DIABETES Flashcards

1
Q

MOST COMMON FORM OF DM IN DOGS AND CATS

A
  • INSULIN DEPENDENT DM
  • Requires daily insulin injections
  • Decreased serum insulin concentration
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2
Q

HOW TO MANAGE NON INSULIN DEPENDENT DM

A
  • May be managed with diet and oral hypoglycemic agents
  • Normal or increased serum insulin concentration
  • 25-30% diabetic cats ?
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3
Q

PATHOPHYSIOLOGY FOR DM

A
  • Islet-specific amyloidosis
  • Beta cell vacuolization
  • Decreased numbers of beta cells
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4
Q

POTENTIAL CAUSES FOR DM

A
  • Obesity
  • Chronic Pancreatitis
  • Drugs (steroids)
  • Concurrent illness
  • Immune destruction?
  • Genetics?
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5
Q

SIGNALMENT FOR DM IN BOTH CATS AND DOGS

A
  • Older animals
    • Dogs: average of 7-9 yrs of age
    • Cats: average of 9-11 yrs of age
  • Dogs: females > males
  • Cats: males > females
  • Any breed or mixed breed
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6
Q

2 TYPES OF PRESENTATION FOR DM

A
  • Non-ketotic (“healthy” or “happy” diabetic)
    • Primary focus of today’s discussion
  • Diabetic ketoacidosis (“sick” or “unhappy” diabetic)
    • Usually some concurrent illness (e.g. pancreatitis) causes counter-regulatory hormone release (e.g., increased epinephrine, cortisol, glucagon, growth hormone)
    • Considered later in course
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7
Q

HISTORY FOR DM

A
  • PU / PD
    • due to glucose which absorb more water
  • Polyphagia
    • they hav the sugar bt cant get it into the cell
  • Obesity with recent weight loss
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8
Q

PE FINDINGS FOR DM

A
  • Often unremarkable
  • May be obese
  • +/-history of weight loss
  • Hepatomegaly
  • Cataracts (dogs)
  • Diabetic neuropathy
  • Cats –“unkempt” haircoat
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9
Q

CBC AND CHEM PANEL FINDINGS FOR DM

A
  • CBC
    • No significant abnormalities
  • Serum chemistry
    • Hyperglycemia
      • if u are nt hyperglycemic u are nt diabetic
      • hyperglycemic is nt enough to say u hav diatedes like in dogs. it could be due to stress
    • Increased ALT, ALP (fat accumulation in liver)
    • Hypercholesterolemia
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10
Q

Collective term for glycated proteins in blood

A
  • Serum Fructosamine
  • Results from irreversible, non-enzymatic binding of glucose to proteins
  • Serves as a marker of mean blood glucose over the circulating lifespan of the proteins (1-3 weeks before sampling)
  • Not affected by acute increases in blood glucose (i.e., stress)
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11
Q

URINALYSIS FINDINGS FOR DM

A
  • Glucosuria
  • Ketonuria
  • Proteinuria
  • Bacteriuria with or without pyuria
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12
Q

MECHANISMS FOR Transient DM in Cats

A
  • Underlying pancreatic islet pathology (e.g. islet cell amyloid)
  • Insulin antagonism
  • Obesity
  • Drugs (e.g. glucocorticoids, megestrol acetate)
  • Hyperglycemia-induced beta cell dysfunction (“vicious cycle”)
  • Occurs in 10-20% of diabetic cats
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13
Q

GOALS OF THERAPY FOR DM

A
  • Resolution of clinical signs (most important!!)
    • PU/PD
    • Polyphagia
    • Weight loss
  • Animal appears healthy and interactive with owner
  • Animal has stable body weight
  • Owner is happy
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14
Q

TX FOR DM

A

Dietary therapy
Insulin therapy
Client education

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15
Q

DISCUSS DIET TX FOR DM

A
  • Promote weight loss if needed
  • Diet characteristics
  • Diet with complex carbohydrates, low in fat, high in fiber
  • Soluble (gums, pectins) preferable to insoluble (lignin, cellulose) fiber
  • Most commercial high fiber diets contain mainly insoluble fiber (still helpful)
  • Adhere to regular feeding schedule (BID meals)
    • Avoid between meal “snacks”
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16
Q

