Hypoadrenocorticism Flashcards

1
Q

Where is glucocorticoids secreted in the adrenal gland?

A

Adrenal cortex, in all 3 layers (zone glomerulus, fasciculata, and reticularis)

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2
Q

Where is aldosterone (mineralocorticoid) secreted in the adrenal gland?

A

In the zone glomerulus only - only place that has aldosterone synthase

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3
Q

What is a possible cause of hypoadrenocorticism in dogs?

A

immune-mediated

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4
Q

Which breeds have familial predisposition to hypoadrenocorticism?

A
  • Leonberger
  • Great Dane
  • Standard Poodle, Portugese Water Dog, Pomeranaina - autosomal recessive
  • Bearded Collie - complex
  • Cocker Spaniels
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5
Q

What’s the definition of primary hypoadrenocorticism in dogs? What’s atypical Addison’s?

A

hypoadrenocorticism = atrophy of adrenal cortices
- so deficient in both mineralocorticoids and glucocorticoids
- Atypical Addison’s = Na+/K+ values remain normal (Addison’s = hyponatremia, and hyperkalemia)
- sometimes atypical Addison’s can progress to full-on Addison’s
- rare have mineralocorticoid deficiency proceed glucocorticoid deficiency
- even more rare to have just aldosterone deficiency

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6
Q

What are some less common causes of hypoadrenocorticism in dogs?

A

Secondary to direct invasion of the adrenal gland
- neoplasia = most common
- infectious: TB, fungal, other granulomatous diseases, infarct

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7
Q

What causes secondary hypoadrenocorticism in dogs?

A
  • dysfunction of the hypothalamus or pituitary gland
  • could be due to neoplasia, infection, inflammation, trauma, infarct
  • will have low CRH or ACTH
  • won’t effect mineralocorticoids
  • difference between that and atypical Addison’s is that secondary hypoadrenocorticism will have low ACTH versus atypical Addison’s will have high ACTH
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8
Q

Which breeds are at a DECREASED risk f hypoadrenocorticism?

A
  • Golden retrievers
  • Yorkies
  • Pitties
  • Chihuahuas
  • Lhasa Apsos
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9
Q

What’s the typical signalment for hypoadrenocorticism in dogs?

A
  • young to mid aged (3-4y = median)
  • female may be at an increased risk
  • breed disposition
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10
Q

**What are some clinical signs of hypoadrenocorticism in dogs?

A

Mostly attributable to lack of cortisol
- decreased appetite
- weigh loss*
- vomiting*
- diarrhea*
- PU/PD**
- lethargy*
- weakness
*
- shaking***
- collapse (extreme)

due to lack of protection of GI mucosa from acidity
**due to lack of mineralocorticoids (aldosterone), leading to Na+ loss
**
due to hypoglycemia

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11
Q

What’s the action of glucocorticoids on glucose homeostasis?

A

In stressful or fasting conditions
- catabolism of glycogen
- stimulates gluconeogenesis

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12
Q

What are some PE abnormalities for hypoadrenocorticism in dogs?

A
  • dehydration (PU/PD, from Na+ excretion)
  • hypotension, mainly systolic (glucocorticoids enhances vascular effects of angiotensin and renin)
  • bradycardia (hyperkalemia, takes longer to repolarize)
  • abdominal pain (glucocorticoids have protective effects on GI mucosa)
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13
Q

What are some common CBC finding for hypoadrenocorticism in dogs?

A
  • increased lymphocyte counts (>2000 = 58% sensitive and 85% specific for hypoadrenocorticism)
  • lower neutrophils
  • higher eosinophils
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14
Q

What electrolyte abnormalities can be seen with hypoadrenocorticism in dogs? Why?

