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Endocrine > Calcium metabolism and disorders > Flashcards

Calcium metabolism and disorders Flashcards

1
Q

How is vitamin D converted in the liver?

A

25-hydoxylase

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2
Q

What is vitamin D converted to in the kidneys?

A

1-hydoxyase

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3
Q

What are the effects of PTH on the kidneys?

A

Stimulates the activation of vitamin D
Promotes phosphate excretion
Reduces calcium resorption

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4
Q

What stimulates the production of PTH?

A

Low calcium
Inhibited by 1,25 (OH)2 vit D
Mg required

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5
Q

What is calcitonins effects on bone?

A

Inhibits osteoclast resorption
Lowers calcium and phosphate
No effect on magnesium

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6
Q

What is the effects of 1,24(OH)2-D on the gut?

A

Increases calcium and phosphate absorption

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7
Q

What are the effect os 1,25(OH)2-d on the kidneys?

A

Increases Ca resorption

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8
Q

What type of receptor is the calcium sensing receptor?

A

G-protein coupled receptor that plays an essential role in regulation of extracellular calcium homostasis

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9
Q

What are the actions of PTH?

A

Calcium resorption from bone
Calcium reabsorption from kidneys
Increase in 1,25(OH)2 vitamin D in kidneys

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10
Q

What are the symptoms of acute hypercalcaemia?

A 
Thirst
Dehydration 
Cofusion 
Polyuria
Coma
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11
Q

What are the symptoms of chronic hypercalcaemia?

A 
Myopathy
Fractures
Osteopaenia
Depression 
Hypertension 
Pancreatitis
Duodenal ulcers
Renal calculi
Shortened QT
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12
Q

Diagnose:
Hypercalcaemia
High PTH
Increased urinary excretion of calcium

A

Primary/tertiary hyperparathyryoidism

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13
Q

Diagnose:
Hypercalcaemia
High PTH
Decreased urinary excretion

A

Familial Hypocalciuric Hypercalcaemia

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14
Q 
Diagnose: 
Hypercalcaemia
Low PTH
High phosphate
Increased ALP
A

Bone pathology:
Bone mets
Sarcoidosis
Thyrotoxicosis

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15
Q 
Diagnose: 
Hypercalcaemia
Low PTH
High phosphate
Decreased ALP
A

Myeloma
Vit D toxicity
Milk-alkali

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16
Q

What does a high PTH with hypercalcaemia indicate?

A

Thyroid issue

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17
Q

What does a low PTH with hypercalcaemia indicate?

A

Bone pathology

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18
Q

What drugs can cause hypercalcaemia?

A

Vit D

Thiazide duiretics - reduce the ability to excrete calcium

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19
Q

How can malignancy cause hypercalcaemia?

A

Metastatic bone destruction
PTHrp from solid tumours
Osteoclast activation factor

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20
Q

How is hypercalcaemia of malignancy diagnosed?

A 
Raised calcium and alk phos
X-ray 
CT
MRI 
Isotope bone scan
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21
Q

Why will hypercalcaemia lead to dehydration?

A

Induces renal resistance to vasopressin, leading to nephrogenic DI
Dehydration in turn lead to a corresponding further increase in calcium conc

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22
Q

How is vitamin D3 synthesized in the skin?

A

Reaction of its cholesterol with UVB

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23
Q

How is vitamin D metabolised within the body?

A

D3 is converted to 25-hydroxy metabolite by hepatic pathways and a second hydroxylation to calcitrol (1,25-dihydroxyvitamin D3) occurs in the renal parenchyma

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24
Q

Where is the majority of calcium found?

A

In bone and intracellular compartments

25
Q

How is acute hypercalcaemia managed?

A

0.9% saline 4-6L within 24hrs
Consider loop diuretics once rehydrated to bring calcium down
Bisphosphonate - single dose with lower calcium over 2/4 days
Steroids (pred 40-60mg) for sarcoid

26
Q

How is primary hyperparathyroidism manged?

A

Surgery - not always

Cinacalet

27
Q

What is the mechanism of action of cinacalcet?

A

Calcium mimic on the calcium receptor and causes reduced PTH output

28
Q

What are the indications of a parathyriodectomy?

A 
Very high calcium (>2.85) 
Under age of 50 
eGFR <60 mL/min
End organ damage: bone disease (osteolitis fibrosa cystica; brown tumors/ pepper pot skull) 
Gastric ulcers
Renal stones
Osteoporosis
29
Q

What is primary hyperparathyroidism and what is the biochem?

A

Primary overactivity of the parathyroid gland i.e. adenoma
High calcium
High PTH
High urinary calcium excretion

30
Q

What is secondary hyperparathyroidism and what is the biochem?

A

Physiological response to low calcium or vit D
Low calcium/lower half of normal
High PTH

31
Q

What is tertiary hyperparathyroidism and what is the biochem?

A

Parathyroid becomes autonomous after many years of overactivity e.g. renal failure
High calcium
High PTH

32
Q

What genetic syndromes are associated with hyperparathyroidism?

