The document summarizes information about the thyroid and parathyroid glands. It discusses the anatomy, physiology, diseases and treatment of hypothyroidism and hyperthyroidism. It also covers the anatomy, regulation, actions and diseases including hypoparathyroidism and hyperparathyroidism of the parathyroid glands. Evaluation and management of thyroid and parathyroid disorders is outlined.

1. Presented by :
Mr. Nirav S. Vachhani
M.Pharm Pharmacology (Sem-2)
Guided by:
Dr. Rina H. Gokani
S. J. Thakkar pharmacy college, Rajkot.

2. 2

3. Introduction:
The thyroid gland was described by Galen
and was named "glandulae thyroidaeae" by
Wharton in 1656.
The thyroid gland is the source of two
fundamentally different types of hormones.
The iodothyronine hormones include
1. Thyroxine (T4) and
2. 3,5,3’-triiodothyronine (T3)
They are essential for normal growth and
development and play an important role in
energy metabolism.
3

4. Anatomy:
4

5. Physiology:
Biosynthesis of Thyroid Hormones :
5

6. Regulation of Thyroid Function :
6

7. The ratio of T4 and T3 secreted :- 10:1
Approximate Values for Thyroid Hormone
Plasma Concentrations and Various Kinetic
Parameters.
T4 T3
Plasma concentration
Total 7.77 mg/dL 0.14 mg/ dL
Free 1.554 ng/dL 0.389 ng/dL
Total hormone in free form 0.02% 0.3%
Plasma half-life 6.7 days 0.75 days
Volume of distribution 10 L 40 L
Metabolic clearance rate 1.1 L/day 24 L/day
Total production rate 85.47 mg/day 33.6 mg/day
From thyroid secretion 100% 20% 7

8. Actions of Thyroid Hormones :
8

9. Evaluation of Thyroid Diseases:
Thyroid Function test :
commonly in use for estimating the iodine,
TBG, free T4 and free T3 concentrations are as
follow:
• Protein-bound iodine:
It is a measure of organically bound iodine
in blood (normal 4-8 ug/dl: myxoedema
2ug/dl; thyrotoxicosis 10-12 ug/dl).
• Serum T4:
It is measured by radio-immuno assay
(normal 5-12 ug/dl). Serum T3 assay can also
be done (normal 80-180 ng/dl).
9

10. •Serum TBG:
It is measured by radio-immuno assay or immuno
electrophoresis, and the ratio of T4 to TBG is used
as an index of free hormone activity.
• Free thyroxine index and effective thyroxine ratio:
These are calculated from the serum T4 and
serum TBG level. There is a good correlation
between these values and free T4 levels. Direct
free T4 measurement are tedious and difficult.
• Scintillography:
The radio iodine uptake by the gland is recorded
photographically and scanned.
10

11. • T3 suppression test:
In the standard test, the pretreatment
radioactive iodine uptake (RAIU) is determined.
Then T3 (as Cytomel) 25 ug tid, is given for 7-10
days. On the last day a repeat RAIU is
performed. In a normal person the RAIU will be
suppressed by 50% or less of the original value.
Whereas in Graves’ disease there is no suppresion
as the thyroid is functioning autonomously.
Clinical history and physical
examination :
11

12. Thyroid Imaging :
• Radioactive imaging
• Ultrasound waves
• CT/MRI scan
12

13. Diseases of the Thyroid :
Two significant functional disorders
characterized by distinct clinical syndromes
are :
I. Hyperthyroidism :
Associated with excessive release of
Thyroid hormones.
II. Hypothyroidism :
Associated with Thyroid hormone
deficiency.
13

14. 1) Hyperthyroidism :
The term hyperthyroidism is restricted to those
conditions in which thyroid hormone production
and release are increased due to gland hyper
function.
The condition is more frequent in females and is
associated with rise in both T3and T4 levels in
blood, though the increase in T3 is generally
greater than that of T4.
Etiopathogenesis :
Primary : Graves’ disease
Toxic multi-nodular goiter
Toxic adenoma
Secondary : TSH hyper secretion by a
pituitary tumor 14

