Adrenal diseases- Hyperadrenocorticism (Cushing’s) and Hypoadrenocortoisism Flashcards
What are the two forms of hyperadrenocorisism and which one is most common
Pituitary- dependent HAC which is most common (85% of cases) and Adrenal dependent HAC
Explain how pituitary dependent HAC works
There is typically a microadenoma which has formed on the anterior pituitary causing an uncontrolled (no negative feedback) increase in ACTH secretion resulting in continual stimulation to release cortisol
Explain how adrenal-dependent HAC works
There is an adenoma/adenocarcinoma that has formed on the adrenal gland stimulating it to release cortisol and interrupting the negative feedback system. Usually the mass is unilateral so one adrenal gland is large and the contralateral one is small
What are the five most common signs of Cushing’s
Polyuria/polydipsia
Polyphagia
Panting (dogs only)
Pendulous abdomen (and enlarged liver, muscle wasting, and odd fat distribution)
Poor hair coat (alopecia, bilateral, truncal, non-pruritic, calcinosis cutis)
What are 3 common biochemical changes with Cushing’s
Mature neutrophilia and lymphopenia (stress leukogram)
elevated ALP
Low USG (<1.020)
Why is proper patient selection crucial for hyperadrenocortisism testing/diagnosis
The cortisol tests are not perfect and are prone to false positives. You shouldn’t test a patient that is already stressed or sick and you should also have 2 or more clinical or biochemical abnormalities before you test
What is important about a highly sensitive test and what is a useful one for Cushing’s
The more sensitive a test the more you can trust a negative test and the more confident you can rule out the patient having the disease (however you can’t trust a positive test, lots of false positives). For Cushing’s the urine cortisol: creatinine ratio (UC:CR) test is good for ruling out HAC, used for animals without many clinical signs but maybe has one or two and you just need to rule it out
How is a UC:CR test preformed
the urine is collected over 2-3 days from the patient when they are not stressed (ideally at home) and then the samples are pooled and submitted to test for urine cortisol, if above range then do LDDST or ACTH stim
How is a low-dose dex suppression test done
It is also highly sensitive and moderately specific, but less specific if the animal is already stressed or sick
You need to get a baseline blood sample (red top) to get a baseline cortisol when the animal isn’t stressed. Then you give dexamethasone IV. Then you get 4 and 8 hour samples.
How do you interpret a LDDST
If the 8 hour sample is >/= 1.4 ug/dL then the animal has Cushing’s (most likely)
If there is any suppression present (must have over 50% of the baseline surpassed at hour 4) but sample still greater than 1.4 then it is likely pituitary dependent
If there isn’t suppression (over 50%) then the diagnosis is just hyperadrenocortisism (you can’t differentiate)
How do you run a ACTH stimulation test
This is a moderately sensitive and specific test but it is better for animals that are stressed or sick
You use synthetic ACTH. You get a baseline cortisol sample and then give sACTH and then get a 1 hour post sample (this is diagnostic)
How do you interpret a ACTH stim test
At the 1 hour mark for cortisol concentrations-
6-17 ug/dL is normal
17-22 ug/dL is questionable (grey zone)
>22 ug/dL suggests HAC (can’t differentiate if PDH)
In cats >15 ug/dL suggests HAC
How can an ultrasound of the adrenal glands help differentiate between the types of Cushing’s
If the adrenal glands are both normal or bilaterally enlarged (or plump) it is probably pituitary dependent (greater than 0.74 cm), but with ADH there is usually a mass or nodule that is causing the increased release of cortisol so one adrenal will be large and the other won’t
so bilateral enlargement= PDH and unilateral enlargement= ADH usually
Explain how measuring endogenous ACTH can differentiate between types of Cushing’s
if the endogenous ACTH is high it is PDH because the pituitary gland is stimulating the adrenals via an increase in ACTH
If the endogenous ACTH is low it is ADH because the negative feedback is working on the pituitary glands and they aren’t releasing much ACTH but the adrenals aren’t responding
How do you preform a UCCR dexamethasone test
You collect urine samples in the morning for 2 days, then you give 0.1mg/kg of dexamethasone orally every 6-8 hours for 3 doses and then you collect another urine sample the following morning and you submit these samples (day 1 and 2 pooled together and day 3 separate) and you measure the UCCR
What is the treatment for hyperadrenocortisism and how does it work
trilostane (Vetoryl) and it blocks the cortisol production by inhibiting 3-beta-hydroxysteroid dehydrogenase (enzyme involved in synthesizing cortisol)
How do you monitor for trilostane and what are the goals ?
