Thyroid Gland: Functions and Hormone Synthesis

THYROID GLAND
By Dr. Saurabh Yadav
Assistant Prof.
Department of Kriya
Sharir
HAMC&H
 
INTRODUCTION
 
Thyroid is a one of the
largest gland of the
endocrine gland.
Location -  Below the
larynx on each side of
trachea and anterior to
the trachea.
It has two lobes, which
are connected in the
middle by an isthmus.
Weight – 10-20 gm in
adults.
 
MICROSCOPIC FEATURES
 
    
Thyroid gland contain about 3 million follicles. These
follicles are lined with cuboidal epithelial cells called
follicular cells. Follicular cavity is filled with a colloidal
substance known as thyroglobulin (TG), which is
secreted by follicular cells. TG is a protein and thyroid
hormones are obtains from TG. In between the
follicular cells, parafollicular cells are present, which
secrete calcitonin.
 
SYNTHESIS OF THYROID HORMONE
 
About 93 % of hormones secreted by the
thyroid gland is thyroxine (T
4
), and 7 %
triiodothyronine (T
3
).
 
Iodine is very essential for the formation of
thyroid hormones. Iodine is consumed through
diet. iodine is converted into iodide and
absorbed from GI tract.
 
For the synthesis of normal quantities of thyroid
hormones, approximately 1 mg of iodine is
required per week or about 50 mg per year.
 
 
 
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.
 
 
    Synthesis of thyroid hormone occurs in five stages –
 
Iodide trapping
Transport of iodide into follicular cavity
Oxidation of iodide
Iodination of tyrosine ( organification)
Coupling reaction
 
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.
 
Transport of iodide into follicular cavity 
From the follicular cells, iodide is transported
into the follicular cavity by an iodide-
chloride pump called pendrin.
 
 
 
Oxidation of iodide 
Inside the follicular cavity, iodide is oxidized
to iodine by the help of an enzyme called
thyroperoxidase and its accompanying
hydrogen peroxide. Iodide must be oxidized
to iodine, because only iodine is capable of
combining with tyrosine to form thyroid
hormones. Absence or inactivity of this
enzyme stops the synthesis of thyroid
hormones.
 
 
 
Iodination of tyrosine ( organification) 
 The binding of iodine with the thyroglobulin
molecule is called organification of the
thyroglobulin. Then, iodine (I) combines with
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.
 
Coupling reaction 
One molecule of DIT and one molecule of
MIT combine to form triiodothyronine (T3).
Two molecules of DIT combine to form tetrai-
odothyronine (T4) or thyroxine.
 
STORAGE OF THYROID HORMONES
 
After synthesis, the thyroid hormones remain
in the form of vesicles within thyroglobulin
and are stored for long period.
Each thyroglobulin molecule contains up to
30 thyroxine molecules and a few
triiodothyronine molecules. In this form, the
thyroid hormones are stored in the follicles
for 2 to 3 months.
 So, when the synthesis of thyroid hormone
stops, the signs and symptoms of deficiency
do not appear for about 2 to 3 months.
 
RELEASE OF THYROID HORMONES FROM
THE THYROID GLAND
 
Thyroglobuline itself is not released into the
circulating blood. the hormones are first
cleaved from the thyroglobulin and then
these free hormones are released.
1.
Follicular cell sends foot-like extensions called
pseudopods, which close around the
thyroglobulin 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 and
enter into follicular cell.
 
3. Then, lysosomes of the cell fuse with these
vesicles.
4.  Digestive enzymes such as proteinases
present in         lysosomes digest (proteolysis)
the thyroglobulin molecules and release the
hormones.
5. Now, the hormones diffuse through base of
the follicular cell and enter the capillaries.
          Blood and various organs in our body
notably liver, kidney, heart and skeletal
muscle convert the T
4 
into T
3
 by an enzyme
called monodeiodinase. Most of the T
3 
found
in blood is the T
3
 derived from T
4
 by these
organs. A small amount of T
4
 is converted into
reverse T
3
.
 
