Calcium Flashcards

(32 cards)

1
Q

write out what the activated form of vitamin D is called

A

1,25-Dihidroxyvitamin D3 1,25(OH)2-D

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2
Q

what bloods should be requested when suspect vitamin D deficiency?

A

Ca, PO4, Mg, AlkP (LFTs), U&Es, 25(OH)VitD

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3
Q

If a patient has a raised ALP, and low Ca and PO4, what is the likely diagnosis? What would you expect the 25(OH)VitD and PTH results to be?

A
Osteomalacia.
Expect 25(OH)D to be under 25nmol/L and an elevated PTH. If 25(OH)D is above 25 nmol/L or PTH is not elevated there may be a more complicated picture or alternate diagnosis to simple vitamin D deficiency.
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4
Q

List 4 potential features of clinical presentation of acute severe hypocalcaemia

A
  • Peri-ral and digital paraesthesiae;
  • Tetany and carpopedal spasm;
  • Laryngospasm;
  • Seizure.
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5
Q

What changes on ECG may be a feature of hypocalcaemia?

A

prolonged QT interval; arrhythmia

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6
Q

What adjusted calcium level defines acute severe hypocalcaemia?

A

< 1.9 mmol/L

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7
Q

What is the primary cause of acute severe hypocalcaemia?

A

thyroidectomy (disrupting parathyroid glands)

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8
Q

other than thyroidectomy, list 7 causes of acute severe hypocalcaemia

A
  • selective parathyroidectomy (usually transient and mild hypocalcaemia) / hypoparathyroidism;
  • severe vitamin D deficience;
  • Mg deficiency (consider PPI-associated hypomagnesaemia);
  • Cytotoxic drugs;
  • Pancreatitis;
  • Rhabdomyolysis;
  • Large volume blood transfusions.
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9
Q

What seven blood tests should you send for in acute severe hypocalcaemia? Which of these is most important for identifying the cause?

A
  • PTH (the most important for establishing cause);
  • Serum calcium (adjusted for albumin);
  • Phosphate;
  • U&Es;
  • 25(OH)VitD;
  • Mg;
  • ALP.
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10
Q

Describe the emergency treatment of acute severe hypocalcaemia

A
  • IV Calcium gluconate (bolus of 10-20mL of 10% calcium gluconate in 50-100mL of 5% dextrose IV over 10 minutes and infusion of 100mL 10% calcium gluconate [which is ten vials] in 1L of 0.9% saline or 5% dectrose, infused at 5 to 100 mls/h );
  • ECG monitoring (continuous during administration of IV bolus);
  • Monitor adjusted calcium levels;
  • Start concomitant oral calcium supplements;
  • Treat hypomagnesaemia and/or vitamin D deficience.

(there are different specific renal guidelines for patients with end stage renal failure or haemodialysis)

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11
Q

What is the initial daily dose of active vitamin D to use for replacement in treatment of hypocalcaemia if a patient doesn’t have PTH due to hypoparathyroidism (eg post op hypocalcaemia)?

A

0.25 - 0.5 mcg daily of 1,25(OH)2 VitD (be sure to monitor with frequent blood tests in stabilisation phase of treatment because active vit D metabolites can cause hypercalcaemia).

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12
Q

What is the normal range for corrected calcium?

A

2.12-2.60 mmol/L

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13
Q

what level of hypercalcaemia requires urgent correction and why?

A

> 3.5mmol/L needs to be corrected urgently because of risk of dysrhythmia and coma

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14
Q

what ophthalmic sign may be a clinical feature of hypercalcaemia?

A

band keratopathy

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15
Q

what ECG findings may be a feature of hypercalcaemia?

A

shortened QT and dysrhythmias

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16
Q

what are ninety percent of cases of hypercalcaemia due to?

A

primary hyperparathyroidism or malignancy

17
Q

name a familial cause of hypercalcaemia

A

familial hypocalciuric hypecalcaemia

18
Q

DDx high calcium and high PTH?

A

primary or tertiary hyperparathyroidism

19
Q

what co-morbidity do patients with tertiary hyperparathyroidism often have?

A

chronic end stage renal failure

20
Q

what PTH level would you expect to see in somebody with hypercalcaemia due to malignancy?

A

low PTH (appropriately)

21
Q

describe the first line management of acute severe hypercalcaemia

A

rehydrate with intravenous 0.9% saline, 4-6litres in 24 hours (monitor for fluid overload especially in renal impairment or in elderly patients);

may need to consider dialysis if severe renal failure;

then after rehydrationadminister intravenous bisphosphonates: eg 4mg zolendronic acid over 15 mins (give more slowly and consider dose reduction in renal impairment);

monitor serum calcium response well: will reach nadir at 2 to 4 days: beware potential for hypocalcaemia especially if vitamin D deficiency or suppressed PTH eg due to malignancy.

22
Q

what is the role of loop diuretics in management of acute symptomatic hypercalcaemia?

A

rarely used: only if fluid overload develops (not effective for reducing serum calcium).

23
Q

if somebody has acute symptomatic hyperglycaemia and lymphoma (or other granulomatous diseases or 15OHvitD poisoning) what should you administer as a second line treatment?

A

glucocorticoids: 40mg prednisolone daily, usually effective in 2 to 4 days

24
Q

what is the mechanism of glucocorticoids when used as second line treatment for acute symptomatic hypercalcaemia?

A

inhibits 1,25(OH)2VitD production

25
when might you consider using glucorticoid as a second line treatment for acute symptomatic hypercalcaemia?
lymphoma; other granulomatous disease; 25OHvitD poisoning
26
when might you consider calcitonin as a second line treatment in acute symptomatic hypercalcaemia?
if poor response to bisphosphonates
27
in the context of acute symptomatic hypercalcaemia, for what conditions are calcimimetics licensed?
hypercalcaemia due to primary hyperparathyrodism, parathyroid carcinoma, or renal failure.
28
Name a calcimimetic
cinacalcet
29
when might you consider parathyroidectomy in an acute presentation of symptomatic hypercalcaemia?
in a situation of acute presentation of primary hyperparathyroidism with severe hypercalcaemia and poor response to other measures.
30
describe the effect of hypomagnesaemia on vitamin D levels?
hypomagnesaemia inhibits PTH release, causing low PTH levels and therefore inadequate vitamin D action
31
what cells release calcitonin?
parafollicular C cells in the thyroid
32
what is the function of calcitonin?
to lower blood calcium when there are high calcium levels by inhibiting osteoclast reabsorption of bone