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Hypercalcaemia >10.5mg/dL (clinical features (bodys response…
Hypercalcaemia >10.5mg/dL
distribution of calcium
99% bones
(calcium-phosphate) hydroxyapetite
parathyroid hormone
when extracellular calcium is low
Bones
release calcium into the blood
Kidney
resorbs calcium in the DCT
kidney
activates calcitriol
GIT
in response to Calcitriol increases absorption of calcium from the diet.
.99% extracellular
Diffusable
free-ionised
roles
neuronal action, all muscle contraction, hormone secretion and blood regulation
complexed
roles
normal in small amounts, electrically neutral not used for processes
non-diffusable: bound to albumin
bound to albumin and not involved in cellular processes, cannot cross cell wall.
albumin binding
albumin is net neg charge. balanced COO- and COOH. changes with bodily acidity
acidic blood
many protons, bind to free COO- and become COOH and becomes positively charged. +ve ca2+ cannot bind as they repel eachother, results in
increased ionised calcium
dehydration
causes psuedohypocalcaemia because of a resultant increase in albumin concentration. free ionised calcium stays the same because of hormonal regulation.
.01% intracellular
too much intracellular calcium results in apoptosis
calcium resides in organelles like the mitochondria and the Smooth ER.
controlling what enters the cell are voltage gated and ligand gated channels. to get Ca out are Na+Ca++ exchangers and ATP-CA pumps. responsible for maintaining intracellular calcium for electrical membrane potential.
the role of calcium in the cell
is to stabilise the resting state of the sodium channels on the cell membranes. which prevents the cell from spontaneously depolarising.
high levels of extracellular calcium = sodium channels less likely to open. sodium cannot enter the cell. cell cannot depolarise
results in neurons being less excitable and harder to reach depolarisation
investigations
PHT, Vitamin D, albumin, phosphorus, magnesium
treatment
decrease calcium with IV saline to increase sodium.
loop diuretics
inhibit calcium resorption resulting in all calcium being excreted.
glucocorticoids
inhibit GIT absorption of ca.
bisphosphinates
/
calcitonin
prevent bone resorption, by inhibiting osteoclasts.
phosphate binders
clinical features
bodys response
dehydration
kidney tries to dump excess calcium and in the process also excretes excess water.
calciuria
excess calcium binds to oxalate and forms stones
PNS
slower or absent reflexes
CNS
confusion, hallucinations, stupor.
muscles
slower muscle contraction = constipation and muscle weakness.
ECG
short QT interval, osborne wave, bradycardia and AV block. hypertension. aotric murmur sclerosis.
Bones and joint
gout and psuedogout and bone pain
urinary:
frequency diruesis and polydipsia. renal failure.
causes
increased osteoclastic resorption
excess vitamin D from diet and supps
thiazide diuretics, estrogen, theophyline, resorption in the DCT
dehydration
Acidity
thyrotoxicosis