A
  • hyponatremia (lack of aldosterone leading to Na+ excretion)
  • hyperkalemia (Lack of aldosterone leading to K+ retention)
  • hypochloremia (follow Na+ from blood to urine)
  • hypercalcemia (glucocorticoids facilitates calciuresis, maybe acidic environment [lack of aldosterone = lack of H+ secretion] displaces Ca+ from albumin due to competition). But it’s usually total Ca elevated, not iCa
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15
Q

What’s the MOA of abnormal glucose level in dogs with hypoadrenocorticism?

A

lack of glucocorticoids = decreased gluconeogenesis and glycogen catabolism
- the hypoglycemia tend to mild, and seizure in uncommon

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16
Q

What’s the reason of increased liver enzymes, low albumin, and low cholesterol for dogs with hypoadrenocorticism?

A
  • it’s not due to liver dysfunction
  • likely due to acute GI ischemia
17
Q

What’s the likelihood of resolving severe serum biochemistry abnormalities in dog with hypoadrenocorticism?

A

they almost always completely resolve with treatment!

18
Q

What are some ECG changes noted with hyperkalemia?

A

lack of P wave, wide QRS, tall T waves
- heart block

19
Q

Can AUS be used to assess adrenal function?

A

No, but dog with hypoadrenocorticism, adrenals are typically <3mm

20
Q

**What is the best test to confirm hypoadrenocorticism in dogs?

A

ACTH stim
baseline and post ACTH cortisol level would be <1mcg/dL

21
Q

Can resting cortisol alone be enough to diagnose hypoadrenocorticism in dogs?

A

no, but you can do cortisol: endogenous ACTH ratio
it’s a good rule out screening test

22
Q

What are some ddx for hypoadrenocorticism?

A

severe GI diseases can lead to electrolyte abnormalities –> tricuriasis, salmonellosis
- periparturient iillness
- chylothorax

23
Q

**How to treat an acute hypo adrenal crisis in dogs?

A

1 = fluids! 0.9% NaCl, though acidic, it has more NaCl than K. The acidosis usually will correct itself

  • if the electrolyte imbalance remains, need to correct Na+ slowly to ovoid osmotic shift
  • can use IV dextrose to stimluate endogenous insulin secretion to drive the K+ intracellular
  • IV insulin only used if glucose level is above 11mmol/L, watch for hypoglycemia
  • hyperglycemia can also decrease Na+ level due to fluid shifting (dilution)
  • if severe acidosis is not resolved, can consider doing bicarbonate
  • can also give DOCP once ACTH stim done and other ddx excluded
  • usually steroids are not needed in the acute setting and can complete ACTH stim first
  • if really need steroids, use dexamethasone instead (won’t cross react with cortisol assay and acts quickly), but can suppress endogenous ACTH/CRH, and effect ACTH stim results
24
Q

What’s the long term treatment for hypoadrenocorticism in dogs?

A

maintenance therapy can usually begin 24-48h post crisis.
Goals = supplement glucocorticoids and mineralocorticoids
- Glucocorticoids: prednisone. initially start high, and taper to lowest effective dose
- Mineralocorticoids: DOCP. SQ injection done every 3 weeks. Monitor Na:K ratio half way and on the day it’s due. If >32, then skip. If < 28, give. Adjust dosage and interval as needed
- fludrocortisone: has both glucocorticoid and mineralocorticoid activity, but it’s harder to tailor to minimize the side effects of steroids
- DOCP is more effective vs fludrocortisone in decreasing the plasma renin activity, increasing Na and decreasing K

25
Q

How is hypoadrenocorticism monitored?

A
  • frequent blood work monitoring the Na:K ratio
  • PU/PD could be a sign of steroid side effect, HA, or other common conditions
  • need to monitor atypical Addison’s closely too as they progress to typical Addison’s
26
Q

What’s the long term prognosis for hypoadrenocorticism in dogs?

A

Excellent, once recovered from acute crisis

27
Q

Give a brief description of hypoadrenocorticism in cats.

A

Rare in cats. but similar presentation and test abnormalities as dogs. Same treatment but prognosis is not as good as dogs.
Can have pseudo hyponatremia and hyperkalemia from peritoneal effusion