Canine Adrenal Flashcards
In 85% of hyperadrenocorticism cases, excess cortisol is secreted due to a pathology of what gland?
Pituitary
*Most cases are pituitary dependent. Otherwise, some cases are caused by an adrenal tumor, and some are iatrogenic (from administration of glucocorticoids)
Why won’t a baseline cortisol level diagnose pituitary dependent HAD?
Cortisol levels are variable.
*ACTH secretory bursts
A Schnauzer presents for PU/PD and weight gain. You note a pot-bellied appearance and crusty skin lesions.
Significant blood and urine results:
Stress leukogram
ALP, ALT, Chol, Glu and Na+ elevated
K+ decreased
USG: 1.012
What lab test is the screening test of choice for diagnosis of the suspected disease?
Low dose dexamethasone suppression
*Although ACTH stim is the gold standard for iatrogenic HAD, it doesn’t work with the other forms. LDDS is the test of choice for HAD that is not iatrogenic.
A LDDS test on a suspected Cushing’s patient shows no suppression. You know this can mean either PDH or ADH (since ADH patients won’t suppress and 25% of PDH patients won’t suppress). You perform an ultrasound to look at the adrenals and find that they are bilaterally enlarged. What kind of HAD does this patient have?
Pituitary dependent
A LDDS test is run on a patient you suspect to have Cushing’s disease. The 8 hour result is within normal range. What type of HAC does this patient have?
It doesn’t. Supression at 8 hours indicates a negative result.
A LDDS test is run on a patient you suspect to have Cushing’s disease. Baseline cortisol is 3.5ug/dL. The 8 hour result is 2.3ug/dL (< 1.0ug/dL) and the 4 hour result is 3ug/dL. What type of HAD does this patient have?
Either PDH or ADH
You run a LDDS test on a patient suspected of Cushing’s disease. Baseline cortisol is 5ug/dL. The 8 hour result is 4ug/dL (< 1ug/dL) and the 4 hour result is 1.7 ug/dL. What type of HAD does this patient have?
Pituitary dependent
*The patient did not suppress at 8 hours, but did supress at 4 hours. Although the result is still higher than the reference range of 1.5ug/dL, it is less than 50% of the baseline cortisol level. This indicates PDH. (remember that 25% of PDH patients will not supress at the 4 hour interval)
Endogenous ACTH level on a Cushing’s patient is decreased. What type of HAD does this patient have?
ADH
*ACTH is decreased in adrenal cases and normal to increased in pituitary cases.
What is the best way to visualize a pituitary microadenoma?
MRI
You have just diagnosed a patient with adrenal dependent hyperadrenocorticism. You suggest removal of the affected adrenal gland but the owner would prefer medical management. What do you prescribe?
Trilostane
*blocks synthesis of adrenal and gonadal steroid hormones
What are the disadvantages to using Trilostane instead of surgery to treat ADH?
Adrenals continue to enlarge and may become necrotic.
MST of only 14 months
What is the MOA of Mitotane and why is this a major disadvantage when using it to treat ADH?
Adrenocorticolytic
Must monitor ACTH closely or risk overtreatment, leading to hypoadrenocorticism
When 90% of the adrenal cortex is destroyed, patients start to show clinlcal signs for what disease?
Hypoadrenocorticism
In typical hypoadrenocorticism, mineralocorticoids and glucocorticoids are deficient. How does atypical hypoAC present?
Deficient glucocorticoids
*Destruction of only the zone fasciculata. Mineralocorticoids normal.
How does hypoadrenocorticism cause hypovolemia, hypotension and cardiac excitability?
Inability to conserve Na+ leads to decreased circulating volume (no concentration of urine).
Lack of aldosterone causes K+ retention and excess, which causes myocardial excitability.
