Syllabus07 PDF

MEDICAL
PHYSIOLOGY
2007
LECTURE SYLLABUS
MEDICAL PHYSIOLOGY
2007
COURSE ADMINISTRATION
PERSONNEL
DEPARTMENT CHAIR
MICHAEL L. JENNINGS, Ph.D.
PROFESSOR
Office: Biomedical Research II
206-2 686-5123
Fax # 686 - 8167
COURSE DIRECTOR
JAMES N. PASLEY, Ph.D.
PROFESSOR
Assistant Dean
Office: Shorey 6S/12 686-5128
Fax # 526 -7605
COURSE ADMINISTRATIVE ASSISTANTS

STACY A. MAJOR
DANNY McKAY
TABLE OF CONTENTS
INTRODUCTION
I. Course Objectives
II. Course Materials
III. Classes
IV. Examinations
Test Validation Procedure
V. Lecture Schedule
Key Physiology Equations
Laboratory Values
MUS # 1
MUS # 2
MUS # 3
MUS # 4
CV #1
CV #2
CV #3
CV #4
CV #5
CV #6
CV #7
CV #8
CV #9
EX #1
EX # 2
CV #12
CV#13
CV #14
CV #15
CV #16
CV #17
RS #1
RS #2
RS #3
RS #4
RS #5
RS #6
RS #7
Mechanics Of Skeletal Muscle Contraction

Functional Properties Of Skeletal Muscle
Neuromuscular Junction
Smooth Muscle
Introduction To Cardiovascular Physiology
Electrophysiology
Cardiac Cycle
Ventricular Function and Energetics
Basic Electrocardiography I
Basic Electrocardiography II
Cardiac Output
The Peripheral Vascular System
Arterial Blood Pressure Regulation
Cardiovascular Responses To Exercise
Skeletal Muscle Respon. and Fuel Use During Exercise.
Hemodynamics
Microcirculation
Blood Coagulation, Hemostasis and Thrombosis
Venous Return
Cardiovascular Intrinsic and Extrinsic Control
Cardiovascular Pathophysiology
Airways; Ventilation; Properties Of Gases
Pulmonary Gas Exchange; O2 Transport
Tissue Gas Exchange; CO2 Transport
Muscles Of Breathing; Pulmonary Pressures
Lung & Thorax Compliance, Airway Resistance
Regulation Of Breathing
Pulmonary Blood Flow; Fluid Balance
Pasley
Page
3
3
4
4
7
8
98
99
Cornett
Cornett
Cornett
Cornett
Soulsby
Soulsby
Soulsby
Soulsby
Alan
Alan
Soulsby
Soulsby
Soulsby
Coker
Coker
Ware
Ware
Ware
Soulsby
Soulsby
Soulsby
Jennings
Jennings
Jennings
Jennings
Jennings
Jennings
Jennings
14
15
16
17
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
RS #8
RS #9
R #1
R #2
R #3
R #4
R #5
R #6
R #7
R #8
A/B #1
A/B #2
A/B #3
GI #1
GI #2
GI #3
GI #4
GI #5
GI #6
GI #7
GI #8
Endo #1
Endo #2
Endo #3
Endo #4
Endo #5
Endo #6
Endo #7
Endo #8
Endo #9
Endo #10
Endo #11
Endo #12
Endo #13
Ventilation/Perfusion Relations (Air/Blood Matching)

Pulmonary Pathophysiology
Body Fluid Compartments
Renal Anatomy and Function
Tubular Fluid Processing
Controlling and Measuring Renal Function
Renal Concentrating and diluting Mechanisms
Regulation of extracellular fluid osmolarity and Na+
concentration
Electrolyte Balance
Diuretics and Renal Related Diseases and Syndromes
Introduction To Acid-Base Balance
Regulation Of Acid-Base Balance
Renal Regulation Of Hydrogen Ion Balance
Introduction Of GI Physiology
Mastication and Swallowing
Swallowing Abnormalities and Gastric Motility
Gastric Secretion and Small Intestinal Motility
Pancreatic, Biliary and Intestinal Secretion
Digestion and Absorption Of Macronutrients
Water, Electrolyte, Vitamin and Mineral Absorption
Lg. Bowel Motility, Gas In The Gut and Dietary Fiber
Temperature Regulation
Energy Balance and Obesity
Neuroendocrine Hormones; Pituitary
Endocrine Control Of Calcium Metabolism
Endocrine Pancreas I
Endocrine Pancreas II
The Thyroid Gland
Adrenal Gland I
Adrenal Gland II
Male Reproductive Physiology
Female Reproductive Physiology I
Female Reproductive Physiology II
Neonatal Physiology
Jennings
Jennings
Kurten
Kurten
Kurten
Safirstein
Safirstein
Safirstein
Kurten
Safirstein
Wight
Wight
Wight
Pasley
Pasley
Pasley
Pasley
Pasley
Pasley
Pasley
Pasley
Conaway
Conaway
Conaway
Conaway
Conaway
Conaway
Conaway
Conaway
Conaway
Gaddy
Gaddy
Gaddy
Jennings
43
44
46
48
50
52
53
55
56
58
60
61
62
64
65
67
69
71
73
75
76
79
80
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MEDICAL PHYSIOLOGY (PHYSIOLOGY 500V)

SPRING SEMISTER 2006
I. COURSE OBJECTIVES
II.
To provide students with an understanding of the normal function of cells,

tissues, or organ systems of the human body
To provide examples of how organ systems are integrated to maintain a
normal physiological state.
To provide students with knowledge on the topics of general cell physiology,
cardiovascular, respiratory, renal, gastrointestinal and endocrine physiology.
To provide both basic factual knowledge of fundamental concepts of
physiology as well as clinical correlates of these concepts as applied to
humans.
To provide basic physiological principles that establish a solid foundation for
future learning of pathophysiological and pharmacological concepts.
COURSE MATERIALS
Required Textbook: The following textbook is required for the course:

- Medical Physiology, Guyton and Hall, 11th Ed., 2006
Other Recommended Concise Textbooks:
-
Costanzo, Linda S., Physiology, W.B. Sanders, Philadelphia, 1998

Pasley, J.N., USMLE Road Map: Physiology, Lange/McGraw-Hill, 2006
Seidel, C., Basic Concepts in Physiology: A Students Survival Guide,
McGraw-Hill, 2002
West J.B., Respiratory Physiology: The Essentials, 5th Edition, LWW,
Philadelphia, 1995
William Ganong, Review of Physiology, Lange/McGraw-Hill, 2005
Learning Resource Center Reverences. The Learning Resource Center (located

on the 5th floor of Ed. II bldg.) has a variety of audiovisual material covering various
aspects of medical physiology. Recommended tapes and CAI presentations are
listed below and in the syllabus under specific lectures.
Interactive Physiology: Cardiovascular
Interactive Physiology: Urinary
Interactive Physiology: Respiratory
Interactive Physiology: Musculoskeletal
Interactive Physiology: Fluid and Electrolytes/Acid Base
Essentials of Physiology
Arterial Blood Gas
SimBioSys Physiology Clinic
Must stay in the LRC
SimBioSys Physiology Lab Must stay in the LRC
Mac & PC CD
Mac & PC CD
Mac & PC CD
Mac & PC CD
Mac & PC CD
Mac & PC CD
CD
Mac & PC CD
Mac & PC CD
Syllabus. A new vigilance on the part of publishers regarding the copyright of their
materials requires us to redefine our policies on the distribution of course materials.
Thus, the printed syllabus has been reduced to general information and lecture
outlines to complement reading assignments and the lecture. Instructors may
choose to cover all or only part of the material contained in the syllabus during a
lecture period, particularly when the text adequately presents the same material.
3
Conversely, topics not mentioned in the syllabus but are in the textbook may be
covered by course exams.
Faculty use of copyrighted materials complies with the law as outlined in the
Guidelines for Fair Use of Copyrighted Materials and is restricted to the use
intended. You, the enrolled student, have certain rights under Fair Use. You may
print or make a copy of the information FOR YOUR OWN USE but this information
CANNOT BE DUPLICATED or copied to give to anyone else.
III. Classes
Lectures. Lectures will be approximately 50 minutes in length and generally will
conform to the classical didactic pattern. Instructors have designed their lectures
to present physiological principles in an organized and comprehensive fashion.
Students are encouraged to ask questions during lecture periods. The course
schedule in the syllabus indicates the dates, times, and location of all lectures. It is
strongly recommended that students read the associated syllabus material and
reading assignments prior to a scheduled lecture.
Clinical Correlation Lectures. Clinical Correlation lectures are presented by
clinicians (either UAMS faculty or private practice physicians) whose subspecialties are related to the organ system under discussion. These presentations
are designed to demonstrate the relationship between medical physiology and
clinical medicine. In addition, the Whitney Memorial Lecture is presented by a
distinguished physiologist each year.
PBL Case Conferences. For these conferences, the class will be divided into 10
small groups of 16 and will meet with assigned faculty members to discuss the
designated case. Cases will be available on the web site approximately one week
ahead. Attendance at these sessions is required.
Group assignments will be posted on the web and the wailing wall.
SIM -MAN PBL groups will be posted on the web and the wailing wall the
location for the SIM MAN PBLs will be on the second floor of the OLD hospital
room 2D/31. Attendance at these sessions is required.
Review Sessions. Question based reviews will be presented at the end of each
topic block prior to examination.
Tutoring Sessions. Will be announced via certified mail and e-mail for students
requiring further assistance.
Students in academic jeopardy are required to attend all tutorial sessions until their
cumulative percent score is consistent with a C letter grade. Students in academic
jeopardy are also encouraged to meet with Dr. Judy Garrett, Office of Educational
Development for individual counseling.
IV. EXAMINATIONS
Midterm Examinations. Four didactic computerized exams will be administered in
the Computer Laboratories on the 8th Floor of the Education II Building. Student
room assignments will be distributed either via the Medical Physiology web site
and/or on the Wailing Wall on the G level of the Education II building prior to each
examination.
4
Computerized Examination Instruction Summary:

1. Students should arrive 10 minutes prior to the start of the exam. Books, notes, paper,
coats, backpacks, etc. are to be left outside or in the back of the examination room.
Late students will Not be given extra time.
2. Type your social security number in the box on the initial screen. Use the number keys
at the top of the keyboard NOT the numeric keys on the right.
3. In the next box, type in your unique password. Your password will be given to you upon
entrance into the exam room on a piece of scratch paper. Read the instructions and
begin the examination. The scratch paper may be used for making notes during the
exam but must be turned in before leaving the room. Follow all instructions, and be
sure to use the scroll boxes to be sure you have read all of the question and examined
all of the possible choices of answers. READ CAREFULLY!
4. Click on the ONE BEST response to each question. Click the Next Question
button when you are ready to leave the current question.

5. Students encountering problems with the computer, should notify the proctor in
the examination room. Queries regarding examination questions will not be

addressed during an examination.
6. When you have completed answering the questions, you will be allowed to return to
questions you have not answered as well as review all questions on the examination by
clicking on the "Go To" button.
7. Warning screens will appear to indicate time remaining at 10, 5 and 1 minutes. When
you type "QUIT" at the end of the examination, you cannot re-enter the examination.
After quitting, you will be permitted to see your unofficial score, if you wish.
8. You may leave at any time after completing the examination.
The final examination in the course (the 5th examination) will be the National Board
Subject Examination in Medical Physiology, and it will be administered in the 8th
Floor laboratories (8A, 8C, 8B and 8D) in the Education II Building.
Midterm # 1
Midterm # 2
Midterm # 3
Midterm # 4
Quizzes
Final Examination
TOTAL
20%
15%
21%
14%
5%
25%
100%
TEST ITEM VALIDATION PROCEDURE

(STUDENT INFORMATION)
The faculty believes that detecting flawed questions on exams is the responsibility
of the faculty and not the students. It is unfair to ask students to research a question
for possible flaws. In a student appeal system, a student must take valuable time
researching a question, when he or she may have an exam the next day in another
course. Consequently, the following methods will be used to assure that all
questions on exams are valid: 1) Questions will be faculty peer reviewed prior to
each exam. 2) After exams, performance data on questions will be studied. 3)
Any questions that fall within a pre-defined range of performance data that suggests
a problem will be reviewed by both the question author and the Course Director. At
this time, questions identified as weak, or flawed, will be deleted from the exam.
After this process, which could take several days, a VALID KEY will then be posted.
This validation process will assure with high probability that all items counted toward
a students score on a test are without significant fault or flaw.
ONLY IN CASES OF CLEAR AND OBVIOUS FLAWS OR ERRORS IN A TEST
ITEM WILL ANY CHANGE IN TEST SCORES BE MADE.
BECAUSE OF THE AUTOMATIC SCREENING OF TEST ITEM QUALITY, IT
SHALL RARELY BE THE CASE THAT ANY ITEM WITH A CLEAR OR
OBVIOUS FLAW REMAINS IN THE TEST AFTER THE SCREENING
PROCESS.
CONCEIVABLE ALTERNATE INTERPRETATIONS OF THE ITEMS STEM
AND/OR ITS OPTIONS (i.e., ALTERNATIVE ANSWERS PROVIDED IN THE
TEST) NEED NOT BE BROUGHT TO THE COURSE DIRECTORS ATTENTION
(UNLESS SIMPLY FOR THE INTELLECTUAL EXERCISE) BECAUSE SUCH
COMMENTS AND OBSERVATION SHALL NOT BE JUDGED OF SUFFICIENT
MERIT TO JUSTIFY ANY CHANGES IN THE SCORING OF ANY TEST ITEM.
This procedure obviates any need for a routine, formal student test item appeal
process. Any student believing that a question counted toward the total test score
was significantly flawed or faulty should bring that opinion to the attention of the
Course Director in a prompt and timely manner. Comments regarding questions
which you believe are flawed and were not deleted from the VALID KEY can be
e-mailed or by filling out a form available in the LRC or Course Office in Shorey.
Comments are due in the Course Office by 4:00 p.m. 48 hours following the
posting of the VALID KEY.
As soon as a final computer rescoring is completed (about one or two more days),
student percent scores will be posted. Final letter grades will be assigned based
upon the following scale.
Letter Grade
Overall Score
85.50 100%
75.50 85.49%
65.50 75.49%
60.00 65.49%
0 59.99%
A
B
C
D
F
MEDICAL PHYSIOLOGY SPRING 2007 SCHEDULE

All lectures will be held in Education Building 2 (G-131 A/B)
(The schedule is subject to change without prior notice)