DIET THEARAPY FOR DM CATS

A
  • Recent studies support role for “low-carbohydrate, high-protein” diet for cats with diabetes mellitus
  • Based on “strict” carnivorous nature of cats
  • Better regulation in many cats
  • Some cats may no longer require insulin
  • Must consider role of “transient” diabetes in outcome
17
Q

TYPE OF INSULIN U SHOULD GIVE TO DOGS

A

PORCINE

HOG DOG

18
Q

TYPE OF INSULIN U SHOULD GIVE TO CATS

19
Q

WHICH TYPE OF INSULIN IS SHORT ACTING

A

REGULAR

FOLLOWED BY MPH

20
Q

THIS TWO TYPES OF INSLIN Contain protamine and zinc to delay insulin absorption from SQ site of injection

A
  • NPH and PZI
  • Lente insulins
    • Depend on zinc content to delay insulin absorption from SQ site of injection
21
Q
  • THIS DRUG
  • HAS Long duration of action (up to 18 hrs in cats) can contribute to “carry over” effect
  • nt used in dogs good for cats
A
  • Glargine (Lantus®)
  • May facilitate remission in cats if used with low carbohydrate diet*
  • Minimal effectiveness in dogs (unreliable)
22
Q

Highly purified porcine insulin suspension GOOD FOR DOGS

A
  • aninsulin
  • Resembles Lente in composition
23
Q

INSULINS FOR DOGS

A
  • Humulin N (NPH): 0.25 to 0.5 U/kg SQ q12h
  • Vetsulin: 0.25 to 0.5 U/kg SQ q12h
24
Q

INSULIN TYPES FOR CAT

A

Beef/pork PZI: 0.25 to 0.5 U/kg SQ q12h or q24h
Glargine (Lantus): 0.25 to 0.5 U/kg SQ q 12h or 24h

25
COMPLICATIONS FOR DM
* Difficulty in regulation (dogs & cats) * Insulin-induced hypoglycemia (Somogyi effect) * Persistent clinical signs (PU, PD, weight loss) * Cataracts (dogs) * Peripheral neuropathy (cats) * Pancreatitis (dogs & cats) * Bacterial infections (dogs & cats) * Ketoacidosis (dogs & cats) * Hepatic lipidosis (dogs & cats) * Hypertension (dogs)
26
PATHOPHYSIOLOGY FOR CATARACT
* Glycolysis oversaturated in lens and leads to glucose metabolism via polyol pathway * Sorbitol and fructose not freely permeable and attract water into lens * Older cats have very low aldose reductase (hence don’t get diabetic cataracts)
27
(Complications indicating poor control of dm
* Dog: cataracts * Cat: peripheral neuropathy
28
When is a glucose curve done?
7 -14 days after starting insulin therapy
29
(lowest blood glucose achieved on glucose curve
Glucose nadir Reflects dosageof insulin
30
\*Duration of insulin action (time in “target zone”) tells u what
Reflects typeof insulin 
31
Time from injection to glucose nadir tells u wat
Reflects type of insulin Onset of insulin action (time from injection until blood glucose begins to fall) also Reflects type of insulin
32
Problems Identified by BG Curve
* Somogyi effect * Short duration of insulin action * Insulin resistance * Stress
33
explain the somogmi effect
* High dose of insulin administered * Animal becomes hypoglycemic (not seen by owner) * Counter-regulatory hormones released and cause hyperglycemia * epinephrine, cortisol, glucagon, growth hormone * Counter-regulatory hormones cause transient (24-72 hrs) insulin resistance potentially leading to erroneous conclusion that animal needs more insulin
34
when should u suspect somogmi effect
* Morning blood glucose \> 400-450 mg/dL * Continued clinical signs: PU, PD, weight loss * Symptoms of hypoglycemia (often unrecognized) * Insulin dosage \> 2.2 U/kg (dog) or \> 5 U (cat) * Wide fluctuations in glycemic control
35
when should u suspect somogmy effect
* Hypoglycemia (\< 65 mg/dL) and hyperglycemia (\> 300 mg/dL) in one 24-hour period after insulin administration