Page 34 - VetCPD Jnl Volume 7, Issue 4

VETcpd - Internal Medicine
Peer Reviewed
Kerry Peak BVSc(Hons) BSc(Hons) CertAVP(SAM) MRCVS
Kerry graduated from the University of Bristol in 2010 with degrees in Anatomical Science and Veterinary Science. Following graduation she worked in Sussex
initially before moving to the Isle of Wight, where she spent seven years working in first opinion practice. Here, she developed a keen interest in medicine, and was awarded the RCVS Certificate of Advanced Veterinary Practice in Small Animal Medicine in 2014. Kerry joined Anderson Moores Veterinary Specialists in July 2018 to undertake a three year residency in Small Animal Internal Medicine, accredited by the American College of Veterinary Internal Medicine. Kerry is interested in all aspects of medicine but particularly enjoys endocrine disease and haematological medicine.
David Walker BVetMed(Hons) DipACVIM DipECVIM-CA FRCVS
David graduated from The Royal Veterinary College (RVC) in 2003, where he subsequently completed an internship and medicine residency following some time
in small animal practice. David is a diplomate of the American and European Colleges of Veterinary Internal Medicine and is an RCVS recognised specialist in Small Animal Internal Medicine.
David was a lecturer at the RVC for one year following his residency and since 2009 he has worked in private referral practice. He is the Director at Anderson Moores Veterinary Specialists, a large multidisciplinary specialist referral practice in Hampshire.
Canine
Hypoadrenocorticism
Hypoadrenocorticism can be defined as a lack of adrenocortical steroid production and this typically includes both glucocorticoids and mineralocorticoids. Hypoadrenocorticism can be classified as primary or rarely secondary; it can
be typical or atypical (isolated hypocortisolaemia). The physiological roles of cortisol and aldosterone can explain the clinical signs and clinico-pathological abnormalities. A good understanding of the hypothalamic-pituitary-adrenal (HPA) axis and the physiological effects of glucocorticoids and mineralocorticoids helps in the understanding of the diagnosis and treatment of canine hypoadrenocorticism. Many cases can be diagnosed and managed in general practice; however, because of the vague and sometimes intermittent signs cases are easy to ‘miss’. Although treatment is required life-long, dogs can often be managed successfully and maintain a good quality of life. With diligent owners, the long-term prognosis is generally excellent. This article aims to address diagnosis and treatment by answering some
of the most common questions that are posed by clinicians.
Key words: hypoadrenocorticism, canine endocrinopathy, atypical Addison’s
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Page 32 - VETcpd - Vol 7 - Issue 4
Introduction
The mammalian adrenal glands consist
of an outer cortex and inner medulla (Figure 1). Hypoadrenocorticism can be defined as a lack of adrenocortical steroid production and this typically includes both glucocorticoids and mineralocorticoids.
Cortisol, the primary glucocorticoid secreted by the adrenal glands, has important roles in maintaining the gastrointestinal mucosal barrier
and regulating insulin and calcium balance. Aldosterone, the primary mineralocorticoid secreted by the adrenal gland, regulates potassium excretion and plasma volume via controlling sodium retention. Secretion of aldosterone
is primarily stimulated by the renin- angiotensin system and hyperkalaemia, with adrenocorticotropic hormone (ACTH) playing only a minor role. Cortisol secretion is mediated by the hypothalamic-pituitary-adrenal (HPA) axis (Figure 2), with ACTH providing the primary control.
Primary or secondary?
Hypoadrenocorticism can be further classified as primary or secondary (Figure 3).
Primary hypoadrenocorticism
Immune-mediated destruction of the adrenal cortex is considered to be the main cause of primary hypoadrenocorticism, although auto-antibodies have only been identified in 24% of dogs (Boag et al.
2015).There appear to be certain breed predispositions to disease, with Portuguese Water Dogs, Standard Poodles, Bearded Collies, Cairn Terriers and Cocker Spaniels over-represented (Hanson et al. 2016). Bilateral neoplastic infiltration
(for example lymphoma), fungal disease, trauma and coagulopathy can also cause primary hypoadrenocorticism. Iatrogenic primary hypoadrenocorticism can occur as the result of drugs such as mitotane. Occasionally, there may be isolated destruction of the zona fasciculata in which case serum electrolytes remain normal, resulting in what is sometimes termed ‘atypical’ hypoadrenocorticism or isolated hypocortisolaemia.This concept will be discussed more thoroughly later in this article.
Secondary and tertiary hypoadrenocorticism
Secondary and tertiary hypoadrenocorticism occur rarely
in dogs and are a result of decreased ACTH secretion by the pituitary gland
or decreased corticotrophin-releasing hormone (CRH) secretion by the hypothalamus.This can occur secondary to inflammation, trauma, neoplasia or congenital abnormalities.Alternatively iatrogenic secondary hypoadrenocorticism may occur following rapid withdrawal
of exogenous corticosteroids. Feedback inhibition from exogenous glucocorticoids suppresses anterior pituitary secretion of ACTH, which in turn leads to atrophy