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Year 2 Clinical > Calcium Homeostasis and Disorders of Calcium Metabolism > Flashcards

Calcium Homeostasis and Disorders of Calcium Metabolism Flashcards

1
Q

Movement of calcium in the body?

A

Calcium is absorbed from the gut (Vitamin D is essential for this) into the blood and shuttles between here and bone

Some calcium is excreted via the kidneys

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2
Q

Factors that affect calcium homeostasis?

A

Diet

Gut absorption, which is affected by:

  • Age
  • Hormones (pregnancy/lactation)
  • Bowel pathology

PTH, which is affected by:

  • Hyper/hypoparathyroidism
  • Malignant hypercalcaemia (PTHrP)

Vitamin D, which is affected by:

  • Diet and absorption
  • Renal and liver status
  • UVB exposure
  • Drugs
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3
Q

Effects of PTH?

A
  • Ca2+ release from bone
  • Absorption from the gut

These both result in increased serum calcium

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4
Q

Regulation of PTH release?

A

Calcium binds to CaSR on the parathyroid gland, which STOPS PTH release and all of its effects

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5
Q

Physiology of vitamin D?

A

Dehydro-cholesterol (in the skin) is converted, by the sun, into:

  • Cholecalciferol (D3) then to
  • 25 (OH) vitamin D (in the liver) then to
  • 1,25 (OH) vitamin (in the kidneys)

1,25 (OH) vitamin D stimulates:

  • PTH release
  • Gut absorption
  • Bone release of Ca2+
  • Kidneys
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6
Q

Acute symptoms of hypercalcaemia?

A
  • Thirst, dehydration and polyuria (as hypercalcaemia can induce nephrogenic diabetes mellitus)
  • Confusion
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7
Q

Chronic symptoms of hypercalcaemia?

A
  • Proximal myopathy
  • Osteopaenia and fractures
  • Depression
  • Hypertension
  • Abdominal pain (due to pancreatitis, ulcers and renal stones)
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8
Q

Phrase to remember symptoms of hypercalcaemia?

A

“Stones, groans, bones and psychic moans”

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9
Q

Single test requires to assess calcium state?

A

PTH:

  • If normal/high - there is a problem with Ca2+ handling
  • If low - there is a bone problem, usually malignancy

Can also check urinary Ca2+:

  • If high, likely to be primary/tertiary hyperparathyroidism
  • If low - FHH (as, if Ca2+ is high, it would normally be excreted in the urine)
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10
Q

Algorithm for hypercalcaemic Ix and diagnoses?

A
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11
Q

Ix for bone pathology (following a result of suppressed PTH and high phosphate)?

A

Alkaline phosphatase

If high:

  • Bone metastases
  • Sarcoidosis
  • Thyrotoxicosis

If low:

  • Myeloma
  • Vitamin D excess
  • Mild-alkali syndrome (due to, e.g: thyrotoxicosis, sarcoidosis, raised HCO-3)
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12
Q

2 main causes of hypercalcaemia?

A
  1. Primary hyperparathyroidism
  2. Malignancy
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13
Q

Other causes of hypercalcaemia?

A

Drugs:

  • Vitamin D
  • Thiazides (stop Ca2+ excretion)

Granulomatous disease, e.g:

  • Sarcoidosis
  • TB

Familial Hypocalciuric Hypercalcaemia (FHH)

High turnover, e.g:

  • Bedridden
  • Thyrotoxic
  • Paget’s disease

Tertiary hyperparathyroidism

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14
Q

What is FHH?

A

FH (autosomal dominant) of hypercalcaemia, typically assoc. with loss of function mutations in the CaSR (calcium sensing receptor)

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15
Q

Ix and result with PRIMARY hyperparathyroidism?

A

Class triad of:

  • Raised serum Ca2+
  • Raised serum PTH (or inappropriately normal)
  • Increased urine calcium excretion (for this to be accurate, the patient must have correct Vitamin D levels)
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16
Q

Mechanisms by which malignancy causes hypercalcaemia?

A
  1. Metastatic bone destruction
  2. PTHrp (PTH related protein) from solid tumours, which acts like PTH
  3. Osteoclast activating factors
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17
Q

Ix and results with hypercalcaemia due to malignancy?

A

Raised Ca2+ and alkaline phosphatase

X-ray, CT, MRI

Isotope bone scan

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18
Q

Acute treatment of hypercalcaemia?

