hypoadrenocorticism Flashcards
Classic findings of Addison’s disease:
- Absent stress leukogram
- Hyperkalemia
- Hyponatremia
- Na+/K+ ratio < 27
- Azotemia
- Mild to moderate metabolic acidosis
- +/- hypercalcemia (30% of cases)
what is addisons disease? common? signalment?
HYPOADRENOCORTICISM
* Dysfunction of the adrenal cortex
* Uncommon endocrinopathy
* Most prevalent in:
> Young to middle aged
> Female dogs
Addison’s disease means deficient secretion in:
Mineralocorticoids
* Aldosterone
> Na+, K+ & water regulation
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Glucocorticoids
* Cortisol
> Stress response
adrenal cortex zones, and what they do?
- Zona glomerulosa:
* Synthesizes & secretes mineralocorticoids
> Aldosterone
<><> - Zona fasciculata:
* Synthesizes & secretes the glucocorticoids
> Cortisone & cortisol
<><> - Zona reticularis:
* Synthesizes & secretes sex hormones
> Androgens & estrogens
* Secretes the same glucocorticoids as the zona fasciculata
categories of hypoadrenocorticism - primary vs secondary
Primary hypoadrenocorticism
* Adrenal atrophy or destruction
<><>
Secondary hypoadrenocorticism
* Deficiency in pituitary ACTH production
* Lack of stimulation of the adrenal glands
types of primary hypoadrenocorticism
- typical
- atypical
- iatrogenic
types of secondary hypoadrenocorticism
- uncommon
- iatrogenic
primary hypoadrenocorticism - how common? what happens?
- Typical, most common presentation
- Bilateral atrophy or destruction of all 3 layers of the
adrenal cortices
> Glucocorticoid & mineralocorticoid secretion affected
primary hypoadrenocorticism causes
- Immune-mediated destruction
- Infiltrative disease
> Fungal infections, neoplasia
> Amyloidosis
> Hemorrhagic disorders / coagulopathies
<><> - Iatrogenic
> secondary to mitotane / trilostane therapy
atypical addisons - what is it? difference from classic / typical?
- Atypical Addison’s disease
> Subgroup of 1° hypoadrenocorticism
<><><> - Bilateral destruction of zona fasciculata & zona reticularis only
> Glucocorticoids affected; Mineralocorticoids spared
> Electrolyte disturbances not appreciated - Gradually progressive disorder
what is secondary hypoadrenocorticism? how does it often come about? what is affected?
Deficiency in ACTH production from the pituitary
* Other pituitary dependent hormones frequently
also affected
* Rare ie. head trauma
<><><>
At the level of the adrenals
* Glucocorticoid production affected
* Mineralocorticoid production usually preserved
> No electrolyte abnormalities
Drug induced hypoadrenocorticism - causes
Administration of drugs that:
* Directly inhibit glucocorticoid production
> Secondary
OR
* Adrenocorticol lysis
> Primary
Primary iatrogenic hypoadrenocorticism - how it arises? what is affected?
- Mitotane / trilostane therapy for Cushing’s disease
- Administration of drugs that produce adrenocorticol lysis
- Both Glucocorticoid & Mineralocorticoid deficiency
Secondary iatrogenic hypoadrenocorticism - how it arises? what do we see?
- Administration of drugs that directly inhibit glucocorticoid production
- Ie. Corticosteroid administration
<><><> - Corticosteroids, via a negative feedback system, depress ACTH production
- Lack of ACTH causes bilateral adrenal atrophy
- On rapid discontinuation of corticosteroids, adrenals unable to respond adequately
> Glucocorticoid deficiency only
> Electrolyte disturbances not appreciated
hypothalamic pituitary adrenal axis - how it works?
- relationship to prednisone, exogenous corticosteroids?
stressors cause hypothalamus to release CRH
> CRH causes release of ACTH from anterior pituitary
> ACTH causes release of cortisol from adrenal gland
> metabolic effects…..
> cortisol acts on AP and hypothalamus to stop them from secreting ACTH and CRH respectively (negative feedback)
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- PREDNISONE = Exogenous ’cortisol’
- always wean corticosteroids!
- On rapid discontinuation of corticosteroids, adrenals unable to respond adequately
Addison’s Predisposed breeds:
Great Dane
Poodle (all sizes)
West Highland White Terrier
Familial predispositions to addison’s in what breeds?
- Portuguese Water Dog
- Leonberger
- Nova Scotia Duck Tolling Retriever
- Bearded Collie
Acute Addisonian Crisis
- significance?
- clinical findings?
Life threatening emergency
<><><>
Clinical findings:
* Shock / Hypovolemia
* Collapse
* Bradycardia
* Hypotension
* Hypothermia
* Pale or injected mucous membranes
* GI hemorrhage
> Hematochezia / Melena
types of signs we can see from addison’s, in broad categories
- Acute Collapse Shock
- Waxing & Waning Non-Specific Signs
signs we would see in an acute case of addisons
Acute Collapse Shock
* Hypothermia
* Slow CRT
* Injected vs pale mucous membranes
* Weak Pulse / Hypotension
* Bradycardia
* GI hemorrhage
* Painful Abdomen
waxing and waning, non-specific signs we might see from addison’s
- Lethargy / depression
- Anorexia / weight loss
- Vomiting
- Diarrhea
- Weakness
- PU/PD
- Hair loss
- Previous response to therapy
how do we diagnose addisons?
Given that the historical & clinical findings are vague, non-specific, often intermittent & found with many other disease processes
* High Index of Suspicion
why is addison’s known as ‘the great pretender’? what can Addison’s look like?
- No pathognomonic signs
> Waxing & Waning illness - Signs are common to a wide variety of more
prevalent diseases - Duration
> Chronic progressive signs (up to 1 year) - May culminate in fulminant acute adrenal crisis
clinical abnormalities seen in addisons?
- electrolytes
- CBC
- urinalysis
- increased K+
- decreased Na+
- Na+/K+ ratio <27
- decreased Cl-
- increased Ca2+
- increased Phos
- Azotemia
- Hypoglycemia
<><>
CBC: - Anemia
- Eosinophilia
- Lymphocytosis
- Lack of stress leukogram
<><>
Urinalysis - USG < 1.030
