Diabetes/DKA/hypoglycemia

Question 1

Type 1 diabetes affects which species?

Answer 1

Dogs

Insulin-dependent

Question 2

Type 2 diabetes affects which species?

Answer 2

Cats
Non-insulin dependent.
May spontaneously become non-diabetic.

Question 3

What are the causes of secondary diabetes?

Answer 3

Pancreatic diz
Hormonal
Drug-induced
Insulin receptor abnormalities
Specific genetic syndromes

Question 4

Insulin doses in intact dogs will be _______ due to hormonal influence.

Answer 4

Increased.

Recc. OVH after diagnosis to allow for better glucose management.

Question 5

S/S of DM

Answer 5

PU/PD, wt loss.

Sick patients: dehydration, depression, anorexia, tachypnea, vomiting.

Question 6

Dx of DM is made based off what clinical criteria?

Answer 6

Persisting hyperglycemia, with glucosuria.

Question 7

Types of intermediate acting insulins

Answer 7

Vetsulin
NPH (dogs)
Humalin N

Question 8

How frequently should intermediate and long acting insulin be given?

Answer 8

Maintenance dose given SQ, divided into BID dose.

Begin at 0.5 U/kg (daily)

Question 9

Types of ultra long acting insulins:

Answer 9

PZI (cats)

Protamine zine and iletin.

Question 10

Fructosamine testing can tell you what?

Answer 10

Give you an idea of the average BG over the last 1-3 weeks.
Pitfall is that patient could be relatively hyperglycemia half the time and hypo glycemia the other half and fructosamine would fall in well regulated range. Should still do blood glucose curves on patients having issues.

Question 11

Common causes of insulin resistance in dogs:

Answer 11

estrus and diestrus
progestagen Rx
acromegaly
hypercortisolism
bacterial infection

Question 12

Criteria to dx DKA:

Answer 12

hyperglycemia, glucosuria, and ketones in urine (+/- serum ketones - only because will show up in urine 1st).

Question 13

Common blood work changes in DKA patients

Answer 13

KETONES…
+/-: ^ALT, ALP, Chol.
Potassium can be inc, dec, or normal. Other electrolytes may be low.
Azotemia, d/t to dehydration or renal failure. Urine should be cultured as UTI can lead to DKA in diabetics.

Question 14

Goals of DKA treatment

Answer 14

Correct dehydration
Correct acidosis (reducing ketone bodies)
Restore normal lytes

Question 15

What type of fluids should be used in initial stabilization of DKA patient?
Insulin?

Answer 15

Isotonic fluids

Regular insulin, b/c of it’s rapid onset and short duration.

Question 16

Regular insulin (Humulin-R) characteristics

Answer 16

Can be given any route.
Onset 30m-1h.
Peak effect 3-6hr
Duration 6-10h
*Initial dose is 0.5 U/kg

Question 17

Regular insulin via the SQ route in DKA patients.

Answer 17

Begin @ 0.5 U/kg
Patient should not be severely hypovolemic.
Titrate appropriately.
Will deter ketogenesis.
Glucose will decline before ketones do.

Question 18

Regular insulin via the IV route in DKA patients:

Answer 18

Begin CRI at 0.1 U/kg/hr.
Reduce to 0.05 U/kg when BG is 250 or less.
Close monitoring essential. Potassium should be supplemented in most cases of DKA because as insulin is given and glucose is driven intracellularly, potassium follows.

Question 19

Why do you want to avoid correcting hyperglycemia too quickly?

Answer 19

Avoid cerebral osmotic dysequilibrium.

Question 20

When managing a DKA patient, when should you begin to supplement dextrose?

Answer 20

When the BG is in the 200-250 range you should start supplementing with 2.5-5% dextrose.
Rate of BG decline should not exceed 75-100 mg/dl/hr.

Question 21

Causes of hypokalemia during DKA treatment?

Answer 21

Dilution
Renal tubular losses
GI losses w/ vomiting
Cellular influx of K+ (cause by acidosis correction and insulin)

Question 22

Protocol for potassium supplementation:

Answer 22

Mild hypokal (3-3.5) - give 30mEq KCl per liter
Moderate (2.5-3) - 40 mEq KCl/L
Severe (<2.5) - 60 mEq KCl/L.
NOTE max infusion rate is 0.5-1.5 mEq/kg/hr.

Question 23

When should sodium bicarb be used in DKA patients?

Answer 23

When pH <7.1 and patient is critical….. Dr. S’s rule is if the patient can stand he trys to avoid giving.

Question 24

When to treat hypophosphatemia?

Answer 24

When serum P <2.0 mg/dl.

Use KPhos. Replenish at 0.06-0.18 mM/kg given over 6 hours. Discontinue when Phos reaches 2 to avoid calcium binding.

Question 25

Pathogenesis of hyperosmolar nonketotic DM:

Answer 25

Insulinized liver deters ketone production. Peripheral insulin depletion = decreased glucose utilization.
Enhanced gluconeogenesis.

Question 26

NKHDS features:

Answer 26

Extreme dehydration.
Brain dysfunction.
Marked hyperglycemia.
Absent ketones.
Decreased renal function.
BG is often above 1000!

Question 27

How do you calculate serum osmolarity?

Answer 27

2(Na + K) + Glu/18 + BUN/2.8

Normal: 290-310 mosm/kg

Question 28

Treatment of NKHDS

Answer 28

0.9% NaCl if hypotensive.
0.45% NaCl, if normotensive.
Regular insulin - CRI at 0.1 U/kg/hr.
KCL

Question 29

What is the definition of hypoglycemia?

Answer 29

<70 mg/dl.

Signs usually don’t occur until <50.

Question 30

Common causes of hypoglcemia:

Answer 30

Insulinoma
Extrapancreatic tumors
Addison's
Liver disease
Sepsis
*Insulin O.D. (most common)
Starvation in young.

Question 31

S/S of hypoglycemia

Answer 31

Anxiety
Tachycardia
Bizarre behavior
Weakness and ataxia
Muscle twitching
Dementia
Seizures

Question 32

Tx for insulin OD

Answer 32

Glucose 0.5 g/kg
Karo syrup PO.
Dextrose 50% (0.5g/ml) @ 1g/kg IV.
Glucagon - 0.25-1mg IM or 0.03 IV

Question 33

Insulinoma info

Answer 33

Beta cell adenocarcinoma most common in dogs. Prognosis is guarded.
Middle and older aged animals.
No breed predilection.

Question 34

Dx of insulinoma

Answer 34

Inappropriate hyperinsulinemia.
Concomitant hypoglycemia.
Use amended insulin - glucose ratio:
I/G = (Insulin u U/ml x 100)/(BG -30). 
>50 suggests insulinoma when expected s/s present.

Question 35

Medical Tx for insulinoma:

Answer 35

Frequent feeding
Diazoxide
Prednisone
Many other drugs to treat symptoms.

Question 36

What is the most common site for metastasis of insulinomas?

Answer 36

Liver

Question 37

Hypoglycemia in sepsis, mechanism?

Answer 37

Gram - bacteria and endotoxins.

• inhibits gluconeogenesis.
• hepatic glycogen depletion
• shift to anaerobic metabolism.