Disorders of Calcium Metabolism Flashcards

1
Q

What are the clinical manifestations of hypercalcaemia?

A

stones, bones, abdominal moans and psychic groans

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2
Q

What is primary hyperparathyroidism?

A

autonomous inappropriate PTH overproduction leading to hypercalcaemia

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3
Q

What is secondary hyperparathyroidism?

A

appropriate PTH increase in response to hypocalcaemia

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4
Q

What is tertiary hyperparathyroidism?

A

Gland has become overactive after initial secondary hyperparathyroidism

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5
Q

What are the main causes of primary hyperparathyroidism?

A

adenoma, hyperplasia, carcinoma (rare)

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6
Q

How do we diagnose primary hyperparathyroidism?

A

high calcium and PTH
phosphate, bicarbonate low (excreted)
ALP normal (increased if severe)
imaging

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7
Q

How do we treat primary hyperparathyroidism?

A

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)

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8
Q

What are the main reasons of malignant disease causing hypercalcaemia?

A

PTHrP released from solid tumours, or have 1-hydroxylase activity (synthesis calcitriol)

bone tumours stimulate osteoclast activation (cytokines) –> bone resorption

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9
Q

How do we diagnose malignancy?

A

raised calcium
suppressed PTH
ALP very high

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10
Q

What are the treatment principles of malignant hypercalcaemia?

A

rehydration
then drugs
treat underlying malignancy (srugery, chemotherapy)

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11
Q

How does factitious hypercalcaemia occur?

A

raised calcium due to high plasma albumin

due to dehydration, venous stasis, or xs IV albumin

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12
Q

how does sarcoidosis lead to hypercalcaemia?

A

hydroxylation of vitamin D in granulomas, leads to high calcium, low PTH
affects lungs mainly (ass. symptoms) and skin (ulcers, lumps, discolouration)

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13
Q

What is the mechanism behind familial hypocalciuric hypercalcaemia (FHH)?

A

parathyroid calcium sensor less sensitive to calcium PTH suppression

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14
Q

What are the clinical manifestations of hypocalcaemia?

A

increased neuromuscular excitability

mental change

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15
Q

What are the two signs used to test for hypocalcaemia?

A

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

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16
Q

What are the causes/risk factors for vitamin D deficiency?

A

lack of sun, diet, malabsorption, chronic renal or liver disease, defective enzymes in vitamin D metaobolic pathway, tanned/dark skinned

17
Q

What are the clinical features of vitamin D deficiency?

A

low calcium, high PTH

osteomalacia - bones soft, pain, fractures, defective mineralisation/calcification

18
Q

What are the causes of vitamin D deficiency?

A
Rickets
Inherited causes 
- deficient 1-ydroxylase
- defective calcitriol receptor
- hypophosphataemic Rickets (mutation, excessive urine loss)
- hypophosphatasia (low ALP)
19
Q

What are the causes of hypoparathyroidism?

A

acquired - surgery, suppresed secretion

inherited - developmental parathyroid problems, genetic disorders

20
Q

What are the biochemical features of hypoparathyroidism?

A

low calcium, low PTH (inappropriate), phosphate high

21
Q

What are treatments for hypocalcaemia?

A

acute - IV calcium
oral calcium, vitamin D intramuscular injection if malabsorption present, sometimes magnesium

close monitoring of plasma [calcium] necessary

22
Q

What is factitiuous hypocalcaemia?

A

Due to low plasma albumin caused by malnutrition/malabsorption/liver disease (reduced synthesis)

23
Q

What is osteoporosis?

A

reduced bone mineral density leading to increased risk of fracture
often age associated

24
Q

What is the MAIN difference between osteoporosis and osteomalacia?

A

osteoporosis DOESN’T AFFECT routine biochemistry or histology

osteomalacia has abnormal biochemistry, histology