endocrinology (primary hypoadrenocorticism) Flashcards

1
Q

what is the pathophysiological mechanism for primary hypoadrenocorticism

A

primary hypoadrenocorticism or Addison’s disease results from the deficient adrenal production of mineralocorticoids and glucocorticoids due to adrenal cortex destruction or more rarely hypophyseal dysfunction

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2
Q

what is the epidemiology of the disease

A

the disease is rare in cats

no sex, breed or age predisposition

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3
Q

what are the clinical signs for hypoadrecorticism

A

non-specific, waxing/waning clinical signs predominate

lethargy and weakness are very commonly seen in cats

other clinical findings commonly reported include anorexia, weight loss, dehydration and hypothermia

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4
Q

what findings are very suggestive of hypoadrecorticism on thoracic radiographs

A

pulmonary hypoperfusion and/or microcardia van be seen as a result of the hypovolemia associated with hypoadrenocorticism

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5
Q

what are the main laboratory changes encountered with hypoadrenocorticism

A

hyponatremia and hyperkalemia are the hallmark biochemical findings, with a sodium to potassium ratio of less than 27:1 considered to be highly suggestive of hypoadrenocorticism
- the degree of hyperkalemia is often mild, while the hyponatremia may be mild to marked

azotemia, hyperphosphatelia and hypochloremia are also common findings

on hematology, lymphocytosis is sometimes seen

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6
Q

explain why there may be poor renal concentrating ability in the face of azotemia and dehydration

A

the hyponatremia in hypoadrenocorticism impairs renal concentrating ability by decreasing the medullary solute gradient, and possibily also interferes with vasopressin release

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7
Q

how would you confirm the diagnosis

A

an ACTH stimulation test is required to confirm a diagnosis of hypoadrenocorticism
- the presence of a low basal cortisol level with little or no response to exogenous ACTH administration is diagnostic for this condition

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8
Q

explain the procedure for an ACTH stimulation test

A

cortisol levels must be determined before and both 60 and 180 minutes following IV injection of 0.125 mg ACTH

lack of response to ACTH (with low basal cortisol level) is seen in both primary and iatrogenic hypoadrenocorticism
- therefore, it is important to review medical therapy to rule out the latter

aldosterone concentrations can also be determined pre- and post-ACTH injection and will usually be low and remain low in hypoadrenocorticism

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9
Q

does pure glucocorticoid-deficient hypoadrenocorticism exist in cats

A

it has not been reported in cats, however, in iatrogenic hypoadrenocorticism, aldosterone levels are typically normal

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10
Q

what is the treatment for hypoadrenocorticism

A

initial treatment requires aggressive IV fluid therapy to replace circulating blood volume and correct electrolyte imbalances (e.g., NaCl 0.9% at a rate of 2-3 times maintenance) in addition to glucocorticoid supplementation

hydrocortisone CRI at 0.5 mg/kg/h IV can be used and is preferable to dexamethasone (0.5-1 mg/kg IV) as it is faster acting
- improvement may be seen over 3-5 days

maintenance therapy is aimed at daily steroid replacement, usually with the mineralocorticoid fludrocortisone acetate (0.1 mg once daily) or desoxycorticosterone pivalate (2.2 mg/kg IM or SC every 25 days) along with physiological glucocorticoid doses such as prednisolone at 0.25 mg/kg PO daily or methylprednisolone acetate (10 mg IM once a month)

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