4. INTRODUCTION
• An endocrine gland , at the root of neck on either side of trachea.
• Two lobes connected by isthmus
HISTOLOGY
• Composed of large number of closed follicles , lined with follicular cells , in
between are present parafollicular cells.
• Follicular cells secrete thyroglobulin( colloidal
substance)which fills follicular cavity and also
secretes T4 and T3 .
• Both T4 and T3 are derivatives of amino acid
tyrosine.
5. HORMONES
• Secretes 3 hormones :-
I. Tetraiodothyronine or ( thyroxine ) T4 ------90% of secretion
II. Tri-iodothyronine or T3 -------9% to 10% of secretion
III. Calcitonin
• Strength of T3 is four times more than T4 but duration of T4 action is four
time more than T3 action .WHY??? Reason is less affinity of T3 for plasma
protein , combines loosely with them so released quickly while T4 binds
strongly and is released slowly.
• Degradation of thyroid hormones occur in kidney , liver and muscles.
• Synthesis takes place in thyroglobulin , tyrosine and iodine are essential .
6. STAGES OF SYNTHESIS OF THYROID
HORMONES
Synthesis occurs in 6 stages
1) Thyroglobulin synthesis:- ER and Golgi apparatus in follicular cells synthesize
and secrete thyroglobulin .After synthesis, it stores in follicles .
2) Iodide trapping:- Iodide is actively transported from blood to follicular cells ,
against EC gradient ,along with Na+ through Na-iodide symport pump.
3) Oxidation of iodide:- Iodide oxidizes to iodine inside follicular cells in
presence of thyroid peroxidase because only iodine combines with tyrosine
to form hormone.
7. 4 ) Transport of iodine to follicular cavity:- Transported from follicular cells to
follicular cavity through iodide –chloride pump called pendrin.
5 ) Iodination of tyrosine :- Iodine binds with thyroglobulin, process called
organification . Iodine combines with tyrosine in thyroglobulin , process called
iodination .Iodination of tyrosine occurs in different stages: tyrosine first
transform to mono-iodothyronine (MIT) and later into tri-iodothyronine (DIT).
6 ) Coupling reaction :- the coupling reaction in different configuration, gives
rise to different thyroid hormones.
8.
9. STORAGE OF HORMONES
• Can be stored up to 4 months, remains in form of vesicles in thyroglobulin.
• Only endocrine gland which stores its hormones for long periods, so sign and
symptoms of deficiency don’t appear before 4 months.
RELEASE FROM THYROID GLAND
• Not released in blood directly, hormones are first cleaved from thyroglobulin and then
released.
• Only T3 and T4 are released into blood stream. MIT and DIT are not released in blood
stream, they are deiodinated by enzyme . During congenital absence of enzyme, MIT
and DIT are secreted in urine and iodine deficiency develops.
10. FUNCTIONS OF THYROID GLAND
• Increases basal metabolic rate(BMR) by increasing O2 consumption except in
brain , retina, spleen, testes and lungs.
• Increase synthesis of protein in cells ,and cardiovascular activity and
carbohydrates metabolism.
• Decrease fat storage by mobilizing from adipose tissue and fat depots , increase
the fatty acid level in blood.
• Decreases cholesterol , phospholipids and triglycerides level in plasma. In
hyposecretion of T4, cholesterol level increase ,results in atherosclerosis.
11. • Increase heat production in body, called thyroid hormone-induced
thermogenesis
• Increase growth in children, promote brain development in fetal life, deficiency
leads to mental retardation .
• Decrease body weight, accelerate erythropoietic activity .polycythemia is
common in hyperthyroidism.
• Increase GIT activity ,hypersecretion cause diarrhea, hypo-- cause constipation.
• Maintain normal sleep, hyposecretion cause somnolence .
• Affect muscular activity, hypersecretion cause thyrotoxic myopathy and tremors.
12. • Increase formation of many enzymes, vitamins are
essential. vitamin deficiency is possible during
hyposecretion of T4.
