Diabetes mellitus and Insulin (Endocrine) Flashcards
Lower insulin concentrations
Insulin dependent cells can’t utilize blood glucose
Insulin independent cells can utilize blood glucose (neurons)
Diabetes Mellitus: Type 1
Dogs, B cell destruction
Progressive complete insulin insufficiency
Caused by pancreatic destruction and hereditary
Diabetes Mellitus: Type 2
Cats, obesity (60%)
Insulin resistance, dysfunctional B cells, ↑ hepatic gluconeogenesis
Pancreatic neoplasia and hyperadrenocorticism (10-20%)
Diabetes Mellitus CS
PU/PD
Polyphagia
WL
DX of Diabetes Mellitus
Difficult
Persistent fasting hyperglycemia (>200 mg/dL)
Glycosuria, ketonuria
Diabetes Mellitus dietary therapy
↑ or insoluble fiber can delay GI glucose absorption
High protein/ low carbs
Commercial diets (hills and purina)
Diabetes Mellitus drug therapy (insulin)
Maintains blood glucose concentrations, eliminate CS of diabetes
Short acting IV
Challenges to drug therapy
Integration with meals, exercise, owner need and lifestyle
1-2 large doses instead to respond to glucose concentrations
Insulin preps
Grouped by time of onset and duration of action
Affects antigenicity
Cattle and swine traditional
Bacterial produced recombinant products (more potent in cats)
Intermediate insulin lente
Insulin and high concentrations of zinc (10x greater than reg insulin)
Vetsulin (only insulin approved for dogs)
Insulin, zinc and protamine
Long acting insulin
Poorly soluble after SQ injection (slow onset, long duration of action)
Designer recombinant insulins
Long acting insulin
Amino acid structure of protein altered to change PK profile
Glargine
Long acting insulin in cats
Structure changes cause a constant systemic absorption
Rapid onset
Detemir
Long acting insulin
Peak effect more predictable than glargine
Longer duration of action
Hypoglycemia
Complication of insulin therapy
CS: neurologic (disorientation, weakness, seizure, blindness)
What causes hypoglycemia
Insulin overdose
Failure to eat
Vomiting
↑ exercise
Treating hypoglycemia
Feeding normal meal (mild)
Feeding/ rubbing on mm sugar/ syrup (moderate)
Slow IV 50% dextrose with CRI 5% dextrose until patient fed (severe)
Insulin resistance
Marked hyperglycemia throughout the day despite insulin doses
Diabetic Ketoacidosis (DKA)
Catabolic disorder
Relative or absolute insulin deficiency
Development: ↑ secretion of stress hormones (cortisol, progest. and GH)
DKA CS
Dehydration and prerenal azotemia
V/D (complicate acid-base and electrolyte disorders)
Weakness, ataxia and seizures
Bloodwork for DKA
Severe acidosis
Blood glucose >300 mg/dL
Hypokalemia, hypophosphatemia, hypomagnesemia
Ketonuria
Aggressive DKA treatment
Restore water and electrolyte (IVFT)
Correct acidosis (bicarbonate)
Insulin supplementation (begin low)
Carb substrate
Isotonic, Na containing fluids
Effects of IVFT
Enhances renal blood flow, promote urinary excretion, ↓ effects of stress hormones
Pancreatic exocrine insufficiency
Poor digestion
↓ trypsin, amylases, lipases
Enzyme replacement