15. Mainly referable to
1. Hypermetabolic state
2. Over activity of the
sympathetic nervous
system
15

16. Diagnosis :
Autonomous thyroid function
 Low TSH
 Elevated T3 / T4
Thyroid scan
 diffuse elevated iodine uptake
Thyroid ultrasound
16

17. Treatment :
Choices:
1. Antithyroid drugs
2. Radioactive iodine therapy
3. Surgery
Choice depends on:
1. Age
2. Severity of the disease
3. Size of the gland
4. Coexistent pathology (Ophthalmoplegia)
5. Other factors:
 Patient’s preference
 Pregnancy
17

18. 1. Antithyroid drugs :
 Propyl thiouracil (PTU) = 100-300 mg TID
 Methimazole (Tapazole) = 10-20 mg TID then OD
 Carbimazole = 40 mg OD
MOA :
 Inhibits the organic binding of iodine and
coupling of iodotyrosine
 PTU can also lower conversion of T4 to T3; it can
also decrease thyroid autoantibody levels.
18

19. Disadvantages of these drugs :
Crosses the placenta --> inhibits fetal thyroid
function
Excreted in breast milk
Side effects:
 Skin rashes
 Fever
 Peripheral neuritis
 Polyarthritis
 Granulocytopenia (reversible)
19

20. 2. Radioactive Iodine Therapy :
MOA :
131
I is taken up and trapped
Emission of α-particle
Destroy thyroid tissue
Advantages :
i. Avoidance of surgery (no injury to nerve /
parathyroid gland)
ii. Reduce cost & ease of treatment
20

21.  Disadvantages :
i. Lifelong thyroxin replacement therapy
ii. Slower correction of hyperthyroidism
iii. Higher relapse rate
iv. Adverse effect of ophthalmopathy
v. Development of Hypothyroidism after
thyroid ablation
 Suitable for :
i. Small or moderate size goiter
ii. Relapse after medical and surgical therapy
iii. Antithyroid drug and surgery are
contraindicated
 Contraindicated :
i. Pregnant / breast feeding
ii. Ophthalmopathy (progression of eye signs)
iii. Young age (children/adolescence)
----> Infertility / carcinoma
21

22. 3. Thyroid Surgery :
 Mainly Suitable for :
i. Young patient
ii. With Graves’ ophthalmopathy
iii. Pregnant
 Advantages :
i. Immediate cure of the disease
ii. Low incidence of hypothyroidism
iii. Potential removal of coexisting thyroid
carcinoma
 Disadvantages :
i. Complication ---> nerve injury (1%) and
hypoparathyroidism (13% transient/ 1%
permanent).
ii. Hematoma
iii. Hypertrophic scar formation
22

23. 2) Hypothyroidism :
Hypothyroidism is a hypometabolic clinical state
resulting from either
i. Inadequate production of thyroid hormones
for prolonged periods,
ii. From resistance of the peripheral tissues to the
effects of thyroid hormones (rarely).
Depending on whether the hypothyroidism arises
from an intrinsic abnormality in the thyroid or
results from hypothalamic or pituitary disease,
divided into primary and secondary categories.
23

24.  Causes of hypothyroidism :
Primary
Postablative (after surgery or radioiodine therapy)
Primary idiopathic hypothyroidism
Hashimoto thyroiditis*
Iodine deficiency*
Congenital biosynthetic defect (dyshormonogenetic goiter)*
Secondary
Pituitary or hypothalamic failure (uncommon)
24

25. Mainly referable to
1. Cretinism
2. Myxoedema
25

26.  Cretinism :
A cretinism is a child with severe
hypothyroidism present at birth or developing
within first two years of postnatal life.
 Clinical features :
• Impaired development of skeletal system & CNS
• Severe mental retardation
• Coarse facial features
• A protruding tongue
• Umbilical hernia
26

