The PowerPoint presentation is on the thyroid gland and it's function

1. PRINCE ABUBAKAR AUDU
UNIVERSITY,ANYIGBA.
P.M.B 1008 ANYIGBA KOGI STATE.
COLLEGE OF HEALTH SCIENCES.
SEMINAR PRESENTATION:
TOPIC: THYROID Gland, FUNCTIONS AND CLINICAL
CORRELATION
Outlines
 Introduction
 Mechanism of thyroid gland
 Synthesis of thyroid hormones
 Storage of thyroid hormones
 Release of thyroid gland
 Transport of thyroid hormones in the blood
 Functions of thyroid hormones
 Regulations of thyroid hormones
 Clinical correlation
INTRODUCTION

2. The thyroid gland is a butterfly-shaped gland located
in the front of the neck, It is an endocrine gland that
produces hormones that regulate various metabolic
processes throughout the body, such as growth and
development, temperature regulation, and energy
production.
The thyroid gland produces two major hormones,
thyroxine (T4) and triiodothyronine (T3), which are
responsible for regulating metabolism. The production and
release of these hormones is regulated by the pituitary
gland, which is located in the brain.
The thyroid gland is made up of thousands of small,
spherical follicles that are filled with a protein-rich fluid
called colloid. Each follicle is lined with follicular cells,
which produce T4 and T3 and store them in the colloid.
When the body needs more thyroid hormones, the thyroid
gland releases T4 and T3 into the bloodstream, where they
travel to target tissues and cells.
The thyroid gland also produces calcitonin, a hormone that
regulates calcium metabolism and helps to lower blood
calcium levels when they get too high.

3. Mechanism of thyroid gland
Synthesis of thyroid hormones
Synthesis of thyroid hormones takes place in thyroglobu lin,
present in follicular cavity. Iodine and tyrosine are essential for
the formation of thyroid hormones. Iodine is consumed
through diet. It is converted into iodide and absorbed from GI
tract. Tyrosine is also consumed through diet and is absorbed
from the GI tract.For the synthesis of normal quantities of

4. thyroid hormones, approximately 1 mg of iodine is required per
week or about 50 mg per year. To prevent iodine deficiency,
common table salt is iodized with one part of sodium iodide to
every 100,000 parts of sodium chloride.
„ STAGES OF SYNTHESIS OF THYROID HORMONES
Synthesis of thyroid hormones occurs in five stages:
1. Thyroglobulin synthesis
2. Iodide trapping
3. Oxidation of iodide
4. Transport of iodine into follicular cavity
5. Iodination of tyrosine
6. Coupling reactions.
1. Thyroglobulin Synthesis: Endoplasmic reticulum and
Golgi apparatus in the follicular cells of thyroid gland
synthesize and secrete thyroglobulin continuously.
Thyroglobulin molecule is a large glycoprotein containing
140 molecules of amino acid tyrosine. After synthesis,
thyroglobulin is stored in the follicle.
2. Iodide Trapping;Iodide is actively transported from blood
into follicular cell, against electrochemical gradient. This
process is called iodide trapping. Iodide is transported into the
follicular cell along with sodium by sodium-iodide symport
pump, which is also called iodide pump. Normally, iodide is 30

5. times more concentrated in the thyroid gland than in the blood.
However, during hyperactivity of the thyroid gland, the
concentration of iodide increases 200 times more.
3. Oxidation of Iodide: Iodide must be oxidized to elementary
iodine, because only iodine is capable of combining with
tyrosine to form thyroid hormones. The oxidation of iodide into
iodine occurs inside the follicular cells in the presence of
thyroid peroxidase. Absence or inactivity of this enzyme stops
the synthesis of thyroid hormones.
4.Transport of Iodine into Follicular Cavity :from the follicular
cells, iodine is transported into the follicular cavity by an iodide-
chloride pump called pendrin.
5. Iodination of Tyrosine :combination of iodine with tyrosine is
known as iodination. It takes place in thyroglobulin. First, iodine
is transported from follicular cells into the follicular
cavity,where it binds with thyroglobulin. This process is called
organification of thyroglobulin. Then, iodine (I) combines with
ith tyrosine, which is already present in thyroglobulin Iodination
process is accelerated by the enzyme iodinase, which is
secreted by follicular cells.
Iodination of tyrosine occurs in several stages. Tyrosine is
iodized first into monoiodotyrosine (MIT) and later into di-
iodotyrosine (DIT). MIT and DIT are called the iodotyrosine
residues.

