This document provides information about a case study on a 32-year-old female patient presenting with symptoms of hyperthyroidism. Lab tests show an irregular heartbeat and signs point to a diagnosis of Graves' disease. The document then provides details on the anatomy and function of the thyroid gland, including how it traps iodine, produces thyroglobulin, and synthesizes and secretes the thyroid hormones T3 and T4. Signs and treatment of both hyperthyroidism and hypothyroidism are discussed.

1. CASE STUDY ON ENDOCRINE
PHYSIOLOGY TOPIC- THYROID GLAND
Presentation by-
2ND YEAR MD
LINCOLN UNIVERSITY COLLEGE

2. HISTORY OF PATIENT:
 Age- 32 years old
 Gender- Female
 Height- 5 feet
 Weight- 39 kg
 Heart rate- 140 bpm
 BP- 130/85 mm of Hg
 Respiratory rate-28/min
 Protruding eyeballs (looks cachectic)
 Palpitation
 Sweating
 Severe anxiety

3. SYMPTOMS(SX):
 Heat Intolerance
 Irregular Menstruation
 Insomnia
 Weight Loss
 Excessive Hunger
 Muscle wasting
 Swelling (anterior part of neck)

4. LAB REPORTS OF THIS PATIENT:
 Hb-10.8 gm/dl
 TLC - 6000 Cu mm
 CXR – NO Abnormality
 ECG- Irregularly irregular
heart reathm.

5. PROBABLE DIAGNOSIS:
 HYPERTHYROIDISM-GRAVES DISEASES

6. THYROID GLAND:
THE THYROID GLAND LIES POSTERIOR TO THE STERNOTHYROID AND
STERNOHYOID MUSCLES, WRAPPING AROUND THE CRICOID CARTILAGE AND
TRACHEAL RINGS. IT IS LOCATED INFERIOR TO THE LARYNGEAL THYROID
CARTILAGE, TYPICALLY TO THE VERTEBRAL LEVELS C5-T1.

7. MICROSCOPIC APPEARANCE OF THE
THYROID GLAND

8. SYNTHESIS AND SECRETION OF THE
THYROID HORMONES
 1.Iodide Trapping(Iodide Pump—the Sodium-Iodide
Symporter).
 2.Formation and Secretion of Thyroglobulin by the
Thyroid Cells.
 3.Oxidation of the Iodide Ion.
 4.“Organification” of Thyroglobulin.(Iodination of
Tyrosine and Formation of the Thyroid Hormones).
 5.Storage of Thyroglobulin.
 6.Release of T3 and T4 from the Thyroid Gland.

9. CELLULAR MECHANISMS

10. (IODIDE TRAPPING)
IODIDE PUMP—THE SODIUM-IODIDE SYMPORTER
 The first stage in the formation of thyroid hormones is
transport of iodides from the blood into the thyroid
glandular cells and follicles.
 The basal membrane of the thyroid cell has the specific
ability to pump the iodide actively to the interior of the cell.
This is achieved by the action of a sodium-iodide
symporter (NIS), which co-transports one iodide ion along
with two sodium Ions into the cell.
 This process of concentrating the iodide in the cell is called
iodide trapping.
 TSH stimulates and hypophysectomy greatly diminishes
the activity of the iodide pump in thyroid cells.
 Iodide is transported out of the thyroid cells across the
apical membrane into the follicle by a chloride-iodide ion
counter-transporter molecule called pendrin.

11. THYROGLOBULIN AND
T3 FORMATION
 The endoplasmic reticulum and Golgi apparatus
synthesize and secrete into the follicles a large
glycoprotein molecule called thyroglobulin(MW-
335,000)
 Each molecule of thyroglobulin contains about 70
tyrosine amino acids, and they are the major
substrates that combine with iodine to form the
thyroid hormones.

12. OXIDATION OF THE IODIDE ION
 The first essential step in the formation of the
thyroid hormones is conversion of the iodide ions to
an oxidized form of iodine, either nascent iodine (I0)
or I3 - , that is then capable of combining directly
with tyrosine.
 This oxidation of iodine is promoted by the enzyme
peroxidase and its accompanying hydrogen
peroxide, which provide a potent system capable
of oxidizing iodides.
 The oxidized iodine at exactly the point in the cell
where the thyroglobulin molecule issues forth from
the Golgi apparatus and through the cell membrane
into the stored thyroid gland colloid.

13. “ORGANIFICATION” OF
THYROGLOBULIN:
 The binding of iodine with the thyroglobulin
molecule is called or ganification of the
thyroglobulin.
 rapidly as the thyroglobulin molecule is released
from the Golgi apparatus or as it is secreted
through the apical cell membrane into the follicle,
iodine binds with about one sixth of the tyrosine
amino acids within the thyroglobulin molecule.

14. STAGES OF IODINATION OF TYROSINE:

15. FINAL FORMATION OF T3 & T4:
 Tyrosine + I = MIT
 MIT + I = DIT
 DIT + MIT = T3
 MIT + DIT = Reverse T3
 DIT + DIT = T4
 (N:B- MIT & DIT- Mono & diiodotyrosine)

16. STORAGE OF THYROGLOBULIN
 After synthesis of the thyroid hormones has
run its course, each thyroglobulin molecule
contains up to 30 T4 molecules and a few
T3 molecules.
 In this form, the thyroid hormones are stored
in the follicles in an amount sufficient to
supply the body with its normal
requirements of thyroid hormones for 2 to 3
months.

