Calcium and Phosphate regulation Flashcards

1
Q

Describe the process of phosphate reabsorption

A

Phosphate is reabsorbed via sodium phosphate transporter into the proximal convoluted tubule cells

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2
Q

How dos PTH regulate phosphate reabsorption

A

Inhibits renal phosphate reabsorption by inhibiting the sodium phosphate co-transport

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3
Q

How dos FGF23 regulate phosphate reabsorption

A

Inhibits the sodium phosphate co-transporters and inhibits calcitriol synthesis, reducing phosphate reabsorption from the gut

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4
Q

Explain how the parathyroid gland responds to calcium levels in the blood

A

Calcium binds to a receptor in high calcium conc.
Receptor activates
Inhibition of PTH secretion

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5
Q

How is calcitriol synthesised

A
  1. UV light converts 7-dehydrocholesterol into cholecalciferol/vit D3 (obtained from the diet via ergocalciferol)
  2. Synthesis of 2,5-hydroxy-cholecalciferol in the liver (+2 OH groups)
  3. PTH stimulates 1𝛼 hydroxylase
  4. synthesis of 1,25-di-hydroxycholecalciferol in the kidney
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6
Q

What does calcitriol / 1,25(OH)2D3 stimulate

A

Ca2+ absorption in the gut
Ca2+ maintenance in the bone
Increased renal Ca2+ reabsorption
-ve feedback on the PTH

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7
Q

What are the causes of vitamin D deficiency

A
Diet 
Lack of sunlight (UVB)
GI malabsorption (coeliac, IBS)
Renal failure
Liver failure 
Vit D receptor defects
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8
Q

Describe vitamin D receptor defects

A

Autosomal recessive
Rare
Resistant to vit D treatment

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9
Q

How do changes in extracellular calcium affect nerve and skeletal muscle excitability

A

Hypercalcaemia = calcium blocks Na+ influx -> less membrane excitability

Hypocalcaemia = enables greater sodium influx -> more membrane excitability

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10
Q

What are the signs symptoms of hypocalcaemia

A
Parasthesia (hands, mouth, feet , lips)
Convulsions
Arrhythmias
Tetany
Muscle cramps/tingling
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11
Q

What is chvostek’s sign

A

Tap facial nerve just below the zygomatic arch
+ve response = twitching of facial muscles
Indicates neuromuscular irritability due to hypocalcaemia

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12
Q

What is trousseau’s sign

A

Inflation of BP cuff for several minutes induces carpopedal spasm = neuromuscular irritability due to hypocalcaemia

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13
Q

What are the causes of hypocalcaemia

A

Vitamin D deficiency
Low PTH levels (hypoparathyroidism)
PTH resistance (pseudohypoparathyroidism)
Renal failure

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14
Q

What causes hypoparathyroidism

A

Surgical – neck surgery
Auto-immune
Magnesium deficiency

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15
Q

How does renal failure cause hypocalcaemia

A

Impaired 1a hydroxylation ->decreased production of 1,25(OH)2D3

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16
Q

What is the normal range of calcaemia

A

2.2-2.6 mmol/L

17
Q

What are the renal effects of hypercalcaemia (signs and symptoms)

A

Renal stones
polyuria
polydipsia

18
Q

What are the causes of hypercalcaemia

A

Primary hyperparathyroidism
Malignancy - tumours/metastases often secrete a PTH-like peptide
Conditions with high bone turnover (hyperthyroidism, Paget’s disease of bone – immobilised patient)
Vitamin D excess (rare)

19
Q

How is primary hyperparathyroidism diagnosed

A

Raised calcium
Raised PTH
Low phosphate

20
Q

How is hypercalcaemia of malignancy diagnosed

A

Raised calcium

Suppressed PTH

21
Q

What is the definition of vitamin D deficiency and what are the states in children and adults

A

Lack of mineralisation in bone

children - rickets
Adults - osteomalaxcia

22
Q

What does vitamin D deficiency result

A

Results in softening of bone
Bone deformities
Bone pain
Severe proximal myopathy.

23
Q

What is the treatment of primary hyperparathyroidism

A

parathyroidectomy

24
Q

How is secondary hyperparathyroidism diagnosed

A

Low calcium

Increased PTH

25
Q

What are the biochemical findings in vitamin D deficiency

A

Plasma [25(OH)D3] is low
Plasma Ca2+ is low
Plasma phosphate low
PTH high

26
Q

How is vitamin D deficiency treated when the patient has normal renal function

A

Give 25 hydroxy vitamin D (25 (OH) D)
Patient converts this to 1,25 dihydroxy vitamin D (1,25 (OH)2 D) via 1a hydroxylase
Ergocalciferol 25 hydroxy vitamin D2
Cholecalciferol 25 hydroxy vitamin D3

27
Q

How is vitamin D deficiency treated when the patient is in renal failure

A

Give Alfacalcidol - 1a hydroxycholecalciferol

28
Q

What can vitamin D excess lead to

A

Can lead to hypercalcaemia and hypercalciuria due to increased intestinal absorption of calcium

29
Q

What can vitamin D excess (intoxication) occur as a result of

A

excessive treatment with active metabolites of vitamin D eg Alfacalcidol
granulomatous diseases such as sarcoidosis, leprosy and tuberculosis (macrophages in the granuloma produce 1a hydroxylase to convert 25(OH) D to the active metabolite 1,25 (OH)2 D

30
Q

What are the actions of PTH on the kidney

A

Increased calcium reabsorption
Increased phosphate excretion
Stimulates 1alpha-hydrolxylase activity -> calcitriol synthesis

31
Q

What are the actions of PTH at the small intestine

A

Increased Ca2+ absorption

Increased phosphate absorption

32
Q

What are the actions of PTH in the bone

A

Stimulation of osteoclasts and inhibition of osteoblasts

Increased bone resorption (decreased bone mass)

33
Q

What are the GI effects of hypercalcaemia (signs and symptoms)

A
Abdominal moans 
Anorexia 
Nausea
Dyspepsia 
Constipation
Pancreatitis
34
Q

What are the CNS effects of hypercalcaemia (signs and symptoms)

A
Psychic groans 
Fatigue 
Depression 
Impaired concentration 
Altered mentation
Coma