Parathyroid anatomy, the causes and features of primary, secondary and tertiary hyperparathyroidism, hypercalcaemic crisis, localisation scans, parathyroidectomy and its complications.
UHS PGET syllabus: Breast and endocrine (6 MCQs, both groups), Parathyroid gland (Breast and endocrine): anatomy, hyperparathyroidism (primary, secondary, tertiary), hypercalcaemia, localisation and parathyroidectomyUpdated October 2026Share on WhatsApp
In 30 seconds
Primary hyperparathyroidism = high calcium with a PTH that is not suppressed; about 85% are a single adenoma; most patients today are found incidentally and the commonest symptomatic feature is renal stones.
Diagnosis is biochemical; scans (sestamibi and neck ultrasound) only localise the gland for a focused (minimally invasive) parathyroidectomy.
Secondary HPT is a response to chronic kidney disease (low or normal calcium, high phosphate); tertiary is autonomous PTH after a renal transplant (high calcium).
On this page
Overview
Parathyroid hormone (PTH) keeps the blood calcium normal. Too much PTH (hyperparathyroidism) is the commonest cause of high calcium in outpatients, while cancer is the commonest cause in hospital patients.
For PGET, know how to diagnose primary hyperparathyroidism, how to localise the gland, the operations, and how to tell primary, secondary and tertiary disease apart. One MCQ usually comes from this topic.
Surgical anatomy
Feature
Superior gland
Inferior gland
Origin
4th pharyngeal pouch
3rd pharyngeal pouch (with the thymus)
Descent
Short
Long, so position varies more
Usual site
Back of the upper lobe, near where the RLN crosses the inferior thyroid artery, close to the cricothyroid joint
Near the lower pole of the thyroid; can lie in the thymus or anterior mediastinum
Usually four glands, each about 30 mg, yellow-brown ("Portland brick") in colour, sitting in a little pad of fat.
Some people have a fifth (supernumerary) gland.
Blood supply of both glands comes mainly from the inferior thyroid artery. Damage to this end-artery supply during thyroidectomy causes hypoparathyroidism.
Calcium control in brief
PTH raises calcium: more bone resorption, more calcium reabsorbed in the kidney, less phosphate reabsorbed, and more 1,25-dihydroxyvitamin D (which raises gut absorption).
Calcitonin (from thyroid C cells) is its physiological opposite and lowers calcium slightly.
Worked example: corrected calcium
Measured calcium 2.40 mmol/L, albumin 30 g/L Corrected Ca = 2.40 + 0.02 × (40 − 30) = 2.40 + 0.20 = 2.60 mmol/L → high-normal to raised
Chronic kidney disease (also vitamin D deficiency, malabsorption)
Low or normal
High (in CKD)
High
Tertiary
Long-standing secondary HPT where glands become autonomous, usually seen after renal transplantation
High
Low or normal
Very high
Memory hook
Primary = gland is the problem; Secondary = gland is responding to low calcium; Tertiary = gland forgot to stop after the cause was fixed.
Primary hyperparathyroidism (PHPT)
Causes and associations
Solitary adenoma in most cases; double adenomas in 2-4%.
Multigland hyperplasia: linked to MEN 1, MEN 2A and long-term lithium.
Parathyroid carcinoma: rare (about 1%).
Only known environmental risk factor: previous neck irradiation.
Women are affected about three times as often as men, usually in the 5th to 6th decades.
Clinical features
Classic mnemonic: "bones, stones, abdominal groans and psychiatric overtones".
System
Features
Renal
Kidney stones (the commonest symptomatic presentation), nephrocalcinosis, polyuria, thirst
Bone
Osteoporosis (especially the distal third of the radius), bone pain; in advanced disease osteitis fibrosa cystica, brown tumours, subperiosteal resorption of the phalanges, "pepper-pot" (salt and pepper) skull
Hypertension; band keratopathy (calcium in the cornea, now rare)
High-yield
Most patients now are found incidentally on a routine calcium test and have no or vague symptoms. Among symptomatic patients, renal stones are the commonest feature.
Diagnosis (biochemical)
High calcium (corrected or ionised) with a PTH that is raised or inappropriately normal (it should be suppressed).
Low phosphate, normal creatinine; alkaline phosphatase raised if there is bone disease.
24-hour urinary calcium to exclude familial hypocalciuric hypercalcaemia (FHH).
Check vitamin D (deficiency can mimic or coexist).
Exam trap
Imaging does not make the diagnosis. A positive scan does not confirm PHPT and a negative scan does not exclude it. Scans are for localisation before surgery only.
Exam trap
FHH (an inherited calcium-sensing receptor defect) gives mild high calcium with low urinary calcium. It is not a surgical disease; parathyroidectomy does not help.
Other causes of high calcium to exclude
Malignancy: bone metastases, myeloma, and PTH-related peptide (PTHrP) from squamous cancers (lung, head and neck, oesophagus), renal cancer. PTH is suppressed.
Granulomas (sarcoidosis, TB), vitamin D or A excess, milk-alkali syndrome, thyrotoxicosis, immobilisation, thiazides, lithium.
Localisation
Test
Comment
Technetium-99m sestamibi scan
Most reliable single study; adenoma cells (oxyphil-rich) retain tracer after the thyroid washes out; good for ectopic glands
Neck ultrasound
First-line with sestamibi; also checks the thyroid
4D-CT
When the first two disagree or before re-operation
Selective venous sampling for PTH
Re-operative cases
Indications for surgery
All symptomatic patients (stones, bone disease, pancreatitis, neuropsychiatric).
