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Diabetes mellitus and D inspidus

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Diabetes mellitus and D inspidus

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Diabetes mellitus and D inspidus

  1. 1. Submitted by: Dr. Kanwarpal Singh Dhillon M.V.Sc (Medicine)
  2. 2.  Diabetes mellitus is a chronic disorder of carbohydrate metabolism due to relative or absolute insulin deficiency  Diabetes is a life-long disease marked by high levels of glucose in the blood  It can be caused by too little insulin, resistance to insulin, or both.
  3. 3.  Insulin (beta cells) ◦ stimulates the uptake of glucose by body cells thereby decreasing blood levels of glucose ◦    Glucagon (alpha cells) ◦ stimulates the breakdown of glycogen and the release of glucose, thereby increasing blood levels of glucose ◦  Glucagon and insulin work together to regulate & maintain blood sugar levels
  4. 4.  Enables glucose to be transported into cells for energy for the body  Converts glucose to glycogen to be stored in muscles and the liver  Facilitates conversion of excess glucose to fat  Prevents the breakdown of body protein for energy
  5. 5.  Multitude of mechanisms ◦ Insulin  Regulation  Secretion  Uptake or breakdown ◦ Beta cells  damage
  6. 6.  1. Immune-mediated destruction of islets occurs leading to B-islet cell dysfunction  relative or absolute deficiency of insulin.  2. severe pancreatitis in dogs  3. Insulin resistance due to hyperadrenocorticism  4.chronic use of glucocorticoids
  7. 7.  5.pregnancy and diestrus .  6.Obesity .  In dogs ,progesterone causes release of growth hormones leading to hyperglycemia which develop insulin resistance.
  8. 8.  Multifactorial: ◦ Obesity: 4 X more likely to develop DM ◦ Pancreatitis ◦ Genetics ?? ◦ Amyloidosis of the pancreatic cells
  9. 9.  Factors lead to impaired insulin action in liver, muscle and adipose tissue and β–cell failure hyperglycemia  If some β–cell function exists, diabetes may be transient
  10. 10. • Occur in middle-aged dogs(7-9yr) and cats • In dogs: female > Males • In cats: Male> Female • More susceptible dog breeds: Miniature Poodles, Dachshunds, Schnauzers, Cairn Terriers, and Beagles Prevalence increasing over time: aging population, obesity, physical inactivity
  11. 11.  There are two major types of diabetes: ◦ Type 1 Diabetes ◦ Type 2 Diabetes
  12. 12. Aetiology of DiabetesAetiology of Diabetes  Type One Diabetes  results when the body’s immune system destroys its own beta cells in the pancreas. No insulin production is then possible.  Type Two Diabetes results from either  Insulin resistance (overweight patients)  Inadequate insulin production (lean patients)  A combination of both
  13. 13.  Insulin levels may be normal, elevated or depressed ◦ Characterized by insulin resistance, ◦ Diminished tissue sensitivity to insulin, ◦ Impaired beta cell function (delayed or inadequate insulin release
  14. 14. What is Insulin Resistance?  Condition in which the body does not utilise insulin efficiently  Insulin resistance is the decreased response of the liver and peripheral tissues (muscle, fat) to insulin  Insulin resistance is a primary defect in the majority of patients with Type 2 diabetes
  15. 15. Characteristics of Diabetes Type 1 Type 2  Rapid onset  Normal or underweight  Little or no insulin  Ketosis common  Autoimmune plus environmental factors  Low familial factor  Treated with insulin, diet and exercise  Gradual onset  80% are overweight  Most have insulin resistance  Ketosis rare  Part of metabolic insulin resistance syndrome  Strongly hereditary  Diet & exercise, progressing to tablets, then insulin
  16. 16. In Dogs:  Polydipsia  Polyuria  Polyphagia  Weight loss and weakness  Ketotic breath  Bilateral cataract  Osmotic diuresis  Recurrent infections, hepatomegaly
  17. 17.  Decreased resistance to bacterial and fungal infections  Develop prostatitis, bronchopneumonia, dermatitis  Emphysematous cystitis… Proteus, Aerobacter aerogens, E. coli  Impaired chemotactic, phagocytic, antimicrobial activity due to decreased neutrophilic function  Hepatomegaly due to lipid accumulation
  18. 18.  In addition to high glucose levels, acutely ill type 1 diabetics have high levels of ketones. ◦ As cells cannot get glucose, they burn fats as an alternate energy source ◦ Ketones are produced by the breakdown of fat and muscle, and are toxic at high levels ◦ Ketones in the blood cause a condition called "acidosis” or “ketoacidosis" (low blood pH) ◦ Urine testing detects ketones in the urine ◦ Blood glucose levels are also high.
