Parathyroid Flashcards

1
Q

What cells secrete parathyroid hormone?

A

Cheif cell

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2
Q

When the parathyroid hormone is produced by parathyroid glands?

A

In response to low calcium (hypocalcaemia)

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3
Q

How does PTH act to increase calcium levels in the blood?

A

Parathyroid hormone acts to raise blood calcium level by:

  • 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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4
Q

Relation of PTH and vitamin D

A
  • Vitamin D 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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5
Q

Primary hyperparathyroidism:

  • cause
  • what happens to Ca++ levels
A

Cause: a tumour in parathyroid gland -> secretion of excess of PTH

Result: hypercalcaemia (high Ca++ in the blood)

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6
Q

Treatment for primary hyperparathyroidism

A

Surgical resection of the tumour

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7
Q

Secondary parathyroidism

  • cause
  • what happens to parathyroid gland
A

Cause: insufficient vitamin D or renal function -> low Ca++ absorption from intestines, kidney and bones

PTH gland responds: production of excess PTH -> hyperplasia of PTH gland -> serum calcium low/normal and PTH high

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8
Q

PTH and Ca++ serum levels in secondary hyperparathyroidism

A
  • PTH - high
  • Ca++ either low or normal (normal if compensated by PTH excess production in response to serum hypocalcaemia that is due to kidney or vit D failure)
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9
Q

Treatment of secondary hyperparathyroidism

A
  • vitamin D replacement
  • renal transplant (if renal failure is a cause)
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10
Q

What’s the cause of tertiary hyperparathyroidism?

What happens to Ca++ levels?

A
  • It is on the background to secondary hyperparathyroidism (when the hyperplasia of PTH gland occurs)
  • In tertiary: even is a cause of secondary hyperparathyroidism is treated -> we will have excess of PTH due to PTH gland hyperplasia
  • Result: high absorption of Ca++ in kidney, intestine and bone -> hypercalcaemia
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11
Q

Treatment for tertiary hyperparathyroidism

A

resection of part of the parathyroid gland

(so less PTH will be produced -> to normalise Ca++ levels)

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12
Q

Primary hyperparathyroidism

  • cause
  • levels: PTH and Ca++
A
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13
Q

Secondary hyperparathyroidism

  • cause
  • levels of PTH and Ca++
A
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14
Q

Tertiary hyperparathyroidism

  • cause
  • levels of PTH and Ca++
A
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15
Q

Primary hypoparathyroidism

  • cause
A

Low PTH secretion

Cause: due to thyroid surgery

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16
Q

Serum levels abnormalities in primary hypoparathyroidism

A

low PTH -> low Ca++ and high phosphate

17
Q

Treatment of primary hypoparathyroidism

A

Alfacalcidol

(vitamin D3)

18
Q

Symptoms of hypoparathyroidism (5)

A

Symptoms are secondary to hypocalcaemia

  • tetany (muscles twitching, camping and spasm)
  • Trousseau sign
  • Chvostek sign
  • chronic: depression, cataracts
  • ECG: prolonged QT interval
19
Q

What are Torsseau and Chvostek signs?

A

Signs of hypocalcaemia

  • Trousseau sign: carpal spasm when brachial a. occluded by inflated BP cuff with pressure above systolic
  • Chvostek sign: tapping over parotid -> facial muscles twitch
20
Q

Pathophysiology of pseudohypoparathyroidism

A
  • abnormality in protein G -> target cells are insensitive to PTH
  • Result: high PTH, low calcium, high phosphate
21
Q

Associations of pseudohypoparathyroidism (symptomatic features)

A
  • low IQ
  • short stature
  • short 4th and 5th metacarpals
22
Q

Diagnosis of pseudohypoparathyroidism

  • investigations
  • result for: a) hypoparathyroidism b) pseudohypoparathyroidism
A

infusion of PTH -> then measuring urinary levels of cAMP and phosphate

a) hypoparathyroidism: infusion of PTH will cause an increase in both cAMP and phosphate
b) pseudohypoparathyroidism: infusion of PTH will not cause an increase in cAMP and phosphate (as target cells not responsive to PTH)

23
Q

What’s pseudopseudohypoparathyroidism?

A

It’s similar phenotype to pseudohypoparathyroidism (abnormalities in G protein and insensitivity to PTH), but normal biochemistry