Diabetes mellitus and D inspidus

1. Submitted by: Dr. Kanwarpal Singh Dhillon
M.V.Sc (Medicine)

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.  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

5.  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

6.  Multitude of mechanisms
◦ Insulin
 Regulation
 Secretion
 Uptake or breakdown
◦ Beta cells
 damage

7.  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

8.  5.pregnancy and diestrus .
 6.Obesity .
 In dogs ,progesterone causes release of growth
hormones leading to hyperglycemia which
develop insulin resistance.

9.  Multifactorial:
◦ Obesity: 4 X more likely to develop DM
◦ Pancreatitis
◦ Genetics ??
◦ Amyloidosis of the pancreatic cells

10.  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

11. • 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

12.  There are two major types of diabetes:
◦ Type 1 Diabetes
◦ Type 2 Diabetes

13. 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

15.  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

16. 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

18. 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

20. In Dogs:
 Polydipsia
 Polyuria
 Polyphagia
 Weight loss and weakness
 Ketotic breath
 Bilateral cataract
 Osmotic diuresis
 Recurrent infections, hepatomegaly

21.  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

22.  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.

23.  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.


24. • 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

25. • 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

26.  Hyperthyroidism
 Hepatic disease
 Renal disease
 Pancreatitis
 Hyperadrenocorticism

27.  CBC: +/- normal, anemia, stress leukogram
 Profile: hyperglycemia, ↑ ALT/SAP,
↑ cholesterol, ↑ bilirubin (cats)
 UA: proteinuria, pyuria

28.  Combination of – Insulin therapy
 Diet
 Weight reduction
 Oral hypoglycemics

29. 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

30.  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.

31.  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.

32. 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

33.  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

34.  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.

35.  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

36.  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

37.  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.

38.  Sulfonylureas  Glipizide @ 2.5mg,bid
 Cats  Glimepiride @2mg sid
 Alpha-Glucosidase inhibitors  acarbose in cats
@12.5-25mg,bid-tid in conjunction with diet

39.  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.

40. Diabetes Management
 Healthy eating/ nutrition
 Exercise
 Monitoring
 Medication/Insulin

41.  Primary Goal – improve metabolic
control
 Blood glucose
 Lipid (cholesterol) levels
 CATS: low carbohydrate, high protein, mod-high
fiber
 DOGS: low fat, high fiber

42.  Increase fiber
◦ >12% slowly fermentable , insoluble fiber or
 >8% moderately fermentable fiber.
 Royal Canin Diabetic HF
 Royal Canin Calorie Control CC High Fibre (obese )

43.  To encourage weight loss
 To decrease insulin resistance induced by obesity

44.  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.

45. 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.

46.  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.

47.  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:

48.  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

49.  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

50.  Diabetes mellitus: glycosuria and high urine sp gr
 Chronic nepthritis : usually associated with renal
failure
 Hyperadrenocorticism.

51.  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.