Cushing's, Addison's and Pheochromocytoma Flashcards
85-95% of endogenous cushing’s dogs and cats are due to ____.
Pituitary-induced micro or macroadenoma
Cushing’s pathogenesis
XS ACTH made in pituitary –> adrenals –> hypercortisolemia (pituitary escape from negative inhibition)
Adrenal steroidogenesis
ACTH –> adrenal cortex –> aldosterone, cortisol and sex steroids.
Atypical cushing’s
normal cortisol levels, cushings symptoms caused by xs intermediate metabolites from steroidogenesis
What are the three zones of the adrenal cortex?
Glomerulosa
Fasciculata
Reticularis
What hormone is made in the zona glomerulosa?
aldosterone
What hormone is made in the zona fasciculata?
cortisol
What hormone is made in the zona reticularis?
ketosteroids and cortisol
Aldosterone has an effect on _____.
Na and K production in the body
Pathophysiologic effects of xs cotisol?
Muscle/bone/tendon - weakness
liver - glycogen deposition; steroid hepatopathy
gut - hyperacid secretions
immune system - suppressed, prone to secondary infection (silent UTIs)
kidney - PU/PD because ^GFR and renal plasma flow
Brain - hyperirritable. Dog: panting!
Bloodstream - mature neutrophilia, lymphopenia, eosinopenia, monocytosis, thrombocytosis, and increased RBCs
Lipid metabolism - increased cholesterol
Breed and age incidence of Hyperadrenocorticism?
toy and miniature breeds (poodles and dachshunds)
age: 3-13 range, avg 8 years old
main endogenous causes of Hyperadrenocorticism?
pituitary dependent (high ACTH, high cortisol) adrenal dependent (low ACTH, high cortisol)
exogenous cause of Hyperadrenocorticism?
iatrogenic - large doses of glucocorticoids (act like cortisol)
** must wean off these drugs because will have trouble making cortisol with removal of drug.
Physical features of Hyperadrenocorticism?
Panting (dogs)
PU/PD
pendulous abdomen (due to muscle weakness)
stria (stretch marks) from weakening/thinning of skin
truncal alopecia with hyperpigmentation
acne formation - keratin plugging of hair follicles
easily bruise
calcinosis cutis
cushings wrinkles
general muscle weakness- myotonia!
lethargy
polyphagia
testicular atrophy and hepatomegaly in the dog due to glycogen accumulation
hypercoagulable
Other: pulmonary calcification, prothrombotic tendency, hypertension, proteinuria, glomerulopathy (can be permanent)
Hyperadrenocorticism lab findings?
mature neutrophilia, eosinopenia, and lymphopenia
Polycythemia
high liver enzymes (hepatomegaly due to glycogen accumulation)
glucose (if also have DM)
+/- pyuria —> UTI
+/- hematuria
Proteinuric (glomerulopathy)
hypertension (glomerulopathy)
high cholesterol/TGs (lipemia)
high cortisol
adrenal/pulmonary calcification (gritty lungs on necropsy)
Cushing’s imaging
radiographs early phase pyeologram arteriography abdominal U/S pituitary CT/MR
If unilateral adrenal tumor is resected, the ipsilateral adrenal will be atrophied so expect _____ post-op.
adrenocortical insufficiency - supplement glucocorticoids
pituitary macroadenomas are hard to resect; try to remove whole pituitary which means will have _____ post-op.
diabetes insipidus (no renal ADH) or another hypoendocrinopathy
Cushing’s diagnosis
Urine cortisol/Cr ratio (if negative, rules out cushing's, if positive, could be something other than cushing's) ACTH stim test*** LDDT - low dose dex suppression HDDT Plasma ACTH - \$\$$ and time
Most common signs of cushing’s in a dog?
PU/PD, pendulous abdomen, and panting
ACTH stim test
hyperstimulation of ACTH (cortisol) is positive for cushings. (>20)
Doesn’t specify if pituitary or adrenal cushings, do LDDT/HDDT to determine which.
LDDT and HDDT
should suppress cortisol to <1.7
If suppresses but not below 1.7, then pituitary cushings.
If does not suppress at all, then adrenal tumor.
20% of PDH will not suppress HDDT
cushing’s treatment?
- surgical removal of hypothalamus or adrenal gland
- medical - OPDDD (dogs) and Trilostane (dogs and cats) suppress cortisol production. Lysodren and Metotane are OPDDD drugs.
- Iatrogenic - stop the steroids (taper off)
How to prove iatrogenic cushing’s?
hold off pred, do ACTH stim test –> no response
OPDDD drug interactions?
It is metabolized in the liver by cytochrome P450 so anything that affects this will affect its metabolism.
Phenobarbital makes OPDDD ineffective because enhances P450 metabolism
OPDDD cytotoxicity?
Adrenocorticolytic –> if destroy adrenal cortex, end up with Addison’s.