6
. Remain MIT & DIT are iodinated tyrosines &
free from the thyroglobulin molecules.
 
7. They are not secreted into the blood,
Instead,  their iodine is cleaved from them
by a de-iodinase enzyme & again this iodine
is recycled to form additional thyroid
hormones.
 
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.
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 great affinity for thyroxine
and about one third of the hormone
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. 
Albumin –
    Albumin transports about one tenth of the
thyroid hormones.
 
 
POTENCY AND DURATION OF ACTION 
The potency of T3 is four times more than that
of T4.
T4 acts for longer period than T3.
Duration of T4 action is four times more than
T3 action. This is because of the difference in
the affinity of these hormones to plasma
proteins.
T3 has less affinity for plasma proteins and
combines loosely with them, so that it is
released quickly.
T4 has more affinity and strongly binds with
plasma proteins, so that it is released slowly.
Therefore, T3 acts on the target cells
immediately and T4 acts slowly.
 
CELLULAR ACTION OF THYROID HORMONE
 
Thyroid hormone enter cells through membrane
transporter protein. Within the cell, most of the T
4
 is
deiodinated to form T
3
.
Now, thyroid hormones enter the nucleus of cell
and bind with thyroid hormone receptors (TR),
which are either attached to DNA genetic strands
or in close proximity to them.
TR is always bound to another receptor called
retinoid X receptor (RXR).
The receptors become activated and initiate the
transcription process. Then large numbers of
different types of messenger RNA are formed,
which activate the ribosomes to synthesize the
new proteins.
 
REGULATION OF THYROID HORMONE
SECRETION
 
    Secretion of thyroid hormones is controlled by
anterior pituitary and hypothalamus through
feedback mechanism.
ROLE OF HYPOTHALAMUS 
    Hypothalamus regulates thyroid secretion by
controlling TSH secretion through thyrotropic-
releasing hormone (TRH).
    Median eminence of hypothalamus secrets
TRH and TRH is transported through the
hypothalamo-hypophyseal portal vessels to the
anterior pituitary. After reaching the pituitary
gland, the TRH causes the release of TSH.
 
ROLE OF PITUITARY GLAND 
    Thyroid-stimulating hormone (TSH) secreted
by anterior pituitary is the major factor
regulating the synthesis and release of
thyroid hormones.
1.
Increased the number of follicular cells of
thyroid.
2.
Increased the conversion of cuboidal cells
into columnar cells in thyroid gland and
thereby it causes the development of
thyroid follicles.
3.
Increased size and secretory activity of
follicular cells.
4.
Increased activity of the iodide pump and
iodide trapping in follicular cells.
 
 
5. Increased thyroglobulin secretion into
follicles
.
6. Increased Iodination of tyrosine and
coupling to form the hormones.
7. Increased proteolysis of the thyroglobulin,
by which release of hormone is enhanced
and colloidal substance is decreased.
FEEDBACK CONTROL  
-
       Increased thyroid hormone in the body
fluids decreases secretion of TRH from
hypothalamus and TSH from anterior
pituitary.
 
 
FUNCTIONS OF THE THYROID HORMONES
 
ACTION ON BASAL METABOLIC RATE (BMR) 
Thyroid hormone increases the metabolic
activities in most of the body tissues, except
brain, retina, spleen, testes and lungs. It
increases BMR by increasing the oxygen
consumption of the tissues. The action that
increases the BMR is called calorigenic
action.
Hyperthyroidism, BMR increases - 60% to
100% above the normal level.
Hypothyroidism, BMR falls - 20% to 40% below
the normal level.
 
