Calcium Abnormalities Flashcards
Causes of Hypecalcaemia? (7)
Malignancy (mets, myeloma, osteosarcoma)
Hyperparathyroidism (primary, secondary, tertiary)
Hyperthyroidism
CKD
Drugs: thiazides, lithium, Ca, Vit D
Vitamin D excess: iatrogenic, granulomatous disease (e.g. Sarcoid)
FHH (Familial hypocalciuric hypercalcaemia), MEN1, MEN2A (all AD)
Hypercalcaemia symptoms?
Bones, abdominal groans, psychic growns, stones, heart aches
GI: Abdominal pain, PUD, N+V, pancreatitis, constipation
Psych: confusion, tiredness, weakness
Renal stones
Join pain (pseudogout)
Cardiac: shortend QT, bradycardia, HTN.
Hypercalcaemia examnation?
BP (Phaeochromocytoma)
Neck scar (parathyroid surgery)
Cachexia, lymphadenopathy, organomegaly
Lung signs for sarcoid, TB, histoplasma
Evidence of renal failure
Bradycardia
Signs of thyrotoxicosis
Joint for pseudogout
How would you investigate Hypercalcaemic paient?
Serum Ca, Vitamin D, PTH and ALP first.
- PTH - If elevated primary hyperPTH is most likely
- If PTH is low consider:
- FHH
- Hypervitaminosis D
- Sarcoidosis
- Multiple myeloma → normal ALP suggests MM
- Bone metastases → raised ALP suggests bone mets
- ALP (if raised osteomalacia, Paget’s, Ca)
If malignancy suspected, PTHrP, serum/urine EPG and immunofixation, CT-CAP
24 h urine Ca fpr FHH (hypocalcaeuria)
At what Ca level does symptom develop?
>3mmol/L.
Higher levels are associated with risk of renal failure
Once it reaches 4 mmol/L - Cardiac arres can occur.
If you suspect FHH, 2 test you can do?
24hour urine for Calcium
Alternatively, spot urine Ca/Cr clearance ratio (<0.01 sugestive of FHH)
When would you consider parathyroidectomy for patient with Hyperparathyroidism? (primary) and how would you manage long-term hypocalcaemia that follows? (2)
- Symptomatic
- Renal stones
- Reduced bone density
Pre-operative localisation is sometimes done with USS and Sestamibi to enable minimally invasive surgery.
Need life-long Vit D after surgery or reimplant tissue in the arm
Treatment options for Primary Hyperparathyroidism? (3)
Bisphosphonates
Calcimimetics (e.g. Cinacalcet)
Parathyroidectomy
How would you manage malignant hypercalcaemia?
Treat underlying tumour
IVF + Furosemide once rehydration complete
Monitor Ca, K, Mg 4 hourly
IV Bisphosphonates - need repeat doses in 3 days if no response
Denosumab if renal failure of poor response with Pamidronate - must ensure Vitamin D replete. Contact renal before use.
Consider Steroids - if due to Sarcoid or Lymphoma.
How would you decide whether this patient’s hypercalaemia is due to malignancy and what investigations would help?
Review history and previous investigations re: malignancy.
I’d expect - low PTH.
ALP if raised suggest bone mets, if normal MM
PTHrP would be helpful.
Do electrophoresis and CTCAP
How would you manage this patient with hypercalcaemia detected on a routine blood test?
Confirm Dx
A: investigate for causes - Vitamin D (deficiency), PTH, ALP. If PTH is low, investigate for Hypercalcaemia of malignancy, Sarcoid, Myeloma.
Screen for complications of disease: look for evidence of psychiatric disturbances, AXR, lipase (constipation, pancreatitis), EUC (and USS renal if impaired to rule out stones)
T: mainly pharmacological. Cessation of causative drugs (lithium, thiazides), IVF - aiming UO 100-150mls/h, Lasix, Bisphosphonates (if malignancy associated or failure to improve with IVF/Lasix in 12 hours), Denosemab (if no response to Pamidronate)…ec.
Ensure F/U and monitor progress. 4h monitor of Ca, Mg, K. Monitor for signs of overload.
What are the typical biochemical profile of primary hyperparathyroidism?
Raised PTH and Calcium or
Even when PTH is inappropriately normal or only mildly elevated, primary hyperparathyroidism is still most likely diagnosis (although FHH is also possibe - but this is very rare - familial hypocalciuric hypercalcaemia)
If you suspect primary hyperparathyroidism, how would you proceed with your investigation?
Diagnosis of primary hyperparathyroidism is biochemical.
Localisation studies should only be performed if patient is being considered for surgery (parathyroidectomy) - as they have high false positive rates and not useful for diagnostic purposes.
a) SESTA-MIBI - to identify hyperfunctioning parathyroid tissue. highest PPV, but often require complementary studies if inconclusive
b) USS + doppler - to identify parathyroid adenoma (hypoechogenicity + extra-thyroidal feeding vessel)
c) Methionine PET/CT
So patient has biochemical primary hyperparathyroidism and +ve SESTAMIBI. What do you do next?
NOT biopsy. You go straight to surgery if an appropriate candidate.
If patient has a strong biochemical primary hyperparathyroidism but negative imaging studies, and patient is surgical candidate, then what do you do?
Bilateral neck exploration by an experienced endocrine surgeon with the use of intraoperative PTH monitoring to localise the disease further.