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Week 9 - Phase 3 > Hypercalcaemia > Flashcards

Hypercalcaemia Flashcards

1
Q

What are the functions of calcium in the body?

A
  • Muscle contraction
  • Stabilisation of membranes
  • Bone growth and remodeling
  • Second messenger signaling
  • Secretion of hormones e.g. insulin
  • Enzyme co-factor e.g. in blood co-agulation.
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2
Q

Where is calcium found in the body?

A

99% in skeleton

  1. 01% intracellular e.g. ER, mitochondria
  2. 99% extracellular - 45% free, 55% bound
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3
Q

What does calcium bind to in the blood?

A

55% - albumin, lactate and phosphate.

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4
Q

Where are the parathyroid glands found?

A

Posterior surface of the thyroid gland

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5
Q

How many parathyroid glands are there?

A

Normally 4, can vary

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6
Q

What artery supplies the parathyroid glands?

A

Inferior thyroid artery.

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7
Q

What is the basic function of parathyroid hormone

A

Raise blood calcium

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8
Q

How does parathyroid hormone act in the kidney?

A
  • Reabsorbs calcium in the DCT
  • Internalises sodium-phosphate co-transporters at the PCT
  • Inhibits Na/H leading to bicarbonate wasting
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9
Q

How does PTH act on bone?

A
  • Increased number and activity of osteoclasts
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10
Q

How does PTH act in the gut?

A
  • Stimulates synthesis of active Bit D in kidney and therefor increases calcium absorption in the gut.
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11
Q

Where is PTH stored?

A

Chief cells in PT glands

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12
Q

What controls PTH secretion and how?

A

Calcium sensing receptor - if high calcium inhibits transcription of the PTH gene and PTH secretion is inhibited.

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13
Q

What breaks down PTH when there is high blood calcium?

A

Calcium sensing proteases.

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14
Q

How do calcimimetic drugs work?

A

Inhibit the Calcium sensing receptor and inhibit PTH secretion.

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15
Q

Where in the body in the calcium sensing receptor found? What is its role?

A
  • Kidney: Increases urinary calcium and magnesium excretion, increases sodium, potassium and chloride excretion.
  • Thyroid: Expressed in C-cells and stimulates calcitonin secretion.
  • Brain, intestine and bone but role not understood.
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16
Q

What kind of hormone is vitamin d?

A

Steroid hormone so needs to bind to a nuclear receptor.

17
Q

How does vitamin D affect calcium?

A

Acts to increase serum calcium levels.

18
Q

Outline vitamin D production?

A
  • 7-dehydrocholesterol is converted to cholecalciferol by UV light.
  • Ergosterol from diet e.g. fish is converted to ergocalciferol.
    Both are converted to calcidol and stored in the liver.
  • Becomes active calcitriol in the kidney.
19
Q

What is the role of Calcitriol (1-25 dihydroxycholecacliferol) ?

A
  • Increased calcium and phosphate absorption from the gut
  • Increases muscle strength
  • Bone mineralization and mobilizes calcium stores
  • Reduces insulin resistance
  • immunomodulation (B and T lymphocytes)
  • Interacts with RAAS. Possible role in prevention of CVD
20
Q

List symptoms of hypercalcaemia?

A
  • Muscle weakness
  • Bone pain or osteoporosis
  • Anorexia
  • Nausea
  • Constipation
  • Pancreatitis
  • Confusion, depression, fatigue, coma
  • Shortening of QT complex, bradycardia
  • Hypertension
  • Polyuria
  • Nephrogenic diabetes insipidus
  • Kidney stones
21
Q

What level is serum calcium if hypercalcaemia symptoms are present?

A

> 3mmol/L

22
Q

What are PTH-mediated (PTH normal/elevated) causes of hypercalcaemia?

A
  • Primary hyperparathyroidism
  • Familial syndromes MEN-1
  • Familial hypocalciuric hypercalcaemia
23
Q

What are PTH-independant (undetectable PTH) causes of hypercalcaemia?

