Page 885 - Small Animal Internal Medicine, 6th Edition
P. 885

CHAPTER                               50
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                                    Disorders of the


                                       Adrenal Gland













            HYPERADRENOCORTICISM IN DOGS                         ADRENOCORTICAL TUMORS
                                                                 Adrenocortical tumors causing hyperadrenocorticism
            Etiology                                             (adrenal-dependent hyperadrenocorticism [ADH]) account
            Hyperadrenocorticism (Cushing’s disease) is classified as   for the remaining 15% to 20% of dogs with spontaneous
            pituitary dependent, adrenocortical dependent, or iatrogenic   hyperadrenocorticism.  Adrenocortical adenoma and car-
            (i.e., resulting from excessive administration of glucocorti-  cinoma occur with approximately equal frequency. No
            coids by the veterinarian or client).                consistent clinical or biochemical features can help dis-
                                                                 tinguish dogs with functional adrenal adenomas from
            PITUITARY-DEPENDENT                                  those with adrenal carcinomas, although large adreno-
            HYPERADRENOCORTICISM                                 cortical masses (maximum width  >4 cm) are more likely
            Pituitary-dependent hyperadrenocorticism (PDH) is the   to be carcinomas. Adrenocortical carcinomas may invade
            most common cause of spontaneous hyperadrenocorti-   adjacent structures (e.g., phrenicoabdominal vein, caudal
            cism, accounting for approximately 80% to 85% of cases. A   vena cava, kidney, body wall) or may metastasize to the
            functional  adrenocorticotropic  hormone  (ACTH)–secret-  liver and lung—findings that are not consistent with
            ing pituitary tumor is found at necropsy in approximately   adrenocortical adenomas.
            85% of dogs with PDH. Adenoma of the pars distalis is   Bilateral adrenocortical tumors can occur in dogs, but
            the most common histologic finding, with a smaller per-  this is uncommon. A nonfunctional adrenocortical tumor or
            centage of dogs diagnosed with adenoma of the pars inter-  ADH with a pheochromocytoma in the contralateral gland
            media and a few dogs diagnosed with functional pituitary   is a more common cause of bilateral adrenal masses in dogs.
            carcinoma. Approximately 50% of dogs with PDH have   Macronodular hyperplasia of the adrenals has also been
            pituitary  tumors  measuring  less  than 3 mm  in diam-  identified in dogs. The adrenals in such animals are usually
            eter, and most of the remaining dogs, specifically those   grossly enlarged, with multiple nodules of varying sizes
            without central nervous system (CNS) signs, have tumors   within the adrenal cortex. The exact pathogenesis of this
            3 to 10 mm in diameter at the time PDH is diagnosed.   latter syndrome is unclear, although most cases in dogs are
            Approximately 10% to 20% of dogs have pituitary tumors   presumed to represent an anatomic variant of PDH. Adre-
            (i.e.,  macrotumors)  exceeding  10 mm in diameter at  the   nocortical tumors can also secrete one of the precursor hor-
            time PDH is diagnosed. These tumors have the potential   mones involved in adrenal steroid synthesis (e.g., progesterone
            to  compress  or  invade  adjacent  structures  and  cause  neu-  and 17-OH-progesterone; see the section on occult [atypical]
            rologic signs as they expand dorsally into the hypothala-  hyperadrenocorticism, p. 878).
            mus  and thalamus  (i.e., pituitary  macrotumor  syndrome)    Adrenal tumors causing ADH are autonomous and func-
            (Fig. 50.1).                                         tional, and randomly secrete excessive amounts of cortisol
              Excessive secretion of ACTH causes bilateral adrenocor-  independent of pituitary control. The cortisol produced by
            tical hyperplasia and excess cortisol secretion from the zona   these tumors suppresses circulating plasma ACTH concen-
            fasciculata of the adrenal cortex (Fig. 50.2). Because normal   trations, causing cortical atrophy of the uninvolved adrenal
            feedback inhibition of ACTH secretion by cortisol is missing,   and atrophy of all normal cells in the involved adrenal (see
            excessive ACTH secretion persists despite increased adreno-  Fig. 50.2). This atrophy creates asymmetry in the size of
            cortical secretion of cortisol. Episodic secretion of ACTH   the adrenal glands, which can be identified on abdominal
            and cortisol is common and results in fluctuating plasma   ultrasonography. Most, if not all, of these tumors appear to
            concentrations that, at times, may be within the reference   retain ACTH receptors and respond to administration of
            range.                                               exogenous ACTH. Adrenocortical tumors causing ADH are

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