Endocrinology_1

Endocrinology_1

DIABETES MELLITUS
1. INSULIN DEFICIENCY
  1. HYPERGLYCAEMIA
    1. DIABETIC KETOACIDOSIS
      1. Body cannot use glycogen as an energy source. KETONES are used instead.
        Ketones: ORGANIC ACIDIC BLOOD
        Aim: To reduce blood ketone level quickly and efficiently
        TREATMENT: I/v fluid therapy Short-acting insulin (i/v or i/m) Antiemetics Antibiotics
        MONITOR AND SUPPORT: Check electrolyte levels, haematology, provide high fibre/low carb diet, comfortable environment, general nursing care, T/P/R regularly, blood pressure monitoring, blood glucose meter
        PROGNOSIS: Good if responsie and successfully treated with adequate management of Diabetes Mellitus
        CLINICAL SIGNS: Collapse Inappetence Dehydration Shock Tachycardia Hypotension
        Diagnosis as with Diabetes Mellitus including abdominal ULTRASONOGRAPHY
  2. Insulin is produced by Beta cells in the PANCREAS (Islet of Langerhans)
    1. Glucose + Insulin = Glycogen Stored in liver and muscle cells
2. CLINICAL SIGNS: Polyuria/polydipsia Polyphagia Cataracts (Dogs) Plantigrade posture (Cats)
  1. MORE SEVERE CLINICAL SIGNS: Vomiting Diarrhoea Depression Lethargy
3. Blood haematology, biochemistry and urinalysis
  1. Fructosamine/ketone presence
4. TREATMENT: Insulin administration
  1. Requires regular monitoring; glucose curves, urine output, weight control. Adjust insulin admin accordingly.
    1. PROGNOSIS: Good with adequate management.
    2. INSULIN OVERDOSE
      1. HYPOGLYCAEMIA
        CLINICAL SIGNS: Weakness, exercise intolerance, collapse, seizures, coma
        DIAGNOSIS; Haematology, biochemistry, glucometer (blood glucose levels)
        TREATMENT; i/v glucose fluid therapy, offer food, glucose solution on gums
        Aim: To raise overall blood glucose levels
        PROGNOSIS
        HYPOADRENOCORTICISM (ADDISON'S DISEASE)
        Deficient in mineralocorticoid (aldesterone) and glucocorticoid (Cortisol)
        CORTISOL: Metabolism of fats, protein, carbohydrates and involved in stress response
        ALDESTERONE: Maintain electrolyte balance (specifically potassium)
        Less aldesterone, increased blood potassium levels
        HYPERKALAEMIA
        Above 5.5 mmol/l is perceived as high
        CLINICAL SIGNS: Bradycardia, poor pulse quality, sluggish electrical conduction >> ECG changes
        DIAGNOSIS: Potassium serum level tests, ECG
        TREATMENT: find underlying cause, fluid therapy is ESSENTIAL
        i/v calcium gluconate, i/v insulin and dextrose, i/v fluid therapy
        CLINICAL SIGNS; Collapse, weakness, lethargy, PUPD, bradycardia, pale MMs, poor pulse quality
        DIAGNOSIS: Haematology, biochemistry, urinalysis, ACTH stimulation test, ECG
        TREATMENT: I/v fluid therapy, hormone replacement therapy
        CLIENT SUPPORT
        HYPERCALCAEMIA
        Increased blood calcium as renal ultrafiltration compromised (Muls et al., U/D)
        CLINICAL SIGNS: Anorexia, PUPD, depression, vomiting, tremors, prolonged = renal failure
        DIAGNOSIS: Haematology, biochemistry, urinalysis, diagnostic imaging
        TREATMENT: i/v NaCl, furosemide, calcitonin
        Underlying cause MUST be identified
  2. Aim: To reduce blood glucose level by supplementing insulin to convert to glycogen.
  3. SUPPORT: Owner communication, low carb/high fibre diet, insulin therapy, exercise as normal
    1. CLIENT SUPPORT: 1-on-1 demonstration of insulin administration, sufficient literature, out-of-hours number, increased client contact with familiar staff

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