Parathyroid Disorders Flashcards

1
Q

What is hyperparathyroidism?

A

Involves overactivity of the parathyroid glands with high levels of parathyroid hormone (PTH)

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2
Q

What is hyperparathyroidism?

A
  • Caused by uncontrolled parathyroid hormone produced directly by a tumour of the parathyroid glands
  • This leads hypercalcaemia - fatigue, depression, bone pain, myalgia, nausea, thirst, polyuria, renal stones, osteoporosis
  • Treated by surgically removing the tumour
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3
Q

What is secondary hyperparathyroidism?

A
  • Insufficient vitamin D or chronic renal failure leads to low absorption of calcium from the intestines, kidneys and bones
  • This causes hypocalcaemia
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4
Q

What is tertiary hyperparathyroidism?

A

This happen when secondary hyperparathyroidism continues for a long period of time (e.g. renal failure), leading to hyperplasia of the glands

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5
Q

What are the functions of PTH?

A
  • Activates osteoclasts - increased bone reabsorption, releases calcium
  • Increased reabsorption of calcium by renal tubules
  • Increased urinary phosphate excretion
  • Increased synthesis of active forms of vitamin D
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6
Q

How is parathyroid hormone regulated?

A
  • Normally the above functions would increase serum calcium, so inhibit PTH secretion
  • PTH secretion is not terminated in hyperparathyroidism - continued osteoclasis
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7
Q

What is fibrosa cystica?

A
  • The result of unchecked hyperparathyroidism, which results in an overproduction of PTH and continued osteoclasis
  • Osteoporosis, brown tumours and osteitis
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8
Q

What is the management of hyperparathyroidism?

A
  • Primary hyperparathyroidism is treated by surgical removal of the tumour
  • Secondary hyperparathyroidism is treated by correcting the vitamin D deficiency or performing a renal transplant to treat renal failure
  • Tertiary hyperparathyroidism is treated by surgical removal of part of the parathyroid tissue to return the parathyroid hormone to an appropriate level
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9
Q

What is hypercalcaemia?

A

High calcium levels in the blood serum

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10
Q

What is the aetiology of hypercalcaemia?

A

Excessive parathyroid (PTH) hormone secretion

  • Primary hyperparathyroidism - caused by a single adenoma (>80%) or diffuse hyperplasia of the parathyroid glands (15-20%)
  • Tertiary hyperparathyroidism

Malignant disease

  • Metastatic bone destruction
  • PTHrp from solid tumours
  • Osteoclast activating factors produced by tumours

Genetic syndromes

  • MEN1 and 2 - will almost always have developed a parathyroid adenoma with hypercalcaemia at a young age
  • Familial isolated hyperparathyroidism - adenoma as in primary hyperparathyroidism
  • Familial hypocalciuric hypercalcaemia - autosomal dominant deactivating mutation in the calcium sensing receptor which results in decreased sensitivity of the receptor to calcium
    • Usually benign/asymptomatic

Others

  • Drugs - Vit. D, thiazides
  • Granulomatous disease e.g. sarcoid, TB
  • High turnover - bedridden, thyrotoxic, Paget’s
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11
Q

What is the general presentation of hypercalcaemia?

A
  • Gallstones (STONES)
  • Bone pain (BONES)
  • Abdominal pain (GROANS)
  • Psychiatric disturbances (PSYCHIC MOANS)
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12
Q

What is the acute presentation of hypercalcaemia?

A
  • Thirst
  • Dehydration
  • Confusion
  • Polyuria
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13
Q

What is the chronic presentation of hypercalcaemia?

A
  • Myopathy
  • Fractures
  • Osteopenia
  • Depression
  • Hypertension
  • Pancreatitis
  • Duodenal ulcers
  • Renal calculi
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14
Q

What are the investigations of hypercalcaemia?

A

Biochemistry

  • Raised calcium
  • Serum PTH
    • Hallmark of primary hyperparathyroidism is hypercalcaemia and hypophosphatemia with detectable or elevated intact PTH levels during hypercalcaemia
    • Undetectable PTH with hypercalcaemia requires further investigation for malignancy
  • Serum alkaline phosphatase - raised in hypercalcaemia of malignancy

Imaging for malignancy

  • X-ray, CT, MRI, PET
  • Isotope bone scan

Familial hypocalciuric hypercalcaemia

  • Bloods - mild hypercalcaemia, reduced urine calcium excretion, PTH may be (marginally) elevated
  • Genetic screening
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15
Q

What is the management of acute severe hypercalcaemia?

A
  • Fluids - rehydrate with 0.9% saline 4-6L in 24 hours
  • Consider loop diuretics once rehydrated (avoid thiazides)
  • Bisphosphonates - single dose will lower Ca2+ over 2-3 days, max. effect at 1 week
  • Steroids occasionally used e.g., prednisolone 40-60mg/day for sarcoidosis
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16
Q

What is the management for hypercalcaemia in primary hyperparathyroidism?

