Hypercalcaemia And Hypocalcaemia Flashcards
Which form of calcium is active
- ionised
2 main pools of calcium
- bone and ECF
What form of calcium is present in bone
Calcium hydroxyapatite (very poorly exchangeable)
Which pool of calcium is measurable
> ECF
- calcium bound LOOK UO
How are calcium levels maintained?
- uptake through GIT (normal uptake needs normalGI function, active absorption from the diet)
- majority stored in skeleton (Osteoclasts -> Ca and PO4 release =)
- excreted renally ( as is phosphate) BUT CaPO4 is INSOLUBLE
What is calcium levels controlled by
- PTH
- metabolites of Vit D (most active 1,25 dihydroxycholecalciferol)
- calcitonin
Actions of PTH
- ^ ca resorption kidney
- promotes conversion 25D3 to 1,25D3
- ^ osteoclasts activity to free ca to bone
- enhanced Ca respotion from the gut mainly via 1,25D3
- PROMOTES PHOSPHATURIA
Outline vitamin D metabolism. What is th active form?
- need sunlight to produce vit D3 (cholecalciferol)
- need liver to produce 25- hydroxycholecalciferol
- need kidney to produce 1,25 hydroxycholecalciferol (calcitriol or active vit D)
Actions of calcitriol
> ^ serum calcium through number of mechanisms
- ^ GI absorption of calcium
- facilitates renal resorption of calcium
- mobilise Ca and PO4 from bone
calcitriol negative feedback inhibits PTH secretion
also has an important immune function (bacteriostatic/cidal in deep sea organisms)
3 main regulators of calcium homestasis. What are these responding to? Which one NEVER causes a clinical problem?
Calcitonin rarely causes a problem
LOOK UP
How much calcium exists in each form? Which forms can be excreted?
> ultrafilterable calcium - ionised ~50% - complexed ~20% > non filterable - protein bound ~30%
What should you always look at if calcium levels changed?
Albumin
What measurement of calcium is prone to artefact?
Ionised calcium - need to keep pH same (^ protein binding) - no exposure to air - agitation > becoming easier to measure at bedside
Why does PHOSPHATURIA result from PTH
- calcium mobilised form bone also produced a lot of PO4
- needs to be excreted quickly
What must be disrupted to cause disturbance of calcium ?
- hormonal control of calcium
- organs involved in absorption, storage or excretion of calcium
2 hormones that control calcium concentration
- PTH
- 1,25 D3 calcitriol
What needs to always be measured alongside calcium?
Phosphate
- 1,25D3 -> ^ phosphate
- PTH -> v phosphate
Which situiation is most urgent wrt Hypercalcaemia and phosphate
^ phosphate and ^ ca
- will mineralise out and lead to soft tissue calcification (likely to be irreversible)
- calcium phosphate product can be measured
When should Hypercalcaemia be investigated?
ALWAYS if repeatable
- even in the ABSCENCE of clinical signs
> can cause irreversible damage to many organs esp kidneys
Clinical signs of Hypercalcaemia
- PUPD
- Weakness, lethargy, depression
- inappetnce, vomiting, diarrhoea, constipation
- facial pruritis and oral dysfunction
- muscle fasciculations
- cardiac tachydysrhymthimas
- sudden death
NO CLINICAL SIGNS POSS
USG of urine before entering collecting duct?
1.001
What is needed for collecting ducts to work normally?
ADH
normal tissue sensitivity
How does calcium interfere with renal function
- impaired renal tonicity
- impaired sensitivity of tissues (collecting duct) to ADH -> impaired water resorption
> USG AZOTAEMIA - can also cause structural renal disease if also has ^phosphate (CaPo4 product >5-6)
* therefore Hypercalcaemia easily confused for structural kidney disease as produces v USG and azotaemia.. Always check ca*
How may CKD be linked to calcium?
Can cause calcium AND phosphate abnormalities
Non-pathological reasons for Hypercalcaemia
- rapidly growing young dogs ( transitive
- hyperalbumenaemia
- hemoconcentration
What 2 reasons will Hypercalcaemia be caused pathologically?
> ^ PTH or PTH rp activity
- low phosphate expected
unrelated to PTH activity
Pathologic, causes of hyper calcium
- ^ PTH activity (1* hyperparathyroidism)
- ^ PTH-like activitty (humoral hypercalcaemia of malignancy, lymphosarc, anal sac adenocarcinoma, multiple myeloma)
- unrelated to PTH (non PT causes)
What is seen clin path with hypercalcaemia d/t ^ PTH/PTH like activity?
- ionised hypercalcaemia AND low or non-elevated phosphate
- serum PTH likely inappropriately NOT SUPPRESSED (should be BELOW ref with ^ Ca) /^ serum PTH-rp
- some PTH like substances are not measurable
Causes of calcium NOT related to PTH activity?
> Vit D toxicity - excessive supplement - rodenticides - psoriasis creams > granulomatous dz - macrophages contain 1,25D3 > hypoadrnocorticsm > CKD - grape intoxication > idiopathic - cats > significant osteolysis
Which breed are pdf 1* hyoerparathyroidism?
Keeshonds
- autosomal dominant
- age related prevalence, rare cats
- calcium negative feedback lost
- ^ autonomous PTH production functional neoplasia (adenoma)
Clinical signs 1* hyoerparathyroidism
- often well, incidental finding
- unremarkable PE
- urolithiasis and LUTD signs (dysuria, pollakiuria, Haematuria)
- uncommon for other signs of Hypercalcaemia to be present
Role of calcium. Where is ca concentration high and low?
- nerve conduction, neuromuscular transmission
- muscle contrction
- intracellular messenger pathways
- coagulation
> intracellular calcium very low
> extracellular 10,000x higher §
How is hypercalcaemia related to CKD?
- MOST azotaemic CKD animals will have Ca in ref
- more likey for cats to be hypercalcaemic than dogs
- more likely to be an ionised hypercalaemia in cats than dogs, but still much more likely to be a NON-ionised hypercalcaemia
- HYPERphosphataemia also likely
- NOT 2* renal hyperparathyroidism as these patients have a NORMAL calcium
Most common cause of hypercalcamiea in cats. What should be monitored and how can this be managed?
Idiopathic
- generally middle aged
- commonly develop calcium oxalate urolths
- monitor calcium, USG, renal function
- management: Diet
- correct unlying causes (IF poss)
- IVFT
- frusemide
- bisphosphonates (pamidronate, alendronate)
Is hypocalcaemia a common finding? What can this mean?
> clinically insignificant - if d/t hyoalbumenaemia > ionised hypocalcaemia significant - d/t CKD - pancreatitis - 1* hypO-PT - iatrogenic hypO-PT - ecalmpsia > NOT DIETARY!!
Clinical signs of hypocalcaemia
> neuro > neuromuscular > GI - panting, anxiety, behavioural changes - weakness, stiff and stilted gait - inappettance/vomiting - hyperthermia - muscle tremors, cramps, pain
Management of hypocalcamiea
> if clinically significant THIS IS LIFE THREATENING
- correct potetnial underlying cause
- acute IV 10% calcium gluconate (bolus then CRI)
- subacute oral medication (calcitriol tapered, AT-10 tapered)
What should always be looked at when assessing calciurm?
- Phosphate
- Albumen
- Level of azotaemia
What is the major damage causig efect of caclium?
Calcification of soft tissues if calcium phosphate product >4.8-6.5
Top 2 causes of hypercalcaemia in DOGs and CATs
>dogs - neoplasia - 1* hyperPT > cats - CKD - idiopathic
