This document provides information about the parathyroid gland, including its anatomy, physiology, diseases, and presenting problems. It discusses the following key points: - The parathyroid glands regulate calcium levels in the blood through secretion of parathyroid hormone (PTH). High calcium levels decrease PTH secretion while low calcium increases it. - Primary diseases include primary hyperparathyroidism from overactive parathyroid glands and hypoparathyroidism from underactive glands. - Hyperparathyroidism causes hypercalcemia and is usually treated by surgically removing the overactive gland(s). Hypoparathyroidism causes hypocalcemia and is treated with calcium and vitamin

1. Parathyroid gland
By: Sabir Abdulrahman

2. Objectives
• Anatomy
• Physiology
• Presenting problems
• Diseases of parathyroid
• Parathyroid neoplasms

3. Anatomy
• The parathyroid glands are four
glands, usually located on the posterior
aspect of the thyroid gland
• Arterial supply is chiefly via the inferior
thyroid artery
• Venous drainage is into
the superior, middle, and inferior
thyroid veins.
• The lymphatic drainage
to paratracheal and deep cervical
nodes.
• Nerves
• sympathetic nerves derived
from thyroid branches of the
cervical ganglia.

4. Physiology
Cell types
– Adipocytes ∼ 50%))
– Parathyroid cells (parathyroid
chief cells
• Produce and secrete PTH
• Have calcium
sensing receptors which
detect changes in calcium
concentration and
modulate PTH secretion
– Oxyphil cells: function not
clear

5. Actions of parathyroid hormone

6. – ↓serum Ca2+ →↑PTH
secretion
– ↑serum PO43−→ ↑PTH
secretion
– ↓ serum Mg2+→↑ PTH
secretion
– ↓ ↓ serum Mg2+→ ↓ PTH
secretion
Regulation of parathyroid hormone

7. Presenting problem
Hypercalcaemia :The normal serum calcium ranges from
8.8 mg/dL-10.8 mg/dL. Primary hyperparathyroidism
and malignancy accounts for 90% of the cases of
hypercalcemia

8. Presenting problem
Hypocalcemia: total serum calcium
concentration < 8.5 mg/dL (< 2.12 mmol/L), or ionized
(free) calcium concentration < 4.65 mg/dL (< 1.16
)mmol/L)
• Seizures
• Tetany
• Paresthesias
• Psychiatric manifestations such as anxiety,
depression
• Chvostek's sign
• Trousseus sign
• QTc prolongation

9. Diseases of parathyroid

10. hyperparathyroidism
➢ Primary
hyperparathyroidism (pHPT): Hypercalcemia r
esults from abnormally active parathyroid
gland
➢ Secondary
hyperparathyroidism (sHPT): Hypocalcaemia r
esults in reactive overproduction of PTH
➢ Tertiary
hyperparathyroidism (tHPT): Hypercalcemia re
sults from untreated sHPT with continuously
elevated PTH levels.

14. Imaging
➢X-ray: decreased bone mineral
density,
o 1-Cortical thinning
o 2-Salt-and-pepper skull: granular
decalcification
o 3-Rugger-jersey spine sign
o 4-Osteitis fibrosa cystica: cyst-like
brown tumors located in
osteolytic spaces
➢Ultrasound/nuclear imaging
(Tc99m-sestamibi scan)
3 4

15. Management of hyperparathyroidism
• The treatment of choice for primary
hyperparathyroidism is surgery parathyroidectomy
should be considered.
• Cinacalcet is a calcimimetic that enhances the
sensitivity of the calcium-sensing receptor, so reducing
PTH levels,
• ocasionally, primary hyperparathyroidism presents
with severe life-threatening hypercalcaemia. This is
often due to dehydration and should be managed
medically with intravenous fluids and
bisphosphonates,

17. Hypoparathyroidism
Etiology
• Post-operative :most common
• Autoimmune
• Infiltrative diseases like Wilson disease
• Radiation induced destruction
• Congenital like DiGeorge syndrome

18. Hypoparathyroidism

19. management of hypoparathyroidism
• Treat the underlying cause
• Persistent hypoparathyroidism and
pseudohypoparathyroidism are treated with
oral calcium salts and vitamin D

20. Familial Hypocalciuric Hypercalcemia
• Familial hypocalciuric hypercalcemia (FHH) is a rare
autosomal dominant condition. It occurs as a result
of mutations in the calcium-sensing receptor gene
(CASR) causing decreased receptor activity. Patients
have mild hypercalcemia, hypocalciuria,
hypermagnesemia, hypophosphatemia.
Parathyroid hormone is normal or mildly elevated

21. Familial hypocalciuric hypercalcaemia
Defective G-coupled Ca2+-sensing receptors in
multiple tissues (e.g., parathyroid, kidneys). Higher
than normal Ca2+ levels required to suppress PTH.
Excessive renal Ca2+ reabsorption mild hypercalcemia
and hypocalciuria with normal to PTH levels.

22. Pseudohypoparathyroidism
• autosomal dominant, maternally
transmitted mutations
(imprinted GNAS gene). when
PTH binds to its receptor end-
organ resistance (kidney and
bone) to PTH.
• Physical findings: Albright
hereditary osteodystrophy
• Labs: PTH high , Ca2+ low ,
PO43– high .

23. Parathyroid adenoma

24. Parathyroid carcinoma