Lyrics · 完整歌詞
Calcium balance reflects coordinated exchanges between bone, kidney and intestine,
regulated principally by parathyroid hormone and active vitamin D.
Parathyroid hormone resorbs bone, retains calcium in the kidney,
excretes phosphate and activates vitamin D.
Active vitamin D absorbs both calcium and phosphate from the gut.
Calcitonin and FGF-23 pull the other way,
and every calcium disorder leaves the residue of this contest.
Because PTH and vitamin D both raise calcium
but move phosphate in opposite directions,
the phosphate is the second number to read.
High calcium with low phosphate points to parathyroid hormone;
high calcium with high phosphate tells a different story.
Primary hyperparathyroidism is a single adenoma in about 80 per cent of cases.
Its signature is high calcium, low phosphate and high chloride,
with a hyperchloraemic acidosis.
An inappropriately raised
or even normal PTH in the presence of hypercalcaemia confirms the diagnosis.
Outpatient hypercalcaemia is usually parathyroid; inpatient hypercalcaemia is usually malignancy.
Cancer raises calcium through PTH-related peptide, and the true PTH is suppressed.
Familial hypocalciuric hypercalcaemia mimics the adenoma,
but an inactivating CASR mutation keeps the urine calcium-to-creatinine clearance ratio below 0.01,
and it never needs surgery.
Chronic kidney disease drives secondary hyperparathyroidism with low or normal calcium
and high phosphate.
Once the glands become autonomous,
calcium flips upward and the disease is tertiary.
Calcium balance reflects coordinated exchanges between bone, kidney and intestine,
regulated principally by parathyroid hormone and active vitamin D.
The clinical picture is stones, bones, groans and psychiatric overtones.
Polyuria arises from calcium-induced nephrogenic diabetes insipidus,
bone pain from osteitis fibrosa cystica.
Hypercalcaemia depresses neuromuscular function, causing weakness, constipation, drowsiness and a short QTc.
Hypocalcaemia excites it, producing paraesthesia, tetany,
Chvostek and Trousseau signs and a long QTc.
Reversing these two directions is the commonest examination error.
Severe hypercalcaemia, above 3.5 mmol/L with symptoms, is an emergency,
and the treatment order is a chain of logic.
Dehydration lowers the filtration rate and traps calcium,
so intravenous saline restores volume and flushes calcium first.
Thiazides are absolutely contraindicated because they reduce urinary calcium excretion.
Loop diuretics are added only for overload.
Zoledronic acid treats the cause by suppressing osteoclasts,
but it takes two to four days.
Calcitonin acts within hours and fades within two days,
so it bridges the gap.
Denosumab serves refractory or renal cases, glucocorticoids treat lymphoma and granulomatous disease,
and dialysis rescues the failing kidney.
Hypocalcaemia is assessed in a fixed order.
Corrected calcium equals measured calcium plus 0.02 multiplied by 40 minus the
albumin in grams per litre.
Then PTH separates parathyroid failure from downstream causes.
Then magnesium is checked, because hypomagnesaemia suppresses PTH and blocks its action,
so calcium cannot be replaced until magnesium is.
Alkalosis binds calcium to albumin and lowers ionised calcium,
which is why hyperventilation causes tetany.
Osteoporosis is diagnosed at a T-score of minus 2.5 or below,
or clinically after a hip or vertebral fragility fracture.
Antiresorptives suppress osteoclasts, whereas intermittent teriparatide builds bone,
because continuous PTH erodes and pulsed PTH restores.
Calcium balance reflects coordinated exchanges between bone, kidney and intestine,
regulated principally by parathyroid hormone and active vitamin D.