Anatomy, Head and Neck, Parathyroid

Article Author:
Ali Ilahi
Article Editor:
Tahir Ilahi
Updated:
12/28/2018 5:43:57 PM
PubMed Link:
Anatomy, Head and Neck, Parathyroid

Introduction

The parathyroid glands are endocrine glands located at the posterior medial aspect of the thyroid gland.  There are four individual small and round glands that divide into pairs.  There are two glands located superiorly called the superior parathyroid gland and a pair that are located inferiorly- referred to as the Inferior parathyroid glands.  

Superior Parathyroid glands: These glands derive from the fourth pharyngeal pouch.  They are located about 1 cm superior to where the inferior thyroid arteries enter the thyroid gland.  

Inferior Parathyroid glands: They derive from the third pharyngeal gland.  The majority of the time these glands are located near the inferior poles of the thyroid glands, though in a small percentage of individuals they are found as low as the superior mediastinum.[1]

Structure and Function

The parathyroid glands have two distinct types of cells: chief cells and the oxyphil cells.

  • Chief cells: The chief cells manage the secretion of the parathyroid hormone (PTH). When the cells are viewed there contain prominent Golgi apparatus and a developed endoplasmic reticulum to help with the synthesis and secretion of the hormone. While the chief cells are smaller than the oxyphil cells, they are more abundant.
  • Oxyphil cells: The purpose of these cells is not entirely understood. They are larger than the chief cells and seem to increase in number with age.   

Function

The parathyroid glands help regulate the calcium level in the blood. When the calcium levels in the blood decrease the parathyroid gland releases a hormone called parathormone or parathyroid hormone (PTH). PTH is initially produced as a polypeptide hormone that initially forms as a pre-proparathyroid hormone (115 amino acids), then becomes a proparathyoid hormone (90 amino acid) and eventually to the final form which comprises 84 amino acids. When secreted, the PTH effects select target organs; which are the kidneys, intestine and the skeletal system.  

  • Kidney: The PTH helps with an increase in calcium reabsorption and excretion of phosphate. The reabsorption is promoted at the ascending loop of Henle, distal tubule and the collecting tubules. Prevention of phosphate reabsorption occurs at the proximal tubule. PTH also promotes 25-hydroxyvitamin D conversion to its active form (1,25-dihydroxy vitamin D-3) via activation of 1-hydroxylase in the proximal tubules.
  • Intestine: The activated vitamin D promotes the absorption of calcium because of the increase formation of the calcium-binding protein in the intestinal epithelial cells.
  • Bone: Rapid Phase- The PTH effects the osteoblastic and osteoclastic cells.  When the PTH binds to the cellular receptors, it allows the pumping of calcium from the osteocytic membrane.  This causes an immediate effect and allows for the rise of calcium to occur in minutes. Slow Phase: The slow phase takes several days to precipitate an increase in blood serum calcium. This process occurs via the osteoblast, as mature osteoclasts do not have receptors for PTH. This activation of the mature osteocytes by the osteoblast is via cytokines. The proliferation of osteoclasts also occurs.[2]

PTH Regulation

Increase of Blood Calcium

PTH regulation is by the negative feedback cycle via the chief cells' unique G- protein calcium receptor.  Increase in blood calcium allows the calcium to bind to G protein and increase production of phosphoinositide molecules. This molecule prevents the secretion of PTH. Vitamin D also helps in the regulation of PTH.  Vitamin D also acts directly on the gland to decrease the transcription of the PTH gene leading to decreased PTH synthesis.

Decrease of Blood Calcium

When there is a detected decrease in blood calcium, there is less calcium binding to the G-protein of the chief cells. This decreased binding subsequently leads to a decreased production of the phosphoinositide molecule allowing more secretion of PTH. A decrease in vitamin D permits an increase in PTH synthesis due to the activation of the transcription of the PTH gene.[3]

Embryology

The parathyroid gland originates from the third and fourth pharyngeal pouches of the endoderm with contributions from the neural crest and the ectoderm.  It is at six weeks in which there is an elongation of the pouch.  The pouch is initially hollow, but with further development, cell proliferation occurs allowing for solidification.

