Paper II
Question
Discuss the etiopathogenesis and morphology of multinodular goitre.
Answer
Etiopathogenesis
- Multinodular goitre develops from recurrent episodes of hyperplasia and involution of the thyroid gland, typically evolving from a pre-existing simple (diffuse) goitre
- Underlying causes include relative iodine deficiency, dietary goitrogens, or subtle enzymatic defects that impair the efficiency of thyroid hormone synthesis
- Impaired hormone synthesis stimulates TSH secretion, causing follicular epithelial hyperplasia
- The response to this stimulation is non-uniform across the gland — some follicles/lobules respond more vigorously than others, leading to focal proliferation, involution, and haemorrhage/scarring occurring asynchronously across the gland, producing a heterogeneous, nodular architecture over time
- Some proliferating follicles develop autonomous function independent of TSH, which can lead to toxic multinodular goitre (with hyperthyroidism) in some patients
Morphology
Gross
- Markedly enlarged, multinodular thyroid, asymmetrically enlarged, with variable nodule sizes
- Cut surface shows irregular nodules, some solid, some cystic (colloid-filled), with areas of haemorrhage, fibrosis, and calcification
Microscopic
- Variably sized follicles, some large and colloid-distended, others small with hyperplastic epithelium
- Areas of follicular epithelial hyperplasia alternating with areas of colloid involution/regression
- Fibrosis and haemorrhage (including old haemorrhage with haemosiderin deposition)
- Degenerative changes: cystic change, calcification
Clinical significance
- Most patients remain euthyroid, but the goitre can cause cosmetic concerns, compressive symptoms (dysphagia, dyspnoea from tracheal compression, particularly with retrosternal extension), or progress to toxic multinodular goitre (hyperthyroidism from autonomous nodules)