You start it and then recheck with ACTH stim in 10-14 days. You want to give the sACTH 4-6 hours after the pill is given. Ideally the medicine controls the cortisol levels and at the 1-hour check the cortisol level goal is around 5 ug/dL
After 30 days you reassess. If the cortisol level with an ACTH stim is >5.0 AND the animal has clinical symptoms still then you can increase the dose. If they don’t have clinical symptoms, even if the cortisol is >5.0, you can leave it alone it is controlled. If it is <5.0 and the animal is still clinical you should look for other causes of the symptoms.
What do you do if a patient has developed iatrogenic hypocortisolism (looks like depression, lethargy, pu/pd, V/D, anorexia) because of trilostane
First do a diagnosis with an ACTH stim- pre and post cortisol may be <1.0 ug/dL. You would treat with dexamethasone tablets and supplement with steroids as needed (may need a break from trilostane or to restart later at a lower dose)
describe typical vs. atypical Addison’s disease (hypoadrenocorticism)
Typical is a deficiency of both glucocorticoid (cortisol) and mineralocorticoid (aldosterone) deficiency
Atypical is just having a glucocorticoid deficiency
What does aldosterone do
It causes sodium and water absorption and potassium and hydrogen excretion
What happens to cause Addison’s
> 90% loss of adrenocortical function from autoimmune destruction of both adrenals, often considered idiopathic
What breed is the poster child for Addison’s and what is different about the signalment compared to most endocrinopathies
Standard Poodle! around 4 years of age (weird because most endocrinopathies are older, like 8 years) and more likely to be females
What are 3 main clinical signs and some biochemical changes with Addison’s
Decrease in cortisol which causes lethargy, hypoglycemia, GI upset, hypotension
Decrease in aldosterone which causes hypovolemia, polyuria, and acidosis
Clinical signs- Episodic GI signs (especially following stress), Polyuria and polydipsia
Biochemical changes- lack of stress leukogram, hyperkalemia, hyponatremia, azotemia, liver enzyme elevation, metabolic acidosis
Why is Addison’s called the great imitator
because it has very vague signs like GI upset and azotemia and liver enzyme elevation- looks like a lot of different things!
What is the screening test for Addison’s
basal cortisol concentration, if the cortisol is >2.0 ug/dL then the animal does not have Addison’s
How do you definitely diagnose Addison’s
Use a ACTH stim test and see if the animal responds by making cortisol
What is delta cortisol
The difference between the peak and basal cortisol levels
How do you treat Addison’s
You give prednisone to replace the glucocorticoids (0.2-0.4 daily and 0.5mg/kg before stressful events). you give Desoxycorticosterone pivalate (an injection every 25-28 days) or Fludrocortisone (a daily med) to replace the mineralocorticoids
How do you monitor Addison’s once the animal is on medication
monitor electrolytes and clinical signs
What is the most important acute therapy in an Addisonian crisis
IV fluids
What are the doses of prednisone for physiologic replacement, anti-inflammatory effects, and immunosuppression
physiologic replacement- 0.2-0.4 mg/kg/day
anti-inflammatory effects- 0.5-1.0 mg/kg/day
immunosuppression- 2.0-4.0 mg/kg/day
What are the doses of dexamethasone for physiologic replacement, anti-inflammatory effects, and immunosuppression
physiologic replacement- 0.02-0.04 mg/kg/day
anti-inflammatory effects- 0.05-0.1 mg/kg/day
immunosuppression- 0.2-0.4 mg/kg/day