Exam 1 / Week 1
Date
Day
Time
Lecture
Title
Instructor
1/02
TU
10
Introduction to Medical Physiology
Pasley
1/02
TU
11
Role of Physiology in Clinical Medicine
Marsh
1/03
MUS # 1
Mech. of Skeletal Muscle Contraction
Cornett
1/04
TH
11
MUS # 2
Funct. Properties of Skeletal Muscle
Cornett
1/05
MUS # 3
Neuromuscular Junction
Cornett
1/05
11
MUS # 4
Smooth Muscle
Cornett
Exam 1 / Week 2
Date
Day
Time
Lecture
Title
Instructor
1/08
1/08
1/09
1/10
M
M
TU
W
9
11
10-12
9
CC 01
CV # 1
PBL 01
CV # 2
Physiology Lecture
Introduction to CV
PBL : Muscle
Electrophysiology
Soulsby
Staff
Soulsby
1/11
TH
CV # 3
The Cardiac cycle
Soulsby
1/11
TH
11
CV # 4
Ventricular Function and Energetics
Soulsby
1/12
10
CV # 5
Basic Electrocardiography I
Allan
1/12
11
CV # 6
Basic Electrocardiography II
Allan
Exam 1 / Week 3
Date
Day
Time
1/15
1/16
1/16
1/17
TU
TU
W
9
11
9
1/18
TH
10-12
1/19
1/19
Exam 1 / Week 4
Date
Day
Lecture
Title
HOLIDAY
Instructor
Martin Luther King Day
CV # 7
CV # 8
CC 02
Cardiac Output
The Peripheral Vascular System
Clinical Correlation: CV
Soulsby
Soulsby
Smith
9 C/D LAB
EKG LAB
Staff
CV # 9
Arterial Blood Pressure Regulation
Soulsby
11
EX # 1
Cardiovascular Responses to Exercise
Coker
Time
Lecture
1/22
11
EX # 2
1/22
CV # 12
1/23
1/25
1/26
TU
TH
F
10-12
11
9
PBL 02
CV # 13
CV # 14
1/26
10
Title
Skeletal Muscle Resp. and Fuel Use
During Exercise
Hemodynamics
PBL: CV / Exercise
The Microcirculation
Blood Coagulation, Hemostasis and
Thrombosis
Physiology Review
Instructor
Coker
Ware
Soulsby
Ware
Ware
Staff
Exam 1 / Week 5
Date
Day
Time
Lecture
Title
Instructor
1/29
8-10 :50
8C LAB
EXAM 1
1/30
TU
CV # 15
Venous Return
Soulsby
1/30
TU
11
CV # 16
Cardiovascular Intrinsic and Extrinsic Control
Soulsby
1/31
11
CV # 17
Cardiovascular Pathophysiology
Soulsby
2/01
2/01
TH
TH
9
11
RS # 1
RS # 2
Airways; Ventilation; Properties of Gases

Pulm. Gas Exchange; O2 Transport
Exam 2 / Week 6
Date
Day
Time
Lecture
Title
Jennings
Jennings
Instructor
2/05
RS # 3
Tissue Gas Exchange; CO2 Transport
Jennings
2/05
RS # 4
Jennings
2/06
TU
RS # 5
2/06
TU
11
RS # 6
Airways; Muscles of Breathing; Pulm.

Pressures
Lung & Thorax Compliance, Airway
Resistance
Regulation Of Breathing
2/08
TH
10-12
9C/D Lab
Mechanics Of Breathing Lab
Staff
2/09
10
CC 03
Pediatric Pulmonary Mechanics
Heulitt
2/09
11
RS # 7
Pulmonary Blood Flow; Fluid Balance
Jennings
Exam 2 / Week 7
Date
Day
Time
2/12
M
11
Lecture
RS # 8
Instructor
Jennings
2/12
2/13
M
TU
1-5
8
PBL 03
RS # 9
Title
Ventilation/Perfusion Relations (Air/Blood
Matching)
SIM - MAN
Pulmonary Pathophysiology
2/13
TU
1-5
PBL 04
SIM - MAN
Staff
2/14
CC 04
Adult Respiratory Diseases
Anderson
2/16
10
SIM - MAN Review
Staff
2/16
11
Review
Staff
Exam 2 / Week 8
Date
Day
Time
2/19
M
Lecture
HOLIDAY
Jennings
Jennings
Staff
Jennings
Title
PRESIDENTS DAY
Instructor
8C LAB
EXAM 2
Renal Anatomy and Function
Renal Blood Flow and Glomerular Filtration
Tubular Transport in Nephron Segments
Renal Concentrating and Diluting
Mechanisms
Fluid Shifts and Water Balance
Kurten
Kurten
Kurten
Safirstein
2/20
TU
8-10:50
2/21
2/21
2/22
2/23
W
W
TH
F
9
11
10
10
R#1
R#2
R#3
R#4
2/23
R#5
Safirstein
Exam 2 / Week 9
Date
Day
Time
2/27
TU
10
Lecture
R#6
Sodium Balance
Instructor
Safirstein
2/27
TU
1-3
PBL 05
PBL: Renal Case Conference
Staff
2/28
R#7
Potassium Balance
Kurten
2/28
11
CC 05
Clinical Correlation: Renal
Andreoli
3/01
TH
10
R#8
Safirstein
3/02
TH
11
A/B # 1
Ca2++, Mg2++, and PO4 Balance and the

Urinary Tract
Introduction To Acid Base
Exam 3 / Week 10
Date
Day
Time
Title
Lecture
Title
Wight
Instructor
3/06
TU
10
A/B # 2
Regulation Of Acid-Base Balance
Wight
3/06
TU
11
A/B # 3
Renal Regulation Of Hydrogen Ion Balance
Wight
3/06
TU
1-3
PBL 06
PBL A/B Computer
Staff
3/07
CC 06
Clinical Correlation:
Wheeler
3/07
10
Physiology Lecture
TBA
3/07
11
Physiology Lecture
TBA
Exam 3 / Week 11
3/10 3/18 SPRING BREAK
Exam 3 / Week 12
Date
Day
Time
Lecture
Title
Instructor
3/19
GI # 1
Introduction to Gastrointestinal Physiology
Pasley
3/19
11
GI # 2
Mastication and Swallowing
Pasley
3/20
TU
10
GI # 3
Pasley
3/22
TH
10
GI # 4
Swallowing Abnormalities and Gastric

Motility
Gastric Secretion and Small Intestinal Motility
Pasley
3/23
GI # 5
Pancreatic, Biliary and Intestinal Secretion
Pasley
3/23
11
Whitney Lecture
Schuster
10
Exam 3 / Week 13
Date
Day
Time
3/26
M
11
Lecture
GI # 6
Title
Digestion and Absorption of Macronutrients
Instructor
Pasley
3/27
TU
11
GI # 7
Pasley
3/27
TH
1-3
PBL 07
Water, Electrolyte, Vitamin and Mineral

Absorption
PBL- GI Case Conference
3/28
GI # 8
Pasley
3/29
TH
CC 07
Lg. Bowel Motility, Gas in the Gut and

Dietary Fiber
Clinical Correlation
3/29
TH
11
Exam 3 / Week 14
Date
Day
Time
Staff
Staff
Review
Lecture
Title
Instructor
4/02
1-4
8C Lab
EXAM 3
4/03
4/04
TU
W
10
9
Endo # 1
Endo # 2
Temperature Regulation
Energy Balance and Obesity
Conaway
Conaway
4/05
TH
10
Endo # 3
Neuroendocrine Hormones: Pituitary
Conaway
4/05
TH
11
CC 08
Clinical Correlation: Pituitary
TBA
4/06
10
Endo # 4
Endocrine Control Of Calcium Metabolism
Conaway
Exam 3 / Week 15
Date
Day
Time
Lecture
Title
Instructor
4/09
11
Endo # 5
Endocrine Pancreas I
Conaway
4/10
4/10
4/11
TU
TU
W
10
11
9
Endo # 6
CC 09
Endo # 7
Endocrine Pancreas II
Clinical Correlation: Diabetic Ketoacidosis
The Thyroid Gland
Conaway
Straub
Conaway
4/12
TH
10
CC 10
Clinical Correlation: Thyroid
Straub
4/12
TH
11
Physiology Lecture
TBA
Exam 4 / Week 16
Date
Day
Time
Lecture
Title
Instructor
4/17
4/18
TU
W
10
10
Endo # 8
Endo # 9
Adrenal Gland I
Adrenal Gland II
Conaway
Conaway
4/19
TH
10
CC 11
Clinical Correlation: Adrenal
TBA
4/19
TH
1-3
PBL 08
Problem Based Learning
Staff
4/20
10
Endo # 10
Male Reproductive Physiology
Gaddy
4/20
Endo # 11
Female Reproductive Physiology I
Gaddy
11
Exam 4 / Week 17
Date
Day
Time
Lecture
Title
Instructor
4/23
10
Endo # 12
Female Reproductive Physiology II
Gaddy
4/24
4/26
TU
TH
10
9
Endo # 13
Neonatal Physiology
Physiology Lecture
Jennings
TBA
4/26
TH
11
CC 11
Clinical Correlation: Reproduction
Kemp
4/26
TH
1-3
PBL 09
Problem Based Learning
Staff
4/27
10
Exam 4 / Week 18
Date
Day
Time
Physiology Review
Lecture
4/30
8-12
8C LAB
5/4
8-12
G-131
Exam 5 / Week 19
Date
Day
Time
5/7
8-12
Title
EXAM 4
NBME REVIEW
Lecture
Title
8C LAB
NBME EXAM
PBL Rooms In Education Building II

B 106
B 108
G 108
G 110
G 112
MEDICAL PHYSIOLOGY SPRING 2007 WEB PAGE

BOOKMARK THIS PAGE AND USE IT TO REACH LECTURE MATERIAL
NEW INFORMATION WILL BE POSTED ON THIS PAGE ONLY
http://www.uams.edu/physiology/MedPhys/MedPhys.htm
12
MUSCLE PHYSIOLOGY
L.E. CORNETT, Ph.D.
13
Title of Lecture: (MUS-1) Mechanisms of Skeletal Muscle Contraction

Instructor: Dr. Lawrence E. Cornett
Biomedical Research Building II 159-2; lcornett@uams.edu;
686-5441
Required Reading:
Medical Physiology, Guyton and Hall; 11th Ed., 2006,

Chapter 6, pp 72-84
Suggested Reading: Diseases of the Skeletal Muscle, Ed., R.L. Wortmann,

Lippincott, Williams and Wilkins, 2000
Objectives:
Describe the relevant cellular structures and proteins involved in muscle
contraction
Describe the events that at the cellular level during the production of the force
Lecture Outline:
I.
Introduction
Muscle typesskeletal, smooth and cardiac
Shared characteristics
II.
Skeletal muscle filaments and associated proteins

Thick filamentmyosin
Thin filamentactin and tropomyosin/troponin complex
III.
Contraction cycle
Sliding filament hypothesis
Ratchet theory of muscle contraction
Biochemical events that occur during a contraction cycle
14
Title of Lecture:
(MUS-2) Functional Properties of Skeletal Muscle

686-5441
Required Reading: Medical Physiology, Guyton and Hall; 11th Ed., 2006,
Chapter 6, pp 72-84
Suggested Reading: Exercise Physiology: Energy, Nutrition and Human
Performance, Eds., W.D. McArdle, F.I. Katch and V.L.
Katch, Lippincott, Williams and Wilkins, 2001
Objectives:
Describe the molecular basis of the length-tension and force-velocity
relationships
Define a motor unit and its functional characteristics
Identify energy sources used to produce ATP for muscle contraction
Classify skeletal muscle fiber types and their functional characteristics
Lecture Outline:
IV.
Mechanical properties of skeletal muscle

Length-tension relationship
Force-velocity relationship
V.
Motor units
The functional unit of a muscle
Motor unit recruitment
VI.
Summation and tetanus

Cumulative effect of repeated stimulation of a muscle
Tetanuselectrophysiological explanation
Treppe or the staircase effect during repetitive stimulation of muscle
contraction
VII.
Energy sources for skeletal muscle contraction

Short-term regeneration of ATP
Anerobicglycolysis
AerobicKrebs Cycle/Oxidative Phosphorylation
VIII.
Skeletal muscle fiber types

Fast twitchGlycolytic (White)
15
Title of Lecture: (MUS-3) The Neuromuscular Junction

686-5441
Chapter 7, pp 85-91
Suggested Reading: Diseases of the Skeletal Muscle, Ed., R.L. Wortmann,
Lippincott, Williams and Wilkins, 2000
Objectives:
Describe the microanatomy of the neuromuscular junction
Explain the mechanism of the end-plate potential and its function in
generating the muscle action potential
Describe the effects and sites of action of drugs and toxins that affect
neuromuscular transmission
Explain the molecular basis of myasthenia gravis
Lecture Outline:
I.
Anatomy and development

Specialized cellular and subcellular structures
Trophic factors that influence neuromuscular junction development
II.
Biosynthesis and metabolism of the neurotransmitter acetylcholine

Synthesisthe key metabolic enzyme is choline-O-acetyltransferase
Degradationacetylcholine esterase terminates the action of released
acetylcholine
III.
Neuromuscular transmission
Ionic basis of the resting membrane or end-plate potential
Nicotinic acetylcholine receptors transduce the signal initiated by
acetylcholine
Excitation-contraction coupling
Latent period
Subcellular structures that carry the action potential to sarcoplasmic
reticulum
Calcium recycling
Miniature end plate potentials
Electrophysiological properties
Physiological function
Pathophysiology
Changes in neuromuscular transmission following motor nerve section
Toxins and other pharmacological agents that act on the neuromuscular
junction
Myasthenia gravis
IV.
V.
VI.
16
Title of Lecture:
(MUS-4) Smooth Muscle

686-5441
Chapter 8, pp 92-100
Suggested Reading: Cellular Aspects of Smooth Muscle Function, Eds., C.Y.
Kao, M.E. Carsten, Cambridge University Press, 1997
Objectives:
Describe the microanatomy of the smooth muscle
Distinguish the functional differences between visceral and multi-unit smooth
muscle
Describe the differences in excitation-contraction coupling between smooth
and skeletal muscle
Lecture Outline:
I.
Structure of smooth muscle

Cellular characteristics favor response to circulating hormones
Individual smooth muscle cells can be functionally linked by gap junctions
II.
Physiology of smooth muscle

Visceral smooth muscle
Multi-unit smooth muscle
III.
Innervation of smooth muscle

Diffuse junctions
Contact junctions
17
CARDIOVASCULAR / EXERCISE
PHYSIOLOGY
M. E. SOULSBY, Ph.D.
M.C. ALLAN, M.D.
R. COKER, Ph.D.
J. WARE, Ph.D.
18
Title of Lecture: (CV-1) Introductory Overview