A

FLUIDS (0.9% saline) - rehydrate with 4-6 l in 24 hours

Once rehydrated, consider loop diuretics (avoid thiazides)

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19
Q

Acute treatment of hypercalcaemia?

A

FLUIDS (0.9% saline) - rehydrate with 4-6 l in 24 hours

Once rehydrated, consider loop diuretics (avoid thiazides)

Bisphosphonates

For sarcoidosis, steroids are used (Prednisolone 40-60 mg/day for)

Salmon calcitonin is rarely used

Chemotherapy, for malignancy, may reduce calcium, e.g: myeloma

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20
Q

Use of bisphosphonates to lower Ca2+?

A

A single dose lowers Ca2+ over 2-3 days

Maximum effect is at 1 week

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21
Q

Sestamibi scan?

A

Shows thyroid and parathyroid uptake, e.g: a pinhole appearance may indicate a parathyroid adenoma (which is benign)

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22
Q

Mx of primary hyperparathyoidism?

A

SURGERY OR NOTHING (surgery is not always required)

Diet and drugs show no proven benefit; however, drinking plenty of fluids reduces risk of renal stones

Cinacalcet is a Ca2+ mimic, so it reduced PTH, and is used in:

  • Tertiary hyperparathyroidism
  • Parathyroid carcinoma
23
Q

Indications for parathyroidectomy?

A

End-organ damage:

  • Bone disease
  • Gastric ulcers
  • Renal stones
  • Osteoporosis

Very high Ca2+ (>2.85 mmol/l)

<50 years old

eGFR <60 ml/min

24
Q

Types of end-organ complications of bone?

A

Osteitis Fibrosa et cystica (AKA brown tumours / pepper pot skull appearance on X-ray)

25
Q

What are primary, seconary and tertiary hyperparathyroidism?

A

Primary:

• Primary over-activity of the parathyroid, e.g: with an adenoma

Secondary:

• Physiological response to low Ca2+

Tertiary:

• Parathyroid becomes autonomous after many years of secondary hyperparathyroidism

26
Q

Ix results in primary, secondary and tertiary hyperparathyroidism?

A

Primary:

  • PTH raised
  • Ca2+ raised

Secondary:

  • Ca2+ low
  • PTH raised

Tertiary:

  • Ca2+ raised
  • PTH raised
27
Q

Genetic syndromes that are assoc. with hyper hypercalcaemia?

A

MEN1/2 - have a parathyroid adenoma (consider if the patient is young)

FHPT (familial hyperparathyroidism) - this is not the same as FHH

28
Q

Symptoms of FHH?

A

Usually benign or asymptomatic and tends to be an incidental finding (in which case, the urine Ca2+ excretion must be checked and, if FHH, it will be low)

29
Q

Ix results with FHH?

A

Mild hypercalcaemia

Reduced urine calcium excretion (IF THIS IS THE CASE, WITH NO/FEW SYMPTOMS, THINK FHH)

PTH may be marginally elevated Genetic screening

30
Q

Symptoms of HYPOcalcaemia?

A

Paraesthesia (esp. in the fingers, toes and perianal region)

Muscle weakness, cramps and tetany

Fatigue

Bronchospasm or laryngospasm

Fits

31
Q

Signs of HYPOcalcaemia?

A

Chovsteks sign (tapping over the facial nerve)

Trousseau sign (capopedal spasm)

32
Q

Ix and results for hypocalcaemia?

A

ECG shows QT prolongation (can be fatal if untreated)

33
Q

3 main causes of hypocalcaemia?

A
  1. Hypoparathyroidism
  2. Vitamin D deficiency:
  • Osteomalacia
  • Rickets
  1. Chronic renal failure
34
Q

Other causes of hypocalcaemia?

A
  • Pancreatitis
  • Hyperventilation
  • Osteoblastic bone metastases
  • Rhabdomyolysis
35
Q

Treatment of acute hypocalcaemia?

A

EMERGENCY IV calcium gluconate - 10ml, 10% over 10 minutes (in 50ml saline/dextrose

Infusion - 10ml, 10% in 100ml infusate at 50ml/hour

36
Q

Causes of hypoparathyroidism?

