Adrenal Excess - Aldosterone Flashcards

1
Q

Which layer of the adrenal gland produces aldosterone?

A

Zona glomerulosa

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2
Q

Aldosterone’s main goal

A

increase intravascular volume

kidneys reabsorb Na+ and secretion of K+ and H+
Regulated by K+ and RAAS
System is triggered by stress, hypovolemia, and hyperkalemia

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3
Q

Do tumors usually result in hypersecretion or suppression of endocrine system?

A

Hypersecretion

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4
Q

Primary Aldosteronism Causes

A
  • Aldosterone-producing adenoma 90%
  • Bilateral Idiopathic Hyperplasia or Primary Adrenal Hyperplasia (60%)

Other: Aldosterone-producing renin-responsive adenomas, ovarian or nephritic neoplastic ectopic secretion of aldosterone (rare)

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5
Q

Primary symp of hyperaldosteronism

A
  • SS related to HTN & Hypokalemia
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6
Q

When to screen HTN pts for Hyperaldosteronism

A

if they have HTN + Hypokalemia

Hyperaldosteronism is a secondary cause of HTN

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7
Q

Hyperaldosteronism WU

A

aldosterone-to-renin ratio

Ratio of aldosterone to plasma renin activity (PRA)
As aldosterone incr, PRA should decr
Aldosterone producing adenomas are unresponsive to a rise in renin, so aldosterone falls
In IHA, the rise in renin causes a rise in aldosterone

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8
Q

Primary Aldosteronism

Which will have higher BP: Adenoma or Hyperplasia?

A

tumors have higher BP than hyperplasia

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9
Q

Imaging order for Aldosteronism

A

Abd CT to r/o cancer

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10
Q

aldosterone-producing adenoma (APA) Trmnt

A

Tumors should be removed laparoscopically. After removal of an adenoma, serum potassium normalizes and blood pressure decreases in all patients; complete normalization of the blood pressure without the need forantihypertensive treatment occurs in 50 to 70% of patients.

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11
Q

Who gets it? Patho? Trmnt?

Bilateral Idiopathic Hyperplasia or Primary Adrenal Hyperplasia

A
  • More common in older men
  • Bilateral adrenal cortex hyperplasia results in elevations of aldosterone
  • HTN and low potassium
  • Tx: spironolactone (potassium sparing diuretic/androgen receptor blocker) to retain potassium and reduce water/Na
  • Eplerenone-aldosterone antagonist* long term management for men due to no gynecomastia/ED like spironolactone
  • Most will require additional HTN meds for control
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12
Q

What is it? causes?

Aldosterone Insufficiency/Hypoaldosteronism

A

component of Addison
Drug induced –NSAIDs, heparin
Diabetes
Kidney failure (GFR<15)

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13
Q

Addison Disease (Adrenocortical insufficiency) typically affects which parts of the adrenal gland?

A

Candy shell (zona glomerulosa and fasiculata)

So it affects Glucocorticoids and Mineralocorticoid function. Usu affects both but can be just one layer

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14
Q

Hypoaldosteronism is due to a decreased _____ secretion

A

Renin

Note: Diseased kidneys fail to detect decreased ECF volume, decreased NaCl, and decreased arterial BP so RENIN is not secreted adequately.
There is no increased angiotensin and no increase in aldosterone

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15
Q

Will Hypoaldosteronism cause hyper or hypo K+?

A

Hyperkalemia

Also metabolic acidosis due to kidneys not producing enough bicarb

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16
Q

Hypoaldosteronism Trmnt

A
  • Maximize medical management of cause
  • Kidney failure – remove all medication that affect kidneys
  • Dialysis if needed
  • Hyperkalemia – loop diuretic if volume can tolerate being dropped
  • Emergently, can give .9NS bolus and loop diuretic
  • may need to address bicarb, depending on kidney function
  • DM – better control
  • Addison – add Fludrocortisone/Florinef if not already being replaced
17
Q

what? ET?

Pheochromocytoma

A
  • Catecholamine-secreting tumor (chromaffin cells of adrenal gland)
  • 30% due to hereditary syndromes

von Hippel-Lindau (VHL) syndrome
multiple endocrine neoplasia type 2(MEN 2)
neurofibromatosis type 1(NF1)

18
Q

Pheochromocytomas secrete what?

A

Catecholamines: norepi, epi, +/- dopamine

MOST pheochromocytomas secrete norepi predominantly

19
Q

What do Catecholamines do?

A
  • Stimulate alpha-adrenergic receptors resulting in vasoconstriction -> Incr BP
  • increased cardiac contractility ->Incr Pulse
  • glycogenolysis, gluconeogenesis -> Incr Blood Sugar
  • GI tract stimulation -> increased mucus, motility and relaxed sphincter tone
  • Stimulation of beta-adrenergic receptors results in incr in HR and contractility
20
Q

which endocrine disorder causes H/A, Diaphoresis, and Palpitations + Severe HTN?

A

Pheochromocytoma

The spells may vary from monthly to several times per day, and the duration may vary from seconds to hours. Typically, they worsen with time, occurring more frequently and becoming more severe as the tumor grows.

21
Q

Pheochromocytoma WU

A
  • Biochemical Testing -> plasma free metanephrines or urinary fractionated metanephrines
  • CMP for gluc, high Ca+
  • CBC for erythrocytosis

Biochemical Tests
- if (+) -> order CT
- plasma free metanephrine level may be measured in a standard venipuncture sample, drawn about 15-20 minutes after intravenous catheter insertion.
- a 24-hour urine collection for creatinine, total catecholamines, vanillylmandelic acid, and metanephrines.
- Cannot be on beta blockers, TCAs, amphetamines, buspirone, Dopamine agonists, alcohol (all inc metanephrines)

22
Q

If pheochromocytoma biochemical test is (+) -> order ______

Biochemical tests -> plasma free metanephrines or urinary fractionated metanephrines

A

CT

23
Q

Pheochromocytoma Trmt

A
  • Endo referral
  • Laparoscopic Adrenalectomy

Prior to Sx
- Alpha-adrenergic antagonist (BP control to prevent HTN crisis. High catecholamines stim alpha receptors on blood vessels -> vasoconstriction)
- BBs (if signficant tachycardia occurs after alpha antagonist. Don’t start until alpha antagonist is stable)

Sx resection cures HTN