Instructor: Dr. Michael E. Soulsby
Biomedical 241B-2; MSoulsby@uams.edu;
686-5127
Required Reading: Medical Physiology, Guyton and Hall, 11th Ed., 2006,
Chapter 9; pp. 103-104 and Chapter 14; pp. 161-167.
Suggested Reading: Medical Physiology, Guyton and Hall., 10th Ed., pp. 144-151.
Objectives:
Appreciate the series arrangement of right and left hearts
Appreciate the parallel arrangement of the systemic circulation
Appreciate the blood pressures and oxygen content around the heart
Become familiar with the hemodynamic equivalent of OHMs Law
Learn the relation between blood flow and blood velocity
Lecture Outline:
I. Heart in the Systems Center
A. Pressures
B. Volumes
C. Oxygen Saturations
II. Hemodynamic equivalent of OHMs Law
A. Pressure
B. Flow
C. Resistance
III. Pressures Around the Circuits
IV. Velocities Around the Circuits
19
Title of Lecture: (CV-2) Electrophysiology

686-5127
Chapter 5; pp. 66-68, and Chapter 9; pp. 103-106;
Chapter 10; pp. 116-122.
Suggested Reading: Medical Physiology, Guyton and Hall; 10th Ed., pp. 64-64,
107-112.
Objectives:
Recognize the varied myocardial action potential forms
Know the phases of these action potentials
Associate transmembrane ion movements with phases
Appreciate the importance of the relationship between myocardial electrical
(refractory) and mechanical periods
Differentiate firing frequency from conduction velocity
Lecture Outline:
I.
Myocardial Fibers
II.
Gap Junctions and the Functional Syncytium
III.
Myocardial Fiber Types

A. Fast Response with Phases
B. Slow Response with Phases
IV. Firing Frequency versus Conduction Velocity
20
Title of Lecture: (CV-3) The Cardiac Cycle

686-5127
Chapter 6; pp. 77-78, Chapter 9; pp. 106 - 111.
Suggested Reading: Medical Physiology, Guyton and Hall; 10th Ed., pp. 100
106.
Objective:
Appreciate the events of a cardiac cycle from the perspective of the
electrocardiogram, the phonocardiogram, pressures, volumes, and events.
Become familiar with the cardiac pressure - volume loop.
Lecture Outline:
I.
Physiologic Parameter Relationships
II.
Preload and Afterload
III.
The Cardiac Cycle PressureVolume Loop
21
Title of Lecture: (CV-4) Ventricular Function And Energetics

686-5127
Chapters 9; pp. 110 -114.
Suggested Reading: Medical Physiology, Guyton and Hall, 10th Ed., pp. 99-106.
Objectives:
Appreciate how changes in preload and afterload can influence stroke
volume.
Learn what is described as the cardiac function relationship
Learn the energy requirements of the cardiac function
Lecture Outline:
I.
Use of Starlings Mechanism to develop the Ventricular Function Relationship
II.
Myocardial Energetics
A. Dynamic Work Energetics
B. Static Work Energetics
C. The Law of Laplace
22
Title of Lecture: (CV-5 & 6) Basic Electrocardiography

Instructor: Dr. M. Christian Allan, M.D.
Chief Fellow in Cardiology
Department of Medicine, UAMS
Chapters 11, 12, 13; pp. 123 -157.
Suggested Reading: Medical Physiology, Guyton and Hall, 10th Ed., pp. 114-142.
Objectives:
Learn the concept of a vector
Appreciate the principles of measurement of the vector from the surface of
the organism
Appreciate the relationship between vector and lead
Appreciate the types and locations of leads.
Lecture Outline:
I.
Principles of Voltage Recording in a Volume Conductor
II.
Recording Standards and Conventions
III.
Vector Analysis of ECGs
23
Title of Lecture: (CV-7) Cardiac Output

686-5127
Chapter 20; pp. 232-236; Chapter 20; pp. 243-245.
Suggested Reading: Medical Physiology, Guyton and Hall; 10th Ed.,
pp. 210-221.
Objectives:
Recognize what alters the cardiac function relationship
Appreciate the equality between cardiac output and venous return
Understand the Fick principle for measurement of cardiac output.
Lecture Outline:
I.
Factors Affecting Stroke Volume

A. Preload
B. Afterload
II.
Factors affecting Cardial Output

A. Heart Rate
B. Myocardial Contractility
C. Total Peripheral Resistance
III.
Measurement of Cardiac Output

A. Ficks Principal
B. Thermodilution
24
Title of Lecture: (CV-8) The Peripheral Vascular System

686-5127
Chapters 15; pp. 171 -180.
Suggested Reading: Medical Physiology, Guyton and Hall 10th Ed., pp. 152-160.
Objectives:
Appreciate what is meant by compliance
Learn the various arterial pressures
Learn the changes in flow velocity from central to peripheral arteries and back
through veins
Lecture Outline:
I.
Arterial Wall Compliance

A. Hydraulic filter
B. Changes with Aging
C. Arteries Versus Veins
II.
Arterial Pressures
A. Systolic
B. Diastolic
C. Pulse
D. Mean
III.
Arterial Pressure Regulation
IV.
Regional Velocity of Blood Flow
25
Title of Lecture: (CV-9) Arterial Blood Pressure Regulation

686-5127
Required Reading: Medical Physiology, Guyton and Hall, 11th Ed., 2006.
Chapter 17, pp. 195-203 ; Chapter 18, pp. 204 214;
Chapter 19, pp. 216-231.
Suggested Reading: Medical Physiology, Guyton and Hall, 10th Ed.;
pp. 184-193,195-208.
Objectives:
Appreciate the factors regulating arterial blood pressure
Recognize the temporal relationship of these factors
Recognize the relative gains of these factors
Lecture Outline:
I. Arterial mean pressure regulation
A.
Chemoreceptors
B. Volume Receptors
C. Dual Innervation & Negative Feedback
D. Endocrine Regulation
1. Renin Angiotensin Aldosterone
2. Atrial Natriuretic Factor
II. Integration of Mechanisms
A.
In time
B.
Relative gains
26
Title of Lecture: (EX-1) Cardiovascular Responses to Exercise.

Instructor: Robert Coker, Ph.D.
Center on Aging, CokerRobert@uams.edu
526-5707
Required Reading: Guyton and Hall, Textbook of Medical Physiology, 11th Ed.,
2006. Chapter 21, pp. 246-249.
Supplemental Reading: Physiology of Sport and Exercise, 2nd Ed., 1999. Eds.:
Wilmore and Costill, Human Kinetics.
Textbook of Work Physiology, 4th Ed., 2003. Eds.:
Astrand, Rodahl, Dahl, and Stromme, Human Kinetics.
Human Cardiovascular Control, 1993. Ed.: Rowell, Oxford
University Press.
Objectives:
Describe the Fick principle and the concept of oxygen uptake during rest and
exercise
Describe the methodologies used to measure oxygen uptake during exercise.
Describe the components of oxygen uptake and how they change with
exercise training.
Describe the influence of posture and gravity on the cardiovascular
responses to exercise.
Lecture Outline:
I. Fick principle of oxygen uptake
Submaximal
Maximal
II. Measurement of the energy cost of exercise
Direct
Indirect
III. Changes in the components of oxygen uptake with exercise
Maximal oxygen consumption
Oxygen requirement
Blood volume
Heart rate
Stroke volume
Cardiac output
Arteriovenous difference
Comparison: Untrained, Trained, and Mitral Stenosis
IV. Postural and gravitational influences on the cardiovascular system
Rest
Exercise
27
Title of Lecture: (EX-2) Skeletal Muscle Responses and Fuel Use During Exercise.
Instructor: Robert Coker, Ph.D.
Center on Aging, CokerRobert@uams.edu
526-5707
Required Reading: Guyton and Hall, Textbook of Medical Physiology, 11th Ed.,
2006. Chapter 84, pp 1055-1066.
Supplemental Reading: Physiology of Sport and Exercise, 2nd Ed., 1999. Eds.:
Wilmore and Costill, Human Kinetics.
Textbook of Work Physiology, 4th Ed., 2003. Eds.:
Astrand, Rodahl, Dahl, and Stromme, Human Kinetics.
Objectives:
Describe the concept of classification of muscle by fiber type and their
associated characteristics.
Describe the general adaptations of muscle to increased and decreased
activity.
Describe the fuel stores in the body available for energy expenditure during
exercise.
Describe the response to feeding during and between exercise bouts.
Lecture Outline:
I. Skeletal muscle fiber types
Type I
Type IIa
Type IIx
II. Skeletal muscle responses to activity
Aerobic training
Strength training
Disuse or immobilization
III. Fuel stores in the body
Carbohydrate
Fat
Protein
IV. Fuel use during exercise
Effects of feeding during exercise
Effects of feeding before and after exercise
28
Title of Lecture: (CV-12) Hemodynamics

Instructor: Dr. Jerry Ware
Biomedical Research Building II, 263-2; jware@uams.edu;
526-6096
Chapter 14, pp. 161 170.
Objectives:
Learn factors regulating blood velocity
Appreciate the hemodynamic equivalent of OHMs Law
Learn the Poiseuille Equation
Calculate resistance to flow in parallel and series circuits
Learn the significance of murmurs, turbulence and bruits
Lecture Outline:
I.
Factors Affecting Velocity of Blood Flow

A. Poiseuille-Hagan Relationship
II.
Factors Affecting Resistance to Flow

A. Series circuits
B. Parallel circuits
III.
Turbulence
C. Reynolds Factors
D. Murmurs
E. Bruits
29
Title of Lecture: (CV-13) The Microcirculation

526-6096
Required Reading: Medical Physiology, Guyton & Hall, 11th Ed.
Chapter 16 pages 181 194 The Microcirculation and the
lymphatic system: capillary fluid exchange, interstitial fluid and
lymph flow
Objectives:
1. Understand the capillary structure critical to function
2. Understand the forces that regulate capillary filtration and reabsorption
3. Understand the role of the lymphatic system in controlling interstitial fluid
protein concentration, interstitial fluid volume and the interstitial fluid
pressure
Lecture Outline:
I. Structure of the microcirculation and capillary system
II. Exchange of water, nutrients, and other substances between the blood and
interstitial fluid
III. Fluid filtration across capillaries and the forces involved
IV. Lymphatic System
30
Title of Lecture: (CV-14) Blood coagulation, Hemostasis and Thrombosis

526-6096
Required Reading: Medical Physiology, Guyton & Hall, 11th Ed.
Chapter 36 pages 457 - 468 Hemostasis and Blood
Coagulation
Objectives:
1.
To distinguish between hemostasis and thrombosis
2.
To understand the differing contributions of coagulation and plateletmediated hemostasis to the arrest of blood flow
3.
To define the temporal sequence of events that constitutes the platelet

functional triad (adhesion, activation and aggregation) and the
consequences of thrombocytopenia or aspirin ingestion
4.
To distinguish between the intrinsic and extrinsic pathways of blood

coagulation
5.
To understand the importance of vitamin K for blood coagulation and

the effects of Coumadin (warfarin)
6.
To have a brief understanding of the importance of the following

proteins for hemostasis; collagen, von Willebrand factor, integrins,
fibrinogen, fibrin, factor V, factor V (Leyden), factor VIII, factor IX, and
thrombin
7.
To understand the importance of fibrinolysis in blood coagulation,

specifically tissue plasminogen activator (TPA), protein C, protein S,
antithrombin III and heparin
Lecture Outline:
I.
The temporal sequence of events leading to hemostasis
II.
The role of the platelet in hemostasis and thrombosis
III.
The protease-mediated events of blood clotting
IV.
The fibrinolytic system and its relevance to coagulation
V.
The molecular basis of bleeding disorders
31
Title of Lecture: (CV-15) Venous Return

686-5127
Chapter 20, pp. 238 243.
Suggested Reading: Medical Physiology, Guyton and Hall, 10th Ed.,
pp. 215-220.
Objectives:
Appreciate the development of the vascular function (venous return)
relationship
Learn those factors influencing the basic relationship
Appreciate factors regulating venous return
Lecture Outline
I.
Development of the Vascular Function Relationship
II.
Factors Affecting the Relationship

A. Vasoconstriction
B. Venoconstriction
C. Skeletal Muscle Pump
D. Respiration
32
Title of Lecture: (CV-16) Cardiovascular Intrinsic and Extrinsic Control

686-5127
Chapter 17, 18, 19 ; pp. 195 -231.
Suggested Reading: Medical Physiology, Guyton and Hall, 10th Ed.,
pp. 175-182, 253-263.
Objectives:
Become familiar with local factors regulating vascular control
Appreciate characteristics of flow through special tissues
Lecture Outline:
I. Intrinsic Factors
A. Local tissue Metabolism
B. Properties of Vascular Muscle
C. Humeral Control
D. Ionic Control
II. Special Circulations
A. Kidney
B. Brain
C. Coronary
D. Splanchnic
E. Skin
F. Lung
33
Title of Lecture: (CV-17) Cardiovascular Pathophysiology

686-5127
Chapter 20; pp. 234-238; Chapter 22, 23, 24 ; pp. 258 -288.
Suggested Reading: Medical Physiology, Guyton and Hall 10th Ed., 203-206,
229-262.
Objectives:
Apply what you have learned to pathological states:
Heart failure
Low pressure shock
High pressure hypertension
Know the types of:
Shock
Hypertension
Heart failure
Lecture Outline:
I. Shock
A.
B.
C.
D.
E.
Reversible
Irreversible
Types (Causes)
Hypertension
Types
II. Goldblatt Models

A. Heart Failure
B. Cardiac Function Changes
C. Vascular Function Changes
D. Combined Functional Changes
34
RESPIRATORY
PHYSIOLOGY
M.L. JENNINGS, Ph.D.
35
Title of Lecture: (Resp.-1) Airways; Ventilation; Properties of Gases

Instructor: Dr. M.L. Jennings
Biomedical 209-2; JenningsMichaelL@uams.edu
296 - 1438
Reading Assignment: Guyton and Hall 11th Edition pp. 475-482; 491-494
Additional Reading: West pp. 1-18; 89-116
Vander pp. 463-467; 475-477
Rhoades and Tanner, pp. 309-311;313-314; 316-318;
319-322
Objectives
Understand the functions of conducting airways.
Know the definitions of lung volumes and capacities.
Understand the meaning of anatomic dead space and its effect on alveolar
ventilation.
Understand the meaning of partial pressure and gas solubility.
Understand the principles governing diffusion of a gas between air and liquid.
Lecture Outline
Functions of conducting airways:
Conduct air in and out of alveoli
Warm, humidify inspired air
Remove inspired particulates by filtration, impaction, mucociliary escalator
Geometry of conducting airways
Pulmonary Volumes: Inspiratory Reserve, Tidal, Expiratory Reserve, Residual
Pulmonary Capacities (Sums of Volumes):
Total Lung Capacity
Vital Capacity
Functional Residual Capacity
Effect of Anatomic Dead Space on Alveolar Ventilation
Each inspired breath, new air to alveoli = Tidal Vol. Anat. Dead Space
Properties of Gases
Gas Law PV = nRT applies to each gas in mixture, e.g., PO2 = nO2RT/V
Partial pressure difference drives diffusion between gas and liquid
Gas Solubility: Dissolved gas conc. = Partial pressure x solubility coeff.
36
Title of Lecture: (Resp.- 2) Pulmonary Gas Exchange; O2 Transport

