Dental Syllabus

HOWARD UNIVERSITY
SOPHOMORE DENTAL PHARMACOLOGY
SYLLABUS
Spring 2004
Coordinator: Martha I. Dávila-García, Ph.D.

Department of Pharmacology
Office Phone: (202)806-7834
Co-Coordinator: Philip Gatti, Ph.D.

Department of Pharmacology
Office Phone: (202)806-9767
DENTAL PHARMACOLOGY
Spring 2004
TABLE OF CONTENTS
Page
Course Format............................................................................................................. 4
Methods and Material of Instruction .......................................................................... 4
Course Description...................................................................................................... 5
Course Organization ................................................................................................... 5
Course Prerequisites.................................................................................................... 5
Measurement and Evaluation...................................................................................... 6
Procedures Governing Examinations ......................................................................... 7
Guidelines for Absences from Intrasessional and Final Examinations ...................... 8
Course Outline .......................................................................................................9-11
Departmental Roster ............................................................................................12-13
Lecture Schedule .................................................................................................14-18
Lecture Objectives
Lecture 1, Introduction and Dose –Response curves. .........................................19-20
Lecture 2, Drug Absorption. ..................................................................................... 22
Lecture 3, Drug Distribution. ................................................................................... 23
Lecture 4, Drug Metabolism..................................................................................... 24
Lecture 5, Drug Elimination..................................................................................... 25
Lecture 6, Pharmacogenetics. .................................................................................. 26
Lecture 7, Pharmacology of the Autonomic Nervous System................................... 27
Lecture 8, Cholinergic Neurotransmission I, Cholinomimetics. .............................. 28
Lecture 9, Cholinergic Neurotransmission II, Inhibitors of Cholinesterase............ 29
Lecture 10, Cholinergic Neurotransmission III, Muscarinic Blocking Drugs......... 30
Lecture 11, Adrenergic Neuroransmission I, Sympathomimetics ............................ 31
Lecture 12, Adrenergic Neuroransmission II, Adrenergic Antagonists. ................. 32
Lecture 13, Ganglionic and Neuromuscular Blocking Agents. ................................ 33
Lecture 14, General Anesthesia...........................................................................34-35
Lecture 15, Local Anesthesia.................................................................................... 36
Lecture 16, Pharmacology of Oxygen/Nitrous Oxide. ............................................. 37
Lecture 17, Respiratory System and Asthma. ........................................................... 38
Lecture 18, Opiate Analgesics and Antagonists..................................................39-40
Lecture 19, Clinical Correlates of Pain Management and Anesthesia ...............41-42
Lecture 20, Parkinson’s Disease and other movement Disorders. .......................... 43
Lecture 21, Antipsychotics...................................................................................44-45
Lecture 22, Antidepressants and Antimanic Drugs .................................................. 46
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DENTAL PHARMACOLOGY
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Lecture 23, Sedative/Hypnotics and Anxiolytics. ..................................................... 47

Lecture 24, Epilepsy and Anticonvulsants...........................................................48-49
Lecture 25, CNS Stimulants. ..................................................................................... 55
Lecture 26, Drugs of Abuse. ................................................................................52-55
Lecture 27, Cardiovascular Pharmacology, Cardiac Gangliosides. ....................... 56
Lecture 28, Antiarrythmics. .................................................................................57-58
Lecture 29, Antianginals......................................................................................59-60
Lecture 30, Diuretics. ..........................................................................................61-62
Lecture 31, Anticoagulants. ...................................................................................... 63
Lecture 32, Antihypertensives..............................................................................64-65
Lecture 33 Inflammation I ...................................................................................66-67
Lecture 34, Inflammation II. ................................................................................66-67
Lecture 35, Immunopharmacology ........................................................................... 68
Lecture 36, Antimicrobials I, Sulfonamides & Trimethoprime. ............................... 69
Lecture 37, Antimicrobials II, Agents fro Urinary tract Infection. .....................70-71
Lecture 38, Antimicrobials III, Penicillin and other Inh.of Cell Wall Synthesis. .... 72
Lecture 39, Antimicrobials IV, Aminoglycosides. .................................................... 73
Lecture 40, Antimicrobials V, Tetracyclines. ......................................................74-75
Lecture 41, Antimicrobials VI, Erythromicin and Misc. Agents. ............................. 76
Lecture 42, Antimicrobials VII, TB........................................................................... 77
Lecture 43, Antivirals................................................................................................ 78
Lecture 44, Antifungals............................................................................................. 79
Lecture 45, Cancer Chemotherapy........................................................................... 80
Lecture 46, Antiseptics.............................................................................................. 81
Lecture 47, Agents affecting Ca2+ metabolism. ...................................................... 82
Lecture 48, Endocrine Pharmacology I, GH, ADH and Prolactin. ....................83-84
Lecture 49, Endocrine Pharmacology II, ACTH and Glucocorticoids. ..............85-86
Lecture 50, Endocrine Pharmacology III, Thyroid and Antithyroid Drugs .......87-88
Lecture 51, Endocrine Pharmacology IV, Estrogen, Progestin,
Oral Contraceptives and Androgens. ..................................................................89-90
Lecture 52, Endocrine Pharmacology V, Insulin and hypoglycemics.................91-92
Lecture 53, Anticaries, Antiplaque, Gingivitis Agents. ............................................ 93
Lecture 54, Toxicology. .......................................................................................94-96
Lecture 55, Prescription Writing. ............................................................................. 97
Lecture 56, Adverse Effects. ..................................................................................... 98
Lecture 57, Drug-Drug Interactions......................................................................... 98
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DENTAL PHARMACOLOGY
Spring 2004
Course Format
Title: Pharmacology
Level: Sophmore
Class Size: 75 students
Methods and Material of Instruction
Number of Times Administered per Academic Year: Once, in the Spring
Clock Hours: 72 hrs Lecture

2 hrs Intrasessional Exam
2 hrs Midterm Exam
2 hrs Final Exam
Lectures: 58
Lectures may include slides, overheads, power point presentations and handouts.
Syllabus
This syllabus contains the objectives for each lecture. The students are expected to
read from the assign books and reading materials. Examinations will be from the
material covered during lecture, assigned reading material and additional sources as
stated in each lecture by the instructor.
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DENTAL PHARMACOLOGY
Spring 2004
Course Description
This course discusses general principles of drug action and the pharmacology of therapeutic
agents. Emphasis will be placed on specific drugs used in routine clinical dentistry when appropriate.
Agents used for non-dental indications will also be covered since they can influence dental treatment
directly or indirectly. Finally, the course offers a thorough review on prescription writing.
The course objective is for the student to understand, define and explain:
• Drug classes available to treat the medical problem.
• Mechanisms of drug action.
• Pharmacokinetic factors which influence each drug.
• Drug-induced alteration in cellular responsiveness (e.g. tolerance, desensitization, dependence).
• Drug usefulness relative to patient’s therapeutic goals.
• Contraindications (absolute and relative).
• Adverse (side) effects including drug-drug interactions.
• Drug abuse-related symptoms.
• Drug induced alterations of clinical laboratory tests.
• Therapeutic index: risk/benefit ratio of therapy.
Course Organization
The first part of the course will deal with General Principles of pharmacology, how drugs are
absorbed, distributed, metabolized and eliminated from the body.
The second part will be on Systemic Pharmacology and will involve discussions of drug classes
and specific pharmacological agents and the systems where they act. (See course Outline page )
Course Prerequisites
Prerequisites for this course include a thorough knowledge of biochemical, physiological and
antimicrobial principles as well as the ability to perform basic scientific calculations and interpret
information presented graphically.
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DENTAL PHARMACOLOGY
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Measurement and Evaluation

All examinations will consist of multiple choice, case history and matching-type questions.
There will be one intra-sessional exam, one midterm exam and one final examination.
To pass the course students must answer correctly 65% of the total questions asked.
The composition of exams are approximately as follows:
1st Intrasessional 100 questions 32% GRADING SYSTEM:

Midterm 90 questions 29% Scaled grading
Final 120 questions 39% (65 % correctly answered questions = 70)
310 100%
Score Grade
90-100 A
80-89 B
70-79 C
< 70 D
Each examination and all grades are subjected to departmental faculty review and verification.
Each student is assured of equal, fair and impartial departmental consideration. The course
coordinator’s functions include scheduling of lectures and reviews, examination assembly, verification
of grading and presentation of grades to the department for approval and submission to the Office of the
Dean.
Exam Dates:
INTRASESSIONAL
Examination I Tuesday Feb. 3, 2004 Will cover material from: Tues. January 6 to
Fri. January 30, 2004
MIDTERM
Midterm Monday March 1, 2004 Will cover material from: Wed. February 4 to
Fri. February 27, 2004
FINAL
Final Examination Wednesday April 28, 2004 Will cover material from: Tues. March 16 to
Thurs. April 15, 2004
Contacts:
Dr. Martha Dávila-García, Course Coordinator, (202) 806-7834
Dr. Philip Gatti, Course Co-Coordinator, (202) 806-9767
Dr. Robert E. Taylor, Chairman, Department of Pharmacology

Department of Pharmacology Faculty
Department of Pharmacology Office, (202) 806-6311
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Spring 2004
Procedures Governing Examinations

1. Students should be seated at least five minutes before the scheduled starting time.
2. No food, radios, books, notes, cell phones or earphones, palm books, or computers will be
allowed at examination seats. Materials brought to the examination room must be placed in the
front or back of the room.
3. Only calculators and writing utensils (pencils and pens) and erasures will be allowed in the
examination seats.
4. The doors will close promptly at the time the examination is scheduled to begin. Students arriving
late will not be admitted to the examination room while examination materials and instructions are
being distributed to the punctual students. Those students arriving late will not be given
additional time to complete the examination.
5. During the course of the examinations, students will remain in their assigned seats. Questions and
needs of individual students will be attended to by proctors who will come to the student’s seat
when the student raises his/her hand.
6. Entrance to the examination will not be allowed for students who enter the room more than 30
minutes late.
7. Upon completion of the examination, the student is to remain seated and raise his/her hand. The
examination materials will be collected by the proctors.
8. After collection of the examination materials, the student will immediately leave the examination
room as well as the immediate area.
9. Students may review their exam results by appointment within 2 weeks after the exam. No
copying of exam questions are allowed.
10. Challenge to individual exam questions must be made within the 2 week after the exam was taken.
Use of these procedures is intended to assure:
a) maximum available time for students to take examinations; and
b) the best possible environment in which student will take examinations.
All students are being asked to become familiar with and to carefully observe these procedures.
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DENTAL PHARMACOLOGY
Spring 2004
Guidelines for Absences from Intrasessional, Midterm and Final Examinations
1. Students may be excused from intrasessional, midterm and final examinations only for reasons of
illness, serious injury, or death in the immediate family.
2. All absences due to illnesses, injury or death in the immediate family that result in or cause the
student to miss an examination must be reported immediately to the Dean’s Office and to the
Department of Pharmacology (Suite 3408, Adams Bldg. (202)806-6311). A report must be made
and an absence request submitted no later than the end of the day of the scheduled examination.
Only official excuses from the Dean, College of Dentistry will be accepted to reschedule a missed
examination.
3. Illness or injury resulting in missed examinations must be certified by a physician.
4. Problems other than those stated above which result in a missed examination must also be
immediately reported to the Dean’s Office and to the Department of Pharmacology for
consideration.
5. All cases will be handled in an individual basis.
6. Makeup examinations not due to serious injury or illness must be taken within 72 hours of the
original examination date and be accompanied by a written excuse from the Dean’s Office.
7. The makeup examination will cover the same lecture material but the questions may be different
from the missed examination. The exam will not be returned to the student.
Failure to comply with set policies may result in a failing grade.
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Course Outline
I. Introduction
A. Pharmacodynamics
1. Dose-Response curves
B. Pharmacokinetics
1. Drug Absorption
2. Drug Distribution
3. Drug Metabolism
4. Drug Elimination
C. Clinical Uses of Drugs
II. Pharmacology of the Autonomic Nervous System
A. Cholinergic Neurotransmission
1. Cholinergic Neurotransmission I, Cholinomimetics
2. Cholinergic Neurotransmission II, Inhibitors of Cholinesterase
3. Cholinergic Neurotransmission III, Muscarinic Blocking Drugs
B. Adrenergic Neuroransmission
1. Adrenergic Neuroransmission I, Sympathomimetics
2. Adrenergic Neuroransmission II, Adrenergic Antagonists
C. Ganglionic and Neuromuscular Blocking Agents
D. General Anesthesia
E. Local Anesthesia
III. Respiratory Pharmacology
A. Pharmacology of Oxygen/Nitrous Oxide.
B. Respiratory System and Asthma.
IV. Pharmacology of Pain
A. Opiate Analgesics and Antagonists.
B. Clinical Correlates of Pain Management and Anesthesia.
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DENTAL PHARMACOLOGY
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V. CNS Pharmacology
A. Parkinson’s Disease and other movement Disorders.
B. Antipsychotics
C. Antidepressants and Antimanic Drugs
D. Sedative/Hypnotics and Anxiolytics
E. Epilepsy and Anticonvulsants
F. CNS Stimulants
G. Drugs of Abuse
VI. Cardiovascular Pharmacology
A. Cardiac Gangliosides
B. Antiarrythmics
C. Antianginals
D. Diuretics
E. Anticoagulants
F. Antihypertensives
VII. Inflammation
VIII. Immunopharmacology
IX. Chemotherapy
A. Antimicrobials I, Sulfonamides & Trimethoprime
B. Antimicrobials II, Agents fro Urinary tract Infection
C. Antimicrobials III, Penicillin and other Inh.of Cell Wall Synthesis
D. Antimicrobials IV, Aminoglycosides
E. Antimicrobials V, Tetracyclines
F. Antimicrobials VI, Erythromicin and Misc. Agents
G. Antimicrobials VII, TB
H. Antivirals
I. Antifungals
J. Cancer Chemotherapy
X. Antiseptics
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XI. Endocrine Pharmacology

A. Agents affecting Ca2+ metabolism
B. Endocrine Pharmacology I, GH, ADH and Prolactin
C. Endocrine Pharmacology II, ACTH and Glucocorticoids
D. Endocrine Pharmacology III, Thyroid and Antithyroid Drugs
E. Endocrine Pharmacology IV, Estrogen, Progestin,
F. Oral Contraceptives and Androgens
G. Endocrine Pharmacology V, Insulin and hypoglycemics
XII. Special Topics in Clinical Pharmacology
A. Anticaries, Antiplaque, Gingivitis Agents
B. Toxicology
C. Prescription Writing
D. Adverse Effects
E. Drug-Drug Interactions.
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DENTAL PHARMACOLOGY
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Department of Pharmacology,
Suite 3408 Adams Bldg.
520 W. St. NW
(202)806-6311
Pharmacology Faculty Roster
Donnell Bowen, Ph.D.
Room 3224, Adams Bldg. (202) 806-9769
e-mail: dbowen@howard.edu
Office Hours: Wednesday 3:00 p.m. - 5:00 p.m. & by appointment
Joseph Cohen, Ph.D.