6. 6. Coupling Reactions :Iodotyrosine residues get coupled with
one another. The coupling occurs in different configurations, to
give rise to different thyroid hormones.
Coupling reactions are:
i. One molecule of DIT and one molecule of MIT combine to
form tri-iodothyronine (T3).
Storage of thyroid hormones
Thyroid hormones are stored in the follicles of the thyroid gland.
The thyroid gland consists of numerous follicles, which are
small, hollow structures lined with follicular cells. These cells
produce and store thyroid hormones.
The process of storing thyroid hormones begins with the
uptake of iodine by the follicular cells from the bloodstream.
Iodine is a crucial component for the synthesis of thyroid
hormones. Within the follicular cells, iodine is combined with
an amino acid called tyrosine to form the two main thyroid
hormones, thyroxine (T4) and triiodothyronine (T3).
After their synthesis, the newly formed thyroid hormones are
stored within the follicles in a colloid, which is a gel-like
substance composed of thyroglobulin. Thyroglobulin is a large

7. protein produced by the follicular cells and serves as a storage
form for thyroid hormones.
When the body requires thyroid hormones, signals from the
brain, specifically the hypothalamus and pituitary gland,
stimulate the release of thyroid-stimulating hormone (TSH).
TSH binds to receptors on the follicular cells, triggering the
release of stored thyroid hormones into the bloodstream.
Release of thyroid
hormones
Thyroglobulin itself is not released into the bloodstream. On
the other hand, the hormones are first cleaved from
thyroglobulin and release into the bloodstream
Sequence of Events
1. Follicular cell sends foot-like extensions called
pseudopods, which close around the thyro
globulin hormone complex. This process is mediated by a
receptor-like substance called megalin, which is present in
the membrane of follicular cell
2. Pseudopods convert thyroglobulin-hormone complex
into small pinocytic vesicles
3. Then, lysosomes of the cell fuse with these vesicles

8. 4. Digestive enzymes such as proteinases present
in lysosomes digest (proteolysis) the thyroglobulin and
release the hormones
5. The hormones diffuse through base of the follicular cell
and enter the capillaries. Only T3 dnd T4are released into
the blood. In the peripheral tissues, T4 is converted into T3.
A small amount of inactive reverse T3 is also formed. It is
the biologically inactive form of T3 and it is produced
when T4 is converted into T3MIT and DIT are not released
into blood. These iodotyrosine residues are deiodinated by
an enzyme called iodotyrosine deiodinase, resulting in the
release of iodine. The iodine is reutilized by the follicular
cells for further synthesis of thyroid hormones. During
congenital absence of iodotyrosine deiodinase, MIT and
DIT are excreted in urine and the symptoms of iodine
deficiency develop.
Transport of thyroid hormones
in the blood
Thyroid hormones are transported in the blood by three types
of proteins:
1. Thyroxine-binding globulin (TBG)
2. Thyroxine-binding prealbumin (TBPA)
3. Albumin.

9. 1. Thyroxine-binding Globulin (TBG)
Thyroxine-binding globulin is a glycoprotein and its
concentration in the blood is 1 to 1.5 mg/dL. It has a geat
affinity for thyroxine and about one third of the hormones
combines strongly with this protein
2. Thyroxine-binding Prealbumin (TBPA)TBPA transports one
fourth of the thyroid hormones. It is also called transthyretin
(TTR).
3. AlbuminAlbumin transports about one tenth of the thyroid
hormones.
Functions of thyroid gland
Hormones
The thyroid gland, one of the largest endocrine glands in the
body, is responsible for producing hormones that regulate
various metabolic processes throughout the body. These
hormones are critical for many essential physiological functions,
including growth and development, temperature regulation,
energy production, and metabolism.
The physiological effects of thyroid hormone are listed
below:

10. 1. Regulating Metabolism: The thyroid gland plays a primary
role in regulating the body’s metabolic rate. The hormones
produced by the gland, namely thyroxine (T4) and
triiodothyronine (T3), play a crucial role in determining how
quickly the body burns calories and uses energy.
2. Regulating Heart Function: The thyroid gland also plays a key
role in regulating heart function by influencing the heart rate
and force of contraction. Thyroid hormones affect the electrical
activity of the heart, which is essential for proper heart function.
3. Regulating the Central Nervous System: The thyroid gland
also plays a role in regulating the central nervous system.
Thyroid hormones are necessary for brain development, and a
deficiency in these hormones during critical periods of brain
growth and development can lead to irreversible
developmental delays.
4. Maintaining Body Temperature: The thyroid gland influences
body temperature by regulating the body's basal metabolic rate.
When thyroid hormone levels are too low or too high, the
body's natural ability to regulate temperature can be affected.
5. Increases the basal metabolic rate.
6. In children, thyroid hormones act synergistically with growth
hormone to stimulate bone growth.
Regulations of thyroid Hormone

