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CEP > L15 - Calcium and parathyroid gland > Flashcards

L15 - Calcium and parathyroid gland Flashcards

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1
Q

What is the function of bone?

A
  1. Protect vital organs
  2. Support muscles
  3. Reservoir or calcium
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2
Q

What is the percentage composition of calcium like?

A
  • 50% of serum calcium free (ionised)

- 50% bound to albumin (so cannot diffuse into cells)

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3
Q

What are the actions of parathyroid hormone?

A
  1. INC calcium reabs in renal distal tubule
  2. INC intestinal calcium abs (via activation of vitamin D)
  3. INC calcium release from bone (stimulates osteoclast activity)
  4. DEC phosphate reabs
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4
Q

Parathyroid hormone is secreted in response to what?

A
  1. Low calcium

2. High phosphate

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5
Q

Function of parathyroid glands?

A

Regulate calcium and phosphate levels

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6
Q

What happens when there is increased PTH secretion from parathyroid glands in hypocalcaemia?

A 
Bone: 
- INC bone resorption
Kidney: 
- INC urinary phosphate
- DEC urinary calcium
- INC 1,25D3 production
Intestine: 
- INC calcium absorption
- INC phosphate absorption

–> INC SERUM ACLCIUM

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7
Q

What is parathyroid hormone?

A
  • 84 aa peptide but biological activity in first 34 aa
  • Half life of 8 mins
  • Cleaved to smaller peptides
  • Assayed by two site assay (to avoid detecting fragments)
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8
Q

How does PTH work?

A

Binds to GPCR mainly in kidney and osteoblasts

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9
Q

What is the effect of PTH in the kidneys?

A
  1. PTH inc distal tubule reabs of calcium
    - Inhibition of PO4 reabs
  2. Stimulates prod of active form of vit D (1,25D3)
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10
Q

What is the negative feedback relating to PTH?

A
  1. PTH transcription (mRNA production) in inhibited by 1,25D3
  2. PTH translation (mRNA to protein synthesis) s inhibited by increased serum calcium
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11
Q

What is bone resorption?

A

The process by which osteoclasts break down the tissue in bones and release the minerals, resulting in a transfer of calcium from bone tissue to the blood

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12
Q

What is the precursor form of vitamin D?

A

25D3

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13
Q

What is the origin of vitamin D2 and vitamin D3?

A

D2 = Plant origin
D3 = Animal origin
- Numbers after name reflect origin

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14
Q

What do the numbers before the name of vitamin D mean?

A

Numbers before the name reflect changes (hydroxylations) in vitamin D that dramatically change its biological activity (1,25D3 binds to the vitamin D receptor VDR - a steroid hormone receptor)

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15
Q

What are the different sources of vitamin D?

A
  1. UV radiation

2. Diet: eggs and fish

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16
Q

Where does vitamin D get converted into its active form?

A

In the kidneys

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17
Q

Which cells produce calcitonin?

A

Calcitonin is produced by thyroid C-cells (parafollicular)

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18
Q

When is calcitonin released?

A

Calcitonin released in HYPERcalcaemia

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19
Q

What is the function of calcitonin?

A

Opposes the action of PTH

  • Inhibits bone resorption by direct effect on osteoclasts
  • Not essential to life (post thyroidectomy no calcium problems)
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20
Q

What is FGF23 (fibroblast growth factor 23)?

A
  • Protein coded by FGF23 gene

- Responsible for phosphate and vit D metabolism

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21
Q

Which cells produce FGF23?

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A

FGF23 produced by bone cells (osteocytes and maybe osteoblasts)

22
Q

What is the action of FGF23?

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A

Increases renal excretion of PO4 and suppresses renal synthesis of active vitamin D (1,25D3)

23
Q

When is FGF23 released?

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A

Released in response to high serum PO4

- Main inducer of FGF23 is 1,25D3

24
Q

What is bone made of?

