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?

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

Tertiary = CKD

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
What might ABG show in primary hyperparathyroidism?
Hyperchloraemic acidosis with normal anion gap (PTH inhibition of renal absorption of HCO3-)
26
Compare calcium, PTH, vitamin D and phosphate in primary vs secondary vs tertiary hyperparathyroidism.
- 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
What are some differential diagnoses for hyperparathyroidism? (10)
- 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
How do we treat primary hyperparathyroidism definitely?
**Total parathyroidectomy** (if asymptomatic with surgical indications or symptomatic) If asymptomatic with no surgical indications - monitoring, parathyroidectomy 2nd line
29
What medical management can we use for primary hyperparathyroidism? (2)
- calcimimetics (cinacalcet) - inhibits PTH release - IV fluids to treat hypercalcaemia
30
How do we treat secondary hyperparathyroidism?
Treat the underlying cause (i.e. vitamin D deficiency, CKD) If vitamin D deficiency - ergocalciferol/cholecalciferol
31
How do we manage osteoporosis in hyperparathyroidism?
Bisphosphonates (alendronic acid)
32
What drug do we avoid in hyperparathyroidism?
Thiazide diuretics
33
How do we manage acute hypercalcaemia in hyperparathyroidism? (4)
- IV fluids - avoid factors that exacerbate hypercalcaemia e.g. thiazide diuretics - maintain adequate hydration - moderate calcium and vitamin D intake
34
What are some complications of hyperparathyroidism? (7)
- neck haematoma after surgery - recurrent and superior laryngeal nerve injury after surgery - hypocalcaemia after surgery - pneumothorax after surgery - osteoporosis - bone fractures - nephrolithiasis (hypercalcaemia)