Non-cortisol-secreting Adrenocortical Tumours and Incidentalomas Flashcards
What can cytology of adrenal tumour determine?
Cortical vs medullary (neuroendocrine) origin
- cannot determine malignancy
Can echogenicity and mineralization determine the malignancy of adrenal tumours?
No
If the adrenal tumour represents metastasis, which cancer types would be most likely?
- pulmonary carcinoma
- mammary CA
- prostatic CA
- gastric CA
- pancreatic CA
- melanoma
What are some AUS evidence suggestive of malignancy of adrenal tumours?
- size, >2cm
- (vascular) invasion
- tortuous vessels
- heterogenous contrast enhancement
What are some signs of adrenal tumour malignancy on CT scans?
- poor demarcation
- heterogenous contrast enhancement
- non-homogenous texture
- vascular invasion: 92% sensitivity, 100% specificity
What’s the MOA of aldosterone?
- it promotes Na reabsorption, K+ & H+ excretion @ the distal nephrons
- therefore, it increases blood volume/ blood pressure
- activated by angiotensin II- decreased blood pressure –> sensed by the kidneys –> stimulates synthesis and excretion of renin –> with angiotensin II –> releases aldosterone
What’s the difference between primary vs secondary hyperaldosteronism?
Primary = autonomous excessive secretion of aldosterone
Secondary = due to an underlying condition (ex. heart failure, CKD) –> associated with enhanced renin concentration
What’s the common signlaments of feline primary hyperaldosteronism?
- median age = 13yo
- no breed or sex predilection
What’s the typical presenting complaint/ physical exam findings?
associated with hypokalemia and hypertension
Hypokalemia
- weakness, lethargy, plantigrade stance
- PU/PD (reversible nephrogenic diabetes insipidus)
Hypertension
- vision issues (retinal detachment, tortuous retinal vessels)
- hemorrhage
- edema
- heart murmur (L sided ventricular hypertrophy)
if also secreting glucocorticoids: skin fragility, alopecia, pot belly
What are some changes noted on routine blood work?
hypokalemia = main finding
- hypernatremia is usually not evident –> hypertension and volume expansion lead to natriuresis
- increased CK due to hypokalemic myopathy
- metabolic alkalosis (increased H+ excretion)
- about 85% of cats are persistently hypertensive
Which imaging modality is useful?
AUS
- cytology can determine if it’s cortical vs medullary
- cytology cannot determine function or malignancy
How is hyperaldosteronism confirmed?
Demonstration of elevated aldosterone level
- but the value does overlap between primary and secondary hyperaldosteronism
- with very early clinical course aldosterone may still in the upper reference limit
What specific blood work can be done to differentiate between primary and secondary hyperaldosteronism?
Testing for plasma renin activity
- in primary hyperaldosteronism, renin should be normal or decreased, due to compensatory mechanism of hyperaldosteronism and hypertension
- in secondary hyperaldosteronism, renin level will stay increased
However, no commercial testing kit available and required large amount of plasma that need to be frozen instantly
What other endocrine tests are available for diagnosing feline hyperaldosteronism?
Urine creatinine aldosterone ratio
- give fludrocortisone for 4 days, should significantly suppress aldosterone in healthy cats
- so for hypertensive cats without hypokalemia, it will rule out hyperaldosteronism if the UCAR suppression is >50% of baseline
- it is difficult to collect urine
- even with a short course of fludrocortisone, significant suppression can occur –> post testing supplementation may be needed
What’s the treatment of choice for feline hyperaldosteronism?
Adrenalectomy
- but it’s risky and challenging
- need thorough workout
- if other hormones (glucocorticoids, progesterone) are secreted too, transient cortisol deficiency can be noted
- K level should be corrected prior to Sx
- electrolyte levels need to be monitored closely post-op (Na+, K+)
- MST = 1297 days (3.5 years)
What are some medical management options for cats with hyperaldosteronism?
Hypertension:
- amlodipine
- spironolactone (competitive aldosterone receptor antagonist)
low K+
- K+ supplementation
- survival ranges from 7m to 2.6 years
What’s the signalment for canine hyperaldosteronism?
middle age + dogs
What are the common presenting signs for canine hyperaldosteronism?
- lethargy
- anorexia
- weakness
- PU/PD
How is canine hyperaldosteronism diagnosed?
- hypokalemia
- hypertension
- metabolic alkalosis
- uncommonly will also have signs related to excessive glucocorticoids
- correlate with imaging findings and clinical signs
- increased aldosterone with normal/decreased renin + exclusion of other causes of hypokalemia
- urine creatinine aldosterone ratio = limited to no value (unlike cats)
- no commercial canine plasma renin assay available
What’s the treatment of choice for canine hyperaldosteronism?
Adrenalectomy
- want to stabilize/ correct as much as the electrolyte imbalance/ hypertension as possible prior to surgery
- (same as in cats)
- amlodipine, spironolactone. oral K+
Post-op
- monitor for Na+, K+ levels
- watch for hypomagnesemia
- supplement mineralocorticoids if hyperkalemia and hyponatremia >72h
- systemic hypertension usually improves 2-3d post op
What’s the prognosis for canine hyperaldosteronism?
adrenalectomy = good to excellent prognosis for adenoma
- carcinoma = guarded
- metastatic sites = persistent clinical signs
- risk of recurrence = slow growing though so can still have a year or so
- mastectomy can be successful
What are the clinical signs associated with excessive progestin secretion?
Progestin can bind to glucocorticoid receptors or displace cortisol from its binding protein –> increased free cortisol serum concentration
- in dogs, progestin will suppress ACTH secretion and lead to adrenal gland atrophy, consistent with glucocorticoid activities
When should sex hormone-secreting adrenal tumours be considered?
Signs of hypercortisolism
- cats: skin fragility, poor hair coat, dermal atrophy
- dogs: also signs of Cushing’s
BUT incompatible ACTH stim or LDDST test results
- ie. cortisol level = low
- then likely due to increased progestin
In cats, increased androgens also reported
- aggression, urine marking, changes in urine odour
How is sex hormone-secreting adrenal tumour treated?
Adrenalectomy
- less info for dogs
How does estradiol level changes with ACTH stim?
It doesn’t change
watch in dogs as estradiol typically has a very wide range of variation in healthy dogs
What are some medical management options for sex hormone-secreting adrenal tumour?
Aminoglutethimide: inhibits the enzymatic conversion of cholesterol to D5-pregnenolone, resulting in a decrease in the production of adrenal glucocorticoids, mineralocorticoids, estrogens, and androgens
- transient response noted in cats
- trilostane can also have some transient response