AC
TION ON PROTEIN METABOLISM 
    Thyroid hormone increases the synthesis of
proteins in the cells
.
ACTION ON CARBOHYDRATE METABOLISM 
    Thyroid hormone stimulates almost all
aspects of carbohydrate metabolism.
↑ glucose absorption from GI tract.
↑ glucose uptake by the cells, by
accelerating the transport of glucose
through the cell membrane.
↑ breakdown of glycogen into glucose.
↑ gluconeogenesis.
Hyperthyroidism – blood glucose ↑
Hypothyroidism – blood glucose ↓
 
ACTION ON FAT METABOLISM 
    Thyroid hormone decreases the fat storage by mobilizing it from
adipose tissues and fat depots. The mobilized fat is converted into
free fatty acid and transported by blood.
↑ free fatty acid level in blood.
ACTION ON PLASMA AND LIVER FATS 
    Increase thyroid hormone decreases the concentrations of
cholesterol, phospholipids, and triglycerides in the plasma, even
though it increases the free fatty acids.
Hypothyroidism - cholesterol level in plasma increases, resulting in
atherosclerosis.
Thyroid hormone increases deposition of fats in the liver, leading
to fatty liver.
Thyroid hormone decreases plasma cholesterol level by
increasing its excretion from liver cells into bile.
 
ACTION ON VITAMIN METABOLISM 
     Thyroid hormone increases the formation of many enzymes
and vitamins form essential parts of the enzymes.
Hyperthyroidism – vitamin deficiency
ACTION ON GROWTH 
Thyroid hormone accelerates the growth of the body,
especially in growing children. Lack of thyroid hormone arrests
the growth.
In hyper secretion of thyroid hormone, excessive skeletal
growth often occurs, causing the child to become taller at an
earlier age.
Thyroid hormone causes early closure of epiphysis. So, the
height of the individual may be slightly less in hypothyroidism.
Thyroid hormone is more important to promote growth and
development of brain during fetal life and first few years of
postnatal life. Deficiency of thyroid hormones during this
period leads to mental retardation and the brain remains
smaller than normal.
 
ACTION ON BODY WEIGHT 
Increase thyroid hormone secretion
decreases the body weight and fat storage.
Decrease thyroid hormone secretion
increases the body weight because of fat
deposition.
 
ACTION ON BLOOD 
Thyroid hormone increases erythropoietin
production and increases blood volume.
Polycythemia is common in hyperthyroidism.
 
ACTION ON CARDIOVASCULAR SYSTEM 
Thyroid hormone acts directly on heart and increases
the heart rate. It is an important clinical investigation
for diagnosis of hypothyroidism and hyperthyroidism.
Due to its effect on enzymatic activity, thyroid
hormone increases the force of contraction of the
heart. In hyperthyroidism or in thyrotoxicosis, the
heart may become weak due to excess activity and
protein catabolism. So, the patient may die of
cardiac decompensation.
Thyroid hormone causes vasodilatation by increasing
the metabolic activities.
Thyroid hormone increase in rate and force of
contraction of the heart, increase in blood volume
and blood flow, increase in cardiac output. This in
turn, increases the blood pressure. But, generally, the
mean pressure is not altered. Systolic pressure
increases and the diastolic pressure decreases.
 
ACTION ON RESPIRATION 
The increased rate of metabolism increases
the utilization of oxygen and formation of
carbon dioxide. These two factors stimulate
the respiratory centers to increase the rate
and depth of respiration.
ACTION ON GASTROINTESTINAL TRACT 
Thyroid hormone increases the appetite and
food intake. It also increases the secretion of
digestive juices and movements of GI tract.
So, hypersecretion of thyroid hormone
causes diarrhea and the lack of thyroid
hormone causes constipation.
 
ACTION ON CENTRAL NERVOUS SYSTEM 
Thyroid hormone promote growth and development of the brain
during fetal life and during the first few years of postnatal life.
Thyroid deficiency in infants results in abnormal development of
synapses, defective myelination and mental retardation.
during the hypersecretion of thyroid hormone, there is excess
stimulation of the CNS. So, the person is likely to have extreme
nervousness and may develop psychoneurotic problems such as
anxiety complexes, excess worries or paranoid thoughts.
Hyposecretion of thyroxine leads to lethargy and somnolence
(excess sleep).
ACTION ON SKELETAL MUSCLE 
when the quantity of hormone becomes excessive, the muscles
become weakened because of excess protein catabolism.
lack of thyroid hormone causes the muscles to become sluggish,
and they relax slowly after a contraction.
 
