Pathophysiology of the Thyroid Gland

Updated: May 23

The Thyroid Gland is a butterfly-shaped gland found in the lower front part of the neck. Its lobes (the butterfly wings) wrap around the trachea and are connected at the centre by an Isthmus. The thyroid gland’s primary function is to secrete hormones that regulate our metabolic rate, protein synthesis and growth. These notes will outline the Physiology of the Thyroid Gland for nursing and health care students, but before reading this mak e sure that you’ve understood the:

  1. Anatomy of the Thyroid Gland

  2. Physiology of the Thyroid Gland

 

Pathophysiology of the Thyroid Gland Part 1: Congenital Hypothyroidism


Congenital Hypothyroidism (CH) is a condition that occurs from a deficiency of thyroid hormones during the foetal or neonatal development stage. Its global incidence is approximately 1 in 3500 live births. Given that the thyroid hormones play a vital role in our bodies’ development, growth, and metabolism, having CH can inhibit physical growth and neurological development. This means that individuals with CH would have stunted growth and intellectual disabilities if the condition is left untreated.


Thankfully, most hospitals have implemented a protocol for newborn screening that would detect CH right after birth. Research has shown that the effects of CH can be fully reversed if the condition is detected before the second week of life. In rare cases where CH would have been very severe, the individual might develop mild neurological or motor deficits.


80% of Congenital Hypothyroidism is caused by an irregularity in the development of the thyroid gland known as Thyroid Dysgenesis. The rest of the cases are typically caused by an abnormality of thyroid hormone biosynthesis called Dyshormonogensis, with only 2-5% of cases occurring from genetic mutations.


CH might also be transient, meaning a temporary condition. This occurs in cases where the pregnant mother would be taking anti-thyroid medications or has thyroid blocking antibodies. It could also happen in cases where an infant is born in an Iodine-poor region, such as countries in Africa and South-East Asia. Or when infants are exposed to excess amounts of Iodine, such as Iodine containing Antiseptics or Radiographic contrasts. These issues can temporarily inhibit the synthesis of the thyroid hormone through an effect known as the Wolff-Chaikoff Effect and cause Hypothyroidism.


Lastly, CH can occur from decreased stimulation of the pituitary or hypothalamic gland, known as Central Congenital Hypothyroidism.


Pathophysiology of the Thyroid Gland Part 2: Adult Hypothyroidism

Adult Hypothyroidism is a condition that occurs from decreased levels of thyroid hormone in the blood, and it is divided into two main categories:

  1. Primary Hypothyroidism: Occurs when the thyroid gland cannot produce adequate amounts of thyroid hormone. It is the most common form of adult hypothyroidism, and it often stems from Iodine Deficiency, Autoimmune Thyroid Diseases or Hashimoto Thyroiditis. It can also occur in post-partum women, patients receiving radioactive iodine treatment, post thyroid removal or as a side effect of certain drugs.

  2. Secondary/Central Hypothyroidism: Occurs when the thyroid gland is normal, and the irregularity is coming from the pituitary gland or hypothalamus. The most common causes of central Hypothyroidism include Pituitary Tumours or tumours compressing the Hypothalamus, Sheehan Syndrome, Thyroid Releasing Hormone (TRH) Resistance or TRH deficiency. Or as a side effect of dopamine, prednisone or opioids.

The manifestations of Hypothyroidism depend primarily on the individual patient. Some might go unnoticed and simply have lethargy, while others might have severe cases resulting in myxoedema coma. Diagnosing Hypothyroidism is done through a blood test and once confirmed, it can be treated with oral Levothyroxine Monotherapy.


Pathophysiology of the Thyroid Gland Part 3: Hyperthyroidism

In contrast with the two previous thyroid conditions, Hyperthyroidism occurs when an individual has excess thyroid hormone production.


The most common cause of Hyperthyroidism in young adults is an AutoImmune Disorder known as Graves Disease, where Thyroid Stimulating Immunoglobins bind to the TSH Receptors and replicate TSH effects. Hence stimulating the production of thyroid hormones. In addition to the hyperthyroidism features, Graves Disease also presents with protrusion of the ocular globes and Pretibial myxoedema.


However, the senior population is less likely to have Graves Disease and would likely develop Hyperthryoidism secondary to Toxic Multinodular Goiter. This condition leads to excess thyroid hormones from autonomous ectopic tissue, thus leading to clinical thyrotoxicosis. Patients with Toxic Multinodular Goiter would typically present with palpable thyroid nodules.


Other common causes of Hyperthyroidism include:

  1. Iodine-Induced Hyperthyroidism

  2. Thyroid Adenomas

  3. De Quervain Thyroiditis

  4. Postpartum Thyroiditis

  5. Factitious Thyroiditis (misuse of thyroid replacement hormones for weight-loss purposes)

The treatment of Hyperthyroidism is divided into two categories:

The first category is Symptomatic Therapy, which aims to suppress the symptoms of Hyperthyroidism, such as palpitations, anxiety, and tremors. The treatment of choice for symptomatic therapy is usually Beta-Adrenergic Antagonists, but if the patient has any contraindications, they can be given Calcium-Channel Blockers.


The second category of treatment is the Definitive Therapy which aims to regulate the thyroid hormone level. These include:

  1. Radioactive Iodine Therapy (RAI)

  2. Thionamide Therapy

  3. Subtotal Thyroidectomy

All three definitive therapy approaches have been proven to stop the excess production of thyroid hormones. However, despite their effectiveness, all therapies leave the patients at risk of developing long term hypothyroidism. This means that the patient would need to monitor their T4 levels regularly and possibly take thyroid replacing hormones indefinitely.

References

  1. Bowden SA, Goldis M. Congenital Hypothyroidism. [Updated 2021 Aug 2]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK558913/

  2. Patil N, Rehman A, Jialal I. Hypothyroidism. [Updated 2022 Feb 6]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK519536/

  3. Mathew P, Rawla P. Hyperthyroidism. [Updated 2021 Dec 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK537053/

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