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Year2 Endo > Calcium Dysregulation > Flashcards

Calcium Dysregulation Flashcards

1
Q

How is Vitamin D made

A

Synthesised in skin or intake via diet

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2
Q

Where is parathyroid hormone secreted

A

Parathyroid glands

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3
Q

What things increase serum calcium and phosphate

A

Vitamin D , Parathyroid hormone ( PTH)

–> regulate calcium and phosphate homeostasis via actions on kidney , bone and gut

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4
Q

How does Vit D and PTH increase serum calcium and phosphate

A

Regulate calcium and phosphate homeostasis via actions on kidney , bone and gut

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5
Q

What molecule decreases serum caclcium and phosphate

A

Calcitonin ( Regulates calcium acutely but no negative ect if parafollicular cells are removed ie thyroidectomy)

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6
Q

Where is calcitonin made

A

Secreted by thyroid parafollicular cells

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7
Q

How can you measure vit D

A

measure serum 25-OH cholecalciferol vit D

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8
Q

What is the active form of vitamin D

A

Calcitriol ( 1,25(OH)2-Cholecalciferol)

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9
Q

How is Vitamin D made

A

2 types : D2 from diet and D3 from sunlight

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10
Q

How is calcitriol made

A

1) UVB hits skin cells
2) Pre-Vitamin D3
3) Vitamin D3
made in skin cells
4) Vitamin D3 then goes to the gut which combines with Vit D2 from the diet
5) They both then go to liver where they are converted into 25(OH)- cholecalciferol using 25 hydroxylase
6) 25 (OH)- cholecalciferol –> 1,25(OH)2Cholecaliferol ( calcitriol using 1 alpha-hydroxylase in the kidney (renal step)
8) 1,25(OH)2cholecalciferol = active form of Vitamin D = calcitriol
9) 1,25(OH)2 vitamin D (calcitriol) regulates its own synthesis by decreasing transcription of 1-alpha hydroxylase

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11
Q

How does Vit D ( calcitriols) regulate it’s self

A

1,25(OH)2 vitamin D (calcitriol) regulates its own synthesis by decreasing transcription of 1-alpha hydroxylase

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12
Q

What are the effects of calcitriol

A

1) acts on bone to increase osteoblast activity ( remember blast not clast –> increases bone synthesis
2) Acts on kidney to increase Ca2+ and PO43- reabsorption
3) Acts on gut to increase Ca2+ absorption and PO42- absorption

note ( increased Ca2+ absorption increases osteoblast activity)

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13
Q

what are the actions of PTH

A

1) Increased Ca2+ reabsorption from bone
( stimulates osteoclast activity –> opposite of calcitriol)
2) Acts on kidney to : increase ca2+ reabsorption, increase PO43- excretion , increase 1-alpha hydroxylase activity
3) Increased 1-a hydroxylase increases calcitriol synthesis
4) Increased calcitriol —> increased Ca2+ absorption and increased Phosphate absorption in the gut

note excretion of PO43- by kidney and reabsorption by gut balance each other out

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14
Q

How does PTH regulate serum cal and phos levels

A

1) acts on liver to increase Ca2+, PO43- reabsorption ( will increase plasma Ca2+
2) Acts on liver to increase 1,25(Oh)2D3 synthesis
3) increased calcitriol increases Ca2+ absorption + PO43- absorption in gut ( increases plasma Ca2+)
4) Increase ca2+ mobilisation increases plasma Ca2+

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15
Q

How does FGF23 regulate serum phosphate

note FGF 23 made by osteocytes

A

1) FGF23 and PTH both inhibit phosphate reabsorption in the kidney through blocking the Na/PO4 cotransporter in the PCT epithelium –> more Na+ and PO43- excretion in urine
2) FGF23 also inhibits calcitriol synthesis which decreases absorption of phosphate from the gut

note( Calcitriol can block the phosphate transporter by stimulating FGF23 (FGF23 has a –ve feedback on calcitriol levels though)

Overall : FGF23 works in 2 ways:
Inhibits PO43-/Na+ cotransporter → increases po43- excretion
Inhibits calcitriol action → DECREASES pO43- REABSORPTION IN GUT

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16
Q

What does hypocalcaemia do to muscles

A

Sensitives excitable tissues , causing muscle cramps , tetany ( involuntary contraction of muscles , tingling)

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17
Q

What are the signs of Hypocalcaemia

A

1) Paraesthesia ( hands, moth , feet and lips)
2) Convulsions
3) Arrhythmias
4) Tetany
( mneumonic CATS go numb)

5) Chvostek’s’ sign – facial paraesthesia
6) Trousseau’s sign - carpopedal spasm

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18
Q

What is chvostk’s sign

A

Facial paraesthesia

caused by hypocalcaemia

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19
Q

What is trousseau’s sign

A

Carpopedal spasm

caused by hypocalcaemia

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20
Q

What are the causes of hypocalcaemia

A 
1) Low PTH ( hypoparathyridsm)  due to 
Surgical – neck surgery
Auto-immune
Magnesium deficiency
Congenital (agenesis, rare)

2) Low Vitamin D levels due to : Deficiency – diet, UV light, malabsorption, impaired production (renal failure)

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21
Q

what is hypoparathyroidism

A

Low PTH levels

22
Q

What can cause hypoparathyroidism

A

Neck surgery
Auto immune
Magnesium deficiency
Congenital ( agenesis , rare)