27.  Treatment of Cretinism :
Iodine only if iodine deficiency is the cause.
Levothyroxine (T4):
 Average dose 1.6 ug/kg
 Age > 50-60 or cardiac disease:
must start at a low dose (25 ug/d)
 Recheck thyroid hormone levels every 4-6
weeks after a dose change
 Aim for a normal TSH level
Liothyronine (T3):
 Tablet (Cytomel®) : 5-10 ug/d (starting)
: 25 ug/d (maintenance)
 Injection (Triostat®) : 50-100 ug
27

28.  Myxoedema :
Myxoedema coma is a rare syndrome that
represents the extreme expression of severe, long-
standing hypothyroidism.
Common precipitating factors include :
1. Pulmonary infections,
2. Cerebrovascular accidents,
3. Congestive heart failure
 Clinical features :
• Hypothermia, which may be profound;
• Respiratory depression
• Unconsciousness
• Dry & rough skin
28

29.  Treatment of Myxoedema :
Levothyroxine
500 mg/day
Livothyronine
75 mg/day
Other
 Rewarming with blankets
 Correction of hyponatremia
 Treatment of the precipitating incident
29

30. 30

31. Introduction:
 The parathyroid glands are usually 4 in number:
1. The superior pair derived from the 3rd
branchial pouch
2. Inferior pair from the 4th branchial pouch of
primitive foregut
31

32. Anatomy:
 composed of solid
sheets and cords of
parenchymal cells
32

33. Regulation of Parathyroid Function
:
33

34. Actions of Parathyroid Hormones :
34

35. Diseases of the Parathyroid :
The major parathyroid disorders are its
functional disorders:
1. Hypoparathyroidism
2. Hyperparathyroidism
35

36. 1) Hypoparathyroidism :
When the parathyroid glands do not secrete
sufficient PTH, the osteocytic reabsorption of
exchangeable calcium decreases and the osteoclasts
become almost totally inactive.
As a result, calcium reabsorption from the bones is
so depressed that the level of calcium in the body
fluids decreases.
When the parathyroid glands are suddenly
removed, the calcium level in the blood falls from
the normal of 9.4 mg/dl to 6 to 7 mg/dl within 2 to 3
days.
36

37.  Aetiology:
Most common cause : Surgery for thyroid diseases
Neck exploration
Adenoma
 Clinical manifestation:
Most of due to Hypocalcaemia
Increased neuromuscular excitablity
Major symptoms
• Numbness around mouth
• Muscle spasm
• Irritability
• Cataract
• Positive chvostek’s sign
• Positive trousseau’s sign 37

38.  Treatment:
For sever, acute treatment:
10% calcium gluconate IV injection
For chronic treatment:
PTH therapy (not currently practised)
Maintenance treatment:
Vitamin D preparations
38

39. Drug Preparations Activity
Ergocalciferol Calciferol injection 7.5 mg Requires renal and
(3000000 units/ml) hepatic activation
( calciferol, vitamine D2)
Calciferol tablets 250µg (10000
units) and 1.25mg (50 000 units)
Calcium and ergocalciferol tablet
(2.4 mmol of calcium + 400 units
of ergocalciferol)
Colecalciferol • A range of preparation Requires renal and
containing calcium (500-600mg) hepatic activation
( vitamin D3)
and colecalciferol (200-440 units)
39

40. Alfacalcidiol Alfacalcidiol capsule 250ng, Requires hepatic
500ng and 1µg activation
(1α-hydroxycolecalciferol)
Alfacalcidiol injection
2µg/ml
Calcitriol (1, 25 – Calcitriol capsule 250ng Active
dihydroxycolecalciferol) and 500 ng
Calcitriol injection 1µg/ml
Dihydrotachysterol • Dihydrotachysterol oral Requires hepatic
injection 250mg/ml activation
40

