calcium and bone Flashcards
calcium regulation: explain the hormonal regulation of blood calcium ion concentration; list the causes and clinical features of hypercalcaemia and hypocalcaemia
diagram of calcium homeostasis: interaction between PTH and vitamin D
diagram; PTH to increase serum Ca2+: increases Ca2+ reabsorption from bone, causes kidney to reabsorb Ca2+, regulates production of active vitamine D (calcitriol); inactive vitamin D (calcidiol) is from liver and undergoes 1a hydroxylation under control of PTA, increasing serum Ca2+ by increasing Ca2+ absorption from gut
phosphate absorption regulation
Na+/PO43- absorbed via cotransporter from urine in proximal convoluted tubule; PTH from blood inhibits this, as does fibroblast growth factor 23 (FGF23 - from osteocytes); this also inhibits calcitriol synthesis, reducing PO43- reabsorption from gut
where does phosphate reabsorption occur
via gut and kidneys
what does increase phosphate reabsorption cause to Na+
less Na+ excretion in urine (as co-transported in)
effect on serum PO43- in hyperparathyroidism
low as increased urine phosphate excretion (PTH inhibits Na+/PO43- transporters)
regulation of PTH secretion: high [Ca2+] ECF
Ca2+ binds to Ca2+ sensin receptor on parathyroid cell -> receptor activation leads to inhibition of PTH secretion
regulation of PTH secretion: low [Ca2+] ECF
Ca2+ not bound to Ca2+ sensin receptor -> no inhibition -> PTH secreted -> PTH action in body leads to increased [Ca2+] ECF
role of vitamin D in calcium homeostasis
diagram
where is vitamin D obtained from
vitamin D obtained from diet (ergocalciferol to inactive vitamin D calcidiol in liver) or sunshine (UVB light); in kidney, 1a-hydroxylase (stimulated by PTH) produces calcitriol (active vitamin D)
effect of cacitriol on PTH, and Ca2+
negative feedback on PTH; increases Ca2+ gut absorption, maintenance in bone, renal Ca2+ reabsorption
5 causes of vitamin D deficiency
malabsorption or dietary insufficiency, lack of sunlight (block UVB light), liver disease (can’t convert to calcidiol), renal disease (no stimulation of renal 1a-hydroxylase by PTH to convert to calcitriol), receptor defects in gut, bone, kidney and parathryoid gland
2 examples of diseases causing GI malabsorption of vitamin D
coeliac, inflammatory bowel
inheritance and prevalence of vitamin D receptor defects, and response to treatment
autosomal recessive, rare, resistant to vitamin D treatment
high EC Ca2+ (hypercalcaemia) effect on nerve and skeletal muscle excitability
Ca2+ blocks Na+ influx as more competition, so less membrane excitability
low EC Ca2+ (hypocalcaemia) effect on nerve and skeletal muscle excitability
enables greater Na+ influx as less competition, so more membrane excitability