomnia, fever, constipation, cough, fainting, visual changes

Antiretrovirals: Client Teaching

* Wash hands frequently; avoid crowds
* Increase fluid intake; empty bladder frequently
* Abstinence or barrier contraception
* Do not share needles
* Take medications as ordered
* Sufficient rest and sleep; healthy diet
* Keep all scheduled appts and lab visits

Perinatal HIV Transmission
Discuss pharmacotherapy for the prevention of perinatal transmission.

Occupation Exposure
* Identify risk factors for occupational exposure to HIV.
* Describe post HIV exposure prophylaxis.

Herpesvirus Infections
* HSV-1
* HSV-2
* CMV
* VZV
* EBV
* Herpesvirus 6
o Children: roseola
o Immunocompromised: hepatitis or encephalitis

Herpesvirus Infections
* Triggering events:
o Immunosuppression
o Physical challenges
o Emotional stress

* Pharmacologic goals:
o Relieve acute symptoms
o Prevent recurrences

Antivirals: NCs
* Baseline: VS, wt, CBC, viral cultures, LFTs, RFTs
* Cautiously: pre-exisiting renal or liver dysfunction
* Judiciously: pregnancy
* Routes: IV, oral, topical, inhalation
o instruct re: proper technique
o Emphasize compliance

Antivirals: NCs
* Generally well tolerated:
o Take with food if GI upset
* Severe adverse reactions:
o Renal Failure, Thrombocytopenia
* More frequently side effects:
o Headache
o Fatigue
o Dizziness

Antivirals: Client Teaching

* Meds do not prevent transmission
o avoid activities that may transmit
* Immediately report: hematuria, bruising, jaundice, fever, chills, confusion, nervousness, dizziness, nausea, vomiting
* Complete full course of treatment
* Keep scheduled appts and lab visits

Antivirals: Client Teaching

* Caution while performing hazardous activities
* No other prescription, OTC, herbals or supplements without HCP approval
* Apply topicals with applicator or glove
* No other creams, ointments, or lotions to infected sites

Influenza

* Describe the characteristics of influenza.
* Differentiate between primary and secondary pharmacotherapy for influenza infections.
* Differentiate between antiviral and neuroaminidase inhibitor therapy.

Viral Hepatitis
* Caused by several different viruses with unique clinical features
* All cause inflammation and necrosis of liver cells
* Acute
o Fever, chills, fatigue, anorexia, nausea, vomiting
* Chronic
o Prolonged fatigue, jaundice, liver cirrhosis, hepatic failure

Viral Hepatitis

* Differentiate between Hepatitis A, Hepatitis B, and Hepatitis C.
* Compare and contrast pharmacotherapy for Hepatitis A, Hepatitis B, and Hepatitis C.

Viral Hepatitis Exposure
Compare and contrast post-exposure prophylaxis for Hepatitis A, Hepatitis B, and Hepatitis C.

Drugs for Viral Infections.ppt

Read more...

13 January 2010

Amino Acid Metabolism



Amino Acid Metabolism
by:Hanley N. Abramson
Professor of Pharmaceutical Sciences
Wayne State University

December 2009

Dynamics of Protein And Amino Acid Metabolism
Dietary Proteins Digestion to Amino Acids
Digestion of Proteins
Stomach: Pepsinogen Pepsin (max. act. pH 2)
Small Intestine: Trypsinogen Trypsin
Trypsin cleaves:
Chymotrypsinogen to chymotrypsin
Proelastase to elastase
Procarboxypeptidase to carboxypeptidase
Aminopeptidases (from intestinal epithelia)

Enteropeptidase
Lumen
Amino Acids Oligopeptides
Intestinal Absorption
Oligopeptides
Amino Acids
Peptidases
Blood
Transport
Protein
Incorporation of NH4+ Into Organic Compounds
Carbamoyl
Phosphate
Synthase I
(CPS-I)
Glutamate
dehydrogenase
a-Ketoglutarate
Glutamate
TCA Cycle
mitochondria
Glutamine
Glutamate
Glutamine
Synthase
Mg++
N of glutamine donated to other compounds in synthesis of purines, pyrimidines, and other amino acids
Biosynthesis of Amino Acids: Transaminations
Glutamate a-Ketoglutarate
Oxaloacetate Aspartate
Glutamate-Pyruvate
Aminotransferase
(Alanine Transferase ALT)
Glutamate-Oxaloacetate
Aminotransferase
(Aspartate Transferase AST)
Blood levels of these aminotransferases, also called transaminases, are important indicators of liver disease
Metabolic Classification of the Amino Acids
* Essential and Non-essential
* Glucogenic and Ketogenic
Non-Essential Amino Acids in Humans
* Not required in diet
* Can be formed from a-keto acids by transamination and subsequent reactions
* Alanine
* Asparagine
* Aspartate
* Glutamate
* Glutamine
* Glycine
* Proline
* Serine
* Cysteine (from Met*)
* Tyrosine (from Phe*)
* Essential amino acids
Essential Amino Acids in Humans
* Required in diet
* Humans incapable of forming requisite carbon skeleton
* Arginine*
* Histidine*
* Isoleucine
* Leucine
* Valine
* Lysine
* Methionine
* Threonine
* Phenylalanine
* Tryptophan