296 - 1438
Reading Assignment:
Guyton and Hall 11th Edition pp. 492-499; 502-503
Additional Reading: West pp. 21-30

Vander et al. pp. 501-509
Rhoades and Tanner, pp. 309-311; 322-323; 350-355
Objectives
Know the relationships among O2 content, partial pressure, total Hb, and
saturation.
Know the events that take place during diffusion of O2 from air to pulmonary
capillary blood.
Understand the effect of alveolar ventilation on alveolar gas composition.
Know the relationship (alveolar gas equation) among inspired PO2, PACO2,
and PAO2.
Lecture Outline
Diffusion of O2 from air to blood
Diffusion of O2 into alv. capillary (equilib. when PO2 in air and blood equal)
Diffusion of O2 into RBC and binding to hemoglobin (4 steps)
Saturation vs PO2 is sigmoid (positive cooperative) relationship.
P50 is PO2 at 50% Saturation; P50 increased by:
High temp, low pH, high CO2, high 2,3-bisphosphoglycerate (2,3-DPG)
Pulse oximeter measures Saturation (%), not the amount (content) of O2
Oxygen content (ml O2/100 ml blood) depends on
Saturation (which depends on PO2 and dissociation curve)
Total concentration of Hb (g Hb/100 ml blood)
Rate of Diffusion from air to blood:
Proportional to surface area of barrier
Inversely proportional to thickness of barrier
Both PO2 and PCO2 reach equil. with air by the time blood is ~ 1/3 through capillary
Steady state:
PACO2 = 40; PAO2 = 100 mm Hg (only minor fluctuations breath to breath)
(PACO2)x(Alveolar Vent.)/760 = Rate of CO2 Production (ml/min)
If Ventilation decreases, PACO2 increases and PAO2 decreases
37
Title of Lecture: (Resp.- 3) Tissue Gas Exchange; CO2 Transport

296 - 1438
Reading Assignment:
Guyton and Hall 11th Edition pp. 503-513

Vander pp. 483-490
Rhoades and Tanner pp. 354-355; 357-358
Objectives
Understand the relationship (Fick Principle) among blood flow, arterial O2
content, venous O2 content, and O2 consumption.
Understand the effect of the HbO2 dissociation curve on tissue O2 delivery.
Know the various forms of CO2 in blood.
Know the relationship between CO2 content and PCO2 in arterial and venous
blood.
Understand the relationship between the Bohr effect and Haldane effect.
Lecture Outline
Mitochondrial PO2 of only ~ 3-5 mm Hg needed for maximal respiration
Blood PO2 must be much higher than 3-5 mm Hg because of diffusion gradient
High arterial PO2 does not, by itself, ensure adequate tissue oxygen supply
Factors important for tissue oxygenation:
O2 consumption and blood flow. Fick : VO2 = O2 Conta-v x Blood flow
Arterial PO2
HbO2 Dissociation curve (ability of Hb to release O2 at high PO2)
Different tissues have very different local (capillary and venous) PO2
Mixed venous PO2 is about 40 mm Hg; weighted average of all venous return
Two safety factors in Dissociation curve:
Flat at high PO2 ensures nearly complete loading in lungs
Steep portion at PO2 < 40 to ensure more O2 delivery for small drop in PO2
Many conditions cause abnormal O2 content vs. PO2
Anemia
Genetic Hb variant with shifted P50
CO poisoning (more in Lecture 9)
Blood doping (high Hct.)
Cyanide poisoning does not interfere with Hb but instead blocks O2 use
38
Title of Lecture: (Resp.-4) Muscles of Breathing; Pulmonary Pressures

296 - 1438
Reading Assignment: Guyton and Hall 11th Edition pp. 471-475
Additional Reading: West pp. 1-18; 89-116;
Vander pp. 467-473
Rhoades and Tanner, pp. 312-316; 326-330
Objectives
Identify the muscles of inspiration and expiration.
Know the reasons for the collapse tendency of the lung and the significance
of pulmonary surfactant.
Know the definitions and relationships among pleural, alveolar, and
transpulmonary pressures.
Understand the effects of muscle paralysis on the maximum inspiratory and
expiratory pressures.
Lecture Outline
Muscles of breathing
Inspiration: Diaphragm, External Intercostals, other accessory muscles
Expiration: Internal Intercostals, abdominals
Collapse tendency of lung:
Elastic fibers
Surface tension
Surface tension normally minimized by presence of pulmonary surfactant
Surfactant secreted by type II alveolar epithelial cells, late in gestation
Inadequate surfactant causes infant respiratory distress syndrome
Mechanical pressures in lung are all expressed relative to atmospheric
Pleural pressure Ppl (normally negative, i.e., subatmospheric)
Alveolar pressure PA (negative during inspiration, positive during exp.)
Transpulmonary Ptp = PA Ppl (pressure that determines lung inflation)
Examples: pressures generated by positive and negative pressure ventilators
Function of resp. muscles can be tested by measuring max. insp., exp. pressures
39
Title of Lecture: (Resp.- 5) Lung Compliance, Thorax Compliance; Airway

Resistance
296 - 1438
Reading Assignment: Guyton and Hall 11th Edition pp. 473; 478-481
Additional Reading: West pp. 1-18; 89-116;
Vander pp. 472-475;
Rhoades and Tanner pp. 323-326;330-331
Objectives
Know the definitions of lung and thorax compliance.
Understand the definition of the compliance of the lungs and thorax combined.
Know the changes in pleural pressure and alveolar pressure that take place
during normal breathing.
Know the factors that influence airway resistance.
Be able to distinguish between compliance work and resistance work of
breathing.
Lecture Outline
Lung compliance, CL = Volume/ Ppl; signs are defined to make CL positive
At high lung volume, CL is low (lung is stiffer and harder to expand further)
Gravity affects degree of inflation of vertical lung:
At apex, Ptp is higher, and local compliance is lower, than at base
Thorax wall also has compliance (similar to lung compliance at FRC)
Compliance of lung/thorax combined: 1/CCombined= 1/CL + 1/CThorax
Pneumothorax (air in lung): Lung collapses and thorax springs outward
Airway Resistance: Ohms Law, Force = Flow X Resistance
Driving force for airflow is Alveolar Pressure, so Airway R = Flow/PA
As is true of compliance, airway resistance is always a positive number
Laminar vs turbulent Flow
Flow is laminar (layered) when velocity is low, as in smaller airways
Flow is turbulent at higher flow rates, as in upper airway
Main sites of resistance are nose and large to medium bronchi (turbulent flow)
If lung volume increase, airway resistance decreases because caliber increases
Many factors influence airway resistance via effects on bronchial smooth muscle:
Beta adrenergic agonists, nitric oxide cause relaxation, R decreased
Cholinergic agonists, histamine, PGF2: contraction, R increased
Resistance Work of Breathing: Minimized by slow breathing
Compliance Work of Breathing: Minimized by shallow breathing
40
Title of Lecture: (Resp.- 6) Regulation of Breathing

296 - 1438
Reading Assignment:
Guyton and Hall 11th Edition pp. 514-523
Additional Reading: West pp. 117-132;136-140
Vander pp. 490-498; 500
Rhoades and Tanner pp. 363-374
Objectives
Identify the major centers in brain that are responsible for regulation of
breathing.
Know the locations and functions of central and peripheral chemoreceptors.
Know the integrated ventilatory responses to changes in arterial PO2 and PCO2.
Know the main features of Cheyne-Stokes breathing.
Know the mechanisms of effects of high altitude on ventilation.
Lecture Outline
Respiratory Centers (Brain Stem)
Pontine Respiratory Group (Pneumotactic Center, Apneustic Center)
Medullary Respiratory Centers (Central Pattern Generator)
Ventral Respiratory Group (VRG)
Dorsal Respiratory Group (DRG)
Central Inspiratory Activity Integrator
Input from inspiratory off-switch neurons and chemoreceptors
Normal output is inspiratory ramp, followed by termination of insp.
Pulmonary receptors: Stretch, Irritant, C-fiber (Juxtacapillary)
Central Chemoreceptors
Not stimulated by hypoxia
Respond to local (interstitial fluid and CSF) H+, which depends on PaCO2
If PaCO2 increases, central chemoreceptors stimulated and VA increases
Peripheral chemoreceptors (carotid and aortic bodies)
Stimulated by low pH and/or low PaO2, esp. PaO2 below ~80 mm Hg
Solely responsible for stimulation of breathing during hypoxemia
Response is to PaO2, not O2 content; insensitive to anemia or CO
Integrated responses
Response to low O2 and high CO2 (low pH) are interdependent
If PaO2 is low, response to high CO2 is exaggerated
Examples of regulation of breathing under special circumstances
Sleep, High altitude, Periodic breathing, Oxygen therapy, Exercise
41
Title of Lecture: (Resp.-7) Pulmonary Blood Flow; Fluid Balance

296 - 1438
Vander pp. 399-400; 465-466; 500
Rhoades and Tanner, pp. 337-345
Objectives
Know the major similarities and differences in blood pressures and vascular
resistances between pulmonary and system circulations.
Understand the effect of gravity on regional blood flow in the vertical lung.
Learn the factors influencing pulmonary vascular resistance.
Understand the factors regulating fluid balance in the lung.
Learn the major metabolic functions of the pulmonary circulation.
Lecture Outline
Blood pressures in the pulmonary circuit: much lower P than systemic
Pulmonary wedge pressure: Estimates left atrial pressure
Pulmonary vascular resistance much lower than systemic
If cardiac output increases, pulm. vasc. R decreases, for two reasons
Recruitment of new open vessels
Distension of previously open vessels
Low pressure implies that gravity has major effect on blood distr. in lung
Very low flow at apex of upright lung
Hypoxic Vasoconstriction: Observed only in the pulmonary circuit
Effect of lung volume on pulmonary vascular resistance R
Increasing or decreasing lung volume increases total pulm. vasc. R
Low volume: R high in larger (extra-alv.) vessels, loss of radial traction
High lung volume: R high in small (alveolar) vessels
Fluid exchanges in pulmonary capillaries
Same principles (Starling forces) apply as in systemic circulation
Imbalance between capillary fluid filtration and lymph removal: Edema
Edema caused by High capillary Pressure, high capillary permeability, loss of
surfactant, severe hypoxia, lymphatic blockage
Functions of pulmonary circulation other than gas exchange
Filtration to prevent emboli from reaching brain, other organs
Metabolic functions: Hormone removal; conversion of angiotensin by ACE
42
Title of Lecture: (Resp.-8) Ventilation/Perfusion Relations (Air/Blood Matching)

296 - 1438
Vander p. 483
Rhoades and Tanner pp. 346-348; 359-361
Objectives
Understand that the ratio of ventilation to perfusion determines local gas
composition.
Understand the effect of air-blood mismatch on the alveolar to arterial (A-a)
PO2 difference.
Know the distinction between absolute and physiologic (right to left) shunt.
Understand the reason why air-blood mismatch has a larger effect on arterial
O2 than on CO2.
Know the definition of physiologic dead space.
Lecture Outline
Normally there is only a small alveolar to arterial (A-a) PO2 gradient
In many pulmonary diseases, there is a large A-a PO2 gradient
Cause of A-a PO2 gradient is usually regional mismatch between ventilation (VA) and
blood flow (perfusion, Q)
Local PO2 in lung depends on the ratio of ventilation to perfusion
VA/Q high (> 0.8), PO2 > 100; PCO2 < 40
VA/Q low (< 0.8), PO2 < 100; PCO2 >40
Blood from poorly ventilated parts of the lung cause PaO2 to be low (A-a gradient)
Extreme example of VA/Q mismatch: absolute right to left shunt:
Systemic venous blood mixes with arterial; Venous admixture lowers PaO2
Bronchial circulation normally causes ~ 2% absolute shunt
Less extreme: regions with very low (but not zero) VA/Q: physiologic shunt
Still causes low PaO2 and A-a PO2 gradient
Breathing pure O2 has large effect on PaO2 in physiologic shunt
Overventilating rest of lung does not correct low PaO2 caused by local low VA/Q
VA/Q mismatch has only minor effect on PaCO2
Normal vertical lung has small VA/Q mismatch because of effect of gravity on Q
Physiological dead space (wasted ventil.): Caused by regions with high VA/Q
Sometimes (e.g., pulmonary embolism), there will be large physiologic shunt and
physiologic dead space present at the same time.
43
Title of Lecture: (Resp.-9) Pulmonary Pathophysiology

296 - 1438
Additional Reading: Rhoades and Tanner pp. 318-319; 331-334; 355-356; 358-361
West pp. 133-149
Vander pp. 498-499
Objectives
Understand the conditions that can cause arterial hypoxemia, tissue hypoxia,
and elevated tissue CO2.
Know the factors that determine PAO2, the A a PO2 difference and the a-v PO2
difference.
Understand the nature of carbon monoxide poisoning and the effects of
maternal CO on oxygen delivery in the fetal circulation.
Understand the use of the forced expiration test and the information derived
from this test.
Know the potential dangers of O2 therapy.
Lecture Outline
Resp. muscles, lung and pulmonary circulation normally maintain PaO2, PaCO2
Hypoventilation causes low PAO2 and low PaO2 but does not increase A-a gradient
Hypoventilation always causes elevated PACO2 and PaCO2 (hypercapnia)
Other causes of hypoxemia, none of which cause major hypercapnia:
Diffusion impairment (pure diffusion impairment is unusual)
V/Q mismatch (always causes increased A-a PO2 gradient):
Absolute shunt
Physiologic shunt (underventilated parts of lung, VA/Q very low)
Pulmonary embolism (part of lung with VA/Q extremely high)
Tissue hypoxia can be present even if PaO2 is normal; low tissue PO2 caused by:
Inadequate blood flow relative to metabolic demand (Fick Principle)
Left-shifted hemoglobin (need more PO2 drop to release O2
Anemia (if not compensated by increased blood flow)
Carbon monoxide poisoning (less total O2 and also left-shift)
Forced Expiration Test
FEV1 is volume of air expired in 1 sec at max effort
Normally FEV1 is about 80% of FVC (forced vital capacity)
Forced expiration text characterized by flow-volume loop
During forced expiration, dynamic airway collapse limits airflow
Hazards of oxygen therapy
Removal of ventilatory drive in patients with COPD
Absorption atelectasis (collapse) is more rapid when breathing high O2
44
RENAL / ACID BASE