41. 2) Hyperparathyroidism :
Hyperparathyroidism is the clinical state that
results from increased production of PTH by the
parathyroid gland.
Hyperparathyroidism is further categorized as
follow:
1. Primary Hyperparathyroidism
2. Secondary Hyperparathyroidism
3. Tertiary Hyperparathyroidism
41

42. I. Primary Hyperparathyroidism:
 Aetiology:
Cause of primary hyperparathyroidism is a
tumor of one of the parathyroid gland.
Much more frequently in women.
Common causes:
Parathyroid adenomas 80%
Carcinoma of parathyroid 2-3%
Primary hyperplasia 15%
 Clinical features:
 Elevated levels of parathyroid hormone
 Hypercalcaemia
 Hypercalciuria
 Kidney stones 42

43. II.Secondary Hyperparathyroidism:
 In secondary hyperparathyroidism, high levels of
PTH occur as a compensation for hypocalcemia
rather than as a primary abnormality of the
parathyroid glands.
 Etiology:
Chronic renal insufficiency
Vitamin D deficiency
Intestinal malabsorption syndromes
 Clinical features:
 Mild hypocalcaemia
 Renal osteodystrophy
 Soft tissue calcification
43

44. III.Tertiary Hyperparathyroidism:
 Tertiary hyperparathyroidism is a complication
of secondary hyperparathyroidism in which
hyper function in spit of removal of the cause of
secondary hyperplasia.
 Possibly, hyperplastic nodule in the parathyroid
gland develops which becomes partially
autonomous and continue to secrete large
quantities of parathyroid hormone without
regard to the needs of the body.
44

45.  Treatment of Hyperparathyroidism:
(i) Surgical removal of the diseased gland.
(ii) Intravenous saline infusion to correct
dehydration.
(iii) Intravenous infusion of 0.1 M solution of basic
sodium phosphate to promote calcium excretion.
(iv) Isotonic sodium sulphate and sodium chloride
administered intravenously to induce calciuresis.
(v) Disodium edetate (EDTA). It chelates calcium, but
is too toxic for routine use. In an emergency 50
mg/kg in 500 ml saline may be given
intravenously.
(vi) Mithramycin. It is a cytotoxic agent and reduces
serum calcium levels. In an emergency 25
mcg/kg/day may be given IV for 3 to 4 days.
45

46. (vii) Calcitonin 5 to 25 mcg/kg may be of therapeutic
value, but experience with this agent is limited.
(viii) Glucocorticosteroids may be tried. They are
claimed to be effective in hypercalcaemia of
vitamin D therapy.
(ix) Haemodialysis may be of value when all other
measures have failed.
 Thus, effective pharmacotherapy for
hyperparathyroidism is not available. Mainly the
treatment is operative.
46

47. Summery:
 The thyroid gland is the source of two
fundamentally different types of hormones.
1. Thyroxine (T4) and
2. 3,5,3’-triiodothyronine (T3)
 The ratio of T4 and T3 secreted :- 10:1
 The evaluation of Thyroid function is maninly done
by Thyroid function test.
 Diseases of Thyroid include
1. Hyperthyroidism
2. Hypothyroidism
 Treatment of these include
1. Antithyroid drugs
2. Radioactive iodine therapy
3. Surgery 47

48.  Parathyroid :
• The Parathyroid gland gland derived from 3rd and
4th bronchial pouch.
• The gland mainly secrets the Pararthyroid hormone.
• The main action of PTH on the Kidney, Bone and
Small intestine.
• There are two main diseases related to PTH.
1) Hypoparathyroidism
2) Hyperparathyroidism
• Treatment:
•Hypothyroidism •Hyperparathyroidism
Ergocalciferol Surgery
Colecalciferol IV infusin of NaPO4
Alfa Calciferol Disodium Edetate
Calcitriol Mithramycine
Dihydrotachysterol Calcitonin 48

49. References:
49

50. 50