Feline Adrenal Gland Disease (Rolph) Flashcards

1
Q

What’s unusual about feline hypoadrenocorticism?

A
  • Primary hypoadrenocorticism = rare
    • Majority idiopathic, occasionally secondary to neopalsia/trauma
  • Secondary hypoadrenocorticis
    • _​_Frequently post-administration of corticosteroids or megestrol acetate
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2
Q

Describe the signalment for feline hypoadrenocorticism.

A
  • 18 mos. - 14 yrs.
  • No gender or breed disposition
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3
Q

What are some clinical signs associated with feline hypoadrenocorticism?

A

Up to 4 mos., waxing/waning

  • Lethargy
  • Depression
  • Anorexia
  • Weight loss
  • Collapse
  • Weakness
  • Dysphagia
  • Vomiting
  • PU/PD
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4
Q

What would CBC and biochemistry results look like for feline hypoadrenocorticism?

A

Often normal

  • Occasionally normocytic, normochromic, non-regenerative anemia, lymphocytosis and eosinophilia
  • Azotemia (pre-renal)
  • Hyperphosphatemia
  • Mild increases in ALT, ALP, tBil
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5
Q

What would urinalysis results look like in feline hypoadrenocorticism?

A

USG typically < 1.030

  • Due to medullary washout from hyponatremia and lack of vasopression
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6
Q

What are expected electrolyte abnormalities in feline hypoadrenocorticism?

A

** OFTEN TELL-TALE SIGNS **

  • Hyponatremia
  • Hypochloremia
  • Hyperkalemia
  • Occasionally hypochloremia and hypo/hypercalcemia
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7
Q

How do you diagnose feline hypoadrenocorticism?

A

ACTH Stimulation Test ± ACTH assay

  • Elevated ACTH concentration in a cat w/ hypoadrenocorticism CONFIRMS primary disease
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8
Q

Describe treatment for feline hypoadrenocorticism?

A

Same as for dogs

  • Aggressive IVF
  • Address hyperkalemia/dysrhythmias
  • Glucocorticoid replacement (IV dexamethasone, prednisolone)
  • Mineralocorticoid replacement (fludrocortisone acetate or DOCP IM)
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9
Q

How long does it take for patients to respond to feline hypoadrenocorticism treatment?

A

About 3-5 days

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10
Q

What’s the prognosis for cats surviving feline hypoadrenocorticism?

A

Excellent (can live for many months/years)

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11
Q

What is feline hyperaldosteronism?

A

Hyperplasia or neoplasia of adrenal glands → overproduction of aldosterone

  • Also known as Conn’s syndrome
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12
Q

Where is aldosterone released from, what does it affect, and what does it stimulate?

A
  • Released from zona glomerulosa (mediated by AngIII, increased K+, corticotrophin)
  • Affects mineralocorticoid receptors in distal renal tubules, colon, salivary glands
  • Stimulates: Na reabsorption, K and hydrogen excretion
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13
Q

What is aldosterone’s role in the kidneys?

A

Traditionally as hormone controlling Na+ reabsoprtion and K+ excretion by acting on:

  • Late distal convoluted tubule
  • Connecting tubules
  • Principle cells of collecting ducts
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14
Q

In the kidney, what does aldosterone activate?

A
  • Epithelial Na+ Channel (ENaC)
  • Sodium chloride co-transporter (NCC)
  • Na,K-ATPase
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15
Q

What’s the relationship between aldosterone and vasoconstriction?

A

Aldosterone MEDIATES vasoconstriction

  • Increases prostacyclin production
  • Potential role in upregulating ET production (ET-1: vasopressor)
  • Upregulates ACE, local production of AngII
  • Upregulates the AT1 receptors
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16
Q

What are some clinical signs of feline hyperaldosteronism?

A
  • Hypokalemia (inappetance, weakness)
  • Hypertension (yowling at night; retinal detachment, ocular hemorrahge, kidney damage, cardiac hypertrophy)
17
Q

How do you diagnose hyperaldosteronism?

A
  • High aldosterone (ALDO)
  • Low plasma renin activity
  • U/S or CT to identify and characterize tumors
18
Q

How do you treat hyperaldosteronism (Conn’s syndrome)?

A

Stabilize medically first!

  • Unilateral: adrenalectomy (post stabilization)
  • Bilateral (or prior to surgery): manage hypertension and potassium loss (spironolactone, K+ supplementation, amlodipine)
19
Q

What is the prognosis of feline hyperaldosteronism (Conn’s syndrome)?

A

Median: 2-3 years if treated (medically or surgically)

  • Irrespective as to whether or not carcinoma/adenocarcinoma or uni/bilateral