Calcium Part II Flashcards
List some symptoms of hypercalcaemia.
- Polyuria/polydipsia
- Constipation
- Confusion, seizures, coma → NOTE: these tend to occur when calcium level >3 mmol/L
Bones, stones, abdominal groans, psychiatric moans
What are the main causes of primary hyperparathyroidism?
- Parathyroid adenoma
- Parathyroid hyperplasia (associated with MEN1)
- Parathyroid carcinoma
Outline the serum biochemistry features of primary hyperparathyroidism.
- High calcium
- Inappropriately raised PTH (could be within normal range but this is still inappropriate in hypercalcaemia)
- Low phosphate (phosphate trashing hormone)
Outline the pathophysiology of familial benign hypercalcaemia.
A mutation in the calcium-sensing receptor (CaSR) leads to a reduced threshold for PTH release (leads to mild hypercalcaemia)
Why don’t patients with familial benign hypercalcaemia get kidney stones?
PTH causes increased renal calcium absorption, thereby reducing urine calcium
Familial hypocalcuric hypercalcaemia
What are the three types of hypercalcaemia of malignancy?
- Humoral hypercalcaemia of malignancy (e.g. small cell lung cancer) → high calcium caused by PTHrP release
- Bone metastases (e.g. breast cancer) → high calcium caused by local bone osteolysis
- Haematological malignancy (e.g. myeloma) → high calcium caused by cytokines
List some other non-PTH driven causes of hypercalcaemia.
- Sarcoidosis (sarcoid tissue expresses 1 alpha hydroxylase)
- Thyrotoxicosis (increases bone resorption)
- Hypoadrenalism (reduced renal Ca2+ transport)
- Thiazide diuretics (reduced renal Ca2+ transport)
- Excess vitamin D (e.g. sun beds)
Outline the management of hypercalcaemia.
- Fluids, fluid and more fluids! (0.9% normal saline, 1L over 1 hour)
- Bisphosphonates but only if there is cancer (stops cancer from eating bone)
- Treat the underlying cause.
List some symptoms and signs of hypocalcaemia
- Neuromuscular excitability (Chvostek’s sign, Trousseau’s sign)
- Stridor (due to laryngeal spasm)
Recall some differentials for hypocalcaemia when the PTH is high
This is an appropriate response to low calcium - SECONDARY HYPERPARATHYROIDISM
Could be due to:
- Vit D deficiency (most common cause)
- CKD (as low renal alpha-1-hydroxylase)
- Pseudohypoparathyroidism (gene deficit –> PTH resistance)
Recall some differentials for hypocalcaemia when the PTH is low
This is an inappropriate response (low calcium should cause high PTH)
Could be due to:
- Surgical - iatrogenic injury during thyroidectomy, or parrathyroidectomy
- Post-radiation
- Autoimmune hypoparathyroidism (rare)
- Di George syndrome (even rarer! Agenesis of parathyroids)
- Magnesium deficiency - can be caused by OMEPRAZOLE
- Pseudohypoparathyroidism (PTH resistance), rare
What does prolonged primary hyperparathyroidism lead to?
Parathyroid bone disease
- Cortical bone lost if -> inc fractue risk
- Osteitis fibrosa cystica
- Rare due to modern mx
What does prolonged secondary hyperparathyroidism lead to?
Renal osteodystrophy
- Due to seconday hyperparathy + retention of aluminium from dialysis fluid
- Rare due to modern mx
Paget’s - what is it? Signs/symptoms?
Increased burn turnover leading to poorly disorganised bone
This is increased activity of both osteoclasts and osteoblasts
Bone pain, deformity, fractures, compression leading to deafness, blindness
Frequently affects pelvis, femur, skull, tiba
Pagets - Ix? Mx?
Ix:
Isolated raised ALP on bloods
X-ray
Mx:
Bisphosphonates for pain
What to suspect in a patient post-op thyroidectomy and tingling?
Suspect damage to parathyroid glands -> leading to hypocalcaemia
In Paget’s disease, what 2 proteins/enzymes do osteoclasts produce?
Osteocalcin and ALP
What cell is responsible for ALP rise in Paget’s
Osteoclasts
What type of hearing loss is associated with Paget’s?
BOTH conductive and sensorineural
Conductive -> since Paget’s affects the ossicles (malleus, incus, stapes)
Nerve -> CNVIII is compressed by bone growth
What scan is used to investigate bone in Paget’s disease?
99Technetium bisphosphonate scan
Are ALP and calcium low or high in osteomalacia?
ALP: high, due to increased bone formation (2ndary hpt attempts to stimulate bone formation)
Calcium: low
What are the vitamin D levels in primary hyperparathyroidism, and why?
Low (or normal)
Because it is all consumed by PTH activating 1-alphaa-hydroxylase
