Hypocalcaemia Flashcards

1
Q

What are the main groups of differentials for low Ca?

A

Low albumin
hypoparathyroidism
Vit D disorders
redistribution

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2
Q

What types of hypoparathyroidism are there?

A

Primary - either atrophy/ lymphocytic infiltrate of galnd or infarction of an adenoma
Secondary - From sx (normally thyroidectomy), can be from parathyroidectomy. cervical trauma

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3
Q

What vitamin D pathologies are there?

A

AKI/ CKD
Nutritional secondary hyperparathyroidism - eg. raw food, common in young animals fed diets with inappropriate Ca to phos ratio)

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4
Q

What are the main dzs of redistribution causing low calcium?

A
Eclampsia
Alkalinising treatment
Blood transfusions (excess citrate)
Feline lower urinary tract obstruction
Sodium Phosphate enemas
Frusemide
Ethylene glycol toxicity
Pancreatitis - due to saponification of peripancreatic fat, often subclinical
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5
Q

Compare low calcium with AKI and CKD

A

AKI - high phos, low Ca. Rapid progression, may see high K, acidosis
CKD - High phos, Ca may be high or low iCa often low to normal

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6
Q

What is eclampsia most common in?

A

small dogs or cats post whelping, within 3 weeks

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7
Q

Outline nutritional secondary hyperparathyroidism

A
Unbalanced diet
Mineral deficiencies
Low Ca Concentration
high PTH secretion
Bone mobilisation
Pain and fractures

On bloods it is rare to see low Ca

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8
Q

What are the main clinical signs of low Ca?

A
tetany/ seizures
facial rubbing/ twitching/ cramps/ stiffness/ fasiculation
High temp
hehaviour changes - aggression/ increased sensitivity/ disorientation/ 
Panting
Prolapsed TE
Increase salivation (cats)
Increased HR and arrythmias
PUPD
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9
Q

When is treatment for hypocalcaemia not needed?

A

When no c/s

If cause is low alb, renal, iCa is normal

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10
Q

Outline initial treatment for hypo Ca

A

IV calcium gluconate. When giving, place ECG, if bradycardia develops, need to stop infusion/ slow as can risk cardiac arrest
Can take 6 hours for signs to disappear

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11
Q

Outline in hospital management of low Ca after initial stabilisation

A

Ca gluconate as CRI or subcut every 6-8 hours. monitor iCa BID
If giving SC then mix 1:1 saline (can get cutaneous reactions)
Monitor lytes - caution when phos is high as may precipitate together in soft tissues
If MG is low then Hypo Ca can be refractory to tx

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12
Q

When is oral maintenance treatment needed for hypo Ca and how is this done

A

Needed for hypoarathyroidism
Vit D needed, give oral Ca whilst Vit D taking effect
Normal vit d given is vit D3 - calcitriol - takes 1-4 days for effect
Give Ca carbonate during this time, then very slowly taper

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13
Q

How will the PTH glands respond to different concentrations of calcium?

A

PTH secretion will dramatically increase when iCa is low;

when iCa is high, PTH secretion will decrease

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14
Q

How does PTH act in the main target organs (kidney, gut, bone)

A

In the kidney, PTH will increase calcium reabsorption and phosphorus excretion. It also increases the activity of 1α-hydroxylase, the enzyme responsible for converting 25-hydroxyvitamin D (25OHD) to 1,25-dihydroxyvitamin D3 (1,25[OH]2 D3 ) (calcitriol).

Calcitriol then acts on the gastrointestinal tract to increase calcium and phosphorus absorption.

In bone, PTH induces osteoclastic bone resorption, which increases calcium and phosphorus resorption.

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15
Q

How useful are the PTH tests for cats

A

Not brilliant, can be affected by lots of things. Treat results with caution

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16
Q

What are the differentials for nutritional secondary hyperparathyroidism?

A

renal secondary hyperparathyroidism
osteogenesis imperfecta
rickets.

17
Q

How do you diagnose secondary renal hyperparathyroidism?

A

High PTH with an animal with CKD

Ca and Phos are variable

18
Q

How do you treat secondary renal hyperparathyroidism?

A

Low phosphate diet +/- phosphate binders

19
Q

What is the danger value for hypocalcaemia?

A

0.8

20
Q

What does calcitriol do?

A

Increase Ca and phose absorption from the intestines and kidney

21
Q

Outline calcitonin

A

secreted from C cells in the thyroid gland in response to hypercalcaemia. Calcitonin inhibits osteoclastic activity, which in turn decreases bone resorption. It can also increase renal excretion of calcium via decreased tubular reabsorption. GI hormones such as gastrin can stimulate the secretion of calcitonin, and this mechanism is considered to help regulate postprandial hypercalcaemia. Calcitonin may also have an important role in regulating bone turnover.