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CEP > L15 - Calcium and parathyroid gland > Flashcards

L15 - Calcium and parathyroid gland Flashcards

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?

A

FGF23 produced by bone cells (osteocytes and maybe osteoblasts)

22
Q

What is the action of FGF23?

A

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

23
Q

When is FGF23 released?

A

Released in response to high serum PO4

- Main inducer of FGF23 is 1,25D3

24
Q

What is bone made of?

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
Q

What are some examples of non-collagenous protein?

A
  1. Osteocalcin
  2. Osteonectin
  3. Osteopontin
26
Q

What are osteocytes?

A
  • Embedded in calcified bone matrix

- Have long processes which contact other osteocytes and osteoblasts

27
Q

What are osteoblasts?

A
  • Bone forming cells which produce matrix constituents and aid calcification
  • Originate from mesenchymal stem cells (bone marrow stem cells or CT mesenchymal cells)
28
Q

What are osteoclasts?

A
  • 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
Q

What are the classical markers of osteoblasts?

A
  • Alkaline phosphatase

- Osteocalcin

30
Q

What are the classical markers of osteoclasts?

A
  • Carbonic anhydrase
  • Tartrate-resistant acid phosphatase (TRAP)
  • Receptor for RANK ligand (RANK)
  • Calcitonin receptor
31
Q

What happens in the activation phase of the bone remodelling cycle (trabecular bone)?

A
  1. Pre-osteoclasts are attracted to the remodelling sites

2. Pre-osteoclasts fuse to form multinucleated osteoclasts

32
Q

What happens in the resorption phase of the bone remodelling cycle (trabecular bone)?

A
  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
Q

What happens in the reversal phase of the bone remodelling cycle (trabecular bone)?

A
  1. Mesenchymal stem cells, pre-cursors to osteoblasts, appear along the burrow or pit where they
  2. Proliferate and differentiate into pre-osteoblasts
34
Q

What happens in the formation phase of the bone remodelling cycle (trabecular bone)?

A
  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
Q

What happens in the quiescence phase of the bone remodelling cycle (trabecular bone)?

A
  1. The remodelling site (now new bone tissue) remains dormant until the next cycle
36
Q

What is primary hyperparathyroidism?

A
  • Parathyroid tumour (usually benign adenoma)
  • Causes hypercalcaemia and low serum phosphate
  • Loss of negatve feedback from hypercalcaemia
37
Q

What is secondary hyperparaythyroidism?

A
  • 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
Q

What would the treatment for primary hyperparathyroidism be?

A

Surgery

39
Q

What would the treatment for secondary hyperparathyroidism be?

A

Phosphate binders or vitamin D analogues

40
Q

What is tertiary hyperparathyroidism?

A
  • Long-standing secondary HPT leads to irreversible parathyroid hyperplasia
  • Usually seen when renal disease corrected e.g. by transplantation
41
Q

What would the treatment for tertiary hyperparathyroidism be?

A

Surgery

42
Q

What are the clinical features of primary HPT?

A
  1. Lethargy/ confusion
  2. Thirst/ polyuria
  3. Renal stones
  4. Constipation
  5. Pancreatitis
  6. Joint pain
  7. Fracture
  8. Depression
  9. Hypertension
43
Q

What is the difference between osteomalacia (rickets) and osteoporosis?

A
  • 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
Q

Cause of osteomalacia?

A
  • Failure to absorb sufficient calcium from the GIT
  • Dietary/ lack of sunlight
  • Rarely inherited
  • Leads to bone pain and pseudofractures
45
Q

Cause of rickets?

A
  • Osteoid at growth plate is weak leading to bow legs

- Growth plate expands to compensate (swollen joints)

46
Q

What treatment would be given to a patient with rickets/ osteomalacia?

A

Vitamin D replacement (dietary or through sunlight)

47
Q

What is osteoporosis of ageing?

A

Male and females show gradual decline in bone density from early adult peak

48
Q

What is postmenopausal osteoporosis?

A

Rapid decline in female bone density following decline in oestrogen at menopause

49
Q

What is the consequence of oestrogen deficiency?

A

Increases bone remodelling and bone resorption

50
Q

What is the treatment of osteoporosis?

A
  • Hormone replacement (oestrogen)
  • Bisphosphates osteoclast poisons)
  • Denosumab (RANK ligand antibody)
  • PTH (but only intermittent)
  • These treatments reduce bone remodelling

CEP (16 decks)

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