Room 4406, Adams Bldg. (202) 806-9774
e-mail: jcohen@howard.edu
Office Hours: Tuesday 1:00 p.m. - 2:00 p.m.
Robert L. Copeland, Jr. Ph.D.

Room 3512H, Adams Bldg. (202) 806-6363
e-mail: rlcopeland@howard.edu
Office Hours: Monday & Friday 2:00 p.m. - 4:00 p.m.
Keith Crawford, Ph.D.

Pharmacy School (202) 806-7262
e-mail: kcrawford@howard.edu
Office Hours: Wednesday 12:00 p.m. - 1:00 p.m.
Martha I. Dávila-García, Ph.D. COURSE COORDINATOR

Room 1322I, Adams Bldg. (202)806-7834
e-mail: mdavila-garcia@howard.edu
Office Hours: Monday 3:00 p.m. – 5:00 p.m. & by appointment
Clifford Ferguson, M.D.

Room 411, Mudd Bldg. (202) 806-4322
e-mail: cferguson@howard.edu
Office Hours: Monday 12:00 p.m. - 1:00 p.m.
Philip Gatti, Ph.D. COURSE CO-COORDINATOR

Room 3512F, Adams Bldg. (202) 806-9767
e-mail: pgatti@howard.edu
Office Hours: Monday 3:00 p.m. - 5:00 p.m. & by appointment
V. John Massari, Ph.D.

Room 3512C, Adams Bldg. (202) 806-7902
e-mail: vmassari@howard.edu
Office Hours: Wednesday 11:00 a.m. - 1:00 p.m. & by appointment
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DENTAL PHARMACOLOGY
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Sonya K. Sobrian, Ph.D.

Room 308, Seeley Mudd Bldg. (202) 806-7902
e-mail: ssobrian@howard.edu
Office Hours: Wednesday 11:00 a.m. - 1:00 p.m. & by appointment
Robert E. Taylor, M.D., Ph.D.

Chairman, Department of Pharmacology
Room 3408, Adams Bldg. (202) 806-6311
e-mail: rtaylor@howard.edu
Office Hours: Monday 3:00 p.m. - 5:00 p.m.; Friday 3:00 p.m. - 5:00 p.m.
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DENTAL PHARMACOLOGY
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SOPHMORE DENTAL PHARMACOLOGY SCHEDULE
SPRING 2004
TUESDAYS 8-9:50 A.M. Held in Lecture Hall 3 of the Dental School (5th floor)
WEDNESDAYS 1-1:50 P.M. Held in Lecture Hall SCR of the Dental School (5th floor)
THURSDAYS 8-8:50 A.M. Held in Lecture Hall 3 of the Dental School (5th floor)
FRIDAYS 10-11:50 A.M. Held in Lecture Hall 3 of the Dental School (5th floor)
COURSE COORDINATOR: Dr. Martha I. Dávila-García (806-7834) - Room 1322I, Numa P.G. Adams Bldg.
CO-COORDINATORS: Dr. Philip J. Gatti (806-9767) - Room 3512F, Numa P.G. Adams Bldg.
OFFICE HOURS: Dr. Martha I. Dávila-García Tuesday 3-5 p.m.

Dr. Philip J. Gatti Mondays 3-5 p.m.
REQUIRED TEXTBOOK: Yagiela, J.A., Neidle, E.A., Dowd, F.J. (1998) Pharmacology & Therapeutics for
Dentistry, 4th Edition.
SUGGESTED TEXTBOOKS: Katzung, B.G. (2003) Basic and Clinical Pharmacology, 9th Edition.
Hardman, J.G. and Limbrid, L.E. (2001) Goodman and Gilman's: The
Pharmacological Basis of Therapeutics. 10th ed. McGraw Hill.
DEPARTMENTAL WEB-SITE: http://www.hucmlrc.howard.edu/Pharmacology/default.htm

___________________________________________________________________________________________________
DATE DAY TIME L.No. SUBJECT LECTURER_____
Jan. 6 Tues. 8-8:15 Course Objectives, Class & Exam DÁVILA-GÁRCÍA

Schedules, Evaluations, Books
UNIT I: GENERAL PRINCIPLES IN PHARMACOLOGY
Jan. 6 Tues. 8:15-8:50 1A Introduction to Pharmacology BOWEN/COPELAND

Divisions of Pharmacology
Mechanisms of Action:
Drug receptor interactions. Dose-response
relationship. Potency vs. Efficacy.
Jan. 6 Tues. 9-9:50 1B Introduction to Pharmacology BOWEN/COPELAND

Divisions of Pharmacology/Mechanisms of Action
Jan. 7 Wed. 1-1:50 2 Drug absorption. Characteristics of biological COPELAND

membranes. Biotransport mechanisms.
Routes of administration.
Jan. 8 Thurs. 8-8:50 3 Drug distribution. Volume of distribution, FERGUSON

Protein binding and storage; redistribution.
Jan. 9 Fri. 10-10:50 4 Drug metabolism. Biotransformation. COHEN
Jan. 9 Fri. 11-11:50 5 Drug elimination. Kinetics of absorption FERGUSON

and elimination. Multiple compartment models.
Jan. 13 Tues. 8-8:50 6 Clinical use of drugs. Factors modifying FERGUSON

the effect of drugs. Pharmacogenetics.
Patient factors: body weight,
Sex, age, genetic factors, diet.
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DENTAL PHARMACOLOGY
Spring 2004
___________________________________________________________________________________________________
UNIT II: PHARMACOLOGY OF THE AUTONOMIC NERVOUS SYSTEM
Jan. 14 Wed. 1-1:50 7 Introduction to Pharmacology of the MASSARI

Autonomic Nervous System (ANS).
Jan. 15 Thur. 8-8:50 8 Cholinergic neurotransmission: COHEN

Cholinomimetics. (esters & alkaloids).
Jan. 16 Fri. 10-10:50 9 Cholinergic neurotransmission: COHEN

Inhibitors of cholinesterase.
Jan. 16 Fri. 11-11:50 10 Muscarinic blocking drugs and their COHEN

therapeutic values in Dentistry.
Jan. 20 Tues. 8-8:50 11 Adrenergic neurotransmission, COHEN

sympathomimetic drugs and their uses in Dentistry.
Jan. 20 Tues. 9-9:50 11 Adrenergic neurotransmission. (cont’d) COHEN
Jan. 21 Wed. 1-1:50 12 Adrenergic receptor antagonists. MASSARI
Jan. 22 Thurs. 8-8:50 13 Ganglionic and neuromuscular blocking MASSARI

drugs.
Jan. 23 Fri. 10-10:50 14 General anesthesia. Clinical approaches CRAWFORD

to the use of general anesthesia.
Jan. 23 Fri. 11-11:50 14 General anesthesia. Individual agents (cont'd) CRAWFORD
Jan. 27 Tues. 8-9:50 15 Local anesthesia. History. General COPELAND

classifications and chemistry.
Mechanism of actions.
Jan. 28 Wed. 1-1:50 16 Pharmacology of Oxygen/Nitrous Oxide JACKSON
Jan. 29 Thurs. 8-8:50 17 Respiratory System and Asthma TYLER/MATHEW
Jan. 30 Fri. 10:00-11:50 18 Opiate analgesics and antagonists. COPELAND

Morphine and related alkaloids.
Methadone and congeners.
Feb. 3 Tues. 8-9:50 FIRST INTRASESSIONAL EXAMINATION

LECTURE HALL 2/3 DENTAL SCHOOL
Covers materials from:
Jan 6 - Jan 30, 2004
Feb. 4 Wed. 1-1 :50 19 Clinical correlations of pain management & JACKSON
anesthesia
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DENTAL PHARMACOLOGY
Spring 2004
____________________________________________________________________________________________
DATE DAY TIME L.No. SUBJECT LECTURER
UNIT III: PHARMACOLOGY OF THE CENTRAL NERVOUS SYSTEM
Feb. 5 Thurs. 8-8:50 20 Therapeutic approach to management MASSARI

of Parkinson's Disease and other
Movement Disorders.
Feb. 6 Fri. 10-11:50 21 Epilepsy and Anticonvulsants DÁVILA-GARCÍA
Feb. 10 Tues. 8-9:50 22 Antidepressants and Antimanic drugs DÁVILA-GARCÍA
Feb.11 Wed. 1-1:50 23 Sedative/Hynotics and Anxiolytics MASSARI
Feb. 12 Thurs. 8-8:50 24 Drug treatment of psychoses SOBRIAN
Feb. 13 Fri. 10-11:50 25 CNS stimulants: cocaine, methylphenidate COPELAND

the methylxanthines.
Feb. 17 Tues. 8-9:50 26 Drugs of Abuse DÁVILA-GARCÍA
UNIT IV: CARDIOVASCULAR
Feb. 18 Wed. 1-1 :50 27 Introduction to cardiovascular pharmacology FERGUSON

cardiac glycosides. Pathophysiology
of congestive heart failure.
Feb. 19 Thurs. 8-8:50 27 Cardiac glycosides (cont'd) FERGUSON
Feb. 20 Fri. 10-11:50 28 Review of arrhythmia, electro- GATTI

physiology of the heart.
Antiarrhythmic drugs,
29 Antianginals
Feb. 24 Tues. 8-9:50 30 Diuretics FERGUSON
Feb. 25 Wed. 1-1:50 31 Anticoagulants TAYLOR
Feb. 26 Thur. 8-8:50 31 Anticogulants (cont'd) TAYLOR
Feb. 27 Fri. 10-11:50 32 Antihypertensive drugs. Drug therapy of GATTI

hypertension. Drugs altering the central
Sympathetic activity.
Vasodilators. Adrenergic Receptor blocking agents
Mar. 1 Mon. 8:00-10:00 MIDTERM EXAMINATION

LECT. HALL 2/3 DENTAL SCHOOL
Covers material from lectures:
Feb. 4 - Feb. 27, 2004
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DENTAL PHARMACOLOGY
Spring 2004
___________________________________________________________________________________________________
Mar. 1-5 MIDTERM WEEK
Mar. 8-12 SPRING RECESS
UNIT V: CHEMOTHERAPY
Mar. 16 Tues. 8-9:50 33 Inflammation I CRAWFORD
Mar. 17 Wed. 1-1:50 34 Inflammation II, Histamine & Antihistamines CRAWFORD
Mar. 18 Thurs. 8-8:50 35 Immunopharmacology SOBRIAN
Mar. 19 Fri. 10-10:50 36 Antimicrobials I. Introduction. BOWEN

Basic concepts in chemotherapy of
microbial disease. Sulfonamides, Trimethoprime.
Mar. 19 Fri. 11-11:50 37 Antimicrobials II. Agents for urinary BOWEN

tract infections.
Mar. 23 Tues. 8-8:50 38 Antimicrobials III. Penicillins and other BOWEN

inhibitors of cell wall synthesis.
Mar. 23 Tues. 9-9:50 38 Inhibitors of cell wall synthesis (cont'd) BOWEN
Mar. 24 Wed. 1-1:50 39 Antimicrobials IV. Aminoglycosides. FERGUSON
Mar. 25 Thurs. 8-8:50 40 Antimicrobials V. Tetracyclines. COPELAND
Mar. 26 Fri. 10-10:50 41 Antimicrobials VI. Erythromycin & FERGUSON

Misc.
Mar. 26 Fri. 11-11:50 42 Antimicrobials VII. TB. COPELAND
Mar. 30 Tues. 8-8:50 43 Antiviral TBA
Mar. 30 Tues. 9-9:50 44 Antifungal agents. BOWEN
Mar. 31 Wed. 1-1:50 46 Antiseptic, disinfectant, hemostatic, COPELAND

and caustic agents.
Apr. 1 Thurs. 8-8:50 47 Agents affecting Ca2+ metabolism, para- FERGUSON

thyroid hormones, calcitonin, vitamin D
and other agents.
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DENTAL PHARMACOLOGY
Spring 2004
___________________________________________________________________________________________________
DATE DAY TIME L.No. SUBJECT LECTURER
UNIT VI: ENDOCRINE PHARMACOLOGY
Apr. 2 Fri. 10-10:50 48 Introduction to endocrine pharmacology, TIZABI

growth hormone, prolactin.
Apr. 2 Fri. 11-11 :50 49 ACTH and glucocorticoids TIZABI
Apr. 6 Tues. 8-8:50 50 Thyroid and Antithyroid drugs TIZABI
Apr. 6 Tues. 9-9:50 51 Estrogen, progestin I. Oral TIZABI

contraceptives, androgens.
Apr. 7 Wed. 1-1:50 51 Estrogen, progestin II TIZABI
Apr. 8 Thurs. 8-8:50 52 Insulin and oral hypoglycemics I CRAWFORD
Apr. 9 Fri. 10-10:50 52 Insulin and oral hypoglycemics II CRAWFORD
UNIT VII: SPECIAL TOPICS IN CLINICAL PHARMACOLOGY
Apr. 9 Fri. 11-11 :50 53 Anticaries, antiplaque, antigingivitis FERGUSON

agents.
Apr. 13 Tues. 8-8:50 54 Toxicology. Heavy metal toxicology: COPELAND

mercury and lead antagonists.
Apr. 13 Tues. 9-9:50 55 Prescription writing, components of FERGUSON

prescription, drug names. Scheduled
substances and rules and regulations.
Apr. 14 Wed. 1-1 :50 56 Adverse drug reactions of prescription FERGUSON

drugs.
Apr. 15 Thurs. 8-8:50 57 Clinically important drug interactions. FERGUSON
Apr. 16 Fri. 10-11:50 REVIEW
Apr. 16-20 READING PERIOD
Apr. 28 Wed. 1:00-3:00 FINAL EXAMINATION

LECT. HALL 2/3 DENTAL SCHOOL
Will cover material from: Tues. March 16
to Thurs. April 15, 2004
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DENTAL PHARMACOLOGY
Spring 2004
Dr. Donnell Bowen/Dr. Robert L. Copeland, Jr.
Introduction
Lecture 1A
Objectives:
Define the following terms:
1. Absorption
2. Drug
3. Permeation
4. Pharmacodynamics
5. Pharmacology
6. pKa
7. Special Carrier
8. Toxicology
9. Weak acid, weak base
You should:
Predict the relative ease of permeation of a weak acid or base from knowledge of its
pKa and the pH of the medium.
Required Reading:
Yagiela, J.A., Neidle, E.A., Dowd, F.J. (1998) Pharmacology & Therapeutics for
Dentistry, 4th Edition. Pages xi - xii, 3-9.
Suggested Reading:
Hardman, J.G. and Limbrid, L.E. (2001) Goodman and Gilman's: The Pharmacological
Basis of Therapeutics. 10th ed. McGraw Hill.
B.G. Katzung. (2001) Basic & Clinical Pharmacology, 8th Edition, Appleton and
Lange.
19
DENTAL PHARMACOLOGY
Spring 2004
Dr. Donnell Bowen/Dr. Robert L. Copeland, Jr.
Introduction
Dose-Response relationships
Lecture 1B
Objectives:
Chemical antagonist ▪ Partial agonist