Asymptomatic patients who meet any consensus criterion:
calcium raised by 0.25 mmol/L (1 mg/dL) or more over the normal range
osteoporosis (T score −2.5 or less) or vertebral fracture
creatinine clearance below 60 mL/min, high urinary calcium or stones
age under 50 years
Operations
Focused (minimally invasive) parathyroidectomy: when one adenoma is clearly shown on concordant imaging; removed through a small (under 3 cm) incision. Cure rates are similar to a full exploration, with less hypocalcaemia.
Intraoperative PTH may be measured: PTH has a half-life of only 3-5 minutes, so it should fall sharply once the adenoma is out.
Bilateral neck exploration (all four glands): when imaging is negative or discordant, and in familial or multigland disease. Traditional cure rate is 95-98%.
Multigland hyperplasia:subtotal (three and a half gland) parathyroidectomy, or total parathyroidectomy with autotransplantation of a small piece into the forearm muscle.
Complications of parathyroidectomy
Complication
Points
Transient hypocalcaemia
Common; perioral tingling, cramps, Chvostek (tapping the facial nerve) and Trousseau (cuff causes carpal spasm) signs
Hungry bone syndrome
After surgery for severe bone disease (high ALP): bones avidly take up calcium, giving severe, prolonged low calcium, phosphate and magnesium
Permanent hypoparathyroidism
About 0.5% after surgery for PHPT; higher after surgery for secondary HPT
RLN injury
Under 1%
Persistent or recurrent HPT
Persistent = calcium stays high in the early weeks after surgery; recurrent = rises again after a normal spell, beyond 6 months
High-yield
Acute symptomatic hypocalcaemia is an emergency: give 10 mL of 10% calcium gluconate slowly IV, then oral calcium and vitamin D. Check and correct magnesium.
Hypercalcaemic crisis
Calcium usually above 3.5 mmol/L; confusion, abdominal pain, vomiting, dehydration, polyuria then oliguria; ECG shows a short QT; once it passes about 4.5 mmol/L the patient risks coma or cardiac arrest.
Treatment:
1. IV 0.9% saline to rehydrate (the most important step) and keep urine output high. 2. Loop diuretic (furosemide) only after the patient is fully filled. 3. IV bisphosphonate (e.g. zoledronate or pamidronate) to stop bone resorption; works over days. 4. Calcitonin as a quick short bridge; steroids for vitamin D excess, sarcoidosis or myeloma. 5. Treat the cause (parathyroidectomy for PHPT).
Familial (genetic) syndromes
Syndrome
Parathyroid disease
Other parts
MEN 1 (menin gene)
Multigland hyperplasia in almost all, young onset
Pituitary adenoma, pancreatic/duodenal endocrine tumours (gastrinoma, insulinoma): the "three Ps"
MEN 2A (RET)
Mild HPT in a minority
Medullary thyroid cancer, phaeochromocytoma
HPT-jaw tumour (HRPT2)
Often cystic; higher risk of carcinoma
Ossifying fibromas of the jaw, renal lesions
In MEN 1, do a bilateral exploration with subtotal or total parathyroidectomy (plus cervical thymectomy).
In MEN 2A, always exclude phaeochromocytoma first.
Secondary and tertiary hyperparathyroidism
Secondary: CKD causes phosphate retention and low active vitamin D, so calcium falls and PTH rises. Glands become hyperplastic.
Treatment is medical first: low-phosphate diet, phosphate binders, active vitamin D (calcitriol, alfacalcidol), and the calcimimetic cinacalcet.
Surgery for very high PTH, bone pain, calciphylaxis (painful skin necrosis from vascular calcification), or failure of medical treatment: subtotal or total parathyroidectomy with autotransplant.
Tertiary: after a successful kidney transplant, the glands keep over-secreting and calcium rises. Surgery (usually subtotal parathyroidectomy) if it persists.
Parathyroid carcinoma
Rare; equal sex ratio, younger patients.
Clues: very high calcium (often around 3.75 mmol/L or more), very high PTH (several times normal), palpable neck mass, bone and kidney disease together.
Treatment: en bloc removal without breaching the capsule (to avoid seeding), often with the adjacent thyroid lobe.
Low calcium, high phosphate, low PTH; long QT; basal ganglia calcification in long-standing cases.
Treat with calcium and active vitamin D (calcitriol or alfacalcidol).
Exam focus
Expect: the commonest cause (single adenoma) and commonest symptomatic presentation (renal stones) of primary hyperparathyroidism, the biochemistry (high calcium, unsuppressed PTH, low phosphate), excluding FHH by urinary calcium, sestamibi scanning, focused versus four-gland surgery, indications for surgery in asymptomatic patients, hungry bone syndrome, the first step in hypercalcaemic crisis (IV saline), secondary HPT in CKD, tertiary HPT after transplant, embryology of the glands and the MEN syndromes.
Quick revision
PHPT: high calcium + unsuppressed PTH + low phosphate; 85% single adenoma.
Stones are the commonest symptom; most patients are asymptomatic.
Diagnose biochemically, then localise with sestamibi and ultrasound.
Focused parathyroidectomy for a localised single adenoma; four-gland exploration otherwise.
FHH: low urinary calcium; no surgery.
Crisis: saline first, then bisphosphonate.
Hungry bones: low calcium, phosphate and magnesium after surgery for bone disease.