A

Congenital absence, e.g: in DiGeorge syndrome

Destruction, due to e.g: surgery, radiotherapy or malignancy

Autoimmune

Hypomagnesaemia

Idiopathic

37
Q

Long-term Mx of hypocalcaemia?

A

Ca2+ supplementation:

• >1-2 g per day

Vitamin D:

  • Tablets - 1α-calcidol (0.5-1 mcg)
  • Depot injection - cholecalciferol (300,000 units 6 monthly)
38
Q

Consqeuences of hypomagnesaema, in terms of calcium?

A

Calcium release from cells is dependent on Mg; if deficient, intracellular Ca2+ is high, as there is less release PTH release is therefore inhibited (requires Ca2+ binding)

Skeletal and muscle receptors become less sensitive to PTH

39
Q

Treatment of hypomagnesaemia, that is causing hypocalacemia?

A

If low, replace with Ca2+ and Mg

40
Q

Causes of hypomagnesaemia?

A

Alcohol

Drugs:

  • Thiazide
  • PPI

GI illness

Pancreatitis

Malabsorption

41
Q

What is pseudohypoparathyroidism?

A

GENETIC defect in GNAS1 causes dysfunction of the Gs protein α-subunit

There is low calcium but PTH conc. is ELEVATED, this this PTH is less effective, due to resistance; the symptoms are the same as in hypoparathyroidism

42
Q

Consequences of pseudohypoparathyroidism?

A

There is a specific phenotype that has been described (Albright’s hereditary osteodystrophy):

  • Bone abnormalities
  • Obesity
  • Subcutaneous calcification
  • Learning disability
  • Brachdactyly (shortened 4th metacarpal)
43
Q

What is pseudo-pseudohypoparathyroidism?

A

Same as Albright’s but the CALCIUM is NORMAL

Note: patients can shift change from pseudo to pseudo-pseudo

44
Q

Causes of rickets and osteomalacia?

A

Vitamin D deficiency due to:

  • Dietary deficiency
  • Malabsorption, e.g: form gastric surgery, coeliac disease, liver disease, pancreatic failure
  • Chronic renal failure
  • Lack of sunlight
  • Drugs, e.g: anti-convulsants
45
Q

X-ray appearance of Rickets and osteomalacia?

A

Bow-legged in children

Looser zones - wide, transverse lucencies traversing part way through a bone, usually at right angles to the involved cortex; this is surrounded by a sclerotic area

46
Q

Clinical presentation of osteomalacia?

A

Proximal myopathy and muscle wasting

Dental defects (caries, enamel)

Bone tenderness, fractures, rib and limb deformity

47
Q

What is Vitamin D resistant rickets?

A

AKA X-linked hypophosphataemia; both genders can develop this but females develop a less severe form It is due to a PHEX or FGF23 mutation, which regulates phosphate levels in plasma and is secreted by osteocytes (in response to calcitriol), i.e: these people have a low phosphate and a high vitamin D

It has the same phenotype as rickets but vitamin D does not help

48
Q

Treatment of vitamin D resistant rickets?

A

Phosphate and vitamin D supplementation (1,25 - OH vitamin D3)

+/-

Surgery

49
Q

Consequences of chronic renal disease?

A

Vitamin D deficiency and secondary hyperparathyroidism

They may have high 25-OH vitamin D, as they cannot hydroxylate it into 1,25-OH vitamin D (this must be CHECKED)

50
Q

Treatment of chronic renal disease?

A

Titrate treatment to PTH levels and do not forget phosphate binders

51
Q

Typical Ix results with osteomalacia?

A

Low Ca2+ and high PTH

Low phosphate

High alkaline phosphatase

Low vitamin D (25-OH)

52
Q

Long-term effects of vitamin D deficiency?

A

Bone demineralisation and fractures

Osteomalacia/rickets

Malignancy (esp. of the colon)

Heart disease

Diabetes,

53
Q

Chronic treatment of vitamin D deficiency?

A

Supplement vitamin D:

  • Vitamin D3 tablets (400-800 IU/day after loading with 3200 IU/day for 12 weeks)
  • Calcitriol (1,25-dihydroxycholecalciferol)
  • Alfacalcidol (1α - hydroxycholecalciferol)

Combined calcium + vitamin D, e.g: Adcal D3

54
Q

Summary of the biochemistry of each condition?

A

Year 2 Clinical (119 decks)

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