Competitive antagonist ▪ Physiologic antagonist
Coupling protein ▪ Quantal dose-response curve
Drug efficacy ▪ Receptor
Intrinsic activity ▪ Spare receptor
Drug potency ▪ Therapeutic index
ED50, TD50, LD50 ▪ Certain safety factor and margin of safety
Effector
Effector mechanism
Insurmountable antagonism
You should be able to:

Specify whether an antagonist is competitive or irreversible on the basis of its effect
on the dose-response curve of the agonist.
Compare the efficacy and potency of drugs on the basis of their dose-response
curves.
Predict the effect of a partial agonist on a system in the presence and in the absence
of a full agonist.
Name an important inert binding site protein in blood.
Give examples of partial agonists, competitive and non-competitive antagonists, and
physiologic and chemical antagonists.
Name 4 methods by which drug-receptor signals bring about effects.
Know the binding forces in the drug-receptor complex.
Identify the components of a dose-response curve.
Required Reading:
Yagiela, J.A., Neidle, E.A., and Dowd, F.J. (1998) Pharmacology & Therapeutics for
Dentistry, 4th Edition. Pages 9-14 and 61-68.
Suggested Reading:
Lange.
20
DENTAL PHARMACOLOGY
Spring 2004
Dr. Robert L. Copland, Jr.
Drug Absorption
Lecture 2
Drug Absorption and Routes of Administration
Objectives:
To understand the process of drug absorption
Discuss the effect of pH on the absorption of weak acids and bases.
To discuss enteral, parenteral, transdermal and other routes of drug administration and
list their advantages and disadvantages.
Drug Absorption
A. Definition:
Drug absorption refers to the passage of a drug from its site of administration into the
circulation. In the gut, lungs, and skin, drugs must first be absorbed through a layer of
epithelial cells that have tight junctions. Drugs that are injected into the subcutaneous
tissue and muscle bypass the epithelial barrier and are more easily absorbed.
B. Processes of absorption
1. Passive diffusion: Most drugs are absorbed by passive diffusion into the
circulation. Drugs may be absorbed passively by lipid diffusion or by aqueous
diffusion.
Lipid diffusion is facilitated by a high degree of lipid solubility.
Aqueous diffusion occurs by passage through aqueous pores in cell
membranes and is restricted to drugs with a low molecular weight.
2. Other types of diffusion: A few drugs are absorbed by active transport or by

facilitated diffusion.
Routes of Drug Administration
A. Enteral administration: Enteral routes of administration are those in which the drug is
absorbed from the gastrointestinal tract.
1. In sublingual administration, a drug product is placed under the tongue. In

buccal administration, the drug is placed between the cheek and the gums.
Sublingual and buccal administration enable the rapid absorption of certain drugs
and are not affected by first-pass drug metabolism.
2. Oral administration refers to drug administration by mouth. Absorption of orally

administered drugs is variable because of the interaction of drugs with food and
gastric acid, the varying rates of gastric emptying and intestinal transit, and the
21
DENTAL PHARMACOLOGY
Spring 2004
varying rates of tablet disintegration and dissolution. Oral administration is not

suitable for use by patients who are sedated, comatose, or suffering from nausea
and vomiting.
3. Rectal administration of drugs may result in either a localized effect or a

systemic effect. Suppositories are useful when patients cannot take medications
by mouth, such as in the treatment of nausea and vomiting. Drugs absorbed from
the rectum undergo relatively little first-pass metabolism in the liver.
B. Parenteral administration: Parenteral administration refers to drug administration with

a needle and syringe or with an intravenous infusion device.
1. Intravenous administration is often preferred for drugs that have short half-
lives and for drugs whose dosage must be carefully titrated to the physiologic
response.
2. Intramuscular administration and subcutaneous administration are suitable for

drug solutions and suspensions.
3. Intrathecal administration refers to injection of a drug through the theca of the

spinal cord and into the subarachnoid space.
C. Transdermal administration: Transdermal administration refers to the application of

drugs to the skin for absorption into the circulation. Transdermal administration bypasses
first-pass hepatic inactivation.
D. lnhalational administration: lnhalational administration may be used to produce either

a localized effect on the respiratory tract (for example, when a drug is used to treat asthma)
or to produce a systemic effect (for example, when a drug is used for general anesthesia).
E. Topical administration: Topical administration refers to the application of drugs to the

surface of the body to produce a localized effect on the skin, eyes, nose, mouth, throat,
rectum, or vagina.
Required Reading:
Dentistry, 4th Edition. Pages 15-23.
Suggested Reading:
Lange.
22
DENTAL PHARMACOLOGY
Spring 2004
Dr. Clifford Ferguson
Drug Distribution
Lecture 3
Drug Distribution, Clearance and Time Course
This lecture series will discuss the pharmacokinetic parameters of Distribution and
Excretion as well as time profiles of drug concentrations during its stay in the body.
Pharmacokinetic can be thought of as what the body does to the drug. This is compared to
pharmacodynamic which can be thought as what the drug does to the body.
Distribution
Irrespective of the route of administration, after a drug gains access to the systemic
circulation, it must be distributed to different tissues and organs in the body before it can
manifest its pharmacologic activity. This lecture will discuss some of the variables that
influences the ability of a drug to travel from its site of entry into the body to its destination
for storage or pharmacologic activity and subsequent elimination. We will explore several
different factors that influence distribution including blood flow, extent of binding to tissue
proteins, physicochemical properties of drugs (including state of ionization, size and lipid
solubility), and the degree and extent to which drugs penetrate physiologic barriers.
Objectives: After the completion of this lecture and reading of the assigned material in the
text book, the student will be able to:
Define distribution
Define volume of distribution
Identify factors that will influence the ability of a drug to enter and leave a tissue,
including capillaries
Understand physiologic barriers to drug distribution such as blood brain barrier,
placental transfer, diffusion into specialized tissues such as the testis, aqueous
humor and lymph.
Understand factors that affect distribution into water versus fat
Use volume of distribution to determine loading doses and make dose adjustments.
Required Reading:
Suggested Reading:
Lange.
23
DENTAL PHARMACOLOGY
Spring 2004
Dr. Joseph Cohen
Drug Metabolism
Lecture 4
Lecture Goal -The goal of this lecture is to inform the listener that the action of most drugs
is terminated through biotransformation of their molecules.
Lecture Objectives -
1. Define drug metabolism and its consequences.

2. Define the phases of drug metabolism.
3. Describe the cytochrome P450 oxidative pathway illustrated in figure 2-9 of
Pharmacology and Therapeutics for Dentistry.
4. Know the major isoenzymes of cytochrome P450 illustrated in figure 2-9.
5. Describe the phase 1 metabolic pathway. Review the reactions of table 2-3 and be able
to recognize them.
6. Describe the phase 2 metabolic pathways. Review the reactions of table 2-4 and be
able to recognize them.
7. Know microsomal enzymatic pathways and nonmicrosomal enzymatic pathways.
8. Describe various factors that affect drug metabolism and the consequences thereof.
Required Reading:
Read pages 27-34 before the lecture on drug metabolism. Review and study all diagrams
and tables. Slides and transparencies will not be used. Internet resources will not be used
and should be ignored.
Books are to be brought to class.
24
DENTAL PHARMACOLOGY
Spring 2004
Drug Elimination
Lecture 5
Overview
Elimination and Time Course of drugs in the Body
The pharmacologic activity of a drug is dependent on what happens to the drug during
its transit and stay in the body. This segment of the lecture series will discuss the behavior
of drugs in the body with respect to accumulation and elimination. The concepts of half-life,
steady-state, compartmental models, First- and Zero-Order kinetics, clearance and
extraction ratios will be introduced and discussed. We will discuss the interrelationships
between these parameters and will look at clinical applications.
Objectives
At the completion of these lectures and reading of the material, the student will be able to:
- Define Steady-state
- Define Half-life
- Define Clearance
- Determine half-life
- Determine clearance
- Define Zero-order kinetics
- Define First-order kinetics
- Discuss differences between one-, two-, and multiple-compartment open.
- Discuss the relationships between half-life, clearance, and volume of distribution.
- Determine how long it take a drug to reach steady-state levels.
- Determine how long it takes a drug to be removed from the body base on its half-life
and steady state levels.
- Discuss the differences in drug removal when the drug follows zero-order elimination
kinetics as opposed to first-order elimination kinetics.
- Determine Ideal Body Weight.
- Determine estimated Creatinine clearance.
- Determine the extraction rates of drugs.
- Discuss the changes that occur in maximum concentration achieved (Cmax) and the
time to reach the maximum concentration (Tmax) for a drug following first-order kinetics
with dose changes.
Required Reading:
Suggested Reading:
Lange.
25
DENTAL PHARMACOLOGY
Spring 2004
Clinical uses of Drugs

Lecture 6
Objectives:
This lecture will explore clinical use of drugs. Topics discussed will include both host
and drug effects. After reading the material in the text and attending the lecture, students
will have an understanding of the following:
Host factors that mediate drug response
Different types of drug reactions and interactions
Monitoring and surveillance of drug effects and adverse effects
Pathophysiology of cancer and its treatment
Required Reading:
Dentistry, 4th Edition.
Suggested Reading:
Hardman, J.G. and Limbrid, L.E. (2001) Goodman and Gilman's: The
Lange.
26
DENTAL PHARMACOLOGY
Spring 2004
Dr. V. John Massari
Pharmacology of the Autonomic Nervous System

Introduction
Lecture 7
Objectives
Introduction to Autonomic Pharmacology
You should be able to draw a schematic diagram of the parasympathetic,

sympathetic, cardiac, and enteric nervous systems, including: efferent and afferent
circuits, locations of ganglia, appropriate neurotransmitters within each circuit, and
major receptors found on ALL autonomically innervated target organs.
Understand the locations and actions of presynaptic receptors.
You must also understand the physiological consequences that result from the
activation or inhibition of any receptor on any given target organ.
You should also be able to compare, in general, the effects of parasympathetic
stimulation (inhibition) vs sympathetic stimulation (inhibition) of any autonomic
effector.
Be absolutely clear about the baro-receptor reflex.
Be able to define the biosynthetic pathways for the synthesis of acetylcholine and
epinephrine.
Required Reading:
Suggested Reading:
Lange.
27
DENTAL PHARMACOLOGY
Spring 2004
Dr. Joseph Cohen
Cholinergic Neurotransmission and Pharmacology

Cholinomimetics
Lecture 8
Lecture Goal –
Associate receptor activity of drugs with the responses to parasympathetic
stimulation listed in table 5-1 on page 73 of Pharmacology and Therapeutics for Dentistry
and discussed in the lecture entitled, “Introduction to Pharmacology of the Autonomic
Nervous System.”
Lecture Objectives –
Know the mechanisms of actions, the pharmacological responses and therapeutic
applications of the drugs listed in figure 8-1, figure 8-2, the formulary on page 124,
and the outline.
Know the chemical characteristics of these agents. Know the cascade of events
illustrated in Figure 8-3.
Required Reading:
Additional Resources –
None. No use will be made of handouts, transparencies, slides, or materials from
the internet. References will be made from the textbook.
The textbook should be brought to class.
28
DENTAL PHARMACOLOGY
Spring 2004
Dr. Joseph Cohen

Inhibitors of Acetylcholinesterase
Lecture 9
Lecture Goal-
Understand how inhibition of acetylcholinesterase generate responses that mimic
those elicited by stimulation of parasympathetic nerves listed in Table 5-1 on page 73 of
Pharmacology and Therapeutics for Dentistry and discussed in the lecture entitled,
"Introduction to Pharmacology of the Autonomic Nervous System."
Know the chemical characteristics of these agents.
Know the mechanism of actions of drugs in figures 8-4, 8-5, 8-6 and 8-7.
Know the pharmacological responses to these drugs and their therapeutic
applications.
Explain the uses of the agents (how the effects are produced) in table 8-1.
Explain the means by which these agents produce the effects in table 8-2.
Know the application of these agents for use as insecticides and nerve gas
poisoning.
Required Reading:
None. No use will be made of handouts, transparencies, slides, or materials from the
internet. References will be made from the textbook.
29
DENTAL PHARMACOLOGY
Spring 2004
Dr. Joseph Cohen

Muscarinic Blocking Drugs and Their Therapeutic Values in Dentistry
Lecture 10
Lecture Goal-
Be able to assign pharmacological effects of muscarinic receptor blockade to each
organ site listed in Table 5-1 on page 73 and discussed in the lecture, "Introduction to
pharmacology of the Autonomic Nervous System."
Know the chemical characteristics of the agents in table 9-1, table 9-5, and the drugs
listed in the formulary on page 132. For table 9-2 appreciate the differences in the
sensitivity of organs to atropine and scopolamine. For table 9-3, appreciate the relative
susceptibilities of organs to muscarinic receptor blockade.
Required Reading:
Dentistry, 4th Edition. Pages 133- 132.
30
DENTAL PHARMACOLOGY
Spring 2004
Dr. Joseph Cohen
Adrenergic Neurotransmission and Pharmacology

Sympathomimetics
Lecture 11
Lecture Goal –
Be able to assign pharmacological responses to adrenergic receptor stimulation at
the organ sites listed in table 5-1 and discussed in the lecture, "Introduction to
Pharmacology of the Autonomic Nervous System".
Objectives –
Know the chemical characteristics of the drugs listed in table 6-1 and figure 6-1 and
the structure-activity relationships.
Know which agents are catecholamines and which are not.
Appreciate the differences in receptor potency of different adrenergic agents.
Be able to explain figures 6-3, 6-4, 6-5, and 6-6.
Appreciate tables 6-3 and 6-4.
Know the drugs listed in the formulary on page 97.
Required Reading:
Dentistry, 4th Edition. Pages 85- 99.
31
DENTAL PHARMACOLOGY
Spring 2004
Dr. V. John Massari
Adrenergic Neurotransmission
Adrenergic Receptor Antagonists
Lecture 12
Pharmacology of Alpha and Beta Adrenergic Receptor Antagonists
Objectives:
You must understand the cardiovascular, pulmonary, ocular, or metabolic effects of

alpha 1 (α1), alpha 2 (α2), beta 1 (β1), beta 2(β2), and beta 3 (β3) receptor
antagonists.
Be able to describe the mechanisms of action, pharmacokinetics, major therapeutic

uses, and major toxic effects of: phenoxybenzamine, phentolamine, tolazoline,
prazosin, terazosin, doxazosin, tamsulosin, propranolol, nadolol, timolol, labetolol,
metoprolol, atenolol, esmolol.
Required Reading:
Dentistry, 4th Edition. Pages 85-99 and 100-113.
Suggested Reading:
Lange.
32
DENTAL PHARMACOLOGY
Spring 2004
Dr. V. John Massari
Ganglionic and Neuromuscular Blocking Drugs

Lecture 13
Pharmacology of Ganglionic and Neuromuscular Transmission
Objectives:
Be able to describe the pharmacology of Nicotine and describe in some detail the
potential effects of nicotine on parasympathetic functions, sympathetic functions, the
CNS, and the skeletal neuromuscular junction.
Locate and identify appropriate nicotinic receptors.
Understand the potential effects of nicotinic agonists or antagonists on the

baroreceptor reflex.
Know the pharmacokinetics of nicotine, and treatment of nicotine poisoning.

uses, and major toxic effects of: d-tubocurarine, metocurine, pancuronium,
doxacurium, pipecuronium,Vecuronium, atracurium, rocuronium, rapacuronium,
Mivacurium, and Succinylcholine.
Understand important drug interactions discussed in the lecture.
Required Reading:
Dentistry, 4th Edition. Page 133-144 .
Suggested Reading:
Lange.
33
DENTAL PHARMACOLOGY
Spring 2004
Dr. Keith W. Crawford
General Anesthetics
Lecture 14
Objectives:
I. Understand Uptake, Distribution and Elimination of Inhalational Anesthetics.