PHYSIOLOGY
R. KURTEN, Ph.D.
R. SAFIRSTEIN, M.D.
P. WIGHT, Ph.D.
45
Title of Lecture: (Renal 1) Body Fluid Compartments

Instructor: Richard C. Kurten, Ph.D.
Biomed B212C; KurtenRichardC@uams.edu
686-8269
Required Reading: Medical Physiology 11th ed., Guyton and Hall;
Chapter 25
Objectives
Identify the body water compartments and understand the nature of fluid
shifts between them
Use the indicator dilution method to measure the size of different body
water compartments
Calculate fluids shifts after infusion of different solutions
Understand clinical conditions that are associated with fluid shifts
Understand the nature and sources of edema
Lecture Outline
Fluid intake and output are balanced at steady state
Sources of water
Water losses
Body fluid compartments
Intracellular fluid
Extracellulular fluid: interstitial fluid, plasma
Measuring body fluid compartment volumes by indicator dilution
Fluid shifts between compartments
Osmosis and osmotic pressure
Concept of osmotic equilibrium
Osmolarity of body fluids
Isotonic, hypotonic, hypertonic fluids
Isosmotic, hyperosmotic, hypo-osmotic fluids
Calculating fluid shifts after infusion of:
Isotonic saline
Hypertonic saline
Hypotonic saline
46
Hyponatremia and hypernatremia

Hypo-osmotic dehydration (contraction): Diarrhea, Vomitting, Overuse of
diuretics, Addisons disease
Hypo-osmotic overhydration (expansion): Excessive secretion of argninine
vasopressin
Hyperosmotic dehydration: diabetes insipidus, excessive sweating
Hyperosmotic overhydration: Cushings disease, primary aldosteronism
Edema
Intracellular edema
Extracellular Edema
Factors that increase capillary filtration
Lymphatic blockage
Some conditions that cause edema
Heart failure
Decreased renal excretion of salt and water
Decreased plasma proteins
Safety factors that prevent edema
Low compliance of the interstitium in the negative pressure range
Increased lymph flow
Washdown of interstitial fluid protein
Edema in potential spaces is called effusion: ascites
47
Title of Lecture: (Renal 2) Renal Anatomy and Function

686-8269
Required Reading: Medical Physiology 11th ed., Chapter 26
Objectives
Know the functions of the kidneys
Review gross and microscopic anatomy of the kidneys
Understand the micturition process
Know the basic renal processes
Understand how renal blood flow and glomerular filtration are
autoregulated
Lecture Outline
Functional Renal Anatomy
The nephron is the basic unit of renal structure and function
Not all nephrons are alike
The kidneys have a rich blood supply and innervation
Micturition
Physiologic anatomy and connections of the bladder
Ureters transport of urine from the kidney into the bladder
The cystemetrogam plots pressure in the bladder as it fills and shows pressure
waves caused by micturition reflexes
Abnormalities of micturition
Atonic bladder
Automatic bladder
Uninhibited neurogenic bladder
The formation of urine
Urine is formed by the combined effect of filtration, reabsorption and
secretion
Large amounts of solutes are filtered and then reabsorbed for rapid
homeostasis
48
The formation of urine: Step 1. Glomerular Filtration

Glomerular filtration rate (GFR), filtration fraction and the filtered load
The glomerular filtration barrier has three layers
Size, shape and electrical charge affect the filterability of macromolecules
GFR is determined by Starling forces
The pressure profile along a glomerular capillary is unusual
Several factors can affect GFR
The glomerular ultrafiltration coefficient
Glomerular capillary hydrostatic pressure
Hydrostatic pressure in Bowmans capsule
Glomerular capillary colloid osmotic pressure
Renal Blood Flow
The kidneys have a high blood flow
Blood flow is higher in the renal cortex than in the renal medulla
The kidneys autoregulate GFR and blood flow
Renal sympathetic nerves and various hormones change renal blood
flow
Importance of autoregulating GFR in preventing extreme changes in renal
excretions
Tubuloglomerular feedback and the juxtaglomerular apparatus
Macula densa feedback mechanism
Myogenic autoregulation of renal blood flow and GFR
Effects of a high protein diet and elevated blood glucose on renal blood
flow and GFR
49
Title of Lecture: (Renal 3) Tubular Fluid Processing

686-8269
Required Reading: Medical Physiology 11th ed., Chapter 27, pages 327-339
Objectives
Understand the mechanisms for transport across the tubule epithelium
Describe the major transport process occurring at each part of the tubule
Understand the Starling forces responsible for peritubular capillary
reabsorption and how they relate to those responsible for glomerular
filtration
Understand the mechanisms for pressure diuresis and natriuresis
Lecture Outline
The formation of urine: Step 2. Tubular processing of the glomerular filtrate
Key Concept: Excretion = Filtration Secretion + Reabsorption
Tubular reabsorption is selective and quantitatively large
Mechanisms for tubular reabsorption
Transcellular and paracellular routes
Primary active transport
Secondary active transport
Glucose
Amino acids
Hydrogen ions
The transport maximum describes the rate at which a substance can be
transported
Graphical description of renal glucose handling (Figure 27-4)
Water reabsorption is passively coupled to sodium reabsorption
Reabsorption of other solutes by passive diffusion
Tubular secretion
Transport along the tubule
Transport in the Proximal Tubule
The proximal convoluted tubule reabsorbs about 65% of the
filtered load of sodium and water
Proximal tubular fluid is essentially iso-osmotic to plasma
Contransporters reabsorb glucose and amino acids
The proximal tubule secretes organic acids and bases
50
Tubular transport in the loop of Henle

Descending and ascending limbs differ in water permeability
The luminal cell membrane of the thick ascending limb contains
a 1-Na+, 2-Cl-, 1-K+ co-transporter that is the target for the
powerful loop diuretics
Tubular transport in the distal nephron
The luminal cell membrane of the distal convoluted tubule
contains a Na+, Cl- cotransporter
Late distal tubule and cortical collecting tubule
Composed of intercalated cells and principal cells
Principal cells reabsorb sodium and secrete potassium in
response to aldosterone and other factors
Water reabsorption is regulated by vasopressin to regulate the
degree of urinary concentration or dilution
Medullary Collecting Ducts
Water reabsorption is regulated by vasopressin to regulate the
degree of urinary concentration or dilution
Capable of secreting hydrogen ions against a large
concentration gradient
Glomerulotubular balance: Where do the transported fluids and solutes
go?
Starling forces in the peritubular capillaries and the renal
interstitial fluid
Regulation of peritubular capillary Starling forces
Pressure natriuresis and pressure diuresis mechanisms
51
Title of Lecture: (Renal 4) Controlling and Measuring Renal Function

686-8269
Objectives
Understand the hormones that regulate renal function and their
mechanisms of action
Understand the clearance concept and how it is used to calculate GFR and
renal blood flow
Use the clearance concept to determine if a compound undergoes net
secretion or reabsorption by the kidney
Lecture Outline
Hormonal control of tubular reabsorption
Angiotensin II is a potent vasoconstrictor that also increases Na+ and
water reabsorption
Aldosterone increases Na+ reabsorption and increases K+ secretion
Vasopressin increase water reabsorption
Atrial natriuretic peptide decreases sodium and water reabsorption
Parathyroid hormone increases calcium reabsorption and reduces
phosphate reabsorption
Sympathetic nervous system activation increases sodium reabsorption
Using clearance methods to quantify kidney function
The clearance rate equation
Inulin clearance as an estimate of GFR
Creatinine clearance and plasma creatinine concentration as estimates of
GFR
Applying the Fick principle to PAH handling
Using PAH clearance to estimate renal plasma flow
Use the hematocrit to convert plasma flow to blood flow
Calculating the filtration fraction
Calculating tubular reabsorption or secretion rates from clearances
Fractional excretion can be used clinically to understand what the kidney is doing.
52
Title of Lecture: (Renal 5) Renal Concentrating and Diluting Mechanisms

686-8269
Objectives
Understand how the kidney produces a dilute urine
Know the relation between cortico-medullary osmotic gradient in the
interstitium and concentrating ability
Understand the concept of active countercurrent multiplication
Know how NaCl reabsorption in the thick ascending limb of the loop of
Henle relates to formation of concentrated and dilute urine
Know how and where arginine vasopressin (AVP) acts on the nephron
Know what is meant by passive countercurrent exchange in the vasa
recta
Know the role of urea in the formation of concentrated urine
Understand the concepts of osmolar and free-water clearance
Lecture Outline
Renal mechanism for excreting a dilute urine
Rapid diuresis follows the ingestion of a large volume of water
Tubular fluid remains iso-osmotic in the proximal tubule (~300 mOsm/L
Tubular fluid becomes dilute in the ascending loop of Henle (~100
mOsm/L)
In the absence of vasopressin, tubular fluid is further diluted in the distal
and collecting tubules (~50 mOsm/L)
Renal mechanism for concentrating urine
Obligatory urine volume
Requirements for excreting a concentrated urine: vasopressin and
hyperosmotic medullary interstitium
The countercurrent multiplier mechanism produces the hyperosmotic
medullary interstitium
countercurrent flow in the loop of Henle
differential permeability of the loop of Henle and collecting
tubules/ducts to water, NaCl and urea
critical role of the 1 Na+- 2 Cl--1 K+co-transporter
53
Relative contribution of the distal tubule and the collecting ducts

Urea contributes significantly (40-50%) to the interstitial hyperosmolality
Countercurrent arrangement of the vas recta preserves hypertonicity
Mechanism of action for vasopressin
Using clearance to quantify urine concentration and dilution
Osmolar clearance
Free water clearance
54
Title of Lecture: (Renal 6) Regulation of extracellular fluid osmolarity and Na+

concentration
686-8269
Objectives
Know how changes in plasma osmolality influence the release of vasopressin
Know how changes in blood volume or blood pressure influences
vasopressin release
Know some stimuli that arouse thirst
Know what is meant by diabetes insipidus and how to distinguish between
central and nephrogenic forms
Lecture Outline
Extracellular fluid sodium concentration and osmolarity are tightly linked
Relationship between sodium concentration and extracellular fluid osmolarity
At steady-state, water input and output are equal
Arginine vasopressin is critical in the control of renal water output and
plasma osmolality
Factors affecting AVP release
Osmoreceptor-ADH feedback mechanism
Cardiovascular reflexes
Other stimuli
Interaction between stimuli affecting AVP release
Habit and thirst govern water intake
CNS centers for thirst
Stimuli for thirst
Osmolar threshold for thirst
Integration of the osmoreceptor-ADH and thirst mechanisms in controlling ECF
osmolarity
Disorders of urinary concentrating ability
Central diabetes insipidus: inappropriate vasopressin secretion
Nephrogenic diabetes insipidus:
Defects in the countercurrent mechanism
Inability of the kidney to respond to vasopressin
Administration of vasopressin can be used to distinguish between central
and nephrogenic diabetes insipidus
55
Title of Lecture: (Renal 7) Electrolyte Balance

Instructor: Robert Safirstein, M.D.
VA6A116; SafirsteinRobertL@uams.edu
257-5866
Objectives
Understand how the kidneys handle potassium and factors that
influence potassium excretion
Understand how the kidney regulates plasma [Mg++]
Understand how PTH regulation of TMP04 regulates plasma phosphate
levels
Know the tubular mechanisms for reabsorption of Na+ and the relative
amounts reabsorbed by each nephron segment
Know the concept of glomerulotubular balance as it pertains to Na+
Know the factors that influence Na+ excretion
Know the mechanisms that detect and respond changes in volumes of
ECF and blood.
Know what stimuli causes release of renin and how renin is related to
sodium balance
Know what stimulates secretion of atrial natriuretic peptide (ANP) and
possible actions of ANP
Know how GFR, Starling forces and endocrine mechanisms are
integrated to adjust renal Na+ excretion
Lecture Outline
Regulation of potassium excretion and extracellular K+ concentration
Special problems related to the predominantly (98%) intracellular
distribution of K+
Factors regulation the internal distribution of K+
Insulin
Aldosterone
-adrenergic stimulation
acid-base abnormalities
cell lysis, strenuous exercise
increased extracellular fluid osmolarity
Potassium secretion by principal cells
Cellular mechanisms
Na+-K+-ATPase
Luminal K+ channel (ROMK)
Factors regulating K+ secretion
Stimulated by increased extracellular fluid K+
Stimulated by aldosterone
Stimulated by increases in tubular flow
56
Reduced by acidosis
Potassium reabsorption by intercalated cells
Changes in Na+ excretion do not change K+ excretion
Regulation of renal calcium excretion and extracellular Ca++ concentration
Regulation of renal phosphate excretion
Overflow mechanism
PTH suppresses Tm for phosphate to enhance excretion
Regulation of renal magnesium excretion and extracellular Mg++
concentration
Integration of mechanism for salt and water balance
Two major sensors
Mean arterial pressure
Retain sodium when pressure is low.
Excrete sodium when pressure is high.
Major effector is Angiotensin II
Plasma osmolality
Retain/drink water when osmolality is high.
Excrete water when osmolality is low.
Major effector is vasopressin
Sodium excretion is controlled by altering GFR or tubular sodium
reabsorption rates via a hierarchy of interrelated mechanisms
pressure diuresis and natriuresis
glomerulotubular balance
tubuloglomerular feedback
sympathetic nervous system control baroreceptor and lowpressure stretch receptor reflexes
angiotensin II amplifies the pressure natriuresis mechanism:
elevated angiotensin II makes blood pressure very sensitive to
changes in sodium intake
angiotensin II blockade shifts pressure natriuresis to lower blood
pressure levels
aldosterone stimulates Na+ reabsorption in cortical collecting ducts
aldosterone escape
adrenal insufficiency in Addisons disease leads to increased
excretion of salt and water and a tendency toward volume
depletion
atrial natriuretic peptide
released by stretch of the atria
acts to increase GFR slightly and to suppress collecting duct Na+
reabsorption
Integrated response to increased Na+ intake
Activation of low pressure receptor reflexes (first few hours)
small increases in arterial pressure result in pressure natriuresis
suppression of angiotensin II formation
stimulation of natriuretic systems
57
Title of Lecture: (Renal 8) Diuretics and Renal Related Diseases and Syndromes
Instructor: Robert Safirstein, M.D.

