Calcium, phosphate and magnesium Flashcards Preview

September lectures yr 3 (2018) > Calcium, phosphate and magnesium > Flashcards

Flashcards in Calcium, phosphate and magnesium Deck (31)
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1
Q

What can imbalances in calcium, phosphate and magnesium cause?

A

number of serious clinical complications including arrhythmias, seizures, coma and respiratory arrest

2
Q

What are the roles of calcium?

A

cell signalling and 2nd messenger

neurotransmitter and hormone release

exocytosis of proteins
muscle contraction
blood clotting
biomineralization

3
Q

What are the roles of phosphate ?

A

integral component DNA and RNA

energy source for cellular functions (ATP)

4
Q

What are the roles of magnesium?

A

DNA and protein synthesis, oxidative phosphorylation, enzyme function, ion channel regulation and neuromuscular excitability

5
Q

What are the normal serum conc for Ca,HPO4, Mg?

A
Ca = 2.2-2.6mmol/L
HPO4 = 0.8-15
Mg = 0.7-1
6
Q

What organ systems play an important role in metabolism ?

A

kidney
skeleton
GI tract
parathyroid gland

7
Q

What regulatory factors that play an important role in the metabolism of Ca, HPO4 and Mg?

A
PTH
Vit D
FGF-23
PTH related protein 
calcitonin
8
Q

What is the Ca/Mg sensing receptor?

A

member of G coupled receptor family= important regulator of Ca and Mg homeostasis

9
Q

What does the feedback mechanism for calcium rely on and why is this important?

A

free (ionised) fraction = physiologically important

  • [calcium] depends on [protein]
  • for each g of albumin it binds 0.02 mmol/L calcium
10
Q

What does a low or high pH cause in terms of calcium levels?

A

decreased pH increases Ca

increased pH decreases Ca

11
Q

What are common causes of hypocalcaemia?

A
chronic and acute renal failure 
vit D deficiency 
hypoparathyroidism 
acure pancreatitis 
magnesium deficiency 
artefact - wrong tube
12
Q

What happens when there is low plasma Ca?

A

stimulates PTH release which acts on bone to increase Ca release, acts on Kidney to increase reabsorption of Ca and acts on gut to increase Ca absorption

13
Q

What is rickets/osteomalacia?

A

deficiency of active vit D
- rickets = affects growing skeleton
- osteomalacia = affects adult skeleton
bone is unduly soft in both

lack of mineralization of collagen component of bone (osteoid)
failure to absorb sufficient calcium from GIT

dietary/lack of sunligh, rarely inherited

14
Q

What are the signs/symptoms of rickets and osteomalacia?

A

rickets - osteoid at growth plate is weak = bow legs
growth plate expands to compensate = swollen joints

osteomalacia = bon pain and pseudofractures

tx= vit D replacement

15
Q

How does the treatment of hypocalcaemia vary?

A

type and route of tx depends on:
- state of pt symptoms
(acutely ill with neuromuscular symptoms = IV calcium, whereas mildly symptomatic - oral calcium)
level and duration of calcium
underlying cause - e.g. if vit D deficient then replace that and if hypoparathyroisim then add 1,25 D3 products

16
Q

What happens when you have hypercalcaemia?

A

reduce secretion of PTH and increase calcitonin release to reduce bone resorption
also increase urinary excretion of calcium and reduce ca absorption in the intestine

17
Q

What are the causes of hypercalcaemia?

A
primary hyperparathyroidism (high PTH)
malignancy (low PTH)

rare

  • familial hypocalcuric hypercalcaemia
  • sarcoid (low PTH)
  • drugs - vit D toxicity
  • prolonged immobilisation (low PTH)
  • adrenal failure (low PTH)
  • milk alkali
18
Q

What are the different types of hyperparathyroidism?

A

primary
- increased secretion of PTH = single or multiple adenoma (common), parathyroid hyperplasia (less common), parathytoid carcinoma

Secondary

  • renal failure
  • vit D deficiency

Tertiary
- as a result of prolonged secondary hyperparathyoidism - renal transplant

19
Q

What are the clinical features of primary hyperparathyroidism?

A

most are asymptomatic
younger pts may develop:
- osmotic symptoms = thirst, polyuria, constipation
- aches and pains
- neuropsychiatric = lethargy/depression, confusion/coma
- renal stones, osteoporosis. pancreatitis

20
Q

What are the mechanisms of malignancy associated hypercalcaemia?

A

humoral hypercalcaemia
- PTHrP related or non-PTHrP related

Bone invasion

Rare causes = drug related (retinoids), immobilisation, PTH carcinoma

21
Q

What is the tx for malignancy associated hypercalcaemia?

A

if renal failure = dialysis with low ca bath
aggressive IV hydration - if volume overload then give loop diuretics
IV bisphosphonate +/- calcitonin
refractory cases - gallium nitrate or denosumab

22
Q

What happens when you have low PO4?

A

reduce PTH release so this will increase PO4 reabsorption in the kidney, and also increase release from bone, increase gut absorption

23
Q

What are the causes of hyperphosphataemia?

A

decreased renal excretion
acute phosphate load
redistribution to ECS
pseudohyperphosphataemia

24
Q

What are the clinical features of hyperphosphataemia?

A

most pts are asymptomatic
Acute
- tetany - hypocalcaemia, seizures and hypotension

Chronic
- secondary hyperparathyroidism - soft tissue calcification- kidneys, cornea, skin

25
Q

What are the causes of Mg deficiency?

A

GI disorders
renal loss
endocrine and metabolic disorders

26
Q

What are the clinical manifestations of hypomagnesia?

A

<0.74
non-specific lethargy and weakness
increased neuromuscular excitability e.g. tremors, carpopedal spasm, muscle cramps, tetany, generalised seizures
can cause cardiac arrhythmias - A and V tachycardia, prolonged QT interval and torsades depointes

27
Q

What is usually the cause of hypomagnesemia?

A

decreased oral intake, increased GIT or renal losses
acquired disorder - only in rare instances - does have an underlying hereditary aetiology

urinary magnesium helps to differentiate renal from extrarenal causes of magnesium wasting

28
Q

What is gitelman syndrome?

A

hypomagnesemia and renal magnesium wasting are distinctive features
AR caused by mutation in SLC12A3 gene encoding sodium chloride cotransporter which is expressed in the DCT

29
Q

What causes magnesium excess?

A

acute renal failure
severe diabetic ketoacidosis
addison’s disease
supplements

30
Q

What can be seen clinically with magnesium excess?

A

loss of deep tendon reflexes
increased PR interval
but only a problem when >2

31
Q

How should you monitor patients with severe mineral imbalance?

A
fluid balance
- fluid intake 
- output
- daily weight 
ECG monitor (arrhythmias) 
renal function and electrolytes at least daily

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