ACTION ON SLEEP 
Hypersecretion of thyroid hormone causes excessive
stimulation of the muscles and central nervous system.
So, the person feels tired, exhausted and feels like
sleeping. But, the person cannot sleep because of the
stimulatory effect of thyroid hormone on synapses.
hyposecretion of thyroxine causes somnolence.
ACTION ON SEXUAL FUNCTION 
In men, hypothyroidism leads to complete loss of
libido and hyperthyroidism leads to impotence.
In women, hypothyroidism causes menorrhagia and
polymenorrhea. In some women, it causes irregular
menstruation and occasionally amenorrhea.
Hyperthyroidism in women leads to oligomenorrhea
and sometimes amenorrhea.
 
APPLIED PHYSIOLOGY
 
GOITER
    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.
Goiter in Hypothyroidism 
– Non-toxic Goiter
    Non-toxic goiter is the enlargement of thyroid
gland without increase in hormone secretion.
the non-toxic hypothyroid goiter is classified into
two types.
 1. Endemic colloid goiter
 2. Idiopathic non-toxic goiter.
 
Endemic colloid goiter 
Endemic colloid goiter is the non-toxic goiter
caused by iodine deficiency. Because of
lack of iodine, there is no formation of
hormones.
By feedback mechanism, hypothalamus
and anterior pituitary are stimulated. It
increases the secretion of TRH and TSH.
The TSH then causes the thyroid cells to
secrete tremendous amounts of
thyroglobulin into the follicle. As there are no
hormones to be cleaved, the thyroglobulin
remains as it is and gets accumulated in the
follicles of the gland. This increases the size
of gland.
 
Idiopathic non-toxic goiter 
Idiopathic non-toxic goiter is the goiter due to
unknown cause. Enlargement of thyroid gland
occurs even without iodine deficiency.
It may be due to thyroiditis and deficiency of
enzymes such as peroxidase, iodinase and
deiodinase, which are required for thyroid
hormone synthesis.
 
HYPERTHYROIDISM
Increased secretion of thyroid hormones is called
hyperthyroidism.
Hyperthyroidism is caused by:
1. Graves’ disease
2. Thyroid adenoma
 
 
Graves’ disease 
Graves’ disease is an autoimmune disease and it is the
most common cause of hyperthyroidism. In Graves’
disease, the B lymphocytes (plasma cells) produce
autoimmune antibodies called thyroid-stimulating
autoantibodies (TSAbs). These antibodies act like TSH by
binding with membrane receptors of TSH. This results in
hypersecretion of thyroid hormones. The high
concentration of thyroid hormones caused by the
antibodies suppresses the TSH production also. So, the
concentration of TSH is low.
 
Thyroid adenoma 
Sometimes, a localized tumor develops in the thyroid
tissue. It is known as thyroid adenoma and it secretes
large quantities of thyroid hormones. As far as this
adenoma remains active, the other parts of thyroid
gland cannot secrete the hormone. This is because, the
hormone secreted from adenoma depresses the
production of TSH.
 
 
Symptoms of Hyperthyroidism –
Intolerance to heat
Increased sweating
Mild to extreme weight loss
Varying degrees of diarrhea
Muscle weakness
Nervousness or other psychic disorders
Extreme fatigue but inability to sleep
 
HYPOTHYROIDISM 
    Decreased secretion of thyroid hormones is
called hypothyroidism. Hypothyroidism leads to
myxedema in adults and cretinism in children.
Myxedema
    Where hypothyroidism is present for a long time,
mucopolysaccharides, hyaluronic acid and
chondroitin sulfate, infiltrate into the various
tissues, causing non-pitting edema or myxedema.
symptoms of myxedema –
1. Swelling of the face
2. Bagginess under the eyes
3. on-pitting edema
4. Atherosclerosis
 
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 –
Sluggish movements
Croaking sound while crying
Tongue large and protruding
Broad and flat nose
Umbilical hernia
 
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The thyroid gland is a vital endocrine gland located below the larynx, responsible for producing thyroid hormones essential for regulating metabolism. This gland consists of follicles lined with follicular cells, producing thyroglobulin and thyroid hormones T3 and T4. Iodine plays a crucial role in the synthesis of these hormones, with a detailed process involving iodide trapping, transport, oxidation, and coupling reactions. Understanding the microscopic features and synthesis of thyroid hormones can provide insights into its significance in maintaining overall health.