A. Factors that influence equilibrium of alveolar gas tension with inspired gas
tension.
B. Factors that influence alveolar-blood gas tension equilibrium.
C. Factors that influence blood-tissue gas tension equilibrium.
II. What association exists between blood solubility/tissue solubility of a gas and the
changes in arterial gas tension over time?
III. How do the concentration effect and the second gas effect influence the time to
equilibrium of blood/tissue gas tension?
IV. Understand how the oil-gas partition coefficient of an anesthetic is related to

blood/tissue solubility, to the MAC, and to the uptake kinetics of inhalational
anesthetics.
V. What are the stages of anesthesia and what physiologic assessments are used to
determine stage?
VI. What are some proposed theories on the mechanism of action of general anesthetics?
VII. For the following drugs, know the effect of the drug on cardiovascular function [blood
pressure, cardiac output (heart rate + stroke volume), peripheral vascular resistance]
and Pulmonary function (respiratory rate, tidal volume), skeletal muscle activity, extent
of metabolism:
Halothane enflurane
isoflurane desflurane
sevoflurane nitrous oxide
VIII. What are the most serious toxicities for each drug mentioned?
IX. For the following intravenous anesthetics understand general mechanism of action (if
known), uses, and limitations:
opioids barbiturates
etomidate propofol
ketamine.
Required Reading:
34
DENTAL PHARMACOLOGY
Spring 2004
Suggested Reading:
Lange.
35
DENTAL PHARMACOLOGY
Spring 2004
Local Anesthetics
Lecture 15
OBJECTIVES
1. Define a local anesthetic
2. Describe the general chemical formula for a local anesthetic

a) of the ester group
b) of the amide group
3. Describe the mechanism of action of these drugs.
4. Name two biotoxins which can block nerve conduction.
5. Explain the interaction of the sodium channel, local anesthetic receptor and local
anesthetic.
6. List the types of the nerve fibers affected by local anesthetics.
7. Name the characteristics of a local anesthetic.
8. List the names of:

a) amino ester local anesthetics
b) amino amide local anesthetics
9. Describe the role of vasoconstrictor agents in local anesthesia.
10. Explain the pharmacokinetics of this group of drugs.
11. Indicate which are the toxic effects of local anesthetics and how to manage
the intoxicated patient.
Required Reading:
Suggested Reading:
Lange.
36
DENTAL PHARMACOLOGY
Spring 2004
Dr. Dana Jackson
Pharmacology of Oxygen and Nitrous Oxide

Lecture 13
Required Reading:
Suggested Reading:
Lange.
37
DENTAL PHARMACOLOGY
Spring 2004
TBA
Respiratory Systems and Asthma

Lecture 17
Required Reading:
Dentistry, 4th Edition. Pages .
Suggested Reading:
Lange.
38
DENTAL PHARMACOLOGY
Spring 2004
Opiate Analgesics and Antagonists

Lecture 18
OPIOID ANALGESICS & ANTAGONISTS - Objectives
Opioids are used extensively in the treatment of pain. In this lecture the endogenous
opioids, including enkephalins, endorphins, and dynorphins, are described and
compared with clinically used synthetic opioids. The pharmacological properties,
pharmacokinetics, and side effects of the clinically used opioids are discussed in this
lecture, with emphasis on the advantages and disadvantages of the use of individual
opioid drugs. The structural properties of the three main classes of opioid receptors,
m, d, and k receptors, are described, as are their pharmacological properties, their
selective agonists and antagonists, and their cellular effector systems. Experimental
agents used to investigate the biological roles of opioids in animal models are also
described with regard to their mechanisms of action.
I. Classification & Chemistry
II. Endogenous Opioid Peptides
III. Pharmacokinetics
A. Absorption
B. Distribution
C. Metabolism
D. Excretion
IV. Pharacodynamics
A. Mechanism of Action:
1. Receptors types
2. Relation of physiologic effects of receptor type
3. Cellular actions
4. Receptor distribution and neural mechanisms of analgesia
5. Tolerance and physical dependence
B. Organ System Effects of Morphine and Its Surrogates

1. Central Nervous systems effects
a. Analgesia
b. Euphoria
c. Sedation
d. Respiratory depression
e. Cough suppression
f. Miosis
39
DENTAL PHARMACOLOGY
Spring 2004
g. Truncal rigidity
h. Nausea and vomiting
Required Reading:
Suggested Reading:
Lange.
40
DENTAL PHARMACOLOGY
Spring 2004
Dr. Dana Jackson
Clinical Correlations of Pain Management and Anesthesia

Lecture 19
PAIN AND ANXIETY CONTROL IN GENERAL DENTISTRY
I. Introduction to patient management techniques
A. Methods available in General Dentistry

1. Interpersonal relationship
2. Patient Preparation
3. Techniques
a. oral sedation
b. inhalation
c. Intra muscular
d. Intravenous
e. Rectal
B. Comparison of techniques in General Practice

1. Training necessary
2. Safety
3. Speed of onset
4. Predictability of results
5. Reversibility
C. Patient Evaluation
1. Patient desires
2. Medical history written
3. Medical history oral
4. Review of history and evaluation
5. Physical evaluation
6. Medical Consultation
D. Contraindications for a sedative technique

1. Allergy
2. Pregnancy
3. Patient desires General Anesthesia
4. Psychological
5. Medical contraindications
6. Physical
a. mental retardation
b. physical limitations
• Control
• Cooperation
• Airway
E. Consent
41
DENTAL PHARMACOLOGY
Spring 2004
1. Written
2. Oral
3. Chaperons, room set up, patient observation
F. Premedication Objectives
1. Relieve Anxiety
2. Amnesia for procedure
3. Safety
4. Cooperative Patient
5. Awake Patient
6. Vital signs not effected
7. Recovery time
Required Reading:
Suggested Reading:
Lange.
42
DENTAL PHARMACOLOGY
Spring 2004
Dr. V. John Massari
Therapeutic Approach to Management of Parkinson’s Disease

Lecture 20
Objectives:
Understand the signs and symptoms of Parkinson’s Disease.
Understand the relative organizations of the Pyramidal and Extra-Pyramidal motor

systems.
Understand the relative effects of dopamine and acetylcholine in this disease.

uses, and major toxic effects of: selegiline, l-dopa, Carbidopa, Trihexyphenidyl,
enztropine, Biperiden, Bromocriptine, Pergolide, Ropinirole, pramipexole, and
Amantadine.
Required Reading:
Dentistry, 4th Edition. Page 208-216.
Suggested Reading:
Lange.
43
DENTAL PHARMACOLOGY
Spring 2004
Dr. Sonya K. Sobrian
Antipsychotic Drugs
Lecture 21
Overview
Antipsychotic or neuroleptic drugs are those used to treat very severe psychiatric illnesses,
i.e., the psychoses and mania. These drugs offer effective palliative treatment of both organic
and idiopathic psychotic disorders. They have beneficial effects on mood and thought, but
many standard neuroleptic agents produce characteristic side effects that mimic neurological
diseases, whereas atypical antipsychotics are associated with weight gain and adverse
metabolic effects such as diabetes.
Although clinically effective antipsychotics include a variety of chemically dissimilar agents,
they share many properties with respect to their pharmacology and clinical uses. Typical
agents block dopamine D2 receptors and reduce dopamine neurotransmission in the forebrain
and limbic system. Some also interact with Dl and D4 dopaminergic, 5-HT2A and 5-HT2c
serotonergic, and α -adrenergic receptors.
Objectives
Be able to distinguish the positive and negative symptoms of schizophrenia.
Distinguish between the original and modified dopamine hypothesis of schizophrenia.
Know the current theories regarding the therapeutic mechanism of action of antipsychotic
drugs.
Know the acute and chronic effects of these drugs on major dopaminergic systems in the
CNS.
List the pharmacological properties of antipsychotic drugs.
Distinguish the properties, relative efficacies and side effects of the major classes of
classical (or typical antipsychotic drugs) the low potency and the high potency compounds.
Distinguish side effects by receptor action.
Describe the time course and symptoms of antipsychotic drug- induced acute dystonia,
akathesia, Parkinson's syndrome, tardive dyskinesia, and neuroleptic malignant syndrome.
Explain how atypical antipsychotics differ from classical antipsychotics in their cellular
actions, efficacies and side-effect profiles.
Contrast the mechanisms of action of phenothiazines and haloperidol with clozapine.
risperidone, and olanzapine. Describe the implications for the theories of the mechanism of
antipsychotic action.
Know the hypersensitivity reactions to antipsychotic drugs including those affecting liver,
blood and skin.
Know common drug interactions.
Know the side effects of these drugs that are most likely to impact dental practice.
44
DENTAL PHARMACOLOGY
Spring 2004
Drugs to Consider:
Antipsychotics/Neuroleptics:
CHLORPROMAZINE
CLOZAPINE
FLUPHENAZINE
HALOPERIDOL
OLANZAPINE
quetiapine
RISPERIDONE
sertindole
THIORIDAZINE
thiothixene
ziprasidone
Antimanic drugs:
CARBAMAZEOINE
LITHIUM CARBONATE
VALPROIC ACID
PRIMARY DRUGS - All CAPITAL LETTERS

SECONDARY DRUGS - all small letters
Required Reading:
Suggested Reading:
Hardman, J.G. and Limbrid, L.E. (2001) Goodman and Gilman's The
Pharmacological Basis of Therapeutics. 10th Edition. McGraw Hill.
Katzung, B.G. (2001) Basic and Clinical Pharmacology. Appleton and Lange.
Stamford, CT. 8th Edition.
45
DENTAL PHARMACOLOGY
Spring 2004
Dr. Martha I. Dávila-García
Antidepressants and Antimanic Drugs

Lecture 22
Overview:
Antidepressant drugs are used to treat serious, continuing mental depression that
interferes with a person's ability to function. Everyone feels sad, "blue," or discouraged
occasionally, but usually those feelings do not interfere with everyday life and do not need
treatment. However, when the feelings become overwhelming and last for weeks or
months, professional treatment can help. Although depression is one of the most common
and serious mental disorders, it is also one of the most treatable. According to the
American Psychiatric Association, 80-90% of people with depression can be helped. If
untreated, depression can lead to social withdrawal, physical complaints, such as fatigue,
sleep problems, and aches and pains, and even suicide.
Objectives:
Understand the characteristics and diagnosis of depression.
Know the classification of depression and mania.
Understand the multiple causes of depression (such as thyroid problems or drug-
induced depression).
Know the biological correlates of depression.
Know the monoamine hypothesis of depression.
Know the classification of Antidepressant drugs.
Understand the pharmacokinetic and pharmacodynamic properties of
Antidepressants.
Know the mechanism of action of Antidepressant drugs.
Know the drugs used in the treatment of mania.
Understand the pharmacokinetic and pharmacodynamic properties of Antimanic
Drugs.
Know the mechanism of action of Antimanic drugs.
Know which drugs are use to treat other conditions, such as obsessive compulsive
disorder, premenstrual syndrome, chronic pain, and eating disorders.
Reading Material:
Dentistry, 4th Edition.Pages 157-167.
Suggested Reading:
Katzung, B.G. (2001) Basic and Clinical Pharmacology. 8th ed. Appleton and Lange.
Stamford, CT.
Brody, T.M., Larner, J., and Minneman, K.P. (1998) Human Pharmacology:
Molecular to Clinical. 3nd ed. Mosby-Year Book Inc., St. Louis, MO.
Hardman, J.G. and Limbrid, L.E. (2001) Goodman and Gilman's The
46
DENTAL PHARMACOLOGY
Spring 2004
Dr. V. John Massari
Sedative Hypnotics and Anti-Anxiety Drugs

Lecture 23
Objectives:
Be able to distinguish between sedative, hypnotic, and anxiolytic effects.
Be able to describe the mechanisms of action, pharmacokinetics, major therapeutic uses,

and major toxic effects of: diazepam, chlordiazepoxide, Alprazolam, clonazepam, and
lorazepam, Triazolam, oxazepam, Zaleplon and Zolpidem, Flumazenil, amobarbital,
butabarbital, pentobarbital, secobarbital, thiopental, methohexital, phenobarbital,
mephobarbital, Buspirone, gepirone, and ipsaperone.
Be able to compare and contrast the pharmacology of the benzodiazepines with that of the
barbiturates.
Understand the reasons that benzodiazepines are the drugs of choice for hypnosis.
Required Reading:
Yagiela, J.A., Neidle, E.A., Dowd, F.J. (1998) Pharmacology & Therapeutics for Dentistry,
4th Edition. Pages 168-184 and 185-196 and 623-633.
Suggested Reading:
B.G. Katzung. (2001) Basic & Clinical Pharmacology, 8th Edition, Appleton and Lange.
47
DENTAL PHARMACOLOGY
Spring 2004
Epilepsy and Anti-convulsants