VA6A116; SafirsteinRobertL@uams.edu
257-5866
Objectives
Understand the mechanisms of action of diuretics
Be able to distinguish causes and consequences of acute and chronic
renal failure
Understand the role of the renin in clinical hypertension
Recognize the condition, molecular basis and clinical features arising
from inherited defects in kidney tubule epithelial cells
Lecture Outline
Diuretics increase urinary output and are used to reduce extracellular fluid
volume
osmotic diuretics: alter driving forces for bulk flow of water
loop diuretics: block the 1 Na+- 2 Cl--1 K+co-transporter
thiazide diuretics: block a Na+-Cl-co-transporter in the distal tubule
carbonic anhydrase inhibitors: proximal tubule
aldosterone antagonists (K+-sparring): principal cell
collecting tubule Na+ channel blockers (K+-sparring)
Acute renal failure
Prerenal acute renal failure
Intrarenal acute renal failure
Postrenal acute renal failure
Physiological effects of acute renal failure
Chronic renal failure
Viscous circle leading to end-stage renal disease
The most common causes of end-stage renal disease are Diabetes
mellitus and hypertension
Injury to the vasculature
Injury to the glomeruli
Injury to the interstitium
Nephrotic Syndrome
58
Effects of renal failure on the body fluids

Hypertension and renal disease
Renal lesions that reduce the ability of the kidneys to excrete sodium and
water promote hypertension
Goldblatt hypertension
Hypertension caused by patchy renal damage and renin secretion
Hypertension caused by excessive Na+ reabsorption: Liddles syndrome
Inherited Defects in Tubular Epithelium
Condition
renal glucosuria
cystinuria
Bartters syndrome
Gitlemans syndrome
Molecular Defect
Na+-dependent glucose
cotransporter
amino acid cotransporter
Na-K-2Cl cotransporter,
K channel or Cl channel
in TAL
thiazide sensitive Na-Cl
cotransporter in DCT
Liddles syndrome
increased open time and

number of ENAC
pseudohypoaldosteronism
type I
decreased activity of
ENAC
distal renal tubular

acidosis type I
intercalated cell Cl/HCO3- exchanger, H+

ATPase
vasopressin-2 (V2)
receptor or aquaporin-2
nephrogenic diabetes
insipidus
59
Clinical Features
glucosuria, polydipsia
kidney stone disease
salt wasting, hypokalemic
metabolic alkalosis
salt wasting, hypokalemic
metabolic alkalosis,
hypocalciuria
hypertension,
hypokalemic metabolic
alkalosis
salt wasting,
hyperkalemic metabolic
acidosis
metabolic acidosis,
osteomalacia
polyuria, polydipsia
Title of Lecture: (AB-1) Introduction To Acid-Base Balance

Instructor: Dr. P. Wight
Biomedical Research Center B212B; pwight@uams.eu
686-5366
(Acid-Base lectures I-III) Chapter 30, pp. 383 - 400
Suggested: Understanding Acid-Base, Benjamin Abelow, 1st Ed. (1998)
Objectives:
Identify the normal range of pH values in the bodys fluids compartments, and
the upper and lower limits of pH compatible with life
Understand the difference between volatile and nonvolatile acids, the average
daily amount of acid produced via ingestion and cellular metabolism, and the
mechanisms by which the body rids itself of this daily acid load
Understand the role of buffers in regulating (maintaining) pH and their relative
importance (amounts) in the different fluid compartments
Understand the concepts of buffer strength, buffer capacity, and the isohydric
principle
Lecture Outline:
I.
Overview of Acid-Base Balance
II.
Definition of Acid and Base
III.
Henderson-Hasselbalch equation
IV.
Buffering Power
V.
Isohydric Principle
VI.
Body Buffers
60
Title of Lecture: (AB-2) Regulation Of Acid-Base Balance

Instructor: Dr. P. Wight
686-5366
pp. (Acid-Base lectures I-III) Chapter 30, pp. 383 - 400
Objectives:
Know the 3 lines of defense to minimize changes in plasma pH
Know the 4 primary disturbances in acid-base balance
Know what is meant by the term compensation
Know the role of the respiratory system in regulating [H+]
Understand the tubular mechanisms for reabsorption of filtered HCO3- and the
factors that influence it
Lecture Outline:
I.
Introduction to Body Buffering
II.
Chemical Buffering (Bicarbonate Buffer System)
III.
Regulation of Arterial PCO2
IV.
Primary Respiratory Acid-Base Disturbances & Compensation
V.
Metabolic Production of Acids and Bases
VI.
Bicarbonate Reabsorption & Factors That Influence Bicarbonate
VII.
Reabsorption
61
Title of Lecture: (AB-3) Renal Regulation Of Hydrogen Ion Balance

Instructor:
Dr. P. Wight
686-5366
(Acid-Base lectures I-III) Chapter 30, pp. 383 - 400
Objectives:
Understand the concept of titratable acid
Understand the role of ammonium secretion in the excretion of H+
Know how to analyze acid-base disturbances
Understand how tubular H+ secretion is related to reabsorption of filtered
bicarbonate and the formation of new bicarbonate which is returned to the body
Lecture Outline:
I.
Endogenous Acid Production (EAP) and Renal H+ Excretion
II.
Titratable Acid (T.A.)
III.
Acid Excretion/Bicarbonate Regeneration

T.A. Excretion
Ammonium Excretion
IV.
Metabolic Disturbances
V.
Anion Gap
VI.
Analysis of Acid-Base Disorders
62
GASTROINTESTINAL
PHYSIOLOGY
J.N. PASLEY, Ph.D.
63
Title of lecture: (GI-1) Introduction of Gastrointestinal Physiology

Instructor: Dr. James N. Pasley
Shorey 6/S12; PasleyJamesN@uams.edu;
686-5128
Chapter 62; pp.777-781 ; Chapter 71; pp. 867-872,
Suggested Reading: Gastrointestinal Physiology, L.R. Johnson, 6th Ed. Mosby,
2001
Objectives:
Describe the overall role of the gastrointestinal tract with respect to whole
body caloric needs.
Describe the major constituents and role of splanchnic circulation.
Include major regulatory mechanisms.
Describe the importance of mind/body factors in GI tract health and disease.
Give examples.
Describe CNS and peripheral (gut and metabolic) factors that influence food
intake.
Lecture outline:
I. Function of the GI tract
General tasks
Splanchnic Circulation
II. The GI tract in health and disease

III. Control of food intake
Appetite and hunger
Hypothalamic control factors
Feeding center
Satiety center
Peripheral control factors
64
Title of Lecture: (GI-2) Mastication and Swallowing

686-5128
Chapter 62; pp. 771-777; Chapter 63; pp. 781-784;
Chapter 64; pp. 791-795
Suggested Reading: Gastrointestinal Physiology, L.R. Johnson, 6th Ed.
Mosby, 2001
Objectives:
Contrast sympathetic and parasympathetic modulation of the entire nervous
system and the effect on organs of the GI tract
Contrast the plasma and saliva concentrations of Na+, Cl- and HCO3- at low
and high secretion rates
State substrates and digestion products of salivary amylase
Identify the function of salivary mucus
State the components of saliva that are important in oral hygiene
Discuss stimuli and control salivary secretion
Describe the pressure changes that occur in the esophagus as the bolus
moves from the pharynx to the stomach
Contrast primary and secondary peristalsis in the esophagus
Contrast the patterns of external and internal innervation of the upper, middle,
and lower esophagus
Lecture outline:
I.
Salivary secretion
Anatomical considerations
Secretory composition
Organic constituents
Functions of salivary secretion
Regulation of secretion
65
II.
Musculature of the Digestive Tract
Structure and function
Motility Patterns
Role of Calcium
III.
Enteric Nervous System
IV.
Integration and control of motor activity
V.
Swallowing
Oropharyngeal Phase
Esophageal Phase
Lower Esophageal Sphincter (LES
66
Title of Lecture: (GI-3) Swallowing Abnormalities and Gastric Motility

686-5128
Chapter 63; pp. 784-786; Chapter 66; pp. 819
Suggested reading: Gastrointestinal Physiology, L.R. Johnson, 6th Ed.
Mosby, 2001
Objectives:
Contrast LES pressure; innervation and motility defects between reflux
(GERD) and achalasia
Describe the storage, digestive and motility roles of the stomach
Define receptive relaxation of the stomach and state mechanisms and
consequence of loss
Describe the origin and form of electrical activity and progression of
peristaltic waves across the stomach
Describe the role of peristaltic waves in mixing and propulsion of contents
and how the frequency is changed by volume
Predict the effect of meal content (osmolarity, fat, acid, etc.) particle size, and
volume on the rate of gastric emptying
Know one cause of delayed gastric emptying and increased gastric emptying
Lecture outline:
I. Esophageal Motor Dysfunction
GERD
Achalasia
II. Gastric Motility
Anatomic Considerations
Reservoir Function (Receptive Relaxation)
Pacemaker Activity
67
Contractile activities
Leading Contraction
Trailing Contraction
Stomach emptying (Fed Pattern)
Regulation of Emptying
Kind of Meal
Duodenal Factors
Fasted pattern
Basic Electrical Rhythm (BER)
Migrating Motor Complex (MMC)
Pathophysiology
Delayed Gastric Emptying
Rapid Gastric Emptying
68
Title of Lecture: (GI-4) Gastric Secretion and Small Intestinal Motility

686-5128
Chapter 63; pp. 786-788 ; Chapter 64; pp. 795-799 ;
Chapter 66 ; pp. 819-822
Suggested reading: Gastrointestinal Physiology, L.R. Johnson, 6th Ed.,
Mosby, 2001.
Objectives:
Contrast the Na+, K+, and Cl- concentrations of gastric secretion with that of
plasma at low and high secretion rates
Know how an alkaline tide is produced following a meal
Know the role of the stomach in preventing pernicious anemia
Describe the modulation of gastric acid secretion by vagal stimulation,
gastrin, histamine, and somatostatin
Identify the stimuli that increase and decrease gastrin release
Contrast intestinal motility patterns during the absorptive phase
(segmentation) with that of the interdigestive phase (MMC)
Know the motility changes and CNS areas associated with vomiting
Lecture outline:
I. Gastric secretion
Composition of Gastric Secretion
Two Functional Mucosal Regions
Cell Types
The Two Component Theory of Secretion
Functions of Gastric Secretions
Mechanisms of Control
3 Phases of Secretion
69
Secretagogues
Inhibitors of Secretion
Gastric mucosal barrier
Hypersecretion of acid
Hyposecretion of acid
Pathophysiology
Peptic Ulcer Disease
II. Motility of the small intestine
Overview
Contractile behavior Fed Pattern
Segmentation
Peristalsis
Power Propulsion
Migrating motor complex (MMC) Fasting Patterns
Motor dysfunction
Physiologic Ileus
Vomiting
70
Title of Lecture: (GI-5) Pancreatic, Biliary and Intestinal Secretion

686-5128
Chapter 64; pp. 799-806; Chapter 66; pp. 821-824
Suggested Reading: Gastrointestinal Physiology, L.R. Johnson, 6th Ed.,
Mosby, 2001
Objectives:
Understand pancreatic secretion
Learn secretions of the exocrine pancreas
Know factors regulating pancreatic secretion
Understand biliary tract secretion
Learn the enterohepatic circulation of bile acids
Know factors regulating biliary tract secretion
Understand intestinal secretion
Understand integration of duodenal cluster unit responses
Lecture Outline
I.
Introduction and Overview
II.
Exocrine Pancreatic Fluid Secretion
III.
Enzyme Secretion - acinar cell secretion
V.
Control of Pancreatic Secretion
VI.
Biliary Tract Secretion

A.
Components
B.
Primary & Secondary Bile Acids
C.
Regulation of secretion
71
VI.
D.
Enterohepatic Circulation
E.
Gallbladder Function
F.
Regulation of Secretion
G.
Gallstones
Intestinal Secretion
Types of Secretion
Control
Pathophysiology
72
Title of Lecture: (GI-6) Digestion and Absorption of Macronutrients

686-5128
Chapter 65; pp. 808-814
Mosby, 2001
Objectives:
Know the role of specific secretions in the processes of digestion and
absorption
Know the sites at which digestion of macronutrients occurs
Understand general conditions which may result in macronutrient
maldigestion and/or malabsorption
Lecture outline:
I.
The Absorptive Area of the Small Intestine
II.
Mechanisms of Absorption
III.
Digestion and absorption of carbohydrate
IV.
Digestion in Different Parts of GI Tract
Carbohydrate Transport Mechanisms
Pathophysiology of Carbohydrate Absorption
Digestion and Absorption of Protein
Source of Protein in the Diet

Digestion
73
V.
Transport
Pathophysiology of Protein Absorption
Digestion and Absorption of Fats
Lipid Digestion
Role of Bile Salts
Enterocyte resynthesis
Chylomicron Secretion
Pathophysiology of Lipid Absorption
74
Title of Lecture: (GI-7): Water, Electrolyte, Vitamin and Mineral Absorption

686-5128
Chapter 65; pp. 814-817 ; Chapter 71; pp. 875-879
Mosby, 2001
Objectives:
Know the sites at which absorption of water, electrolytes and minerals occur
Understand the mechanisms mediating absorption of water, electrolytes,
minerals and
water-soluble vitamins
Understand the basic mechanisms governing the absorption of calcium and
iron in the GI tract
Lecture outline:
I. Absorption of Water and Electrolytes
Absorption of water from small intestine
Sodium transport
Chloride and bicarbonate
Potassium transport
Pathophysiological alterations of salt and water absorption
Mechanism of H20 absorption
II. Fat Soluble Vitamins (A, D, E, K)

III. Water soluble vitamins (C, B1, B2, B6, B12, Niacin, Biotin, Folic Acid)
IV. Calcium Absorption
V. Iron Absorption
75
Title of Lecture: (GI-8) Large Bowel Motility, Gas in the Gut and Dietary Fiber
686-5128
Chapter 63; pp 788-791; Chapter 66; pp. 822-823, 825
Suggested Reading: Gastrointestinal Physiology, 6th Ed., L.R. Johnson,
Mosby, 2001
Objectives:
Compare colonic motility with small intestine motility including slow wave
differences
Contrast haustral shuttling with mass movements
Describe the sequence of events occurring during the defecation reflex
including those voluntary and involuntary control
Understand the basic pathophysiology of constipation, diarrhea
Discuss dietary fiber and its effects on the gastrointestinal tract
Compare and contrast Hirschsprungs Disease with Achalasia
Know sources of gas in the gut
Lecture Outline:
I. Motility of colon
Anatomical considerations
Functional differences between right transverse and left colon
Physiology of the rectosigmoid Region
II. Motility of colon

