NSC 217 Human Anatomy 2

NSC 217 HUMAN ANATOMY (II) 2
NSC 217: Human Anatomy II- Urogenital and endocrine anatomy (1–0 –4) =
2 UNITS
It shall cover the gross anatomy, embryology and histology of the kidney, ureter, urinary
bladder and the male and female urethra. The gross anatomy and clinical relevance of
endocrine organs such as pituitary, thyroid, parathyroid, pancreas, gonads and adrenal
glands shall be taught.
COURSE CODE: NSC 217
COURSE TITLE: Human Anatomy II
COURSE UNITS: 2 Credit units (18 hours of instruction online; 6 hours of
Discussion forum online/tutorial; 24 hours of laboratory practical)
YEAR: 2 SEMESTER: First
CON-CURRENT COURSES: NSc 213, 215, 217, 209, 219
SESSION: _______ COURSE WEBSITE: www.noun.edu.ng/
COURSE WRITERS
Dr. Adewole O.S. MBBS, PhD, (Associate Professor).
Dr. Abiodun A. O. MBBS, FWCS, M.Sc. (Senior Lecturer)
Dr. Ayannuga A. A. MBBS, Ph.D (Senior Lecturer)
Dr. Adeyemi D.A. PhD (Senior Lecturer)
Dr. Ojo S. K. MBChB, MSc (Lecturer II); Dr. Arayombo B. E. MBChB, MSc
(Lecturer II)
Department of Anatomy and Cell Biology, College of Health Sciences,
Obafemi Awolowo University, Ile-Ife, Nigeria
Course Facilitators:
1
____________________
COURSE EDITORS: Dr O.O. Irinoye and Dr E.O Oladogba
PROGRAMME LEADER: Professor Mba Okoronkwo OON
COURSE COORDINATOR: _______________________________
COURSE REVIEWER Dr S S Bello MBBS, PhD
Department of Anatomy, FBMS, College of Health Sciences, Usmanu Danfodiyo
University, Sokoto, Nigeria
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COURSE GUIDE
Table of Contents Page
General Introduction 3
Course Aims 3
Course Objectives 3
Working through the Course 3
Course Materials 4
Study Units 4
Reference Textbooks 5
Equipment and Software Needed to Access Course 5
Number and Places of Meeting 6
Discussion Forum 6
Course Evaluation 6
Grading Criteria 6
Grading Scale 7
Schedule of Assignments with Dates 7
Course Overview 7
How to get the most from this Course 8
MODULE 1- Urinary System 9
MODULE 2 The Endocrine System 29
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COURSE GUIDE
GENERAL INTRODUCTION
Welcome to NSC 217 – Human Anatomy II. This is a second year course and runs at
same time with Human Anatomy I (NSC 215). This part will cover the gross anatomy,
embryology and histology of the kidney, ureter, urinary bladder and the male and female
urethra. The gross anatomy and clinical relevance of endocrine organs such as pituitary,
thyroid, parathyroid, pancreas, gonads and adrenal glands. Caring for patients always
require sound understanding of the normal structure of the body organs as to know what
such manifest could be wrong and how. Basic assessments done before planning general
and nursing care usually consider the various organs that function within systems and
as interrelated systems. You will be required to be able to describe these organs and
discuss their clinical correlates to the knowledge of the body parts. You will enjoy
drawing and labelling, as well as seeing some of these organs in real life. You will also
see the variations in normal and diseased organs as you are encouraged to participate in
all laboratory assignments.
COURSE AIM.
The aim of this course is further your understanding of the structural make up of two
(2) of the life supporting systems as such prepares you to apply your knowledge in
planning to meet the care needs of your body and that of your clients as such may relate
to normal and abnormal changes in the various organs that make up the systems.
COURSE OBJECTIVES
At the completion of this course, you should be able to:
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i. Discuss the structure and relations, embryology and histology of the organs in the
following systems:
a. The urinary system
b. The endocrine system
WORKING THROUGH THIS COURSE
The course will be delivered adopting the blended learning mode, 70% of online but
interactive sessions and 30% of face-to-face during laboratory sessions. You are
expected to register for this course online before you can have access to all the materials
and have access to the class sessions online. You will have the hard and soft copies of
course materials, you will also have online interactive sessions, face-to-face sessions
with instructors during practical sessions in the laboratory. The interactive online
activities will be available to you on the course link on the Website of NOUN. There
are activities and assignments online for every unit every week. It is important that you
visit the course sites weekly and do all assignments to meet deadlines and to contribute
to the topical issues that would be raised for everyone ‘s contribution. You will be
expected to read every module along with all assigned readings to prepare you to have
meaningful contributions to all sessions and to complete all activities. It is important
that you attempt all the Self-Assessment Questions (SAQ) at the end of every unit to
help your understanding of the contents and to help you prepare for the in-course tests
and the final examination. You will also be expected to keep a portfolio where you keep
all your completed assignments.
COURSE MATERIALS
Course Guide
5
Course Text in Study Units
Textbooks (Hard and electronic)
Book of Laboratory Practical
Assignment File/Portfolio
STUDY UNITS
This course comprises 2 Modules and 10 units. They are structured as presented:
Module 1- Urinary System
Unit 1- The anatomy of the kidneys
Unit 2- The anatomy of the ureters
Unit 3- The anatomy of the bladder
Unit 4- The anatomy of the urethra
Module 2- Endocrine System
Unit 1 Functions of the Endocrine System
Unit 2 Hormones
Unit 3 Pituitary Gland
Unit 4 Thyroid and Parathyroid Gland
Unit 5 Adrenal Gland
Unit 6 Pancreas
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REFERENCE TEXTBOOKS
1. Sadler T.W (2012), Langman‘s Medical Embryology 12th edition.
2. Philip Tate (2012) Seeley‘s Principles of Anatomy & Physiology 2nd edition.
3. Katherine M. A. Rogers and William N. Scott (2011) Nurses! Test yourself in
anatomy and physiology
4. Kent M. Van De Graff, R.Ward Rhees, Sidney Palmer (2013) Schaum‘s Outline of
Human Anatomy and Physiology 4th edition.
5. Kathryn A. Booth, Terri. D. Wyman (2008) Anatomy, physiology, and
pathophysiology for allied health
6. Keith L Moore, Persuade T.V.N (2018), The Developing Human Clinically
Oriented Embryology 11th Edition Lippincott Williams & Wilkins.
COURSE REQUIREMENTS AND EXPECTATIONS OF YOU
Attendance of 95% of all interactive sessions, submission of all assignments to meet
deadlines; participation in all CMA, attendance of all laboratory sessions with evidence
as provided in the logbook, submission of reports from all laboratory practical sessions
and attendance of the final course examination. You are also expected to:
1. Be versatile in basic computer skills
2. Participate in all laboratory practical up to 90% of the time
3. Submit personal reports from laboratory practical sessions on schedule
4. Log in to the class online discussion board at least once a week and contribute to
ongoing discussions.
5. Contribute actively to group seminar presentations.
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EQUIPMENT AND SOFTWARE NEEDED TO ACCESS COURSE
You will be expected to have the following tools:
1. A computer (laptop or desktop or a tablet)
2. Internet access, preferably broadband rather than dial-up access
3. MS Office software – Word PROCESSOR, Powerpoint, Spreadsheet
4. Browser – Preferably Internet Explorer, Moxilla Firefox
5. Adobe Acrobat Reader
NUMBER AND PLACES OF MEETING (ONLINE, FACE-TO-FACE,
LABORATORY PRACTICALS)
The details of these will be provided to you at the time of commencement of this
course
DISCUSSION FORUM
There will be an online discussion forum and topics for discussion will be available
for your contributions. It is mandatory that you participate in every discussion every
week as will be moderated by your facilitator. Your participation links you, your face,
your ideas and views to that of every member of the class and earns you some mark.
COURSE EVALUATION
There are two forms of evaluation of the progress you are making in this course. The
first are the series of activities, assignments and end of unit, computer or tutor marked
assignments, and laboratory practical sessions and report that constitute the continuous
assessment that all carry 30% of the total mark. The second is a written examination
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with multiple choice, short answers and essay questions that take 70% of the total mark
that you will do on completion of the course.
Students evaluation: The students will be assessed and evaluated based on the
following criteria
 In-Course Examination:
In-course examination will come up in the middle of the semester. These would
come in form of Computer Marked Assignment. This will be in addition to one
compulsory Tutor Marked Assignment (TMA‘s) and three Computer Marked
Assignment that comes after the modules.
 Laboratory practical: Attendance, record of participation and other
assignments will be graded and added to the other scores from other forms of
examinations.
 Final Examination: The final written examination will come up at the end of
the semester comprising essay and objective questions covering all the contents
covered in the course. The final examination will amount to 60% of the total
grade for the course.
Learner-Facilitator evaluation of the course
This will be done through group review, written assessment of learning (theory and
laboratory practical) by you and the facilitators.
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GRADING CRITERIA
Grades will be based on the following Percentages
Tutor Marked Individual Assignments 10%
Computer marked Assignment 10%
Group assignment 5% 30%
Discussion Topic participation 5%
Laboratory practical 10%
End of Course examination 70%
GRADING SCALE
A = 70-100
B = 60 - 69
C= 50 - 59
F = < 49
SCHEDULE OF ASSIGNMENTS WITH DATES
Every Unit has activity that must be done by you as spelt out in your course materials.
In addition to this, specific assignment will also be provided for each module by the
facilitator.
SPECIFIC READING ASSIGNMENTS
To be provided by each module
COURSE OVERVIEW
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Human Anatomy (II)
Human Anatomy (II) is the second of the four volumes of Human Anatomy. The course
that covers some of the major organs that are responsible for life. In this course, two
systems that are responsible for the maintenance of the body will be covered. The
structures and locations of the various organs that make each of the systems will be
studied. These are the urinary and endocrine systems. The course has the theory and
laboratory components that spread over 15 weeks. The course is presented in Modules
with small units. Each unit is presented to follow the same pattern that guides your
learning. Each module and unit have the learning objectives that helps you track what
to learn and what you should be able to do after completion. Small units of contents will
be presented every week with guidelines of what you should do to enhance knowledge
retention as had been laid out in the course materials. Practical sessions will be
negotiated online with you as desirable with information about venue, date and title of
practical session.
HOW TO GET THE MOST FROM THIS COURSE
1. Read and understand the context of this course by reading through this course guide
paying attention to details. You must know the requirements before you will do well.
2. Develop a study plan for yourself.
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3. Follow instructions about registration and master expectations in terms of reading,
participation in discussion forum, end of unit and module assignments, laboratory
practical and other directives given by the course coordinator, facilitators and tutors.
4. Read your course texts and other reference textbooks.
5. Listen to audio files, watch the video clips and consult websites when given.
6. Participate actively in online discussion forum and make sure you are in touch with
your study group and your course coordinator.
7. Submit your assignments as at when due.
8. Work ahead of the interactive sessions.
9. Work through your assignments when returned to you and do not wait until when
examination is approaching before resolving any challenge you have with any unit or
any topic.
10. Keep in touch with your study centre, the NOUN, School of Health Sciences
websites as information will be provided continuously on these sites.
11. Be optimistic about doing well.
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COURSE MATERIALS
NSC 217 - HUMAN ANATOMY II - Urogenital and endocrine anatomy (1–0 –4) =
2 UNITS
Module 1- Urinary System
Unit 1- The anatomy of the kidneys
Unit 2- The anatomy of the ureters
Unit 3- The anatomy of the bladder
Unit 4- The anatomy of the urethra
Module 2- The Endocrine System
Unit 1 Functions of the Endocrine System
Unit 2 Hormones
Unit 3 Pituitary Gland
Unit 4 Thyroid and Parathyroid Gland
Unit 5 Adrenal Gland
Unit 6 Pancreas
MODULE 1- URINARY SYSTEM
Introduction
The urinary system consists of the paired kidneys and ureters and the unpaired bladder
and urethra. This system contributes to the maintenance of homeostasis by a complex
process that involves filtration, active absorption, passive absorption, and secretion.
The result is the production of urine, in which various metabolic waste products are
eliminated.
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Module objectives
At the end of this module, you should be able to:
i. Discuss the anatomy and functions of each component of the urinary system.
CONTENTS
Unit 1: The anatomy of the kidneys
Unit 2: The anatomy of the ureters
Unit 3: The anatomy of the bladder
Unit 4: The anatomy of the urethra
UNIT ONE- THE ANATOMY OF THE KIDNEYS
CONTENT
1.0 Introduction
2.0 Learning objectives
3.0 Main Content
3.1 Developmental anatomy of the kidneys
3.2 The gross anatomy of the kidneys
4.0 Conclusion
5.0 Summary
6.0 Tutor Marked Assignments
6.1 Activity
6.2 Tutor Marked Tests
1.0 Introduction
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The kidneys make up the body‘s main purification system. They control the
composition of blood by removing waste products, many of which are toxic, and
conserving useful substances. The kidneys help control blood volume and consequently
play a role in regulating blood pressure. The kidneys also play an essential role in
regulating blood PH. Approximately one-third of one kidney is all that is needed to
maintain homeostasis. Even after extensive damage, the kidneys can still perform their
life-sustaining functions. If the kidneys are damaged further, however, death results
unless specialized medical treatment is administered.
The urinary system
Fig. 1.1: NSC 201 HUMAN ANATOMY (II) 137
2.0 Learning objectives

