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)