III. Transit Time
76
Anal continence
IV.
Pathophysiologic Disorders
Constipation
Diarrhea
Aganglionosis
V.
Role of dietary fiber in gastrointestinal health
VI.
Gas in the gut
77
ENDOCRINOLOGY
H.H.Conway, Ph.D.
D. Gaddy, Ph.D.
78
Title of Lecture: (Endo-1) Temperature Regulation

Instructor: Dr. Howard H. Conaway
Biomed 241C-2; conawayhowardh@uams.edu ;
686-5125
Required Reading: Medical Physiology, Guyton and Hall, 11th Ed. 2006,
Chapter 73 pp. 889-901.
References: Review of Medical Physiology, Ganong, 22nd Ed., 2005.
pp. 251-255,
Objectives:
Review normal body temperature
Describe heat production, heat loss and temperature regulating mechanisms
Know physiological mechanisms activated by increased and decreased body
temperatures
Understand the theory of fever production
Outline body temperatures under different conditions
Lecture Outline:
I.
Normal body temperature
II
Feedback mechanisms
III.
How the body produces heat
IV
Heat loss
V.
Temperature regulation mechanisms
VI
Set point
VII.
Mechanisms activated by increased body temperature
VIII.
Mechanisms activated by decreased body temperature
IX.
Fever
X.
Body temperatures under different conditions
XI.
Cold-induced vasodilation
79
Title of Lecture: (Endo-2) Energy Balance and Obesity

686-5125
Chapter 71 pp. 871-874, Chapter 72 pp. 884-888,
References: Science, Obesity Declared a Disease, Vol. 227, pp. 1019-1020,
1985. Science, Why Do People Get Fat? Vol. 227, pp. 1327-1328,
1985. Science, Obese Children: A Growing Problem, Vol. 232, pp.
20-22, 1986. Science, Regulation of Body Weight, Vol. 280, pp.
1363-1387, 1998.
Objectives:
Review caloric consumption, energy equivalents of foodstuffs and the
respiratory quotient
Describe basal metabolic rate (BMR)
Define normal weight and obesity
Know risks and health problems associated with obesity
Indicate theories of the causes of obesity
Introduce the hyperinsulinemia of obesity
Review treatments for obesity
Lecture Outline:
I.
Energy expenditure
II.
Energy equivalents of foodstuffs
III.
Basal Metabolic Rate (BMR)
IV.
Normal weight
V.
Obesity
VI.
Risk factors and health problems associated with obesity
VII.
Theories of the cause(s) of obesity
III.
Hyperinsulinemia
IX.
Social consequences of obesity
X.
Treatments for obesity
I.
Energy expenditure:
80
Title of Lecture: (Endo-3) Neuroendocrine Hormones, Pituitary

686-5125
Chapter 75 pp. 918-930.
References: Review of Medical Physiology, Ganong, 22nd Ed. 2005,
pp. 242-252,
Objectives:
Review pituitary anatomy and blood supply
Know posterior pituitary hormones and functions
Understand hypothalamic releasing and inhibiting hormones
Outline anterior pituitary hormones
Describe secretion, function and feedback control of growth hormone
Introduce secretion, function and feedback control of prolactin
Lecture Outline:
I.
The pituitary
II.
Pituitary anatomy
III.
The posterior pituitary and hormones
IV.
The pituitary blood supply and its functional significance
V.
Hypothalamic releasing and inhibitory hormones
VI.
Pre proopiomelanocortin
VII.
Anterior pituitary cells and hormones
VIII.
Growth hormone
IX.
The pituitary
81
Title of Lecture: (Endo-4) Endocrine Control of Calcium Metabolism

686-5125
Chapter 79 pp. 978-995.
References: Review of Medical Physiology, Ganong, 22nd Ed., 2005
pp. 382-395. Principles of Physiology, Berne and Levy, 3rd Ed.
2000, pp. 519-532
Objectives:
Understand calcium balance
Review intestinal absorption of calcium
Describe plasma calcium fractions
Give the different types of bone
List the cells of bone and their functions
Know parathyroid hormone (PTH) actions
Outline calcitriol (1,25(OH)2-vitamin D3) metabolism and functions
Define regulatory controls of plasma Ca++
Explain the relationship of calcitonin to calcium metabolism
Introduce abnormalities involving PTH and plasma Ca++
Lecture outline:
I.
Calcium metabolism
II.
Hormonal regulation of calcium metabolism
III.
Abnormalities involving PTH and serum Ca++
82
Title of Lecture: (Endo-5) Endocrine Pancreas I

686-5125
Required Reading: Medical Physiology, Guyton and Hall, 11th Ed. 2006.
Chapter 78 pp. 961-977
References: Principles of Physiology, Berne an Levy, 3rd Ed., pp. 508-518,
2000. Review of Medical Physiology, Ganong, 22nd Ed. 2005,
pp. 333-355.
Objectives:
Know endocrine hormones of the pancreas
Introduce diabetes mellitus
Describe the insulin molecule
Outline insulin production and release
Know factors influencing insulin release
Discuss possible mechanisms of insulin action
Lecture outline:
I.
Endocrine hormones of the pancreas
II.
Diabetes mellitus
III.
The human insulin molecule
IV.
Insulin production and release
V.
Factors influencing insulin release
VI.
Insulin action
83
Title of Lecture: (Endo-6) Endocrine Pancreas II

686-5125
Chapter 78 pp. 961-977.
References: Review of Medical Physiology, Ganong, 22nd Ed., pp. 333-355, 2005.
Principles of Physiology, Berne and Levy, 3rd Ed., pp. 508-518,
2000.
Objectives:
Know actions of insulin
Understand glucagon secretion and function
Outline insulin, glucagon and somatostatin interactions
Introduce type 1 and type 2 diabetes
Lecture outline:
I.
Insulin action
II.
Specific actions of insulin
III.
Glucagon
IV.
Relationships between insulin, somatostatin and glucagon secretion
V.
Diabetes mellitus
84
Title of Lecture: (Endo-7) The Thyroid Gland

686-5125
Chapter 76 pp. 931-943.
Principles of Physiology, Berne and Levy, 3rd Ed., pp. 548-558,
2000.
Objectives:
Compare inactive and active thyroid follicles
Give structures of thyroxine, T3 and rT3
Understand thyroid hormone biosynthesis
Outline feedback of the thyroid hormones and iodide involvement in thyroid
function
Introduce pharmacological agents altering thyroid function
Show the relationships between production and plasma levels of the thyroid
hormones
Define the importance of the thyroid hormone binding proteins in plasma
Know actions of the thyroid hormones
Lecture outline:
I.
General information
II.
Formation of the thyroid hormones
III.
Iodide uptake and thyroid hormone synthesis
IV.
Feedback and thyroid function
V.
Iodide involvement in thyroid hormone homeostasis
VI.
Pharmacological intervention
VII.
Quantitative aspects of the thyroid hormones
VIII.
Thyroid hormone binding proteins
IX.
Actions of the thyroid hormones
85
Title of Lecture: (Endo-8) Adrenal Gland I

686-5125
Chapter 77 pp. 944-960.
References: Principles of Physiology, Berne & Levy, 3rd Ed., pp. 559-571, 2000.
Review of Medical Physiology, Ganong, 22nd Ed., pp. 356-381, 2005.
Objectives:
Review anatomy of the adrenal gland
Give the hormones secreted by the adrenal gland
Introduce steroid hormone structure
Know biosynthesis of mineralocorticoids, glucocorticoids and adrenal
androgens
Show consequences of adrenal enzyme deficiencies
Understand feedback control of steroid hormones produced by the adrenal
gland
Know biosynthesis and release of adrenal medulla catecholamines
Lecture outline:
I.
The adrenal glands
II.
Steroid hormone structure
III.
Adrenal steroid hormone biosynthesis
IV.
Control of adrenal cortical secretions
V.
Catecholamine hormone synthesis and release
86
Title of Lecture: (Endo-9) Adrenal Gland II

686-5125
Chapter 77 pp. 944-960.
Principles of Physiology, Berne and Levy, 3rd Ed., pp. 559-578, 2000.
Objectives:
Outline adrenocortical hormone transport and excretion
Define permissive, direct and pharmacological actions of the glucocorticoids
Show chemical modifications of the glucocorticoid molecule
Understand feedback recovery of the glucocorticoid axis
Describe glucocorticoid and mineralocorticoid receptors
Review the relationship of the adrenal medulla to the autonomic nervous
system
Give mechanisms of action of the catecholamines
Introduce pheochromocytoma
Compare physiological responses of epinephrine and norepinephrine
Know metabolic actions of epinephrine
Emphasize interactions of the major metabolic hormones
Reference actions mediated by adrenergic receptors
Lecture outline:
I.
Adrenocortical hormone transport and excretion
II.
Glucocorticoid actions
III.
Pharmacology of glucocorticoids
IV.
Steroid-receptor interactions
V.
The adrenal medulla
VI.
Chromaffin tumors - pheochromocytoma
VII.
Metabolic actions of epinephrine
VIII.
Actions mediated by adrenergic receptors

87
Title of Lecture: (Endo-10) Male Reproductive Physiology

Instructor:
Dr. Dana Gaddy

Biomed 2-Rm 210-2; GaddyDana@uams.edu
686-5918
Chapter 80, pp. 996-1009
Suggesting reading: Vander, Sherman and Lucianos Human Physiology, 9th
Edition, by Widmaier, Raff and Strang, 2004
Chapter 17, pp. 671-694
Objectives:
Describe the differentiation of the male reproductive tract including the role of
in utero androgen production and Mllerian Inhibitory Factor
List testosterone induced changes that occur at puberty
Diagram cellular actions of testosterone
Describe the hormonal control of the testis
Describe the hormonal control of spermatogenesis
Know the role of male accessory glands in reproduction
Contrast hypergonadotropic and hypogonadotrophic hypogonadism in the
male
Lecture Outline:
I. Testis
Development
Cryptorchidism
Sertoli cell
Leydig cell
88
II. Testis
III. Male sexual response
IV. Testosterone secretion and effects
Secretion
Metabolism
Cellular action
Androgenic effects
Anabolic effects
Testosterone absence
Before Puberty
After Puberty
V. Hypothalamic/pituitary regulation
Pulsatile GNRH Secretion
Feedback Regulation
89
VI. Fertility Control
VII. Pathophysiology
Hypogonadotropic Hypogonadism
Kallmanns Syndrome
Panhypopituitarism
Hypergonadotropic hypogonadism
Klinefelters syndrome
Testicular feminization (AIS)
5 - reductase deficiency
90
Title of Lecture: (Endo-11) Female Reproductive Physiology

Instructor:
Dr. Dana Gaddy

686-5918
Chapter 81, pp. 1011-1026
Suggested reading: Vander, Sherman and Lucianos Human Physiology, 9th
Chapter 17, pp. 658-671
Objectives:
Pulses of hypothalamic GnRH regulate the secretion of LH and FSH, which
enhance follicular development, steroid genesis, ovulation, and formation
of the corpus luteum.
LH and FSH, in coordination with ovarian theca and granulosa cells,
regulate the secretion of follicular estradiol.
Ovulation occurs as the result of a positive feedback of follicular estradiol
on the hypothalamic-pituitary axis that induces LH and FSH surges.
Follicular development occurs in distinct steps: primordial, primary,
secondary, tertiary, and Graafian (preovulatory) follicle stages.
Follicular rupture (ovulation) requires the coordination of appropriately
timed LH and FSH surges that induce inflammatory reactions in the
graafian follicle, leading to dissolution at midcycle of the follicular wall by
several ovarian enzymes.
Follicular atresia results from the withdrawal of gonadotropin support.
The formation of a functional corpus luteum requires the presence of an
LH surge, adequate numbers of LH receptors, sufficient granulosa cells,
and significant progesterone secretion.
The uterine cycle is regulated by estradiol and progesterone, such that
estradiol induces proliferation of the uterine endometrium, whereas
progesterone induces differentiation of the uterine endometrium and the
secretion of distinct products.
During puberty, the hypothalamus begins to secrete increasing quantities
of GnRH, which increases LH and FSH secretion, enhances ovarian
function, and leads to the first ovulation.
Menopause ensues from the loss of numerous oocytes in the ovary and
the subsequent failure of follicular development and estradiol secretion.
LH and FSH levels rise from the lack of negative feedback by estradiol.
91
Lecture Outline:
I.
Female reproductive system
II.
Hypogonadal axis regulation of reproduction
III.
Follicular development
IV.
2-cell Hypothesis of steroidogenesis
V.
Role of Estrogens
VI.
Role of Progesterone
VII.
Hormonal integration of ovarian cycle with uterine changes
VIII.
In vitro fertilization
IX.
Luteal insufficiency
X.
Ovulation and fertilization
92
Title of Lecture: (Endo-12) Female Reproductive Physiology II

Instructor:
Dr. Dana Gaddy

686-5918
Chapter 82, pp. 1027-1041
Suggested reading: Vander, Sherman and Lucianos Human Physiology, 9th
Chapter 17, pp. 671-694
Objectives:
Fertilization of the ovum occurs in the oviduct. Progesterone and estrogen
released from the ovary prepare the oviduct and uterus for receiving the
developing embryo.
The blastocyst enters the uterus, leaves the surrounding zona pellucida,
and implants into the uterine wall on day 7 of gestation.
Human chorionic gonadotropin (hCG), produced by trophoblast cells of
the developing embryo, activates the corpus luteum to continue producing
progesterone and estradiol beyond its normal life span to maintain
pregnancy.
Shortly after the embryo implants into the uterine wall, a placenta develops
from embryonic and maternal cells and becomes the major steroidsecreting organ during pregnancy.
Major hormones produced by the fetoplacental unit are progesterone,
estradiol, estriol, hCG, and human placental lactogen. Elevated estriol
levels indicate fetal well-being, whereas low levels might indicate fetal
stress. Human placental lactogen has a role in preparing the breasts for
milk production.
The pregnant woman becomes insulin-resistant during the latter half of
pregnancy in order to conserve maternal glucose consumption and make
glucose available for the developing fetus.
The termination of pregnancy is initiated by strong uterine contractions
induced by oxytocin. Estrogens, relaxin, and prostaglandins are involved
in softening and dilating the uterine cervix so that the fetus may exit.
Lactogenesis is milk production, which requires prolactin (PRL), insulin,
and glucocorticoids.
Galactopoiesis is the maintenance of an established lactation and requires
PRL and numerous other hormones. Milk ejection is the process by which
stored milk is released; milk letdown is regulated by oxytocin, which
contracts the myoepithelial cells surrounding the alveoli and ejects milk
into the ducts.
Lactation is associated with the suppression of menstrual cycles and
93
anovulation due to the inhibitory actions of PRL on GnRH release and the
hypothalamic-pituitary-ovarian axis.
The hypothalamic-pituitary axis becomes activated during the late
prepubertal period, resulting in increased frequency and amplitude of
GnRH pulses, increased LH and FSH secretion, and increased steroid
output by the gonads.
Most disorders of sexual development are caused by chromosomal or
hormonal alterations, which may result in in-fertility, sexual dysfunction,
or various degrees of intersexuality (hermaphroditism).
Lecture outline:
I. Pregnancy
Fertilization and implantation
Associated maternal endocrine
changes
Maternal metabolism changes
Fetal metabolic regulation
II. Parturitionhormonal control
III. Chromosomal abnormalities
IV. Lactation regulation
V. Pubertymenarche
Factors involved in timing of puberty
VI. Adrenarche
VII. Menopause
Symptoms
Hormonal changes
Physiological changes
Hormone Replacement Therapy
94
Title of Lecture: (Endo-13) Neonatal Physiology

