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CEP > Parathyroid Hormone, Calcium And Bone > Flashcards

Parathyroid Hormone, Calcium And Bone Flashcards

1
Q

The function of bones:

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

What is the percentage of calcium in bones?

A

99%

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3
Q

What is the role of soluble calcium?

A
  1. Excitable tissue
  2. Muscle/ nerve
  3. Cell Adhesion
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4
Q

What hormones regulate soluble calcium in the body?

A

PTH
Vitamin D
FGF23

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5
Q

What percentage of calcium is free and what percentage is bound to albumin?

A

50% of serum calcium “free” (ionised)
50% bound to albumin (so cannot diffuse into cells)

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6
Q

What is the serum calcium concentration?

A

2.1-2.6 mM

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7
Q

What hormone stimulates calcium absorption from the gut?

A

Vitamin D

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8
Q

What hormone stimulates reabsorption of calcium from the kidney?

A

All the hormones
PTH
Vitamin D
FGF23

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9
Q

What hormone controls release of calcium from the bones?

A

PTH
Vitamin D

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10
Q

Calcium physiology of the bone (calcium input and output)

A

1.0g of calcium
- 0.5 g input per day
- 0.5 g output per day

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11
Q

Calcium physiology of the kidney (input and output)

A

10 gday input
9.8 g/day reabsorbed
0.2 g/day urinary excretion

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12
Q

Calcium physiology of the intestine (input and output)

A

1.0 g/day
0.8 g/day into the serum Ca
0.2 g/day excreted

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13
Q

Biological structure of Parathyroid hormone?

A

84 amino acid peptide but biological activity in first 34 amino acids (PTH 1-34), half life 8 mins

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14
Q

What is the normal range of PTH for an adult?

A

1.6 - 6.9 pmol/L

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15
Q

How does PTH cause an effect?

A

Peptide so cant enter cell and acts extrinsically
Binds to cell membrane G protein coupled receptors mainly in kidney and osteoblasts

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16
Q

What are osteoblasts?

A

Allow bone formation

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17
Q

What are osteoclasts?

A

Carry out bone resorption
Bone cells that break down the tissue in bones and release minerals
Resulting in transfer of calcium in bones into the blood

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18
Q

Mechanism that occurs when someone is hypocalcaemic?

A

Increase in PTH secretion
Acts on kidney and increase in urinary phosphate and decrease in urinary calcium output
Stimulates active form of vitamin D (1,25D3)
Intestine increase in calcium and phosphate absorption
Last resort- stimulates burn turnover (bone resorption)

These actions increase serum calcium

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19
Q

What are the actions of PTH?

A

Acts mainly to restore calcium levels at the cost of phosphate levels
Acts at the level of the kidney

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20
Q

What are the effects of 1,25D3?

A

Wide spread effect
Increases both Ca and PO4 levels
Acts at the level of the intestine

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21
Q

What is the precursor form of vitamin D?

A

7-dehydrocholestrol

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22
Q

What do the numbers after the name reflect about the properties of vitamin D

A

Reflect the origin of the vitamin D
E.g.
Vitamin D2 - the 2 shows its of plant origin (ergocalciferol)
Vitamin D3 - the 3 shows its of animal origin (cholecalciferol)

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23
Q

What does the number before the vitamin D reflect?

A

Represent the hydroxylations of the vitamin D
Hydroxyl groups change biological activity of vit D - make it more active

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24
Q

How does 1,25D3 act on cells?

A

Similar to steroid hormones so bind to VDR nuclear receptors intrinsically
Acts as a transcription regulator

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25
Q

How is the level of vitamin D in the body measured?

A

Inactive form 25D3 measured
Because easier and cheaper

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26
Q

What is the normal range of vit D in the body?

A

Still an ongoing debate
But should be more than 50nmols/L

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27
Q

What are a persons sources of VIT D

A
  • UV radiation
  • Diet (fish eggs)
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28
Q

How is Vit D obtained from UV radiation ?

A

Skin has 7-dehydrocholestrol molecule
That converts UV to vit D3
Then vitamin D3 transported to liver via the blood
Liver converts D3 into inactive 25D3
PTH then activates 25D3 in kidney to 1,25D3

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29
Q

How does negative feedback loop work to maintain optimum serum calcium levels?

A

There are 2 feedback loops
1. When increased PTH secretion activates more 1,25D3 production it feedbacks and switches off PTH secretion
2. When serum calcium increases it feedbacks and decreases PTH secretion

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30
Q

What cells secrete calcitonin

A

Parafollicular (C-cells)
In the thyroid

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31
Q

When is calcitonin secreted?

A

During hypercalcemia
Inhibits bone resorption (inhibits parathyroid effect) by direct effect on osteoclasts

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32
Q

Is calcitonin essential to life?

A

No
Because even post thyroidectomy there are no calcium problems
Unless there is a massive spike in calcium

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33
Q

What are the two ways in which calcitonin lowers calcium levels?