* Essential in children, not in adults

Glucogenic Amino Acids
* Metabolized to a-ketoglutarate, pyruvate, oxaloacetate, fumarate, or succinyl CoA
Phosphoenolpyruvate Glucose
* Aspartate
* Asparagine
* Arginine
* Phenylalanine
* Tyrosine
* Isoleucine
* Methionine
* Valine
* Glutamine
* Glutamate
* Proline
* Histidine
* Alanine
* Serine
* Cysteine
* Glycine
* Threonine
* Tryptophan

Ketogenic Amino Acids
* Isoleucine
* Leucine *
* Lysine *
* Threonine
* Tryptophan
* Phenylalanine
* Tyrosine

Amino Acids Formed From a-Ketoglutarate
Transamination or
Glutamate
Urea Formation
Blood Urea Nitrogen
Synthesis of Nitric Oxide
Nitric oxide synthase (NOS)
Nitric Oxide
Conversion of Serine to Glycine
Sulfur-Containing Amino Acids
Homocysteine
Homocysteinuria
High blood levels of homocysteine associated with cardiovascular disease
Methionine Metabolism: Methyl Donation
Pneumocystis carinii infectons
Creatine and Creatinine
Normal Utilization of Phenylalanine ....

Amino Acid Metabolism.ppt

Read more...

25 September 2009

Opioid Analgesics & Antagonists



Opioid Analgesics & Antagonists

* Pain management

Opioid Analgesics & Antagonists

* Severe or chronic malignant pain opioids are the drugs of choice.
* Opioids are natural or synthetic compounds that produce morphine-like effects; opiates are drugs obtained from the juice of the opium poppy.
* All drugs in this category act through binding to specific opioid receptors in the CNS to mimic the effects of endogenous agents (endorphins & enkephalins) that eliminate many of the symptoms of a pain syndrome.
* Their anxiolytic and euphoric effects have led to their abuse.

Opioid Receptors

* Opioids interact stereospecifically with protein receptors on the membranes of certain cells in the CNS, on nerve terminals in the periphery and on cells of the gastrointestinal tract and the anatomic regions.
* The major effects of opioids are mediated through three receptor families: μ, κ and δ.
* Analgesic properties are mediated mainly via μ receptors and κ receptors of the dorsal horn of the spinal cord.
* Enkephalins interact more selectively with the δ receptors in the periphery.
* All three families are G-protein coupled receptors and inhibit adenylate cyclase.
* They are also involved in postsynaptic hyperpolarization (increasing K+ efflux) or reducing presynaptic Ca++ influx; this inhibits neuronal activity.

Receptor distribution

High densities of opioid receptors have been identified on peripheral nerve fibers, immune cells and five general areas of the CNS:

1. Brainstem: mediating respiration, cough, nausea & vomiting, maintenance of BP, papillary diameter and control of stomach secretion.

2. Medial thalamus: mediating poorly localized deep pain

3. Spinal cord: receptors located in the substantia gelatinosa are involved in the receipt & integration on sensory input leading to the attenuation of painful afferent stimuli.

Receptor distribution

4. Hypothalamus: mediating neuroendocrine secretion.

5. Limbic system: the greatest concentration of receptors are located in the amygdale, these receptors play a major role in emotional behavior & response and little analgesic effect.

Receptor distribution

6. Periphery: Peripheral nerve fibers bind opioids, they inhibit Ca+2 dependent release of excitatory, pro-inflammatory substances (substance P) from nerve endings

7. Immune cells: the role of these receptors in analgesia is undetermined.

Opioid Agonists

* The strongest naturally occurring analgesic drugs are found in opium from the poppy flower, morphine and less potent codeine. These drugs show a high affinity for the μ receptor and less affinity for the κ and δ receptors.