  • Thyroid Gland
  • Hormone Synthesis
  • Endocrine
  • Iodine
  • Metabolism

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  1. THYROID GLAND By Dr. Saurabh Yadav Assistant Prof. Department of Kriya Sharir HAMC&H

  2. INTRODUCTION Thyroid is a one of the largest gland of the endocrine gland. Location - Below the larynx on each side of trachea and anterior to the trachea. It has two lobes, which are connected in the middle by an isthmus. Weight 10-20 gm in adults.

  3. MICROSCOPIC FEATURES Thyroid gland contain about 3 million follicles. These follicles are lined with cuboidal epithelial cells called follicular cells. Follicular cavity is filled with a colloidal substance known as thyroglobulin (TG), which is secreted by follicular cells. TG is a protein and thyroid hormones are obtains from TG. In between the follicular cells, parafollicular cells are present, which secrete calcitonin.

  4. SYNTHESIS OF THYROID HORMONE About 93 % of hormones secreted by the thyroid gland is thyroxine (T4), and 7 % triiodothyronine (T3). Iodine is very essential for the formation of thyroid hormones. Iodine is consumed through diet. iodine is converted into iodide and absorbed from GI tract. For the synthesis of normal quantities of thyroid hormones, approximately 1 mg of iodine is required per week or about 50 mg per year.

  5. Thyroglobulin Synthesis Endoplasmic reticulum and Golgi apparatus in the follicular cells of thyroid gland synthesize and secrete continuously. Thyroglobulin molecule glycoprotein containing 140 molecules of amino acid tyrosine. thyroglobulin is a large

  6. Synthesis of thyroid hormone occurs in five stages Iodide trapping Transport of iodide into follicular cavity Oxidation of iodide Iodination of tyrosine ( organification) Coupling reaction

  7. 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. Transport of iodide into follicular cavity From the follicular cells, iodide is transported into the follicular cavity by an iodide- chloride pump called pendrin.

  8. Oxidation of iodide Inside the follicular cavity, iodide is oxidized to iodine by the help of an enzyme called thyroperoxidase and its accompanying hydrogen peroxide. Iodide must be oxidized to iodine, because only iodine is capable of combining with tyrosine to form thyroid hormones. Absence or inactivity of this enzyme stops the synthesis of thyroid hormones.

  9. Iodination of tyrosine ( organification) The binding of iodine with the thyroglobulin molecule is called organification of the thyroglobulin. Then, iodine (I) combines with tyrosine, which is thyroglobulin. Iodination accelerated by the enzyme iodinase, which is secreted by follicular cells. already present process in is Iodination of tyrosine occurs in several stages. Tyrosine is monoiodotyrosine (MIT) and later into di- iodotyrosine (DIT). MIT and DIT are called the iodotyrosine residues. iodized first into

  10. Coupling reaction One molecule of DIT and one molecule of MIT combine to form triiodothyronine (T3). Two molecules of DIT combine to form tetrai- odothyronine (T4) or thyroxine.

