Calcium Homeostasis and Disorders of Metabolism Flashcards Preview

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Flashcards in Calcium Homeostasis and Disorders of Metabolism Deck (88)
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1

In which 3 ways can serum calcium be increased?

  1. Gut absorption
  2. Bone resorption
  3. Kidney reabsorption

2

Which receptor will serum calcium act on in order to self regulate its level?

Calcium sensing receptor (CaSR)

3

Stimulation of the CaSR will inhibit production of which hormone?

Parathyroid hormone (PTH)

4

What is the overall action of parathyroid hormone?

Increase serum calcium

5

In which 3 key ways does PTH increase serum calcium?

  1. Resorption of bone
  2. Reabsorption by the kidneys
  3. Absorption from the gut

6

Which vitamin is useful in calcium homeostasis?

Vitamin D3

7

What roles does vitamin D3 have on calcium homestasis?

  1. Increases calcium uptake from the gut
  2. Increases bone mineralisation (also increases resorption)
  3. Potentially reduces PTH activity

8

In which ways will hypercalcaemia acutely present?

  1. Thirst
  2. Dehydration
  3. Confusion
  4. Polyuria

9

In which ways will hypercalcaemia acutely present?

  1. Myopathy
  2. Osteopenia
  3. Fractures
  4. Depression
  5. Hypertension
  6. Abdominal pain (pancreatitis, ulcers, renal stones)

Stones, groans, bones and psychic moans

10

What is the most important test to do in someone with suspected hypercalcaemia?

PTH

11

If a patient has hypercalcaemia and high albumin, what will urea levels be like in the following circumstances?

a) Dehydration

b) Cuffed sample

a) Raised urea

b) Normal urea

12

If a patient has hypercalcaemia and normal/low albumin what are the 3 main things to consider?

  1. Familial hypocalciuric hypercalcemia (FHH)
  2. Primary/tertiary hyperparathyroidism
  3. Bone pathology

13

How may a bone pathology be differentiated from either FHH or primary/tertiary hyperparathyroidism in a patient with hypercalcaemia and low/normal albumin?

PTH (and phosphate) levels

(PTH is low and phosphate is high in such patients with bone pathology)

14

If a patient has primary/tertiary hyperparathyroidism or FHH, what levels are both phosphates and PTH expected to be?

PTH - Normal/high

Phosphates - Normal/low

15

How may primary/tertiary hyperparathyroidsm and FHH be differentiated biochemically?

  1. Primary/tertiary hyperparathyroidsm - High urine Ca2+
  2. Familial hypocalciuric hypercalcemia - Low urine Ca2+

(Both conditions have hypercalcaemia, normal/low albumin, normal/high PTH and normal/low phosphates)

16

What are the key biochemical markers which suggest a general bone pathology as the cause of hypercalcaemia?

  1. Hypercacaemia
  2. Normal/low albumin
  3. Low PTH
  4. High phosphates

17

When considering a bone pathology as the cause of hypercalcaemia, what 3 things would a high ALP suggest as the cause?

  1. Bone metastasis
  2. Sarcoidosis
  3. Thyrotoxicosis

18

When considering a bone pathology as the cause of hypercalcaemia, what 3 things would a low ALP suggest as the cause?

  1. Myeloma
  2. Vitamin D excess
  3. Milk-alkali syndrome

19

What causes milk-alkali syndrome?

  1. Excess dietary milk or alkali (e.g. dyspepsia)
  2. Excess calcium supplementation (e.g. in post-menopausal women)

20

What are the main causes for hypercalcaemia?

  1. Primary hyperparathyroidism
  2. Malignancy
  3. Drugs - vitamin D, thiazides
  4. Granulomatous disease - sarcoidosis, TB
  5. Familial hypocalcuric hypercalcaemia
  6. Tertiary hyperparathyroidism
  7. High calcium turnover - bedridden, thyrotoxic, Paget's etc
  8. Dehydration

21

Primary hyperparathyroidsm has which 3 key biochemical abnormalities?

  1. Raised serum calcium
  2. Raised (or inappropriately normal) serum PTH
  3. Increased urine calcium excretion

(such abnormalities would also present with tertiary hyperparathyroidsm)

22

In which 3 main ways can malignancies induce hypercalcaemia?

  1. Parathyroid hormone release protein (PTHrp) release
  2. Metastatic bone destruction
  3. Osteoclast activating factors

23

How is acute hypercalcaemia treated?

  1. Fluids 0.9 saline 4-6L in 24hrs
  2. Loop diuretics once rehydrated
  3. Bisphosphonates 
  4. Steroids (rarely used, e.g. sarcoidosis)
  5. Salmon calcitonin (rarely used)

24

How are the parathyroid glands imaged?

Sestamibi scintigraphy scan

25

What are the treatment menthods for primary hyperparathyroidsm?

  1. Surgery
  2. Cinacalcet

26

How does cinacalet work?

Acts on CaSR as a calcimemetic

Calcium levels are negatively regulated

27

What is secondary hyperparathyroidism?

Excess PTH secretion in response to hypocalcaemia

(this is usually as a result of chronic kidney disease leading to excessive calcium loss)

Hyperplasia of the parathyroid glands is usually implicated

28

Secondary hyperparathyroidism involves:

a) High/Low calcium levels

b) High/Low PTH levels

a) Low calcium levels

b) High PTH levels

 

29

Which genetic syndromes can result in hyperparathyroidism?

  1. MEN 1 and 2
  2. Familial hyperparathyroidism

30

What is the reference interval for serum calcium?

2.2-2.6 mmol/L