Calcium Disorders Flashcards

1
Q

CCM Chapter 52

A

Calcium Disorders

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2
Q

What are the three forms of circulating calcium

A

Ionised, protein bound and complexed to anions

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3
Q

WHat ECG changes may be noted with hypercalcemia?

A

Bradycardia -prolonged PR interval, widened QRS
complex, shortened QT interval, shortened or absent ST segment,
and a widened T wave

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4
Q

What are the three most important hormones in calcium regulation?

A

PTH, Vit D and Calcitonin

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5
Q

What are the three broad ways in which calcium is regulated

A

the absorption of dietary calcium
the extent of ECFCa2+ excretion by the kidney
the relative rate of release and uptake of ECFCa2+ from the bony skeleton which contains a massive reservoir of 99% of ECFCa2+

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6
Q

What is the catalyst for PTH secretion?

A

Secreted by chief cells in the parathyroid in response to hypocalcemia or low calcitriol levels (active form vit D)

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7
Q

What inhibits PTH secretion

A

Hypercalcaemia or high calcitriol levels

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8
Q

What is the principle action of PTH?

A

increase calcium via increased renal tubular reabsorption, increased osteoclastic bone resorption and increased calcitriol production

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9
Q

How is Vit D absorbed and metabolised?

A

Absorbed via diet –> metabolised to calcidiol in the liver then calcitriol in the kidney.
calcitriol is promoted by deceased phos, calcium and calcitriol and increased PTH. All of those substances offer negative feedback mechanisms

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10
Q

What is the role of calcitriol?

A

acts on
intestine -> enhances enterocyte calcium and phos absorption
bone, -> promotes bone formation
kidney -> acts to inhibit calcitriol production and promote calcium and phos resorption
and PTH -> inhibits PTH secretion

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11
Q

What is the role of calcitonin?

A

Produced in the parafollicular cells of the thyroid in response to an increased calcium meal or hyerpcal.
inhibits osteoclastic resorption, and decreases renal calcium absorption

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12
Q

How does pH affect ionised calcium measure?

A

Higher pH means more calcium binding sites available on albumin mean less ionised calcium and more bound

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13
Q

Hypercalcaemia

A
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14
Q

What CSx are associated with hypercalcaemia?

A

PU/PD, anorexia, constipation, lethargy, weakness

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15
Q

WHat ECG changes may be noted with hypercalcemia?

A

Bradycardia - prolonged PR interval, widened QRS
complex, shortened QT interval, shortened or absent ST segment,
and a widened T wave

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16
Q

What are the common differentials associated with hypercalcemia?

A

H - hyperparathyroidism
A - Addisons
R - Renal failure
D - Hypervitaminosis D
I - Idiopathic in cats
O - osteolytic lesions
N - Neoplasia
S - Spurious
G- granulomatous disease

17
Q

A calcium to phos product of what increases the risk of soft tissue mineralisation

A

60

18
Q

How may hypercalcaemia be treated?

A
  1. Treat the cause
  2. IV fluids - 0.9% saline ideal as the sodium ions provide competition for renal tubular resorption of calcium
  3. Diuretics
  4. Steroids - reduces bone resorption, decreased GI absorption, increased renal excretion
  5. Calcitonin - reduces activity and formation of osteoclasts - may cause vomiting,
  6. Haemodyalsis
  7. Bisphosphonates - decrease osteoclastic activity,
19
Q

Hypocalcaemia

A
20
Q

What CSx are associated with hypocalcaemia

A

Muscle tremors
Cramping
Stiff gait
Restlessness
seizres
panting
pyrexia
lethargy
Prolapse third eyelid in cats
tachycardia

21
Q

What ECG changes may occur in hypocalcaemia?

A

prolonged QT interval (because of prolonged
ST segment), deep, wide T waves, or atrioventricular block

22
Q

What differentials commonly result in hypocalcaemia ?

A
  • Chronic renal failure
  • Eclampsia
  • Acute kidney injury
  • Pancreatitis
  • Soft tissue trauma or rhabdomyolysis
  • Hypoparathyroidism
  • After sudden reversal of chronic hypercalcemia
  • Secondary to magnesium depletion
  • Ethylene glycol
  • Phosphate enema
  • Bicarbonate administration
  • Improper sample anticoagulant (EDTA)
  • Infarction of parathyroid gland adenoma
  • Rapid IV infusion of phosphates
  • Acute calcium-free IV infusion
  • Intestinal malabsorption, PLE, starvation
  • Hypovitaminosis D
  • Blood transfusion (with citrate-containing anticoagulant)
  • Hypomagnesemia (PTH secretion and receptor effects)
  • Nutritional secondary hyperparathyroidism
  • Acute tumor lysis syndrome
  • Chelating agents
  • Excessive bisphosphonate treatment
23
Q

When do you decide to treat hypocalcaemia?

A

If Csx are present or if it is severe/moderate and progressive

24
Q

Why should calcium not be given SQ?

A

can cause skin necrosis and
abscess formation severe enough to warrant euthanasia, even when
diluted calcium preparations are administered.

25
Q

What should be monitored during calcium admin?

A

Heart rate and ECG should be monitored
closely during administration to look for bradycardia; prolonged
PR interval; widened QRS complex; shortened QT interval;
elevated, shortened, or absent ST segment; and widened T wave, all
of which may indicate cardiac toxicity. It is important to note that it
may take up to 30 to 60 minutes for all clinical signs to resolve after
correction of hypocalcemia, and some behavioral changes and
panting may persist during this time.

26
Q

What options exist for longer term supplimentation?

A

Cacitriol (vit D)
Oral calcium