• Essential for normal sexual function. In males ,
hyposecretion cause loss of libido and
hypersecretion cause impotence .In women,
hypersecretion cause oligomenorrhea and
amenorrhea, hyposecretion cause
polymenorrhea and menorrhagia.
13. DISORDERS OF THYROID GLAND
HYPERTHYROIDISM
Increased secretion of thyroid gland .Caused by Graves disease and thyroid adenom
GRAVES’ DISEASE :- Autoimmune disease ,most common cause of hyperthyroidism
B-Lymphocytes produce thyroid stimulating autoantibodies (TBAbe).these antibiotics
act as TSH by binding with membrane receptors and activating cAMP systems of
thyroid follicular cells , results in hyperthyroidism.
THYROID ADENOMA :- sometimes, localized tumor develops in thyroid tissues and
secretes large quantity of thyroid hormones. Not associated with autoimmunity, the
hormone secreted from adenoma depresses the TSH production.
14. Exophthalmos :-
• Most but not all hyperthyroid patient develops Exophthalmos (bulging of eyes)
• Caused due to swelling of retro-orbital tissues and degenerative changes in
extraocular muscles.
• Leads to blindness due to stretch and damage to optic nerve and due to
constant exposure to atmosphere cause dryness ,infection and irritation.
15. HYPOTHYROIDISM
Decreased secretion of thyroid hormone ,leads to myxedema in adults and
cretinism in children.
MYXEDEMA :- edematous appearance. Caused due to thyroid gland , genetic
disorder or iodine deficiency .Common cause is autoimmune disease called
hashimoto’s thyroiditis,common in middle aged
Women.
Sign and symptoms includes features like:-
Swelling of face, bagginess under eyes ,Non-
Pitting type of edema , atherosclerosis.
16. CRETINISM :- Occurs due to congenital absence of thyroid gland, genetical
disorder , or lack of iodine
Features of cretinism include babies with sluggish
movements, croaking sound, mental retardness.
skeleton growth is more affected than soft tissue.
big tongue with dripping saliva.
18. GOITER
Means enlargement of thyroid gland ,Occurs both in hypothyroidism and
hyperthyroidism.
Goiter in hyperthyroidism ---- Toxic goiter :-
Enlarged thyroid gland with increased hormone secretion,
caused by thyroid tumor.
Goiter in hypothyroidism ---- nontoxic goiter :-
Enlarged thyroid gland without increased thyroid
hormone secretion.
19. Based on cause ,nontoxic goiter classified into two types :-
Endemic colloid goiter :- due to iodine deficiency(less than 50ug/day),no
formation of hormones, thyroglobulin accumulates in follicles, increase size of gland
Idiopathic non-toxic goiter :- due to unknown cause, gland enlarges
without iodine deficiency, suggested due to thyroiditis and deficiency of enzymes
(peroxidases, deiodinase…etc.)required for hormone synthesis. some foodstuffs
(turnips,cabbage..etc.) contain goitrogenic substances which suppress hormone
synthesis.
20. TREATMENT OF THYROID DISORDERS
TREATMENT FOR HYPERTHYROIDISM :-
I. BY USING ANTITHYROID SUBSTANCES : Drugs which suppresses hormone
secretion e.g. Thiocyanate ,thiourylenes ,high cons of inorganic iodides.
II. BY SURGRICAL REMOVAL : when antithyroid substances are not possible ,this
process is called thyroidectomy.
TREATMENT FOR HYPOTHYROIDISM :-
Only treatment is administration of thyroid extract or ingestion of pure thyroxine
in form of tablets ,orally.
21. THYROID DIAGNOSTIC TESTS
Functional status of thyroid gland can be assessed by following tests :-
i. Measurement of plasma level of T3 and T4 : measure concentration of
“free” thyroid hormone in plasma.
ii. Measurement of TRH and TSH : these hormones will be total absent in
hyperthyroidism dur to –ive feedback by increased level of thyroid hormone
iii. Measurement of basal metabolic rate : In hyperthyroidism rate increased
by 30% to 60%. In hypothyroidism rate decrease by 20% to 40% .