Morphine


Mechanism of Action:

* Opioids exert their major effects through interaction with central & peripheral opioid receptors, binding results in hyperpolarization, inhibition of nerve firing and presynaptic inhibition of transmitter release.
* Morphine acts at the κ receptors in lamina I & II of the substantia gelatinosa of the cord and decreases the release of substance P, it also inhibits the release of excitatory transmitters from nociceptive nerve terminals centrally and in the cord.

Actions:

Analgesia:

* Opioids cause pain relief by both raising the pain threshold at the spinal cord level and altering the central perception of pain. Awareness of pain remains but it loses its unpleasant character.

Euphoria:

* Opioids produce a sense of contentment and well being, this may be

related to stimulation of the central tegmental tract.

Respiration:

* Opioids cause respiratory depression by decreasing the sensitivity of central respiratory neurons to CO2. This occurs at therapeutic doses and as dose increases respiratory arrest will occur.

Suppression of cough reflex

* Antitussive properties do not correlate with analgesic or respiratory depression effects; this appears mediated via a different receptor complex.

Actions:

Miosis:

* This results from stimulation of μ and κ receptors located in the Edinger-Westphal nucleus of CN III, this is resistant to tolerance, pin point pupils remain after most other opioid effects have developed tolerance.

Emesis:

* Opioids directly stimulate the chemoreceptor trigger zone in the area postrema that causes vomiting.

GI tract:

* Opioids relieve diarrhea by decreasing gut motility and increasing the tone of intestinal smooth muscle. Constipation is also resistant to tolerance. Biliary spasm is exacerbated by increasing biliary tone with sphincter of Oddi spasm.

Cardiovascular:

* At large doses morphine produces hypotension & bradycardia.

Actions:

Histamine release:

* Morphine causes mast cell degranulation with the release of histamine causing urticaria, itching, diaphoresis and vasodilation. In asthmatics it may precipitate bronchospasm.

Hormonal Actions:

* Morphine inhibits the release of GnRH, CRH and deceases the release of LH, FSH & ACTH and β-endorphin. Testosterone and cortisol levels decrease. Prolactin and GH release are increased via suppression of dopamine levels centrally. ADH release is also diminished.

Therapeutic Uses

* Analgesia: Few drugs are as effective as morphine for the relief of pain.
* Treatment of diarrhea
* Anti-tussive: codeine and dextromethorphan are congeners with greater antitussive effects.
* Pulmonary edema: IV morphine dramatically relieves the dyspnea associated with pulmonary edema due to LV failure.

Pharmacokinetics

1. Administration: Morphine is poorly absorbed orally; codeine is a much more effective oral analgesic. Both undergo extensive first pass metabolism in the liver. Inhalation is an effective route but has found favor only with non-medicinal administration.

2. Distribution: Morphine readily enters all body tissues except the brain; morphine is the least lipid soluble of the opiates (fentanyl, methadone and heroin all enter the CNS much more quickly).

3. Metabolism: Conjugated in the liver, morphine–6-glucuronide is a much more potent analgesic; however morphine-3-glucuronide is less analgesic. Both are excreted in the urine with small amounts excreted in the bile. Hepatic & renal dysfunction both prolong the normal 4-6 hour duration of action when administered systemically.

Adverse effects

* Severe respiratory depression can occur and is the mechanism of dearth in most opiate overdose. Vomiting, dysphoria and allergic reactions are also common adverse effects.
* Caution must be exercised when opiates are used in those with liver or renal failure.

Tolerance & Physical Dependence

Repeated use produces tolerance to the effects of respiratory depression, analgesia, euphoria and sedation. Tolerance does not develop to miosis and constipation. Physical & psychological dependence readily occur with morphine and other opiates. Withdrawal induces a syndrome associated with autonomic, motor and psychological responses that are incapacitating, rarely are these life threatening.

Meperidine

* Meperidine (Demerol) is a synthetic opioid structurally unrelated to morphine.
* Mechanism: It binds to μ receptors with some binding at κ receptors.
* Actions: It causes respiratory depression similar to morphine but has no significant cardiovascular effect when given orally. IV administration produces a decrease in PVR resulting in increased peripheral blood flow. It causes papillary dilation via an atropine –like effect.