  19. 19.  Develop frequently in dogs  Related to unique sorbitol pathway by which glucose is metabolized in the lens leading to Edema of lens and opacity.  Rare in cats. 
  20. 20. • Based on persistent fasting hyperglycemia and glycosuria • Normal fasting Glucose….75-125mg/dL • In Cats stress induced hyperglycemia…. So take multiple samples • Serum glycosylated Hb or fructosamine help to DDx stress induced hypergylcemia and DM
  21. 21. • Hypercholesterolemia • Hypertriglyceridemia • Increased ALP……coz of hepatic lipidosis • Increased ALT…….hepatocellular stress • Ketonemia…beta hydroxy butyrate increased • Hematology…. Not diagnostic • Urinalysis  SG > 1.025  Glycosuria  Variable ketonuria  Proteinuria  Bacteruria
  22. 22.  Hyperthyroidism  Hepatic disease  Renal disease  Pancreatitis  Hyperadrenocorticism
  23. 23.  CBC: +/- normal, anemia, stress leukogram  Profile: hyperglycemia, ↑ ALT/SAP, ↑ cholesterol, ↑ bilirubin (cats)  UA: proteinuria, pyuria
  24. 24.  Combination of – Insulin therapy  Diet  Weight reduction  Oral hypoglycemics
  25. 25. 1) Short acting (upto 6 hours)– neutral insulin 2) Intermediate (upto 16 hours)  Isophane (neutral protamine Hagedorn NPH)  Lente (mixed insulin Zn suspension)  Biphasic (mixed isophane and neutral) 3) Long acting(upto 24 hours)  PZI (protamine zinc insulin)  Insulin Galargine
  26. 26.  Dogs and cats  BID dosing needed with 2 meals of equal calories  DOGS: 0.25-0.5 units/kg BID  Diet high in simple sugars should be provided.
  27. 27.  In dogs with poor control of diabetes on NPH or lente insulin use of basal insulin detemir should be considered.  Starting dosage is 0.1U/kg , bid with reassessment of clinical signs in 1 wk.
  28. 28. INSU LIN ORIGIN INDICATI ONS ROU TE FREQUEN CY DOG CAT Regul ar crysta lline Recombina nt human Treat DKA IV Continuous infusion -- -- NPH Recombina nt human Treat diabetes at home SC q12h 8-14hr 6-12hr Lente Pure pork Good initial insulin for dogs SC q12h 8-14hr 8-14hr PZI 90% beef 10% pork “ SC q12h - 10-14hr Glargi ne Insulin analog Treat diabetes at home SC q12-24h 10- 16hr 10-16hr
  29. 29.  Dog may be hospitalized for up to 24 hours  Food and insulin injection(s) will be given according to the usual schedule at home (pet owner’s normal regime followed)  This includes insulin injections, size, type and timing of meals and exercise routine  A blood sample will be taken prior to feeding and insulin injection  Blood samples will then be taken every 1-2 (or 4 hours) for up to 24 hours  Blood glucose will be measured in each of these samples
  30. 30.  The blood glucose levels are plotted against time to produce a curve. This curve indicates the changes in blood glucose levels after the insulin is injected.
