Hyperparathyroidism + Hypoparathyroidism + Diabetes Insipidus Flashcards

1
Q

Physiology of the parathyroid glands

A

There are four parathyroid glands situated in four corners of the thyroid gland. The parathyroid glands, particularly the chief cells in the glands, produce parathyroid hormone in response to hypocalceaima.

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2
Q

How does parathyroid hormone act to raise blood calcium levels?

A
  • Increases osteoclast activity in bones
  • Increases calcium absorption from gut
  • Increases calcium absorption from kidneys
  • Converts vitamin D into active forms, vitamin D increases calcium absorption from intestines
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3
Q

Symptoms of hypercalcaemia

A

Renal stones, painful bones, abdominal groans and psychiatric moans.

  • Renal stones
  • Painful bones
  • Abdominal groans refers to symptoms of constipation, nausea and vominting
  • Psychiatric moans refers to symptoms of fatigue, depression and psychosis
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4
Q

Pathophysiology of primary hyperparathyroidism

A

Primary hyperparathyroidism is caused by uncontrolled parathyroid hormone produced directly by a tumour of the parathyroid glands. This leads hypercalcaemia.

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5
Q

Management of primary hyperparathyroidism

A

Surgical removal of the tumour

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6
Q

Pathophysiology of secondary hyperparathyroidism

A

Insufficient vitamin D or chronic renal failure leads to low absorption of calcium, resulting in hypocalcaemia.

Parathyroid hyperplasia occurs. Parathyroid hormone will be high.

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7
Q

Management of secondary hyperparathyroidism

A

Correct vitamin D deficiency or perform renal transplantation to treat renal failure.

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8
Q

Pathophysiology of tertiary hyperparathyroidism

A

This happens when secondary hyperparathyroidism continues for a long period of time.

It leads to hyperplasia of the glands and increased parathyroid hormone levels.

When the cause of the secondary hyperparathyroidism is treated the parathyroid hormone level remains inappropriately high leading to hypercalaemia.

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9
Q

Management of tertiary hyperparathyroidism

A

Surgical removal of part of the thyroid tissue

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10
Q

Cause of hypoparathyroidism

A

Iatrogenic: neck surgery or radiation (the vast majority)

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11
Q

Clinical features of hypoparathyroidism

A

Hypocalacemia

  • Muscle twitching
  • Lethargy
  • Muscle spasma
  • Psychosocial changes
  • Prolonged QT interval
  • Chovostek sign: twitching of the facial muscles on tapping the cheek
  • Trousseau sign: spasm of the muscles of the hand on application of a BP cuff (rare)
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12
Q

Describe pseudohypoparathyroidism

A

Hypocalcaemia is present but PTH is elevated, primarily because of end organ receptor insensitivity to the effect of PTH.

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13
Q

Investigations for hypoparathyroidism

A
  • Decreased serum calcium
  • Elevated phosphate
  • Decreased PTH
  • Normal alkaline phosphatase (ALP)
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14
Q

Management of hypoparathyroidism

A
  • Severe hypocalcaemia
    • IV calcium gluconate is indicated
  • Long term management
    • Calcium and vitamin D replacement
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15
Q

What is the role of anti diuretic hormone?

Pathophysiology of diabetes insipidus?

A

ADH acts on the collecting ducts in the kidneys, allowing them to reabsorb water from the urine.

Diabetes insipidus prevents kidneys from concentrating urine resulting in polydipsia and polyuria.

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16
Q

What are the two classes of causes of diabetes insipidus?

A

Nephrogenic (collecting ducts don’t respond to ADH)

or

cranial (hypothalamus does not produce ADH)

17
Q

Differential diagnosis of diabetes insipidus

A

Primary polydipsia (patient drinks excessive amount of water)

18
Q

Causes of nephrogenic diabetes insipidus

A
  • Lithium
  • Genetic (AVPR2 gene on X chromosome)
  • Intrinsic kidney disease
  • Electrolytes (↓K+, ↑Ca2+)
19
Q

Causes of cranial diabetes insipidus

A
  • Idiopathic
  • Brain tumour
  • Head injury
  • Brain surgery
  • Radiotherapy
  • Infection eg meningitis, encephalitis, TB
20
Q

Clinical features of diabetes insipidus

A
  • Polyuria
  • Polydipsia
  • Dehydration
  • Postural hypotension
  • Hypernatraemia
21
Q

Diabetes insipidus investigations

A
  • U&Es: hypernatraemia
  • Urine osmolality: low urine osmolality (<300mol/kg)
  • Serum osmolality: high
  • Water deprivation test
22
Q

Describe the water deprivation test

A
23
Q

Urine osmolality after water deprivation and after desmopresin injection in cranial DI and nephrogenic DI

A
  • Cranial DI:
    • After water deprivation: low urine osmolality
    • After desmopressin: high urine osmolality
  • Nephrogenic DI:
    • After water deprivation: low urine osmolality
    • After desmopressin: low urine osmolality
24
Q

Management of cranial DI

A

Desmopressin

25
Q

Management of nephrogenic DI

A

More difficult to treat

  • Drink adequate fluid
  • Low sodium diet/low protein diet
  • Thiazide diuretics