Week 11 - Thyroid disorders

Question 1

What are the two main hormones produced by the thyroid gland and their functions?

Answer 1

• T3 (Triiodothyronine): Active form, increases metabolism and oxygen use.
• T4 (Thyroxine): Precursor to T3.

(Also produces Calcitonin, which lowers blood calcium.)

Question 2

How does the hypothalamus–pituitary–thyroid (HPT) axis regulate thyroid hormone production?

Answer 2

Hypothalamus releases TRH → stimulates pituitary to release TSH → stimulates thyroid to secrete T3/T4.

Elevated T3/T4 inhibit TRH and TSH (negative feedback).

Question 3

What is the most common cause of hypothyroidism worldwide and in iodine-sufficient regions?

Answer 3

Worldwide: Iodine deficiency.
Iodine-sufficient areas: Hashimoto’s thyroiditis.

Question 4

List four common causes of hypothyroidism.

Answer 4

• Iodine deficiency
• Hashimoto’s thyroiditis
• Thyroid surgery or radioiodine therapy
• Congenital defects

Question 5

What happens to TSH and thyroxine levels in primary hypothyroidism?

Answer 5

↓ T3/T4 (thyroxine)

↑ TSH (compensatory pituitary response)

Question 6

What are the main clinical features of hypothyroidism?

Answer 6

• Weight gain, lethargy
• Cold intolerance, pale/dry skin
• Bradycardia, low cardiac output
• Constipation, dry hair
• Non-pitting oedema (myxedema), coarse features, deep voice
• In infants: Cretinism

Question 7

What causes myxedema in hypothyroidism?

Answer 7

Accumulation of hydrophilic mucopolysaccharide substances in skin and tissues causing non-pitting oedema.

Question 8

What is Cretinism and when does it occur?

Answer 8

Congenital or early-childhood hypothyroidism → causes growth failure and mental retardation, often due to iodine deficiency.

Question 9

What is Hashimoto’s thyroiditis?

Answer 9

An autoimmune destruction of the thyroid gland leading to hypothyroidism and possible goitre.

Question 10

Describe the pathogenesis of Hashimoto’s thyroiditis.

Answer 10

Autoimmune response against thyroid antigens → lymphocytic infiltration → follicular destruction and fibrosis → ↓ T3/T4 → ↑ TSH.

Question 10

Who is most commonly affected by Hashimoto’s thyroiditis?

Answer 10

Women aged 45–65 years, with a female:male ratio of 10–20:1.

Question 11

What is Hashitoxicosis?

Answer 11

A transient hyperthyroid phase in Hashimoto’s due to follicular disruption and release of stored hormones before hypothyroidism develops.

Question 12

What are the typical hormone findings in Hashimoto’s thyroiditis?

Answer 12

↓ T3 and T4

↑ TSH

Question 13

What is secondary hypothyroidism?

Answer 13

Underproduction of thyroid hormones due to pituitary or hypothalamic dysfunction (↓ TSH stimulation).

Question 14

What are the hormone changes in secondary hypothyroidism?

Answer 14

Both TSH and T3/T4 are decreased.

Question 15

What is the primary cause of hyperthyroidism?

Answer 15

Graves’ disease (autoimmune stimulation of the thyroid).

Question 16

List four causes of hyperthyroidism.

Answer 16

• Graves’ disease
• Toxic multinodular goitre
• Toxic adenoma
• Iodine-induced hyperthyroidism

Question 17

What are the main clinical features of hyperthyroidism?

Answer 17

• Heat intolerance, sweating
• Weight loss with increased appetite
• Tachycardia, palpitations
• Tremor, irritability, anxiety
• Diarrhoea
  -Lid lag, staring gaze

Question 18

What is Graves’ disease and who does it affect most?

Answer 18

An autoimmune hyperthyroid condition due to TSH receptor–stimulating antibodies, most common in women aged 20–40.

Question 19

What autoantibodies are produced in Graves’ disease?

Answer 19

1. Thyroid-Stimulating Immunoglobulin (TSI) – mimics TSH
2. Thyroid Growth-Stimulating Immunoglobulin – enlarges thyroid
3. TSH-Binding Inhibitor Immunoglobulin – prevents normal TSH binding

Question 20

What is the classic triad of features in Graves’ disease?

Answer 20

Diffuse goitre (thyrotoxicosis)
Exophthalmos (eye protrusion)
Pretibial myxedema (skin thickening over shins)

Question 21

What lab results are seen in Graves’ disease?

Answer 21

↑ T3 and T4
↓ TSH

Question 22

What are the main treatment options for hyperthyroidism?

Answer 22

Antithyroid drugs (block hormone synthesis)

Radioiodine therapy (destroys tissue)

Surgery (thyroidectomy)

Question 23

What is Diffuse Multinodular Goitre (DMG)?

Answer 23

An enlarged thyroid gland with multiple nodules caused by impaired hormone synthesis (usually due to iodine deficiency).

Question 24

Describe the pathophysiology of DMG.

Answer 24

↓ T3/T4 → ↑ TSH → follicular hypertrophy & hyperplasia → colloid accumulation → fibrosis & nodule formation over time.

Question 25

What are the two main types of DMG?

Answer 25

Endemic: due to dietary iodine deficiency. Sporadic: occurs in women at puberty or pregnancy due to increased demand for T4.

Question 26

Why does the thyroid gland enlarge in DMG?

Answer 26

Persistent TSH stimulation causes follicular cell hypertrophy and hyperplasia.

Question 27

What are the main clinical signs and symptoms of DMG?

Answer 27

- Visible neck swelling - Dysphagia or airway obstruction - SVC compression - Usually euthyroid, but 10% progress to toxic multinodular goitre (hyperthyroid).

Question 28

How can DMG lead to both hypothyroidism and hyperthyroidism?

Answer 28

Early: impaired synthesis → hypothyroidism. Later: autonomous nodules produce excess hormone → hyperthyroidism (Plummer’s syndrome).

Question 29

What are the management options for multinodular goitre?

Answer 29

Small goitre: annual monitoring. Large goitre: surgery if compressive or cosmetic. Toxic goitre: radioiodine therapy.