Adrenal Disease Flashcards
a 10 yo FS lab presents for recurrent UTIs, PUPD, and increased panting. on urinalysis, the USG is 1.018 and the UPC is 1.5. On blood chemistry she has a high ALT, AST, and ALP. Differentials?
hyperadrenocorticism (cushings)
which kind of cushings is more common in dogs, pituitary or adrenal?
pituitary depndent (85), usually a small pituitary pars distalis tumor.
iatrogenic cushings is caused by
giving steroids for long periods of time
what are the most common clinical signs of cushings in dogs?
PUPD
alopecia
pendulous abdomen
hepatomegaly
polyphagia
pituitary dependent cushings is more common in younger or older dogs? larger or smaller dogs?
younger and small dogs: pituitary
adrenal is often older and bigger dogs
true or false: most cushings dogs come to you happy and not ill
true! some owners might not bring the pet in because their dog seems just fine at home and they think it’s just overweight or changes more common in old dogs like accidents in the house and PUPD
a 12 yo cockapoo comes to you with PUPD, a big belly, and some bilateral alopecia on the flank. You suspect cushings. what changes on chemistry and urinalysis panel would confirm your suspcision?
high ALP, high ALT, hyperlipidemia, USG lower than 1.020, UPC>1 (proteinuria)
list some diferentials for an ALP that is higher than an ALT?
endocrinopathy, diabetes mellitus, cholangitis, cholestatis disease, cholecystolith, steroids, phenobarb, chronic hepatopathies, neoplasia
why do dogs with cushings have a high ALP, high ALT, high lipids, and isosthenuria?
ALP: steroid isoenzyme is induced with cortisol
ALT: swollen hepatocytes and glycogen accumulation
Lipids: lipolysis=high TG and high cholesterol
isosthenuria: diruesis
**note we dont know why they get proteinuria
besides CBC/chem and urinalysis, what are some other diagnostics to confirm cushings in dogs?
blood pressure: many will be hypertensive
urine culture: up to half of dogs have UTIs that are silent due to flushing
screen for hypothyroid, make sure they dont have it
what might you suspect to see on ultrasound in a suspected cushing dog?
hepatomegaly, can check for gallbladder mucocele, can check adrenal gland size
why do cushings dogs show bronchial and tracheal ring mineralization and potential pulmonary thromboembolism?
they are in a hypercoagulable state from the cortisol which increases a bunch of the coagulation factors
what is the difference between a screening test and a differentiating test for cushings? list examples of tests under both categories
screning: do they have cushings or not?
- LDDST (sensitive), ASTH stim (specific), urine cortisol creatinine test (sensitive)
differentiating: what kind of cushing do they have?
- LDDST (4 hr suppression), abdominal ultrasound, HDDST (almost never done anymore)
explain the urine cortisol to creatinine ratio test for cushings
it’s not the best test, although it’s sensitive, it is not very specific (anything causing stress can make it high), I am unlikely to use this test but is an option, owner can bring a urine sample from home
describe the ACTH stim test for cushings
measures the response of adrenal glands in response to ACTH, it tests the adrenal reserve. in cushings dogs they will have an exaggerated response (except if it’s iatrogenic).
You give synthetic ACTH and then collect blood at 1 hour post.
think of the dog knocking on the doors and the doors open and overflow with excess cortisol. adrenals are JACKED ASF
the ACTH stim test is specific but not sensitive, which means
you can miss some cushings but if it’s positive, the patient likely has cushings
true or false: ACTH stim test can differentiate between pituitary and adrenal cushings
false
describe the LDDST 8hr test for cushings?
low dose dex suppression test: the bread + butter test :)
normal animals, if given dex (a steroid), should have negative feedback and suppress ACTH and therefore suppress cortisol
in cushings animals there is little or no suppression
it is sensitive but less specific so if it’s negative it’s less likely to be cushings
proper way to interpret a LDDST?
sample at 4hrs and 8 hrs
look at the 8 hr number first: it’s considered cushings if cortisol is higher than the lab reference
then look at the 4 hr number: most of the time if there is suppression at 4 hr with an increase at 8 hr this indicates pituitary dependent (essentially it dips down and then goes back up, 50% suppression or greater)–>pituitary dependent retains some ability for negative feedback with exoogenous steroids. this does not happen with adrenal dependent
how does an endogenous ACTH test work
with pituitary cushings, endogenous ACTH is high because the pituitary is producing it
with adrenal cushings, endogenous ACTH is low because of the negative feedback and excessice cortisol production
why isn’t the endogenous ACTH test done more?
it’s super expensive and the samples are fragile and need to be shipped in a special vial, it is not practical
the main treatments used for cushings are
trilostane*** and mitotane–>reduce adrenal reserves to what you need. this takes weeks to months to work
could do a hypophysectomy but it’s complicated and not often done
how does trilostane work? what are some potential complications of the drug?