  11. STORAGE OF THYROID HORMONES After synthesis, the thyroid hormones remain in the form of vesicles within thyroglobulin and are stored for long period. Each thyroglobulin molecule contains up to 30 thyroxine molecules triiodothyronine molecules. In this form, the thyroid hormones are stored in the follicles for 2 to 3 months. So, when the synthesis of thyroid hormone stops, the signs and symptoms of deficiency do not appear for about 2 to 3 months. and a few

  12. RELEASE OF THYROID HORMONES FROM THE THYROID GLAND Thyroglobuline itself is not released into the circulating blood. the hormones are first cleaved from the thyroglobulin and then these free hormones are released. 1. Follicular cell sends foot-like extensions called pseudopods, which thyroglobulin 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 and enter into follicular cell. close around the

  13. 3. Then, lysosomes of the cell fuse with these vesicles. 4. Digestive enzymes such as proteinases present in lysosomes digest (proteolysis) the thyroglobulin molecules and release the hormones. 5. Now, the hormones diffuse through base of the follicular cell and enter the capillaries. Blood and various organs in our body notably liver, kidney, heart and skeletal muscle convert the T4 into T3 by an enzyme called monodeiodinase. Most of the T3 found in blood is the T3 derived from T4 by these organs. A small amount of T4 is converted into reverse T3.

  14. 6. Remain MIT & DIT are iodinated tyrosines & free from the thyroglobulin molecules. 7. They are not secreted into the blood, Instead, their iodine is cleaved from them by a de-iodinase enzyme & again this iodine is recycled to form additional thyroid hormones.

  15. 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. 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 great affinity for thyroxine and about one third of the hormone combines strongly with this protein.

  16. 2. Thyroxine-binding Prealbumin (TBPA) TBPA transports one fourth of the thyroid hormones. It is also called transthyretin (TTR). 3. Albumin Albumin transports about one tenth of the thyroid hormones.

  17. POTENCY AND DURATION OF ACTION The potency of T3 is four times more than that of T4. T4 acts for longer period than T3. Duration of T4 action is four times more than T3 action. This is because of the difference in the affinity of these hormones to plasma proteins. T3 has less affinity for plasma proteins and combines loosely with them, so that it is released quickly. T4 has more affinity and strongly binds with plasma proteins, so that it is released slowly. Therefore, T3 acts on the target cells immediately and T4 acts slowly.

  18. CELLULAR ACTION OF THYROID HORMONE Thyroid hormone enter cells through membrane transporter protein. Within the cell, most of the T4 is deiodinated to form T3. Now, thyroid hormones enter the nucleus of cell and bind with thyroid hormone receptors (TR), which are either attached to DNA genetic strands or in close proximity to them. TR is always bound to another receptor called retinoid X receptor (RXR). The receptors become activated and initiate the transcription process. Then large numbers of different types of messenger RNA are formed, which activate the ribosomes to synthesize the new proteins.

  19. REGULATION OF THYROID HORMONE SECRETION Secretion of thyroid hormones is controlled by anterior pituitary and hypothalamus through feedback mechanism. ROLE OF HYPOTHALAMUS Hypothalamus regulates thyroid secretion by controlling TSH secretion through thyrotropic- releasing hormone (TRH). Median eminence of hypothalamus secrets TRH and TRH is transported through the hypothalamo-hypophyseal portal vessels to the anterior pituitary. After reaching the pituitary gland, the TRH causes the release of TSH.

  20. ROLE OF PITUITARY GLAND Thyroid-stimulating hormone (TSH) secreted by anterior pituitary is the major factor regulating the synthesis and release of thyroid hormones. 1. Increased the number of follicular cells of thyroid. 2. Increased the conversion of cuboidal cells into columnar cells in thyroid gland and thereby it causes the development of thyroid follicles. 3. Increased size and secretory activity of follicular cells. 4. Increased activity of the iodide pump and iodide trapping in follicular cells.

  21. 5. Increased thyroglobulin secretion into follicles. 6. Increased Iodination of tyrosine and coupling to form the hormones. 7. Increased proteolysis of the thyroglobulin, by which release of hormone is enhanced and colloidal substance is decreased. FEEDBACK CONTROL - Increased thyroid hormone in the body fluids decreases secretion of TRH from hypothalamus and pituitary. TSH from anterior

  22. FUNCTIONS OF THE THYROID HORMONES ACTION ON BASAL METABOLIC RATE (BMR) Thyroid hormone increases the metabolic activities in most of the body tissues, except brain, retina, spleen, testes and lungs. It increases BMR by increasing the oxygen consumption of the tissues. The action that increases the BMR is called calorigenic action. Hyperthyroidism, BMR increases - 60% to 100% above the normal level. Hypothyroidism, BMR falls - 20% to 40% below the normal level.

