Calcium disorders in SA Flashcards

1
Q

Use a diagram to illustrate calcium homeostasis?

A
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2
Q

Draw an in depth diagram of how calcium homeostasis is managed in the SA?

A
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3
Q

What forms of calcium are there in the body?

A
  • total vs. ionised vs. bound vs. complexed
  • Standard serum tube gives just a total calcium. The only form that is relevant is the ionised form as this is only bit that will change performance of the cells.
  • The bound form tends to be related to albumin. If there are changes in total protein levels our bound level will change.
  • Total calcium concentrations are affected by total protein concentrations.
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4
Q

How do we measure ionised calcium?

A
  • Must be correct pH and temp and oxygen free when collected if possible
  • Careful with heparin samples as it binds calcium.
  • Ionised calcium is very labile so getting an accurate value is very hard. Needs to be in machine very quickly before it clots.
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5
Q

Create a diagram that shows distribution of calcium?

A
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6
Q

Total calcium measurements include?

A
  • bound (to albumin; ~40%)
  • complexes (~10%)
  • free/ionised (~50%)
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7
Q

If albumin concentrations decrease, then total calcium decreases because?

A

Ionised calcium is in equilibrium with the interstitial fluid and is regulated by PTH.

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8
Q

What influences the measured calcium concentration?

A

If you get a hypercalcemia you didn’t expect probs due to the below:

  • Lipaemia
  • Haemolysis
  • pH
  • Albumin concentration
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9
Q

What is the impact of pH on the ionised calcium concentration?

A
  • Alkalosis (not common in dogs, can happen in respiratory disease with hyperventilation) – tends to increase the binding of calcium and therefore tends to cause ionised hypocalcaemia
  • Acidosis – tends to reduce the binding of calcium to albumin and therefore tends to cause ionised hypercalaemia
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10
Q

Why is the concentration of (ionised) calcium important in the body?

A

Action potentials. Things that influence resting and acting potential. Potassium and calcium change the threshold potential. Changes the point at which membrane potential needs to get to before it can fire off. Hypercalcaemia decreases threshold potential: ability to fire and AP has increased.

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11
Q

What are the clinical signs of hypercalcaemia?

A
  • Renal: PU/PD*
  • General: Muscle weakness, lethargy, depression, and tremors (neuromuscular)
  • Gastrointestinal: Anorexia, vomiting, and constipation
  • Cardiac (rare): Arrhythmias secondary to myocardial calcification

*Decreased sensitivity of the renal tubules to ADH and tubular changes secondary to mineralization of the basement membranes, degeneration, and interstitial fibrosis

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12
Q

What are the differentials for hypercalcaemia?

A

HOGS IN YARDL

Hyperparathyroidism

Ostolytic lesions

Granulomatous disease (monocyttil/ macrophage inflammatory based disease)

Spurious

Idiopathic

Neoplasia

Young

Addison’s

Renal failure

Vitamin (D) toxicity

(Lungworm angistrongylum)

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13
Q

The four major differential diagnoses for hypercalcaemia in the dog are?

A
  • Hypercalcaemia of malignancy*
    • most common: lymphosarcoma and anal sac adenocarcinoma. Palpate anal sacs of animal that come in hypercalcaemic and PU/PD.
  • Hypoadrenocorticism (Addison’s disease; A)
  • Primary hyperparathyroidism (H)
  • Chronic kidney disease*

Most common in *

  • *HHM – humoral hypercalcaemia of malignancy
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14
Q

How does cancer cause hypercalcaemia?

A

Note: not all cancers cause hypercalcaemia

By which mechanisms does cancer cause hypercalaemia?

  • PTHrP (parathyroid hormone related protein) production (NB low PTH)
    • Lymphoma
    • Carcinomas
  • Vitamin D production (lymphoma)
  • Ectopic PTH secretion (humans mainly)
  • IL-1 and TGF-b can both stimulate bone resorption
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15
Q

Why do you see hypercalcaemia associated with granulomatous disease?

A
  • Autogenous production of active vitamin D (calcitriol) by macrophages.
  • Similar action to 1α-hydroxylase in the kidney.
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16
Q

Show how pattern of phosphate and calcium gives you a strong suspicion of pathological cause?

A
17
Q

Describe hypervitaminosis D?

A
  • diet/medication history;
  • low PTH concentration
  • If vitamin D toxicosis:
    • Intoxication with Dovonex™ anti-psoriasis medication (vitamin D analogue)
    • Excessive vitamin D supplementation
    • E.g. salmon oil
    • Intoxication with Vit D rodenticide
18
Q

The two major differential diagnoses for hypercalcaemia in the cat are?

A
  • Hypercalcaemia of malignancy (N)
    • most common; usually lymphosarcoma
  • Idiopathic hypercalcaemia (I)
19
Q

What is the major secondary complication of idiopathic hypercalcaemia?

A

Renal damage; calcium oxalate urolithiasis

20
Q

A number of treatments exist for hypercalcaemia list them?

A

Intravenous fluid therapy (0.9% saline) Na encourages release of calcium in kidney

Diuretics (furosemide) Increase renal excretion of calcium (sodium encourages calcium excretion)

Glucocorticoids (prednisolone or dexamethasone) Decrease absorption of calcium from intestine, reduce bone resorption of calcium, and enhance calcium excretion from kidneys

Mithromycin

Bisphosphonates (pamidronate or zoledronate) Treatment for osteoarthritis Inhibit osteoclast activity and induce osteoclast apoptosis

21
Q

Hypocalcaemia

Although lower than normal calcium concentrations are often detected and corrected with fluid therapy, clinical hypocalcaemia is a rare occurrence in small animals.

When clinical signs are detected, serum total calcium concentrations are often <1.5 mmol/L and treatment must be initiated as quickly as possible.

Clinical signs of hypocalcaemia in dogs and cats include:

A
  • Focal muscle spasms or fasciculations (antebrachial fasciulations)
  • Ataxia or spasticity
  • Tetany and generalized seizures
  • Anorexia, vomiting, and diarrhoea
  • Nervousness
  • Prolongation of the ST segment and QT interval; arrhythmias
  • Prolapse of the third eyelid (cats)
22
Q

Eclampsia (puerperal tetany) is a manifestation of hypocalcaemia.

Clinical features include:

A
  • Lactational hypocalcaemia
  • Acute life-threatening condition
  • Plasma total calcium concentrations <1.5mmol/L
  • Most common in small dogs
  • Tetany observed
  • Fever can develop as muscle contraction generates heat
  • Develops as a result of extreme hypocalcaemia in bitches and queens.
  • More common in small dogs (less common in larger dogs and cats).
  • Clinical signs depend on rate of decline of serum calcium.
23
Q

When is eclampsia seen most frequently?

A

Most frequently seen in first 21 days of nursing

24
Q

What is the aetiology of eclampsia?

A
  • Loss of calcium into the milk and foetal skeleton
  • Poor dietary use of calcium
  • Reduced appetite due to stress of parturition
  • Parathyroid atrophy (poor diet/dietary supplements)
  • Hypomagnasaemia effects how hypocalcaemia can be treated
25
Q

What is the treatment approach for eclampsia?

A
  • Administer 10% calcium gluconate solution IV slowly (don’t give it in hartmanns as you’ll end up with a chalky patient.
  • 5 to 15 mg/kg IV slow over 10 to 20 min; equivalent to 0.5 to 1.5 ml/kg
    • Want to get calcium above 0.6-0.7mmol/l
  • Continue with CRI – 2.5-3.75mg/kg/hr of elemental calcium
  • But then need to review and address cause:
    • e.g. if hypoparathyroid or pancreatitis or ethylene glycol