Ch. 8 Incidentally Discovered Adrenal Mass on CT Scan Flashcards
What is the differential diagnosis of hypercortisolism? (4)
What is the clinical presentation of an adrenal nodule that hypersecretes aldosterone?
HTN + hypokalemia
(Aldosterone acts on DCT to inc. sodium reabsorption. This causes passive reabsorption of water and increases extracellular volume and BP. To balance positively charged sodium ions, potassium is excreted in urine).
What is the clinical presentation of pheochromocytoma?
Sustained or episodic HTN
Symptoms: headache, flushing, palpitations
What signs and symptoms should raise suspicion for an adrenocortical carcinoma?
Highly lethal malignancies (5-year survival <25%)
Most common hormone hypersecretion associated with adrenocortical carcinoma = Cushing’s Syndrome (then virilization)
Pts with non-functional tumors may present with:
- Abdominal mass
- Abdominal pain
- Nausea
- Anorexia
- Early satiety
- Weight Loss
Approximately 75% of adrenocortical carcinomas are >6 cm at the time of presentation
Adrenal Incidentaloma
- What is it?
- What is the incidence?
- What is the most common cause?
- Indications for removal of adrenal incidentaloma < 6 cm?
- What tumor must be r/o prior to biopsy or surgery for any adrenal mass?
- Incidentally discovered mass seen on imaging performed for an unrelated reason
- Approximately 5% of patients who undergo an abdominal CT scan will have an incidentally discovered adrenal mass.
- Nonfunctioning adenoma (>75% of cases)
- **HORMONALLY ACTIVE
- Pheo (24-hr urine for catecholamine, VMA, metanephrines)
What is the most common adrenal mass?
Non-functional benign adrenocortical adenoma
Only 15% of adrenal adenomas are associated with hormone hypersecretion
What are the zones of the adrenal gland and what hormones do they produce?
Cortex:
- Glomerulosa –> aldosterone
- Fasciculata –> cortisol
- Reticularis –> androgen (DHEA, DHEA-S, androstenedione)
Medulla:
- Catecholamine sx
What are the systemic effects of normal and excessive cortisol secretion?
Cortisol binds to intracellular cytoplasmic receptors and influences transcriptional activation of genes, specifically affecting glucose metabolism, intravascular volume, and immune modulation.
Primary action of cortisol:
- Inc. blood glucose levels via inhibition of insulin-mediated cellular glucose uptake
- Glycogenolysis
- Hepatic gluconeogenesis
- Proteolysis
- Lipolysis
Therefore, excess cortisol:
- Hyperglycemia
- Muscle wasting
- Fat redistribution –> central obesity
Additional effects:
- Inhibits cytokine production
- Inhibits T-cell activation
- Impairs monocyte and neutrophil chemotaxis
Therefore, impairs wound healing and increases risk of infection
- Inc. renal reabsorption of sodium, raising peripheral vascular resistance –> HTN
Algorithm for workup and mgmt of incidental adrenal mass
Laboratory testing for:
Hypercortisolism (Cushing’s syndrome)
Hyperaldosteronism (Conn’s syndrome)
Catecholamine hypersecretion (pheochromocytoma)
What laboratory testing can identify hyperaldosteronism?
Pts with hyperaldosteronism generally have increased aldosterone levels (>20 ng/dL), but the most sensitive screening test is to calculate the ratio between the serum aldosterone level / PRA
Normal ratios are 4-10 range while pts with hyperaldosteronism have ratios >30.
May also see hypokalemia + inc. urinary potassium excretion
To confirm dx: inappropriate aldosterone secretion should be seen after salt loading (b/c under normal physiology, high sodium load to DCT should suppress renin secretion, thereby reducing aldosterone secretion)
What is the best imaging modality to evaluate an adrenal nodule? What is another option?
Contrast-enhanced CT scan with fine cuts
MRI = alternative
What imaging characteristics help to differentiate a benign from malignant lesion?
Benign on CT scan:
- size <4 cm
- homogenous appearance
- well-defined borders
- high levels of intracellular lipid
- rapid washout of contrast
- low amount of vascularity
Malignancy:
- size > 6 cm
- irregular borders with necrosis
- calcification and/or hemorrhage within the mass
- ill-defined borders with possible invasion into adjacent structures
- low levels of intracellular lipid
- high vascularity
Mgmt:
What is the treatment for a nonfunctional adrenal mass? How does size impact mgmt?
Mgmt based on likelihood of malignancy
Lesions smaller than 4 cm with benign imaging have very low risk of malignancy (<5%) –> observe with interval CT scanning
Lesions greater than 6 cm or those with concerning imaging features should be resected –> adrenalectomy
What is the surveillance protocol for an adrenal nodule that will not be resected?
Follow-up should consist of repeat imaging at 6, 12, and 24 mo, as well as repeat biochemical evaluation for hormone levels yearly for 4 yrs
What are the key surgical principles during an adrenalectomy? Prognosis?
What is the arterial/venous supply/drainage of the adrenal gland?
Laparoscopic adrenalectomy = standard surgical tx for most adrenal tumors
Operation can be performed either transabdominally or retroperitoneally
Excellent prognosis –> adrenalectomy for aldosterone-secreting adenoma results in HTN improvement in 70-90% pts
Arterial supply:
- Inferior phrenic artery (superiorly)
- Aorta (medially)
- Renal artery (inferiorly)
Venous drainage:
- From L adrenal vein empties into L renal vein
- From R adrenal vein empties directly into IVC
E. Increased serum aldosterone concentration
Decreased perfusion pressure in the stenotic kidney causes increased production of renin which then causes increased serum aldosterone concentration… renin converts angiotensinogen to ATI in the renal arterioles NOT the veins… renin also stimulates production of aldosterone
