Page 917 - Small Animal Internal Medicine, 6th Edition

CHAPTER 50 Disorders of the Adrenal Gland 889

require small amounts of prednisone or prednisolone, if usually returns within 2 to 4 weeks after the medication is
any. However, when stressed or ill, these same animals may discontinued, unless long-acting depot forms of glucocorti-
VetBooks.ir require large amounts of prednisone or prednisolone (i.e., coids are used.
Glucocorticoid-deficient hypoadrenocorticism is usually
0.25-0.5 mg/kg) given twice a day. Failure to provide ade-
quate quantities of glucocorticoids can lead to persistent and
cats with chronic, vague gastrointestinal clinical signs
worsening lethargy, inappetence, and vomiting. The amount identified during the diagnostic evaluation of dogs and
of prednisone or prednisolone required to offset the deleteri- such as lethargy, anorexia, vomiting, diarrhea, and weight
ous effects of stress and illness is variable and unpredictable. loss. Results of routine blood and urine tests are typically
Therefore it is always better to err on the high end of the normal. Diagnosis requires an ACTH stimulation test (see
dosage range and then gradually decrease the dosage over p. 870). Therapy involves the administration of glucocorti-
the ensuing weeks. coids, as previously described for the treatment of primary
hypoadrenocorticism. The exception is secondary adrenal
Prognosis insufficiency induced by the overzealous administration of
The prognosis in dogs and cats with adrenal insufficiency is glucocorticoids, in which case treatment revolves around
usually excellent. The most important factors in determining a gradual reduction in the dose and frequency of admin-
an animal’s long-term response to therapy are client educa- istration, with eventual discontinuation of the medica-
tion about the disease and client dedication to treatment. If tion. Dogs and cats with secondary adrenal insufficiency
client–veterinarian communication is good, if frequent should not have mineralocorticoid deficiency. Periodic
rechecks are performed, and if clients are conscientious measurement of serum electrolytes is advisable because
about carrying out therapy, dogs and cats with adrenal insuf- primary glucocorticoid-deficient adrenal insufficiency
ficiency can have a normal life expectancy. may progress to mineralocorticoid deficiency weeks to
months after glucocorticoid-deficient hypoadrenocorticism
ATYPICAL HYPOADRENOCORTICISM is diagnosed.

Some dogs with hypoadrenocorticism present to the veteri- PHEOCHROMOCYTOMA
narian with clinical signs of glucocorticoid deficiency but
with serum electrolyte concentrations within the reference Etiology
range at initial presentation. A deficiency in glucocorticoid Pheochromocytoma is a catecholamine-producing tumor
but not mineralocorticoid secretion is referred to as atypical derived from the chromaffin cells of the adrenal medulla.
hypoadrenocorticism, a syndrome identified in up to 30% of Pheochromocytomas are uncommon in dogs and rare in
dogs with hypothyroidism. Glucocorticoid deficiency may cats. Pheochromocytomas are usually solitary tumors
be adrenocortical in origin (primary atypical hypoadreno- ranging in size from nodules of less than 0.5 cm in diameter
corticism; most common) or may result from impaired to masses greater than 10 cm in diameter. Pheochromocy-
secretion of ACTH by the pituitary gland (secondary hypo- toma involving both adrenal glands, pheochromocytoma
adrenocorticism). Baseline endogenous plasma ACTH con- involving one adrenal gland with a functional adrenocortical
centrations are normal or increased when the primary tumor in the contralateral gland, and pheochromocytoma
problem is adrenal in origin and are decreased when the with concurrent PDH have also been identified in dogs.
primary problem is pituitary in origin (see Table 50.6). Glu- Pheochromocytomas have an unpredictable growth pattern,
cocorticoid but not mineralocorticoid deficiency of adrenal ranging from slow to rapid, and infiltration of the phren-
origin may be seen in a dog in the early stages of develop- icoabdominal vein, caudal vena cava, and surrounding soft
ment of typical primary hypoadrenocorticism with destruc- tissue structures can occur when the tumor is relatively small
tion of the zona fasciculata more advanced than destruction (<2.5 cm in maximum width; see Fig. 50.8). In one report,
of the zona glomerulosa. Mineralocorticoid deficiency and 87% of pheochromocytomas in 38 dogs were greater than
abnormal serum electrolyte concentrations develop weeks to 2.5 cm in width, 45% were greater than 5 cm in width, and
months later. In some dogs and cats glucocorticoid defi- most (62%) involved the right adrenal gland. Pheochromo-
ciency does not progress to mineralocorticoid deficiency. cytoma should always be considered a malignant tumor in
The cause of this form of hypoadrenocorticism is not known, dogs and cats. Distant sites of metastasis include the liver,
although drugs such as mitotane, trilostane, and megestrol lung, regional lymph nodes, bone, and CNS. Paragangliomas
acetate (cats) are known to play a part. are tumors arising from chromaffin cells located outside the
Glucocorticoid deficiency resulting from pituitary dys- adrenal medulla, most commonly near the sympathetic
function is called secondary hypoadrenocorticism. Destruc- ganglia; they are rare in dogs and cats.
tive lesions (e.g., neoplasia, inflammation) involving the
pituitary gland or hypothalamus and long-term administra- Clinical Features
tion of exogenous glucocorticoids are the most common Pheochromocytomas occur most commonly in older dogs
recognized causes of secondary adrenal insufficiency. Adre- and cats, with a median age of 11 years at the time of diag-
nocortical atrophy may develop after the injectable, oral, or nosis in dogs. There is no apparent sex- or breed-related
topical administration of glucocorticoids. Adrenal function predisposition.