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Parathyroid Hormone, Calcium And Bone Flashcards

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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
How is the level of vitamin D in the body measured?
Inactive form 25D3 measured Because easier and cheaper
26
What is the normal range of vit D in the body?
Still an ongoing debate But should be more than 50nmols/L
27
What are a persons sources of VIT D
- UV radiation - Diet (fish eggs)
28
How is Vit D obtained from UV radiation ?
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
29
How does negative feedback loop work to maintain optimum serum calcium levels?
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
30
What cells secrete calcitonin
Parafollicular (C-cells) In the thyroid
31
When is calcitonin secreted?
During hypercalcemia Inhibits bone resorption (inhibits parathyroid effect) by direct effect on osteoclasts
32
Is calcitonin essential to life?
No Because even post thyroidectomy there are no calcium problems Unless there is a massive spike in calcium
33
What are the two ways in which calcitonin lowers calcium levels?
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
34
Mechanism that occurs during hypercalcaemia?
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
35
Where does absorption of Ca and PO4 occur?
In intestines
36
Which areas of the body help control calcium and PO4 levels
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
Where is fibroblast growth factor 23 (FGF23) produced?
Produced by bone cells (osteocytes and maybe osteoblasts)
38
When is FGF23 released?
Released in response to high serum PO4
39
What are the 2 effects of FGF23
1. Increases renal excretion of PO4 2. Suppresses renal synthesis of active vitamin D (1,25D3)
40
What is the main inducer of FGF23
1,25D3 through feedback control
41
Mechanism that happens in response to hyperphosphataemia?
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
What kind of hormones are PTH and vitamin D
PTH peptide hormone Vit D steroid hormone
43
4 bone and mineral disorders:
1. Primary hyperparathyroidism 2. Rickets/ osteomalacia 3. Secondary hyperparathyroidism 4. Osteoporosis
44
What causes primary hyperparathyroidism?
Parathyroid tumour (usually benign adenoma
45
What are the effects of primary hyperparathyroidism?
Causes hypercalcaemia and low serum phosphate Loss of negative feedback so PTH constantly secreted
46
How is primary hyperparathyroidism treated?
Surgery Removal of tumour
47
Clinical features of primary hyperparathyroidism
Neuro: Lethargy/ confusion Renal: Thirst/ Polyuria, renal stones GI: Constipation, pancreatitis Rheumatic: Joint pain, fracture Neuropsychiatric: Depression Cardiac: Hypertension
48
Rheumatic meaning?
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
The effects of no negative feedback loop:
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
Where is calcium and PO4 absorbed from
Intestines due to action pf 1,25D3
51
Effect of increased PTH?
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
What happens during rickets
Lack of mineralisation of collagen component of bone (osteoid) Failure to absorb sufficient calcium from the GI tract - hypocalcaemia
53
Difference btw rickets and osteomalacia
Rickets - affects growing skeleton (children) Osteomalacia - affects adult skeleton Bone unduly soft in both situations
54
What causes rickets?
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
Hows is vitamin D activated in the body?
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
What are the clinical effects of Rickets?
- Osteoid at growth plate is weak Causes bow legs - growth plate expands to compensate Swollen joints
57
What is osteoid?
The unmineralised component of a bone
58
Clinical effects of osteomalacia
- Bone pain - Psuedofractures Because bones fully grown in adults
59
Treatment for rickets and osteomalacia?
Vitamin D replacement (dietary or sunlight)
60
What is the primary defect of rickets/ osteomalacia?
Insufficient vitamin D Hence insufficient 1,25D3
61
What is secondary hyperparathyroidism?
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
How to treat secondary hyperparathyroidism?
1. Phosphate binders (prevent body from absorbing phosphorus from food) 2. Vitamin D analogues (synthetic form of 1,25D3)
63
How does secondary hyperparathyroidism cause bone loss?
Renal disease causes decrease in 1,25D3 Which causes hypocalcaemia Which increases PTH secretion Which causes increases in bone turnover
64
How does each bone disease affect the bones specifically?
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
What marker is used to identify Renal disease?
FGF23 Increased secretion due to high serum PO4 Less urinary output from kidneys because they are unfunctional
66
Definition of hypophosphatemia
Blood of low levels of serum PO4
67
What is oncogenous osteomalacia?
Benign tumour in the body That secretes FGF23 And causes hypophosphatemia Also low serum 1,25D3
68
What is X linked hypophosphataemia?
PHEX targets FGF23 Mutations on the PHEX gene lead to elevated FGF23 and suppressed 1,25D3
69
What is the role of PHEX
Breaks down FGF23
70
What is the most common bone disease?
Loss of bone mass/ density = mineral and non mineral bone decreased Normal bone but less of it
71
Osteoporosis leads to increased fracture risk where?
Wrist Spine Hip
72
3 scenarios in which osteoporosis can occur?
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
How does oestrogen affect bone health?
Activates osteoblasts which produce bone Inhibits bone resorption
74
Post menopausal osteoporosis?
Decline in oestrogen Causes increased bone resorption More loss of bone minerals So more susceptible to fractures
75
Is peak in bone strength bigger in male or females?
Males
76
Is age range of fracture threshold bigger in males or females?
Females More susceptible to osteoporosis because of menopause
77
What is a kyphotic spine?
Curvature of spine that makes top of back more rounded
78
Treatment of osteoporosis?
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
What does oestrogen deficiency do to the bones?
Increases bone remodels and bone resorption
80
How does denosumab work to treat osteoporosis?
Rank ligand antibody Blocks rank ligands on osteoblasts from interacting with rank on osteoclasts Resulting in decreased differentiation of pre-osteoclasts
81
What are some types of biphosphonates?
Etidronate Risedronate Clodronate Alendronate
82
How do biphosphonates work to treat osteoporosis
Disrupt Intracellular enzymes required for osteoclast activity Which decrease bone resorption
83
How can intermittent use of PTH be used to treat osteoporosis
Anabolic Stimulates osteoblasts> osteoclasts Tetriparatide - first 34 amino acids of PTH is anabolic stimulator for bone formation
84
Osteoporosis prevention options:
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
What is hyperparathyroidism?
Increased secretion of PTH
86
Why is negative feedback important in calcium homeostasis?
Because increased PTH secretion increases bone resorption which can compromise the bone
87
Causes of secondary hyperparathyroidism
- 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.

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