Diabetes Mellitus Flashcards

1
Q

What cells create insulin?

Side effects of no insulin

A

Beta cells in pancreas

  • Glucose cannot enter cells
  • Cell “starvation”
  • Hyperglycemia
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2
Q

Type I: Insulin dependent diabetes mellitus (IDDM) is due to what?

What % of dogs have this type? cats?

A

Beta cell destruction

  • > Virtually ALL DOGS
  • > 30-‐50% of cats
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3
Q

Type II: Non‐insulin dependent diabetes mellitus (NIDDM)

A

Insulin resistance and/or beta cell dysfunction

  • > 50‐70% of cats; Note: The term “non‐insulin dependent” is misleading
  • We should instead be thinking of the pathophysiology
  • Likely have some residual beta cell function
  • Insulin resistance, impaired insulin secretion; - Keep in mind - most of these cats are treated with insulin
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4
Q

Causes of DM

A

 Genetics  Immune-‐mediated;  Insulin-‐antagonizing drugs;  Progesterone, cortisol  Obesity;  Pancreatitis

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5
Q

Dog DM Signalment

A

Dogs:;  4-‐14 years (7-‐9 y peak)  Female > male;  Breed predispositions;  Aust Terrier  Schnauzers  Beagles;  Samoyeds  Etc

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6
Q

Cat DM Signalment

A

 Cats:;  Usually >9 y (peak 10 y)  Male neutered;  No breed predispositions (?)

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7
Q

Common features of DM

A

 Common:  PU/PD;  Weight loss;  If diabetic ketoacidosis, can have history and PE reflecting systemic illness; - UTIs (50% of dogs);  May be obese or low body condition;  ± dull hair coat;  ± hepatomegaly;  ± cataracts (dogs);  ± plantigrade stance (cats)

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8
Q

Other differentials for DM

A

 Cats  DM;  Hyperthyroidism  Renal insufficiency

 Dogs:  DM;  Hyperadrenocorticism  Renal insufficiency;

      Also consider:;  Urinary tract infections, hypercalcemia, liver disease, etc
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9
Q

Initially document 3 things for diagnosing DM

A
  1. Consistent clinical signs
  2. Persistent fasting hyperglycaemia
  3. Glucosuria
    When BG approx. \> 12 mmol/L in dogs
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10
Q

Differentials for DM (Pathologic, Physiologic, Pharmacologic)

A
  1. Pathological  Diabetes mellitus  Pancreatitis;  Hyperadrenocorticism
  2. Physiological  Post-‐prandial ( < 2 hours)  Stress/excitement  Diestrus
  3. Pharmacological/ toxicity
       Dextrose-‐containing IV fluids
    
       Steroids
    
       Progesterone
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11
Q

Things to rule out with DM

A

 Rule out stress hyperglycemia especially in cats;  Document glucosuria and/or elevated fructosamine

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12
Q

Goals of initial DM diagnosis

A
  1. Identify persistent hyperglycemia & glycosuria
  2. Diagnose DM
  3. Identify any contributing causes of DM
  4. Concurrent problems that make glucose regulation difficult
  5. Complications that may be secondary to persistent hyperglycemia
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13
Q

Recommended DM Diagnostics

A
  • CBC
  • Biochemical profile
  • Urinalysis
  • Urine culture & sensitivity
  • ± Fructosamine level
  • ± cPLI or fPLI (pancreatic lipase immunoreactivity)
  • ± Abdominal ultrasound
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14
Q

Common Clinicopathologic Findings for DM - CBC/Biochem

A
  • CBC usually unremarkable
  • Biochemistry profile
    • Hyperglycemia
    • incr ALP & ALT (especially in dogs)
      • Mild-moderate ( < 500 U/L)
      • Usually due to DM effects on liver (lipidosis, etc)
    • incr cholesterol, triglycerides
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15
Q

Common Clinicopathologic Findings - Urinalysis

A
  • Glucosuria (a.k.a. “glycosuria”)
  • ± Ketonuria
  • ± Proteinuria
  • ± Bacteriuria, RBCs, WBCs
  • UTI’s common
  • May have unremarkable urine sediment, no clinical signs
  • Urine culture / sensitivity recommended in all patients
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16
Q

Goals of DM treatment

A
  1. Minimize/eliminate clinical signs
  2. Delay/prevent DM-associated complications
  3. Prevent hypoglycemia secondary to treatment
    • Want to control [glucose] within/close to normal range
    • Address hyperglycemia
    • Insulin or oral hypoglycemic agents (cats only)
    • Diet
    • Consistent exercise
    • Control concurrent diseases that can lead to insulin resistance
17
Q

Intermediate acting therapy for DM

A

NPH; Caninsulin; (Vetsulin in USA - not currently available)

18
Q

Longer acting therapy for DM

A

Glargine; Protamine zinc insulin (PZI) - currently available in USA, approval pending in Canada

19
Q

Cats vs dogs in insulin response

A

 Cats usually require a longer-‐acting insulin than dogs;  And have a more unpredictable response

20
Q

Insulin Treatment; - Concentrations; - Amount of therapy (x times a day); Typical doses; Method of dose

A

Note different concentrations;  U‐40 (Caninsulin) versus U‐100 (most other insulins);  Require different syringes;  Most patients will require twice daily therapy;  Typical starting doses for most insulins:;  0.25-‐0.5 U/kg of lean body weight twice daily ;  SQ injection over truncal region;  Alternate sides each injection

21
Q

NPH

A

 Human recombinant product ;  U‐100 product (100 U per mL) ;  Typical duration of activity:;  2‐8 h in cats (may be too short);  Usually < 12 hours in dogs

22
Q

Caninsulin; Length of duration

A

 Veterinary‐approved product (cats & dogs);  Combination of a short & intermediate acting insulin ; - 30% amorphous zinc (short-‐acting); - 70% crystalline zinc (long-‐acting);  Porcine product;  U-40 insulin (40 units per mL);  Typical duration of action: ; - 2-‐10 hours in cats; - Close to 12 hours in dogs

23
Q

Protamine Zinc Insulin

A

 Long-‐acting insulin;  Recombinant human PZI;  Approved for cats in US, approval pending in Canada;  U-‐40 product (40 U per mL);  Compounded PZI (bovine) not recommended;  Typical duration of action: ; - 4-‐14 hours in cats; - >12 hours in dogs (maybe too long acting?)