it is a competitive inhibitor of beta hydroxysteroid dehydrogenase enzyme which inhibits the production of progesterone and therefore the production of cortisol (and a little bit aldosterone)
possible adrenal suppression for months if overdosed, adrenal necrosis, mild hyperkalemia from aldosterone suppression, adrenal atrophy
you diagnose a 10 yo dog with cushings and decide to start the dog on trilostane. how will you monitor the dog going forward?
start at 1mg/kg q12 with food, then recheck in 7-10 days, 4-6 hours after the morning dose. We want to see the results of the ACTH stim to be decreased ( we are trying to decrease the adrenal reserves).
if it’s between 70 and 250 and there’s improved clinical signs, keep the dose the same. If it’s between 70 and 250 and there’s no improvement in clinical signs, give it one more month and recheck. If it’s higher than 250, increase dose by 25% and re check in a week. And if it’s below 70, stop the med and start pred (youve given the dog addisons now)
how does mitotane work?
it has a cytotoxic effect on the adrenal cortex and kills the adrenal glands
it is considered the “old” drug and it can induce addisons
should you use trilostane or mitotane?
depends on owner compliance, cost, and comfort. Trilostane is way more expensive but is the “newer” drug. Both treat the disease well, and both can have complications. Trilostane is often chosen first
an owner brings their dog Pal to you and you diagnose cushings. the owner is very overwhelmed and explains to you they have very limited funds and cannot afford trilostane. What treatment options are there?
we focus on treating the most common complications: hypertension and proteinuria. the dog will however continue to be PUPD and polyphagic.
true or false and explain why: cushings is a benign disease
false!!
common complications: hypertension, bladder stones (more calcium excretion, calcium stones), UTIs, proteinuria, diabetes due to insulin resistance, hypercoagulability, mucocele
true or false: feline cushings is common
false, but when it happens, it’s really bad. they are usually also diabetic
what’s the difference between typical addison’s and atypical addisons?
typical: deficiency of both mineral and glucocorticoids, way more common
atypical: deficinecy of just glucocorticoids
why are addison’s dogs “sick”?
mineralocorticoids normally cause sodium reabsroption and potassium secretion
glucocorticoids normally control metabolism, cellular stability, and the stress response. essentially effects anything.
addison’s patients dont have enough of either of these
what causes addison’s?
immune mediated adrenalitis most commonly
iatrogenic (gave too much steroids and cause adrenal atrophy)
common signalment for addison’s?
poodles, duck tollers, protugese water dog, bearded collie
females
young dogs, average 4 years
clinical signs of addisons?
vague waxing and waning signs: anorexia, vomiting, lethargy, diarrhea, weight loss, weakness, shivering, dehydration, bradycardia, shock
it can be ANYTHING
a 4yo poddle named Booger comes to you with waxing and waning vomiting and diarrhea. Her heart rate is 60 and she has a body condition score of 3/9. What CBC/chem findings would you expect based on the top differential?
lack of a stress leukogram, hyperkalemia, azotemia (dehydration), USG less than 1.030 (they dont have enough sodium), could have hyponatremia, hyperphosphetemia, many more too.
you do a CBC chem on Booger and find lack of a stress leukogram and an Na/K ratio of 18. what diagnostic test will you do now?
ACTH stim test: if post cortisol is above 55 it’s unlike to be addisons, and if its below the detection limit, Booger has addisons.
could also consider a baseline cortisol test: if it’s below detection limit, addison’s is confirmed.
if the Na/K ratio is less than 24, you should ALWAYS do what test
an ACTH stim because this is highly suggestive of addison’s
a duck toller named Fwimsy comes to you in shock. the owner says she’s been vomtting recently on and off and has been acting a bit lethargic. You suspect addions disease. how will you treat Fwimsy in her acute crisis? (assume typical addisons)
IV fluids: treat the shock with a 10ml/kg bolus over 5 mins and restore normal electrolytes
Dexamethasone: 0.1-0.1mg/kg IV (dex does not interfere with cortisol testing)
fix the hyperkalemia: calcium gluconate, dextrose, insulin, can start mineralocorticoids but not right away
usually 1-2 days in hospital and then can go home.
why dont we use 0.9% NaCl to treat addisons?
it is acidifying, it squishes bicarb
what mineralocorticoid options are there for addisons patients?
Fludrocortisone and DOCP
DOCP is often chosen most of the time, it is an injection every 25 days and it’s easier than pills. You give them pred at the same time. more expensive.
Fludcrocortisone is an oral pill and there’s only 1 size so big dogs need like 6 pills twice a day. more annoying. also has some gluco action not just mineralo. So you could consider stopping pred on this one.
true or false: owners should increase the pred dose during stressful situations for addison’s patients
true! double the dose the day before, during, and the day after. this mimics normal physiology
how often should you monitor addions’s patients?
1 month after discharge: do bloodwork, we want Na/K above 27 (if it’s below 24 you may need to increase DOCP dose). then every 3-6 months at the time of a DOCP injection
true or false; there is no way to effectively monitor atypical addions
true! just based on clinical signs
true or false: pred interferes with cortisol testing
true