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At the end of this unit, you should be able to:
i. Describe the functions of the kidneys
ii. Describe the embryology of the kidneys
iii. Describe the anatomy of the kidneys
iv. Understand some clinical conditions related to the kidneys
3.0 Main Content
3.1 Developmental anatomy of the kidneys
Knowledge of the development of the urinary tract will enable you to understand how
abnormalities can easily occur while the foetus is growing and why young babies have
difficulties with fluid challenges. The system develops from the intermediate mesoderm
on either side of the dorsal (back) body wall, which gives rise to three successive
nephric structures (filtering units) of increasingly advanced design. The kidney changes
three times before it is completed! The first kidneys are transitory, non-functional
segmental nephrotomes in the cranial region which regress in the fourth week on day
twenty-four to twenty-five. After this, an elongated pair of mesonephros appear in the
thoracic and lumbar region either side of the vertebral column. These structures are
functional, as they have complete nephrons and drain caudally via the Wolffian ducts
to the urogenital sinus. By week five the ureteric buds sprout from the Wolffian ducts
and develop into the definitive kidneys that will serve the child for life. The bladder
expands from the superior urogenic sinus, and the inferior section gives rise to the
urethra in both sexes. Ureters are then emplaced on the bladder wall. This articulation
can give rise to multiple ureters forming or joining with the bladder ineffectively. At
week six, germ cells migrating from the yolk sac induce the mesonephros to
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differentiate into Sertoli cells in the male and follicle cells in the female. At the same
time a new Müllerian duct develops parallel to the mesonephric duct. It is in week six,
when the Y chromosome exerts its effect, that a development cascade then sees the
forming of the male or female external genitalia and the kidneys ascending to their
lumbar site in the abdomen, the right being lower than the left due to the presence of
the liver.
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Fig. 1.2: The kidney bud position
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By the tenth week, the foetal kidney is functional and commences urine production.
Foetal urine is important, not to get rid of waste products from the blood as the placenta
regulates fluid and electrolyte homeostasis, but to supplement the production of
amniotic fluid. Amniotic fluid is vital to the foetal development as it contains proteins,
carbohydrates, lipids and phospholipids, urea and electrolytes. It is a clear slightly
yellow liquid round the foetus and increases during the pregnancy to 800 ml at thirty-
four weeks. It is constantly circulated by the foetus as it swallows and “inhales” the
fluid, replacing it by “exhalation” and urination. The amniotic fluid protects the foetus
by cushioning it from outside crushing, allows it to move and develop its muscular-
skeletal system, keeps it at an even temperature and allows the lungs and gut to mature.
The kidney and urine production at birth
The neonate has an immature kidney function at birth which makes it vulnerable to
water loss and fluid gain, such as losing fluid through rapid breathing or failure to feed.
The neonate‘s kidneys weigh about 23 g but have their full complement of filtering
units (nephrons); this weight will double in six months and treble by the end of the first
year eventually growing to its adult size by puberty which shows a ten-fold increase
from birth. The growth of the kidney depends on its work; if one kidney is removed the
other will double in size and take on the function of both. When the infant is born the
loss of placenta flow, followed by a rapid increase in the infant ‘s own renal blood flow,
causes a high vascular resistance in the neonate kidney. This results in a temporarily
reduced renal blood flow and filtration through the filtering units to produce urine;
however, as the infant starts to feed and the load presented to the kidney increases, 95
per cent of infants will pass urine in the first twenty-four hours after birth. The neonate
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will pass 20–35 ml of urine four times a day while intake is low and milk production
establishes in the mother, but this soon rises to 100–200 ml ten times a day by the tenth
day of life. The urine that is first produced shows reduced urea excretion because of the
overall tissue growth rate in the infant that uses the protein rather than allowing it to be
broken down in the liver. Also, in the first few days, urea is deposited in the kidney
medulla to create the concentration gradient for the Loop of Henle function in adjusting
water and sodium in the blood. Growth is thus sometimes referred to as the third kidney.
The kidney capillary network resistance reduces over the first few weeks of life, which
allows increasing filtration ability by the glomeruli, however, the newborn kidney
glomeruli capsules are formed of cuboid epithelium and are not fully replaced by thin
pavement epithelium and fully functional until after the first year.
3.2 The gross anatomy of the kidneys
The kidneys excrete the end products of metabolism and excess water (regulate the fluid
and electrolyte balance of the body). The kidneys also have endocrine functions
producing and releasing erythropoietin which affects red blood cell formation, renin
which influences blood pressure, 1,25-dihydroxycholecalciferol, which is involved in
the control of calcium metabolism.
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Fig. 1.3:
The two kidneys are reddish brown, bean-shaped organs. They lie retroperitoneally on
the posterior abdominal wall, within the paravertebra gutters resting on the muscles of
the posterior abdominal wall. They are largely under cover of the costal margin. They
lie craniocaudally at the level of the T12 - L3 vertebrae. The hilum is about 5 cm from
the midline at the level of L1.
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Fig.1.4:
Dimension and Weight
A normal kidney measures approximately 10 - 12 cm in length, 5 - 6 cm in width, and
2.5 - 3 cm in thickness (AP dimension). The average weight in adult males is about 150
g while in females it is about 135g
External Topography
Each kidney has 2 borders (medial and lateral) 2 surfaces (anterior and posterior) and 2
poles (superior and inferior).
The upper pole of the right kidney usually lies slightly (about 2.5 cm) inferior to that of
the left kidney, probably owing to its relationship to the bulk of the right lobe of the
liver.
Relations
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Relations of the kidney could be described in respect of its anterior and posterior
surfaces
Posterior Relations
Posteriorly, the right and left kidneys are related to similar structures with a little
exception. They include: the diaphragm, psoas major, quadratuslumborum,
aponeurosis of the transversus abdominis muscles, 12th rib, transverse process of L1
vertebra, subcostal vessels (artery and vein), Subcostal iliohypogastric and ilio-
inguinal nerves. The posterior surface of the left kidney is related to the eleventh rib.
Anterior Relations of the right and left
kidney Right
Right Left
right suprarenal gland left suprarenal gland
 liver and is separated from it by  stomach
hepatorenal recess  spleen
 the descending part of the  body and tail of the pancreas
duodenum  left colic flexure and the
 right colic flexure beginning of the descending
colon,
 Proximal parts of the jejunum.
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Fig. 1.5a: Posterior Relation of the Kidney Fig.1.5b: Anterior Relation of the
right and left Kidney
Renal hilum and renal pelvis
The renal hilum is a deep vertical opening on the medial margin of each kidney through
which renal vessels, lymphatics, nerves and ureter enter and leave the substance of the
kidney. Internally, the hilum is continuous with the renal sinus. Perinephric fat
continues into the hilum and sinus and surrounds all structures.
The Renal pelvis is the funnel shaped commencement of the ureter. It is normally the
most posterior of the three main structures in the hilum. The capacity of the average
pelvis is less than 5 ml.
Arterial supply: the arterial supply to the kidneys is from the renal arteries which arise
as a lateral branch of the abdominal aorta at the level of L2. Each renal artery divides
into five segmental arteries at the hilum which, in turn, divide sequentially into lobar,
interlobar, arcuate and cortical radial branches. The cortical radial branches give rise
to the afferent arterioles which supply the glomeruli and go on to become efferent
arterioles. The differential pressures between afferent and efferent arterioles lead to the
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production of an ultrafiltrate which then passes through, and is modified by, the nephron
to produce urine.
Veinous Drainage: The kidneys are drained by the right and left renal veins. Each
renal vein drains into the IVC.
Lymphatic Drainage is to the para-aortic lymph nodes.
Innervation: The innervations of the kidney is from renal plexus which have
sympathetic and parasympathetic parts. The sympathetic contribution is from the
leastsplanchnic nerve and lumbar splanchnic nerve while the parasympathetic supply is
from the vagal trunk.
General structure of the kidneys
Each kidney consists of an outer renal cortex and an inner renal medulla. The renal
cortex lies beneath the renal capsule. It is a continuous band of pale tissue that
completely surrounds the renal medulla. Extensions of the renal cortex called the renal
columns (of Bertin) project into the inner aspect of the kidney; they divide the renal
medulla into discontinuous aggregations of striated triangular-shaped tissue called the
renal pyramids. The bases of the renal pyramids are directed outward, towards the renal
cortex, while the apex of each renal pyramid projects inward, towards the renal sinus as
renal papilla. The renal papilla is surrounded by a minor calyx. The minor calices
receive urine and represent the proximal parts of the tube that will eventually form the
ureter. In the renal sinus, several minor calices unite to form a major calyx, and two or
three major calices unite to form the renal pelvis, which is the funnel-shaped superior
end of the ureters.
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Fig. 1.6: The general structure of the kidney
Clinical correlates
Kidney Stones
i. Kidney stones are hard objects usually found in the renal pelvis of the kidney. They
are normally 2–3 mm in diameter, with a smooth or a jagged surface. About 1% of all
autopsies reveal kidney stones, and many of the stones occur without causing
symptoms. The symptoms associated with kidney stones occur when a stone passes into
the ureter, resulting in intense referred pain down the back, side, and groin area. The
ureter contracts around the stone, causing the stone to irritate the epithelium and
produce bleeding. Kidney stones can also block the ureter, cause ulceration in the ureter,
and increase the probability of bacterial infections. About 65% of all kidney stones are
composed of calcium oxylate mixed with calcium phosphate, 15% are magnesium
ammonium phosphate, and 10% are uric acid or cystine. The cause of kidney stones is
usually obscure. Predisposing conditions include a concentrated urine and an
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abnormally high calcium concentration in the urine, although the cause of the high
calcium concentration is usually unknown.
ii. Renal failure can result from any condition that interferes with kidney function.
Acute renal failure occurs when kidney damage is extensive and leads to the
accumulation of urea in the blood and to acidosis. In complete renal failure, death can
occur in 1–2 weeks. Acute renal failure can result from acute glomerular nephritis, or it
can be caused by damage to or blockage of the renal tubules. Some poisons, such as
mercuric ions or carbon tetrachloride, which are common to certain industrial processes,
cause necrosis of the nephron epithelium. If the damage does not interrupt the basement
membrane surrounding the nephrons, extensive regeneration can occur within 2–3
weeks. Severe ischemia associated with circulatory shock resulting from sympathetic
vasoconstriction of the renal blood vessels can cause necrosis of the epithelial cells of
the nephron.
Chronic renal failure results when so many nephrons are permanently damaged that
the nephrons that remain functional cannot adequately compensate.
iii. Diabetic nephropathy is a disease of the kidney associated with diabetes mellitus,
and it is the principal cause of chronic renal failure. It damages renal glomeruli and
ultimately results in the destruction of functional nephrons through progressive scar
tissue formation, which is mediated in part by an inflammatory response.
iv. Other causes of renal failure can include: chronic glomerular nephritis, trauma to the
kidneys, the absence of kidney tissue caused by congenital abnormalities, tumors,
urinary tract obstruction by kidney stones, damage resulting from pyelonephritis
(inflammation of the renal pelvis).
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Self-Assessment Exercises (SAEs)
1. Describe the functions of the kidneys
ii. Describe the embryology of the kidneys
iii. Describe the anatomy of the kidneys
4.0 Conclusion
The kidney is the major organ of excretion in the body, it is a paired organ located at
the posterior aspect of the lumber region. About 30-50% of one kidney is sufficient for
the body to function normally. The kidneys filter about 180litters of fluid daily and over
99% of the filtrate are reabsorbed.
5.0 Summary
In this unit, you have learnt that:
i. The urinary system consists of the paired kidneys and ureters and the unpaired bladder
and urethra.
ii. The functions of the urinary system include excretion, regulation of blood volume
and pressure, regulation of concentration of solutes in the blood, vitamin D synthesis
and regulation of red blood cell synthesis.
iii. The anatomy and histology of the kidneys
iv. Clinical conditions associated with kidney malfunctions.
Some patients with hypertension are kept on a low-salt (low- sodium) diet. Propose an
explanation for this therapy
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7.0 References and other resources
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UNIT TWO- ANATOMY OF URETER
CONTENT
1.0 Introduction
2.0 Objectives
3.0 Main Content
3.1 Gross anatomy of the ureters
3.2 Vasculature of the ureters
3.3 Histology of the ureters
4.0 Conclusion
5.0 Summary
6.1 Activity
1.0 Introduction
The ureters are muscular tubes whose peristaltic contractions convey urine from the
kidneys to the urinary bladder. Each measures 25 cm in length and it comprise of the
renal pelvis, abdominal, pelvic and intravesical portions. Its luminal diameter is 3 mm
but is slightly less at three areas of constriction including: the pelvi-ureteric (uretero-
pelvic ) junction, where it crosses the common iliac vessels at the pelvic brim and where
it runs within the wall of the urinary bladder, which is its narrowest part.
2.0 Objectives
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At the end if this unit, you should be able to:
i. Describe the course of the ureters
ii. Describe in details the relations of the ureters
iii. Discuss the vasculature of the ureters
3.0 Main Content
3.1 Gross anatomy of the ureters
Each descends slightly medially anterior to psoas major, and enters the pelvic cavity
where it curves laterally, then medially as it runs down to open into the base of the
urinary bladder.
Relations
Abdominal ureter
In the abdomen, both ureters courses anterior to the psoas major, tip of lumbar process,
genitofemoral nerve and posterior to gonadal (testicular & ovarian) vessels. The right
ureter courses lateral to the inferior vena cava and posterior to the descending part of
duodenum, right colic and ileocolic vessels, lower part of mesentery and terminal ileum.
The left ureter courses posterior to the left colic vessels, loops of jejunum, sigmoid
colon and mesentery, medial to the aorta and lateral to the inferior mesenteric vessels.
At the pelvic brim the ureter courses anterior to the bifurcation of the common iliac
artery and the sacroiliac joint
Pelvic ureter
The ureter in both sexes runs anterior to lateral wall of the lesser pelvis, internal iliac
artery (IIA), commencement of anterior trunk of IIA and anteromedial to umbilical
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artery, inferior vesical artery and middle rectal artery. In males the ureter courses
inferior to the vas deferens and anterosuperior to the seminal vesicle; while in females
it courses posterior to the ovary, posteroinferior (and later lateral) to the uterine artery,
lateral uterus and then anterior vagina
3.2 Vasculature of the ureters
Arterial supply
The ureters receive arterial branches from adjacent vessels as they pass towards the
bladder. These vesssels include ureteric branches of the renal arteries; abdominal aorta,
the testicular or ovarian arteries, and the common iliac arteries; the internal iliac arteries
(i.e. superior vesical and uterine arteries). In all cases, arteries reaching the ureters
divide into ascending and descending branches, which form longitudinal anastomoses.
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Fig. 2.1:
Venous drainage
Veins draining the abdominal part drain into the renal and gonadal (testicular or ovarian)
veins. Veins draining the pelvic part drain into the internal iliac veins
Lymphatic drainage
Lymphatic drainage of the ureters follows a pattern similar to that of the arterial supply.
Lymph from the upper part of each ureter drains to the lumbar nodes; those from the
middle part of each ureter drains to lymph nodes associated with the common iliac
vessels; while lymph from the inferior part of each ureter drains to lymph nodes
associated with the external and internal iliac vessels.
33
Innervation
The innervations is autonomic having sympathetic and parasympathetic contributions
from T10 – L1 segment of the spinal cord and pelvic splanchnic nerve (S2 – S4)
respectively.
3.3 Histology of the ureters
The wall of the ureter is composed of an external adventitia, a smooth muscle layer and
an inner mucosal layer. The mucosal layer consists of the urothelium (transitional
epithelium) and an underlying connective tissue lamina propria. It has no muscularis
mucosae. The muscle bundles are so arranged that morphologically distinct longitudinal
and circular layers cannot be clearly distinguished.
Self Assessment
i. Describe the course of the ureters
ii. Describe in details the relations of the ureters
iii. Discuss the vasculature of the ureters
iv. Describe the phenomenon ―water under the bridgeǁ
4.0 Conclusion
The Ureter are the paired tubes that convey the excreted urine from the kidney to the
bladder. It has two parts viz: Abdominal and pelvic parts. Histologically the ureter is
lined by transitional epithelium.
5.0 Summary
34
i. The ureters are muscular tubes whose peristaltic contractions convey urine from the
kidneys to the urinary bladder. Each measures 25 cm in length and it comprise of the
renal pelvis, abdominal, pelvic and intravesical portions.
ii. The ureters receive arterial branches from adjacent vessels as they pass towards the
bladder.
iii. Lymphatic drainage of the ureters follows a pattern similar to that of the arterial
supply
iv. The venous drainage depends on the part of the ureter been drained.
Clinical correlates
Ureteric stones:
Ureteric stones are kidney stones that gradually move down the urinary system from
the kidneys to the bladder.
6.1 Activity: As provided by the facilitator

