Hyperparathyroidism Flashcards

1
Q

Which cells produce PTH

A

Chief cells in the glands, produce parathyroid hormone in response to hypocalcaemia (low blood calcium).

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2
Q

How does PTH raise blood calcium

A

Increasing osteoclast activity in bones (reabsorbing calcium from bones)

Increasing calcium absorption from the gut

Increasing calcium absorption from the kidneys

Increasing vitamin D activity

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3
Q

How does vitamin D increase blood calcium levels

A

Acts to increase calcium absorption from the intestines.

Parathyroid hormone acts on vitamin D to convert it into active forms. So vitamin D and parathyroid hormone act together to raise blood calcium levels.

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4
Q

Symptoms of hypercalcaemia

A

Renal stones
Painful bones
Abdominal groans refers to symptoms of constipation, nausea and vomiting

Psychiatric moans refers to symptoms of fatigue, depression and psychosis

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5
Q

What is primary hyperparathyroidism caused by

A

Uncontrolled parathyroid hormone produced directly by a tumour of the parathyroid glands.

This leads to hypercalcaemia

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6
Q

How is primary hyperparathyroidism treated

A

Surgical removal of tumour

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7
Q

What is secondary hyperparathyroidism

A

Where 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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8
Q

Why is there raised PTH in secondary hyperparathyroidism

A

The parathyroid glands reacts to the low serum calcium by excreting more parathyroid hormone.

Over time the total number of cells in the parathyroid glands increase as they respond to the increased need to produce parathyroid hormone.

This is called hyperplasia. The glands become more bulky. The serum calcium level will be low or normal but the parathyroid hormone will be high.

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9
Q

How is secondary parathyroidism treated

A

Correcting the vitamin D deficiency or performing a renal transplant to treat renal failure.

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10
Q

What causes tertiary hyperparathyroidism

A

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

It leads to hyperplasia of the glands. The baseline level of parathyroid hormone increases dramatically.

Then when the cause of the secondary hyperparathyroidism is treated the parathyroid hormone level remains inappropriately high.

This high level of parathyroid hormone in the absence of the previous pathology leads to high absorption of calcium in the intestines, kidneys and bones and causes hypercalcaemia.

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11
Q

How is tertiary hyperparathyroidism treated

A

Surgically removing part of the parathyroid tissue to return the parathyroid hormone to an appropriate level.

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12
Q

Pathophys of paget’s disease of bone

A

There is excessive bone turnover due to excessive activity of both osteoblasts and osteoclasts leading to sclerosis and lysis

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13
Q

Presentation of paget’s disease

A

Bone pain
Bone deformity
Fractures
Hearing loss can occur if it affects the bones of the ear

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14
Q

X-ray findings in paget’s disease of the bone

A

Bone enlargement and deformity
Osteoporosis circumscripta
Cotton wool appearance of skull
V-shaped defects

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15
Q

What is osteoporosis circumscripta

A

Describes well defined osteolytic lesions that appear less dense compared with normal bone

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16
Q

What does cotton wool appearance of skull in paget’s disease refer to

A

describes poorly defined patchy areas of increased density (sclerosis) and decreased density (lysis)

17
Q

What are V-shaped defects in Paget’s disease of the bone

A

“V-shaped defects” in the long bones are V shaped osteolytic bone lesions within the healthy bone

18
Q

Biochem findings in Paget’s disease of the bone

A

Raised alkaline phosphatase (and other LFTs are normal)
Normal calcium
Normal phosphate

19
Q

Predisposing factors for Paget’s disease of the bone

A

increasing age
male sex
northern latitude
family history

20
Q

Management of Paget’s disease of the bone

A

Bisphosphonates
NSAIDs for bone pain
Calcium and vitamin D supplements
Surgery rarely

21
Q

Complications of Paget’s disease of the bone

A
deafness (cranial nerve entrapment)
osteosarcoma 
fractures
skull thickening
high-output cardiac failure
Spinal stenosis
22
Q

Initial management of hypercalcaemia

A

IV fluid therapy(3-4l/day)

Following rehydration bisphosphonates may be used

23
Q

Other options for management of hypercalcaemia

A

calcitonin - quicker effect than bisphosphonates

steroids in sarcoidosis

24
Q

What is osteomalacia

A

Osteomalacia is a condition where there is defective bone mineralisation causing “soft” bones

This results from insufficient vitamin D

25
Q

What are looser zones

A

Fragility fractures that go partially through the bone

26
Q

Risk factors for osteomalacia

A

Darker skin
Low exposure to sunlight
Colder climates
Time indoors

27
Q

Interpretation of serum 25-hydroxyvitamin D levels

A

<25 nmol/L – vitamin D deficiency

25 – 50 nmol/L – vitamin D insufficiency

75 nmol/L or above is optimal

28
Q

Treatment of osteomalacia

A

Treatment is with supplementary vitamin D