  23. ACTION ON PROTEIN METABOLISM Thyroid hormone increases the synthesis of proteins in the cells. ACTION ON CARBOHYDRATE METABOLISM Thyroid hormone stimulates almost all aspects of carbohydrate metabolism. glucose absorption from GI tract. glucose uptake by the cells, by accelerating the transport of glucose through the cell membrane. breakdown of glycogen into glucose. gluconeogenesis. Hyperthyroidism blood glucose Hypothyroidism blood glucose

  24. ACTION ON FAT METABOLISM Thyroid hormone decreases the fat storage by mobilizing it from adipose tissues and fat depots. The mobilized fat is converted into free fatty acid and transported by blood. free fatty acid level in blood. ACTION ON PLASMA AND LIVER FATS Increase thyroid hormone decreases the concentrations of cholesterol, phospholipids, and triglycerides in the plasma, even though it increases the free fatty acids. Hypothyroidism - cholesterol level in plasma increases, resulting in atherosclerosis. Thyroid hormone increases deposition of fats in the liver, leading to fatty liver. Thyroid hormone decreases plasma cholesterol level by increasing its excretion from liver cells into bile.

  25. ACTION ON VITAMIN METABOLISM Thyroid hormone increases the formation of many enzymes and vitamins form essential parts of the enzymes. Hyperthyroidism vitamin deficiency ACTION ON GROWTH Thyroid hormone accelerates the growth of the body, especially in growing children. Lack of thyroid hormone arrests the growth. In hyper secretion of thyroid hormone, excessive skeletal growth often occurs, causing the child to become taller at an earlier age. Thyroid hormone causes early closure of epiphysis. So, the height of the individual may be slightly less in hypothyroidism. Thyroid hormone is more important to promote growth and development of brain during fetal life and first few years of postnatal life. Deficiency of thyroid hormones during this period leads to mental retardation and the brain remains smaller than normal.

  26. ACTION ON BODY WEIGHT Increase thyroid hormone secretion decreases the body weight and fat storage. Decrease thyroid hormone secretion increases the body weight because of fat deposition. ACTION ON BLOOD Thyroid hormone increases erythropoietin production and increases blood volume. Polycythemia is common in hyperthyroidism.

  27. ACTION ON CARDIOVASCULAR SYSTEM Thyroid hormone acts directly on heart and increases the heart rate. It is an important clinical investigation for diagnosis of hypothyroidism and hyperthyroidism. Due to its effect on enzymatic activity, thyroid hormone increases the force of contraction of the heart. In hyperthyroidism or in thyrotoxicosis, the heart may become weak due to excess activity and protein catabolism. So, the patient may die of cardiac decompensation. Thyroid hormone causes vasodilatation by increasing the metabolic activities. Thyroid hormone increase in rate and force of contraction of the heart, increase in blood volume and blood flow, increase in cardiac output. This in turn, increases the blood pressure. But, generally, the mean pressure is not altered. Systolic pressure increases and the diastolic pressure decreases.

  28. ACTION ON RESPIRATION The increased rate of metabolism increases the utilization of oxygen and formation of carbon dioxide. These two factors stimulate the respiratory centers to increase the rate and depth of respiration. ACTION ON GASTROINTESTINAL TRACT Thyroid hormone increases the appetite and food intake. It also increases the secretion of digestive juices and movements of GI tract. So, hypersecretion of thyroid hormone causes diarrhea and the lack of thyroid hormone causes constipation.

  29. ACTION ON CENTRAL NERVOUS SYSTEM Thyroid hormone promote growth and development of the brain during fetal life and during the first few years of postnatal life. Thyroid deficiency in infants results in abnormal development of synapses, defective myelination and mental retardation. during the hypersecretion of thyroid hormone, there is excess stimulation of the CNS. So, the person is likely to have extreme nervousness and may develop psychoneurotic problems such as anxiety complexes, excess worries or paranoid thoughts. Hyposecretion of thyroxine leads to lethargy and somnolence (excess sleep). ACTION ON SKELETAL MUSCLE when the quantity of hormone becomes excessive, the muscles become weakened because of excess protein catabolism. lack of thyroid hormone causes the muscles to become sluggish, and they relax slowly after a contraction.