35
36
UNIT THREE- URINARY BLADDER
CONTENT
1.0 Introduction
2.0 Objectives
3.0 Main Content
3.1 Gross anatomy of the urinary bladder
3.2 Vasculature of the urinary bladder
3.3 Histology of the urinary bladder
4.0 Conclusion
5.0 Summary
6.1 Activity
1.0 Introduction
Infants are expected to be incontinent, but the ability to control voiding of urine depends
on a complete and functioning renal system, maturation of the nervous supply,
opportunity/support given to the child to void and cultural expectations. Children can
become anxious and regress if expectations are beyond their ability and control. The
maturation of control mechanisms usually takes up to five years for healthy children to
be dry in the day and overnight. The urinary bladder is a complex organ made of
specialised muscle layers and enervated by a reflex arc to the spine and central
37
coordination in the brain. Remember that if the child does not want to void, for whatever
reason, they can override the messages to their brain from their distending bladder.
2.0 Objectives
i. Discuss the Gross anatomy of the urinary bladder
ii. Explain Vasculature of the urinary bladder
iii. Explain Histology of the urinary bladder
3.0 Main Content
3.1 Gross anatomy of the urinary bladder
The urinary bladder is a hollow viscus with strong muscular wall characterized by its
distensibility. It is a temporary reservoir for urine. It varies in size, shape, position and
relations, according to its content and the state of neighbouring viscera. When empty,
the adult urinary bladder lies entirely in the lesser pelvis posterior to the pubic bones
but as it distends it expands anterosuperiorly into the abdominal cavity and may ascend
to the level of the umbilicus when fully distended. In infant and children, the urinary
bladder lies in the abdomen even when empty. The bladder usually enters the greater
pelvis by 6 years of age; It enters the lesser pelvis after puberty. When empty, it is
pyramidal in shape and has an apex, a base, two inferolateral surfaces, a superior surface
and the neck as shown in the diagram below.
38
Fig. 3.1:
The apex of the pyramid points forwards and from it a fibrous cord, the urachus, passes
upwards to the umbilicus as the median umbilical ligament. The base (posterior
surface, fundus) is triangular. In the male, the seminal vesicles lie on the outer posterior
surface of the bladder and are separated by the vas deferens. The rectum lies behind the
seminal vesicle. In the female, the vagina intervenes between the bladder and rectum.
Fig. 3.2:
39
The inferolateral surfaces are related inferiorly to the pelvic floor and anteriorly to the
retropubic fat pad and pubic bones.
The superior surface is triangular. In males it is completely covered by peritoneum
which posteriorly reflects on to the rectum as the rectovesical pouch while in females,
it is largely covered by peritoneum, which is reflected posteriorly onto the uterus at the
level of the internal os to form the vesicouterine pouch.
The bladder neck fuses with the prostate in the male whereas it lies directly on the
pelvic fascia (which surrounds the upper urethra) in the female. The pelvic fascia is
thickened in the form of the puboprostatic ligaments (male) and pubovesical ligaments
to hold the bladder neck in position.
Bladder Interior
The mucous membrane of the bladder is thrown into folds called rugae when the bladder
is empty except for the membrane overlying the trigone which is smooth.
Trigone is a triangular area on the interior of the base of the bladder. The superior angles
of the trigone mark the openings of the ureteric orifices while its inferior angle
corresponds to the internal urethral meatus.
3.2 Vasculature of the urinary bladder
Arterial supply: superior and inferior vesical arteries (branches of the internal iliac
artery.
Veinous drainage: The vesical veins coalesce around the bladder to form a plexus that
drains into the internal iliac vein.
40
Lymph drainage: lymphatic vessels from the superolateral aspects of the bladder pass
to the external iliac lymph nodes whereas those from the fundus and neck pass to the
internal iliac lymph nodes.
Nerve supply (Vesical Plexus): Sympathetic fibers are conveyed from inferior thoracic
and upper lumbar spinal cord levels to the vesical plexuses primarily through the
hypogastric plexuses and nerves, parasympathetic fibers from sacral spinal cord levels
are conveyed by the pelvic splanchnic nerves and the inferior hypogastric plexus. Motor
input to the detrusor muscle is from efferent parasympathetic fibres from S2–4. Fibres
from the same source convey inhibitory fibres to the internal sphincter so that co-
ordinated micturition can occur. Conversely, sympathetic efferent fibres inhibit the
detrusor and stimulate the sphincter.
Histology of the urinary bladder
The wall of the urinary bladder consists of three layers: an outer adventitial layer of soft
connective tissue (which in some regions possesses a serosal covering of peritoneum);
a smooth muscle coat composed of a triple layer of trabeculated smooth muscle known
as the detrusor muscle; and an inner mucosal layer which lines the interior of the bladder
with a transitional epithelium. The detrusor is thickened at the bladder neck to form the
internal urethra sphincter.
4.0 Conclusion
The Bladder is located in the pelvic cavity, just behind the pubic bone. It serve as a
storage tank for urine before the time of micturition. The prostate is locate at the neck
of the bladder. Histologically the bladder is lined by transitional epithelium.
41
5.0 Summary
i. The urinary bladder is a muscular organ that serves as a reservoir for urine and the
interior is made up of mucous membrane thrown into folds called rugae when the
bladder is empty with the exception of the membrane overlying the trigone which is
smooth.
ii. The Arterial supply to the bladder are the superior and inferior vesical arteries
(branches of the internal iliac artery).
iii. The veinous drainage includes The vesical veins coalesce around the bladder to form
a plexus that drains into the internal iliac vein.
iv. The Lymph drainage includes the lymphatic vessels from the superolateral aspects
of the bladder pass to the external iliac lymph nodes whereas those from the fundus and
neck pass to the internal iliac lymph nodes.
Clinical correlates
Urinary Bladder Cancer
In the United States, urinary bladder cancer affects more than 60,000 new patients each
year and is among the 10 most common cancers in men and women. Half the diagnosed
cases of urinary bladder cancer can be attributed to cigarette smoking, even 10 years or
more after cessation of smoking. When bladder cancer is detected early (the cancer is
confined to the bladder), the survival rate is 94%, whereas, if it is detected late (after it
has spread to other areas), the survival rate is 6%. Unfortunately, early detection of
urinary bladder cancer is especially challenging due to its rapid growth rate. Frequently,
blood in the urine is a symptom but, because this symptom is also associated with other,
42
less serious problems, it tends to be ignored. What is the statistics of bladder cancer in
Nigeria?
6.1 Activity – See Laboratory Manual or instruction as provided by the Facilitator
6.2 Please answer the following questions:
i. Discuss the Gross anatomy of the urinary bladder
ii. Explain Vasculature of the urinary bladder
iii. Explain Histology of the urinary bladder
iv. Describe the concept of urinary incompetence
43
UNIT FOUR- THE URETHRA
CONTENT
1.0 Introduction
2.0 Objectives
3.0 Main Content
3.1 Anatomy of the male urethra
3.2 Anatomy of the female urethra
3.3 Histology of the male and female urethra
4.0 Conclusion
5.0 Summary
6.1 Activity
1.0 Introduction
The urethra is a tube that exits the urinary bladder inferiorly and anteriorly. It carries
urine to the outside of the body. In males, the urethra extends to the end of the penis. In
females, it opens into the vestibule anterior to the vaginal opening. The female urethra
is approximately 4 cm in length, whereas the male urethra is approximately 20 cm.
2.0 Objectives
i. Discuss the anatomy and the functions of the urethra
ii. Discuss the differences between the male and female urethra
44
3.0 Main Content
3.1 Anatomy of the male urethra
The male urethra is approximately 20 cm long. It is considered in three parts:
Prostatic urethra (3 cm): bears a longitudinal elevation (urethral crest) on its posterior
wall. On either side of the crest a shallow depression, the prostatic sinus, marks the
drainage point for 15–20 prostatic ducts. The prostatic utricle is a 5 mm blind ending
tract which opens into an eminence in the middle of the crest at the verumontanum. The
ejaculatory ducts open on either side of the utricle.
Fig. 4.1:
Membranous urethra (2 cm): lies in the urogenital diaphragm and is surrounded by
the external urethral sphincter (sphincter urethrae).
Penile urethra (15 cm): traverses the corpus spongiosum of the penis to the external
urethral meatus.
45
Fig.4.2:
Vasculature of the male urethra
Arterial supply:
The blood supply is from the vessels of prostate, sphincter urethra and the corpus
spongiosum as it passes through them. They include branches of the inferior vesical
artery, middle rectal artery and internal pudendal artery.
Innervation:
The mucous membrane of the penile part receives a branch from the perineal nerve,
while the more proximal parts are innervated by the inferior hypogastric plexus having
sympathetic contribution from sacral sympathetic trunk and parasympathetic fibres
from the pelvic splanchnic nerve S2-S4.
Lymphatics
Lymphatic drainage is into the internal and external iliac lymph nodes.
3.2 Anatomy of the female urethra
The female urethra is a narrow membranous canal, about 4cm long, extending from the
internal urethra orifice at the lower angle of the trigone of the bladder to the external
46
urethra orifice. It is placed behind the symphysis pubis, embedded in the anterior wall
of the vagina and its direction is obliquely downward and forward. Its diameter when
undialated is about 6mm. It perforates the fascia of the urogenital diaphragm and its
external orifice is situated directly in front of the vagina opening and about 2.5cm
behind the clitoris.
Vasculature of the female urethra
Blood Supply
The upper part of the female urethra is supplied by the vagina arteries while the lower
end receives contribution from the internal pudendal artery.
The veins drain into vesical plexus and the internal pudendal veins.
Lymphatics
Lymph vessels pass mainly into the internal iliac lymph nodes but some reach the
external iliac groups of nodes.
Nerve Supply
Nerve supply is from the inferior hypogastric plexus and the perineal branch of the
pudendal nerve.
4.3 Histology of the male and female urethra
The urethra is composed of mucous membrane, supported by sub-mucous tissue which
connects it with the various structures through which it passes.
The mucous membrane, is lined by transitional epithelium (typical of urinary tract)
except at the navicular fossa (in males) and external urethra orifice where the mucosa
is lined by a non-keratinised stratified squamous epithelium. The urethra mucosa has
numerous mucous urethra glands (of Littre).
47
4.0 Conclusion
The Urethra is the tubes that convey the excreted urine from the bladder to the outside
of the body. In males it is about 20cm long while in female it is just 5cm long.
Histologically the urethra is also lined by transitional epithelium.
5.0 Summary
i. The urethra as a tube that exits the urinary bladder inferiorly and anteriorly. In
males, the urethra extends to the end of the penis. In females, it opens into the
vestibule anterior to the vaginal opening.
ii. The male urethra has 3 parts - prostatic, membranous and penile urethra.
6.1 Activity – As directed by the Facilitator
6.2 Please answer the following questions:
i. Discuss the anatomy and the functions of the urethra
ii. Describe with the aid of a diagram the difference between the male urethra and the
female urethra.
iii. From your experience what are the implications of the different structures of the
urethra for males and females in clinical care?
7.0 Reference and other resources
48
49
MODULE 2 THE ENDOCRINE SYSTEM
Unit 1 Hormones
Unit 2 Pituitary Gland and Hypothalamus
Unit 3 Thyroid and Parathyroid Glands
Unit 4 Adrenal Glands
Unit 5 Pancreas
Unit 6 Other Endocrine Glands
UNIT 1 HORMONES
CONTENTS
1.0 Introduction
2.0 Objectives
3.0 Main Content
3.1 Functions of the endocrine system
3.2 Transport of hormones in the blood
3.3 Interaction of hormones with their target tissues
3.4 Clinical correlates
4.0 Conclusion
5.0 Summary
6.0 Tutor-Marked Assessment
7.0 References/Further Reading
50
1.0 INTRODUCTION
The endocrine system is composed of endocrine glands, which are ductless glands
secreting chemical messengers into the circulatory system. In contrast, exocrine glands
have ducts that carry their secretions to surfaces. The term endocrine is derived from
the Greek words endo, meaning within, and krino, to separate. The term implies that
cells of endocrine glands produce chemical messengers within the glands that influence
tissues separated from the glands by some distance. The chemical messengers secreted
by endocrine glands are called hormones, a term derived from the Greek word hormon,
meaning to set into motion. Thus, hormones stimulate responses from cells.
2.0 OBJECTIVES
• describe the functions of the endocrine system
• define the terms endocrine gland and hormone
• explain how the regulation of hormone secretion is achieved
• describe the means by which hormones are transported and excreted.
3.1 Functions of the Endocrine System
The main regulatory functions of the endocrine system are the following:
1. Metabolism and tissue maturation. The endocrine system regulates the rate of
metabolism and influences the maturation of tissues, such as those of the nervous
system.
2. Ion regulation. The endocrine system helps regulate blood pH, as well as Na+, K+,
and Ca2+ concentrations in the blood.
51
3. Water balance. The endocrine system regulates water balance by controlling the
solute concentration of the blood.
4. Immune system regulation. The endocrine system helps control the production of
immune cells.
5. Heart rate and blood pressure regulation. The endocrine system helps regulate the
heart rate and blood pressure and helps prepare the body for physical activity.
6. Control of blood glucose and other nutrients. The endocrine system regulates blood
glucose levels and other nutrient levels in the blood.
7. Control of reproductive functions. The endocrine system controls the development
and functions of the reproductive systems in males and females.
8. Uterine contractions and milk release. The endocrine system regulates uterine
contractions during delivery and stimulates milk release from the breasts in lactating
females.
3.2 Transport of Hormones in the Blood
Hormones can be defined as chemicals secreted by a cell that affect the functions of
other cells. Once released, most hormones enter the bloodstream where they are carried
to their target cells. The target cells of a hormone are the cells that contain the receptors
for the hormone. A hormone cannot affect a cell unless the cell has receptors for it.
Many hormones in the body are derived from steroids. Steroids are soluble in lipids and
can therefore cross cell membranes very easily. Once a steroid hormone is inside a
cell, it binds to its receptor, which is commonly in the nucleus of the cell. The hormone-
receptor complex turns a gene on or off. When new genes are turned on or off, the cell
begins to carry out new functions, and this is ultimately how steroid hormones affect
52
their target cells. Examples of steroid hormones are estrogen, progesterone,
testosterone, and cortisol. Non -steroid hormones are those that are made of amino
acids or proteins. Proteins cannot cross the cell membrane easily. Therefore, these
hormones bind to receptors on the surface of the cell. The hormone-receptor complex
in the membrane usually activates a G-protein. The G-protein causes enzymes inside
the cell to be turned on. Different chemical reactions then begin inside the cell. The cell
now takes on new functions. Prostaglandins are local hormones. They are derived from
lipid molecules and typically do not travel in the bloodstream to find their target cells.
Instead, their target cells are located close by. They have the same effects as other
hormones and are produced by many body organs, including the kidneys, stomach,
uterus, heart, and brain.
Transport of Hormones in the Blood
Water-soluble hormones (peptides and catecholamines) are dissolved in the plasma and
transported from their sites of synthesis to target tissues, where they diffuse out of the
capillaries, into the interstitial fluid, and ultimately to target cells. Steroid and thyroid
hormones, in contrast, circulate in the blood mainly bound to plasma proteins. Usually
less than 10 percent of steroid or thyroid hormones in the plasma exist free in solution.
For example, more than 99 percent of the thyroxine in the blood is bound to plasma
proteins. However, protein-bound hormones cannot easily diffuse across the capillaries
and gain access to their target cells and are therefore biologically inactive until they
