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After the MSA > Parathyroid gland and calcium > Flashcards

Parathyroid gland and calcium Flashcards

1
Q

What are the cells of the parathyroid gland?

A
  • Chief cells

* Oxyphilic cells

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2
Q

What is the primary action of the parathyroid gland?

A

Maintenance of plasma Ca2+

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3
Q

What increases plasma Ca2+?

A
  • PTH

* Vitamin D3

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4
Q

what decreases plasma Ca2+?

A

Calcitonin

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5
Q

Describe the distribution of Ca2+ in the body

A
  • 99% in the bone and teeth
  • 0.1% in the plasma - 1/2 is free, 45% bound to proteins, 5% chelated to di-carboxylic acids
  • Rest intracellular
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6
Q

What are the physiological functions of Ca2+?

A
  • Prosthetic group for many enzymes and structural proteins
  • Structure of the plasma membrane - needed for the structure of the Na+ channel
  • Excitation coupling in the muscle
  • Excitation-secretion coupling at axonal terminals and in endocrine and exocrine glands
  • Blood coagulation
  • Major intracellular second messenger
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7
Q

What are the symptoms of hypocalcaemia?

A
  • Muscle cramps/twitches
  • Numbness in fingers/toes
  • Brittle nails
  • Irritability
  • Reduced mental capacity
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8
Q

Levels of calcium - hypocalcemia

A
  • Ca<8mg/dl in the plasma

* Less than 1.6mmol/l are lethal

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9
Q

What are the causes of hypocalcemia?

A

no/low PTH:
• Post surgical hypoparathyroidism
• Inherited hypoparathyroidism

Signalling mechanism of PTH disrupted:
• Pseudo-hypoparathyroidism
• Pseudo-pseudo-hypoparathyroidism

• Vitamin D related

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10
Q

Calcium levels - hypercalcemia

A
  • Total plasma calcium >10.6mg/dl

* Lethal if >3.8mmol/l

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11
Q

What are the symptoms of hypercalcemia?

A
  • Anorexia
  • Various GI tract disturbances
  • Lethargy
  • Depression
  • Confusion
  • Aches/pains
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12
Q

What are the causes of hypercalcemia?

A
  • Hyperparathyroidism/ adenoma in the parathyroid gland or ectopic tumour raising PTH/PTHrP levels
  • High vitamin D intake
  • Familial hypocalciuric hypercalcemia
  • Sarcoidosis/granuloma
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13
Q

Which cell is responsible for PTH release?

A

Chief cells

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14
Q

Describe the release of PTH

A
  • G protein coupled receptor in the chief cell binds calcium
  • This binds to Gq, activates phospholipase C which hydrolyses PIP2-> IP3 + DAG
  • IP3 binds to IP3 receptors which opens calcium channels and calcium then leaves the ER
  • DAG activates protein kinase C which phosphorylates a number of proteins
  • The rise of calcium inhibits the exocytosis of PTH
  • When calcium drops you get constitutive release of PTH
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15
Q

Describe the processing of PTH

A
  • Pre-pro PTH
  • Signal sequence gets cleaved making pro-PTH
  • Then the pro-sequence gets cleaved making PTH which gets secreted
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16
Q

Describe the processing of calcitonin

A
  • In the parafollicular C cells within the thyroid or brain neurones
  • CCP = calcitonin C terminal peptide
  • CGRP= calcitonin gene related peptide - potent neurotransmitter in the brain
  • In the thyroid CCP and calcitonin are synthesised
  • In the brain CGRP is synthesised
17
Q

In which part of the bone does most calcium turnover take place?

A

Trabecular bone on the outside

18
Q

Osteoblasts

A
  • Lay down new bone
  • Secrete osteoid (range of bone proteins - 90% type 1 collagen)
  • Some proteins in osteoid bind calcium and phosphate and promote the development of hydroxyapatite crystal
  • When they are surrounded by bone they become osteoclasts
19
Q

How are osteocytes connected to each other?

A

Canaliculi

20
Q

Describe the action of osteoblasts when the levels of PTH are low

A
  • Osteoblasts (in the presence of vitamin D) secrete osteoid and release calcium and phosphate in high concentrations
  • Hydroxyapatite - collagen fibres and proteins stimulate bone growth
21
Q

Describe the action of osteoblasts when the levels of PTH are high

A
  • Osteoblasts release cytokines e.g. Il-6, RANK ligand, M-CSF
  • Binds to circulating stem cells and causes them to differentiate in to osteoclast precursors and cause osteoclasts-> mononuclear osteoclasts -> RANK)
  • Stimulates bone reabsorption
22
Q

Describe bone resorption by osteoclasts

A
  • Integrins bind to vitronectins on the bone sealing apical surface
  • Bone reabsorption is promoted
  • Increased carbonic anhydrase acid is secreted into the apical surface (HCO3- is exchanged for chloride)
  • Exocytosis of proteolytic enzymes from the cytosol via lysosomes fusing with the apical surface - stimulated by cytokines
  • Collagen is broken down into amino acids
  • Hydroxyapatite is broken down into calcium and phosphate which is taken up into the cell on the apical surface and is released on the basolateral surface into circulation
23
Q

Where do we get vitamin D from?

A

Mainly from the diet, some as a byproduct of cholesterol biosynthesis (in the presence of UV light in the skin)

24
Q

Where do we get vitamin D3 from?

A
  • Milk
  • Eggs
  • Some fish
25
Q

Where do we get vitamin D2 from?

A
  • Mainly plants

* Ergocalciferol

26
Q

What are the enzymes involved in vitamin D metabolism?

A
  • In the liver: a-25 hydroxylase

* In the kidney 1 hydroxylase

27
Q

Describe the intestinal absorption of Ca2+

A
  • In the intestine, the uptake of calcium is dependent on vitamin D3/D2- it stimulates the synthesis of proteins needed for calcium uptake and calbindin
  • Ca2+ is accumulated in the cytosol by binding to calbindin which transmits the calcium to two places- an ATPase and a calcium exchanger
  • Because of calbindin, free intracellular Ca2+ remains very low
  • Ca2+ is exchanged for 3 Na+ at the calcium exchanger and for a H+ (and ATP-> ADP) at the ATPase
28
Q

Describe the intestinal absorption of phosphate

A
  • Co-transporter: 2Na+ and HPO4 2-

* unknown ion channel transports HPO42- or H2PO4- out of the cell into the interstitial fluid

After the MSA (22 decks)

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