Endocrine Flashcards
Pathophysiology of canine diabetes mellitus
Pancreas does not make insulin (similar to type I in people). Usually immune-mediated or secondary to pancreatitis. Middle-aged dogs predisposed.
Canine diabetes mellitus treatment
Goal: control clinical signs and improve quality of life
No remission possible
Tx: Insulin (vetsulin) begin at 0.25-0.5 U/kg q12h, high fiber diet, glucose curves to guide treatment (helps void underdosage/overdosage)
How would glucose curves help identify the somogyi effect?
The somogyi effect is when the animal is on too much insulin. This leads to a drop in BG which the body responds by releasing glucagon to spike BG. On “spot checks” this may lead us to think the patient is being UNDERdosed.. but in reality the patient is being OVERdosed!
DKA pathophysiology
Mismanaged DM leading to a lack of insulin for glucose uptake. The cells are starved leading to fat breakdown and ketone build-up
DKA clinical pathology findings
Glucose ___
Potassium ___ or ___
Na ___
AG ___
Glucose HIGH
Potassium HIGH (no cellular uptake) or LOW (anorexia)
Sodium LOW (fluid shift into vasculature)
AG HIGH (KLUE)
DKA Treatment
IV fluids
Electrolyte correction
Fast acting insulin (CRI)
Dextrose (resolve the ketonemia)
Potassium ALWAYS given with insulin CRI
Hyperadrenocorticism (Cushings) etiology
Pituitary dependent tumor (85%) PDH
Adrenal dependent tumor (15%) ADH
Iatrogenic (excessive corticosteroids)
Cushing’s clinical signs
muscle weakness/atrophy, alopecia, comedones, abdominal distention, hepatomegaly, thin skin, calcinosis cutis
Cushing’s clinical pathology
_____ leukogram
_____ ALP, ALT, Triglycerides
_____ BUN
_____ Creatinine
stress leukogram (neutrophils and monocytes HIGH, lymphocytes and eosinophils LOW)
LOW BUN (cortisol inhibits ADH causing washout)
LOW Creatinine d/t muscle wasting
LDDST (how to perform, expected results for PDH vs ADH)
Baseline, 4 hr, 8 hr sample
PDH - will see suppression (drop in 4 hr) and then huge spike in 8 hr
ADH - will NOT see any suppression for any sample
ACTH stimulation test (expected results for cushings vs addisons)
Cushings - will see exaggerated response
Addisons- no response
Cushing’s Tx (two main drugs & their mechanism)
Mitotane - cytotoxic adrenocortical destruction
Trilostane - inhibit cortisol synthesis
can ultrasound abdomen to look for adrenal mass
Addison’s disease gender predelection
70% Female
Addison’s pathophysiology and clinical signs
Decreased production of cortisol and aldosterone
Anorexia, lethargy, thin condition, PU/PD, diarrhea, collapse, bradycardia (tall T waves), shaking, low SG
Addison’s clinical pathology
Anemia
Lack of ____ leukogram
K __
Na/Cl __
ALT/AST/ALP __
USG __
Lack of stress leukogram
High potassium
Low na/cl
High liver enzymes
USG < 1.030