L11 - Calcium Homeostasis COPY Flashcards
HYPOCALCEMIA
i) what effect does it have on neurons?
ii) what can it cause to happen?
iii) name two signs of hypocalcaemia and explain each
iv) what causes these signs ionically?
i) destabilises them
ii) can cause seizures
iii) 1) carpopedal spasm (Trousseau’s sign)
- low calcium makes nerons more likely to fire
2) Chvosteks sign
- tap facial nerve (superficial) and check response
- can happen in 10% of normal people
iv) low plasma calcium increases the permeability of neuronal membranes to sodium therefore they fire APs more easily causing seizures/spasm
CONSEQUENCES OF HYPERCALCAEMIA
i) name three acute symptoms
ii) name five chronic consequences
iii) what may a patient with high calcium be at risk of in their kidneys?
iv) how does hypercalcemia affect the bones?
i) thirst, polyuria and abdominal pain
- abdo pain due to less NS firing therefore constipation etc
ii) constipation, osteoporosis, MSK weakness, renal problems, neurobehav symptoms
iii) high calcium can increase risk of kidney stone formation
iv) hypercalcaemia can cause body to wee out calcium then you can get osteoporosis as its lost from the bones
MEASURING SERUM CALCIUM
i) what % is protein bound? of which what % is bound to albumin and what % is bound to globulin?
ii) what % is bound to cations? name two cations it may be bound to?
iii) what % is ionised (free)?
iv) what is the normal calcium level measured in the blood?
i) 40% is protein bound
- of which 90% is bound to albumin and 10% to globuli
ii) 10% is cation bound - phosphate and citrate
iii) 50% is ionised/free
iv) 2.15-2.55 mmoles/l
MEASURING CALCIUM - CLINICAL IMPLICATIONS
i) the lab reports total serum calcium corrected for what?
ii) give two scenarios when this may be inaccurate?
iii) in these cases - what should be measured?
i) lab reports total serum calcium corrected for the albumin concentration
ii) may be inaccurate if the albumin conc is <20g/l or in severe acute illness
iii) measure ionised calcium directly
CONTROL OF CALCIUM IN THE BLOOD
i) which hormone is the main controller of keeping calcium in the normal range?
ii) which gland and cells is this hormone released from?
iii) what determines this hormones release?
i) parathyroid hormone
ii) made in the parathyroid glands in the chief cells
iii) serum calcium concentration (free calcium in the blood)
- drop in calcium triggers PTH release
CALCIUM AND PTH SECRETION
I) which cells sense low plasma calcium ?
ii) what does low calcium levels in the blood cause to happen in these cells? what does this lead to?
iii) which ion is required as a co-factor for PTH secretion? name a drug class that can inhibit this ion
iv) what effect does PTH have on the renal tubule?
i) chief cells in the PTH gland
ii) low blood calcium causes a conformational change in the calcium sensing receptor in the chief cell which causes PTH release
iii) Mg2+ is required as a co-factor for PTH secretion
- proton pump inhibitors can cause low mg2+
iv) PTH acts on the renal tubule when calcium levels in the blood are low and causes reduced calcium excretion
PTH RECEPTOR
i) which recptor does PTH bind to exert is action?
ii) what happens when PTH binds its receptor?
iii) name two places these receptors are found - why?
i) PTH receptor 1
ii) induces a conformational change
iii) bone - lots of calcium stored here
kidney - excretes calcium
PTH ACTION ON BONES
i) what is the rapid effect of PTH on bone? which cells are involved?
ii) which cells are involved in slower release of calcium?
iii) which cytokine is made by these cells that binds the receptor on an osteoclast?
iv) what happens when this cytokine binds an osteoclast?
i) causes calcium release immediately
- osteocytes have projections that can push out fluid with a high calcium concentration into the circulation
ii) osteoblasts and osteoclasts
iii) osteoblasts make a rank ligand which binds its receptor on osteoclasts
iv) when rank binds osteoclast - the osteoclast produces acid/enzymes that dissolve the bone and release calcium into the circulation
ACTION OF PTH ON THE KIDNEY
i) what is the rapid effect of PTH on the kidney? name three places in the nephron where this takes place
ii) how is phosphate reabsorption affected by PTH? why?
iii) which hormone do osteocytes produce that stimulate renal phosphate excretion?
i) reabsorption of calcium in the LOH, DT and CD
ii) decrease in phosphate reabs from the kidney to prevent CaPo4 products building up in the blood
iii) osteocytes produce FGF23 which stimulates phosphate excretion
THE KIDNEY, VITAMIN D AND PTH
i) what is 25 OH vitamin D converted to in the kidney?
ii) which molecules positively and negatively regulate this?
iii) what action does the product of this conversion have on the gut? (2)
iv) why do mesenchymal tumours present with osteomalacia?
i) 25OH vitamin D is converted to 1,25 OH vitamin D in the kidney
ii) positively reg by PTH and negatively reg by FGF23 (from osteocytes)
iii) 1,25OH vit D stimulates calcium transporters and binding proteins in the gut = increases calcium absorption
iv) mesenchymal tumours can produce excess FGF23 which can cause decreased calcium absorption, low PO4 and very low 1,25 vit D = low calcium and vitamin D = SOFT BONES
PRIMARY HYPERPARATHYROIDISM
i) what is seen in relation to serum calcium, serum phosphate and PTH?
ii) name two things that can cause it
iii) name two bone complications - why?
iv) name a renal complication - why?
v) give five indications for a parathyroidectomy
i) high serum calcium, low serum phosphate and very high PTH
ii) all parathyroids can produce excess PTH
or there can be a single nodule that has broken away and is making PTH inappropriately
iii) osteoporosis and bone cysts
- high PTH causes break down of bone
iv) renal stones - lots of calcium reabs from the renal tubule and there may be lots of calcium in urine –> stones
v) osteoporosis (do bone mineral density scan), renal stones, age <50yrs, serum calcium >2.8mmol/l, choice
HYPOPARATHYROIDISM
i) what levels of serum calcium and PTH are seen?
ii) name four causes of primary hypoparathyroidism - which is the most common?
i) low serum calcium and low/normal PTH
ii) iatrogenic is the most common (thyroidectomy or neck surgery for cancer)
- autoimmune
- hypomangesaemia
- genetic mutations
SECONDARY HYPERPARATHYROIDISM
i) what is it? what PTH levels are seen?
ii) what levels of 25 OH vitamin D may be seen? give two reasons for this
iii) how can renal failure cause it?
iv) name two consequences of low vitamin D on bones
v) which group of people find it harder to make vitamin D? what does this predispose them to?
i) high PTH to compensate for low calcium for another reasom - its trying to get low serum calcium back to normal
ii) low serum 25 OH vitamin D will decrease calcium abs
due to lack of sun exposure or GI problems (malabsorption)
iii) renal failure means no 25 to 1,25 OH vitamin D therefore absorption from the gut. may be compromised
iv) low vit D = rickets and osteomalacia
v) elderly struggle to make vit D which can affect the NMJ which increases fall rate and therefore fracture rate
