Hypothyroidism is a disorder of the endocrine system where the thyroid gland does not produce enough thyroid hormone. Hypothyroidism can be due to various etiologies including Hashimoto thyroiditis, postpartum thyroiditis, and congenital hypothyroidism. Hypothyroidism can result in a spectrum of neuropsychiatric symptoms, and can also be caused by psychotropic medications such as lithium.

Remember that the thyroid produces tri-iodothyronine (T3) and thyroxine (T4), which are iodine-containing hormones that control the body’s metabolic rate. T3 binds nuclear receptors with greater affinity than T4, and thus is the “active” hormone.


The mnemonic 7 B's can be used to remember the main functions of thyroid hormone:
  • Basal metabolic rate
  • Blood sugar (increases glycogenolysis and gluconeogenesis)
  • Break down lipids (increases lipolysis)
  • Brain maturation
  • Bone growth (synergism with growth hormone)
  • β-adrenergic effects in heart, which increases contractility (this is why β-blockers alleviate adrenergic symptoms in thyrotoxicosis)
  • Stimulates surfactant synthesis in Babies

Hashimoto thyroiditis (also known as Hashimoto's Disease) is an autoimmune disorder with antithyroid peroxidase (antimicrosomal) and antithyroglobulin antibodies. It is the most common cause of hypothyroidism in iodine-sufficient regions (i.e. - most Western and affluent nations). On physical exam, individuals may have a moderately enlarged, nontender thyroid.

Postpartum thyroiditis is a self-limiting thyroiditis that can last for up to 1 year after delivery. Individuals can go between transient hyperthyroidism or hypothyroidism. Following the self-limited phase, most individuals will return back to a euthyroid state. On physical exam, the thyroid is typically painless and normal in size.

Congenital hypothyroidism in the fetus can occur due to antibody-mediated maternal hypothyroidism, and thyroid dysgenesis.

Self-limited disease often following a viral infection (e.g. - flu). Individuals may be hyperthyroid early in course of illness, followed by hypothyroidism. Hypothyroidism can remain permanent in about 15% of cases. On physical exam, individuals will have jaw pain, and tender thyroid. ESR may also be elevated.

When an individual does not have adequate iodine, the thyroid will progressively enlarge as it tries to keep up with an increased demand for thyroid hormone production. This results in a prominent goiter that develops, and is seen on physical exam. Iodine deficiency is the most common cause of thyroid enlargement and goiter worldwide.

Lithium decreases production and release of thyroxine (T4) from the thyroid gland. It also interferes with de-iodination of T4 to T3 (tri-iodothyronine). T3 is the metabolically active form of thyroid hormone.[1]

Hypothyroidism vs. Hyperthyroidism

Hypothyroidism Hyperthyroidism
Neuropsychiatric Hypo-activity, lethargy, fatigue, weakness, depressed mood, reflexes (delayed, diminished) Hyperactivity, restlessness, anxiety, insomnia, fine tremors (due to increased β-adrenergic activity), reflexes (brisk)
Ocular Periorbital edema Ophthalmopathy in Graves disease (including periorbital edema, exophthalmos), lid lag/retraction
Metabolic Cold intolerance, decreased sweating, weight gain (due to lowered basal metabolic rate), hyponatremia (due to decreased free water clearance) Heat intolerance, sweating, weight loss
Cardiovascular Bradycardia, dyspnea on exertion (cardiac output) Tachycardia, palpitations, dyspnea, arrhythmias (e.g. - atrial fibrillation), chest pain, hypertension
Gastrointestinal Constipation. decreased appetite Diarrhea, increased appetite
Dermatologic Dry cool skin, coarse brittle hair, diffuse alopecia, brittle nails; puffy facies and generalized nonpitting edema (myxedema) Warm moist skin, fine hair, onycholysis, pretibial myxedema in Graves disease
Reproductive Abnormal uterine bleeding, decreased libido, infertility Abnormal uterine bleeding, gynecomastia, decreased libido, infertility
Laboratory Findings • Elevated TSH
• Decreased free T3 and T4
• Hypercholesterolemia (due to decreased LDL receptor expression)
• Decreased TSH
• Elevated free T3 and T4
• Decreased LDL, HDL, and total cholesterol
  • In patients with psychosis, hypothyroidism should be considered as a possible secondary cause of psychosis.[2]
    • This is especially true for patients with a history of thyroid problems or thyroidectomy regardless of the presence of other signs and symptoms of hypothyroidism or the level of T3 and T4 in the thyroid function test.[3]
  • In the absence of symptoms, elevated TSH levels <10 should not be treated.
    • Routine management is to repeat a TSH level in q3-6 months
    • You should however, check an anti-TPO Ab to rule out Hashimoto‘s, as subclinical hypothyroid may be treated if Anti-TPO is high, because there is an increased risk of progression to overt hypothyroidism in the future.[4]