Meperidine

* Therapeutic uses: Severe acute pain, it lacks anti-tussive activity and produces less smooth muscle contraction/spasm than morphine.
* Pharmacokinetics: It is well absorbed form the GI tract; it is most often given IM. It has a shorter duration of action than morphine (2-4 hours). It is demethylated in the liver and excreted in the urine.
* Adverse effects: With large repeated doses normeperidine (demethylated meperidine) accumulates causing anxiety, muscle tremors and convulsions. It causes papillary dilation (vs. miosis with morphine) in large doses. There is cross-tolerance with other opioids.

Methadone

* This is a synthetic orally effective opioid that is equipotent to morphine but induces less euphoria and has a longer duration of action.
* Mechanism of action: Methadone binds to the μ receptor.
* Actions: Methadone is well absorbed orally and is an equipotent analgesic to morphine. It causes miosis, respiratory depression, biliary spasm and constipation just like morphine.

* Therapeutic uses: It is used for controlled withdrawal from heroin & morphine. Methadone is it self addictive but the withdrawal syndrome is somewhat milder but more protracted than with other opioids.
* Pharmacokinetics: Readily absorbed orally it is highly protein bound so remains in tissues for a prolonged period. It is transformed in the liver and excreted by the urine as mostly inactive metabolites.
* Adverse effects: similar to morphine particularly the risk of addiction

Fentanyl

* Chemically related to merperidine fentanyl has 100 times the analgesic potency of morphine. It has a rapid onset of action and a short duration (15-30 minutes. It can be used IV, epidurally or intrathecally. Transmucosal and transdermal preparations are available. Fentanyl is metabolized to an inactive metabolite by the cytochrome p4503A4 system. Drug metabolites are eliminated through the urine. Like morphine fentanyl causes miosis (vs. mydriasis). A particular risk of the transmucosal or transdermal routes is respiratory depression; these delivery routes create a reservoir of drug in the skin or mucosa.
* Sufentanil, Alfentanil & Remifentanil are related to fentanyl they differ in their potency and metabolic disposition. Sufentanil is even more potent than fentanyl.

Heroin


* Heroin is produced by the diacetylation of morphine which results in a three fold increase in its potency. The acetylation allows it to cross the BBB much more rapidly yielding a more pronounced euphoria. It may be used IV or smoked, both allow for rapid distribution, heroin is metabolized to morphine. There is no medical indication for its use in the US.

Moderate Agonists

Codeine

* This is a much less potent analgesic than morphine, it produces less euphoria and has much lower abuse potential and rarely produces physical dependence.
* It is an effective oral analgesic. It does possess significant antitussive effects at subanalgesic doses.
* Codeine is often formulated with either acetaminophen, aspirin of ibuprofen; care but be exerted when these are used with over the counter analgesic to avoid overdose with the non-opioid agent.
* A synthetic congener of codeine dextromethorphan lacks analgesic properties is an effective antitussive available without prescription.

Moderate Agonists

Oxycodone

* This is a semisynthetic derivative of morphine that is orally active; it too is formulated with over-the-counter analgesics. It is metabolized in the liver and excreted via the kidney. Controlled release forms of oxycontin requiring once or twice a day dosing are effective for chronic pain. Crushing these pills disrupts the sustained release mechanism resulting in acute intoxication consistent with opiate overdose.

Moderate Agonists

Hydrocodone is a semi-synthetic opioid derived from two of the naturally occurring opiates, codeine and thebaine. Hydrocodone is an orally active narcotic analgesic and antitussive. It is commonly available in tablet, capsule, and syrup form and is often compounded with other analgesics like acetminophen or ibuprofen

Moderate Agonists

Propoxyphene

* This is a derivative of methadone, it is used for mild to moderate pain; it has ~1/2 the potency of codeine.
* It is often formulated with another over-the-counter analgesic. The combination has greater effect than either drug alone.
* Toxic doses may produce cardio and pulmonary toxicity particularly when taken in combination with alcohol and/or sedatives in addition to CNS depression. Opioid antagonists can reverse the pulmonary and CNS effects but not the cardiotoxixity.

Mixed Agonist-Antagonist and Partial Agonists

Buprenorphine

* This agent is a partial agonist at μ receptors producing morphine-like effects in naïve users but precipitating withdrawal in morphine dependents.
* It is metabolized in the liver and excreted in the urine and bile. This agent may be taken sublingually or parenteral and possess a long duration of action.
* Adverse effects respiratory depression not reversible by naloxone, hypotension and nausea.
* Its main use is in opioid detoxification as its withdrawal syndrome appears less severe and of shorter duration than methadone. It is available outside of the specialized clinic allowed to dispense methadone for opiate withdrawal.

