Diabetes: Insulin Resistance and DKA

Question 1

What is insulin resistance generally defined as?

Answer 1

> 1.5 - 2.0 U/kg in dog
or
3 U/cat

Question 2

disproportionately needs more insulin than it should

Answer 2

Insulin Resistance, some thing else is going on

Question 3

▫Bacterial infections* (periodontal disease, UTI)
▫Major organ failure (heart, liver, kidney)
▫Pancreatitis
▫Concurrent endocrinopathies* (hyperadrenocorticism, acromegaly,
hyperthyroidism, hypothyroidism)

*more steady state and chronic

Answer 3

Main Suspects for Insulin Resistance

Question 4

• Result of too much insulin
• Response to either hypoglycemia
  (BG < 60 mg/dl) or too rapid a decline in BG
• Secretion of counter-regulatory stress hormones
• Can results in an overall increase of BG with
  worsening of Pu/Pd and increased fructosamine

Answer 4

Insulin-induced hyperglycemia/
Somogyi Phenomenon

Question 5

• Pituitary adenoma
• Excessive GH secretion
  →Insulin resistance
  →IGF-1 →Bony and soft tissue overgrowth
  (HCM, kidneys, liver, endocrine glands, DJD, Spondylosis and more…)
• Signs develop slowly

Answer 5

Acromegaly (Hypersomatotropism)

Question 6

abnormal growth of the hands, feet, and face, caused by overproduction of growth hormone by the pituitary gland

Answer 6

acromegaly

Question 7

• CATS: always diabetics
• DM often appears first
• The “typical” physical manifestations are often NOT present or obvious
• Weight loss is NOT a feature despite uncontrolled DM

Answer 7

Acromegaly

Question 8

• ↑Insulin-like Growth Factor-1 (IGF-1)
• Good screening test in a cat that is difficult to regulate when other differentials have been ruled out
• Confirm diagnosis with brain imaging

Answer 8

Acromegaly: Diagnosis

Question 9

Treatment for Acromegaly

Answer 9

• Radiation therapy
• manage with insulin

Question 10

• Clinical signs overlap
  ▫Pu/Pd/PP, distended abdomen, abnormal hair coat
• CBC/Chem/UA overlap
  ▫↑liver enzymes, Chol, TG, dilute urine

Answer 10

Diabetes and Cushing’s disease

Question 11

• In a diagnosed HAC, concurrent DM is easy to confirm (↑BG, glycosuria and ↑fructosamine)
• In diabetics, concurrent HAC is very difficult to confirm: DM causes chronic stress
  ▫DM (especially uncontrolled) will cause false positive results on screening tests for HAC
  ▫Adrenal glands are normal in size in DM but they are not always enlarged in HAC
• Diabetics can and should be controlled (albeit insulin resistance) prior to testing for HAC

Answer 11

Diabetes and Cushing’s disease

Question 12

Could look like Cushing’s because?

Answer 12

The diabetes is causing stress

Question 13

is a serious complication of diabetes mellitus
▫10% mortality in human medicine!

Answer 13

Diabetic ketoacidosis (DKA)

Question 14

are derived from oxidation of fatty
acids by the liver and are used as an energy source
during periods of glucose deficiency (the good)

Answer 14

Ketone bodies

Question 15

Fatty acids in the Liver can be:

Answer 15

• Incorporated into triglycerides
• Metabolized into CO2 and water
• Converted to ketone bodies
  (the good)

Question 16

ketone bodies

Answer 16

acetoacetate, β-
hydroxybutyrate, and acetone

Question 17

Excessive production of _____________, as occurs in uncontrolled diabetes, results in their accumulation in the circulation

Answer 17

ketone bodies
(the bad)

Question 18

are substrates for
energy metabolism when needed

Answer 18

Ketone Bodies
(the bad)

Question 19

• Ketones are weak acids (unmeasured anions) and drive an acid base shift
  
  • High anion gap metabolic acidosis causes sickness

Answer 19

Ketosis (ketonemia, ketonuria)

Question 20

• acid accumulation (ketones), decreased HCO3, and increased Anion Gap

Answer 20

Metabolic Acidosis

Question 21

is a powerful inhibitor of lipolysis and fatty acid oxidation

Answer 21

Insulin

Question 22

Relative or absolute deficiency of insulin “allows” ____________ to increase, thus increasing the availability of fatty acids to the liver and in turn promoting ketogenesis

Answer 22

lipolysis

Question 23

Why did my patient develop DKA?

Answer 23

• untreated diabetic without insulin
• untreated diabetic without insulin and a source of insulin resistance
• treated diabetic without enough insulin due to a source of insulin resistance

Question 24

• Severe acidosis
• Hyperosmolality
• Increased osmotic diuresis
• Dehydration
• Electrolyte derangements (K, P, Ca, Na)

Answer 24

Consequences of DKA

Question 25

• Hyperglycemia
• Glycosuria
  *Ketonemia/Ketonuria
• Metabolic Acidosis

Answer 25

Making the diagnosis for DKA

Question 26

▫CBC
▫Biochemistry
▫Urinalysis

Answer 26

Standard Diagnostics

Question 27

▫Blood Gas
▫Pancreatic testing
▫Abdominal imaging
▫Urine culture
▫ANY tests indicated by patient abnormalities

Answer 27

Second Tier Diagnostics

Question 28

1. Replace dehydration deficit and supply fluid needs
2. Manage electrolyte abnormalities
3. Initiate insulin therapy to help reduce glucose levels and reverse ketone production in DKA
4. Treat underlying diseases if present

Answer 28

Goals of DKA Therapy

Question 29

How much do I give in fluid therapy?

Answer 29

▫Maintenance fluid requirement
- Start hourly maintenance based on your patient
▫Ongoing losses
- Estimate ongoing losses based on clinical status
▫Correct Dehydration
- Estimate dehydration and correct aggressively

Question 30

What do I give in fluid therapy?

Answer 30

Buffered isotonic replacement CRYSTALLOID
- LRS, Plasmalyte, Normosol?
- 0.9% NaCl?

Question 31

refers to a state of low extracellular fluid volume, generally secondary to combined sodium and water loss

Answer 31

hypovolemia

Question 32

Insulin therapy should not begin until the patient’s
_____________ is corrected and electrolytes
supplemented!

Answer 32

hypovolemia

Question 33

Goals of insulin therapy

Answer 33

▫Slowly decrease blood glucose levels
▫Inhibit further lipolysis and ketogenesis

Question 34

the breakdown of fats and other lipids by hydrolysis to release fatty acids

Answer 34

lipolysis

Question 35

For regular Insulin people are using?

Answer 35

IV continuous rate infusion (CRI) protocol

Question 36

Regular insulin protocols should be continued until what?

Answer 36

Until the animal is eating, at which time the patient is moved to a long-acting insulin

Question 37

• Daily vitals
• Physical examinations and hydration assessments 2-4 times per day
• Recheck electrolytes every 6-24 hours depending on severity
• Recheck phosphorus every 24 hours

Answer 37

Patient Monitoring