Thyroid And Parathyroid Pathology
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Direct answer
Thyroid pathology covers Graves disease with diffuse hyperplasia and eye signs, Hashimoto thyroiditis with anti-TPO antibodies and Hürthle cells, painful de Quervain thyroiditis, endemic iodine-deficiency goitre and the four carcinomas — papillary with Orphan-Annie nuclei and psammoma bodies is the commonest and most tested. Parathyroid pathology is dominated by primary hyperparathyroidism, usually a single adenoma, causing hypercalcaemia with stones and bone disease; secondary hyperparathyroidism follows chronic kidney disease and tertiary its autonomous escape.
What you must remember
- Graves disease: TSH-receptor stimulating antibodies produce diffuse hyperplasia with papillary infolding; exophthalmos and pretibial myxoedema distinguish it from toxic nodular goitre (Plummer), which lacks eye signs.
- Hashimoto: commonest hypothyroid cause in iodine-sufficient regions; anti-thyroid peroxidase, dense lymphocytic infiltrate with germinal centres and Hürthle change; lymphoma risk. Endemic goitre in India reflects iodine deficiency, addressed by universal iodised salt.
- De Quervain subacute thyroiditis: painful tender gland two to three weeks after a viral illness, giant-cell granulomas, high ESR, transient thyrotoxicosis then recovery. Riedel thyroiditis is a rare woody IgG4-related fibrosing disease mimicking cancer.
- Papillary carcinoma: commonest, young women, childhood irradiation risk; Orphan-Annie eye nuclei, grooves and psammoma bodies; lymphatic spread to cervical nodes; excellent prognosis.
- Follicular carcinoma: diagnosed only on capsular or vascular invasion, spreading haematogenously to bone and lung. Medullary carcinoma: calcitonin-secreting C cells with amyloid stroma, MEN2-RET association, diarrhoea and flushing. Anaplastic carcinoma: elderly, rapidly lethal.
- Primary hyperparathyroidism: single adenoma in the large majority of women beyond the menopause; mostly detected as asymptomatic hypercalcaemia on screening; stones, bones, abdominal groans and psychic moans; high calcium with high or inappropriately normal PTH and low phosphate.
- Bone signatures: osteitis fibrosa cystica with brown tumours, subperiosteal resorption on the radial side of middle phalanges, salt-and-pepper skull. Secondary hyperparathyroidism shows high PTH with low or normal calcium and high phosphate; tertiary emerges as autonomous hypercalcaemia. Surgical hypoparathyroidism causes tetany with Chvostek and Trousseau signs; pseudohypoparathyroidism resists PTH with short fourth-fifth metacarpals.
Common confusion
Papillary spreads lymphatically and follicular haematogenously; both take up radioiodine, unlike medullary and anaplastic. De Quervain is painful, granulomatous and post-viral; Hashimoto is painless, lymphocytic and antibody-rich. High calcium with high PTH is primary, low calcium with high PTH secondary, and rising calcium after long secondary disease tertiary.
Exam-focused takeaway
FMGE asks carcinoma histology by buzzword — Orphan-Annie nuclei, psammoma bodies, amyloid with calcitonin — and parathyroid states by the calcium-PTH pair. Brown tumour and subperiosteal resorption are the bone marks, and the asymptomatic-screening presentation is the modern norm. Hashimoto antibodies and de Quervain pain are standard single-liners.
Frequently asked questions
Which thyroid carcinoma has psammoma bodies?
Papillary carcinoma, with Orphan-Annie nuclei and nuclear grooves; it spreads lymphatically and carries an excellent prognosis even with nodal disease.
What marks medullary carcinoma?
Origin from calcitonin-secreting C cells, amyloid stroma, MEN2 and RET association, with diarrhoea and flushing; calcitonin and CEA serve as tumour markers.
How does de Quervain thyroiditis present?
Painful tender swelling after a viral respiratory infection, with granulomas, raised ESR and transient thyrotoxicosis; it settles with NSAIDs or a short steroid course.
What is a brown tumour?
An osteoclast-rich haemorrhagic focus of osteitis fibrosa cystica in hyperparathyroidism, mimicking a primary bone tumour; treating the parathyroid state heals it.
Why is calcium high in primary but low in secondary hyperparathyroidism?
An autonomous adenoma secretes PTH despite hypercalcaemia, whereas failing kidneys retain phosphate and cut calcitriol, keeping calcium low while PTH rises appropriately; tertiary disease turns autonomous and calcium rises.
Which antibodies mark Hashimoto?
Anti-thyroid peroxidase, often with anti-thyroglobulin, in a lymphocyte-and-Hürthle-cell gland; long-standing disease raises lymphoma risk.