Lecture 24
Overview
Epilepsy is a nervous system disorder that produces sudden, intense bursts of electrical
activity in the brain. This abnormal electrical activity in the brain causes seizures, which may
briefly upset a person's muscle control, movement, speech, vision, or awareness. People with
epilepsy have repeated seizures that usually occur without warning and often for no clear
reason. If epilepsy is not treated, seizures may occur throughout a person's life in some cases,
becoming more severe and more frequent over time. Treatment most often involves
medication. Surgery, a special diet (ketogenic diet), a nerve stimulation device (vagus nerve
stimulator), or a combination of these approaches also may be tried when medication alone
does not control a person's seizures, but will not be covered in class.
Objectives:
• Know the classification of seizures.
• Characterization of Seizures and implications for drug selection.
• Define epilepsy
• Mechanism of action of major antiepileptic drugs.
• Correlation between prescribed oral doses and serum levels.
• Kinetics of phenytoin.
• Biotransformation products of major antiepileptic drugs.
• Know the first and second drugs of choice for each type of epileptic seizure.
• Understand Status epilepticus and its therapeutic control.
• Drug Interactions between major antiepileptic drugs.
• Drug interactions of major antiepileptic drugs and other drugs.
List of Drugs:
Carbamazepine (Tegretol)
Clonazepam (Klonopin)
Diazepam (Valium)
Ethosuximide (Zarontin)
Ethotoin (Peganone)
Fosphenytoin (Cerebyx)
Gabapentin (Neurontin)
Lorazepam (Ativan)
Lamotrigine (Lamictal)
Mephenytoin (Mesantoin)
Mephobarbital (Mebaral)
Metharbital (Gemonil)
Methuximide (Celontin Kapseals)
Paramethadione (Paradione)
Pentobarbital sodium (Nembutal)
Phenacemide (Phenurone)
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Phenobarbital (Luminal sodium)

Phensuximide (Milontin Kapseals)
Phenytoin (Dilantin)
Primidone (Mysoline)
Tiagabine (Gabatril)
Topiramate (Topamax)
Trimethadione (Tridione)
Valproic acid (Depakene, Myproic acid,
sodium valproate, Depakote).
Reading Material:
Yagiela, J.A., Neidle, E.A., Dowd, F.J. (1998) Pharmacology & Therapeutics for Dentistry, 4th
Edition. Pages 197-207.
Suggested Reading:
Katzung, B.G. (2001) Basic and Clinical Pharmacology. 8th ed. Appleton and Lange. Stamford,
CT.
Brody, T.M., Larner, J., and Minneman, K.P. (1998) Human Pharmacology: Molecular to
Clinical. 3nd ed. Mosby-Year Book Inc., St. Louis, MO.
Hardman, J.G. and Limbrid, L.E. (2001) Goodman and Gilman's The Pharmacological Basis of
Therapeutics. 10th ed. McGraw Hill.
Additional resources: The departmental web page has the power point presentation
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DENTAL PHARMACOLOGY
Spring 2004
Dr. Robert L. Copland
CNS Stimulants
Lecture 25
Introduction
A great many substances can cause an increase in neuronal activity of the central nervous
system (CNS) by a variety of mechanisms. The ultimate cause is a disturbance in the normal
balance of excitatory and inhibitory activities of the CNS. This balance fluctuates over narrow
limits in the healthy person. Once a gross, generalized disturbance has developed, whether
initiated by reduced inhibition (e.g., strychnine) or enhanced excitement (e.g.,
pentylenetetrazol), the symptoms of excessive output are similar: generalized tonic-clonic
convulsions. At threshold doses, however, or as the effects of intoxication with various
stimulants, convulsant agents first appear, there are differences in symptom patterns that
reflect the different mechanisms and/or sites of action. These include varied influences on
consciousness and on cognitive and emotional processes.
Drugs classified as CNS stimulants have few therapeutic applications. In the past, one
category of CNS stimulants has been used as analeptics, agents intended to reverse marked
CNS depression, usually from an overdose of barbiturate or other depressant drug.
Unfortunately, the demonstration of effective antagonism of drug-induced depression has been
inconsistent, and the difference between the analeptic dose and convulsant dose for most of
these agents is very narrow. Furthermore, the stimulant phase is often of short duration and is
followed by generalized depression that may then be refractory to further treatment. The
current consensus on the use of analeptics is that they do no good in emergency treatment of
depressant drug overdose and may do considerable harm.
CNS stimulants in this class are also important as toxicological (strychnine) or abuse
(caffeine) problems, as well as being effective diagnostic (pentylenetetrazol) and research
(picrotoxin) tools in the study of synaptic interrelationships in the CNS. These agents qualify as
analeptics in that the lowest effective doses demonstrate CNS stimulation as the major
pharmacological effect. Examples of drugs in other classes that stimulate the CNS in overdose
are the local anesthetics (procaine), antihistamines (pyrilamine), tricyclic antidepressants
(imipramine), and atropine, to name a few.
CLASSIFICATION OF CNS STIMULANTS

CNS stimulants may be classified according to their predominant site of stimulation. The
diversity in chemical structures among this class of drugs defies attempts to establish
structure-activity relationships and suggests that multiple mechanisms are involved in drug-
induced convulsant effects.
The representation of the sites of action for these substances must not be taken too
literally. Most of these drugs appear to cause neuronal excitation of any portion of the CNS,
providing the drug dosage is adequate.
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Classifications of stimulants have also been based on mechanism (e.g., picrotoxin as a

GABA antagonist) and on use or medical consequences of exposure.
Individual Agents to Be Considered:

Strychnine
Picrotoxin
Pentylenetetrazol
Doxapram, Nikethamide,
Amphetamine, Methylphenidate,
Cocaine
Caffeine
Nicotine
Required Reading:
4th Edition. Pages.
Suggested Reading:
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DENTAL PHARMACOLOGY
Spring 2004
Drugs of Abuse
Lecture 26
Overview
Drugs of Abuse and Dependence fall into several groups: those that are prescribed and have
clinical use; those that are manufactured illicitly; and those that are commercially available and
easily obtained. These drugs have a wide spectrum of actions in the brain and body, and they
belong to seven broad classes:
1. Narcotics/Opioids
2. CNS depressants
3. Psychostimulants
4. Psychedelics and hallucinogens
5. Cannabis
5. Phencyclidine and Analogs
6. Anticholinergics
7. Volatile Inhalants
Objectives:
The students will understand the following:
The concepts of abuse, addiction, tolerance, psychological vs physiological
dependence, cross-tolerance, cross-dependence and withdrawal.
Define abstinence and relapse
Classification of drugs of abuse and dependence.
Clinical characteristics of drug dependence.
Systems involved and mechanism of action of major drugs of abuse and dependence.
Symptoms of overdose/intoxication for major drug groups and treatment.
Symptoms of withdrawal for major drug groups and treatment.
Detoxification techniques for different drugs of abuse.
The mortality and morbidity associated with dependence to various drugs.
Define abstinence and relapse.
Drug Interactions between major groups of drugs of abuse and dependence.
Reading Material:
• Yagiela, J.A., Neidle, E.A., and Dowd, F.J. (1998) Pharmacology and Therapeutics for
Dentistry. 4th ed. Mosby-Year Book Inc. pp. 656-670.
Suggested Reading:
th
• Katzung, B.G. (2001) Basic and Clinical Pharmacology. 8 ed. Appleton and Lange.
Stamford, CT. pp 532-547.
• Hardman, J.G. and Limbrid, L.E. (2001) Goodman and Gilman's The Pharmacological
Basis of Therapeutics. 10th ed. McGraw Hill. pp 621-642.
• Joyce H. Lowison, Pedro Ruiz, Robert. B. Millman, and John G. Langrod (1997) Substance
Abuse: A Comprehensive Textbook. 3rd. ed. Williams and Wilkins. pp 956 p.
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Web Sites:
• http://www.drugabuse.gov/DrugsofAbuse.html
• http://www.nida.nih.gov/
• http://www.hucmlrc.howard.edu/Pharmacology/default.htm
• http://www.usdoj.gov/dea/concern/concern.htm
• http://www.clubdrugs.org/
• http://www.nida.nih.gov/DrugPages/DrugsofAbuse.html
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Introduction to Cardiovascular Pharmacology

Cardiac gangliosides
Lecture 27
Treatment of Congestive Heart Failure
Introduction:
Cardiovascular diseases are the number one cause of death in the U.S.A. today. In the
U.S.A., approximately 5 million people suffer from cardiovascular disease. The five year
survival rate is only about 35%. A substantial percentage of the healthcare expenditures,
both economic and manpower is spent on caring for individual with heart disease. Of all
the cardiovascular diseases, the greatest mortality results from congestive heart failure and
its complications. Despite not having a cure for the disorder, many therapeutic strategies
exist. These are designed based on knowledge obtained on factors affecting diastolic and
systolic functioning of the heart. This lecture will discuss therapeutic options available
based on the pathophysiologic derangements causing and resulting from congestive heart
failure.
After attending the lecture and reading material in the text(s), each student should:
Understand the consequence of heart failure
Therapeutic goals in treating heart failure patients
How Congestive Heart Failure treatment impacts dental procedures
Understand the rationale for the use of the following pharmaceutic agents in CHF management
Cardiac glycosides
Angiotensin Converting Enzyme Inhibitors
Angiotensin Receptor Antagonists
Diuretics
Aldosterone Antagonists
Beta Adrenergic Receptor Antagonists
Nitrates
Phosphodiesterase Inhibitors
Sympathomimetic Agents
Required Reading:
Dentistry, 4th Edition. Pages

Suggested Reading:
Basis of Therapeutics. 10th ed. McGraw Hill. Chapter 34.
Lange. Chapter 13.
Online resources:
www.medscape.com and www.pslgroup.com. Both are free but requires registration.
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DENTAL PHARMACOLOGY
Spring 2004
Dr. Philip J. Gatti
Anti-Arrythmics
Lecture 28
I. Review of Cardiovascular Physiology
Review of properties of the heart including membrane responsiveness, automaticity,
refractory period, and conduction; excitation contraction coupling and electrical activity of
the heart including the action potential and electrocardiogram.
II. Cardiac Drugs

A. Anti-Arrhythmic Agents
1) Mechanism of action
Describe the pathophysiologic mechanisms of cardiac arrhythmias: abnormal automaticity,
triggered rhythms, and abnormal impulse conduction.
Describe the phases of the action potential of automatic and non-automatic tissues.
Identify the ionic currents responsible for these phases.
Describe the electrophysiologic actions of antiarrhythmic drugs in normal and abnormal
myocardial and conduction tissue, and their effect on the phases of the cardiac action
potential.
Describe the indications of each class of antiarrhythmic drugs and rationale for using them
in these arrhythmias.
Describe the indirect autonomic actions of these drugs.
Classify antiarrhythmic drugs as to class IA, IB, IC, II, III, IV
2) Pharmacokinetics
Describe the routes of administration, biotransformation and excretion of selected
antiarrhythmic drugs.
3) Therapeutic indications
Describe the use of antiarrhythmic drugs in supraventricular arrhythmias (atrial flutter, atrial
fibrillation, paroxysmal supraventricular tachycardia, junctional arrhythmias).
Describe the use of antiarrhythmic drugs in ventricular arrhythmias (ventricular premature
beats, ventricular tachycardia, ventricular fibrillation).
4) Adverse effects, drug interactions and contraindications

Describe the cardiac and extracardiac manifestations of toxicity from antiarrhythmics.
Describe the possible contraindications of antiarrhythmic drugs in the presence of heart
block or congestive heart failure, and the precautions and contraindications in other
conditions.
Drugs to be considered: Quinidine, procainamide, lidocaine, tocainide, mexiletine, flecainide,

propranolol, sotalol, amiodarone, bretylium, verapamil, diltiazem.
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Required Reading:
4th Edition. Pages 333-348.
Suggested Reading:
Chapter 14.
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DENTAL PHARMACOLOGY
Spring 2004
Dr. Philip J. Gatti
Anti-Anginal Drugs
Lecture 29
Principles and Knowledge objective
1) Mechanisms of action
- Describe the basic pathophysiology of myocardial ischemia.
- Explain the significance of atherosclerotic coronary artery disease and coronary artery
disease and coronary artery spasm (Prinzmetal’s) in the production of myocardial ischemia
and angina pectoris.
- Describe the hemodynamic actions of antianginal drugs, including their coronary and
peripheral vasodilator actions.
- Describe the effects of each antianginal drug or drug class on the determinants of
myocardial oxygen consumption (heart rate, myocardial wall tension, etc.)
2) Actions on organ systems

- Describe the cardiac actions of anti-anginal drugs (electrophysiologic, coronary vasodilator,
inotropic actions).
- Describe the action of anti-anginal drug on the peripheral circulation (arterial, venous) and
their effects on ventricular preload and afterload.
3) Pharmacokinetics
- Describe the routes of administration, biotransformation and excretion of anti-anginal drugs.
- Describe the significance of a “first-pass effect” for orally administered antianginal drugs.
- Describe the time-course of anti-anginal activity (onset and duration of action).
- Describe the problem of dose intervals and tolerance development with the nitrates.
- Describe the use of anti-anginal drugs in classic (effort-related) angina pectoris and
vasospastic angina pectoris.
- Describe the use of “myocardial preservation” and discuss the use of anti-anginal in the
context of acute myocardial infarction.