dissociate from plasma proteins. The relatively large amounts of hormones bound to
proteins serve as reservoirs, replenishing the concentration of free hormones when they
53
are bound to target receptors or lost from the circulation. Binding of hormones to plasma
proteins greatly slows their clearance from the plasma.
3.3 Interaction of Hormones with their Target Tissues
Hormones bind to proteins or glycoproteins called receptors. The portion of each protein
or glycoprotein molecule where a hormone bind is called a receptor site, or binding site.
The shape and chemical characteristics of each receptor site allow only a specific type
of chemical messenger to bind to it. The tendency for each type of chemical messenger
to bind to a specific type of receptor, and not to others, is called specificity. Insulin
therefore binds to insulin receptors but not to receptors for growth hormone. Some
hormones, however, can bind to a number of different receptors that are closely related.
For example, epinephrine can bind to more than one type of epinephrine receptor.
Hormone receptors have a high affinity for the hormones that bind to them, so only a
small concentration of a given hormone results in a significant number of receptors with
hormones bound to them. Hormones are secreted and distributed throughout the body
by the circulatory system, but the presence or absence of specific receptor molecules in
cells determines which cells will or will not respond to each hormone. For example,
there are receptors for thyroid stimulating hormone (TSH) in cells of the thyroid gland,
but there are no such receptors in most other cells of the body. Consequently, cells of
the thyroid gland produce a response when exposed to TSH, but cells without receptor
molecules do not respond to it. In general, the number of functional receptors affects
the amplitude of a cell’s response to a hormone. More receptors produce a larger
response than fewer receptors. The number of functional receptors can be regulated. In
down-regulation, the number of functional receptors is reduced by temporary or
54
permanent removal of receptors from the plasma membrane, inactivation of receptors,
or decreased synthesis of replacement receptors. In up-regulation, the number of
functional receptors is increased through increased receptor synthesis or availability.
Drugs with structures similar to specific hormones may compete with those hormones
for their receptors. A drug that binds to a hormone receptor and activates it is called an
agonist for that hormone. A drug that binds to a hormone receptor and inhibits its action
is called an antagonist for that hormone. For example, drugs exist that compete with
epinephrine for its receptor. Epinephrine agonists activate epinephrine receptors,
whereas epinephrine antagonists inhibit them.
3.4 Clinical Correlates
Lipid- and Water-Soluble Hormones in Medicine
Specific hormones are given as treatments for certain illnesses. Hormones that are
soluble in lipids, such as steroids, can be taken orally because they can diff use across
the wall of the stomach and intestine into the circulatory system. Examples include the
synthetic estrogen and progesterone-like hormones in birth control pills and steroids
that reduce the severity of inflammation, such as prednisone. In contrast to lipid soluble
hormones, protein hormones cannot diffuse across the wall of the intestine because they
are not lipid-soluble. Furthermore, protein hormones are not transported across the wall
of the intestine because they are broken down to individual amino acids by the digestive
system. The normal structure of a protein hormone is therefore destroyed, and its
physiological activity is lost. Consequently, protein hormones must be injected rather
than taken orally. The most commonly administered protein hormone is insulin, which
is prescribed for the treatment of diabetes mellitus.
55
4.0 Conclusion
Hormones are substances produce by endocrine glands in the body, and are transported
in the blood to their organs or tissue of function. All hormones are synthesis from
protein, so good nutrition is required for maximum hormone production.
5.0 SUMMARY
• The main regulatory functions include water balance, uterine contractions and milk
release, metabolism and tissue maturation, ion regulation, heart rate and blood pressure
regulation, control of blood glucose and other nutrients, immune system regulation, and
control of reproductive functions
• Endocrine glands produce hormones that are released into the interstitial fluid and
diffuse into the blood. Hormones act on target tissues, producing specific responses.
The protein group of hormones includes hormones that are proteins, glycoproteins,
polypeptides, and amino acid derivatives. The lipid group of hormones includes
hormones that are steroids and fatty acid derivatives.
• Generalizations about the differences between the endocrine and nervous systems
include the following: (a) The endocrine system is amplitude-modulated, whereas the
nervous system is frequency modulated, and (b) the response of target tissues to
hormones is usually slower and of longer duration than their response to neurons.
• Water-soluble hormones, such as proteins, epinephrine, and norepinephrine, are
rapidly removed from the blood. These hormones regulate activities that have a rapid
onset and a short duration. Lipid-soluble hormones and thyroid hormones are not
quickly removed from the blood. They produce a prolonged effect.
56
6.0 SELF – ASSESSMENT EXERCISE
Given these events:
1. The α subunit of a G protein interacts with Ca2+ channels.
2. Calcium ions diff use into the cell.
3. The α subunit of a G protein is activated.
57
UNIT 2 THE PITUITARY GLAND AND HYPOTHALAMUS
CONTENTS
1.0 Introduction
2.0 Objectives
3.0 Main Content
3.1 Structure of the pituitary gland
4.0 Conclusion
5.0 Summary
1.0 INTRODUCTION
The pituitary gland is located at the base of the brain and is controlled by the
hypothalamus. This gland is well protected by a bony structure called the sella turcica.
Just superior to the gland is the optic chiasm, which carries visual information to the
brain for interpretation. The pituitary is divided into two lobes—the anterior and the
posterior.
The location of the pituitary gland
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The pituitary gland, or hypophysis, secretes nine major hormones that regulate
numerous body functions and the secretory activity of several other endocrine glands.
The hypothalamus of the brain and the pituitary gland are major sites where the
nervous and endocrine systems interact. The hypothalamus regulates the secretory
activity of the pituitary gland. Hormones, sensory information that enters the central
nervous system, and emotions, in turn, influence the activity of the hypothalamus.
2.0 OBJECTIVES
• describe the structure of the pituitary gland
• discuss the hormones of the pituitary gland
3.1 Structure of the pituitary gland
The pituitary gland is roughly 1 cm in diameter, weighs 0.5–1.0 g, and rests in the sella
turcica of the sphenoid bone. It is located inferior to the hypothalamus and is connected
to it by a stalk of tissue called the infundibulum. The posterior pituitary, or
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neurohypophysis is continuous with the brain. It is formed during embryonic
development from an outgrowth of the inferior part of the brain in the area of the
hypothalamus. The outgrowth forms the infundibulum, and the distal end of the
infundibulum enlarges to form the posterior pituitary.
Relationship of the pituitary gland to the brain
Portal vessels are blood vessels that begin in a primary capillary network, extend some
distance, and end in a secondary capillary network. The hypothalamohypophyseal
portal system is one of two major portal systems. The other is the hepatic portal system.
The hypothalamohypophyseal portal system extends from the hypothalamus to the
anterior pituitary. The primary capillary network in the hypothalamus is supplied with
blood from arteries that deliver blood to the hypothalamus. From the primary capillary
network, the hypothalamohypophyseal portal vessels carry blood to a secondary
capillary network in the anterior pituitary. Veins from the secondary capillary network
eventually merge with the general circulation. Hormones, produced and secreted by
neurons of the hypothalamus, enter the primary capillary network and are carried to the
secondary capillary network. There the hormones leave the blood and act on cells of the
anterior pituitary. They act either as releasing hormones, increasing the secretion of
anterior pituitary hormones, or as inhibiting hormones, decreasing the secretion of
anterior pituitary hormones. Each releasing hormone stimulates and each inhibiting
hormone inhibits the production and secretion of a specific hormone by the anterior
pituitary. In response to the releasing hormones, anterior pituitary cells secrete
hormones that enter the secondary capillary network and are carried by the general
circulation to their target tissues. Thus, the hypothalamohypophyseal portal system
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provides a means by which the hypothalamus, using hormones as chemical messengers,
regulates the secretory activity of the anterior pituitary.
There is no portal system to carry hypothalamic hormones to the posterior pituitary.
Hormones released from the posterior pituitary are produced by neurosecretory cells
with their cell bodies located in the hypothalamus. The axons of these cells extend from
the hypothalamus through the infundibulum into the posterior pituitary and form a nerve
tract called the hypothalamohypophyseal tract. Hormones produced in the
hypothalamus pass down these axons in tiny vesicles and are stored in secretory vesicles
in the enlarged ends of the axons. Action potentials originating in the neuron cell bodies
in the hypothalamus are propagated along the axons to the axon terminals in the
posterior pituitary. The action potentials cause the release of hormones from the axon
terminals, and they enter the circulatory system.
Hormones of the pituitary gland
Posterior Pituitary Hormones
The posterior pituitary stores and secretes two polypeptide hormones called antidiuretic
hormone and oxytocin. A separate population of cells secretes each hormone.
Antidiuretic hormone (ADH) is so named because it prevents the output of large
amounts of urine (diuresis). ADH binds to membrane-bound receptors and increases
water reabsorption by kidney tubules. This results in less water loss from the blood into
the urine, and urine volume decreases. ADH can also cause blood vessels to constrict
when released in large amounts. Consequently, it is sometimes called vasopressin.
Oxytocin binds to membrane – bound receptors and causes contraction of the smooth
muscle cells of the uterus and milk ejection, or milk “let-down” from the breasts in
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lactating women. Oxytocin plays an important role in the expulsion of the fetus from
the uterus during delivery by stimulating uterine smooth muscle contraction.
Commercial preparations of oxytocin are given under certain conditions to assist in
childbirth and to constrict uterine blood vessels following childbirth. Oxytocin also
causes the contraction of uterine smooth muscle in non - pregnant women during
menses, which helps expel the uterine epithelium and a small amount of blood.
Oxytocin also promotes the movement of sperm cells through the uterus and uterine
tubes. Oxytocin has been called the great facilitator of life. In addition to its role in
reproduction and lactation, oxytocin produced in the limbic system and other parts of
the brain influences a variety of social and non- social behaviours in females and males.
In many species, oxytocin promotes pair bonding, sexual behaviour, and parental care.
In humans, oxytocin promotes social interactions, feelings of attachment, and maternal
behaviour. Oxytocin also inhibits memory, decreases the stress response, reduces
feelings of anxiety, suppresses appetite, and raises the pain threshold.
Anterior Pituitary Hormones
Releasing and inhibiting hormones that pass from the hypothalamus through the
hypothalamohypophyseal portal system to the anterior pituitary influence anterior
pituitary secretions. The hormones secreted are proteins, glycoproteins, or polypeptides.
They are transported in the circulatory system and bind to membrane-bound receptor
molecules on their target cells. For the most part, each hormone is secreted by a separate
cell type. The major hormones of the anterior pituitary, their target tissues, and their
effects on target tissues are listed in below. Anterior pituitary hormones include growth
62
hormone, thyroid stimulating hormone, adrenocorticotropic hormone and related
substances, luteinizing hormone, follicle-stimulating hormone, and prolactin.
Hormones of the pituitary gland
Mechanism by which hypothalamus controls pituitary secretion
Almost all secretion by the pituitary is controlled by either hormonal or nervous signals
from the hypothalamus. Indeed, when the pituitary gland is removed from its normal
position beneath the hypothalamus and transplanted to some other part of the body, its
rates of secretion of the different hormones (except for prolactin) fall to very low levels.
Secretion from the posterior pituitary is controlled by nerve signals that originate in the
63
hypothalamus and terminate in the posterior pituitary. In contrast, secretion by the
anterior pituitary is controlled by hormones called hypothalamic releasing and
hypothalamic inhibitory hormones (or factors) secreted within the hypothalamus and
then conducted to the anterior pituitary through minute blood vessels called
hypothalamichypophysial portal vessels. In the anterior pituitary, these releasing and
inhibitory hormones act on the glandular cells to control their secretion.
The hypothalamus receives signals from many sources in the nervous system. Thus,
when a person is exposed to pain, a portion of the pain signal is transmitted into the
hypothalamus. Likewise, when a person experiences some powerful depressing or
exciting thought, a portion of the signal is transmitted into the hypothalamus. Olfactory
stimuli denoting pleasant or unpleasant smells transmit strong signal components
directly and through the amygdaloid nuclei into the hypothalamus. Even the
concentrations of nutrients, electrolytes, water, and various hormones in the blood
excite or inhibit various portions of the hypothalamus. Thus, the hypothalamus is a
collecting center for information concerning the internal well-being of the body, and
much of this information is used to control secretions of the many globally important
pituitary hormones.
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Hypothalamic- hypophyseal system
Growth Hormone
Growth hormone (GH) stimulates the growth of most tissues and, through its effect on
the epiphyseal plates of bones, GH plays a role in determining how tall a person
becomes. GH promotes the protein synthesis necessary for growth by increasing the
movement of amino acids into cells and promoting their incorporation into proteins. It
also decreases the breakdown of proteins.
GH plays an important role in regulating blood nutrient levels between meals and
during periods of fasting. GH increases lipolysis, the breakdown of lipids. Fatty acids
released from fat cells into the blood circulate to other tissues and are used as an
energy source. The use of fatty acids as an energy source “spares” the use of blood
glucose, helping maintain blood sugar levels. In addition, GH increases glucose
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synthesis by the liver, which releases glucose into the blood. Thus, through its effects
on adipose tissue and the liver, GH maintains or increases blood sugar levels. GH has
indirect effects on some tissues by stimulating the production of polypeptides called
somatomedins, primarily by the liver but also by skeletal muscle and other tissues.
Somatomedins circulate in the blood, stimulating growth in cartilage and bone and
increasing the synthesis of protein in skeletal muscles. The best known somatomedins
are two polypeptide hormones produced by the liver called insulin-like growth factor
I and II because of the similarity of their structure to insulin. Two hormones released
from the hypothalamus regulate the secretion of GH. Growth hormone– releasing
hormone (GHRH) stimulates the secretion of GH, whereas growth hormone inhibiting
hormone (GHIH) inhibits the secretion of GH. Stimuli that influence GH secretion act
on the hypothalamus to increase or decrease the secretion of the releasing and inhibiting
hormones. Low blood glucose levels and stress stimulate the secretion of GH, and high
blood glucose levels inhibit the secretion of GH. An increase in certain amino acids
stimulates increased GH secretion. Most people have a rhythm of growth hormone
secretion, with daily peak levels occurring during deep sleep. Growth hormone
secretion also increases during periods of fasting and prolonged exercise.
Blood growth hormone levels do not become greatly elevated during periods of rapid