A
  • Malignancy
  • Granulomatous disorders
  • Vitamin D toxicity
  • Drugs: Thiazides, lithium, calcium supplements
  • Adrenal insufficiency
24
Q

What kind of malignancy commonly causes hypercalcaemia?

A

Solid organ tumours and hematological malignancies

25
Q

Why does malignancy cause hypercalcaemia?

A

Through increase bone resorption and calcium release through 3 mechanisms

  1. Osteoclalst metastasis and myeloma
  2. tumor secretion of PTHrP which binds to the PTH receptor and stimulates bone resorption and renal calcium resorption.
  3. Tumor production of 1,25 dihydroxycholecalciferol by activated macrophages. Can occur in lymphoma.
26
Q

Describe management of hypercalcaemia?

A
  1. Stop medicine that contribute
  2. Rehydration: normal saline, 3-4L in first 24h
  3. Loop diruretic: promote calciuria
  4. Bisphosphonates: Inhibite bone resorption e.g. zoledronic acid.
  5. Steroids: Effective in hematological malignancy, granulomatous disease.
27
Q

What is the most common cause of primary hyperparathyroidism?

A

An isolated parathyroid adenoma.

28
Q

What end organ damage can primary hyperparathyroidism cause?

A
  • Bone: osteoporosis, other radiological changes such as bone cysts or subperiosteal resorption.
  • Kidneys: Renal calculi, nephrocaclinosis, renal impairment.
  • Pancreatitis
29
Q

What familial conditions are linked to primary hyperparathyroidism?

A

MEN-1 or MEN-2

30
Q

What is a brown tumor?

A

A collection of osteoclasts, poorly mineralized bone and fibrous tissue.
Occurs as a result of excess osteoclast activity.
‘Brown’ because of appearance due to haemosidrin deposition.

31
Q

What are the management options for primary hyperparathyroidism?

A
  • Parathyrodectomy
  • Observation if no end organ damage. Monitor with DEXA scans and renal ultrasound every 3 years.
  • Medical treatment: Bisphosphonates to preserve bone mass.
    Calcium sensing receptor agonists (e.g. Cinacalcet) which reduces serum calcium but not urine calcium. Doesn’t prevent end organ damage.
32
Q

What are possible complications of parathyroidectomy?

A
  • Vocal cord paresis
  • Haematoma causing thraceal compression.
  • Transient hypocalciua, may need oral calcium/vit D supplement.
  • ‘Hungry bones’: In patient with significant bone disease or very elevated PTH. Sudden withdrawal of PTH leads to imbalance between bone formation and resorption - net increase in uptake of calcium and magnesium by bone. Need calcium and vitamin D supplementation.
33
Q

List causes of Vitamin D deficiency?

A
  • Poor sunlight exposure (elderly, housebound)
  • Malabsorption
  • Gastrecotmy
  • Enzyme inducing drugs e.g. anti-convulsants
  • Renal disease (impairing hydroxylation of Vitamin D)
34
Q

What is osteomalacia?

A

Associated with low Vitamin D.
Failure to ossify bones in adulthood as a result of Vitamin D deficiency.
Hypo-mineralisation of trabecular and cortical bone.

35
Q

How does osteomalacia present?

A

Insidiously with bone pain, proximal myopathy, hypocalciaemia.

36
Q

What blood results would indicate osteomalacia?

A

Low calcium, phosphate and Vit D.

Elevated all phos and PTH.

37
Q

What are ‘looser zones’?

A

Also called cortical infarctions or milkman lines.

They are ‘insufficiency fractures’.

38
Q

What features are seen on x-ray in osteomalacia?

A

Looser zones and osteopenia.

39
Q

Outline management of Vitamin D deficiency?

A

Cholecalciferol (D3): Resore body stores and correct metabolic disturbance.
This will heal bony abnormalities.

Alfacalcidiol (active vit D): In renal impairment and in hypoparathyroidism (can’t activate via D in gut).
Higher risk of hypercalcaemia.

Week 9 - Phase 3 (8 decks)

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