Lecture: Calcium Flashcards
Functions of calcium in the body (8)
Structural role Activator Blood caogulation Skeletal and cardiac muscle contraction Nerve impulse transmission Milk production Regulation of membrane ion transport Cellular secretion
Major sources of dietary calcium
Milk and milk products
Factors affecting the variability in absorption of calcium from the SI
Concentration in the diet pH Presence of activated vitamin D Parathyroid hormone High protein Diet Steatorrhea Age
Storage of calcium in the body
Gut
ECF
Kidney
Bone (highest conc)
What 3 forms is calcium present in serum in
Ionised/free (active)
Complexed
Protein bound (inactive)
What are blood calcium levels influenced by
Parathyroid hormone
Calcitonin
Vitamin D
How many amino acids compose the PTH
84
When is PTH released
When ECF calcium is decreased
What organs/tissues does PTH act on
Bone, kidney and intestine
Describe calcitonin molecule
32 amino acid peptide with one disulphide bond
What secretes calcitonin
C cells of the thyroid in response to an increase in ionised calcium
Three target tissues for activated vitamin D
Intestine, bone and kidney
How much calcium is bound to albumin
50%
Non diseases state total serum calcium level
2.4 mmol/L
When is binding of calcium to protein decreased/increased
Decreased in acidosis states
Increased in alkalosis states
What is normal calcium level required for
Nerve function, membrane permeability and glandular secretion
Does PTH glands recognise unbound or bound calcium
Unbound
Why is “adjusted calcium used”
So patients with low albumin are not mistaken for being hypocalcaemic
and so
patients with normal calcium low albumin are not missed for being hypercalaemic
How to calculate adjusted calcium (mmol/L)
Total calcium + 0.02(47-[albumin])
Causes of hypocalcaemia
Hypoparathyroidism
Vitamin D deficiency
Renal disease
Pseudohypoparathyroidism
Clinical features of hypocalcaemia
Neurological features such as tingling, tetany and mental changes, cardiovascular signs and cataracts
What should adjusted calcium level be
above 2.1 mmol/L
What further tests should be done following measuring Ca and albumin to determine if patient is hypocalcaemic
Measure urea and creatinine for renal disease.
Check PTH is appropriate to serum Ca.
Treatment for hypocalcaemia
Oral calcium supplements
Causes of hypercalcaemia
Primary hyperparathyroidism and hypercalcaemia of malignancy
Clinical features of hypercalcaemia
Neurological and psychiatric features such as lethargy, confusion
Irritability and depression
Gastrointestinal problems such as anorexia, abdominal pain, renal features such as thirst and polyuria
Cardiac arrhytmias
What does a level of 3.5 mmol/L or greater of adjusted calcium mean
Life threatening and action is required immediately
Treatment of hypercalcaemia
Intravenous saline is administered to restore GFR and promote a diuresis
Aminohydroxypropylidene diphosphate is treatment of choice in patients with hypercalcemia of malignancy. (inhibits bone reabsorption)
Average dietary intake of magnesium
15 mmol per day
When is hypermagnesaemia seen
Uncommon but occasionally seen in renal failure
Symptoms of hypomagnesaemia
Impaired muscle function such as tetany, hyperirritability, tremor, convulsions and muscle weakness
Laboratory diagnosis of hypomagnesaemia
Spectrophotometric with metallochromic indicators, calmagite and methylthymol blue, formazan dye, magon and phosphoazo III
At what level of magnesium conc. might benefit from magnesium therapy
< 0.7 mmol/L
How to detect intracellular magnesium concentration when Mg is within reference range
Research procedure NMRspectro-scopy to detect free MG 2+ inside cells
What can magnesium supplements cause
Diarrhoea
What is phosphate attached to
Inside cells mostly attached to lipids and proteins
Where is most of the bodys phosphate
In bone
How is control of ECF phosphate concentration achieved
By the kidney where tubular reabsorption is reduced by PTH
Normal phosphate concentration (monohydrogen phosphate and dihydrogen phosphate)
0.8 -1.4 mmol/L
Causes of hyperphosphateaemia
Renal failure
Hypoparathyroidism
Haemolysis
Pseudohypoparathyroidism
Causes of hypophosphataemia
Hyperparathyroidism Congenital defects of tubular phosphate reabsotpion Ingestion of non-absorbabke antacids Treatment of diabetic ketoacidosis Sever dietary deficiency.