- Describe the cardiac and extra-cardiac side-effects of anti-anginal drugs.
- Describe the beneficial and adverse interactions between anti-anginal drugs and between
anti-anginal drugs and other.
Drugs to be considered:
DILTIAZEM NIFEDIPINE
dipyridamole NITROGLYCERIN
isosorbide dinitrate PROPRANOLOL
nadolol timolol
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Required Reading:
Suggested Reading:
Basis of Therapeutics. 10th ed. McGraw Hill. Chapter 32.
Chapter 12.
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DENTAL PHARMACOLOGY
Spring 2004
Diuretics
Lecture 30
DIURETICS AND DRUGS AFFECTING RENAL FUNCTION AND ELECTROLYTE
METABOLISM INCLUDING WATER, SALT AND IONS
1. Review of Renal Physiology/Biochemistry
2. Diuretics
Principles and Knowledge Objectives

Describe and understand the important role of the organic acid secretory system for the
actions of some diuretics and for various interactions of diuretics with other types of drugs.
Describe the sites in the nephron where diuretics and other agents act: i.e., glomerulus,
proximal tubule, loop of Henle (thin limb; medullary and cortical thick ascending limb), distal
tubules and collecting ducts
Explain the mechanism of action of each class of diuretics or other agents.
Compare the effects of prototypical diuretics or agents on excretion of various electrolytes
and compare effects on cardiovascular system as to antihypertensive effects.
Describe the therapeutic uses of these agents, e.g., edema causing dysfunction resulting
from decreased cardiac, liver and renal function, and use in treatment of poisoning. State
appropriate agents to be used in each condition.
Relate absorption, distribution and excretion to particular therapeutic uses; e.g., the use of
osmotic diuretics or vasodilators such as dopamine to increase urine flow in cases of
impending renal failure.
Describe the interactions of diuretics with other drugs such as cardiac glycosides, oral
anticoagulants, oral hypoglycemics, uricosuric drugs, aminoglycoside antibiotics and non-
steroidal anti-inflammatory drugs.
State the adverse effects of diuretics related to and unrelated to water and electrolyte
excretion.
Relate effects of diuretics that would contraindicate their use in certain conditions, e.g., use
of osmotic diuretics in pulmonary edema.
Describe and understand the mechanisms whereby furosemide and thiazides are useful in
the management of various calcium metabolism disorders.
ACETAZOLAMIDE, AMILORIDE, ETHACRYNIC ACID, FUROSEMIDE, bumetanide,
HYDROCHLOROTHIAZIDE, CHLORTHALIDONE, mannitol, POTASSIUM CHLORIDE,
SPIRONOLACTONE, TRIAMETERENE
1. Agents Affecting that Renal Conservation of Water
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Principles and knowledge objectives to be considered:

Describe the site and mechanism of agents used to treat diabetes insipidus.
Describe the adverse effects of hydrochlorothiazide and arginine vasopressin related to
and unrelated to renal function.
Be familiar with other agents such as chlorpropamide and clofibrate that act in antidiuretic
hormone sensitive diabetes insipidus.
Know that demeclocycline is used in water intoxication due to inappropriate secretion of
antidiuretic hormone.
Be aware that lithium compounds cause a syndrome like diabetes insipidus.
Drugs to be considered: benzothiadiazides, desmopressin acetate (DDAVP), dopamine,

demeclocycline
Minimum list of drugs affecting renal function to be considered:

ACETAZOLAMIDE
+AMILORIDE
benzothiadiazides
+bumetanide
+CHLORTHALIDONE
demeclocycline
desmopressin acetate (DDAVP)
dopamine
ETHACRYNIC ACID
+FUROSEMIDE
+HYDROCHLOROTHIAZIDE
INDAPAMIDE
mannitol
+POTASSIUM CHLORIDE (e.g. Slow-K)
SPIRONOLACTONE
+TRIAMTERENE
Required Reading:
Suggested Reading:
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DENTAL PHARMACOLOGY
Spring 2004
Dr. Robert E. Taylor
Anticoagulant, Antithrombotic and Thrombolytic Drugs

Lecture 31
Objectives:
State the appropriate routes of administration of heparin and the oral anticoagulants.
Describe the extent of binding of oral anticoagulants to plasma protein
Explain the pharmacokinetics and pharmacodynamic variability of oral anticoagulants
between patients.
Describe the relationship between the chemical structure of the oral anticoagulants and
vitamin K and its importance in determining the mechanism of action of the oral
anticoagulants. (Post ribosomal gamma carboxylation of Factor II, VII, IX, X in the
hepatocyte).
State the sites of action of heparin in the coagulation process.
Describe the relationship between mechanism of action and speed of onset of action and t-
1/2 of heparin and the oral anticoagulants. State the interaction of heparin with protamine
sulfate.
Consider the problems associated with thrombolytic therapy, e.g., streptokinase inn primary
post MI.
Consider adjuncts to thrombolytic therapy, e.g., antithrombin, antiplatelet.
Describe the use of desmopressin in factor VIII deficiency and Von Willebrands disease.
Describe the side effects of heparin and warfarin.
State the antidotes of heparin and warfarin toxicity.
State the contraindications to anticoagulant therapy.
Describe the mechanism of action, indication, and complications of thrombolytic therapy.
Explain the difference between available thrombolytic agents.
Describe the laboratory monitoring of heparin, warfarin and thrombolytic agents.
2. Drugs to consider:
ACETYLSALICYLIC ACID
sulfinpyrazone
HEPARIN
VITAMIN K
PROTAMINE SULFATE
WARFARIN SODIUM (Coumadin)
STREPTOKINASE
DESMOPRESSIN ACETATE (DDAVP)
LOW MOLECULAR WEIGHT HEPARIN
(Epsilon amino caproic acid)
Tranxenic Acid
APSAC (acylated plasminogen streptokinase complex)
tissue-type plasminogen activator (tPA)
Required Reading:
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DENTAL PHARMACOLOGY
Spring 2004
Dr. Philip J. Gatti
Antihypertensives and Related Drugs

Lecture 32
Principles and knowledge objectives
1) Mechanism of action
- Describe the current views for the etiology of essential hypertension.
- Review the determinants of systemic arterial blood pressure and the pathophysiologic
mechanisms in essential hypertension.
- Describe the mechanism by which each antihypertensive drug or drug class exerts its
therapeutic function.
2) Actions on organs systems

- Describe the relevant action of antihypertensive drugs in other organ systems (CNS, other).
3) Pharmacokinetics
- Describe the routes of administration, biotransformation and excretion of antihypertensive
drugs.
- Describe the time-course of their antihypertensive activity (onset and duration of action) for
each class of agents.
- Describe the use of antihypertensive drugs in mild, moderate and severe essential
hypertension.
- Describe the use of antihypertensive drugs in hypertensive emergencies.

- Describe the cardiac and extracardiac side-effects of antihypertensive drugs.
ANTENOLOL HYDRALAZINE NITROPRUSSIDE

ANGIOTENSIN (I & II) HYDROCHLOROTHIAZIDE phentolamine
betaxolol INDAPAMIDE pindolol
CAPTOPRIL LABETOLOL PRAZOSIN
chlorthalidone lisinopril PROPRANOLOL
CLONIDINE metazolone reserpine
DIAZOXIDE methyldopa spironolactone
DILTIAZEM metoprolol triamterene
ENALAPRIL minoxidil trimethaphan
guanadrel NIFEDIPINE terazosin
guanethidine NITROGLYCERIN (I.V.) timolol
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Required Reading:
Suggested Reading:
Basis of Therapeutics. 10th ed. McGraw Hill. Chapter 31 and 33.
Chapter 11.
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DENTAL PHARMACOLOGY
Spring 2004
Inflammation I and II
Lecture 33 and 34
Objectives
I. Understand how complex pathways interface in the pathogenesis of inflammation.

Specifically, understand the role of:
- vasoactive amines (e.g. histamine, serotonin)
- peptide autocoids (e.g. bradykinin)
- role of the complement system
- NO and cGMP signaling
- Macrophage-derived reactive oxygen species and proteolytic enzymes
- Lipid autocoids ( leukotrienes, prostaglandins)
- Cellular and humoral immune actions
- Inflammatory cytokines (e.g. TNF-alpha, IL-1, IL-6, etc.)
II. Understand physiologic effects of histamine:

A. Specifically, understand the actions of histamine: a) on bronchioles b) on vasculature c) in
the stomach d) in the intestine e) cutaneous effects.
B. Understand the mechanism of histamine release from mast cells (e.g. in allergen-induced
asthma, allergic rhinitis, anaphallaxis) and pharmacologic agents that modulate mast cell
degranulation.
C. Histamine receptor subtypes (H1 and H2), their distributions, physiologic effects they
regulate and signaling pathways activated by each type.
D. Indications for H2 agonists
E. Indications for H1 and H2 antagonists

1. agents (structural classes) that interact with different receptor types
2. distinctions between first and second generation H1 antagonists
Lipid Autocoids
A. Leukotrienes and related compunds
1. Understand the synthetic pathways (including key enzymes) and the biologic activities of
leukotrienes (LTB4, peptidyl leukotrienes).
2. What are the pharmacologic targets for leukotriene synthesis/ action? What are the
indications for
these pharmacologic agents?.
B. Prostaglandins and related compounds.

1. Understand the synthesis (including key enzymes) and physiologic functions of
prostaglandins, prostacyclin (PGI2) and thromboxane.
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2. Understand the distinction between COX-1 and COX-2 and the predominant anatomical
locations of these enzymes.
3. What are the indications for prostaglandin analogues?
4. What are the indications for agents that inhibit COX (NSAIDS)?
5. What are the major potential toxicities encountered with COX-inhibitors and how does
enzyme selectivity influence toxicity profile?.
6. Understand the unique pharmacologic features of acetyl salicylic acid (aspirin), including:
(a) action at COX,
(b) dose-ranges for various indications,
(c) dose-dependent pharmacokinetics, and
(d) presentation and management of salicylate toxicity
7. Mechanism and management of acetaminophen toxicity.
Drugs to consider:
H1- antagonists
Brompheniramine
CHLORPHENIRAMINE
DIPHENHYDRAMINE
promethazine
TERFENADINE
CLEMASTINE
H2 - antagionists
CIMETIDINE
famotidine
NIZATIDINE
RANITIDINE
Required Reading:
4th Edition. Pages 297-319 and 320-332.
Suggested Reading:
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DENTAL PHARMACOLOGY
Spring 2004
TBA
Immunopharmacology
Lecture 35
IMMUNOSTIMULANTS & IMMUNOSUPPRESSANTS
Objectives:
a. Understand the components of immune response.
b. Know the therapeutic uses of the agents.
c. Know the targets for action of the individual agents.
d. Know the pharmacodynamics of individual agents.
e. Know the unwanted effects of the individual agents.
Required Reading:
4th Edition. Page 547-564.
Suggested Reading:
Basis of Therapeutics. 10th ed. McGraw Hill. Pages 621-642.
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DENTAL PHARMACOLOGY
Spring 2004
Dr. Donnell Bowen
Antimicrobials I, Introduction
Sulfonamides & Trimethoprim
Lecture 36
OBJECTIVES

Dihydropteroate synthetase
Dihydrofolate reductase
Sequential blockade
Antimetabolite
Antibacterial synergy

Describe the mechanisms of action of sulfonamides and trimethoprim on bacterial folic acid
synthesis.
Describe the mechanisms of resistance to sulfonamides and trimethoprim. . List the major
clinical uses of sulfonamides and trimethoprim, singly and in combination.
Required Reading:
Suggetsted Reading:
Basis of Therapeutics. 10th ed. McGraw Hill. Pages.
B.G. Katzung. (2001) Basic & Clinical Pharmacology, 8th Edition, Appleton and Lange,
Pages.
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DENTAL PHARMACOLOGY
Spring 2004
Dr. Donnell Bowen
Antimicrobials II
Agents used in the Treatment of Urinary Infection
Lecture 37
Objectives
Describe the mechanisms of antibacterial action of nitrofurantoin, nalidixic acid, and
methenamine salts as urinary antiseptics and describe their toxic effects.
Concepts
Urinary Antiseptics: These agents act in the urine to suppress bacteriuria. They lack systemic
antibacterial effects but may be toxic. They are often administered with acidifying agents, since
bacterial growth in urine is inhibited at a low pH.
(1) Nitrofurantoin is active against many urinary tract pathogens (not Proteus or Pseudomonas
spp), and resistance emerges slowly. Active orally, the drug is excreted in the urine via filtration
and secretion, and it may reach toxic levels in the blood of patients with renal dysfunction.
Adverse effects include gastrointestinal irritation, skin rashes, neuropathies, and hemolysis in
patients with G6PDH deficiency.
(2) Nalidixic acid is a quinolone that acts against many gram-negative organisms (not Proteus or
Pseudomonas spp) by mechanisms that may involve acidification or inhibition of DNA gyrase.
Resistance emerges rapidly. Active orally/the drug is excreted in the urine partly unchanged and
partly as the inactive glucuronide. Toxic effects include gastrointestinal irritation, glycosuria, skin
rashes, photosensitzation, visual disturbance, and CNS stimulation.
(3) Methenamine mandelate and hippurate combine acidification with the release of the
antibacterial compound formaldehyde at pH levels below 5.5. They are not usually active against
Proteus spp because of urinary alkalininzation by such organisms. Insoluble complexes form
between formaldehyde and sulfonamides, and the drugs should not be used together.
(4) Cycloserine inhibits the incorporation of D-alanine into cell wall mucopeptides. It is active
against coliforms, mycobacteria, and Proteus ssp. Clinical use is limited by serious toxicity,
including headache, tremor, vertigo, and psychotic reactions.
Note: Many systemically active antimicrobial agents are effective in the treatment of urinary tract infections:
these agents include penicillins, cephalosporins, sulfonamides, trimethoprimsulfamethoxazole, and
aminoglycosides.
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Required Reading:
Suggetsted Reading:
Pages.
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DENTAL PHARMACOLOGY
Spring 2004
Dr. Donnell Bowen
Antimicrobials III
Penicillins and Other Inhibitors of Cell Wall Synthesis
Lecture 38
OBJECTIVES
Beta-lactam ring structure

Penicillin-binding proteins
Peptidoglycan chains
Beta-Lactamase enzyme activity
Transpeptidases
Hypersensitivity reactions
Describe the mechanism of antibacterial action of beta-lactam antibiotics.