growth, although children tend to have somewhat higher blood levels of growth
hormone than do adults. In addition to growth hormone, genetics, nutrition, and sex
hormones influence growth.
Clinical correlates
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1. Gigantism is a condition of abnormally increased height that usually results from
excessive cartilage and bone formation at the epiphyseal plates of long bones. The most
common type of gigantism, pituitary gigantism, results from excess secretion of GH.
The large stature of some individuals, however, can result from genetic factors rather
than from abnormal levels of GH.
2. Acromegaly is caused by excess GH secretion in adults, and many pituitary giants
develop acromegaly later in life. The GH stimulates the growth of connective tissue,
including bones. Bones in adults can increase in diameter and thickness, but not in
length because the epiphyseal plates have ossified. The effects of acromegaly are most
apparent in the face and hands. Hypersecretion of GH can also cause elevated blood
glucose levels and may eventually lead to diabetes mellitus.
3. Dwarfism, the condition in which a person is abnormally short, is the opposite of
gigantism. Pituitary dwarfism results when abnormally low levels of GH affect the
whole body, thus producing a small person who is normally proportioned.
Achondroplasia, or achondroplastic dwarfism, is the most common type of
dwarfism; it produces a person with a nearly normal-sized trunk and head but shorter-
than-normal limbs. Achondroplasia is a genetic disorder, not a hormonal disorder.
Modern genetic engineering has provided a source of human GH for people who
produce inadequate quantities. Human genes for GH have been successfully introduced
into bacteria using genetic engineering techniques. The gene in the bacteria causes GH
synthesis, and the GH can be extracted from the medium in which the bacteria are
grown.
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4.0 Conclusion
The Pituitary gland is located in cranial cavity, it regulate most of the endocrine
activities in the body. The gland has two parts, the anterior and posterior parts. The
gland is controlled by a feedback mechanisms.
5.0 SUMMARY
• The pituitary gland secretes at least nine hormones that regulate numerous body
functions and other endocrine glands. The hypothalamus regulates pituitary gland
activity through hormones and action potentials.
• The posterior pituitary develops from the floor of the brain and connects to the
hypothalamus by the infundibulum. The anterior pituitary develops from the roof of the
mouth.
• The hypothalamohypophyseal portal system connects the hypothalamus and the
anterior pituitary. Through the portal system, the hormones inhibit or stimulate hormone
production in the anterior pituitary. The hypothalamohypophyseal tract connects the
hypothalamus and the posterior pituitary. Hormones are produced in hypothalamic
neurons. The hormones move down the axons of the tract and are secreted from the
posterior pituitary.
• Antidiuretic hormone (ADH) promotes water retention by the kidneys. Oxytocin
promotes uterine contractions during delivery and causes milk ejection in lactating
women. Growth hormone (GH) stimulates growth in most tissues and is a regulator of
metabolism. GH stimulates the uptake of amino acids and their conversion into proteins
and stimulates the breakdown of fats and the synthesis of glucose.
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SELF – ASSESSMENT EXERCISE
Examine the histological structure of the pituitary gland ad distinguish between the
anterior and posterior pituitary glands.
Tutor Mark Assignment
describe the structure of the pituitary gland
• discuss the hormones of the pituitary gland
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UNIT 3 THE THYROID AND PARATHYROID GLANDS
CONTENTS
1.0 Introduction
2.0 Objectives
3.0 Main Content
3.1 Structure of the thyroid gland
4.0 Conclusion
5.0 Summary
1.0 INTRODUCTION
The thyroid gland consists of two lobes connected by a narrow band called the
isthmus. The lobes are located on each side of the trachea, just inferior to the larynx.
The thyroid gland is one of the largest endocrine glands, with a weight of
approximately20 g. It is highly vascular and appears more red than its surrounding
tissues.
2.0 OBJECTIVES
At the end of this unit, you will be able to:
• describe the anatomy of the thyroid and parathyroid gland
• discuss the thyroid hormones and parathyroid hormones.
3.0 MAIN CONTENT
3.1 Structure of the thyroid gland
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The thyroid gland contains numerous follicles, which are small spheres whose walls are
composed of a single layer of cuboidal epithelial cells. Each thyroid follicle is filled
with proteins, called thyroglobulin which are synthesized and secreted by the cells of
the thyroid follicles. Large amounts of the thyroid hormones are stored in the thyroid
follicles as part of the thyroglobulin molecules. Between the follicles, a delicate network
of loose connective tissue contains scattered parafollicular cells, or C cells.
Calcitonin is secreted from the parafollicular cells and plays a role in reducing the
concentration of Ca2+ in the body fluids when Ca2+ levels become elevated.
Thyroid and parathyroid glands
Thyroid hormones
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The thyroid hormones are triiodothyronine (T3) and tetraiodothyronine (T4).
Another name for T4 is thyroxine. T3 constitutes 10% of thyroid gland secretions and
T4 90%. Although calcitonin is secreted by the parafollicular cells of the thyroid gland,
T3 and T4 are considered to be the thyroid hormones because they are more clinically
important and because they are secreted from the thyroid follicles.
T3 and T4 Synthesis
Thyroid-stimulating hormone (TSH) from the anterior pituitary stimulates thyroid
hormone synthesis and secretion. TSH causes an increase in the synthesis of T3 and T4,
which are then stored inside the thyroid follicles as part of thyroglobulin. TSH also
causes T3 and T4 to be released from thyroglobulin and to enter the circulatory system.
An adequate amount of iodine in the diet is required for thyroid hormone synthesis
because iodine is a component of T3 and T4. The following events in the thyroid
follicles result in T3 and T4 synthesis and secretion:
1. Iodide ions (I−) are taken up by thyroid follicle cells by secondary active transport
(symport). The movement of the I− is against a concentration gradient of approximately
30-fold in healthy individuals. TSH promotes the uptake of I−.
2. Iodide is transported into the follicle lumen and converted into iodine (Io).
3. Thyroglobulin molecules, which contain numerous tyrosine amino acids, are
synthesized, packaged into secretory vesicles, and secreted into the lumen of the follicle.
4. Iodine atoms are bound to a few of the tyrosine amino acids of thyroglobulin,
producing monoiodotyrosine, which has one iodine atom, or diiodotyrosine, which has
two iodine atoms. After the tyrosines are iodinated, two diiodotyrosine combine to form
tetraiodothyronine (T4), which has four iodine atoms. Also, one monoiodotyrosine and
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one diiodotyrosine combine to form triiodothyronine (T3), which has three iodine
atoms. A 2–4 months reserve supply of T3 and T4 is stored within the thyroid follicles
as part of thyroglobulin.
5. Thyroglobulin is taken into the thyroid follicle cells by endocytosis.
6. Lysosomes fuse with the endocytic vesicles, and proteolytic enzymes break down
thyroglobulin to release T3, T4, and amino acids.
7. T3 and T4 are lipid soluble and diff use through the plasma membranes of the follicle
cells into the interstitial fluid and finally into the blood. The remaining amino acids of
thyroglobulin are used again to synthesize more thyroglobulin.
Effects of Thyroid Hormones
Thyroid hormones interact with their target tissues in a fashion similar to that of the
steroid hormones. They readily diffuse through plasma membranes into the cytoplasm
of cells. Within cells, they bind to receptor molecules in the nuclei. Thyroid hormones
combined with their receptor molecules interact with DNA in the nuclei to influence
genes and initiate new protein synthesis. The newly synthesized proteins within the
target cells mediate the cells’ response to thyroid hormones. It takes up to a week after
the administration of thyroid hormones for a maximal response to develop, and new
protein synthesis occupies much of that time. Thyroid hormones affect nearly every
tissue in the body, but not all tissues respond identically. Metabolism is primarily
affected in some tissues, and growth and maturation are influenced in others.
The normal rate of metabolism for an individual depends on an adequate supply of
thyroid hormone, which increases the rate at which glucose, fat, and protein are
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metabolized. The increased rate of metabolism produces heat. Thyroid hormones
increase the activity of N+–K+ pumps, which helps increase the body temperature as
ATP molecules are broken down. Thyroid hormones also alter the number and activity
of mitochondria, resulting in greater ATP synthesis and heat production. The metabolic
rate can increase 60%–100% when blood thyroid hormones are elevated. Low levels of
thyroid hormones lead to the opposite effect. Maintaining normal body temperature
depends on an adequate amount of thyroid hormones.
Normal growth and maturation of organs also depend on thyroid hormones. For
example, bone, hair, teeth, connective tissue, and nervous tissue require thyroid
hormones for normal growth and development. Both normal growth and normal
maturation of the brain require thyroid hormones.
Regulation of Thyroid Hormone Secretion
Thyroid hormone secretion is regulated by hormones produced in the hypothalamus and
anterior pituitary. Thyrotropin – releasing hormone (TRH) is produced in the
hypothalamus. Chronic exposure to cold increases TRH secretion, whereas stress, such
as starvation, injury, and infections, decreases TRH secretion. TRH stimulates TSH
secretion from the anterior pituitary. Small fluctuations in blood levels of TSH occur
on a daily basis, with a small nocturnal increase. TSH stimulates the secretion of thyroid
hormones from the thyroid gland. TSH also increases the synthesis of thyroid hormones,
as well as causing an increase in thyroid gland cell size and number. Decreased blood
levels of TSH lead to decreased secretion of thyroid hormones and thyroid gland
atrophy. Thyroid hormones have a negative-feedback effect on the hypothalamus and
anterior pituitary gland. As thyroid hormone levels increase in the circulatory system,
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they inhibit TRH and TSH secretion. Also, if the thyroid gland is removed or if the
secretion of thyroid hormones declines, TSH levels in the blood increase dramatically.
Calcitonin
In addition to secreting thyroid hormones, the thyroid gland secretes a hormone called
calcitonin produced by the parafollicular cells. Calcitonin secretion is directly regulated
by blood Ca2+ levels.. As blood Ca2+ concentration increases, calcitonin secretion
increases, and, as blood Ca2+ concentration decreases, calcitonin secretion decreases.
Calcitonin binds to membrane-bound receptors of osteoclasts and inhibits them, which
reduces the rate of bone matrix breakdown and the release of Ca2+ from bone into the
blood. Calcitonin may prevent blood Ca2+ levels from becoming overly elevated
following a meal that contains a high concentration of Ca2+. The role of calcitonin in
humans is unclear. It may be important in slowing bone turnover during periods of rapid
growth. Calcitonin helps prevent elevated blood Ca2+ levels, but a lack of calcitonin
secretion does not result in a prolonged increase in blood Ca2+ levels. Other
mechanisms controlling blood Ca2+ levels, such as parathyroid hormone and vitamin
D, are able to compensate for the lack of calcitonin secretion.
Parathyroid glands
The parathyroid glands are usually embedded in the posterior part of each lobe of the
thyroid gland. Usually, four parathyroid glands are present, with their cells organized
in densely packed masses or cords rather than in follicles. The parathyroid glands
secrete a polypeptide hormone called parathyroid hormone (PTH), which is essential
for the regulation of blood Ca2+ levels. PTH is much more important than calcitonin in
regulating blood Ca2+ levels. PTH regulates blood Ca2+ levels by affecting Ca2+
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release from bones, Ca2+ excretion by the kidneys, and vitamin D formation by the
kidneys, which promotes Ca2+ absorption by the small intestine. PTH increases the
release of Ca2+ from bones into blood by increasing the number of osteoclasts in bone,
which results in increased bone breakdown. PTH promotes an increase in osteoclast
numbers by stimulating stem cells in red bone marrow to differentiate and become
osteoclasts. The effect of PTH on osteoclast formation, however, is indirect. PTH binds
to its receptors on osteoblasts, stimulating them. The osteoblasts, through surface
molecules and released chemicals, stimulate osteoclast stem cells to become osteoclasts.
In the kidneys, PTH increases Ca2+ reabsorption from the urine into the blood so that
less calcium leaves the body in urine. PTH also increases the formation of active vitamin
D in the kidneys. The vitamin D is carried by the blood to epithelial cells of the small
intestine, where it promotes the synthesis of Ca2+ transport proteins. PTH increases
blood Ca2+ levels by increasing the rate of active vitamin D formation, which in turn
increases the rate of Ca2+ absorption in the intestine. PTH secretion is directly regulated
by blood Ca2+ levels. As blood Ca2+ concentration increases, PTH secretion decreases;
as blood Ca2+ concentration decreases, PTH secretion increases. This regulation keeps
blood Ca2+ levels fluctuating within a normal range of values.
Clinical correlates
1. Hypothyroidism is reduced or no secretion of thyroid hormones. It can be caused by
inadequate TSH stimulation of the thyroid gland, an inability of the thyroid gland to
produce thyroid hormones, or the surgical removal or destruction of the thyroid gland
for various reasons. Damage to the pituitary gland can result in decreased TSH
secretion. Tumors and inadequate blood delivery to the pituitary because of blood loss
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during childbirth are causes of pituitary insufficiency. Lack of iodine in the diet can
result in decreased thyroid hormone levels because iodine is necessary for the synthesis
of thyroid hormones. Damage to the thyroid gland by drugs, chemicals, or an
autoimmune disease (Hashimoto disease) can also reduce thyroid hormone production.
Hyposecretion of thyroid hormones decreases the rate of metabolism. Low body
temperature, weight gain, reduced appetite, reduced heart rate, reduced blood pressure,
decreased muscle tone, constipation, drowsiness, and apathy are major symptoms.
2. Hyperthyroidism is an abnormally increased secretion of thyroid hormones. After
diabetes mellitus, the most common endocrine disorder is a type of hyperthyroidism
called Graves disease. It is an autoimmune disorder that produces a specific
immunoglobulin, called thyroid-stimulating immunoglobulin (TSI).
3. Goiter is a chronic enlargement of the thyroid gland not due to a tumor. Goiter
eventually develops with chronic hypersecretion of thyroid hormones. TSI in Graves
disease or elevated TSH produced by pituitary tumors results in continual
overstimulation of the thyroid gland. Thyroid hormone synthesis increases and thyroid
gland cells increase in size and number, producing goiter. Hypothyroidism caused by
an iodine deficiency in the diet can also cause goiter. Without adequate iodine to
synthesize thyroid hormones, blood levels of thyroid hormones decrease. The reduced
negative feedback of thyroid hormones on the anterior pituitary and hypothalamus
results in elevated TSH secretion. TSH causes increased thyroid gland cell size and
number and increased thyroglobulin synthesis, even though there is not enough iodine
to synthesize thyroid hormones. Historically, goiters were common in people from areas
where the soil was depleted of iodine. Consequently, plants grown in these areas, called
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goiter belts, had little iodine in them and caused iodine-deficient diets. Iodized salt has
nearly eliminated iodine-deficiency goiters. However, it remains a problem in some
developing countries
4.0 Conclusion
The Thyroid gland is located just below the larynx, it has two lobes and an adjoining
part, the hormones produce by thyroid gland are T3 and T4. The Para-thyroid glands
are 4 smaller glands located in the posterior aspect of the thyroid gland, they produce
para-thyroid hormone.
5.0 SUMMARY
• The thyroid gland is just inferior to the larynx. The thyroid gland is composed of small,
hollow balls of cells called follicles, which contain thyroglobulin. Para-follicular cells
are scattered throughout the thyroid gland.
• Thyroid hormone (T3 and T4) synthesis occurs in thyroid follicles. Iodide ions are
