Adrenal Gland

A

General

• 1.

  Paired, retroperitoneal glands superior and medial to kidney

• 2.

  Weight 4–5 g; yellow in color because of high lipid content

B

Arterial Supply

• 1.

  Superior adrenal artery—branch of inferior phrenic artery

• 2.

  Middle adrenal artery—branch of aorta

• 3.

  Inferior adrenal artery—branch of renal artery

C

Venous Drainage

• 1.

  Single major adrenal vein, 5%–10% of patients with accessory venous drainage

• 2.

  Right adrenal vein—short, drains directly into inferior vena cava (IVC)

• 3.

  Left adrenal vein—longer, empties into left renal vein

D

Cortex

• 1.

  Embryology: It is derived from mesodermal tissue on adrenogenital ridge at the fifth week of gestation near gonads and can have ectopic tissue near sex organs.

• 2.

  Outer portion of gland consists of three zones:

  • a.

    Zona glomerulosa—outer layer, produces mineralocorticoid aldosterone (salt)

  • b.

    Zona fasciculata—middle layer, produces glucocorticoid cortisol (sugar)

  • c.

    Zona reticularis—inner layer, produces androgens (sex)

E

Medulla

• 1.

  Embryology: It is derived from ectodermal tissue arising from the neural crest and can have ectopic tissue in paraaortic/paravertebral locations; organ of Zuckerkandl at aortic bifurcation is a collection of neural crest cells similar to the adrenal medulla.

• 2.

  Inner portion of gland contains chromaffin cells, which produce catecholamine hormones epinephrine and norepinephrine.

A

Physiology

• 1.

  Aldosterone secretion is regulated by renin-angiotensin system.

  • a.

    Juxtaglomerular cells in kidney stimulate renin release with decreased renal blood flow, decreased plasma Na ⁺ , and increased sympathetic tone.

  • b.

    Renin induces conversion of angiotensinogen to angiotensin I.

  • c.

    Angiotensin I is cleaved by angiotensin-converting enzyme (ACE) in lungs to angiotensin II.

  • d.

    Angiotensin II is a potent vasoconstrictor and increases aldosterone synthesis/release.

  • e.

    Aldosterone acts on distal convoluted tubule to increase Na ⁺ reabsorption and H ⁺ /K ⁺ excretion.

B

Primary Aldosteronism/Conn Syndrome

• 1.

  Presentation: presents at 30–50 years of age with hypertension not controlled with multimodal therapy, hypokalemia, muscle weakness and fatigue, polydipsia, polyuria, and headaches

• 2.

  Pathophysiology: 70% single functional adrenal adenoma, 30% bilateral adrenal hyperplasia (BAH), differential includes renal artery stenosis, cirrhosis, congestive heart failure (CHF), and adrenocortical carcinoma

• 3.

  Laboratory evaluation: hypernatremia, hypokalemia, and metabolic alkalosis; elevated aldosterone and low renin activity (ratio >1:30); failure to suppress aldosterone with sodium loading

• 4.

  Imaging: computed tomography (CT) or magnetic resonance imaging (MRI) (less sensitive) with intravenous (IV) contrast to identify adenoma

• 5.

  Selective venous catheterization: used with bilateral gland enlargement and when there is inability to identify an adenoma on imaging; cannulate bilateral adrenal veins and measure aldosterone and cortisol levels after adrenocorticotropic hormone (ACTH) stimulation; greater than fourfold difference in measurements is diagnostic

• 6.

  Scintigraphy: nuclear medicine scan; ¹³¹ I-6-iodomethyl noriodocholesterol (NP-95) is taken up in the adrenal cortex, and adenomas appear as “hot” nodules, whereas BAH has bilateral increased uptake

• 7.

  Treatment: surgical excision after preoperative potassium supplementation and control of hypertension with spironolactone (aldosterone antagonist), amiloride (K ⁺ sparing diuretic), calcium channel blocker, and ACE-inhibitor; patients may require mineralocorticoid replacement; monitor closely for adrenal insufficiency in immediate postoperative period

A