Hypothyroidism

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 Hypothyroidism  

Definition

Hypothyroidism is a condition characterized by an underactive thyroid gland, leading to a deficiency of thyroid hormones triiodothyronine (T3) and thyroxine (T4). These hormones are essential for regulating metabolism, growth, and development.

  • In very rare cases, hormone production may be sufficient, but the hormones fail to exert adequate peripheral effects (peripheral resistance).

  • Hypothyroidism can be congenital or acquired.

Etiology

  1. Primary hypothyroidism (thyroid gland dysfunction – most common form)

    • Autoimmune thyroiditis (Hashimoto disease):

      • The most frequent cause in iodine-sufficient regions such as the US.

      • Associated with HLA-DR3.

      • More common in women (♀ > ♂, about 7:1).

    • Postpartum thyroiditis:

      • A variant of subacute lymphocytic thyroiditis.

      • Occurs within 1 year after delivery in ~5% of women.

    • De Quervain thyroiditis (subacute granulomatous):

      • Viral-mediated damage to follicular cells.

      • Presents with a painful thyroid.

    • Iatrogenic causes:

      • Following thyroidectomy, radioiodine therapy, or drugs such as amiodarone and lithium.

    • Nutritional deficiency:

      • Iodine deficiency is the most common cause worldwide.

    • Riedel thyroiditis:

      • Rare, associated with extensive fibrosis, thyroid becomes hard (“stone-hard”).

    • Wolff-Chaikoff effect:

      • Transient hypothyroidism caused by excessive iodine intake.

  2. Secondary hypothyroidism (pituitary origin)

    • Due to pituitary adenoma, surgery, irradiation, or trauma → ↓ TSH production.

  3. Tertiary hypothyroidism (hypothalamic origin)

    • Impaired TRH secretion → ↓ TSH → ↓ T3/T4.

  4. Congenital hypothyroidism

    • Thyroid dysgenesis (aplasia, hypoplasia, or ectopy).

    • Dyshormonogenesis (enzyme defects such as thyroid peroxidase deficiency).

    • Transplacental maternal antithyroid antibodies.

    • Iodine deficiency during pregnancy.

Pathophysiology

  • Hypothyroidism disrupts the hypothalamic–pituitary–thyroid axis.

    • Primary hypothyroidism: ↓ T3/T4 → ↑ TSH (compensatory).

    • Secondary: ↓ TSH → ↓ T3/T4.

    • Tertiary: ↓ TRH → ↓ TSH → ↓ T3/T4.

  • Main effects:

    • Generalized decrease in basal metabolic rate → ↓ oxygen consumption and ↓ heat production.

    • Skin/appendages: dryness, alopecia.

    • Cardiovascular: bradycardia, decreased cardiac output.

    • GI: constipation due to reduced motility.

    • CNS: lethargy, slowed cognition.

    • Accumulation of glycosaminoglycans (mucopolysaccharides) in dermis → myxedema (non-pitting edema).

    • Hyperprolactinemia due to TRH stimulation of prolactin secretion.

Clinical Features

  1. General symptoms (due to ↓ metabolism):

    • Fatigue, cold intolerance, weight gain (despite reduced appetite).

    • Dry skin, brittle nails, hair loss (Queen Anne’s sign – thinning of outer eyebrows).

    • Decreased sweating, pallor.

    • Bradycardia, reduced exercise tolerance.

    • Constipation.

    • Hypothyroid myopathy, delayed deep tendon reflexes (Woltman sign).

    • Carpal tunnel syndrome (due to mucopolysaccharide deposition).

  2. Features of myxedema (severe cases):

    • Puffy appearance, periorbital edema, hoarseness, macroglossia.

    • Pretibial edema, generalized non-pitting edema.

    • Myxedematous heart disease: bradycardia, cardiomegaly, dilated cardiomyopathy, dyspnea.

    • Myxedema coma: rare but life-threatening emergency with hypothermia, hypoventilation, bradycardia, hypotension.

  3. Reproductive/endocrine features:

    • Women: menstrual irregularities (secondary amenorrhea, menorrhagia).

    • Men: decreased libido, erectile dysfunction, infertility.

  4. Neuropsychiatric:

    • Depression, impaired memory, somnolence.

    • Elderly may present with “pseudodementia” rather than classic hypothyroid features.

Diagnosis

  1. Initial evaluation:

    • TSH: best screening test.

    • FT4: used to confirm diagnosis.

    • Typical findings:

      • Primary hypothyroidism: ↑ TSH, ↓ FT4.

      • Subclinical hypothyroidism: ↑ TSH, normal FT4.

      • Secondary/Tertiary: ↓ TSH and ↓ FT4.

  2. Additional labs:

    • Anti-thyroid peroxidase (anti-TPO) antibodies, anti-thyroglobulin antibodies (TgAb) → Hashimoto.

    • Creatine kinase ↑ (hypothyroid myopathy).

    • Hyponatremia (due to impaired free water clearance).

  3. Imaging:

    • Thyroid ultrasound for goiter/structural abnormalities.

    • Thyroid scintigraphy for functional assessment.

Differential Diagnoses

  • Euthyroid sick syndrome (non-thyroidal illness):

    • Occurs in critically ill patients.

    • Low T3 with normal TSH/FT4 initially; prolonged illness → low T4 also.

  • Depression, chronic fatigue syndrome, and dementia in elderly.

Treatment

  • Lifelong thyroid hormone replacement:

    • Levothyroxine (synthetic T4): preferred. Converted peripherally to T3.

    • Liothyronine (T3): reserved for severe cases or myxedema coma (with levothyroxine IV).

  • Dose adjustments:

    • Higher dose needed in pregnancy (due to increased demand).

    • Monitor TSH/FT4 regularly.

  • Drug interactions (reduced absorption):

    • Proton pump inhibitors, calcium salts, ferrous sulfate, bile acid sequestrants.

  • Overtreatment risks:

    • Thyrotoxicosis, atrial fibrillation, osteoporosis.

Complications

  • Myxedema coma: rare, life-threatening; requires IV levothyroxine + liothyronine.

  • Primary thyroid lymphoma: increased risk in long-standing Hashimoto thyroiditis.

  • Cardiovascular complications: atherosclerosis, pericardial effusion.

Congenital Hypothyroidism

  • Etiology:

    • Thyroid dysgenesis (aplasia, hypoplasia, ectopy).

    • Dyshormonogenetic goiter (enzyme defects).

    • Maternal antithyroid antibodies.

    • Iodine deficiency.

  • Clinical features in neonates:

    • Often asymptomatic at birth (maternal hormones cross placenta).

    • Prolonged jaundice, hypotonia, poor feeding, macroglossia, hoarse cry.

    • Umbilical hernia, large fontanelles, puffy face.

    • If untreated: severe developmental delay, intellectual disability, short stature, skeletal abnormalities (cretinism).

  • Mnemonic: The 7 P’s: Pot-bellied, Pale, Puffy-faced, Protruding umbilicus, Protuberant tongue, Poor brain development, Prolonged jaundice.

  • Screening:

    • Neonatal TSH screening (24–48h after birth) is mandatory in most countries.

    • Early treatment prevents irreversible intellectual disability.

  • Treatment:

    • Lifelong levothyroxine with close monitoring.

 Good luck👍

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