calcium dysregulation Flashcards
What do vitamin D & PTH do? Where are they produced from?
Vitamin D produced in skin. PTH produced in parathyroid gland. Vit D and PTH increase calcium levels
What does calcitonin do and where is it secreted from?
Calcitonin decreases calcium and is secreted from the parafollicular cells.
Where is vitamin D made and from what? Where else can we get vitamin D from and in what form?
Vitamin D made in the skin with UVB light. From precursor to pre-vitamin D3 to vitamin D3. from the diet as vitamin D2
What is required for vitamin D to become active? Where does this happen? What happens if we make too much of the active vitamin D?
hydroxylation steps. 1st hydroxylation step in the liver - enzyme 25 hydroxylase to form 25 OH cholecalciferol. Second hydroxylation step in the kidney with enzyme 1- alpha hydroxylase to form active vitamin D (calcitriol). If we make too much calcitriol negative feedback to decrease transcription of 1-alpha hydroxylase to make less calcitriol.
What are the effects of calcitriol on the bones and on the guts & kidney? What happens in deficiency of vitamin D?
calcitriol affects osteoblasts (bone building cells) in order to build bone. It increases calcium & phosphate reabsorption in both the guts and the kidney. Vitamin D deficiency causes rickets in children and osteomalacia in adults.
Where is parathyroid hormone PTH produced? What are the effects of PTH on bone, gut and kidney in terms of calcium & phosphate?
PTH is produced in parathyroid gland (we have 4). PTH affects osteoclasts (bone breaking) cells releasing calcium from bones. In gut increases calcium & phosphate reabsorption. In kidney increases calcium reabsorption but increases phosphate excretion. Also increases 1-alpha hydroxylase activity in kidney and therefore increases calcitriol which increases calcium & phosphate reabsoprtion.
What is the action of FGF23? Where is it made?
FGF23 is made by osteocytes to regulate phosphate. It inhibits the sodium-phosphate co-transporter in PCT which usually increases phosphate reabsorption, in order to promote phosphate excretion. (PTH also inhibits this transporter). It also inhibits calcitriol formation in order to further decrease phosphate reabsorption from gut and kidney.
What happens to the body when we have hypocalcaemia and why? What are the symptoms associated with it? What is the sign associated with it and what is it?
Hypocalcaemia leads to increased sensitisation of neuronal tissues to sodium. So we get increased neuronal excitability leading to convulsions, tetany, arrhytmias, parasesthetia. Sign is trousseaus sign - carpopedal spasm.
What are potential causes of hypocalcaemia and how are they divided?
- PTH deficiency - magnesium deficiency, agnesis, neck surgery, autoimmune. 2. vitamin D deficiency - deficiency from diet, UV light, malabsorption, or impaired production (kidney failure - second hydroxylation step)
What does hypercalcaemia do to the body and why? What are the signs and symptoms associated with it?
Hypercalcaemia decreases neuronal excitability so leads to stones (renal stones), abdominal moans (constipation, pain, anorexia, nausea), psychic groans (depression, fatigue, coma).
What are potential causes of hypercalcaemia?
- excess PTH - parathyroid adenoma - autonomous production of PTH due to benign adenom due to no negative feedback. 2. metastasis: cancer metastasis to bone can activate osteoclasts to resorb bone and thus increase serum calcium levels. Other cancers can cause PTH -like peptide that binds on PTH receptors to increase calcium reabospriton. 3. vitamin D excess (rare)
What do parathyroid glands do and how do they react to calcium levels?
We have 4 parathyroid glands that sense calcium levels. If calcium low will make more PTH to normalise levels, if calcium high will make less PTH.
What is a parathyroid adenoma and what does it cause?
Paraythyroid adenoma is primary hyperparathyroidism. Benign adenoma of parathyroid gland that produces PTH and has no negative feedback so autonomous PTH production increasing calcium.
What is primary hyperparathyroidism? What would be seen in blood test? What is treatment? If untreated what can happen?
Primary parathryoidism is benign parathyroid adenoma that produces autonomous pTH with no negative feedback. On blood test would see high PTH, high calcium, low phosphate. Treatment is surgery (parathyroidectomy). If left untreated - osteoporosis, kidney stones, psychological impact
What is secondary hyperparathyroidism? What would be seen in blood test? What is treatment and how should this change depending on renal status?
Normal physiological response to low calcium, makes PTH to normalise this. In blood - low calcium, high PTH. Treatment is vitamin D replacement. In those with normal renal function can give inactive vtiamin D (ergocalfierol) because can convert it. In those with renal form need to give calcitriol in its active form (alfacalidol)
