Disorders of Calcium Metabolism Flashcards
What are the clinical manifestations of hypercalcaemia?
stones, bones, abdominal moans and psychic groans
What is primary hyperparathyroidism?
autonomous inappropriate PTH overproduction leading to hypercalcaemia
What is secondary hyperparathyroidism?
appropriate PTH increase in response to hypocalcaemia
What is tertiary hyperparathyroidism?
Gland has become overactive after initial secondary hyperparathyroidism
What are the main causes of primary hyperparathyroidism?
adenoma, hyperplasia, carcinoma (rare)
How do we diagnose primary hyperparathyroidism?
high calcium and PTH
phosphate, bicarbonate low (excreted)
ALP normal (increased if severe)
imaging
How do we treat primary hyperparathyroidism?
rehydration
adenomectomy or drugs
- bisphosphonates (inhibits osteoclasts, bone resorption)
- furosemide (inhibits distal calcium resorption)
- calcitonin (inhibits osteoclast)
- GC (inhibit vit D conversion to calcitriol)
- calcimimetics (bind calcium receptor - inhibit PTH release)
What are the main reasons of malignant disease causing hypercalcaemia?
PTHrP released from solid tumours, or have 1-hydroxylase activity (synthesis calcitriol)
bone tumours stimulate osteoclast activation (cytokines) –> bone resorption
How do we diagnose malignancy?
raised calcium
suppressed PTH
ALP very high
What are the treatment principles of malignant hypercalcaemia?
rehydration
then drugs
treat underlying malignancy (srugery, chemotherapy)
How does factitious hypercalcaemia occur?
raised calcium due to high plasma albumin
due to dehydration, venous stasis, or xs IV albumin
how does sarcoidosis lead to hypercalcaemia?
hydroxylation of vitamin D in granulomas, leads to high calcium, low PTH
affects lungs mainly (ass. symptoms) and skin (ulcers, lumps, discolouration)
What is the mechanism behind familial hypocalciuric hypercalcaemia (FHH)?
parathyroid calcium sensor less sensitive to calcium PTH suppression
What are the clinical manifestations of hypocalcaemia?
increased neuromuscular excitability
mental change
What are the two signs used to test for hypocalcaemia?
Chvostek’s sign: facial nerve in front of tragus tapped causing momentary muscle contraction in face
Trousseau’s sign: brachial artery occluded using BP cuff (3 min) causing neuromuscular irritability which induces spasm of hand and forearm muscles
What are the causes/risk factors for vitamin D deficiency?
lack of sun, diet, malabsorption, chronic renal or liver disease, defective enzymes in vitamin D metaobolic pathway, tanned/dark skinned
What are the clinical features of vitamin D deficiency?
low calcium, high PTH
osteomalacia - bones soft, pain, fractures, defective mineralisation/calcification
What are the causes of vitamin D deficiency?
Rickets Inherited causes - deficient 1-ydroxylase - defective calcitriol receptor - hypophosphataemic Rickets (mutation, excessive urine loss) - hypophosphatasia (low ALP)
What are the causes of hypoparathyroidism?
acquired - surgery, suppresed secretion
inherited - developmental parathyroid problems, genetic disorders
What are the biochemical features of hypoparathyroidism?
low calcium, low PTH (inappropriate), phosphate high
What are treatments for hypocalcaemia?
acute - IV calcium
oral calcium, vitamin D intramuscular injection if malabsorption present, sometimes magnesium
close monitoring of plasma [calcium] necessary
What is factitiuous hypocalcaemia?
Due to low plasma albumin caused by malnutrition/malabsorption/liver disease (reduced synthesis)
What is osteoporosis?
reduced bone mineral density leading to increased risk of fracture
often age associated
What is the MAIN difference between osteoporosis and osteomalacia?
osteoporosis DOESN’T AFFECT routine biochemistry or histology
osteomalacia has abnormal biochemistry, histology
