Hyperparathyroidism (E&M) Flashcards

1
Q

Define hyperparathyroidism.

A

Abnormally high PTH levels in blood due to overactivity of the parathyroid glands

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2
Q

What does PTH do?

A

Increases serum calcium + decreases serum phosphate

  • increase calcium reabsorption (kidney)
  • increase 1-alpha-hydroxylase expression (activates vitamin D = increases calcium reabsorption)
  • increases phosphate excretion (neutral change in phosphate as indirectly increases PO4 via calcitriol)
  • activates osteoblasts to mobilise calcium and differentiate into osteoclasts
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3
Q

What is PTH secretion normally stimulated by?

A

Decrease in serum calcium

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4
Q

What are the effects of calcitriol? (3)

A
  • increased osteoblast activity
  • increased calcium and phosphate absorption (gut)
  • increased calcium and phosphate REabsorption (kidney)
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5
Q

What are the effects of calcitonin? (2)

A
  • decreased osteoclast activity
  • increased calcium, sodium and phosphate excretion (kidney)
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6
Q

What are the effects of FGF23?

A

Inhibits calcitriol production, increased phosphate excretion in kidneys

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7
Q

Which groups does hyperparathyroidism happen to most? (2)

A
  • F>M
  • > 50 years old
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8
Q

What causes primary hyperparathyroidism? (4)

A
  • parathyroid adenoma (benign tumour - 80%)
  • parathyroid hyperplasia (20%)
  • parathyroid carcinoma (<0.5%)
  • MEN syndrome
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9
Q

What causes secondary hyperparathyroidism? (3)

A
  • vitamin D deficiency –> reduced calcium absorption in gut = hypocalcaemia –> increased PTH
  • CKD
  • malnutrition
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10
Q

What causes tertiary hyperparathyroidism?

A

Chronic renal failure - persistent secondary hyperparathyroidism

Hyperplasia of parathyroid glands after correction of underlying renal disorder

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11
Q

What calcium levels do we see in primary vs secondary vs tertiary hyperparathyroidism?

A
  • primary - high (autonomous PTH release from tumour)
  • secondary - low (hypocalcaemia stimulates PTH release)
  • tertiary - high (due to chronic increase in PTH due to persistent secondary hyperparathyroidism)
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12
Q

What are the clinical features of primary hyperparathyroidism?

A

Hypercalcaemia Sx - painful bones, renal stones, abdominal groans and psychic moans

  • bone pain (especially back pain)
  • renal stones
  • constipation, anorexia, abdominal pain, nausea
  • low mood, depression, memory loss, fatigue
  • polydipsia and polyuria
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13
Q

What are the clinical features of secondary and tertiary hyperparathyroidism? (5)

A
  • secondary: hypocalcaemia - CATS go numb (convulsions, arrhythmias, tetany, spasm, paraesthesia)
  • tertiary - Sx of CKD
  • Sx of underlying cause (i.e. renal failure)
  • bone pain
  • increased risk of fractures - osteoporosis/osteopenia
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14
Q

What might you see on examination of secondary hyperparathyroidism? (2)

A

Signs of hypocalcaemia:

  • Chvostek’s sign - twitching of facial muscles when facial nerve is tapped below zygomatic arch
  • Trousseau’s sign - carpopedal spasm when BP cuff inflated for several minutes
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15
Q

What are some risk factors for hyperparathyroidism? (6)

A
  • female sex
  • age >50
  • Fx for primary hyperparathyroidism
  • multiple endocrine neoplasia (MEN) 1, 2A, 4
  • lithium treatment
  • hyperparathyroidism-jaw tumour syndrome
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16
Q

What are the first-line investigations for hyperparathyroidism? (4)

A
  • serum calcium
  • serum intact PTH with immunoradiometric or immunochemical assay
  • serum creatinine
  • serum urea
17
Q

What does serum calcium show in primary, secondary and tertiary hyperparathyroidism?

A
  • high in primary and tertiary
  • low/normal in secondary
18
Q

What does serum phosphate show in hyperparathyroidism?

A
  • low in primary
  • high in secondary if CKD, low if vitamin D deficiency
  • high in tertiary (CKD)
19
Q

What is PTH like in hyperparathyroidism?

A

High

20
Q

How can we tell the difference between primary and tertiary hyperparathyroidism?

A
  • PTH raised or inappropriately normal in primary
  • PTH markedly raised in tertiary
  • ALP may be raised in primary
21
Q

What might ALP show in hyperparathyroidism?

A

May be raised (primary) - susceptible to post-parathyroidectomy hypocalcaemia

22
Q

What would we look for to diagnose secondary hyperparathyroidism? (4)

A
  • low calcium
  • low phosphate if vitamin D deficiency (osteomalacia)
  • high phosphate if CKD
  • high PTH
23
Q

What scan can we do in hyperparathyroidism and why?

A

USS to look for parathyroid gland adenoma

24
Q

What would an X-ray show in hyperparathyroidism? (2)

A
  • Pepperpot appearance
  • osteopenia/erosion of bone
25
Q

What might ABG show in primary hyperparathyroidism?

A

Hyperchloraemic acidosis with normal anion gap (PTH inhibition of renal absorption of HCO3-)

26
Q

Compare calcium, PTH, vitamin D and phosphate in primary vs secondary vs tertiary hyperparathyroidism.

A
  • calcium: high vs low/normal vs high
  • PTH: high/normal vs high vs very high
  • vitamin D: high vs low vs low
  • phosphate: low vs low/high vs high
27
Q

What are some differential diagnoses for hyperparathyroidism? (10)

A
  • familial hypocalciuric hypercalcaemia - Ca:Cr ratio, Fx
  • humoral hypercalcaemia of malignancy - low PTH, mild hypokalaemia hypochloraemic acidosis, high PTH-related peptide
  • multiple myeloma
  • milk-alkali syndrome - excess antacids
  • sarcoidosis - low PTH
  • hypervitaminosis D
  • thyrotoxicosis
  • leukaemia
  • immobilisation
  • thiazide use
28
Q

How do we treat primary hyperparathyroidism definitely?

A

Total parathyroidectomy (if asymptomatic with surgical indications or symptomatic)

If asymptomatic with no surgical indications - monitoring, parathyroidectomy 2nd line

29
Q

What medical management can we use for primary hyperparathyroidism? (2)

A
  • calcimimetics (cinacalcet) - inhibits PTH release
  • IV fluids to treat hypercalcaemia
30
Q

How do we treat secondary hyperparathyroidism?

A

Treat the underlying cause (i.e. vitamin D deficiency, CKD)

If vitamin D deficiency - ergocalciferol/cholecalciferol

31
Q

How do we manage osteoporosis in hyperparathyroidism?

A

Bisphosphonates (alendronic acid)

32
Q

What drug do we avoid in hyperparathyroidism?

A

Thiazide diuretics

33
Q

How do we manage acute hypercalcaemia in hyperparathyroidism? (4)

A
  • IV fluids
  • avoid factors that exacerbate hypercalcaemia e.g. thiazide diuretics
  • maintain adequate hydration
  • moderate calcium and vitamin D intake
34
Q

What are some complications of hyperparathyroidism? (7)

A
  • neck haematoma after surgery
  • recurrent and superior laryngeal nerve injury after surgery
  • hypocalcaemia after surgery
  • pneumothorax after surgery
  • osteoporosis
  • bone fractures
  • nephrolithiasis (hypercalcaemia)