The inferior parathyroid originates from the third pharyngeal pouch, and the superior parathyroid arises from the fourth pharyngeal pouch. The fetal parathyroid hormone cells respond to calcium levels- fetal calcium levels are higher than maternal calcium levels.[1]

Blood Supply and Lymphatics

The thyroid gland and the parathyroid gland share the same blood supply. The inferior thyroid arteries supply the parathyroid gland via its branches.  Collaterals via the superior thyroid artery, thyroid ima artery, laryngeal, tracheal, and esophageal arteries.  Parathyroid veins would drain into the thyroid vein plexus.

Parathyroid lymphatic vessels drain in the deep cervical and paratracheal lymph nodes.  

Nerves

The nerve supply of the parathyroid derives from the branches of the cervical ganglia of the thyroid gland.  The nerve supply to the parathyroid glands is vasomotor.   

Surgical Considerations

Parathyroid glands have inconsistent locations between individuals. Due to these variants, damage to the glands can occur during neck surgery especially thyroidectomy. To prevent this damage, surgeons need to preserve the posterior part of the thyroid gland during thyroidectomy. If preservation of the posterior portion of the thyroid is not possible, then the parathyroid glands should be relocated so that accidental damage cannot occur. Removal of both pairs of the parathyroid gland would cause a decrease in the serum calcium levels, leading to the development of tetany.[4]

Removal of Parathyroid gland due to Pathologies

A hyperfunctioning parathyroid gland may require surgical intervention.  When the parathyroid over-secretes PTH, there are risks associated with high blood calcium. However, many such patients present with incidentally discovered hypercalcemia. These patients only require monitoring, and even mild symptoms can are medically manageable. However, when there are severe symptoms present with hypercalcemia, surgical intervention is needed.[5]

Bilateral Neck Exploration

When surgery is considered the most traditional technique is bilateral neck exploration. During this procedure, the surgeon will locate all four of the glands and based on appearance will determine if partial or complete glandular removal is necessary.

Focused Parathyroidectomy

Another less invasive approach allows limited operation of the diseased gland. This allows the surgeon to target the gland that has been identified after pre-operative localizing tests. Radiographic parathyroidectomy can be considered as a type of focused parathyroidectomy.  The patient receives a small injection of Tc-99m sestamibi the morning of the surgery. A handheld gamma probe is employed in the operating theater by the surgeon to detect the hyperactive gland. After excision of the diseased tissue, the probe can be used again to detect if any overactive tissue remains. 

Clinical Significance

Hyperparathyroidism

Hyperparathyroidism is due to the hyper or overactivity of the parathyroid gland. Hyperparathyroidism can lead to hypercalcemia. Hyperparathyroidism can be broken down into subsequent subgroups.

Primary: Primary hyperparathyroidism is due to direct gland alterations. This can be due to a benign tumor, hyperplasia, or even parathyroid cancer. Excess secretion of the PTH will present with hypoglycemia, osteoporosis, osteitis fibrosa cystica and hypertension. 

Secondary: This is a physiological increase of PTH due to reduced calcium levels in the blood. Causes of decreased calcium levels in the blood include inadequate vitamin D intake or chronic renal failure.

Tertiary: This occurs after prolonged secondary hyperparathyroidism.  Due to the continues chronic increase secretion of PTH, there are structural changes in the parathyroid glands. 

Malignant: Various tumors (bronchial squamous cell carcinomas) can produce a parathyroid-like protein that can mimic PTH function.  Though the protein mimics PTH, reduction of actual PTH levels occurs due to the negative feedback to the parathyroid gland. 

Hypercalcemia

Hypercalcemia can be the result of an overactive parathyroid gland. Symptoms can range from being non-existent to severe.

General

  • headache
  • fatigue

Kidneys

  • kidney stones- leading to back and flank pain
  • excessive urination
  • excessive thirst

Abdomen

  • vomiting
  • constipation
  • nausea
  • decreased appetite
  • abdominal pain

Heart

abnormal electrical rhythms

Muscle

  • twitches
  • cramps
  • weakness

Skeletal system

  • fractures
  • bone pain
  • osteoporosis

Neurological symptoms

  • memory loss
  • irritability
  • depression
  • confusion
  • coma

Hypoparathyroidism

Hypoparathyroidism is due to a reduced activity of the gland.  This condition has primary and secondary classifications. 

Primary: There is a gland failure which results in a decrease in PTH secretion.  Patients who suffer from this disorder will often need calcium supplementation

Secondary: This occurs when there is surgical removal/injury of the parathyroids. This can often be accidental during neck surgery.[6]



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