Ca, Mg, P Flashcards

1
Q

Name 3 hormones that regulate calcium homeostasis

A

• Parathyroid hormone PTH ( bone, kidney)
• vitamin D
. Calcitonin (minor) (from thyroid)

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2
Q

Name 6 causes hypercalcaemia

A

• Primary hyperparathyroidism: sporadic/familial (common)
• malignancy (common)
- humoral hypercalcaemia of malignancy (pthrp)!
-Widespread skeletal metastases ( commonly breast ca)
- haem malignancy: multiple myeloma, adult T cell leukemia/lymphoma
• Granulomatous disease: sarcoidosis, tb, histoplasmosis, leprosy
• vit D toxicity
• renal transplant: tertiary hyperparathyroidism
• thyrotoxicosis

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3
Q

Name 5 functions/ consequences of PTH

A

•Phosphaturia (phosphate exchanged for ca )
• Hypercalciuria (due to “overload”)
• mild acidosis (decreased bicarb reabsorption kidney)
• increased plasma calcium (bone release calcium, kidney reabsorb)
• phosphate also reabsorbed from gut with Ca

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4
Q

Name 2 effects vit D has on calcium levels

A

Calcitriol stimulates:
- gut to absorb Ca and P
- bone to stimulate osteoclasts, only in high concetrations

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5
Q

Name 3 effects of fibroblast growth factor FGF 23

A

Secreted by osteocytes when increased calcitriol and P
- hypophosphataemia
-phosphaturia
-decrease serum calcitriol

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6
Q

Name 5 causes hyperphosphataemia

A
  • renal insufficiency (common), CKD
  • tissue catabolism (common) eg tumour lysis syndrome
  • hypoparathyroidism
  • vit D intoxication
  • acromegaly
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7
Q

Why is hyperphosphataemia clinically NB? (2)

A
  • causes inhibition of 1 alpha hydroxylation of 25 hydroxycholecalciferol in kidneys to Calcitriol (vit D)
  • may combine with Ca, causing metastatic calcium deposits in tissues and hypoCa
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8
Q

Name 3 broad causes and 3 specific causes within each of hypophosphataemia

A

Redistribution
-DKA recovery phase
- enteral/parenteral nutrition with inadequate phosphate; IV glucose
- resp alkalosis

Renal loss
-primary hyperparathyroidism
- renal tubular disease, diuretics
- hypoPhosphataemic rickets, tumour associated osteomalacia (FGF23)

Decrease intake/absorption
-dietary, malabsorption, vomiting
- P binding agents eg Mg, Ca salts
- vit D deficiency
- alcohol withdrawal

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9
Q

Define severe hypophosphataemia and it’s clinical effects (5)

A

<0,3 mmol/L
- myopathy, muscle weakness, rhabdomyolysis
-haemolysis
- decreased phagocytosis and chemotaxis
-thrombocytopenia

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10
Q

Name 2 symptoms of chronic hypophosphataemia

A

Rickets
Osteomalacia

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11
Q

Name 5 causes hypoMg

A
  • prolonged diarrhoea, malabsorption most commonly
  • refeeding syndrome
  • alcoholism - chronic and withdrawal, liver cirrhosis: severe hypoalbuminameia
  • PPIs
  • renal tubular disease (but in advanced kidney disease, hyperMg)
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12
Q

Name 5 clinical features and consequences of of hypoMg

A

-tetany
- agitation, delirium
- ataxia, tremor, choreiform movements, convulsions
- muscle weakness, cardiac arrythmias
- hypocalcaemia (cause and worsen above symptoms)

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13
Q

How calculate adjusted plasma calcium?

A

If albumin <40
Ca + 0,02 x (40- albumin)

If albumin >45
Ca - 0,02 x ( albumin - 45)

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14
Q

Name 2 physiological factors that stimulate the kidney to form calcitriol by 1 alpha hydroxylation of 25-oh cholecalciferol

A

• Increase PTH
• decrease phosphate

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15
Q

Name 4 physiological factors that inhibit the kidney to form calcitriol by 1 alpha hydroxylation of 25-oh cholecalciferol

A

• Decrease PTH
• increase phosphate
• increase fgf-23
• calcitriol production by negative feedback

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16
Q

Most common cause primary hyperparathyroid?

A

Parathyroid adenoma

17
Q

Treatment hyperparathyroid?

A

Surgery

18
Q

How does malignancy affect calcium

A

Hypercalcaemia, even if not metastatic ( PTH related peptide secreted)

19
Q

Define primary hyperparathyroidism

A

Parathyroid glands release too much PTH eg by parathyroid adenoma or hyperplasia
Pth and calcium increased

20
Q

Define secondary hyperparathyroidism and 2 causes

A

Due to decreased synthesis calcitriol (need it for ptH to work on bone) → hypocalcaemia → increase PTH as physiolgical response but no increase in calcium
Due to:
• CKD.
• vitamin D deficiency

High PTH (no neg feedback from calcitriol + high P)
High P! (Excr by kidneys impaired)
Normal/low Ca
Low calcitriol (decr synth by kidneys -> low Ca)

21
Q

Define tertiary hyperparathyroidism and 2 causes

A

Post renal transplant. Established kidney failure → develop autonomous PTH secretions
Sudden ability to metabolise vitamin D normally → hypercalcaemia.

22
Q

If symptoms hypocalcaemia but calcium is normal, which diagnosis should be considered

A

Hypomagnesemia

23
Q

What effect does ph have on calcium

A

Alkalosis = greater binding = free calcium decrease (symptoms hypo Ca)

Acidosis = less binding = free calcium increase

24
Q

Name 9 indications for measuring ionised (free active) calcium

A

Not routinely done.
• CKD and dialysis
• transplantation
• extra corporeal transfusion
• massive transfusion
• critical illness
• hyper parathyroid
• post op period following parathyroïdectomy
•Severe pancreatitis
• hyper Ca of malignancy

25
Q

Approach to hypo Ca ( low total plasma ca) (6)

A

•Plasma albumin and ionized calcium (if hypoalbumin, and or normal ionized/”corrected” calcium, no action needed)
. If ionized calcium low (true hypo ca), do clinical assessment (if positive investigate appropriately)
•If negative, do plasma creatinine (increased = renal impair)

• if normal, do magnesium (low = hypo mg)
.If normal, do plasma PTH
. If PTH low to normal →hypoparathyroid

. If PTH increased, measure phosphate
. If acute high phosphate → hyper p cell lysis; chronic → pseudohypoparathyroid
• if low phosphate, do 25 (oh)d (low =Vit D def)
. If normal/high 25(oh)d, do 1,25 (OH) 2 D
- low: vDDR type 1
- normal/high: osteoblastic metastasis, acute pancreatitis, multiple blood transfusions, inhibitors bone resorption, vDDR type 2

26
Q

What is relationship between mg and Ca

A

Directly proportional
(Mg needed to produce pth)

27
Q

Approach to hyper Ca (5)

A

Do albumin

  • albumin high: do urea
    → high urea = dehydration
    → normal urea = cuffed specimen
  • albumin normal/low: do phosphate, urea, alkaline phosphatase alp
    → low/normal phosphate+ normal urea = primary/tertiary hyperparathyroid (high pth)
    → high/normal phosphate
    > high alp (from increased bone turnover) = bone metastasis (also low chloride,, sarcoidosis, thyrotoxicosis
    > normal alp = myeloma (high plasma protein), excess vitamin D, sarcoidosis, milk alkali syndrome if high HCO3 alkalosis)