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Renal > Hypercalcaemia And Hypocalcaemia > Flashcards

Hypercalcaemia And Hypocalcaemia Flashcards

1
Q

Which form of calcium is active

A
  • ionised
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2
Q

2 main pools of calcium

A
  • bone and ECF
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3
Q

What form of calcium is present in bone

A

Calcium hydroxyapatite (very poorly exchangeable)

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4
Q

Which pool of calcium is measurable

A

> ECF

- calcium bound LOOK UO

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5
Q

How are calcium levels maintained?

A
  • 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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6
Q

What is calcium levels controlled by

A
  • PTH
  • metabolites of Vit D (most active 1,25 dihydroxycholecalciferol)
  • calcitonin
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7
Q

Actions of PTH

A
  • ^ 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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8
Q

Outline vitamin D metabolism. What is th active form?

A
  • 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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9
Q

Actions of calcitriol

A

> ^ 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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10
Q

3 main regulators of calcium homestasis. What are these responding to? Which one NEVER causes a clinical problem?

A

Calcitonin rarely causes a problem

LOOK UP

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11
Q

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

A 
> ultrafilterable calcium 
- ionised ~50% 
- complexed ~20% 
> non filterable
- protein bound ~30%
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12
Q

What should you always look at if calcium levels changed?

A

Albumin

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13
Q

What measurement of calcium is prone to artefact?

A 
Ionised calcium 
- need to keep pH same (^ protein binding) 
- no exposure to air 
- agitation 
> becoming easier to measure at bedside
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14
Q

Why does PHOSPHATURIA result from PTH

A
  • calcium mobilised form bone also produced a lot of PO4

- needs to be excreted quickly

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15
Q

What must be disrupted to cause disturbance of calcium ?

A
  • hormonal control of calcium

- organs involved in absorption, storage or excretion of calcium

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16
Q

2 hormones that control calcium concentration

A
  • PTH

- 1,25 D3 calcitriol

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17
Q

What needs to always be measured alongside calcium?

A

Phosphate

  • 1,25D3 -> ^ phosphate
  • PTH -> v phosphate
18
Q

Which situiation is most urgent wrt Hypercalcaemia and phosphate

A

^ phosphate and ^ ca

  • will mineralise out and lead to soft tissue calcification (likely to be irreversible)
  • calcium phosphate product can be measured
19
Q

When should Hypercalcaemia be investigated?

A

ALWAYS if repeatable
- even in the ABSCENCE of clinical signs
> can cause irreversible damage to many organs esp kidneys

20
Q

Clinical signs of Hypercalcaemia

A
  • PUPD
  • Weakness, lethargy, depression
  • inappetnce, vomiting, diarrhoea, constipation
  • facial pruritis and oral dysfunction
  • muscle fasciculations
  • cardiac tachydysrhymthimas
  • sudden death
    NO CLINICAL SIGNS POSS
21
Q

USG of urine before entering collecting duct?

A

1.001

22
Q

What is needed for collecting ducts to work normally?

A

ADH

normal tissue sensitivity

23
Q

How does calcium interfere with renal function

A
  • 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*

24
Q

How may CKD be linked to calcium?

A

Can cause calcium AND phosphate abnormalities

25
Q

Non-pathological reasons for Hypercalcaemia

A
  • rapidly growing young dogs ( transitive
  • hyperalbumenaemia
  • hemoconcentration
26
Q

What 2 reasons will Hypercalcaemia be caused pathologically?

A

> ^ PTH or PTH rp activity
- low phosphate expected
unrelated to PTH activity

27
Q

Pathologic, causes of hyper calcium

A
  • ^ PTH activity (1* hyperparathyroidism)
  • ^ PTH-like activitty (humoral hypercalcaemia of malignancy, lymphosarc, anal sac adenocarcinoma, multiple myeloma)
  • unrelated to PTH (non PT causes)
28
Q

What is seen clin path with hypercalcaemia d/t ^ PTH/PTH like activity?

A
  • 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
29
Q

Causes of calcium NOT related to PTH activity?

A 
> Vit D toxicity
- excessive supplement 
- rodenticides
- psoriasis creams
> granulomatous dz
- macrophages contain 1,25D3
> hypoadrnocorticsm 
> CKD
- grape intoxication
> idiopathic 
- cats 
> significant osteolysis
30
Q

Which breed are pdf 1* hyoerparathyroidism?

A

Keeshonds

  • autosomal dominant
  • age related prevalence, rare cats
  • calcium negative feedback lost
  • ^ autonomous PTH production functional neoplasia (adenoma)
31
Q

Clinical signs 1* hyoerparathyroidism

A
  • often well, incidental finding
  • unremarkable PE
  • urolithiasis and LUTD signs (dysuria, pollakiuria, Haematuria)
  • uncommon for other signs of Hypercalcaemia to be present
32
Q

Role of calcium. Where is ca concentration high and low?

A
  • nerve conduction, neuromuscular transmission
  • muscle contrction
  • intracellular messenger pathways
  • coagulation
    > intracellular calcium very low
    > extracellular 10,000x higher §
33
Q

How is hypercalcaemia related to CKD?

A
  • 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
34
Q

Most common cause of hypercalcamiea in cats. What should be monitored and how can this be managed?

A

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)
35
Q

Is hypocalcaemia a common finding? What can this mean?

A 
> clinically insignificant 
- if d/t hyoalbumenaemia
> ionised hypocalcaemia significant
- d/t CKD
- pancreatitis
- 1* hypO-PT 
- iatrogenic hypO-PT 
- ecalmpsia 
> NOT DIETARY!!
36
Q

Clinical signs of hypocalcaemia

A 
> neuro
> neuromuscular
> GI 
- panting, anxiety, behavioural changes
- weakness, stiff and stilted gait
- inappettance/vomiting
- hyperthermia
- muscle tremors, cramps, pain
37
Q

Management of hypocalcamiea

A

> 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)
38
Q

What should always be looked at when assessing calciurm?

A
  • Phosphate
  • Albumen
  • Level of azotaemia
39
Q

What is the major damage causig efect of caclium?

A

Calcification of soft tissues if calcium phosphate product >4.8-6.5

40
Q

Top 2 causes of hypercalcaemia in DOGs and CATs

A 
>dogs
- neoplasia
- 1* hyperPT
> cats
- CKD
- idiopathic

Renal (23 decks)

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