- ^ 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

Hypercalcaemia And Hypocalcaemia Flashcards by laura knight

Which form of calcium is active

ionised

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2 main pools of calcium

bone and ECF

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What form of calcium is present in bone

Calcium hydroxyapatite (very poorly exchangeable)

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Which pool of calcium is measurable

> ECF

- calcium bound LOOK UO

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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

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What is calcium levels controlled by

PTH
metabolites of Vit D (most active 1,25 dihydroxycholecalciferol)
calcitonin

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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

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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)

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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)

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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

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How much calcium exists in each form? Which forms can be excreted?

> ultrafilterable calcium 
- ionised ~50% 
- complexed ~20% 
> non filterable
- protein bound ~30%

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What should you always look at if calcium levels changed?

Albumin

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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

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Why does PHOSPHATURIA result from PTH

calcium mobilised form bone also produced a lot of PO4

- needs to be excreted quickly

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What must be disrupted to cause disturbance of calcium ?

hormonal control of calcium

- organs involved in absorption, storage or excretion of calcium

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2 hormones that control calcium concentration

- 1,25 D3 calcitriol

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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 ```