taken into the follicles by secondary active transport (symport), transported to the
follicle lumen, and converted to iodine. Thyroglobulin is secreted into the follicle
lumen. Tyrosine molecules with iodine combine to form T3 and T4 within
thyroglobulin. Thyroglobulin is taken into follicle cells and is broken down; T3 and T4
diff use from the follicles to the blood.
• Thyroid hormones are transported in the blood. Thyroid hormones bind to thyroxine-
binding globulin and other plasma proteins. The plasma proteins prolong the time that
thyroid hormones remain in the blood. T3 and T4 bind with nuclear receptor molecules
and initiate new protein synthesis.T3 and T4 affect nearly every tissue in the body. T3
and T4 increase the rate of glucose, fat, and protein metabolism in many tissues, thus
78
increasing body temperature. Normal growth of many tissues is dependent on T3 and
T4.
• Thyrotropin-releasing hormone (TRH) and thyroid-stimulating hormone (TSH)
regulate T3 and T4 secretion. TRH from the hypothalamus increases TSH secretion.
TRH increases as a result of chronic exposure to cold and decreases as a result of food
deprivation, injury, and infections. Increased TSH from the anterior pituitary increases
T3 and T4 secretion.
• The para-follicular cells secrete calcitonin. An increase in blood calcium levels
stimulates calcitonin secretion. Calcitonin decreases blood Ca2+ levels by inhibiting
osteoclasts.
• The parathyroid glands are embedded in the thyroid gland. Parathyroid hormone
(PTH) increases blood Ca2+ levels. PTH stimulates an increase in osteoclast numbers,
resulting in increased breakdown of bone. PTH promotes Ca2+ reabsorption by the
kidneys and the formation of active vitamin D by the kidneys. Active vitamin D
increases calcium absorption by the intestine. A decrease in blood Ca2+ levels
stimulates PTH secretion.
Examine the slides of the thyroid and parathyroid glands under the microscope in the
histology laboratory
1. Describe events in the thyroid follicles that result in the synthesis and secretion of
thyroid hormones.
2. Describe the actions of thyroid hormones T3 and T4.
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3. What are some common disorders associated with thyroid dysfunction?
4. What two cell types are found in the parathyroid glands?
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UNIT 4 ADRENAL GLANDS
CONTENTS
1.0 Introduction
2.0 Objectives
3.0 Main Content
3.1 Anatomy of the adrenal glands
4.0 Conclusion
5.0 Summary
1.0 INTRODUCTION
An adrenal gland sits on top of each kidney. It is divided into two portions—the adrenal
medulla and the adrenal cortex. The adrenal medulla is the central portion of the gland
and secretes epinephrine and norepinephrine. These hormones produce the same
effects that the sympathetic nervous system produces. They increase heart rate,
breathing rate, blood pressure, and all the other actions that prepare the body for
stressful situations.
2.0 OBJECTIVES
• Describe the anatomy of the adrenal gland
• List the hormones released by the adrenal glands and give the functions of each.
3.0 MAIN CONTENT
3.1 Anatomy of the adrenal glands
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The adrenal glands, or suprarenal (above the kidney) glands, are two small glands that
are located superior to each kidney. Each adrenal gland has an inner part, called the
adrenal medulla (marrow or middle), and an outer part, called the adrenal cortex (bark
or outer). The cortex has three indistinct layers: the zona glomerulosa, the zona
fasciculata, and the zona reticularis.
The adrenal glands
The medulla and the three layers of the cortex are structurally and functionally
specialized. In many ways, an adrenal gland is four glands in one.
1. The zona glomerulosa, a thin layer of cells that lies just underneath the capsule,
constitutes about 15 percent of the adrenal cortex. These cells are the only ones in the
adrenal gland capable of secreting significant amounts of aldosterone because they
contain the enzyme aldosterone synthase, which is necessary forsynthesis of
aldosterone. The secretion of these cells is controlled mainly by the extracellular fluid
82
concentrations of angiotensin II and potassium, both of which stimulate aldosterone
secretion.
2. The zona fasciculata, the middle and widest layer, constitutes about 75 percent of the
adrenal cortex and secretes the glucocorticoids cortisol and corticosterone, as well as
small amounts of adrenal androgens and estrogens. The secretion of these cells is
controlled in large part by the hypothalamicpituitary axis via adrenocorticotropic
hormone (ACTH).
3. The zona reticularis, the deep layer of the cortex, secretes the adrenal androgens
dehydroepiandrosterone (DHEA) and androstenedione, as well as small amounts of
estrogens and some glucocorticoids. ACTH also regulates secretion of these cells,
although other factors such as cortical androgen-stimulating hormone, released from
the pituitary, may also be involved. The mechanisms for controlling adrenal androgen
production, however, are not nearly as well understood as those for glucocorticoids and
mineralocorticoids.
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Secretion of adrenocortical hormones by the different zones of the adrenal cortex and
secretion of catecholamines by the adrenal medulla.
Hormones of the adrenal medulla
Approximately 80% of the hormone released from the adrenal medulla is epinephrine,
or adrenaline. The remaining 20% is norepinephrine. The adrenal medulla consists of
cells derived from the same cells that give rise to postganglionic sympathetic neurons,
which secrete norepinephrine. Epinephrine is derived from norepinephrine. The adrenal
medulla and the sympathetic division function together to prepare the body for physical
activity, producing the “fight-or-flight” response. Some of the major effects of the
hormones released from the adrenal medulla are the following:
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1. Increased breakdown of glycogen to glucose in the liver, the release of the glucose
into the blood, and the release of fatty acids from fat cells. The glucose and fatty acids
are used as energy sources to maintain the body’s increased rate of metabolism.
2. Increased heart rate, which increases blood pressure and blood delivery to tissues.
3. Increased vasodilation of blood vessels of the heart and skeletal muscle, which
increases blood flow to the organs responsible for increased physical activity. The
hormones increase vasoconstriction of blood vessels to the internal organs and skin,
which decreases blood flow to organs not directly involved in physical activity.
4. Increased metabolic rate of several tissues, especially skeletal muscle, cardiac
muscle, and nervous tissue. The release of adrenal medullary hormones primarily
occurs in response to stimulation by sympathetic neurons because the adrenal medulla
is a specialized part of the autonomic nervous system. Several conditions, including
exercise, emotional excitement, injury, stress, and low blood glucose levels, lead to the
release of adrenal medullary hormones.
Hormones of the adrenal cortex
The adrenal cortex secretes three hormone types: mineralocorticoids, glucocorticoids,
and androgens. All are similar in structure in that they are steroids, highly specialized
lipids that are derived from cholesterol. Because they are lipid-soluble, they are not
stored in the adrenal gland cells but diff use from the cells as they are synthesized.
Adrenal cortical hormones are transported in the blood in combination with specific
plasma proteins; they are metabolized in the liver and excreted in the bile and urine.
The hormones of the adrenal cortex bind to nuclear receptors and stimulate the synthesis
of specific proteins that are responsible for producing the cell’s responses.
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Mineralocorticoids
The major secretory products of the zona glomerulosa are the mineralocorticoids. The
mineralocorticoids are so named because they are steroids, produced by the adrenal
cortex, that affect the “minerals” Na+, K+, and H+. Aldosterone is produced in the
greatest amounts, although other, closely related mineralocorticoids are also secreted.
Aldosterone increases the rate of Na+ reabsorption by the kidneys, thereby increasing
blood Na+ levels. Sodium reabsorption can result in increased water reabsorption by
the kidneys and an increase in blood volume, providing ADH is also secreted. Increased
blood volume can increase blood pressure. Aldosterone increases K+ and H+ excretion
into the urine by the kidneys, thereby decreasing blood levels of K+ and H+. When
aldosterone is secreted in high concentrations, it can result in abnormally low blood
levels of K+ and H+. The reduction in H+ can cause alkalosis, an abnormally elevated
pH of body fluids.
Glucocorticoids
The zona fasciculata of the adrenal cortex primarily secretes glucocorticoids. The
glucocorticoids are so named because they are steroids produced by the adrenal cortex
that affect glucose metabolism. The major glucocorticoid is cortisol. The target tissues
and responses to the glucocorticoids are numerous. The two major types of responses
to glucocorticoids are classified as metabolic and anti-inflammatory. Cortisol increases
the breakdown of protein and fat and increases their conversion to forms that can be
used as energy sources by the body. For example, cortisol causes proteins in skeletal
muscles to be broken down to amino acids, which are then released into the circulatory
system. Cortisol acts on the liver, causing it to convert amino acids to glucose, which is
86
released into the blood or stored as glycogen. Thus, cortisol increases blood sugar
levels. Cortisol also acts on adipose tissue, causing fat stored in fat cells to be broken
down to fatty acids, which are released into the circulation. The glucose and fatty acids
released into the circulatory system are taken up by tissues and used as sources of
energy.
Glucocorticoids decrease the intensity of the inflammatory and immune responses by
decreasing both the number of white blood cells and the secretion of inflammatory
chemicals from tissues. Cortisone, a steroid closely related to cortisol, is often given as
a medication to reduce inflammation that occurs in response to injuries. It is also given
to reduce the immune and inflammatory responses that occur as a result of allergic
reactions or diseases resulting from abnormal immune responses, such as rheumatoid
arthritis or asthma. In response to stressful conditions, cortisol is secreted in larger than
normal amounts. Cortisol aids the body in responding to stressful conditions by
providing energy sources for tissues. If stressful conditions are prolonged, however,
immunity can be suppressed enough to make the body susceptible to infections. Cortisol
secretion is regulated through the hypothalamus and anterior pituitary gland. Stress and
low blood glucose levels stimulate increased corticotropin-releasing hormone (CRH)
from the hypothalamus. CRH stimulates increased adrenocorticotropic hormone
(ACTH) secretion from the anterior pituitary gland. ACTH stimulates increased
cortisol secretion.
Clinical correlates
I. Adrenal Tumors
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The two major disorders of the adrenal medulla are both tumors. Pheochromocytoma
is a benign tumor; neuroblastoma is a malignant tumor.
Symptoms, resulting from the release of large amounts of epinephrine and
norepinephrine, include hypertension (high blood pressure), sweating, nervousness,
pallor, and tachycardia (rapid heart rate). The high blood pressure results from the effect
of these hormones on the heart and blood vessels and is correlated with an increased
chance of heart disease and stroke.
II. Chronic adrenocortical insufficiency, often called Addison disease, results from
abnormally low levels of aldosterone and cortisol in the blood. The cause of many cases
of chronic adrenocortical insufficiency is unknown, but it frequently results from an
autoimmune disease in which the body’s defense mechanisms inappropriately destroy
the adrenal cortex. Other causes are infections and tumors that damage the adrenal
cortex.
I. Aldosteronism is caused by an excess production of aldosterone. Primary
aldosteronism results from an adrenal cortex tumor, and secondary aldosteronism
occurs when an extraneous factor, such as an overproduction of renin, a substance
produced by the kidneys, increases aldosterone secretion. Major symptoms of
aldosteronism are hypernatremia (elevated blood Na+), hypokalemia (decreased K+),
alkalosis (decreased H+), and high blood pressure due to the retention of water and Na+
by the kidneys.
IV. Cushing syndrome is a disorder characterized by the hypersecretion of cortisol and
androgens and possibly by excess aldosterone production. Most cases are caused by
excess ACTH production by nonpituitary tumors, which usually result from a type of
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lung cancer. Some cases of increased ACTH secretion do result from pituitary tumors.
Sometimes adrenal tumors or unidentified causes can be responsible for hypersecretion
of the adrenal cortex without increases in ACTH secretion.
4.0 Conclusion
The Adrenal glands are two, located on the superior pole of each kidney, the gland has
two part, the cortex and the medulla. The gland develop from the neural crest cells.
Some of the hormones produce by adrenal gland are Aldosterone and Cortisol.
5.0 SUMMARY
• The adrenal glands are near the superior poles of the kidneys. The adrenal medulla
arises from the same cells that give rise to postganglionic sympathetic neurons.
• The adrenal cortex is divided into three layers: the zona glomerulosa, the zona
fasciculata, and the zona reticularis.
• Epinephrine accounts for 80% and norepinephrine for 20% of the adrenal medulla
hormones. The adrenal medulla hormones prepare the body for physical activity.
• The zona glomerulosa secretes the mineralocorticoids, especially aldosterone.
Aldosterone acts on the kidneys to increase Na+ and to decrease K+ and H+ levels in
the blood.
• The zona fasciculata secretes glucocorticoids, especially cortisol. Cortisol increases
fat and protein breakdown, increases glucose synthesis from amino acids, decreases the
inflammatory response.
• The zona reticularis secretes androgens. In females, androgens stimulate axillary and
pubic hair growth and sexual drive
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I. Examine microscopic slides of the adrenal gland in the histology laboratory
II. Distinguish between the darker cortex with vertically arranged rows of cells and the
lighter medulla.
What controls glucocorticoid secretion?
90
UNIT 5 PANCREAS
CONTENTS
1.0 Introduction
2.0 Objectives
3.0 Main Content
3.1 Anatomy of the pancreas
4.0 Conclusion
5.0 Summary
1.0 INTRODUCTION
The pancreas is located behind the stomach. It is an endocrine gland as well as an
exocrine gland. It is considered an exocrine gland because it secretes digestive enzymes
into a duct that leads to the small intestine. It is considered an endocrine gland because
it contains structures known as islets of Langerhans that secrete hormones into the
bloodstream. The islets of Langerhans secrete two hormones—insulin and glucagon.
2.0 OBJECTIVES
• describe the anatomy of the pancreas
• identify the pancreatic hormones and to explain their physiological effects.
3.0 MAIN CONTENT
3.1 Anatomy of the pancreas
91
The pancreas lies retroperitoneally in roughly the transpyloric plane. For descriptive
purposes it is divided into head, neck, body and tail. The head lies in the C-curve of the
duodenum and sends out the uncinate process which hooks posteriorly to the superior
mesenteric vessels as these travel from behind the pancreas into the root of the
mesentery. Posteriorly lie the inferior vena cava, the commencement of the portal vein,
aorta, superior mesenteric vessels, the crura of diaphragm, coeliac plexus, the left
kidney and suprarenal gland. The tortuous splenic artery runs along the upper border of
the pancreas. The splenic vein runs behind the gland, receives the inferior mesenteric
vein and joins the superior mesenteric to form the portal vein behind the pancreatic
neck.
To complete this list of important posterior relationships, the common bile duct lies
either in a groove in the right extremity of the gland or embedded in its substance, as it
passes to open into the second part of the duodenum. Anteriorly lies the stomach
separated by the lesser sac. To the left, the pancreatic tail lies against the hilum of the
spleen. Blood is supplied from the splenic and the pancreaticoduodenal arteries; the
corresponding veins drain into the portal system.
Pancreatic hormones
Insulin promotes the uptake of glucose by cells. It therefore reduces glucose
concentrations in the bloodstream. It also promotes the transport of amino acids into
cells and increases protein synthesis. Glucagon increases glucose concentrations in the
bloodstream and slows down protein synthesis.
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Effect of Insulin and Glucagon on Their Target Tissues
Insulin