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A
  • Specialised CT
  • Extracellular matrix which is able to calcify
  • Collagen fibres with preferential orientation (approx 90% of protein content)
  • Non-collagenous proteins essential to bone function
  • Contains several types of cells
  • Calcification occurs with formation of HYDROXYAPATITE crystals
25
What are some examples of non-collagenous protein?
1. Osteocalcin 2. Osteonectin 3. Osteopontin
26
What are osteocytes?
- Embedded in calcified bone matrix | - Have long processes which contact other osteocytes and osteoblasts
27
What are osteoblasts?
- Bone forming cells which produce matrix constituents and aid calcification - Originate from mesenchymal stem cells (bone marrow stem cells or CT mesenchymal cells)
28
What are osteoclasts?
- Bone resorbing cells - Usually found in contact with calcified bone surface - in lacunae (cavity/ depression in bone) - Multinucleated - originate from bone marrow lineage - Produce acid (to resorb mineral) and enzymes (to resorb matrix) - Attachment to bone v important - integrins
29
What are the classical markers of osteoblasts?
- Alkaline phosphatase | - Osteocalcin
30
What are the classical markers of osteoclasts?
- Carbonic anhydrase - Tartrate-resistant acid phosphatase (TRAP) - Receptor for RANK ligand (RANK) - Calcitonin receptor
31
What happens in the activation phase of the bone remodelling cycle (trabecular bone)?
1. Pre-osteoclasts are attracted to the remodelling sites | 2. Pre-osteoclasts fuse to form multinucleated osteoclasts
32
What happens in the resorption phase of the bone remodelling cycle (trabecular bone)?
1. Osteoclasts dig out a cavity, called a RESORPTION PIT, in spongy bone or burrow a tunnel in compact bone 2. Calcium can be released into the blood for use in various body functions 3. Osteoclasts disappear
33
What happens in the reversal phase of the bone remodelling cycle (trabecular bone)?
1. Mesenchymal stem cells, pre-cursors to osteoblasts, appear along the burrow or pit where they 2. Proliferate and differentiate into pre-osteoblasts
34
What happens in the formation phase of the bone remodelling cycle (trabecular bone)?
1. The pre-osteoblasts mature into osteoblasts at the surface of the burrow or pit 2. Release osteoid at the site, forming a new soft non-mineralised matrix 3. The new matrix is mineralised with collagen, calcium and phosphorus thus creating the new bone
35
What happens in the quiescence phase of the bone remodelling cycle (trabecular bone)?
1. The remodelling site (now new bone tissue) remains dormant until the next cycle
36
What is primary hyperparathyroidism?
- Parathyroid tumour (usually benign adenoma) - Causes hypercalcaemia and low serum phosphate - Loss of negatve feedback from hypercalcaemia
37
What is secondary hyperparaythyroidism?
- Disease outside parathyroid gland - Kidney damaged from renal disease --> cannot reabs Ca and excrete PO4 --> dec Ca and inc PO4 IN BLOOD --> HYPOcalcaemia/ HYPERphosphataemia --> PTH released --> BUT, kidney damaged, therefore PTH no effect, keep secreting PTH --> leading to HYPERparathyroidism - When kidney dmged, leads to dec activation of vit D as it normally occurs in the kidneys (therefore dec active vit D)
38
What would the treatment for primary hyperparathyroidism be?
Surgery
39
What would the treatment for secondary hyperparathyroidism be?
Phosphate binders or vitamin D analogues
40
What is tertiary hyperparathyroidism?
- Long-standing secondary HPT leads to irreversible parathyroid hyperplasia - Usually seen when renal disease corrected e.g. by transplantation
41
What would the treatment for tertiary hyperparathyroidism be?
Surgery
42
What are the clinical features of primary HPT?
1. Lethargy/ confusion 2. Thirst/ polyuria 3. Renal stones 4. Constipation 5. Pancreatitis 6. Joint pain 7. Fracture 8. Depression 9. Hypertension
43
What is the difference between osteomalacia (rickets) and osteoporosis?
- Osteomalacia is the lack of mineralisation of collagen component of bone (osteoid) - Osteoporosis is the loss of bone mass/ density (BOTH mineral and osteoid decreased); normal bone but less of it - leads to in fracture risk wrist, spine and hip
44
Cause of osteomalacia?
- Failure to absorb sufficient calcium from the GIT - Dietary/ lack of sunlight - Rarely inherited - Leads to bone pain and pseudofractures
45
Cause of rickets?
- Osteoid at growth plate is weak leading to bow legs | - Growth plate expands to compensate (swollen joints)
46
What treatment would be given to a patient with rickets/ osteomalacia?
Vitamin D replacement (dietary or through sunlight)
47
What is osteoporosis of ageing?
Male and females show gradual decline in bone density from early adult peak
48
What is postmenopausal osteoporosis?
Rapid decline in female bone density following decline in oestrogen at menopause
49
What is the consequence of oestrogen deficiency?
Increases bone remodelling and bone resorption
50
What is the treatment of osteoporosis?
- Hormone replacement (oestrogen) - Bisphosphates osteoclast poisons) - Denosumab (RANK ligand antibody) - PTH (but only intermittent) - These treatments reduce bone remodelling

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