Pathology: Normal range for serum Ca2+is 2.25-2.5mmol/l. A large amount of Ca2+ is transported bound toproteins so corrected calcium calculations are used.
Aetiology: Raised PTH:
Primary hyperparathyroidism
Normal PTH:
Malignancy(paraneoplastic or due to bone metastases)
Genetic e.g. familialhypocalciuric hypercalcemia
Endocrine e.g.hyperthyroidism, hypoadrenalism, phaeochromocytoma
Drugs e.g. thiazides,vitamin D and A supplements
Sarcoidosis
TB
Others:
Immobility
AIDS
Milk-alkali syndrome
Symptoms: Mild: Polyuria,polydipsia, dyspepsia.
Moderate: Constipation, anorexia, nausea, fatigue.
Severe: Abdominal pain, lethargy.
Signs: Mild: Mildcognitive impairment.
Moderate: Muscle weakness.
Severe: Dehydration, arrhythmias, coma.
Investigations: Bloods:Corrected Ca2+, PTH, U&Es, LFTs, Vitamin D, Phosphate,Magnesium,
Serum ACE(Sarcoidosis)
Urine: Calcium
Imaging: Renalultrasound, ultrasound neck, SestaMIBI of parathyroids, bone
scan for metastases
Treatment: IV 0.9% saline.
IV bisphosphonates.
Haemodialysis if refractory.
If hyperparathyroidism may need parathyroidectomy.
If other cause treat underlying condition.
Complications: Arrhythmias,shortened QT interval on ECG, pancreatitis, renal stones if chronic, renaltubular acidosis.
Prognosis: Poor in malignant causes,otherwise good with treatment.
Pathology: Very common in hospital patients.Low Ca2+ interferes with the function of neurones and cardiac andskeletal myocytes.
Aetiology: Low PTH:
Hypoparathyroidism - primary or iatrogenic
High PTH(secondary hypoparathyroidism):
Vitamin D deficiency
PTH resistance (pseudohypoparathyroidism,hypomagnesaemia)
Rickets
Fanconi’s syndrome
Normal PTH:
Drugs – blood transfusion,bisphosphonates, phenytoin, ketoconazole,
Acute pancreatitis
Toxic shock syndrome
Hyperventilation
Rhabdomyolysis
Tumour lysis syndrome or scleroticbone metastases
Symptoms: Paraesthesia, muscle cramps andspasms, tetany
Signs: Chvostek’ssign (tapping over facial nerve produces spasm)
Trousseau’s sign (inflation of BP cuff causescarpopedal spasm).
If chronic can cause abnormal dentition, subcapsularcataract, papilloedema, confusion, ectopic calcification.
Investigations: Bloods:Corrected Ca2+, PTH, U&E, Mg2+, phosphate, CK(rhabdomyolysis),
amylase(pancreatitis)
ECG: Prolonged QT and ST intervals
Imaging: Renalultrasound, ultrasound neck, SestaMIBI of parathyroids, bone
scan for metastases
Treatment: Acute: Calcium gluconate IV. If hypomagnesaemia correct thisconcurrently.
Chronic:Supplement vitamin D, oral calcium supplements, adequate dietary
intake.
Complications: Arrhythmias,prolonged QT interval on ECG, laryngospasm, bronchospasm.
Prognosis: Dependant on cause, some willhave unstable calcium levels long term..
Pathology: Excess production ofparathyroid hormone from the parathyroid gland causing hypercalcaemia,calciuria, renal stones, nephrocalcinosis, hypertension, osteoporosis.
Aetiology: Primary:Parathyroid adenoma (85%), multiple gland hyperplasia (10-15%),
parathyroid carcinoma (1-5%). Can bepart of Multiple endocrine
neoplasia (MEN)syndromes
Secondary: Chronicrenal disease and Vitamin D deficiency
Tertiary: Autonomoushyperplasia due to prolonged secondary
hyperparathyroidism
Symptoms: 50% asymptomatic orrelated to high calcium
Signs: Related to high calcium. Could be an incidentalfinding. Also features of chronic kidney disease
Investigations: Bloods: ParathyroidHormone, Calcium Profile, U&E, if MEN suspected then
pituitary profile and serum calcitoninassay (medullary thyroid cancer)
Imaging: ChestX-ray, Abdominal X-ray, Isotope bone scan, CT/MRI, parathyroid
subtraction scan
Treatment: Medical: Bone protection, hydration, bisphosphonates
Surgical: Parathyroidectomyparticularly if adenoma or carcinoma
Complications: Related to highcalcium. Complications from surgery include haemorrhage, incomplete excision, andrecurrent laryngeal nerve injury
Prognosis: Usually good unless underlyingmalignancy or CKD
Disorder
PTH
Calcium
Phosphate
PTH Physiological Change Appropriate or Inappropriate
Primary Hyperparathyroidism
↑
↑
↓
Inappropriate
Secondary Hyperparathyroidism
↑
↓
↓
Appropriate
Tertiary Hyperparathyroidism
↑
↑
↑
Inappropriate
Figure 5.3 Summary Of Physiological Changes in Hyperparathyroidism
PTH
Calcium
Phosphate
PTH Physiological Change Appropriate or Inappropriate
Hypoparathyroidism
↓
↓
↑
Inappropriate
Pseudohypoparathyroidism
↑
↓
↑
Appropriate
Pseudopseudohypoparathyroidism
Normal
Normal
Normal
N/A
Pathology: Failure of development ofparathyroid, failure to secrete, damage to the gland, failure of PTH action
Aetiology: DiGeorge syndrome, hypomagnesaemia,calcium receptor mutation, autoimmune, radiation, damage during thyroid surgery,infiltration, pseudohypoparathyroidism
Symptoms: Paraesthesia,muscle cramps and spasms, tetany
Signs: Signs ofhypocalcaemia
Investigations: Bloods: ParathyroidHormone, Calcium Profile, U&E, magnesium
ECG: ProlongedQT interval
Treatment: Activated vitamin D and calciumsupplements. Aim for low normal calcium. If tetany or severe presentation useIV calcium gluconate.
Complications: Renal stones and nephrocalcinosis fromcalcium supplementation
Prognosis: Usually good. Can be associatedwith mental retardation, cataracts, extrapyramidal symptoms
Figure 5.4 Summary Of Physiological Changes in Hypoparathyroidism
