GIE disorders of the thyroid gland

What is hyperthyroidism and hypothyroidism?

Hyper - too much thyroid hormone in the body

Hypo - too little thyroid hormone in the body

What is hyperthyroidism?

• Autoimmune disease caused by Graves’ disease

• Occurs in 2% of women, 10x more than men

• Antibodies are directed against proteins on the surface of follicular cells

• Drugs that can cause it are amiodarone (arrhythmia) and lithium (bipolar)

What are the symptoms of hyperthyroidism?

• Hot, flushed, heat intolerant

• Enlarged thyroid gland (goitre)

• Exopthalmos - eyes protrude more than normal

• Weight loss

• Muscle weakness and tremor

• Increased pulse, palpitations and sweating

• Hair loss and menstrual changes

How is hyperthyroidism diagnosed?

• Physical exam

• Family history

• Blood tests - TSH levels would decrease, thyroid hormones would increase, thyroid antibodies

  • If they take biotin it can give false highs of T3 and T4 and low TSH, patients should stop 2 days before test

• Thyroid scan - iodine uptake

What can happen after taking drug treatment for hyperthyroidism?

Treatment is for 12-18 months

• Decrease in T hormone secretion

• Allergic reactions - rashes, fever, pains

• Neutrophils decrease, infection risk increases

• Agranulocytosis is rare

• Seek medical attention if: sore throat, mouth ulcers, bruising, fever, malaise or non-specific illness

What do hyperthyroid drugs do?

Inhibit organic binding of iodine

• Iodine and tyrosine make t3 and t4

What are the two main anti-hyperthyroidism drugs?

• Carbimazole - precursor of methimazole, inhibits iodine oxidation and coupling to tyrosine. First line treatment

  • MOA - inhibits thyroperoxidase enzyme

  • Given in high doses until euthyroid (normal levels) → reduce to maintenance dose → withdraw after 1-2 years and monitor

• Propylthiouracil - inhibits peripheral de-iodination of T4 to T3

What type of drugs is given to reduce symptoms of hyperthyroidism?

Beta blockers - propranolol, metoprolol, nadolol

• Reduces tremor, tachycardia and anxiety

• Can cause asthma

Why is radioactive iodine given to some patients for hyperthyroidism?

Destroys extra thyroid tissue by x-ray and beta particle emission

• ¹³¹I is given as an aq solution or capsule

• Taken up by active transport and concentrates in the gland

• First line for some patients or after failure of anti-thyroid drugs/thyroidectomy or for some cancers

What are the side effects of radioactive iodine?

• Slow, progressive effect that is hard to control

  • Can produce hypothyroidism

• Not for people wanting to be pregnant as there’s risk of radiation damage to the developing fetus

  • 6 month wait

What surgery is there for hyperthyroidism?

Thyroidectomy - patients with a large goitre (breathing problems) or iodine failed

• Leaving some gland left leads to a possibility of recurrent thyrotoxicosis or hypothyroidism

What are the possible causes of hypothyroidism?`

• Congenital (disease from birth)

• Autoimmune disease - antibodies to thyroglobulin

• Inflammation of thyroid - Hashimotos thyroiditis

• Dietary iodine deficiency

What are the 3 types of hypothyroidism?

• Hashimotos thyroiditis - inflammation, fibrosis and decreased function of thyroid gland. Goitre evident.

• Myxoedema - hypothyroidism developing in adult life. Adult onset slow and insidious, confused with normal aging process. ⇑ women. In rare cases, becomes medical emergency, requires treatment by T3.

• Congenital - poor mental development, dwarfism.

  • Prevented by RAPID treatment with T4 at birth. Maternal iodine deficiency. Congenital dysfunction in hormone biosynthesis

What are the symptoms of hypothyroidism?

