Diabetes Mellitus

DIABETES MELLITUS
  • Diabetes mellitus is a complex metabolic disorder as result of insufficient insulin secretion or excessive insulin antagonism leading to wide aberrations in carbohydrate, fat and protein metabolism with secondary disturbances in water and electrolytes.

Insulin non-availability

  • Degenerative changes in β cells in pancreatic islets.
  • Reduced effectiveness of hormone due to anti-insulin antibodies or inactive complex.
  • Autoimmune mediated islets cytotoxicity.
  • Inappropriate secretion of hormones by neoplasms in other organs.

Incidence

  • 1:200 total canine patients
  • Spontaneous in mature dogs (8-9 yrs female more affected than male)
  • Susceptibility: miniature Poodle, Dacshunds and Terriers.

Pathogenic mechanism

  • Destruction of islet cells due to severe pancreatitis and subsequent replacement by fibrous tissues. So, the gland becomes firm, multinodular and often has scattered areas of haemorrhage and necrosis.
  • Selective degeneration of Islet cells (more in cats): Stress, obesity, administration of cortisol.

Causes

  • Idiopathic atrophy
  • Virus

Clinical signs

  • Onset is insidious – chronic.
  • Polydipsia, polyuria, increased food consumption but loss of body weight.
  • Bilateral cataract.
  • In diabetes increased concentration of glucose in aqueous and vitreous humour. So glucose penetrates into lens. There, it is metabolized into sorbitol and further into fructose. The increased concentration in lens leads to entry of water into lens fiber and causing swelling.
  • Weakness.
  • Diminished resistance to bacteria and fungal infection. So, recurrent or chronic infection such as suppurative cystitis, prostatitis, Bronchopneumonia and dermatitis.
  • Hepatomegaly due to cirrhosis or accumulation of fat. Rough palpation leads to intra abdominal haemorrhage.
  • Chronic renal disease.
  • Blindness due to microangiopathy.
  • Gangrene.
  • Ketone bodies accumulate in blood. Loss of sodium through urine – H+ conserved – so, acidosis leading to coma.

Laboratory diagnosis

  • Glycosuria (urine more viscid, sweety odour & specific gravity increase.
  • Fasting hyperglycemia - increases to 140 mg/ 100ml.
  • Glucose tolerance test (GTT) (i/v or oral).
  • Ketone in blood and urine and smell in respiratory tract.
  • Elevated serum cholesterol and triglycerides.

Differential diagnosis

  • Chronic nephritis: urine - Low specific gravity, increased protein, no sugar.
  • Diabetes insipidus: Urine - low specific gravity which increase after the administration of antidiuretic hormone.
  • Pyometra: Polyuria, No glucose. Abdominal distension.
  • Acute nephritis: Increased temperature, vomition, occasionally urine contains sugar.
  • Adreno cortical hyper function: Alopecia, hyperkeratosis.
  • Prolonged steroid therapy.

Treatment

  • Uncomplicated - Control hyperglycemia by insulin.
  • Complicated - Correction of dehydration with plasma expanders, electrolyte replacement.
  • Infusion of bicarbonate to control acidosis.
  • If hypokalemia , 'K' to be given.
  • For obese animal - no insulin.
  • In milder cases - Soluble insulin- absorbed quickly, act within 20-30 minutes; reach peak levels within 4 hrs and maintained at these levels for maximum of 8 hrs
  • Protamine Zn insulin s/c : reach peak in 8-12 hrs and this level is maintained for nearly 24-36 hrs
  • Intermediate action: - Lente insulin, Globulin insulin and Isophan insulin. They start acting in 4 hrs, reach peak in 8hrs and maintained for 18-26 hrs.
  • NPH (Neutral Protamine Hagedorn) : 1 unit /kg in morning along with food.
  • Stabilize the patient: To start with 2 units of soluble insulin + 2 units of other types; then 4 + 4; then 6+6 units
  • Check the urine daily.
  • In advanced case – several hundred units i/v.
  • Good grade of canned food and green vegetables + pancreatin – 2 tablet.
  • Oral therapy – unsuccessful.
Last modified: Friday, 20 January 2012, 8:26 AM