17. RELEASE OF T4 AND T3 FROM THE
THYROID GLAND
 The apical surface of the thyroid cells sends out
pseudopod extensions that close around small portions
of the colloid to form pinocytic vesicles that enter the
apex of the thyroid cell.
 Then lysosomes in the cell cytoplasm immediately fuse
with these vesicles to form digestive vesicles containing
digestive enzymes from the lysosomes mixed with the
colloid.
 Multiple proteases among the enzymes digest the
thyroglobulin Molecules and release T4 and T3 in free
form.
 These then diffuse through the base of the thyroid cell into
the surrounding capillaries. Thus, the thyroid hormones
are released into the blood.

18. EFFECT OF THYROID HORMONE IN THE
BODY:
 1. ACTION ON BASAL METABOLIC RATE (BMR)
 ACTION ON PROTEIN METABOLISM
 ACTION ON CARBOHYDRATE METABOLISM
 ACTION ON FAT METABOLISM
 ACTION ON PLASMA AND LIVER FATS
 ACTION ON VITAMIN METABOLISM
 ACTION ON BODY TEMPERATURE
 ACTION ON GROWTH:

19. EFFECTS:CONT.
 ACTION ON BODY WEIGHT : Increase in thyroxine secretion
decreases the body weight and fat storage. Decrease in thyroxine secretion
increases the body weight because of fat deposition.
 ACTION ON CARDIOVASCULAR SYSTEM:
 ACTION ON RESPIRATION:
 ACTION ON GASTROINTESTINAL TRACT:
 ACTION ON SLEEP:Hypersecretion of thyroxine causes
excessive stimulation of the muscles and central nervous system.
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.irregular
menstruation and occasionally amenorrhea.Hyperthyroidism in women leads
to oligomenorrhea and sometimes amenorrhea.

20. REGULATION OF THYROID SECRETION

21. THYROID FUNCTION TESTS:
DIAGNOSIS FOR ANY ABNORMALITY OF
THYROID GLAND:
 1. Measurement of plasma T3 and T4:
measurement of concentration of “free” thyroid
hormones in the plasma, i.e. T3 and T4 to ensure
that is it hypo ? Hyperthyroid ? Diseases.
2. Measurement of TRH & TSH: absence of
these two hormones occurs in hyperthyroidism.
3. Measurement of BMR : In
hythyroidism, basal metabolic rate is increased by
about 30% to 60%. Basal metabolic rate is
decreased in hypothyroidism by 20% to 40%.

22. DISEASES OF THE THYROID
HYPERTHYROIDISM
1.GRAVES DISEASE (EXOPHTHALMIC
HYPERTHYROIDISM) THE MOST COMMON FORM OF HYPERTHYROIDISM,
IS AN AUTOIMMUNE DISEASE .

23. 2. THYROID ADENOMA (A TUMOR):
THAT DEVELOPS IN THE THYROID TISSUE AND SECRETES LARGE
QUANTITIES OF THYROID HORMONE.

24. SIGNS AND SYMPTOMS OF
HYPERTHYROIDISM
(1) a high state of excitability,
(2) intolerance to heat,
(3) increased sweating,
(4) mild to extreme weight loss
(5) varying degrees of diarrhea,
(6) muscle weakness,
(7) nervousness or other psychic disorders,
(8) extreme fatigue but inability to sleep,
(9) tremor of the hand
(10) tachycardia & atrial fibrillzation

25. TREATMENT FOR HYPERTHYROIDISM
 1. By using Antithyroid Substances:
 Antithyroid substances are the drugs which
suppress the secretion of thyroid hormones.
Hyperthyroidism in early stage can be treated by
antithyroid substances-
 i. Thiocyanate
 ii. Thiourylenes
 iii. High concentration of inorganic iodides.

26. TREATMENT CONT….
 2. By Surgical Removal:
 In advanced cases of hyperthyroidism, treatment by
using antithyroid substances is not possible. So,
thyroid gland of these patients must be removed.
Surgical removal of thyroid gland is called
thyroidectomy.

27. HYPOTHYROIDISM
 Endemic Goiter (Caused by Dietary Iodide
Deficiency)
 Myxedema (Hashimoto’s thyroiditis ) In ADULT
 Cretinism In CHILD

28. GENERAL FEATURES OF HYPOTHYROIDISM
1.ENDEMIC GOITER:-(NON TOXIC)

29. 2.PATIENT WITH MYXEDEMA

30. GENERAL FEATURES OF
HYPOTHYROIDISM IN MYXEDEMA
 1. Swelling of the face
 2. Bagginess under the eyes
 3.edema
 4. Atherosclerosis
 Others- Anemia, Fatigue and muscular
sluggishness, body weight Increase, Constipation,

31. GENERAL FEATURES OF HYPOTHYROIDISM IN
3.CRETINISM
1. stunted growth with
bloated body.
2. big tongue obstructs
swallowing and
breathing.
Cretinism (3-month-old
baby)

32. REATMENT FOR HYPOTHYROIDISM
 The only treatment for hypothyroidism is the
administration of thyroid extract or
ingestion of pure thyroxine in the form of
tablets, orally.

33. THANK YOU