Exam 8: L.3: Adrenal/Cushings Flashcards
Adrenal gland
G: Salt (aldosterone)
F: sugar (cortisol)
R: sex (androgens)
Functional adrenal tumor: produces a lot of cortisol despite pituitary decreasing production of ACTH
Hyperadrenocortiscism: etiologies
1) spontaneous
- pituitary -dependent hyperadrenocortiscism (pituitary tumor-most from pars this distalis)
- functional adrenal tumors (FAT)
2) iatrogenic disease (exogenous glucocorticoid administration)
Hyperadrenocortiscism: typical signalment
1) 7-9 years of age
2) PDH: there are high risk breeds
- dogs <20 kg: 85% of HAC is due to PDH
3) FAT: higher risk breeds = GSD, Dachsund, Labrador
- dogs >20 kg: 50% PDH, 50% FAT
Systemic impact of excess glucocorticoids: skin, liver, muscle, CNS
Hyperadrenocortiscism: common presenting complaints (slow onset)
1) PU/PD
2) polyphagia
3) abdominal enlargement-obesity
4) hair loss, skin infection
5) panting*= = >this may be the 1st thing owner’s notice!
6) muscle weakness/lethargy
NOTE: important to note that these dogs are not generally sick
Hyperadrenocortiscism: physical exam
1) conformational changes: hepatomegaly, abdominal muscle weakness, increased intra-abdominal fat, muscle atrophy
= pendulous abdomen*
2) cutaneous changes: symmetrical alopecia, comedones, coat color changes, hyperpigmentation, scale
Hyperadrenocortiscism: associated conditions
1) hypercoagulability: thromboembolism
- thrombocytosis, loss of anti-thrombin in the urine
2) hypertension (>50% of dogs)
- due to excessive secretion of renin
3) hypercalcemia and urinary calculi
4) proteinuria
5) myopathy
6) DM
7) infections
Cushing’s: clinical pathologic funding
1) CBC
- stress leukogram (lymphopenia, neutrophilia, monocytosis)
- hemoconcentration
2) biochem
- elevated ALP (most common abnormality) seen in 85-95% of cases: ALP isomers from bone, liver, glucocorticoids (cortisol)
- increase in plasma glucose
- hypercholesterolemia
- lipemia
Cushing’s: lab data
1) electrolytes
- occasionally increased sodium and decreased potassium
2) urinalysis
- dilute urine (often <1.015) in 85% of cases
- proteinuria in about 50% of dogs (hypertension)
- glucosuria
- evaluate for UTI (50% of cases)
HAC: screening hormone assays/tests
1) ACTH stimulation test
2) low-dose dexamethasone suppression test
3) urine cortisol-creatinine ratio
ACTH stim test
1) administration of a supra-physiologic dose of ACTH causes the adrenals to maximally secrete cortisol
2) dogs with HAC have larger, more active adrenals and will produce more cortisol than unaffected animals**
3) majority of dogs with PDH will show inexcessiveresponse
- dogs with FAT show variable response
Advantage: safe, simple, quick
disadvantage: lower sensitivity them LDDST, cannot differentiate PDH from FAT
ACTH stim
1) ACTH response can be normal in 15-30% of dogs with PDH!
- If you are suspicious of PDH and get a normal ACTH response, do NOT rule out PDH = => do LDDST
2) preferred test for diagnosis of iatrogenic HAC
3) only test recommended for monitoring response to therapy for HAC
Low-dose dexamethasone suppression test
1) measure baseline cortisol
2) give dexamethasone IV
3) measure cortisol at 4 and 8 hours post (normally cortisol should decrease)
4) dogs with PDH show relative resistance to the suppressive effects of dexamethasone on ACTH secretion
5) dogs with FAT: have very low circulating ACTH concentration, dexamethasone has little to no effect on cortisol secretion
6) **may be the single best test to screen for HAC
LDDST
1) **a result of >1.4 ug/dL at the 8 HOUR measurement of cortisol is consistent HAC
2) decrease at the 4 hour measurement
- <1.4 ug/dL OR
- <50% of basal cortisol
- consistent with PDH!
3) no decrease at the 4 hour measurement by above criteria
- cannot differentiate PDH from FAT
- 35% OF DOGS WITH PDH do NOT have a decrease at 4 hour cortisol
Advantages: high sensitivity, differentiates PDH from FAT in 40% of dogs with HAC
disadvantages: lower specificity than ACTH stim; requires 8 hours to complete
Localizing/differentiating tests
1) LDDST (differentiates 40% of canine with PDH)
2) HDDST
3) endogenous ACTH concentrations
4) diagnostic imaging
- if PDH = = > high ACTH levels cause bilateral adrenomegaly
- if FAT will sign = >large functional adrenal tumor with a small contralateral adrenal gland
HDDST
1) protocol is similar to LDDST, but dose of dexamethasone is increased
2) administration of a high dose of dexamethasone does NOT cause cortisol suppression in dogs with FAT
3) 75% of dogs with PDH will suppress at the 4 and/or 8 hour measurement
4) disadvantage of HDDST: it can NEVER confirm the presence of FAT (it will not suppress)