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Renal > Hyprecalcaemia and hypocalcaemia disorders > Flashcards

Hyprecalcaemia and hypocalcaemia disorders Flashcards

1
Q

How is calcium controlled?

A
  • PTH
  • metabolites of vitamin d
  • calcitonin
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2
Q

How does PTH increase Ca?

A
  • KIDNEY:
  • BONE
  • GIT
  • increases urine phosphate excretion (phosphaturia)
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3
Q

Actions of calcitriol

A

Papp

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4
Q

Why is calcium important?

A

Nn conduction and Neuromuscular transmission

  • muscle contraction
  • intracellular messenger involved in any number of cell signalling pathways
  • coagulation
  • vital maintenance of cell membrane integrity
  • second messenger roles
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5
Q

Why is calcium important

A
  • nn conduction and NM transmission
  • mm contraction
  • intracellular messenger involved in any number of cell signalling pathways
  • coagulation
  • intracellular Ca maintained at v low levels: vital for maintenance of cell membrane integrity, second messenger roles
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6
Q

How is Ca distributed in the body?

A
  • 2 main pools: bone and ECF
  • almost all calcium in bone is present as calcium hydroxyapatite (very poorly exchangeable)
  • EC calcium is biologically measurable form, includes: Ca bound to albumin, Ca chelated to various compounds, Ca free in solution or ‘ionised calcium’
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7
Q

Describe Ca uptake in GIT

A

active

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8
Q

How is Ca stored in bones?

A

Ca mobilised by osteoclasts with Ca and phosphate being released

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9
Q

Is calcium phosphate soluble or insoluble?

A

insoluble (calcium and phosphate are excreted separately by kidneys)

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10
Q

Control of Ca

A
  • PTH
  • metabolites of vitamin D (1,25 dihydroxycholecalfierol most active)
  • calcitonin
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11
Q

Outline PTH action

A
  • INCRASES CA at KIDNEY: increases Ca resorpton, promoting conversion of 25 D3 to 1.25 D3
  • INCREASES CA at bones: activation of osteoclast activity
  • INCREASES Ca at GIT: enhanced Ca resorption from gut, mainly mediated through 1,25 D3
  • INCREASES urinary phosphate excretion
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12
Q

Actions - calcitriol

A
  • increases serum Ca through number of mechanisms:
  • increasing GIT absorption of calcium
  • facilitating renal absorption of calcium
  • by mobilising Ca and PO4 ffrom bone
  • calcitriol has negative ffedback on its own secretion, inhibits PTH secretion
  • maintains aspects of immune system
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13
Q

What do PTH, metabolites of vit D and calcitonin respond to?

A

ionised Ca levels

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14
Q

Total serum Ca level = ?

A

2.45-2.83 mmol/L

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15
Q

Describe different calcium states

A
  • ULTRAFILTERABLE CALCIUM: ionised and complexed forms

- Protein bound calcium (1/3, almost exclusively to albumin)

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16
Q

How to measure serum Ca

A
  • prinicipally interested in ionised calcium

- so always also look at albumin levles

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17
Q

What artefacts are ionised calcium measurements prone to?

A
  • any increase in pH increases protein binding and decreases ionised calcium
  • increases in pH can occur through exposure to air, agitation, variation in [heparin]
  • numerous devices can measure this ‘at bedside’
18
Q

T/F: as CaPO4 is insoluble, for the mobilisation of Ca from bone to result in an increase in ionised Ca, the PO4 has to be readily removed

A

True

19
Q

Outline disturbances in Ca balance

A
  • needs to be significant disruption of hormonal control of Ca or the organs involved in absorption/storage/excretion of Ca
  • results in hyper/hypocalcaemia
  • or may result in altered bone metabolism without changes to serum calcium
20
Q

Which 2 hormones are principally involved in controlling clinically signifciant alterations in serum ca concentrations?

A
  • PTH

- 1,25 D3 calcitriol

21
Q

Why do you need to look at the phosphate levels when looking into possible Ca disturbances?

A

it is the calcium phosphate product that is producing irreversible soft tissue calcification (

22
Q

When can hypercalcaemia be ignored?

A

never - repeatable hypercalcaemia should always be investigated, even in absence of obviou CS

23
Q

Result of prolonged untreated hypercalcaemia

A

(especially with normal or increased phosphate) an lead to irreversible damage to many organs especially kidneys.

