CANINE
This section covers the most clinically relevant endocrine disorders in dogs, including hyperadrenocorticism, hypoadrenocorticism, diabetes mellitus, hypothyroidism, and insulinoma. Each condition is explored through its pathophysiology, clinical presentation, diagnostic workup, and treatment protocols to help you build strong clinical reasoning skills and prepare confidently for NAVLE scenarios.
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Canine Endocrinology Flashcards
Question 1:
Which of the following is the most accurate statement regarding the pathophysiology of adrenal-dependent hyperadrenocorticism in dogs?
A. It results from bilateral adrenal hyperplasia secondary to excessive ACTH secretion.
B. It is characterized by an autonomous adrenal tumor leading to suppression of endogenous ACTH.
C. It is caused by iatrogenic suppression of the adrenal cortex following abrupt steroid withdrawal.
D. It originates from a pituitary macroadenoma producing excess cortisol directly.
Question 2:
A dog is suspected of having hyperadrenocorticism. Which of the following diagnostic findings is most consistent with pituitary-dependent hyperadrenocorticism (PDH) based on a Low-Dose Dexamethasone Suppression Test (LDDST)?
A. Cortisol suppression at both 4 and 8 hours post-dexamethasone
B. No cortisol suppression and markedly enlarged unilateral adrenal gland on ultrasound
C. Cortisol suppression at 4 hours but not at 8 hours, with bilaterally enlarged adrenal glands
D. No cortisol suppression and plasma ACTH concentration below reference interval
Question 3:
Which of the following is the most appropriate initial dose and mechanism of action of trilostane in the treatment of canine hyperadrenocorticism?
A. 0.1 mg/kg BID; irreversible inhibitor of 11β-hydroxylase
B. 2–3 mg/kg SID or BID; reversible inhibitor of 3β-hydroxysteroid dehydrogenase
C. 1–2 mg/kg BID; adrenocorticolytic cytotoxic agent causing adrenal necrosis
D. 5 mg/kg SID; ACTH receptor blocker inhibiting pituitary stimulation
Answers
Answer 1:
B. It is characterized by an autonomous adrenal tumor leading to suppression of endogenous ACTH.
Explanation:
Adrenal-dependent hyperadrenocorticism (ADH) occurs due to a functional adrenal neoplasm (adenoma or carcinoma) that autonomously secretes cortisol, independent of pituitary control. This negative feedback leads to suppression of ACTH production by the pituitary and atrophy of the contralateral adrenal gland. In contrast, pituitary-dependent HAC (PDH) involves bilateral adrenal hyperplasia due to chronic ACTH stimulation. Iatrogenic HAC arises from exogenous glucocorticoid administration, not tumor activity.
Answer 2:
C. Cortisol suppression at 4 hours but not at 8 hours, with bilaterally enlarged adrenal glands
Explanation:
LDDST is highly sensitive for detecting HAC. In PDH, partial suppression of cortisol at 4 hours followed by rebound at 8 hours is a classical pattern due to episodic ACTH secretion from a pituitary adenoma. Additionally, bilateral adrenal hyperplasia is typical on imaging. In contrast, ADH usually shows no suppression at either time point and unilateral adrenal enlargement, with suppressed ACTH levels.
Answer 3:
B. 2–3 mg/kg SID or BID; reversible inhibitor of 3β-hydroxysteroid dehydrogenase
Explanation:
Trilostane is a competitive and reversible inhibitor of 3β-hydroxysteroid dehydrogenase, an enzyme critical for cortisol and aldosterone synthesis. It is the most widely used drug for both PDH and ADH. Initial dosing ranges from 2 to 3 mg/kg, administered once or twice daily depending on clinical response and monitoring. It requires regular ACTH stimulation tests to avoid inducing iatrogenic hypoadrenocorticism. Mitotane, by contrast, is a cytotoxic agent that causes adrenal necrosis.
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