Biomedical 209-2; JenningsMichaelL@uams.edu)
296-1438
Chapter 83, pp. 1042-1052
Objectives:
Understand the general time course of growth of the fetus.
Understand the respiratory system changes that occur at birth
Understand the changes in the circulatory/cardiovascular system in the
fetus during gestation and at parturition
Know the functional problems of organ systems that are specific to the
neonate
Understand the major functional consequences of premature birth
Lecture Outline:
I. Fetal Metabolism and Development of Organ Systems
II. Adjustment of neonate to extrauterine life
Breathing at birthcauses, delays and abnormalities
Hypoxia
Lung Expansion, surfactant deficiencyRespiratory Distress Syndrome
III. Circulatory adjustments at birth
Important anatomical structures involved in fetal circulation
Changes in fetal circulation at birth
Altered pulmonary and systemic vascular resistance at birth
Closure of the foramen ovale, ductus arteriosus, and ductus venosus
95
IV. Functional Problems of the neonate

Respiratory system
Circulation
Fluid balance, acid-base balance, renal function
GI and Liver
Metabolic rate and body temperature
Nutritional needs early post-natal: Calcium, Vitamin D, Iron, Vitamin C
V. Problems associated with prematurity
96
Key Physiology Equations

Equation Name
Mean arterial pressure
Resistance
Equation
Pa = CO X TPR
8 1
r 4
Compliance
C = V/P
Cardiac output
CO = SV X HR
Cardiac output
(measurement)
CO =
O2
[O ]
2 pulmonary
vein
Ejection fraction
EF = SV/EDV
Starling equation
J2 = Kf [(Pc Pi) (c - I)]
Physiologic dead space
Alveolar ventilation
VD = VT X
[O ]
2
Paco 2 PECO 2
Paco 2
VA = (VT VD) X breaths/min
Renal clearance
C=
U V
x
Px
GFR
GFR =
Free water clearance
consumption
inulin
Pinulin
C H 2 O = V C osm
Henderson-Hasselbalch
equation
pH = pK + log
Serum anion gap
Anion gap = Na+ - (Cl- + HCO3-)
97
A
HA
pulmonary artery
LABORATORY VALUES
* Included in the Biochemical Profile (SMA-12)
REFERENCE RANGE
BLOOD, PLASMA, SERUM
* Alanine aminotransferase
(ALT, GPT at 30C)
Amylase, serum
* Aspartate aminotransferase (AST,
GOT at 30C)
Bilirubin, serum (adult) Total//Direct
2+
* Calcium, serum (Ca )

* Cholesterol, serum
Cortisol, serum
Creatine kinase, serum

Creatinine, serum
Electrolytes, serum
Sodium (Na+)
Chloride (Cl)
* Potassium (K+)
Bicarbonate(HCO3)
Magnesium(Mg2+)
Estriol, total, serum (in pregnancy)
24-28 wks// 32-36 wks
28-32 wks//36-40wks
Ferritin, serum
Follicle-stimulating hormone,
serum/plasma
Gases, arterial blood (room air)

pH
PCO2
PO2
* Glucose, serum
Growth hormone - arginine

stimulation
SI REFENCE INTERVALS
8-20 U/L
25 -125U/L
8-20 U/L
25 -125U/L
8-20 U/L
8-20 U/L
0.1-1.Omg/dL//0.0-0.3mg/dL
8.4-10.2mg/dL
Rec:<200mg/dL
0800 h: 5-23 g/dL // 1600 h: 3-15
g/dL
2000 h:50% of 0800 h
Male: 25-90U/L
Female: 10-70U/L
0.6-1.2 mg/dL
2-17mol/L// 0-5 mol/L

2.1-2.8 mmol/L
<5.2 mmol/L
138-635 nmol/L // 82-413 nmol
136-145mEq/L
95-105mEq/L
3.5-5.0mEq/L
22-28 mEq/L
1.5-2.0mEq/L
136-145 mmol/L
95-105 mmol/L
3.5-5.0 mmol/L
22-28 mmol/L
1.5-2.0 mmol/L
30-170ng/mL // 60-280ng/mL
40-220ng/mL // 80-350 ng/mL
Male: 15-200ng/mL
Female: 12-150ng/mL
Male:4-25mlU/mL
Female: premenopause 4-30
mlU/mL
midcycle peak 10-90 mlU/mL
postmenopause 40-250 mlU/mL
104-590// 208-970 nmol/L

140-760// 280-1210 nmol/L
15-200 g/L
12-150 g/L
4-25 U/L
4-30 U/L
7.35-7.45
33-45 mmHg
75-105 mmHg
Fasting: 70-110 mg/dL
2-h postprandial: < 120 mg/dL
[H+] 36-44 nmol/L

4.4-5.9 kPa
10.0-14.0 kPa
3.8-6.1 mmol/L
Fasting: <5ng/mL
provocative stimuli: > 7 ng/mL
Fraction of 0800 h: 0.50

25-90 U/L
10-70 U/L
53-106 mol/L
10-90 U/L
40-250 U/L
<6.6 mmol/L
< 5 g/L
> 7 g/L
Immunoglobulins, serum
IgA
IgE
IgG
IgM
Iron
Lactate dehydrogenase, serum
Luteinizing hormone, serum/plasma
76-390mg/dL
0-380 IU/mL
650-1500mg/dL
40-345mg/dL
50-170g/dL
45-90U/L
Male:6-23mlU/mL
98
0.76-3.90 g/L
0-380 klU/L
6.5-15 g/L
0.4-3.45 g/L
9-30 mol/L
45-90 U/L
6-23 U/L
Osmolality, serum
Parathyroid hormone, serum,
N-terminal
* Phosphatase (alkaline), serum (pNPP at 30C)
* Phosphorus (inorganic), serum
Prolactin, serum(hPRL)
* Proteins, serum
Total(recumbent)
Albumin
Globulin
Thyroid-stimulating hormone, serum
or plasma
Thyroidal iodine (120I) uptake
Thyroxine (T4),serum
Triglycerides, serum
Triiodothyronine (T3), serum (RIA)
Triiodothyronine (T3) resin uptake
* Urea nitrogen, serum (BUN)
* Uric acid, serum
Cerebrospinal Fluid
Cell count
Chloride
Gamma globulin
Glucose
Pressure
Proteins, total
Hematologic
Bleeding time (template)
Erythrocyte count
Erythrocyte sedimentation rate
(Westergren)
Hemoglobin A1C
Hemoglobin, blood
Hemoglobin, plasma
Leukocyte count and differential
Leukocyte count
Segmented neutrophils
Bands
Eosinophils
Basophils
Lymphocytes
Monocytes
Mean corpuscular hemoglobin
Mean corpuscular hemoglobin
concentration
Mean corpuscular volume
Partial thromboplastin time (activated)
Female: follicular phase 5-30

mlU/mL
midcycle75-150mlU/mL
postmenopause 30-200 mlU/mL
275-295mOsmol/kg
5-30 U/L
75-150 U/L
30-200 U/L
275-295mOsmol/kg
230-630 pg/mL
230-630 ng/L
20-70 U/L
3.0-4.5 mg/dL
< 20 ng/mL
20-70 U/L
1.0-1.5 mmol/L
<20 g/L
6.0-7.8 g/dL
3.5-5.5 g/dL
2.3-3.5 g/dL
60-78 g/L
35-55 g/L
23-35 g/L
0.5-5.0U/mL
8-30% of administered dose/24 h
0.5-5.0 mU/L
5-12 g/dL
35-160 mg/dL
115-190 ng/dL
25-35%
7-18mg/dL
3.0-8.2 mg/dL
0.80-0.30/24 h
64-155 nmol/L
0.4-1.81 mmol/L
1.8-2.9 nmol/L
0.25-0.35
1.2-3.0 mmol urea/L
0.18-0.48 mmol/L
0-5 cells/mm3
118-132 mEq/L
3-12% total proteins
40-70 mg/dL
70-180 mm H2O
<40 mg/dL
0-5 x 106/L
118-132 mmol/L
0.03-0.12
2.2-3.9 mmol/L
70-180 mm H2O
<0.40 g/dL
2-7 minutes
Male: 4.3-5.9 million/mm3
Female: 3.5-5.5 million/mm3
Male: 0-15 mm/h
Female: 0-20 mm/h
6%
Male: 13.5-17.5 g/dL
Female: 12.0-16.0 g/dL
1-4 mg/dL
2-7 minutes
4.3-5.9 x 1012/L
3.5-5.5 x 1012/L
0-15 mm/h
0-20 mm/h
0.06%
2.09-2.71 mmol/L
1.86-2.48 mmol/L
0.16-0.62 mmol/L
4500-11,00/mm3
54-62%
3-5%
1-3%
0-0.75%
25-33%
3-7%
25.4-34.6 pg/cell
4.5-11.0 x 109/L
0.54-0.62
0.03-0.05
0.01-0.03
0-0.0075
0.25-0.33
0.03-0.07
0.39-0.54 fmol/cell
31-36% Hb/cell
80-100 mm3
4.81-5.58 mmol Hb/L

80-100fl
99
Platelet count
Prothrombin time
Reticulocyte count
Thrombin time
Volume
Plasma
Red cell
SWEAT
Chloride
URINE
Calcium
Chloride
Creatinine clearance
Estriol, total (in pregnancy)
30 wks
35 wks
40 wks
17-Hydroxycorticosteroids
17-Ketosteroids, total
Osmolality
Oxalate
Potassium
Proteins, total
Sodium
Uric acid
25-40 seconds
150,000-400,000/mm3
11-15 seconds
0.5-1.5% of red cells
< 2 seconds deviation from control
25-40 seconds
150-400 x 109/L
11-15 seconds
0.005-0.015
< 2 seconds deviation from control
Male: 25-43 mL/kg

Female: 28-45 mL/kg
Male: 20-36 mL/kg
Female: 19-31 mL/kg
0.025-0.043 L/kg
0.028-0.045 L/kg
0.020-0.036 L/kg
0.019-0.031 L/kg
0.35 mmol/L
0-35 mmol/L
100-300 mg/24h
Varies with intake
Male: 97-137 mL/min
Female 88-128 mL/
2.5-7.5 mmol/24h
Varies with intake
6-18 mg/24h
9-28 mg/24h
13-42 mg/24h
Male: 3.0-10.0 mg/24
Female: 2.0-8.0 mg/24h
Male: 8-20 mg/24h
Female: 6-15 mg/24h
50-1400 mOsmol/kg
8-40 g/mL
Varies with diet
< 150 mg/24h
Varies with diet
Varies with diet
21-62 mol/24h
31-97 mol/24h
45-146 mol/24h
8.2-27.6 mol/24h
5.5-22.0 mol/24h
28-70 mol/24h
21-52 mol/24h
100
90-445 mol/L
Varies with diet
< 0.15 g/24h
Varies with diet
Varies with diet

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MEDICAL

COURSE ADMINISTRATIVE ASSISTANTS

Mechanics Of Skeletal Muscle Contraction

Ventilation/Perfusion Relations (Air/Blood Matching)

MEDICAL PHYSIOLOGY (PHYSIOLOGY 500V)

To provide students with an understanding of the normal function of cells,

Required Textbook: The following textbook is required for the course:

Costanzo, Linda S., Physiology, W.B. Sanders, Philadelphia, 1998

Learning Resource Center Reverences. The Learning Resource Center (located

Computerized Examination Instruction Summary:

button when you are ready to leave the current question.

the examination room. Queries regarding examination questions will not be

TEST ITEM VALIDATION PROCEDURE

MEDICAL PHYSIOLOGY SPRING 2007 SCHEDULE

(The schedule is subject to change without prior notice)

Introduction to Medical Physiology

Role of Physiology in Clinical Medicine

Mech. of Skeletal Muscle Contraction

Funct. Properties of Skeletal Muscle

The Cardiac cycle

Ventricular Function and Energetics

Martin Luther King Day

Arterial Blood Pressure Regulation

Cardiovascular Responses to Exercise

Cardiovascular Intrinsic and Extrinsic Control

Airways; Ventilation; Properties of Gases

Tissue Gas Exchange; CO2 Transport

Airways; Muscles of Breathing; Pulm.

Mechanics Of Breathing Lab

Pediatric Pulmonary Mechanics

Pulmonary Blood Flow; Fluid Balance

Adult Respiratory Diseases

SIM - MAN Review

PBL: Renal Case Conference

Clinical Correlation: Renal

Ca2++, Mg2++, and PO4 Balance and the

Regulation Of Acid-Base Balance

Renal Regulation Of Hydrogen Ion Balance

PBL A/B Computer

Introduction to Gastrointestinal Physiology

Mastication and Swallowing

Swallowing Abnormalities and Gastric

Pancreatic, Biliary and Intestinal Secretion

Water, Electrolyte, Vitamin and Mineral

Lg. Bowel Motility, Gas in the Gut and

Neuroendocrine Hormones: Pituitary

Clinical Correlation: Pituitary

Endocrine Control Of Calcium Metabolism

Clinical Correlation: Thyroid

Clinical Correlation: Adrenal

Problem Based Learning

Male Reproductive Physiology

Female Reproductive Physiology I

Female Reproductive Physiology II

Clinical Correlation: Reproduction

Problem Based Learning

PBL Rooms In Education Building II

MEDICAL PHYSIOLOGY SPRING 2007 WEB PAGE

L.E. CORNETT, Ph.D.

Title of Lecture: (MUS-1) Mechanisms of Skeletal Muscle Contraction

Medical Physiology, Guyton and Hall; 11th Ed., 2006,

Suggested Reading: Diseases of the Skeletal Muscle, Ed., R.L. Wortmann,

Skeletal muscle filaments and associated proteins