In-House Diagnostics Module 2 Flashcards

1
Q

What are the three factions of total Ca

A

Ionised calcium (55%) - physiologically active
Complex calcium (10%)
Protein bound calcium (35%)

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2
Q

Calcium intake/storage?

A

Intake mainly via GI tract with excretion via kidneys - Ca stored in bones can be nobilised during hypocalcaemia

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3
Q

What hormones are part of calcium control?

A
  1. PTH: main hormone to increase Ca
  2. Calcitonin: Decreased Ca by decreased bone absorption
  3. Calcitrol: in response to PTHrp, increases Ca by increased GIT absorption and bone resorption
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4
Q

7 Causes of hypercalcaemia

A
  1. Neoplasia - multiple myeloma, mammary carcinoma, lymphoma, adenocarcinoma
  2. Primary hyperparathyroidism
  3. Acute renal failure
  4. Idiopathic in cats
  5. Granulomatous disease - angiostrongylus, fungal
  6. Vit D. tox
  7. Bone disorders
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5
Q

Clinical signs of hypercalcaemia?

A

inappetent, lethargy
PUPD
V+, constipation
Affects kidneys ability to respond to ADH - pre-renal azotaemia with dilute urine
soft tissue mineralisation

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6
Q

Treatment of hypercalcaemia

A
  • Fluid diuresis - NaCl 4-6ml/kg/hr
  • Frusemide 1-2mg/kg q6-12hrs renal Ca excretion
  • Bisphosphates (decreased bone resorption) - clondronate
  • glucocorticoid at anti-inflam doses
  • Salmon calcitonin - possible anaphylaxis
  • peritoneal/haemodialysis - life threatening Ca
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7
Q

Hypocalcaemia causes?

A
  • Improper sampling
  • Hypoparathyroidism - primary/iatrogenic/nutritional
  • Chronic renal failure
  • Eclampsia
  • Ethylene glycol
  • Acute pancreatitis
  • Malabsorption
  • Iatrogenic - rapid blood product admin, rapid phosphate admin, phosphate enema
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8
Q

Clinical signs of hypocalcaemia

A
  • Increases excitability of neuromuscular tissue: muscle tremors, facial rubbing, behaviour changes, hyperthermia, panting
    –> tetany, ECG changes, hypotension –> resp distress/death
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9
Q

Causes of hypophosphataemia

A

Decreased GI absorption
Refeeding syndrome
Tumor genesis syndrome
Increased urinary loss - diuresis, hyperaldosterone, glucose therapy

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10
Q

Causes of hyperphosphataemia

A
  • most commonly with renal disease
  • secondary renal hyperparathyroidism
  • tumor lysis syndrome
  • rhabdomyolysis
  • Haemolysis
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11
Q

Types of lactate

A

Lactate A - shock and decreased systemic perfusion and increased muscular activity
Lactate B - B1: Underlying disease, B2: Drug or toxin induced, B3: mitochondrial myopathy

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12
Q

What is urea

A

an end-product of protein metabolism
synthesised in liver from ammonium and bicarb
excreted via kidneys
affected by urine flow and dehydration

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13
Q

What is creatinine

A

formed in muscle through degradation of creatine and freely filtered through the glomerulus, small amount through Gi tract

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14
Q

What are conditions that can trigger DKA

A

UTI
Acute pancreatitis
Cushings
Cholangiohepatitis
Neoplasia
Renal failure
Infection
GH

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15
Q

DKA treatment protocol

A
  1. Restore intravascular volume - match to Na levels
  2. K supplementation
  3. Insulin/glucose protocol
  4. monitor for hypophosphataemia
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16
Q

Addisons treatment protocol

A

fluids - NaCl
K+ tx if needed
Dexameth
Zycortal
Maintenance pred