  30. ACTION ON SLEEP Hypersecretion of thyroid hormone causes excessive stimulation of the muscles and central nervous system. So, the person feels tired, exhausted and feels like sleeping. But, the person cannot sleep because of the stimulatory effect of thyroid hormone on synapses. hyposecretion of thyroxine causes somnolence. ACTION ON SEXUAL FUNCTION In men, hypothyroidism leads to complete loss of libido and hyperthyroidism leads to impotence. In women, hypothyroidism causes menorrhagia and polymenorrhea. In some women, it causes irregular menstruation and occasionally Hyperthyroidism in women leads to oligomenorrhea and sometimes amenorrhea. amenorrhea.

  31. APPLIED PHYSIOLOGY GOITER 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. Goiter in Hypothyroidism Non-toxic Goiter Non-toxic goiter is the enlargement of thyroid gland without increase in hormone secretion. the non-toxic hypothyroid goiter is classified into two types. 1. Endemic colloid goiter 2. Idiopathic non-toxic goiter.

  32. Endemic colloid goiter Endemic colloid goiter is the non-toxic goiter caused by iodine deficiency. Because of lack of iodine, there is no formation of hormones. By feedback mechanism, hypothalamus and anterior pituitary are stimulated. It increases the secretion of TRH and TSH. The TSH then causes the thyroid cells to secrete tremendous thyroglobulin into the follicle. As there are no hormones to be cleaved, the thyroglobulin remains as it is and gets accumulated in the follicles of the gland. This increases the size of gland. amounts of

  33. Idiopathic non-toxic goiter Idiopathic non-toxic goiter is the goiter due to unknown cause. Enlargement of thyroid gland occurs even without iodine deficiency. It may be due to thyroiditis and deficiency of enzymes such as peroxidase, iodinase and deiodinase, which are required for thyroid hormone synthesis. HYPERTHYROIDISM Increased secretion of thyroid hormones is called hyperthyroidism. Hyperthyroidism is caused by: 1. Graves disease 2. Thyroid adenoma

  34. Graves disease Graves disease is an autoimmune disease and it is the most common cause of hyperthyroidism. In Graves disease, the B lymphocytes (plasma cells) produce autoimmune antibodies autoantibodies (TSAbs). These antibodies act like TSH by binding with membrane receptors of TSH. This results in hypersecretion of thyroid concentration of thyroid hormones caused by the antibodies suppresses the TSH production also. So, the concentration of TSH is low. called thyroid-stimulating hormones. The high Thyroid adenoma Sometimes, a localized tumor develops in the thyroid tissue. It is known as thyroid adenoma and it secretes large quantities of thyroid hormones. As far as this adenoma remains active, the other parts of thyroid gland cannot secrete the hormone. This is because, the hormone secreted from adenoma depresses the production of TSH.

  35. Symptoms of Hyperthyroidism Intolerance to heat Increased sweating Mild to extreme weight loss Varying degrees of diarrhea Muscle weakness Nervousness or other psychic disorders Extreme fatigue but inability to sleep

  36. HYPOTHYROIDISM Decreased secretion of thyroid hormones is called hypothyroidism. Hypothyroidism leads to myxedema in adults and cretinism in children. Myxedema Where hypothyroidism is present for a long time, mucopolysaccharides, chondroitin sulfate, infiltrate into the various tissues, causing non-pitting edema or myxedema. symptoms of myxedema 1. Swelling of the face 2. Bagginess under the eyes 3. on-pitting edema 4. Atherosclerosis hyaluronic acid and

  37. 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 Sluggish movements Croaking sound while crying Tongue large and protruding Broad and flat nose Umbilical hernia

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