A
  • Surgery (not always required) - indications include end organ damage, calcium >2.85 mmol/l, under age 50 and reduced eGFR (< 60 mL/min)
  • Cinacalcet - calcium mimetic, reduces PTH
    • Can be useful if need treatment but unfit for surgery
    • Licenced but not SMC approved
    • Approved for tertiary hyperparathyroidism and parathyroid carcinoma
17
Q

What is the management of hypercalcaemia in malignancy?

A
  • Treat underlying malignancy
  • Chemotherapy may reduce calcium in malignant disease e.g., myeloma
18
Q

What is hypocalcaemia?

A

Low calcium levels in the blood serum

19
Q

What is the aetiology of hypocalcaemia?

A
  • Chronic kidney disease
  • Congenital absence (DiGeorge syndrome)
  • Destruction (surgery, radiotherapy, malignancy)
  • Autoimmune
  • Hypomagnesaemia - calcium release from cells is dependent on magnesium
  • Idiopathic
  • Pseudohypoparathyroidism and pseudo-pseudohypoparathyroidism
20
Q

What is the presentation of hypocalcaemia?

A
  • Paraesthesia - fingers, toes, perioral
  • Muscle cramps, tetany
  • Muscle weakness
  • Fatigue
  • Bronchospasm or laryngospasm
  • Fits
  • Chovesteks sign - gentle tapping over the facial nerve causes twitching of the ipsilateral facial muscles
  • Trousseau sign - inflation of the sphygmomanometer cuff above systolic pressure for 3 min induces tetanic spasm of the fingers and wrist
  • ECG - QT prolongation
21
Q

What are the investigations of hypocalcaemia?

A

Low serum calcium

22
Q

What s the acute management of severe hypocalcaemia?

A
  • IV calcium gluconate 10 ml, 10% over 10 mins (in 50ml saline or dextrose)
  • Calcium infusion (10ml 10% calcium gluconate in 100ml infusate, at 50 ml/h)
23
Q

What is the management of long term hypocalcaemia?

A
  • Calcium supplement >1-2g PO/day
  • Vitamin D
    • 1 alphacalcidol 0.5-1 mcg PO/day OR
    • Depot injection: cholecalciferol 300 000 units 6 monthly
24
Q

What is hypomagnesemia?

A

Low magnesium levels in the blood serum

25
Q

What is the aetiology of hypomagnesemia?

A
  • Alcohol
  • Drugs - thiazide, PPIs
  • GI illness with diarrhoea
  • Pancreatitis
  • Malabsorption
26
Q

What is the presentation of hypomagnesemia?

A
  • Anorexia
  • Nausea and vomiting
  • Muscle weakness, lethargy
  • Fits
  • Cardiac arrhythmias
  • Positive Chovestek sign and Trousseau sign indicate secondary hypocalcaemia
27
Q

What are the investigations for hypomagnesemia?

A
  • Serum magnesium low
  • Measure other electrolytes, particularly K+ and Ca2+
28
Q

What is the management for hypomagnesemia?

A

Magnesium supplementation, calcium supplementation if needed

29
Q

What are the complications of hypomagnesemia?

A

Secondary hypocalcaemia

  • Calcium release from cells is dependent on magnesium
  • In magnesium deficiency intracellular calcium is high
  • PTH release inhibited
  • Skeletal muscle receptors less sensitive to PTH
30
Q

What is pseudohypoparathyroidism?

A

Condition associated primarily with resistance to the parathyroid hormone

31
Q

What is the aetiology of pseudohypoparathyroidism?

A

Genetic defect - dysfunction of Gs alpha subunit (GNAS 1 gene)

32
Q

What is the pathophysiology of pseudohypoparathyroidism?

A

End organ resistance to PTH due to mutation of the Gs⍺-protein, which is coupled to the PTH receptor

33
Q

What is the presentation of pseudohypoparathyroidism?

A
  • Bone abnormalities (McCune Albright)
  • Obesity
  • Subcutaneous calcification
  • Learning disability
  • Brachydactyly (shortened 4th metacarpal)
34
Q

What are the investigations for pseudohypoparathyroidism

A

Bloods - calcium will be low but PTH concentrations are elevated due to PTH resistance

35
Q

What is pseudo-pseudohypoparathyroidism?

A
  • Describes the phenotypic defects of pseudohypoparathyroidism (Albright’s hereditary osteodystrophy) but without any abnormalities in calcium metabolism
  • Individuals with this condition may share the same gene defect as those with pseudohypoparathyroidism and be members of the same families