Calcium+Phosphate Flashcards

1
Q

What is the most abundant metal in the body?

A

Calcium

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2
Q

What is the storage distribution of calcium like in the body?

A

Unbound’ ionised calcium = biologically active component

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3
Q

What molecules lead to an increase in serum calcium?

A

Parathyroid hormone (PTH) (secreted by parathyroid glands)
Vitamin D
Synthesised in skin or intake via diet
Main regulators of calcium & phosphate homeostasis via actions on kidney, bone and gut

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4
Q

What molecule lead to a decrease in serum calcium?

A

Calcitonin (secreted by thyroid parafollicular cells)
Can reduce calcium acutely, but no negative effect if parafollicular cells are removed eg thyroidectomy

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5
Q

Where is vitamin D2 derived from?

A

Ergocalciferol-Derived from UV irradiation of plants

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6
Q

Where is vitamin D3 derived from?

A

Cholecalciferol-Derived from UV irradiation of skin and certain foods e.g egg yolk

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7
Q

What is a good indicator of vit-D levels that is biologically inactive?

A

Serum 25-OH cholecalciferol

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8
Q

How does 1,25(OH)2 cholecalciferol (calcitriol) regulate its own synthesis?

A

It decreases transcription of 1 alpha-hydroxylase

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9
Q

Give the pathways of 7-dehydrocholesterol and dietary vitamin D2 to 1,25(OH)2 cholecalciferol

A

-UV radiation causes 7-dehydrocholesterol to turn into pre vitamin D3, then into vitamin D3-This moves from skin cells into capillaries

-Vitamin D2 moves into capillaries, converting into vitamin D3

> D3 is converted into 25(OH)cholecalciferol in the liver by 25 hydroxylase
Then into 1,25(OH)2cholecalciferol by 1-a-hydroxylase

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10
Q

What is the active form of vitamin D

A

Calcitriol-Same as 1,25(OH)2-cholecalciferol

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11
Q

What is the major role of calcitriol?

A

Increase Ca2+ and PO4^3- reabsorption from the gut

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12
Q

What cells secrete PTH in parathyroid gland and do they secrete PTH directly?

A

Chief cells
No-Secreted as a large precursor (pre-pro-PTH) & cleaved to PTH

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13
Q

How are Ca2+ levels detected for PTH secretion to be released?

A

G-protein coupled calcium sensing receptor on chief cells detects change in circulating calcium concentration
PTH secretion inversely proportional to serum calcium

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14
Q

What is the function of PTH

A

PTH degrades bone to release Ca2+

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15
Q

How does PTH increase blood Ca2+ and PO4^3- levels

A

Increased bone reabsorption

Increased 1-a-hydroxylase activity
>Increased 1,25(OH)2 D3 synthesis
>Ca2+, PO4^3- gut absorption

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16
Q

What is the effect of PTH on bone?

A

> PTH binds to receptor on osteoblast
Produces OAFs(Osteoclast activating factors)
Conversion into osteoclast
Increased bone resorption

17
Q

How does calcitriol work?

A

(Pretty similarly to PTH)
-Only difference is calcitriol binds to calcitriol receptors

18
Q

How is Ca2+ alone regulated by PTH and calcitriol?

A

PTH-Ca2+ in a negative feedback loop
PTH increases calcitriol production
Calcitriol reduces PTH production
Calcitriol increases serum Ca2+

19
Q

Where is calcitonin produced from?

A

Parafollicular cells

20
Q

What is the impact of calcitonin?

A

Reduces serum Ca2+(with a limited effect)
-Increases Ca2+ excretion
-Decreases osteoclast activity

21
Q

Does a thyroidectomy interfere with serum calcium levels?

A

Nope

22
Q

What is the physiological role of calcitonin?

A

Remains unclear-Something to do with calcium

23
Q

What is the impact/mechanism of FGF23?

A

-Reduces PO4^3- reabsorption
>Inhibits Na+/PO4^3- co-transport in renal tubule
>Reduces production of calcitriol, leading to less PO4^3- reabsorption from gut

24
Q

What are the symptoms for hypocalcaemia?

A
25
Q

Why does hyper/hypocalcaemia alter membrane excitability?

A

HIGH extracellular calcium (HYPERcalcaemia)
Ca2+ blocks Na+ influx, so LESS membrane excitability
LOW extracellular calcium (HYPOcalcaemia)
enables GREATER Na+ influx, so MORE membrane excitability

(Negative inside of membrane normally)
-Ca2+ reduces the amount of Na+ influx needed to generate an AP
26
Q

What is chvosteks’ sign?

A
27
Q

What is trousseaus’ sign?

A
28
Q

What are the causes of PTH deficiency?

A

Hyperparathyroidism
Vit D deficiency

29
Q

How would this process be inhibited, causing vitD deficiency, Ergocalciferol->25-OH D3

A
30
Q

How would this process be inhibited, causing vitD deficiency, 7-dehydrocholesterol->Vit D3

A
31
Q

How would this process be inhibited, causing vitD deficiency, Vit D3->25-OH D3

A
32
Q

How would this process be inhibited, causing vitD deficiency, 25-OH D3->Calcitriol

A
33
Q

How would this process be inhibited, causing vitD deficiency, Calcitriol->(effects of calcitriol)

A
34
Q

What diseases does lack of bone mineralisation(Vit D deficiency) cause in children and adults?

A

Lack of bone mineralisation = ‘soft’ bones
In children – rickets (bowing of bones)
In adults – osteomalacia (fractures, proximal myopathy)

35
Q

What are the symptoms of hypercalcaemia?

A

Signs & symptoms
Stones, abdominal moans and psychic groans’
Reduced neuronal excitability – atonal muscles

Stones – renal effects
Nephrocalcinosis – kidney stones, renal colic

Abdominal moans - GI effects
Anorexia, nausea, dyspepsia, constipation, pancreatitis

Psychic groans - CNS effects
Fatigue, depression, impaired concentration, altered mentation, coma (usually >3mmol/L)

36
Q

What are the causes of hypercalcaemia?

A

Primary hyperparathyroidism
Too much PTH
Usually due to a parathyroid gland adenoma
No negative feedback - high PTH, but high calcium
Malignancy
Bony metastases produce local factors to activate osteoclasts, increasing calcium reabsorption from bone
Vitamin D excess (rare)