Insulin increases the uptake of glucose and amino acids by target cells. Once insulin
binds to its receptors, the receptors cause specific proteins in the membrane to become
phosphorylated. Part of the cell’s response to insulin is to increase the number of
transport proteins in the membrane of cells for glucose and amino acids. The major
target tissues of insulin are the liver, adipose tissue, the skeletal muscles, and the satiety
center within the hypothalamus of the brain. The satiety center is a collection of
neurons in the hypothalamus that controls appetite. Unlike the satiety center, most of
the nervous system does not depend on insulin for the uptake of glucose. Insulin is very
important for the normal functioning of the nervous system, however, because insulin
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regulates blood glucose levels. If blood glucose levels are not maintained within a
normal range, the brain malfunctions because glucose is its primary energy source.
When insulin levels increase, the movement of glucose and amino acids into cells
increases. Glucose molecules that are not immediately used as an energy source are
stored as glycogen in the liver, skeletal muscle, and other tissues, or they are converted
to fat in adipose tissue. Amino acids are used to synthesize proteins.
When insulin levels decrease, the opposite effects are observed. The movement of
glucose and amino acids into tissues slows. Glycogen is broken down to glucose, which
is released from the liver, but not from skeletal muscle. Adipose tissue releases fatty
acids, and proteins are broken down into amino acids, especially in skeletal muscle. The
amino acids are released into the blood, taken up by the liver, and used to synthesize
glucose, which is released into the blood. When insulin levels decrease, the liver uses
fatty acids to make acetoacetic acid, which is converted to acetone and _-
hydroxybutyric acid. These three substances collectively are referred to as ketone
bodies. The liver releases the ketone bodies into the blood, from which other tissues
take them up and use them as a source of energy. The ketone bodies are smaller, more
readily used “packets” of energy than are fatty acids. Ketone bodies, however, are acids
that can adversely aff ect blood pH if too many of them are produced. In addition, when
insulin levels are low, the liver releases cholesterol and triglycerides into the blood.
Glucagon
Glucagon increases blood sugar and ketone levels. Glucagon primarily influences the
liver, although it has some effect on skeletal muscle and adipose tissue. The pancreas
secretes glucagon into the hepatic portal system, which carries blood to the liver from
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the pancreas and intestines. Glucagon binds to membrane-bound receptors, activates G
proteins, and increases cAMP synthesis. In general, glucagon causes the breakdown of
glycogen to glucose and increases glucose synthesis from amino acids. The release of
glucose from the liver increases blood glucose levels.
Regulation of pancreatic hormones
Insulin
Blood levels of nutrients, neural stimulation, and hormones control the secretion of
insulin. Elevated blood levels of glucose directly affect the β cells and stimulate insulin
secretion. Low blood levels of glucose directly inhibit insulin secretion. Thus, blood
glucose levels play a major role in the regulation of insulin secretion. Certain amino
acids also stimulate insulin secretion by acting directly on the _ cells. After a meal,
when glucose and amino acid levels increase in the circulatory system, insulin secretion
increases. During periods of fasting, when blood glucose levels are low, the rate of
insulin secretion declines. The autonomic nervous system also controls insulin
secretion. The parasympathetic stimulation of digestive system organs is associated
with food intake. Parasympathetic stimulation of the pancreas increases its secretion of
insulin and digestive enzymes. Sympathetic stimulation inhibits insulin secretion and
helps prevent a rapid fall in blood glucose levels during periods of physical activity or
excitement. This response is important for maintaining normal functioning of the
nervous system. Gastrointestinal hormones involved with the regulation of digestion,
such as gastrin, secretin, and cholecystokinin, increase insulin secretion.
95
Glucagon
Low blood glucose levels stimulate glucagon secretion, and high blood glucose levels
inhibit it. Certain amino acids and sympathetic stimulation also increase glucagon
secretion. After a high-protein meal, amino acids increase both insulin and glucagon
secretion. Insulin causes target tissues to accept the amino acids for protein synthesis,
and glucagon increases the process of glucose synthesis from amino acids in the liver.
Clinical correlates
Diabetes mellitus results from the inadequate secretion of insulin or the inability of
tissues to respond to insulin. As a result, blood sugar levels increase. The two major
types of diabetes are type 1 and type 2 diabetes. Type 1 diabetes mellitus, also called
insulin dependent diabetes mellitus (IDDM), results from diminished or absent insulin
secretion. It affects approximately 5%–10% of people with diabetes mellitus and most
commonly occurs in young people. Type 1 diabetes mellitus develops as a result of
autoimmune destruction of the pancreatic islets, and symptoms appear after
approximately 90% of the islets have been destroyed. Heredity plays a role in the
condition, although the initiation of pancreatic islet destruction may involve a viral
infection of the pancreas. Type 2 diabetes mellitus, also called noninsulin-dependent
diabetes mellitus (NIDDM), results from insulin resistance, the inability of tissues to
respond normally to insulin. It affects approximately 90%– 95% of people who have
diabetes mellitus and usually develops in people older than 40–45 years of age, although
the age of onset varies considerably. People with type 2 diabetes mellitus have a reduced
number of functional receptors for insulin, or one or more of the enzymes activated by
96
the insulin receptor are defective. Heredity influences the likelihood of developing type
2 diabetes, but it is not as important a risk factor as for type 1 diabetes.
Three potentially life-threatening conditions are associated with untreated diabetes
mellitus: diabetic ketoacidosis, hyperglycaemic hyperosmolar state, and insulin shock.
 Diabetic ketoacidosis (DKA) is the triad of hyperglycemia, ketosis, and
acidosis. Ketosis is the presence of excess ketone bodies in the blood.
 Hyperglycemic hyperosmolar state (HHS) consists of very elevated blood
sugar levels. It is most likely to develop in type 2 diabetics who have enough
insulin to prevent ketosis, but not enough insulin to prevent hyperglycemia.
 Insulin shock occurs when there is too much insulin relative to the amount of
blood glucose. Too much insulin, too little food intake after an injection of
insulin, or increased metabolism of glucose due to excess exercise by a diabetic
patient can cause insulin shock. The high levels of insulin cause target tissues to
take up glucose at a very high rate. As a result, blood glucose levels rapidly fall
to a low level.
4.0 Conclusion
The Pancreas is located in the abdominal cavity, it is retro-peritoneal, and the exocrine
portion of the pancreas produces pancreatic digestive juices. The endocrine portion
consists of the pancreatic islets, the alpha cells secretes glucagon and beta cells secrete
insulin.
5.0 SUMMARY
• The exocrine portion of the pancreas consists of a complex duct system, which ends
in small sacs, called acini, which produce pancreatic digestive juices.
97
• The endocrine portion consists of the pancreatic islets. Each islet is composed of alpha
cells, which secrete glucagon, and beta cells, which secrete insulin.
• Insulin’s target tissues are the liver, adipose tissue, muscle, and the satiety center in
the hypothalamus. The nervous system is not a target tissue, but it does rely on blood
glucose levels maintained by insulin.
• Insulin increases the uptake of glucose and amino acids by cells. Glucose is used for
energy, stored as glycogen, or converted into fats. Amino acids are used to synthesize
proteins. Low levels of insulin promote the formation of ketone bodies by the liver.
• Glucagon’s target tissue is mainly the liver. Glucagon causes the breakdown of
glycogen to glucose and the synthesis of glucose from amino acids. The liver releases
glucose into the blood.
• Insulin secretion increases because of elevated blood glucose levels, an increase in
some amino acids, parasympathetic stimulation, and gastrointestinal hormones.
Sympathetic stimulation decreases insulin secretion.
• Glucagon secretion is stimulated by low blood glucose levels, certain amino acids,
and sympathetic stimulation. Somatostatin inhibits insulin and glucagon secretion.
I. Examine the microscopic slides of the pancreatic tissue in the histology laboratory
and note the pancreatic islets which are the endocrine portion of the pancreas.
II. In the gross anatomy laboratory, study the anatomy of the pancreas and its relations.
6.0 Tutor Mark Assignment
1. What are the physiological effects of the pancreatic hormones?
98
2. What are causes of diabetes mellitus (insulin deficiency)?
99
UNIT 6 OTHER ENDOCRINE GLANDS
CONTENTS
1.0 Introduction
2.0 Objectives
3.0 Main Content
3.1 Pineal body
4.0 Conclusion
5.0 Summary
1.0 INTRODUCTION
There are other hormone producing organs which most people are not aware of or
consider as parts of the endocrine system. They will be discussed in great details in this
chapter, they include the pineal gland, thymus and the hormone – like substances. We
will discuss the testis and ovaries as well.
2.0 OBJECTIVES
• discuss the anatomy and functions of other glands with endocrine functions.
• define autocrine and paracrine agents
• discuss the age-related changes that occur in the endocrinesystem.
100
3.0 MAIN CONTENT
3.1 Pineal body
The pineal gland is a small, pinecone-shaped structure located superior and posterior to
the thalamus of the brain. The pineal gland produces a hormone called melatonin, which
inhibits the functions of the reproductive system in some animals. Melatonin helps to
regulate your circadian rhythms, which is your biological clock. Your biological clock
helps you decide when you should be awake or asleep. Melatonin is also thought to play
a role in the onset of puberty. Tumors that destroy the pineal gland correlate with early
sexual development, and tumors that result in pineal hormone secretion correlate with
retarded development of the reproductive system. It is not clear, however, if the pineal
gland controls the onset of puberty.
The amount of light detected by the eyes regulates the rate of melatonin secretion. The
axons of some neurons in the retina pass from the optic chiasm to the suprachiasmatic
nucleus in the hypothalamus, which influences the pineal gland through sympathetic
neurons. Increased light exposure inhibits melatonin secretion, whereas darkness allows
melatonin secretion. Melatonin is sometimes called the “hormone of darkness” because
its production increases in the dark. In many animals, longer day length (shorter nights)
causes a decrease in melatonin secretion, whereas shorter day length (longer nights)
causes an increase in melatonin secretion. For example, in animals that breed in the
spring, increased day length results in decreased melatonin secretion. With decreased
inhibition of the hypothalamus by melatonin, sex hormone production increases, which
promotes the development of reproductive structures and behavior. In the fall,
101
decreased day length results in increased melatonin secretion, decreased sex hormone
production, atrophy of reproductive
Thymus gland
The thymus is in the neck and superior to the heart in the thorax; it secretes a hormone
called thymosin. Both the thymus and thymosin play an important role in the
development and maturation of the immune system
Thymosin promotes the production of certain lymphocytes.
Other hormone producing organs include:
Cholecystokinins are released from the gastrointestinal tract. They regulate digestive
functions by influencing the activity of the stomach, intestines, liver, and pancreas. The
kidneys secrete a hormone in response to reduced oxygen levels in the kidney. The
hormone is called erythropoietin. It acts on red bone marrow to increase the production
of red blood cells. In pregnant women, the placenta is an important source of hormones
that maintain pregnancy and stimulate breast development. These hormones include
estrogen, progesterone, and human chorionic gonadotropin, which is similar in structure
and function to LH. These hormones are essential to the maintenance of pregnancy
Hormone - like Substances
Autocrine chemical messengers are chemicals released by a cell that affect the cell
producing it or affect nearby cells of the same cell type. Examples of autocrine chemical
messengers include a group of related chemical mediators called eicosanoids, which are
derived from fatty acids. The eicosanoids include prostaglandins, thromboxanes,
prostacyclins, and leukotrienes.
102
Paracrine chemical messengers are chemicals released by a cell that affect nearby cells
of a different cell type. Examples of paracrine chemical messengers include growth
factors, clotting factors, and histamine. Autocrine and paracrine chemical messengers
differ from hormones in that they are not secreted from discrete endocrine glands, they
have local effects rather than systemic effects, or they have functions that are not
understood adequately to explain their role in the body. The schemes used to classify
chemicals on the basis of their functions are useful, but they do not indicate that a
specific molecule always performs as the same type of chemical messenger in every
place it is found. Some chemical messengers, such as prostaglandins, have both
autocrine and paracrine functions. Furthermore, some of these chemicals can also act as
hormones. Testosterone produced in the testes has a paracrine effect on the development
of sperm cells, but it is released into the blood and has an endocrine effect on skeletal
muscle development.
Effects of aging on the endocrine system
Age-related changes to the endocrine system include a gradual decrease in the secretion
of some, but not all, endocrine glands. Some of the decreases in secretion may be due
to a decrease in physical activity as people age. GH secretion decreases as people age,
and the decrease is greatest in people who do not exercise. It may not occur in older
people who exercise regularly. Decreasing GH levels may explain some of the gradual
decrease in bone and muscle mass and some of the increase in adipose tissue in many
elderly people.
103
Administering GH to slow or prevent the consequences of aging has not been
established to be effective, however, and unwanted side effects are possible. A decrease
in melatonin secretion may influence age-related changes in sleep patterns. The
secretion of thyroid hormones decreases slightly with age. Age-related damage to the
thyroid gland by the immune system can occur, and this happens in women more than
in men. Approximately 10% of elderly women have some reduction in thyroid hormone
secretion.
Parathyroid hormone secretion does not appear to decrease with age. Blood levels of
Ca2+ may decrease slightly because of reduced dietary calcium intake and vitamin D
levels. The greatest risk is a loss of bone matrix as parathyroid hormone increases to
maintain blood levels of Ca2+ within their normal range.
Reproductive hormone secretion gradually declines in elderly men, and women
experience menopause.
There are no age-related decreases in the ability to regulate blood glucose levels. There
is an age-related tendency to develop type 2 diabetes mellitus in those who have a
familial tendency to do so, and it is correlated with age-related increases in body weight.
Thymosin from the thymus decreases with age. Fewer immature lymphocytes are able
to mature and become functional, and the immune system becomes less effective in
protecting the body. There is an increased susceptibility to infection and to cancer.
4.0 Conclusion
The other hormone producing organs in the body are; the pineal gland, thymus, the testis
and ovaries. They produce hormones that act locally. The pineal gland produces
melatonin, thymosin by thymus and erythropoietin by the kidney.
104
5.0 SUMMARY
• The pineal gland produces melatonin, which can inhibit reproductive maturation and
may regulate sleep–wake cycles.
• The thymus produces thymosin, which is involved in the development of the immune
system.
• The kidneys produce erythropoietin, which stimulates red blood cell production.
• Autocrine chemical messengers are chemicals that locally affect cells producing them
or affect cells of the same type.
• There is a gradual decrease in the secretion rate of most, but not all, hormones. Some
decreases are secondary to gradual decreases in physical activity.
discuss the anatomy and functions of other glands with endocrine functions.
discuss the age-related changes that occur in the endocrine system
6.0 Tutor Mark Assignment
What are autocrine and paracrine agents
105
106