23
Q

What can cause low vitamin D levels

A

Deficiency –> diet , UV light , malabsorption , impaired production ( renal failure)

24
Q

What does hypercalcaemia do to muscles

A

Makes them atonal ( due to reduced neuronal excitability)

25
Q

What are the symptoms of hypercalcaemia

A

Stones , abdo moans and psychic groans

1) stones – renal effects ( Nephrocalcinosis - kidney stones , renal colic)
2) Abdominal moan - GI effects anorexia , nausea, dyspepsia , constipation , pancreatic
3) Psychic groan - CNS effects ( fatigue , depression , impaired concentration , altered mentation , coma if >3mmol/L)

26
Q

Causes of hypercalcaemia

A

1) primary Hyperparathyroidism ( too much PTH commonly due to parathyroid gland adenoma) –> no negative feedback aka high PTH , high Ca 2+
2) Malignancy (bony metastases prod local factors that activate osteoclasts. Certain cancers ie squamous cell carcinomas secrete PTH related peptide that acts at PTH receptors
3) Excess Vit D ( rare)

27
Q

What happens to PTH levels calcium levels decrease

A

increases ( -ve feedback )

28
Q

What are the different types of hyperparathyroidism

A

1) Primary hyperparathyroidism–> Parathyroid adenoma
ca2+ increase bur no -ve feedback to PTH due to autonomous PTH secretion from parathyroid adenoma

2) 2nary hyperparathyroidism due to hypocalcaemia
3) tertiary hyperparathyroidism due to kidney

29
Q

What does Primary hyperparathyroidism cause

A

High PTH ( not suppressed by hypercalcaemia)

  • -> High calcium
  • -> Low Phosphate ( increase renal phosphate excretion due to inhibition of Na+/PO43- transporter in kidney
30
Q

How to treat hyperparathyroidism

A

1) Parathyroidectomy

31
Q

What complications can occur in untreated hyperparathyroidism

A 
Osteoporosis 
Renal calculi ( stones) 
Phycological impact of hypercalcaemia --> mental function , mood
32
Q

What is primary hyperparathyroidism

A

Parathyroid gland not working

33
Q

What is secondary hyperparathyroidism

A

Physiological response to hypocalcaemia ( problem with calcium not parathyroid gland)

34
Q

What does secondary hyperparathyroidism causes

A

Calcium will be low / low - normal

–> PTH will be high ( hyperparathyroidism) secondary to low ca2+

35
Q

How is secondary hyperparathyroidism different to 1ary in terms of Calcium levels

A 
2nard = ca will by low 
1ary = ca will be high
36
Q

What are causes of 2nary hyperparathyroidism

A

1) Vit D deficiency ( common) due to diet , reduced sunlight

2) renal failure –> can’t make calcitriol due to lack of 1-alpha- hydroxylase by PTH ( uncommon)

37
Q

Treatment of 2nary hyperparathyroidism

A

1) Vit D replacement
( give 25(OH)vit D to pateints with normal renal function so they can convert it to calcitriol

ie ( Ergocalciferol 25(OH) vit D2 and Cholecalciferol 25(OH) vit D3)

2) in pateints with renal failure no 1-a-hyroxylase to must give Alfacalcidol ( 1-a hydroxycholecalciferol)

38
Q

What is tertiary hyperparathyroidism

A

rare
Occurs in chronic renal failure ( can’t make calcitriol)
PTH increases + hyperplasia of parathyroid gland

Autonomous PTH secretion causes hypercalcaemia

39
Q

How do you treat tertiary hyperparathyroidism

A

Parathyroidectomy

40
Q

What are the 3 different types of hyperparathyroidism

A 
1ary = problem with thyroid gland  
2ary = problem with calcium levels 
3ary = problem with kidneys

Primary hyperparathyroidism
Parathyroid adenoma, makes too much PTH
Calcium increases, but PTH stays high (no negative feedback)
Secondary hyperparathyroidism
Normal physiological response to low calcium (commonly caused by low vitamin D)
Calcium low/low-normal, PTH high
Tertiary hyperparathyroidism
Complication of chronic renal failure and prolonged calcitriol deficiency
Initially calcium falls and PTH rises (secondary hyperparathyroidism), but over a long period high PTH drive by enlarged parathyroid glands increases calcium

41
Q

How to diagnose Hypercalcaemia

A

Look at PTH levels ( normal response for hypercalcaemia is decrease in PTH )
Diagnose according to what type of hyperparathyroidism it is

42
Q

What can cause hypercalcaemia

A

Malignancy
Hypercalcaemia due to high ca2+ intake
Low / Supressed PTH

43
Q

What would be the diagnosis of a pateint with hypercalcaemia and high PTH

A

Hyperparathyroidism

1) 1ary if renal function is normal ( cause would be parathyroid adenoma)
2) Tertiary hyperparathyroidism if chronic renal failure ( and PTH gland enlarged )

Remember Not 2ary as that is due to low ca2+ levels

44
Q

How to diagnose vit D deficiency

A

Measure Vit D as 25(OH) cholecalciferol and calcitriol is hard to measure ( will be low)
Calcium will be low / low - normal
PTH will be high ( 2nary hyperparathyroidism)

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Year2 Endo (13 decks)

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