Parathyroid Flashcards

(39 cards)

1
Q

How many parathyroid glands are there?

A

4

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2
Q

Where are they located in relation to the thyroid gland?

A

Posterior aspect of the thyroid gland

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3
Q

Which cells secrete parathyroid hormone?

A

Chief cells

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4
Q

What kind of hormone is parathyroid hormone?

A

A polypeptide

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5
Q

What is the primary stimulus for parathyroid hormone?

A

Hypocalcaemia

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6
Q

What is the primary inhibitor of parathyroid hormone?

A

Hypercalcaemia

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7
Q

What is another name for a parafollicular cell?

A

C-cells

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8
Q

What are parafollicular cells stimulated by?

A

Hypercalcaemia

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9
Q

What are parafollicular cells inhibited by?

A

Hypocalcaemia

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10
Q

Where is calcitonin produced from?

A

Parafollicular cells (or C -cells)

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11
Q

What do parafollicular cells produce?

A

Calcitonin

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12
Q

What stimulates calcitonin release?

A

Hypercalcaemia

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13
Q

What stimulates parathyroid release?

A

Hypocalcaemia

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14
Q

What is a humoral stimulus?

A

Endocrine function which is controlled by change in electrolytes i.e. hypocalcaemia leading to increased parathyroid release

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15
Q

What kind of stimulus causes calcitonin or parathyroid release?

A

Humoral stimuli (calcium)

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16
Q

How does PTH effect the bone?

A

Increase osteoclastic activity by activating osteoblasts to release Rank-ligand, which stimulates Rank receptors on osteoclasts

17
Q

What doe osteoclasts do?

A

Resorb bone - releases calcium into the blood

18
Q

What do osteoblasts do?

A

Bone deposition - takes calcium from the blood to build bone

19
Q

What is the significance of Rank Ligand to PTH?

A

Released by osteoblasts in response to PTH causing activation of the osteoclasts

20
Q

What is released by increased osteoclastic activity?

A

Phosphate and calcium

21
Q

How does PTH affect the blood biochemistry?

A

Increases phosphate and calcium release via increased osteoclastic activity, increased calcium uptake by kidney (phosphate is excreted) and increased synthesis of active vitamin D causing increased uptake in the GI tract of calcium

22
Q

How does PTH affect the kidney?

A

DCT to reabsorb calcium by secondary active transport + increases phosphate excretion + increases the expression of 1-alpha-hydroxalase

23
Q

What is the overall effect of PTH?

A

To increase calcium in the blood

24
Q

How is cholecalciferol formed?

A

UV light activates 7-dehydrocholestrol to cholecalciferol

25
What happens to cholecalciferol in the liver
Converted to 25-hydroxycholecalciferol via 25-hydroxalase
26
What is the role of 1-alpha-hydroxalase in the kidney?
It hydroxalases 25-hydroxycholecalciferol to | 1,25-cholecalciferol (calcitriol)
27
What is another name for calcitriol?
Vitamin D
28
How is Vitamin D produced?
UV light activates 7-dehydrocholesterol which goes to the liver and is converted to 25-hydroxycholecalciferol, which is converted by the kidney to 1,25-cholecalciferol, otherwise known as calcitriol or vitamin D)
29
What is the role of Vitamin D?
Increase calcium uptake from the gi tract via calcium channel proteins
30
What kind of hormone is vitamin D?
A steroid hormone
31
Which mechanisms cause calcium increase by PTH?
Increased GI uptake via vitamin D, Increased osteoclast activity, Increase resorption of calcium in the kidney
32
What is the overall effect of calcitonin?
Reduces blood calcium
33
What does calcitonin do in the bone?
Directly inhibits osteoclastic activity and thereby increases osteoblastic activity
34
Where do the parathyroid glands develop from in embryological development?
Superior glands - pharyngeal pouch 4 | Inferior glands - pharyngeal pouch 3
35
What is the blood supply to the parathyroid gland?
Inferior and superior thyroid arteries
36
Where is the gene for PTH located?
Chromosome 11
37
What is the main cause of primary hyperparathyroidism?
A solitary adenoma of the parathyroid gland
38
What is the main cause of secondary hyperparathyroidism?
Caused by hypocalcaemia secondary to chronic kidney disease or vitamin D deficiency
39
What is the main cause of tertiary hyperparathyroidism?
Prolonged stimulation leads to hyperplasia of the parathyroid gland and insensitivity to calcium levels. This is seen in end stage renal failiure