24
Q

CS - hypercalcaemia

A
  • PD and PU
  • weakness, lethargy, depression
  • inappetence, vomiting, diarrhoea, constipation
  • facial pruritus and oral discomfort
  • mm twitching and fasiculations
  • cardiac tachydysrhythmias
  • sudden death
  • or no detectable CS at all!
25
Q

Clinical pathology - hypercalcaemia

A
  • hypercalcaemia
    +/- disruption to serum phosphate concentration
  • with or without evidence of disruption to renal function
26
Q

Effect of hypercalcaemia on renal function

A
  • hypercalcaemia interferes with tubular function so the animal has trouble concentrating its urine –> USG azotaemia
  • structural renal disease if accompanied by elevated serum phosphate (CaPO4 product of >5-6)
27
Q

Clinical pathology - hypercalcaemia

A
  • hypercalcaemia
  • with or without disruption to serum phosphate concentration
  • with or without evidence of disruption to renal function characterised by azotaemia and IDU (inappropriately dilute urine)
  • impaired renal function can result in alterations to calcium and phosphate metabolsim (hyperphosphataemia and non-ionised hypercalcaemia)
28
Q

Causes - hypercalcaemia

A
  • non-pathological reasons (rapidly growing young dogs, lab error)
  • transient or interpretive (haemoconcentration, hyperalbuminaemia)
  • pathological (d/t increased PTH or PTH-like activity, unrelated to increased PTH activity)
29
Q

Outline pathological causes of hypercalcaemia

A
  • INCREASED PTH ACTIVITY: primary hyperparathyroidism
  • INCREASED PTH-LIKE ACTIVITY: humoral hypercalcaemia of malignancy, lymphosarcoma, anal sac adenocarcinomas, multiple myelomas etc etc
  • UNRELATED INCREASED PTH or PTH1a: non-parathyroid hormone dependent causes of hypercalcaemia
30
Q

Outline increased PTH and PTH-like activity

A
  • ionised hypercalcaemia and low or non-elevated phosphate are typically present
  • serum PTH likely to be ‘inappropriately not suppressed’ or there may be an elevation in serum PTHrP or some other PTH-like compound
  • PTHrP is measurable, others are not:
31
Q

Causes of hypercalcaemia not related to PTH-ish activity

A
  • vitamin D toxicity (excessive supplementation, rodenticides, psoriasis creams)
  • granulomatous inflammation
  • hypoadrenocorticism
  • CKD (grape intoxications)
  • idiopathic (cats)
  • significant osteolysis
32
Q

Describe primary hyperparathyroidism

A
  • keeshund markedly over-represented in developing primary hyperparathyroidism (autosomal dominat, with age-related penetrance)
  • increased and autonomous PTH production by a functional neoplasm (usually solitary adenoma)
  • disease of older dogs, generally over six years, uncommon in cats
  • calcium negative feedback is lost
33
Q

CS - primary hyperparathyroidism

A
  • these dogs often well (hypercalcaemia may be incidental)
  • often unremarkable PE
  • may develop urolithiasis and then show LUT signs - dysuria, pollakiuria, haematuria
  • uncommon for other signs of hypercalcaemia
34
Q

Outline hypercalcaemia of chronic renal disease

A
  • most animals with azotaemic CKD will have serum calcium in the reference range
  • 14% of dogs and 38% cats are hypercalcaemic and it will be an ionised hypercalcaemia in 10% dogs, 28% cats
  • hyperphosphataemia will also be present
  • NOT secondary to renal hyperparathyroidism (all these patients have NORMAL Ca)
35
Q

Outline idiopathic hypercalcaemia

A
  • perhaps commonest cause of hypercalcaemia in cats
  • as idiopathic, is a diagnosis of exclusion
  • generally middle-aged cats
  • commonly develop Ca oxalate uroliths throughout urinary tract
  • monitor Ca, USG, renal function
  • management: try dietary and then other management
36
Q

Outline management of hypercalcaemia

A
  • correct underlying cause or causes
  • consider tx to reduce the degree of hypercalcaemia: fluid therapy, furosemide, bisphosphonates (pamidronate or alendronate)
37
Q

Outline management of hypocalcaemia

A
  • not uncommon as clinically insignificant result of hypoalbuminaemia
  • BUT ionised hypocalcaemia is most frequently (dogs 3-%, cats 50%) associated CRF and:
  • pancreatitis
  • primary hypoparathyroidism
  • iatrogenic hypoparathyroidism
  • eclampsia
38
Q

CS - hypocalcaemia

A
  • abnormal neuro, neuromuscular and GIT function or combinations of all these:
  • panting, anxiety and behavioural changes
  • weakness with a stiff and stilted gait
  • inappetance through to vomiting
  • hyperthermia
  • mm tremors and cramps, mm pains
39
Q

Management - hypocalcaemia

A
  • once you have determined the hypocalcaemia is clinically significant and have corrected a potential underlying cause then:
  • acute IV 10% calcium gluconate
  • subacutely oral medication
40
Q

What does hypercalcaemia in cats seem to be caused by?

A
  • CKD
  • ‘idiopathic’ hypercalcaemia
  • rest
41
Q

What doses hypercalcaemia in dogs seem to be caused by?

A
  • neoplasia
  • primary hyperparathyroidism
  • the rest
42
Q

Management - hypocalcaemia

A
  • frequently an unimportant problem clinically as it can result of other abnormalities
  • must be tx when cause of CS it absolutely needs managing it as life-threatening
  • consequently whenever detected it should ALWAYS be investigated to level that makes you comfortable

Renal (30 decks)

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