Lyrics · 完整歌詞
Two principal cellular lineages provide a useful framework for understanding the major thyroid carcinomas:
follicular epithelial cells and parafollicular C cells.
Follicular epithelium gives rise to papillary, follicular and, by dedifferentiation, anaplastic carcinoma.
Parafollicular C cells stand apart and produce medullary carcinoma.
Papillary carcinoma, the commonest, is diagnosed by nuclear features: ground-glass chromatin,
grooves and intranuclear pseudoinclusions,
often with psammoma bodies and a BRAF V600E mutation.
Prominent nucleoli are not among them.
Follicular carcinoma looks identical to adenoma on cytology,
so capsular or vascular invasion on histology, not aspiration, separates the two.
Anaplastic carcinoma presents as a rapidly enlarging hard mass in an older patient
and carries TP53 mutations.
Medullary carcinoma behaves as its lineage predicts.
C cells secrete calcitonin, deposit amyloid in the stroma,
spread mainly through lymphatics and never trap iodine,
so radioiodine is useless and calcitonin with CEA becomes the follow-up marker.
Thyroglobulin serves the follicular-derived tumours instead.
About a quarter of medullary cancers are hereditary,
driven by germline RET mutations.
MEN2A combines medullary carcinoma, phaeochromocytoma and parathyroid hyperplasia; MEN2B combines medullary carcinoma,
phaeochromocytoma and mucosal neuromas with a marfanoid habitus, but spares the parathyroids.
One rule is absolute:
phaeochromocytoma must be excluded or treated before the thyroid is removed,
or catecholamine release under anaesthesia will provoke a hypertensive crisis.
Two principal cellular lineages provide a useful framework for understanding the major thyroid carcinomas:
follicular epithelial cells and parafollicular C cells.
The parathyroids are read along three axes: calcium, phosphate and PTH.
PTH keeps calcium in and drives phosphate out.
Primary hyperparathyroidism, usually a single adenoma, therefore shows high calcium,
low phosphate and high PTH, with a tendency to hyperchloraemic acidosis.
Secondary hyperparathyroidism in chronic kidney disease shows low or normal calcium,
high phosphate and a compensatory high PTH.
When years of stimulation make the glands autonomous,
calcium flips from low to high and tertiary disease has arrived.
Malignancy raises calcium through PTHrP or bone metastases, and PTH is suppressed,
which separates it from every parathyroid cause.
Cinacalcet sensitises the calcium-sensing receptor, so PTH and calcium both fall.
Removing or bruising the parathyroids reverses the equation.
After thyroidectomy, calcium falls while phosphate rises, nerves become hyperexcitable,
and perioral tingling, Chvostek's and Trousseau's signs and carpopedal spasm appear,
sometimes with a prolonged QT interval.
Symptomatic hypocalcaemia receives intravenous calcium gluconate on a monitor,
followed by oral calcium and calcitriol.
Magnesium must be checked, because hypomagnesaemia blocks PTH release.
Laryngospasm and haematoma both threaten the airway.
Two principal cellular lineages provide a useful framework for understanding the major thyroid carcinomas:
follicular epithelial cells and parafollicular C cells.