24
Q

Glargine

A

 Long-‐acting insulin, U-‐100 product;  Recombinant human insulin product;  Forms a “depot” when injected SQ;  Gives a “peakless” insulin release in humans (flat-‐; line glucose curve)  Not in cats;  Typical duration of action  8-‐18 hours in cats;  >12 hours in dogs

25
Q

3 goals for dietary therapy

A
  1. Correct obesity, maintain appropriate weight; 2. Minimize impact of meal on glucose fluctuations; 3. Two main meals coinciding with injections; - Ideal to offer snacks in between to promote more continuous glucose release rather than two large; spikes per day; - Some pets are grazers (ok)
26
Q

3 principles for dietary therapy in dogs

A
  1. High fiber diets (soluble fibers); - Slow GI glucose absorption; - Contraindicated in thin dogs; - No proven benefit of high fiber diets for diabetic dogs; 2. In general, avoid highly digestible diets ; - E.g., low residue, Gastro (absorbed easily, spike); 3. Moderate fat restriction (fat <30% ME) if: ; - Chronic pancreatitis; - Persistent hypertriglyceridemia
27
Q

Principles for dietary therapy in cats

A

(Cats are carnivores); 1. Carbohydrate-restricted diet preferred; 2. Canned diets have higher protein than kibble; 3. High protein / low carbohydrate diets;  Improve control of DM, improve rate of diabetic remission ;  Some canned over-‐the-‐counter diets that are low carb /high protein;  Preferred to have <7% carbohydrate per dry matter basis

28
Q

Treatment considerations in dogs & cats

A
  1. Control concurrent disease ;  Insulin resistance; 2. Avoid insulin-‐antagonizing drugs or states  Glucocorticoids;  OHE for intact females once stable; (progesterone);  Consistent exercise -> Increases glucose delivery to cells, insulin mobilization; 3. If there are some functional pancreatic beta cells remaining:;  Alternatives to insulin therapy;  Potential for cats to have diabetic remission; 4. No reliable indicators of which diabetic cats have residual beta cell activity
29
Q

When can you use non-insulin treatment

A

 Diabetic cats with remaining beta cell; function may respond to medical therapy:;  Oral “hypoglycemic agent” plus high protein diet;  Very mild cases may respond to high protein diet change alone; -> Selecting candidates: ;  Stable / no DKA;  Mild clinical signs;  Owner’s desires;  Must have a concurrent diet change

30
Q

Glipizide, glyburide

A

 Stimulate insulin secretion from pancreas  Need some functional pancreas remaining

31
Q

Chances of remission in cats, depends on?

A
  1. Cats with remaining beta cell function:;  Resolution of hyperglycemia may allow beta cells to recover function…; 2. Most common within first few weeks-months of treatment;  Depends on early, well regulated glucose control;  Few predictive factors for remission;  Higher remission rates in cats treated with insulin + high protein diet
32
Q

What do you do if remission is suspected?

A

 Gradual withdrawal of insulin;  Avoid rebound hyperglycemia that may induce; glucose toxicity of the recovering beta cells ;  Recommend high protein diet for life;  Some may never require treatment for DM again;  Others become insulin‐dependent within weeks to months

33
Q

Purpose of a Glucose Curve (w.r.t. DM)

A

Curves allow assessment of:;  Insulin efficacy;  Glucose nadir;  Peak insulin effect;  Duration of action;  Degree of fluctuation in BG; Used to evaluate a newly treated patient, recent dose change or if clinical signs are present

34
Q

Drawbacks to glucose curves (w.r.t. DM)

A

 Time‐consuming;  10-‐12 hour curve recommended;  Can be expensive;  Stress hyperglycemia (especially cats);  Natural day‐to‐day variation;  Poor repeatability, highly variable

35
Q

Tecnique to giving a Glucose Curve

A
  1. Breakfast & insulin as usual; 2. To clinic ASAP (if monitoring at home, can start just before breakfast/insulin); 3. Blood samples taken every 1‐2 hours through day; 4. Until next insulin injection; 5. Usually 10‐12 hours in duration; 6. Occasionally a 24‐hour curve recommended
36
Q

Glucometer readings that are acceptable

A
  • Usually underestimate BG by 10-‐15%; - Compared to reference laboratory; - Exception is AlphaTrak (veterinary glucometer - can slightly under or overestimate BG)
37
Q

Bottom part of the glucose curve where it is the lowest is called the

A

Nadir; (Ideal is 5-9 mmol/L)

38
Q

Desired Recheck Results (3 elements)

A
  1. Resolution of clinical signs;  PU/PD, weight loss, etc; 2. Blood glucose curves;  Obtain glucose nadir 5-‐9 mmol/L;  Maintain BG < 16 mmol/L throughout day;  < 13 mmol/L feasible in many cases ; 3. Avoid hypoglycemia;  Hypoglycemia activates counter‐regulatory hormones that may cause a subsequent rapid spike in glucose levels;  “Somoygi” effects