A

Major effect: inhibits osteoclast activity which breaks down the bone
Minor effect: inhibits renal tubular cell reabsorption of calcium and PO4 so excreted in the urine

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34
Q

Mechanism that occurs during hypercalcaemia?

A

Increased secretion of calcitonin
Stops bone resorption by directly acting on osteoclasts

Also decreased PTH secretion
Decrease in urinary phosphate and increase in urinary calcium
Decrease in 1,25D3 production which decreases calcium and PO4 absorption in intestine

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35
Q

Where does absorption of Ca and PO4 occur?

A

In intestines

36
Q

Which areas of the body help control calcium and PO4 levels

A

Thyroid (calcitonin) and parathyroid (PTH) glands
Kidney - excretion of ions and activation of vit D (1,25D3)
Intestine - absorption of ions
Bone - calcium reservoir

37
Q

Where is fibroblast growth factor 23 (FGF23) produced?

A

Produced by bone cells (osteocytes and maybe osteoblasts)

38
Q

When is FGF23 released?

A

Released in response to high serum PO4

39
Q

What are the 2 effects of FGF23

A
  1. Increases renal excretion of PO4
  2. Suppresses renal synthesis of active vitamin D (1,25D3)
40
Q

What is the main inducer of FGF23

A

1,25D3 through feedback control

41
Q

Mechanism that happens in response to hyperphosphataemia?

A

Osteocytes sense high phosphate and increases secretion of FGF23
Stimulates increase in PO4 urinary output
And decreases 1,25D3 production
This decreases serum PO4 levels

PTH secretion increases due to impression of low serum calcium levels

42
Q

What kind of hormones are PTH and vitamin D

A

PTH peptide hormone
Vit D steroid hormone

43
Q

4 bone and mineral disorders:

A
  1. Primary hyperparathyroidism
  2. Rickets/ osteomalacia
  3. Secondary hyperparathyroidism
  4. Osteoporosis
44
Q

What causes primary hyperparathyroidism?

A

Parathyroid tumour (usually benign adenoma

45
Q

What are the effects of primary hyperparathyroidism?

A

Causes hypercalcaemia and low serum phosphate
Loss of negative feedback so PTH constantly secreted

46
Q

How is primary hyperparathyroidism treated?

A

Surgery
Removal of tumour

47
Q

Clinical features of primary hyperparathyroidism

A

Neuro: Lethargy/ confusion
Renal: Thirst/ Polyuria, renal stones
GI: Constipation, pancreatitis
Rheumatic: Joint pain, fracture
Neuropsychiatric: Depression
Cardiac: Hypertension

48
Q

Rheumatic meaning?

A

an umbrella term that refers to arthritis and several other conditions that affect the joints, tendons, ligaments, bones, and muscles (arthritis refers to disorders that mainly affect the joints).

49
Q

The effects of no negative feedback loop:

A

PTH secretion not switched off
Increased PO4 urinary output
Decreased urinary Ca
Increased 1,25D3 production hence increased absorption of calcium and phosphate
Increased bone resorption as well

50
Q

Where is calcium and PO4 absorbed from

A

Intestines due to action pf 1,25D3

51
Q

Effect of increased PTH?

A

Increases bone resorption
Increases urinary PO4
Decreases urinary Ca
Increases prod. Of 1,25D3 hence increases absorption of Ca and PO4 in the intestine

52
Q

What happens during rickets

A

Lack of mineralisation of collagen component of bone (osteoid)
Failure to absorb sufficient calcium from the GI tract - hypocalcaemia

53
Q

Difference btw rickets and osteomalacia

A

Rickets - affects growing skeleton (children)
Osteomalacia - affects adult skeleton
Bone unduly soft in both situations

54
Q

What causes rickets?

A
  1. Dietary/ lack of sunlight
  2. Mutations in vit D receptor VDR
  3. 1 alpha-hydroxylase defects (enzyme that prod. 1,25D3)
  4. X linked hypophosphataemic rickets (affects males only)
55
Q

Hows is vitamin D activated in the body?

A

Vitamin D obtained from sun exposure, foods, and supplements is biologically inert and must undergo two hydroxylations in the body for activation.
- first hydroxylation, which occurs in the liver, converts vitamin D to 25D3
- second hydroxylation occurs primarily in the kidney and forms the physiologically active 1,25D3

56
Q

What are the clinical effects of Rickets?

A
  • Osteoid at growth plate is weak
    Causes bow legs
  • growth plate expands to compensate
    Swollen joints
57
Q

What is osteoid?

A

The unmineralised component of a bone

58
Q

Clinical effects of osteomalacia

A
  • Bone pain
  • Psuedofractures
    Because bones fully grown in adults
59
Q

Treatment for rickets and osteomalacia?

A

Vitamin D replacement (dietary or sunlight)

60
Q

What is the primary defect of rickets/ osteomalacia?

A

Insufficient vitamin D
Hence insufficient 1,25D3

61
Q

What is secondary hyperparathyroidism?