A

MEN1/2

Familial isolated hyperparathyroidism

33
Q 
Clinical Case: 
80 year old man presents to ARU with 1 stone weight loss, cough, back pain
- cCa2+ level= 3.4 (ref 2.2.-2.6mmol/L),
Phosp= 1.4 (0.8-1.5 mmol/L)  , 
Alk Phos= 272 (30-130 U/L)
CXR – LLL (left lower lobe) collapse
What investigations would you want?
A

Spine x-ray
Isotope bone scan
Myeloma screen
Dx: malignant hypercalcaemia

34
Q

Clinical case:
33 year old woman presents to bone clinic with incidental hypercalcaemia
- cCa2+ level= 2.72 (ref 2.2.-2.6mmol/L),
Phosp= 1.0 (0.8-1.5 mmol/L) ,
Alk Phos= 120 (30-130 U/L)
PTH = 7.9 – 6.5/7 is normal
What investigations would you want?

A

Urinary calcium excretion which was 0.02 mmol/L FR

Dx: Familial hypocalciuric hypercalcaemia

35
Q

What is familial hypocalciuric hypercalcaemia?

A

Issue with calcium receptor and therefore increased PTH - increased serum calcium but low calcium excretion in urine

36
Q

What is the mode of inheritance of familial hypocalciuric hypercalcaemia?

A

Autosomal dominant

Usually benign

37
Q

What are the symptoms of signs of hypocalcemia?

A 
Paraesthesia - fingers, toes and perioral
Muscle cramps, tetany
Muscle weakness
Fatigue
Bronchospasm or laryngospasm
Fits
Chvostek's sign
Trousseau sign 
ECG: QT prolongation - risk of VF
38
Q

What is trousseau sign?

A

Carpopedal spasm

39
Q

What is chvostek’s sign?

A

Tapping over facial nerve due to hyperexcitable nerve root endings (motor units)

40
Q

What is the treatment for acute hypocalcaemia?

A

IV calcium gluconate 10ml, 10% over 10 mins (in 50 ml saline or dextrose)
Infusion after bolus (10ml, 10% in 100 ml infuse at 50ml/h)

41
Q

What can cause hypoparathyroidism?

A

Congenital absence (DiGeorge - deletion in 22)
Destruction (surgery, radiotherapy, malignancy)
Autoimmune
Hypomagnesaemia
Idiopathic

42
Q

What is the long term management of hypoparathyroidism?

A

Calcium supplement: 1-2g per day

Vitamin D tablets (alphacalcidol 0.5-1mcg)

43
Q

Why is magnesium important?

A

Calcium release from cells is dependent on magnesium
In magnesium deficiency intracellular calcium is high and PTH release is inhibited
Skeletal and muscle receptors less sensitive to PTH

44
Q

What is the treatment for hypomagnesemia?

A

Replace with calcium and magnesium

45
Q

What can cause hypomagnesaemia?

A 
Alcohol 
Drugs: thiazide, PPI
GI illness
Pancreatitis
Malabsorption
46
Q

What is pseudohypoparathyroidism?

A

Genetic defect - dysfunction of Gs alpha subunit on GNAS 1

47
Q

What is the biochem presentation of pseudohypoparathyroidism?

A

Low calcium

PTH elevated due to PTH resistance

48
Q

What are the clinical symptoms of pseudohypoparathyroidism?

A 
Bone abnormalities (mccune albright = areas of abnormal scar like fibrosis tissue in bones) 
Obesity
Subcutaneous calcification 
Learning difficulty
Brachydactyly
49
Q

What is pseudopseudohypoparathyroidism?

A

Albright’s hereditary osteodystrophy but no alteration in PTH action and thus normal calcium

50
Q

What can cause rickets/osteomalacia?

A 
Gastric surgery
Coeliac disease
Liver disease
Pancreatic failure
Chronic renal failure
Lack of sunlight 
Drugs: anticonvulsants
51
Q

How will osteomalacia present clinically?

A 
Low calcium
Muscle wasting - proximal myopathy
Dental defects - caries, enamel
Bone - tenderness, fractures, rib deformity, limb deformity
Pseudofractures
52
Q

What is the classic sign of osteomalacia?

A

Loosers sign

53
Q

What effects can chronic renal disease have?

A

Vitamin D deficiency

Secondary hyperparathyroidism

54
Q

What are the long term consequences of vitamin D deficiency?

A

Bone disease:
Demineralisation/ fractures
Osteomalacia/ rickets
Malignancy - esp colon

55
Q

What is vitamin D resistant rickets?

A

X -linked hypophosphatemia

PHEX or FGF23 gene mutation

56
Q

What is the FGF 23 gene responsible for?

A

Phosphate levels in plasma and is secreted by osteocytes in response to calcitriol

57
Q

How will vitamin D resistant rickets present?

A

Low phosphate

Vitamin D high

58
Q

How is vitamin D resistance rickets treated?

A

Phosphate and vitamin D supplements +/- surgery

Endocrine (35 decks)

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