Describe the mechanisms underlying the resistance of bacteria to beta-lactam antibiotics.
Identify the important drugs in each subclass of penicillins and describe their antibacterial
activity and clinical uses.
Identify the 4 subclasses of cephalosporins and describe their antibacterial activities and
uses.
List the major adverse effects of the penicillins and the cephalosporins.
Identify the important features of aztreonam and imipenem.
Required Reading:
Suggested Reading Assignment:

Pages.
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DENTAL PHARMACOLOGY
Spring 2004
Antimicrobials IV
Aminoglycosides
Lecture 39
Introduction: This lecture will cover the class of antibiotics called aminoglycoside. A discussion of
clinical uses, mechanisms of actions and adverse effects will be given for the group as a class and
for selected individual agents in the class.
After completion of this lecture and reading the assigned texts, each student should be able to:
Understand the mechanism of action of aminoglycoside.
Understand limitations of use as related to resistance, toxicity and spectrum of activity.
Discuss side effects associated with the drugs and class in general.
Develop strategies for use of aminoglycoside antibiotics.
Understand the role of aminoglycoside antibiotics as part of the therapeutic options
available.
Required Reading:
4th Edition. Pages 482-533. Chapter 37.
Suggested Reading:
Pages.
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DENTAL PHARMACOLOGY
Spring 2004
Antimicrobials V
Tetracyclines & Chloramphenicol
Lecture 40
Tetracyclines
Objectives:
To understand the chemistry of the family of tetracyclines.
Understand the pharmacokinetic property of tetracycline as it relates to its oral
bioavailability, distribution, metabolism, and excretion.
To know the spectrum and indications.
To understand the mechanism and site of drug action.
To understand the development of drug resistance.
To know the adverse effects on:
- Bones and teeth
- Gastrointestinal
- Liver
- Kidney
- Photosensitization
To know the drug interactions
Drugs to be discussed:
Tetracycline
Doxycycline
Minocycline
Oxytetracycline
Chlortetracycline
Demeclocycline
Methacycline
Chloramphenicol
Chloramphenicol is primarily bacteriostatic, although it may be bactericidal to certain
species, such as H. influenzae, N. meningitidis, and Strep. pneumoniae. Chloramphenicol
possesses a fairly wide spectrum of antimicrobial activity. Strains are considered sensitive if they
are inhibited by concentrations of 8 mg/ml or less.
Chloramphenicol is not a first-line antibiotic because of its potential for causing aplastic
anemia. The drug is reserved for patients with serious infections, such as meningitis, typhus, and
typhoid fever, who cannot take safer alternatives because of resistance or allergies. It also is an
effective therapy for Rocky Mountain spotted fever.
I. Antimicrobial Activity
II. Pharmacokinetics
III. Clinical Uses
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DENTAL PHARMACOLOGY
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IV. Adverse Reactions

A. Gastrointestinal Disurbances
B. Bone Marrow Disturbances
C. Toxicity for Newborn Infants
D. Interactions with Other Drugs
Objectives:
Understand the pharmacokinetic property of chloramphenicol as it relates to its oral
bioavailability, distribution, metabolism, and excretion.
To know the spectrum and indications.
To understand the mechanism and site of drug action.
To know the adverse effects on:
- Bone marrow disturbances
- Gastrointestinal
- Newborn infants (Toxicity)
To know the drug interactions
Required Reading:

Suggested Reading:
75
DENTAL PHARMACOLOGY
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Antimicrobials VI
Erythromycin and Miscellaneous
Lecture 41
Introduction:
This lecture will cover antibiotics that collectively called miscellaneous because they have
different mechanisms of actions. Although grouped as miscellaneous, they are widely used in
clinical medicine today and are important in treating a variety of infectious diseases. The
clinical indications and contraindications for use of these agents will be discussed. The
mechanism by which these agents exert their clinical and pharmacologic activity will be
discussed as well as adverse effects. The classes of antibiotics to be discussed include the
macrolide antibiotics (erythromycin, clarithromycin and azithromycin), the lincosamide
clindamycin, metronidazole, the fluoroquinolones (currently there are greater than ten agents
approved for use in the USA and they will be discussed by groups) and a students will be
introduced to a new class of antibiotics agents called ketolides and their role in the ever
changing clinical spectrum. Telithromycin is the first of this new class to be approved in the
USA.
Objectives:
After attending this lecture and reading the material in the assigned texts, the student will be
able to:
Understand the mechanism of action and pharmacokinetics of fluoroquinolone antibiotics.
Understand the mechanism of action of macrolide antibiotics.
Understand the mechanism of action and pharmacokinetics of lincosamide antibiotics.
Understand the mechanism of action and pharmacokinetics of ketolides antibiotics.
Understand the mechanism of action and pharmacokinetics of metronidazole.
Describe and identify adverse effects of the fluoroquinolone, macrolide, lincosamide,
metronidazole and ketolides antibiotics.
Identify and describe the clinical indications for use of the fluoroquinolone, macrolide,
lincosamide, metronidazole and ketolides antibiotics.
Design a dosing regimen for use of the fluoroquinolone, macrolide, lincosamide,
metronidazole and ketolides antibiotics.
Required Reading:
Suggetsted Reading:
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DENTAL PHARMACOLOGY
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Antimicrobials VII
Tuberculosis (TB)
Lecture 42
Antimycobacterial Drugs
Mycobacteria are acid-fast bacilli that cause tuberculosis (TB) arid leprosy. These chronic
infections often require treatment with multiple drugs for months or years. Drugs are used
in combination because of their synergistic effect against mycobacteria and because
combination therapy prevents drug resistance. It is currently estimated that 1/2 of the
world's population (3.1 billion) is infected with mycobacterium tuberculosis. Mycobacterium
avium complex is associated with AIDS related TB.
I. Classification of Drugs
3 Groups depending upon the degree of effectiveness and potential side effects
A. First Line: (primary agents)
Are the most effective and have lowest toxicity.
- Isoniazid
- Rifampin
B. Second Line:
Less effective and more toxic effects
- p-amino salicylic acid
- Streptomycin
- Ethambutol
C. Third Line:
Are least effective and most toxic
- Amikacin
- Kanamycin
- Capreomycin
- Viomycin
- Kanamycin
- Cycloserine
ll. Chemotherapy of TB
III. Chemoprophylaxis of TB
Required Reading:
Suggested Reading:
77
DENTAL PHARMACOLOGY
Spring 2004
TBA
Antivirals
Lecture 43
Objectives:
a. Describe the mechanism of action of antiretroviral agents, purine and pyrimidine
antimetabolites, amantadine, foscarnet and the interferons.
b. Know the agents used non-systemically.
c. Describe the clinical uses of antiviral drugs and list the toxic effects of those used
systemically.
d. Know the antiretroviral agents that are used in monotherapy and in combination therapy.
OVERVIEW. Viruses are obligate intracellular parasites that require for survival the active
participation of the metabolic processes of the invaded cell. Thus agents that are able to kill
viruses often injure host cells as well. Despite this inter-relationship, there is a growing
number of drugs that have substantial therapeutic merit in the treatment of viral infections.
Mechanisms of Action:
1. Adsorption and penetration of the virus
2. Early protein synthesis
Required Reading:
Suggetsted Reading:
C.R. Craig and R.E. Stitzel (eds.). Modern Pharmacology, 4th Edition, Little, Brown and
Company, 1994.
C.M. Smith and A.M. Reynard (eds.). Essentials of Pharmacology. W.B. Saunders
Company, 1995.
78
DENTAL PHARMACOLOGY
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TBA
Antifungal Agents
Lecture 44
ANTIFUNGAL AGENTS
Overview:
Drugs used in the treatment of fungal infections are traditionally divided into two distinct
groups, namely superficial and systemic agents. It should be borne in mind that this
distinction can be arbitrary since some drugs (imidazoles and triazoles, polyenes) may be
used in either manner. Many superficial mycoses maybe treated either systemically or
topically.
Objectives:
Describe the probable mechanisms of action of griseofulvin and of those of antifungal
agents used for systemic infections.
Describe the clinical uses of amphotericin B, flucytosine, griseofulvin, fluconazole,
itraconazole, ketoconazole and terbinafine.
Indicate the major toxic effects of systemic antifungal drugs including griseofulvin.
Identify the main topical antifungal agents.
Know the drug interactions and contraindications.
Required Reading:
Suggested Reading:
Basic and Clinical Pharmacology, 8th Edition, J.G. Katzang (ed.). Appleton and Lange,
2001.
Pharmacology, Lippincott's illustrated Reviews, 2nd Edition, R.A. Harvey, P .C.
Champe,M.J. Mycek, S.B. Gertner and M.M. Perper (eds.). J.B. Lippincott Company, 2000.
Modern Pharmacology, 4th Edition, C.R. Craig and R.E. Stitzel (eds.). Little, Brown
andCompany, 1994.
Essentials of Pharmacology, C.M. Smith and A.M. Reynard (eds.). W.B. Saunders
Company, 1995.
79
DENTAL PHARMACOLOGY
Spring 2004
Dr. Donnell Bowen
Cancer Chemotherapy
Lecture 45
OBJECTIVES
Cell cycle kinetics

Cell cycle-specific (CCS)
Cell cycle-nonspecific (CCNS)
Growth fraction
Log kill hypothesis
Pulse therapy
Rescue therapy

1. Describe the relevance of cell cycle kinetics to the mode of action and clinical use of anticancer
drugs.
2. Identify the major subclasses of anticancer drugs and describe the mechanisms of action of the
main drugs in each subclass.
3. Identify the drugs of choice for the more important neoplastic diseases and describe their
pharmacokinetics and their toxic effects.
4. Understand the strategies of combination chemotherapy and pulse, recruitment, and rescue
therapies.
Required Reading:
4th Edition. Pages 565-581 and 644-655.
Suggested Reading:
80
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Spring 2004
Antiseptic, Desinfectant, Hemostatic, and Caustic Agents

Lecture 46
Overview
Disinfectants, Antiseptics, & Sterilants — Objectives
Infection control is the selection and use of procedures and products to prevent the spread of
infectious diseases. Based on scientific data and recommendations of professional organizations
and government agencies (CDC), this lecture will address the basic principles of infections control
and their application in the dental office.
Antiseptics and disinfectants are chemical agents with antimicrobial activity but no specific site of
action in contrast to antibiotics, antiseptics do not have a specific target, but agents that work
through generally chemical means strong acids and bases are corrosive and can oxidize organic
molecules or denature (unfold) proteins.
Chemical Agents to be described:

I. Alcohols
II. Chlohexidine
III. Halogens
1. Iodine
2. Iodophora
3. Chlorine
IV. Phenolics
V. Quaternary Ammonium Compounds
VI. Aldehydes
VII. Peroxygen Compounds
VIII. Heavy Metals
IX. Strerilants
X. Preservatives
Required Reading:
CDC Recommended Infection-Control Practices for Dentistry in: http://www.med.howard.edu/pharmacology/
Suggested Reading:
81
DENTAL PHARMACOLOGY
Spring 2004
TBA
Agents Affecting Calcium Metabolism

Lecture 47
AGENTS AFFECTING CALCIFICATION
Objectives:
a. Define calcium distribution in humans.
b. Describe synthesis, secretion, regulators and modulators of parathyroid hormone (PTH).
c. List the physiological effects and clinical use of PTH .
d. List the steps in the production of activated vitamin D and its metabolism.
e. List the physiological effects, therapeutic uses and adverse effects of activated vitamin D.
f. Describe the relationship of dihydrotachysterol's structure to that of vitamin D and its
therapeutic use.
g. List the physiologic effects and therapeutic uses of calcitonin.
h. List the secondary agents affecting calcium homeostasis and describe their usefulness.
Required Reading:
Suggested Reading:
Basis of Therapeutics. 10th ed. McGraw Hill. Pages 1715-1743.
Pages 706-722.
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DENTAL PHARMACOLOGY
Spring 2004
Dr. Yousef Tizabi
Introduction to Endocrine Pharmacology

Lecture 48
OBJECTIVES
1. Describe the general mechanism of action of hormones.
2. Describe the anterior and posterior pituitary hormones.
3. Describe the regulatory mechanisms for each of the above hormones.
4. Understand the problems related to hypo- or hyper-secretion of each hormone.
5. Know the pharmacological treatment of each condition.
6. Know the mechanism of action of the drugs and their side effects.
7. Be cognizant of the dental implications of hormonal abnormalities.
8. Be cognizant of the dental implications of pharmacotherapies.
OUTLINE
1. Hypothalamic hormones
a. Chemical Composition
b. Distribution
c. Therapeutic Applications
2. Anterior pituitary hormones

a. Classifications
b. Regulation
c. Pharmacological Applications
3. Posterior pituitary hormones

a. Classifications
b. Regulation
c. Pharmacological Applications
3. Growth Hormone
a. Chemical Structure
b. Regulation
c. Deficiency Symptoms
d. Excess Symptoms
e. Pharmacological Treatments
f. Side effects
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DENTAL PHARMACOLOGY
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4. Prolactin
b. Regulation
c. Excess Symptoms
d. Pharmacological Treatments
e. Side effects
5. Antidiuretic Hormone (ADH) or Vasopressin

b. Regulation
c. Deficiency Symptoms
d. Excess Symptoms
e. Pharmacological Treatments
f. Side effects
Required Reading:
4th Edition.
Suggested Reading:
84
DENTAL PHARMACOLOGY
Spring 2004
Dr. Yousef Tizabi
ACTH and Glucocorticoids

Lecture 49
OBJECTIVES
1. Describe the hypothalamic-pituitary adrenal axis.
2. Know the chemical nature and actions of CRH.
3. Know the chemical nature and actions of ACTH.
4. Know the chemical nature and actions of glucocorticoids.
5. Describe the mechanism of action of glucocorticoids.
6. Describe the therapeutic uses and side effects of CRH.
7. Describe the therapeutic uses of ACTH and side effects.
8. Describe the therapeutic uses of glucocorticoids and their side effects.
9. Be cognizant of the dental relevance of hyper or hypo secretion of ACTH and CRH.
10. Be cognizant of the dental relevance of the drugs that affect HPA axis.
OUTLINE
1. Corticotropin Releasing Hormone (CRH)
b. Distribution
c. Mechanism of action
d. Therapeutic Applications
e. Side effects
2. ACTH (Adrenocorticotropic Hormone)

b. Synthetic analogs (Cosyntropin)
e. Side effects
3. Glucocorticoids
b. Synthetic compounds (Prednisone, Triamcinolone, Dexamethasone)
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DENTAL PHARMACOLOGY
Spring 2004
e. Side effects
4. Drugs for treatment of hyperadrenocorticism

a. Mechanism of action
b. Side effects
Required Reading:
4th Edition.
Suggested Reading:
86
DENTAL PHARMACOLOGY
Spring 2004
Dr. Yousef Tizabi
Thyroid and Anti-Thyroid Drugs

Lecture 50
OBJECTIVES
1. Describe the hypothalamic-pituitary thyroid axis.
2. Know the chemical nature and actions of thyrotropin releasing hormone (TRH).
3. Know the chemical nature and actions of thyroid stimulating hormone (TSH).
4. Know the chemical nature and actions of thyroid hormones.
5. Describe the symptoms associated with hypothyroidism.
6. Know the dental implication of hypothyroidism.
7. Describe the symptoms associated with hyperthyroidism.
8. Describe the drugs used in the treatment of hypothyroidism and their side effects.
9. Describe the drugs used in the treatment of hyperthyroidism and their side effects.
OUTLINE
1) Thyrotropin Releasing Hormone (TRH)
b. Distribution
e. Side effects
2) Hypothyroidism
a. Hypometabolism and associated symptoms (dental implications)
b. Causes
c. Drugs used in treatment of hypothyroidism
d. Side effects
3) Hyperthyroidism
a. Hypermetabolism and associated symptoms
b. Causes
c. Drugs used in treatment of hyperthyroidism
d. Side effects
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DENTAL PHARMACOLOGY
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4) Mechanism of action of propylthiouracil

a. Interference with iodination process
b. Interference with coupling of mono and diiodotyrosine
c. Inhibition of deiodinase (conversion ofT4 to T3)
5) Side effects of propylthiouracil

a. Agranulocytosis
b. Skin rash
c. Increase vascularity
6) Drugs Inhibiting iodide uptake
7) Iodide use and symptoms of iodism (dental relevance, e.g. soreness of teeth and gums)
131
8) I
uses and contraindications
9) Drugs used as a adjunct therapy in hyperthyroidism

a. Beta adrenergic blockers (Propranolol, Atenolol)
b. Calcium channel blockers (Diltiazem)
10) Presurgical Treatments

a. Iodide
b. Dexamethasone
c. Iopanoic Acid
11) Drugs for treatment of hypercortisolemia

b. Side effects
Required Reading:
4th Edition. Pages 464-466
Suggested Reading:
88
DENTAL PHARMACOLOGY
Spring 2004
Dr. Yousef Tizabi
Estrogen, Progestin I. Oral Contraceptives, Androgens