• Weakness, fatigue

• Cold intolerance

• Weight gain (but may have decreased appetite)

• Constipation

• Dry skin, thickened skin

• Brittle hair, alopecia

• Intellectual deterioration, mental and physical lethargy

• Goitre - TSH⇑

• Anaemia

How is hypothyroidism diagnosed?

• Physical exam

• Family history

• Blood tests - TSH levels would increase, thyroid hormones would decrease, thyroid peroxidase antibodies

  • If they take biotin it can give false highs of T3 and T4 and low TSH, patients should stop 2 days before test

• Primary hypo - TSH increased and FT4 is below reference range

• Subclinical hypo - TSH increased by FT4 inside range

• Secondary hypo - TSH not increased and T4 is low

What is the aim of thyroid replacement therapy?

Replace with T4

• Get back function

• Normal physical and mental development

• Reduce goitre - suppress raised TSH

• Single dose, 30-60 mins before breakfast, caffeine and meds can have interactions

What are the signs of T4 overdose?

Life long therapy so always monitor for signs of thyrotoxicosis

• Tremor, agitation, weakness

• Insomnia

• Flushing, sweating, weight loss

• Angina type pain, arrhythmias

• Diarrhoea, vomiting

What drugs are used for thyroid replacement therapy?

Levothyroxine sodium - synthetic T4

• Treatment of choice

• OD dosing

Liothyronine sodium

• Similar action but metabolised quicker

• Used in severe hypothyroid states

• Used IV as part of supportive treatment of thyroid coma

Monitor every 3 months, then annually after return to normal range

What is a thyroid storm?

Complication of severe, untreated, or poorly managed hyperthyroidism

• It causes an extreme surge of thyroid hormones, leading to a sudden, severe hypermetabolic state

• A rapid heartbeat.

• A high temperature.

• High blood pressure (hypertension)

• Yellowing of the skin and eyes (jaundice)

• Severe agitation and confusion.

• Loss of consciousness

Explain the rationale for treatment of disorders of thyroid function with reference to:

• The physiology of thyroid function and control

• The pathology of and effects of thyroid dysfunction

• The mechanism of action of drugs or treatments used

Hyperthyroidism arises when excess thyroid hormones (T3 and T4) are produced or released, most commonly due to Graves’ disease, toxic multinodular goitre, or thyroiditis. Because thyroid hormones normally increase metabolic rate and enhance β‑adrenergic sensitivity, their overproduction leads to symptoms such as tachycardia, heat intolerance, tremor, weight loss, anxiety, and increased bowel frequency. The rationale for treatment is therefore to reduce hormone synthesis, limit hormone release, or block peripheral effects. Thionamides such as carbimazole and propylthiouracil inhibit thyroid peroxidase, preventing iodide oxidation, organification, and coupling reactions, thereby reducing new hormone production. Radioiodine selectively destroys overactive thyroid tissue, providing a definitive reduction in hormone output, while beta‑blockers control adrenergic symptoms and, in the case of propranolol, reduce peripheral T4‑to‑T3 conversion. In severe or acute cases, high‑dose iodine temporarily suppresses hormone release, and surgery may be used when medical therapy is unsuitable or ineffective.

Hypothyroidism occurs when the thyroid gland fails to produce sufficient T3 and T4, most commonly due to Hashimoto’s thyroiditis, iatrogenic causes (radioiodine or surgery), iodine deficiency, or certain medications. Because thyroid hormones normally regulate metabolic activity, low levels lead to fatigue, cold intolerance, weight gain, bradycardia, constipation, cognitive slowing, and hyperlipidaemia. Treatment is based on restoring physiological hormone levels to reverse metabolic slowing and prevent complications such as myxoedema coma or cardiovascular disease. Levothyroxine, a synthetic form of T4, is the standard therapy because it mimics natural thyroid secretion and is converted peripherally to T3 as needed, providing stable and predictable replacement. Dosing is titrated according to TSH levels in primary hypothyroidism, reflecting the underlying negative‑feedback physiology of the hypothalamic–pituitary–thyroid axis.