11. Regulation of thyroid hormone starts at the hypothalamus. The
hypothalamus releases thyrotropin-releasing hormone (TRH)
into the hypothalamic-hypophyseal portal system to the
anterior pituitary gland. TRH stimulates thyrotropin cells in the
anterior pituitary to the release of thyroid-stimulating hormone
(TSH). TRH is a peptide hormone created by the cell bodies in
the periventricular nucleus (PVN) of the hypothalamus. These
cell bodies project their neurosecretory neurons down to the
hypophyseal portal
circulation, where TRH can concentrate before reaching the
anterior pituitary
Disor
der
of
thyro

12. id gland
Hyperthyroidism; Hyperthyroidism, also called overactive
thyroid ;a condition by which thyroid gland release more
hormones (thyrosine) more than the body needs.
Hyperthyroidism is a set of disorders that involve excess
synthesis and secretion of thyroid hormones by the thyroid
gland, which leads to the hypermetabolic condition of
thyrotoxicosis
Cause of hyperthyroidism
1. Graves' disease: In this disorder, the immune system attacks
the thyroid. This makes the thyroid create too much thyroid
hormone. Graves’ disease is a hereditary condition (passed
down through a family).
2 Infllammation (thyroiditis) of the thyroid due to viral
infections
3 Taking too much thyroid hormone (common)
,4 Noncancerous growths of the thyroid gland

13. B Hypothyroidism: hypothyroidism can be defined as an
aplied physiology or a disorder which occurs when there's a
Decrease in secretion of thyroid hormones.
Hypothyroidism leads to myxedema in adults and cretinism in
children.
MYXEDEMA
Myxedema is the hypothyroidism in adults, characterized by
generaliz
ed
edemato
us
appearan
ce.
Causes
for
myxede
ma
Myxedem
a occurs
due to

14. diseases of thyroid gland, genetic disorder or iodine deficiency.
In addition, it is also caused by deficiency of thyroid-stimulating
hormone or thyrotropin-releasing hormone. Common cause of
myxedema is the autoimmune disease called Hashimoto’s
thyroiditis, which is common in late middle-aged women.
Signs and symptoms
It is associated with the following symptoms:
1. Swelling of the face
2. Bagginess under the eyes
3. Non-pitting type of edema, i.e. when pressed, it does not
make pits and the edema is hard.
4. Atherosclerosis: It is the hardening of the walls of arteries
because of accumulation of fat deposits and other substances.
general features of hypothyroidism in adults are:
1. Anemia
2. Fatigue and muscular sluggishness
3. Menorrhagia and polymenorrhea
4. Decreased cardiovascular functions .
5. Increase in body weight.
CRETINISM
Cretinism is the hypothyroidism in children, characterized by
stunted growth.Cretinism occurs due to congenital absence of
thyroid gland, genetic disorder or lack of iodine in the diet.
Features Of Cretinism

15. 1. A newborn baby with thyroid deficiency may appear normal
at the time of birth because thyroxine might have been
supplied from mother. But a few weeks after birth, the baby
starts developing the signs like sluggish movements.
2. Skeletal growth is more affected than the soft tissues. So,
there is stunted growth with bloated body. The tongue
becomes so big that it hangs down with dripping of saliva.
C. Goiter
Abnormal enlargement of the butterfly-shaped gland below the
Adam's apple (thyroid).
A goitre commonly develops as a result of iodine deficiency or
inflammation of the thyroid gland.
Goiter means enlargement of the thyroid gland. It occurs both
in hypothyroidism and hyperthyroidism.
Goiter in Hyperthyroidism – Toxic Goiter ,Toxic goiter is the
enlargement of thyroid gland with increased secretion of
thyroid hormones, caused by thyroid tumor.

16. Based
on the
cause,
the
non-
toxic
hypoth
yroid
goiter
is
classifi
ed into
two
types.
1.
Endemi
c
colloid
goiter
2.
Idiopat
hic
non-
toxic

17. goiter.
1. Endemic colloid goiter
Endemic colloid goiter is the non-toxic goiter caused by iodine
deficiency. It is also called iodine deficiency goiter. Iodine
deficiency occurs when intake is less than 50 µg/day.
2. Idiopathic non-toxic goiter
Idiopathic non-toxic goiter is the goiter due to unknown cause.
Enlargement of thyroid gland occurs even without iodine
deficiency.
Treatment.
A. Hyperthyroidism:Treatment depends on the cause and
severity of symptoms. Hyperthyroidism is usually treated with
one or more of the following:
Antithyroid medicines (propylthiouracil or methimazole)
which reduce or block the effects of the extra thyroid
hormone
Radioactive iodine to destroy the thyroid gland and stop
the excess production of hormones
Surgery to remove the thyroid
B. Hypothyroidism:The treatment for hypothyroidism is the
administration of thyroid extract or ingestion of pure thyroxine
in the form of tablets, orally.

18. C. Goiter
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