Table of Contents
Page created on May 16, 2019. Last updated on May 27, 2022 at 13:47
General
Hypothyroidism is most frequently caused by an underactive thyroid, which produces fewer thyroid hormones than normal. It’s rarely caused by peripheral resistance to thyroid hormones. Goiter is often present, but this depends on the exact condition. Like most thyroid conditions are women more frequently affected than men.
It may be acquired or congenital. The most common cause of hypothyroidism in the western world is Hashimoto’s thyroiditis. The symptoms of it are mostly caused by decreased basal metabolic rate and generalized myxoedema. It’s rarely a severe disease but myxoedema coma, a potentially fatal complication, may occur.
Acquired (“adult”) hypothyroidism
These conditions mostly affect young female adults.
Etiology:
- Primary hypothyroidism
- Hashimoto thyroiditis
- Postpartum thyroiditis
- de Quervain thyroiditis
- Iatrogenic
- Iodine deficiency
- Drugs
- Lithium
- Amiodarone
- Secondary hypothyroidism
- Disorders of the pituitary -> TSH deficiency
- Tertiary hypothyroidism
- Disorders of the hypothalamus -> TRH deficiency
Hashimoto thyroiditis is an autoimmune disease and the most common cause of hypothyroidism in the western world. It involves antibodies against thyroid peroxidase (TPO) and thyroglobulin (Tg), which causes inflammation and destruction of thyroid tissue.
The condition has a genetic background. The age of onset is often in the 20 – 30s, and females are more affected. In the early phase thyrotoxicosis can develop as the thyroid gland is destroyed, which releases thyroid hormones into the circulation. After this the thyroid will be hypofunctional.
Postpartum thyroiditis occurs in around 10% of women giving birth. It occurs 1 – 8 months after delivery and gives a self-limiting hypothyroidism.
de Quervain thyroiditis is a self-limiting hypothyroidism that occurs after a viral upper respiratory tract infection.
Iatrogenic hypothyroidism is a result of the treatment of hyperthyroidism. This treatment can involve surgery, radioiodine therapy or antithyroid drugs that destroy the thyroid.
Iodine deficiency can cause hypothyroidism in severe cases.
Pathomechanism: For unknown reasons will hypothyroidism stimulate deposition of glycosaminoglycans like hyaluronic acid in the dermis and mucous membranes. This may be due to increased TSH due to decreased negative feedback. TSH stimulates fibroblasts, similarly to in Graves disease. This causes generalized myxoedema.
Also due to the increased TSH will prolactin levels increase, as prolactin production is stimulated by TSH. Hyperprolactinaemia suppresses LH, FSH and testosterone production, which causes various symptoms.
Clinical features: The symptoms of hypothyroidism are related to the decreased BMR, to the generalized myxoedema and to the hyperprolactinaemia.
- General symptoms
- Depression
- Goiter (depending on the etiology)
- Hypodynamic circulation (low CO)
- Decreased BMR
- Fatigue
- Cold intolerance
- Cold, dry skin
- Weight gain, despite poor appetite
- Constipation
- Muscle weakness
- Myxoedema
- Doughy, puffy skin
- Generalized oedema, often at the legs
- Hyperprolactinaemia
- Abnormal menstrual cycle
- Galactorrhoea
- Decreased libido (due to decreased testosterone)
The myocardial contractility is reduced and there is bradycardia, resulting in a low cardiac output.
Complications: Myxoedema coma is an acute state of decompensated hypothyroidism with a high mortality rate (50%). Despite the name isn’t outright coma common and myxoedema itself isn’t involved in the pathogenesis, so the condition would probably be better named as hypothyroid crisis.
The main event in myxoedema coma is sudden cardiac decompensation, often triggered by an infection, surgery or trauma. It can also be triggered by a sudden decrease in compliance in treatment. The typical symptoms include:
- Decreased level of consciousness, potentially coma
- Bradycardia
- Hypotension
- Hypothermia
- Hypoventilation
- Myxoedema
Cardiogenic shock may develop, potentially causing death.
Treatment: Lifelong replacement of thyroid hormones with L-thyroxine.
Congenital (“neonatal”) hypothyroidism
Congenital hypothyroidism is mostly idiopathic, although some genetic factors are known. Neonates are screened for hypothyroidism as symptoms rarely appear before a few weeks after birth. Most cases nowadays are caught by screening; only a few are diagnosed based on clinical symptoms.
Etiology:
- Thyroid hypoplasia or dysplasia (majority of cases)
- Peripheral resistance to thyroid hormones (rare)
- Mother has TSH-receptor-blocking antibodies (transient hypothyroidism)
Clinical features: Symptoms rarely affect the infant in utero as the mother’s thyroid hormones to some degree substitute the infant’s hypothyroidism. Symptoms rather appear a few weeks after birth.
- Short extremities
- Mental retardation
- Feeding problems
- Protruding abdomen
- Umbilical hernia
- Prolonged new-born jaundice
Complications: Thyroid hormones are essential for early brain development. Untreated cases of congenital hypothyroidism result in permanent neurological damage.
Untreated congenital hypothyroidism also causes cretinism, a condition characterised by short stature and mental retardation.
Hypothyroidism in elderly
Elderly with hypothyroidism may present with atypical symptoms. These patients often experience dementia and depression rather than the typical hypothyroid symptoms.
Many of the typical hypothyroid symptoms like hypothermia, fatigue and weight gain can occur in healthy elderly and can therefore mask an underlying hypothyroidism.
Hi! Just a little fix. Under clinical features, hyperprolactinaemia it sais: “Abnormal menstrual cycle (due to decreased LH and TSH)”. Is it supposed to be FSH?
From what I can tell, it’s not well known exactly how it occurs. It might be due to decreased LH and FSH, but I would think that such changes would be compensated for and normalised by the endocrine system.
Anyway, it’s not important, so I removed it.
Szia, Nik!
It seems, from various studies, that both TSH and TRH stimulate the synthesis of prolactin.
Hey
Interesting, but luckily it’s probably not very important.