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NSC 217 HUMAN ANATOMY (II) 2

glands shall be taught.

COURSE CODE: NSC 217

COURSE TITLE: Human Anatomy II

COURSE UNITS: 2 Credit units (18 hours of instruction online; 6 hours of

Discussion forum online/tutorial; 24 hours of laboratory practical)

YEAR: 2 SEMESTER: First

CON-CURRENT COURSES: NSc 213, 215, 217, 209, 219

SESSION: _______ COURSE WEBSITE: www.noun.edu.ng/

Dr. Adewole O.S. MBBS, PhD, (Associate Professor).

Dr. Abiodun A. O. MBBS, FWCS, M.Sc. (Senior Lecturer)

Dr. Ayannuga A. A. MBBS, Ph.D (Senior Lecturer)

Dr. Adeyemi D.A. PhD (Senior Lecturer)

Department of Anatomy and Cell Biology, College of Health Sciences,

Obafemi Awolowo University, Ile-Ife, Nigeria

COURSE EDITORS: Dr O.O. Irinoye and Dr E.O Oladogba

PROGRAMME LEADER: Professor Mba Okoronkwo OON

COURSE COORDINATOR: _______________________________

COURSE REVIEWER Dr S S Bello MBBS, PhD

Department of Anatomy, FBMS, College of Health Sciences, Usmanu Danfodiyo

University, Sokoto, Nigeria

Table of Contents Page

Working through the Course 3

Equipment and Software Needed to Access Course 5

Number and Places of Meeting 6

Schedule of Assignments with Dates 7

How to get the most from this Course 8

MODULE 1- Urinary System 9

MODULE 2 The Endocrine System 29

all laboratory assignments.

At the completion of this course, you should be able to:

a. The urinary system

b. The endocrine system

WORKING THROUGH THIS COURSE

meaningful contributions to all sessions and to complete all activities. It is important

all your completed assignments.

Course Text in Study Units

Textbooks (Hard and electronic)

Book of Laboratory Practical

Module 1- Urinary System

Unit 1- The anatomy of the kidneys

Unit 2- The anatomy of the ureters

Unit 3- The anatomy of the bladder

Unit 4- The anatomy of the urethra

Module 2- Endocrine System

Unit 1 Functions of the Endocrine System

Unit 3 Pituitary Gland

Unit 4 Thyroid and Parathyroid Gland

Unit 5 Adrenal Gland

1. Sadler T.W (2012), Langman‘s Medical Embryology 12th edition.

3. Katherine M. A. Rogers and William N. Scott (2011) Nurses! Test yourself in

anatomy and physiology

Human Anatomy and Physiology 4th edition.

5. Kathryn A. Booth, Terri. D. Wyman (2008) Anatomy, physiology, and

pathophysiology for allied health

6. Keith L Moore, Persuade T.V.N (2018), The Developing Human Clinically

Oriented Embryology 11th Edition Lippincott Williams & Wilkins.

COURSE REQUIREMENTS AND EXPECTATIONS OF YOU

Attendance of 95% of all interactive sessions, submission of all assignments to meet