Antagonists

Opioid antagonists bind with high affinity to the μ, κ & δ receptors but fail to transducer. In normal individuals these agents produce no effect but in those with opiates present they induce an acute withdrawal syndrome.

A. Naloxone

* This agent is used to reverse the coma and respiratory depression associated wit opioid overdose. It competes at all receptors with much greater avidity than agonists. IV administration produces a reversal of CNS & respiratory depression within ~30 seconds. It has a relatively short T1/2 (60-100 minutes) so reversal will often abate requiring repeat administration. Binding affinity is 10X greater at the μ receptor than κ; this may explain how naloxone reverses respiratory depression but not analgesia (resulting from agonism of the κ- receptors in the spinal cord).

B. Naltrexone

* This agent has similar actions as naloxone but it is an oral agent with a much longer duration of action, a single dose is able to antagonize the effects of heroin for up to 48 hours.

Opioid Analgesics & Antagonists.ppt

Read more...

26 July 2009

Pharmacology Presentations Part-4



Pharmacology Presentations from Howard University College of Medicine

Drug Abuse – Hallucinogenic Drugs
By:Robert L. Copeland, Jr., Ph.D.

Drugs of Abuse: Opiates
By:Robert L. Copeland, Jr., Ph.D.

Drugs of Abuse Part V Inhalants
By:Martha I. Dávila-García, Ph.D.

Opioid Agonists And Antagonists
By: Dr. Robert L. Copeland

CNS Depressants Sedative/Hypnotics
By:Dr. Martha I. Dávila-García

Non-Metallic Environmental Toxicants
By: Sidney Green Ph.D

Good Laboratory Practices
By:Sidney Green, Ph.D.

Dyslipidemia
By:GETU ASSEFA M.D.

Read more...

Pharmacology Presentations Part-3



Pharmacology Presentations from Howard University College of Medicine

Heavy Metals And Heavy Metal Antagonists 1, 2
By:Robert L. Copeland, Jr., Ph.D.

Therapeutic Gases - Oxygen
By:Robert L. Copeland, Ph.D.

Parkinson's Disease
By:Robert L. Copeland, Ph.D.

Biotransformation of Xenobiotics
By:Barbara M. Davit, PhD, DABT

Drug Metabolism

Pharmacology 1, 2
By:Dr. Martha I. Dávila-García

Drug Development and Regulation
By: Joseph Hanig, Ph.D.

Drugs of Abuse
By:Martha I. Dávila-García, Ph.D.

Drugs of Abuse Part-1
Martha I. Dávila-García, Ph.D.

Read more...

Pharmacology Presentations Part-2



Pharmacology Presentations from Howard University College of Medicine

Introduction to Toxicology 1, 2 , 3
By:SIDNEY GREEN, PH.D.

Alcohols - Monohydroxyl Alcohols
By:Dr. Akinshola

Local Anesthetics
By:Robert L. Copeland, Ph.D

CNS Stimulants 1, 2
1.By:Robert L. Copeland, Ph.D.
2.Martha I. Dávila-García, Ph.D.

Cancer Chemotherapy
By:Jillian H. Davis

Introduction to the Databases of National Library of Medicine
By:Robert L. Copeland,Ph.D.

Drug-Receptor Interactions
By:Dr. Robert L. Copeland

The Parasympathetic Nervous System 1, 2, 3

Cell Wall Inhibitors
By:Robert L. Copeland, Ph.D.

Read more...

Pharmacology Presentations Part-1



Pharmacology Presentations from Howard University College of Medicine

Anticoagulant, Antithrombotic and Anti-Platelet Drugs
By: Robert Taylor, MD, Ph.D.

Antiviral Agents
By:Jillian H. Davis

Antiepileptic Drugs 1, 2, 3, 4
By:Martha I. Dávila-García, Ph.D.

Routes of Drug Administration 1, 2, 3
By:Robert L. Copeland, Ph.D.

Tetracyclines, 2
By:Martha I. Dávila-García, Ph.D.

Pediatric and Perinatal Pharmacology
By: Martha I. Dávila-García, Ph.D.

Antiepileptic Drugs
By:Martha I. Dávila-García, Ph.D

Penetration of drug into the eye after systemic Administration

Antidepressants
By:Martha I. Dávila-García, Ph.D.

Clinical Toxicology
By:Joseph Hanig, Ph.D.

Acid-Peptic Disease PUD/GERD/NSAIDs
By:Duane T. Smoot, M.D., FACP, FACG

Read more...
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