Lecture 51
Overview
Estrogen, Progestin I. Oral Contraceptives, Androgens
OBJECTIVES
1. Describe the hypothalamic-pituitary gonadal axis.
2. Know the chemical nature and actions of GnRH.
3. Know the chemical nature and actions of LH and FSH.
4. Know the chemical nature and actions of Estrogens.
5. Know the chemical nature and actions of Progestin.
6. Know the chemical nature and actions of Androgens.
7. Know the conditions associated with hypo- or hyper secretion of each of the above
hormones.
8. Know the pharmacological applications and side effects ofGnRH or its analogs.
9. Know the pharmacological applications and side effects of estrogenic compounds.
10. Know the pharmacological applications and side effects of progestin compounds.
11. Know the pharmacological applications and side effects of androgenic compounds.
12. Know the chemical nature and mechanism of action of oral contraceptives.
13. Know the side effects of oral contraceptives.
OUTLINE
1. Gonadotropin Releasing Hoffi1one (GnRH)
a. Regulatory Mechanism
b. Synthetic Analogs
e. Side effects
2. Follicular Stimulating Hoffi1one (FSH)

b. Mechanism of action
d. Side effects
3. Luteinizing Hormone (LH)

d. Side effects
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DENTAL PHARMACOLOGY
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4. Estrogen
c. Synthetic Compounds
e. Side effects
5. Progesterone
e. Side effects
6. Androgens
e. Side effects
7. Oral Contraceptives
a. Various preparations (e.g. combinations of estrogenic and progestin compounds)
c. Side effects and contraindications
8. Fertility Drugs
a. Chemical nature
c. Side effects
9. Antiandrogens
b. Side effects
Required Reading:
Suggested Reading:
90
DENTAL PHARMACOLOGY
Spring 2004
Insulin and Oral Hypoglycemics I & II

Lecture 52
Pharmacotherapy of Diabetes Mellitis

Objectives
A. Understand the actions and signaling pathways of the Insulin receptor
B. Understand the diverse physiologic function of Insulin

1. Carbohydrate metabolism
- glucose uptake and utilization
- effects on gluconeogenesis
- effects on glycogen production
2. Lipid Metabolism
- tissue uptake (lipoprotein lipase)
- effects on lipogenesis/lipolysis
- oxidation of lipids/ketone formation
C. How does insulin deficiency influence the physiologic actions modulated by insulin?
D. Understand the patterns of insulin secretion

- post-prandial secretion
- basal/fasting secretion
E. Proposed mechanism on the pathogenesis of IDDM
F. Proposed mechanism of the pathogenesis of NIDDM

1. Risk factors
2. Progression from IGT
3. Contributors to hyperglycemia
- insulin resistance
- impaired insulin secretion
- hepatic glucose production
II. Pharmacotherapy
A. Insulin therapy
Time-Effect profiles for insulin preparations
- rapid/short acting, intermediate acting, long-acting
B. Oral Agents
Understand the mechanism of actions and the components of pathophysiology targeted by
each class
1. sulfonylureas/ meglitinides
2. biguanides
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DENTAL PHARMACOLOGY
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3. alpha-glucosidase inhibitors
4. thiazolidinediones
Required Reading:
Suggested Reading:
92
DENTAL PHARMACOLOGY
Spring 2004
Anticaries, Antiplaque, Antigingivitis Agents

Lecture 53
Objectives:
After reading the assigned chapters and attending the lecture, the students will have an
understanding of:
Causes of dental caries and Gingivitis
Preventative measures for dental caries and gingivitis
Use of fluoride in cavity prevention programs
Different types of antigingivitis treatments and when to use each
Side effects/Adverse actions of agents used in the prevention and treatment of
dental caries and gingivitis.
Required Reading:
Suggested Reading:
93
DENTAL PHARMACOLOGY
Spring 2004
Toxicology
Lecture 54
Heavy Metal Intoxication & Chelators
Objectives:
The environmental metals of greatest concern are lead, mercury, arsenic, and cadmium. In the
past, lead paint was available for use in homes, and lead pipes and/or lead solder delivered water
to some homes. As a result, people can be exposed to lead on a daily basis; this exposure is a
major pediatric concern. Mercury similarly is a contaminant of our environment; human beings are
exposed to mercury in the fish they eat as well as in the amalgam fillings in their teeth. Arsenic is
found naturally in high concentrations in drinking water in various parts of the world. Recently,
cadmium has been classified as a known human carcinogen. This lecture will deal primarily with
the toxic effects of these four metals and the chelators that are used to treat metal intoxication.
Heavy metals exert their toxic effects by combining with one or more reactive groups (ligands)
essential for normal physiological functions. Heavy metals, particularly those in the transition
series, may react in the body with ligands containing oxygen (OH, COO -, OPO3H -, >C=O),
sulfur (SH,S), and nitrogen (NH2 and >NH). The resultant metal complex (or coordination
compound) is formed by a coordinate bond – one in which both electrons are contributed by the
ligand.
Heavy-metal antagonists (chelating agents) are designed specifically to compete with these
groups for the metals, and thereby prevent or reverse toxic effects and enhance the excretion of
metals. A chelate is a complex formed between a metal and a compound that contains two or
more potential ligands. An ideal chelating agent would have the following properties: high
solubility in water, resistance to biotransformation, ability to reach sites of metal storage, capacity
to form nontoxic complexes with toxic metals, ability to retain chelating activity at the pH of body
fluids, and ready excretion of the chelate. A low affinity for Ca2+ also is desirable, because Ca2+
in plasma is readily available for chelation, and a drug might produce hypocalcemia despite high
affinity for heavy metals. The most important property of a therapeutic chelating agent is greater
affinity for the metal than that of the endogenous ligands. The large number of ligands in the body
is a formidable barrier to the effectiveness of a chelating agent. Observations in vitro on chelator-
metal interactions provide only a rough guide to the treatment of heavy-metal poisoning. Empirical
observations in vivo are necessary to determine the clinical utility of a chelating agent.
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DENTAL PHARMACOLOGY
Spring 2004
Toxicology of Heavy Metals

I. Lead
a. Pharmacokinetics
b. Pharmacodynamics
i. Nervous System
ii. Blood
iii. Kidneys
iv. Reproductive Organs
v. Gastrointestinal Tract
vi. Cardiovascular System
c. Major Forms of Lead Intoxication
i. Inorganic Lead Poisoning
1. Acute
2. Chronic
3. Organolead Poisoning
d. Treatment
i. Inorganic Lead Poisoning
ii. Organic Lead Poisoning
II. Arsenic
a. Pharmacokinetics
b. Pharmacodynamics
c. Major Forms of Arsenic Intoxication
i. Acute Inorganic Arsenic Poisoning
ii. Chronic Inorganic Poisoning
iii. Arsine Gas Poisoning
III. Mercury
a. Pharmacokinetics
b. Major Forms of Mercury Intoxication
i. Acute
ii. Chronic
c. Treatment
i. Acute Exposure
ii. Chronic Exposure
Pharmacology of Chelators
I. Dimercaprol (2,3- Dimercaptopropanol, BAL)
a. Indications & Toxicity
II. Succimer (Dimercaptosuccinic Acid, DMSA)
III. Edetate Calcium Disodium (Ethylenediaminetetraacetic Acid; EDTA)
IV. Penicillamine (D- Dimethylcysteine)
V. Trientine (Triethylenetetramine)
VI. Deferoxamine
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DENTAL PHARMACOLOGY
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Required Reading:
Suggested Reading:
96
DENTAL PHARMACOLOGY
Spring 2004
Prescription Writing
Scheduled Substances
Rules and Regulations
Lecture 55
Introduction
This lecture is designed to introduce students to federal laws that impact prescribing of
medications, to the components of a prescription, to rationally prescribing of therapeutic agents
and to the writing of a prescription.
Objectives:
1. Highlight Federal Laws (and Amendments) that relate to drug use and availability in this
country.
Food and Drug Act of 1906
Federal Food, Drug and Cosmetic Act of 1938
Kefauver-Harris Amendment to the 1938 Act (in 1951)
Durham-Humphrey Amendment to the 1938 Act (in 1951)
The Comprehensive Drug Abuse Prevention and Control Act (Controlled Substance Act) of
1970
2. Discuss Scheduled drug classification, purpose and prescribing constraints.
3. Identify and discuss the component of a prescription the prescription.
4. Demonstrate and teach the correct way to write a prescription.
Required Reading:
4th Edition. 696-706.
Suggested Reading:
Basis of Therapeutics. 10th ed. McGraw Hill. Appendix 1, Principles of Prescription writing
and Patient Compliance Instructions.
Pages 1104 -1112.
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DENTAL PHARMACOLOGY
Spring 2004
Clinically Important Drug Interactions

Lecture 56 & 57
Topic:
Adverse Drug Reactions and Drug-Drug Interaction
Introduction:
This lecture is designed to demonstrate the significance of ADRs and drug interactions
from a clinical perspective. Students will be provided concepts that should help them to identify
and hopefully prevent adverse outcomes from the use of drugs as well as mechanisms for
improving care of patients when drug combinations are desired.
Objectives:
1. Define Adverse Drug Reactions (ADRs) and Drug-Drug interactions (DDIs).
2. Identify factors that predispose individuals to ADRs.
3. Classify ADRs and DDls
4. List ways to investigate and prevent the occurrence of ADRs and DDIs.
5. Give examples of ADRs and DDIs from a mechanistic perspective.
Reference:
Lecture notes provided in syllabus and made available on web site.
Required Reading:
4th Edition. Pages 47-60. Appendix P 707.
Other References:
Lecture notes may be found on web site.
Suggested Reading:
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DENTAL PHARMACOLOGY
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REVIEW SESSION
APRIL 18TH, 2004
10:00 to 11:50 am
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HOWARD UNIVERSITY

SOPHOMORE DENTAL PHARMACOLOGY

Coordinator: Martha I. Dávila-García, Ph.D.

Co-Coordinator: Philip Gatti, Ph.D.

Lecture 23, Sedative/Hypnotics and Anxiolytics. ..................................................... 47

Class Size: 75 students

Methods and Material of Instruction

Number of Times Administered per Academic Year: Once, in the Spring

Clock Hours: 72 hrs Lecture

Measurement and Evaluation

The composition of exams are approximately as follows:

1st Intrasessional 100 questions 32% GRADING SYSTEM:

Dr. Robert E. Taylor, Chairman, Department of Pharmacology

Procedures Governing Examinations

Use of these procedures is intended to assure:

a) maximum available time for students to take examinations; and

b) the best possible environment in which student will take examinations.

Guidelines for Absences from Intrasessional, Midterm and Final Examinations

3. Illness or injury resulting in missed examinations must be certified by a physician.

5. All cases will be handled in an individual basis.

Failure to comply with set policies may result in a failing grade.

XI. Endocrine Pharmacology

Joseph Cohen, Ph.D.

Robert L. Copeland, Jr. Ph.D.

Keith Crawford, Ph.D.

Martha I. Dávila-García, Ph.D. COURSE COORDINATOR

Clifford Ferguson, M.D.

Philip Gatti, Ph.D. COURSE CO-COORDINATOR

V. John Massari, Ph.D.

Sonya K. Sobrian, Ph.D.

Robert E. Taylor, M.D., Ph.D.

SOPHMORE DENTAL PHARMACOLOGY SCHEDULE

OFFICE HOURS: Dr. Martha I. Dávila-García Tuesday 3-5 p.m.

DEPARTMENTAL WEB-SITE: http://www.hucmlrc.howard.edu/Pharmacology/default.htm

Jan. 6 Tues. 8-8:15 Course Objectives, Class & Exam DÁVILA-GÁRCÍA

UNIT I: GENERAL PRINCIPLES IN PHARMACOLOGY

Jan. 6 Tues. 8:15-8:50 1A Introduction to Pharmacology BOWEN/COPELAND

Jan. 6 Tues. 9-9:50 1B Introduction to Pharmacology BOWEN/COPELAND

Jan. 7 Wed. 1-1:50 2 Drug absorption. Characteristics of biological COPELAND

Jan. 8 Thurs. 8-8:50 3 Drug distribution. Volume of distribution, FERGUSON

Jan. 9 Fri. 10-10:50 4 Drug metabolism. Biotransformation. COHEN

Jan. 9 Fri. 11-11:50 5 Drug elimination. Kinetics of absorption FERGUSON

Jan. 13 Tues. 8-8:50 6 Clinical use of drugs. Factors modifying FERGUSON

UNIT II: PHARMACOLOGY OF THE AUTONOMIC NERVOUS SYSTEM

Jan. 14 Wed. 1-1:50 7 Introduction to Pharmacology of the MASSARI

Jan. 15 Thur. 8-8:50 8 Cholinergic neurotransmission: COHEN

Jan. 16 Fri. 10-10:50 9 Cholinergic neurotransmission: COHEN

Jan. 16 Fri. 11-11:50 10 Muscarinic blocking drugs and their COHEN

Jan. 20 Tues. 8-8:50 11 Adrenergic neurotransmission, COHEN

Jan. 20 Tues. 9-9:50 11 Adrenergic neurotransmission. (cont’d) COHEN

Jan. 21 Wed. 1-1:50 12 Adrenergic receptor antagonists. MASSARI

Jan. 22 Thurs. 8-8:50 13 Ganglionic and neuromuscular blocking MASSARI

Jan. 23 Fri. 10-10:50 14 General anesthesia. Clinical approaches CRAWFORD

Jan. 23 Fri. 11-11:50 14 General anesthesia. Individual agents (cont'd) CRAWFORD

Jan. 27 Tues. 8-9:50 15 Local anesthesia. History. General COPELAND

Jan. 28 Wed. 1-1:50 16 Pharmacology of Oxygen/Nitrous Oxide JACKSON

Jan. 29 Thurs. 8-8:50 17 Respiratory System and Asthma TYLER/MATHEW

Jan. 30 Fri. 10:00-11:50 18 Opiate analgesics and antagonists. COPELAND

Feb. 3 Tues. 8-9:50 FIRST INTRASESSIONAL EXAMINATION

UNIT III: PHARMACOLOGY OF THE CENTRAL NERVOUS SYSTEM

Feb. 5 Thurs. 8-8:50 20 Therapeutic approach to management MASSARI

Feb. 6 Fri. 10-11:50 21 Epilepsy and Anticonvulsants DÁVILA-GARCÍA

Feb. 10 Tues. 8-9:50 22 Antidepressants and Antimanic drugs DÁVILA-GARCÍA

Chemical antagonist ▪ Partial agonist