  31. 31.  The highest blood glucose concentrations occur at the time of each insulin injection  The lowest spot in the curve is called the nadir.  If the blood glucose nadir is >150mg/dl, the insulin dose may be increased  If the nadir is less than 80mg/dl, the insulin should be decreased  A glucose nadir occurring 12 hr or longer after insulin administration. indicates prolonged duration of insulin effect
  32. 32.  It looks like a bowl  The nadir, appears halfway between insulin injections  If the dog’s blood glucose does not go lower than 100 mg/dl or higher than 300 mg/dl during the observation period, it means that the insulin doses and duration are working well
  33. 33.  In cats ,Glargine is the initial insulin of choice.  It is used in combination with high protein and low carbohydrate diet.  It Is associated with remission of diabetes and discontinuation of insulin therapy in 80-90% cases within 3-4months.
  34. 34.  Sulfonylureas  Glipizide @ 2.5mg,bid  Cats  Glimepiride @2mg sid  Alpha-Glucosidase inhibitors  acarbose in cats @12.5-25mg,bid-tid in conjunction with diet
  35. 35.  Therapy involves – 1. I/V fluids like RL for correcting dehydration and acidosis.  2. giving regular insulin @ 0.2U/kg followed by 0.1U/kg regular at hourly interval.  3.once glucose level comes <250mg/dl then dose of 0.5U/kg is given every 4-6 hr s/c.
  36. 36. Diabetes Management  Healthy eating/ nutrition  Exercise  Monitoring  Medication/Insulin
  37. 37.  Primary Goal – improve metabolic control  Blood glucose  Lipid (cholesterol) levels  CATS: low carbohydrate, high protein, mod-high fiber  DOGS: low fat, high fiber
  38. 38.  Increase fiber ◦ >12% slowly fermentable , insoluble fiber or  >8% moderately fermentable fiber.  Royal Canin Diabetic HF  Royal Canin Calorie Control CC High Fibre (obese )
  39. 39.  To encourage weight loss  To decrease insulin resistance induced by obesity
  40. 40.  Diabetes insipidus is a condition characterised by PD,PU and excretion of large amount of hypotonic urine.   It occurs either due to low level of ADH in the body or due to impaired response of renal tissue to normal level of ADH in body.
  41. 41. Etiology & classification  Central diabetes insipidus: reduced secretion of ADH: ◦ also known as hypophyseal form ◦ Develops due to some lesion in hypothalamus ◦ 1. pituitary neoplasms, ◦ 2. cyst ◦ 3. inflammatory granuloma ◦ 4.trauma etc.  Nephrogenic diabetes insipidus: Kidney fails to respond to normal secretion of ADH.
  42. 42.  PU/PD: Passing large volume of hypotonic urine  Urine osmolality is decreased below normal plasma osmolality (approx 300 m Osm/kg) even during water deprivation.
  43. 43.  History: chronic PU/PD that does not respond to dehydration and is not due to primary renal disease  Water deprivation test  ADH response test ◦ Bladder is emptied and water and food are withheld for 3 to 8 hours ◦ Urine and plasma osmolality is deterimined ◦ At the end: If urine sp gr > 1.025: only a partial ADH deficiency or with antagonism of ADH action by hypercortisolism ◦ Little change in sp gr : Complete lack of ADH:
  44. 44.  Measure urine sp gr. at the start (Normal sp gr of dog urine: 1.020 to 1.040)  Put 2-4 drops of desmopressin acetate in the conjunctival sac  Empty the bladder at 2 hours  Collect urine again at 4,8,12, 18 and 24 hours and measure sp gr  Sp gr. peaks at > 1.026 in animals with a primary ADH deficiency, but show little change with nephrogenic diabetes insipidus
  45. 45.  After water deprivation: ◦ >3 normal animals ◦ 1.6-3 in animals with moderate ADH deficiency ◦ <1.8 in animals with severe ADH deficiency  After ADH administration ◦ > 2 in animals with primary ADH deficiency ◦ Between 1.1-2 in partial ADH deficiency ◦ < 1.1 in unresponsive ADH cases
  46. 46.  Diabetes mellitus: glycosuria and high urine sp gr  Chronic nepthritis : usually associated with renal failure  Hyperadrenocorticism.
  47. 47.  Desmopression acetate (synthetic analog of ADH) ◦ 2 drops on the nasal mucosae or conjunctivae SID to BID for life long  Caution: cardiac patients.  Do not restrict water.

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