A

Secondary to renal disease not due to primary defect in parathyroid glands

This condition causes chronic low calcium levels in your blood and your parathyroid glands have to work extra hard to try to raise your blood calcium level and release more parathyroid hormone. Tests will usually show a raised level of parathyroid hormone and a low blood calcium level.

Phosphate may be high because kidneys cant remove it

62
Q

How to treat secondary hyperparathyroidism?

A
  1. Phosphate binders (prevent body from absorbing phosphorus from food)
  2. Vitamin D analogues (synthetic form of 1,25D3)
63
Q

How does secondary hyperparathyroidism cause bone loss?

A

Renal disease causes decrease in 1,25D3
Which causes hypocalcaemia
Which increases PTH secretion
Which causes increases in bone turnover

64
Q

How does each bone disease affect the bones specifically?

A

Primary hyperparathyroidism - increase PTH secretion causes bone resorption
Rickets - lack of Bone mineralisation of the bone due to low vit D
Secondary - renal disease increases PTH secretion so increased Bone turnover
Osteoporosis - lack of bone density both mineral and non mineral. Normal bone but less of it.

65
Q

What marker is used to identify Renal disease?

A

FGF23
Increased secretion due to high serum PO4
Less urinary output from kidneys because they are unfunctional

66
Q

Definition of hypophosphatemia

A

Blood of low levels of serum PO4

67
Q

What is oncogenous osteomalacia?

A

Benign tumour in the body
That secretes FGF23
And causes hypophosphatemia
Also low serum 1,25D3

68
Q

What is X linked hypophosphataemia?

A

PHEX targets FGF23
Mutations on the PHEX gene lead to elevated FGF23 and suppressed 1,25D3

69
Q

What is the role of PHEX

A

Breaks down FGF23

70
Q

What is the most common bone disease?

A

Loss of bone mass/ density = mineral and non mineral bone decreased
Normal bone but less of it

71
Q

Osteoporosis leads to increased fracture risk where?

A

Wrist
Spine
Hip

72
Q

3 scenarios in which osteoporosis can occur?

A
  1. Osteoporosis of aging
  2. Post menopausal osteoporosis - due to decline in oestrogen
  3. Steroid enhanced osteoporosis - e.g. glucocorticoids such as prednisolone as a therapy for inflammatory diseases
73
Q

How does oestrogen affect bone health?

A

Activates osteoblasts which produce bone
Inhibits bone resorption

74
Q

Post menopausal osteoporosis?

A

Decline in oestrogen
Causes increased bone resorption
More loss of bone minerals
So more susceptible to fractures

75
Q

Is peak in bone strength bigger in male or females?

A

Males

76
Q

Is age range of fracture threshold bigger in males or females?

A

Females
More susceptible to osteoporosis because of menopause

77
Q

What is a kyphotic spine?

A

Curvature of spine that makes top of back more rounded

78
Q

Treatment of osteoporosis?

A
  1. Hormone replacement - oestrogen
  2. Inhibition of osteoclast development - Denosumab
  3. Inhibition of osteoclast activity - biphosphonates
  4. Stimulation of osteoblast activity - intermittent use of PTH
79
Q

What does oestrogen deficiency do to the bones?

A

Increases bone remodels and bone resorption

80
Q

How does denosumab work to treat osteoporosis?

A

Rank ligand antibody
Blocks rank ligands on osteoblasts from interacting with rank on osteoclasts
Resulting in decreased differentiation of pre-osteoclasts

81
Q

What are some types of biphosphonates?

A

Etidronate
Risedronate
Clodronate
Alendronate

82
Q

How do biphosphonates work to treat osteoporosis

A

Disrupt Intracellular enzymes required for osteoclast activity
Which decrease bone resorption

83
Q

How can intermittent use of PTH be used to treat osteoporosis

A

Anabolic
Stimulates osteoblasts> osteoclasts
Tetriparatide - first 34 amino acids of PTH is anabolic stimulator for bone formation

84
Q

Osteoporosis prevention options:

A
  1. Diagnosis of osteoporosis risk is made based on assessment of low Bone Mineral Density (BMD) using DEXA or ultrasound and laboratory investigations. Optimal BMD may prevent osteoporotic fracture
  2. Exercise - enhances osteocyte activity through bone stress
  3. Vitamin D and Calcium - help maintain general bone health
  4. Avoid smoking and high alcohol alcohol intake
85
Q

What is hyperparathyroidism?

A

Increased secretion of PTH

86
Q

Why is negative feedback important in calcium homeostasis?

A

Because increased PTH secretion increases bone resorption which can compromise the bone

87
Q

Causes of secondary hyperparathyroidism

A
  • If you have an intestinal or gut condition, such as Crohn’s Disease, you may have a problem absorbing calcium from your food into your blood causing persistently low calcium levels.
  • Vitamin D deficiency (which can cause rickets in children or osteomalacia in adults) is another common cause of chronic low level of calcium in your blood.
  • The most common cause of Secondary Hyperparathyroidism is kidney disease. It occurs in nearly all people who are on long-term kidney dialysis because of kidney failure. Because you have kidney failure, your blood calcium level can become chronically low.

CEP (12 decks)

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