2-6: 5/12: Hyperaldosteronism

Front 1

Decreased blood volume and _________ increase aldosterone.

Back 1

High potassium
ACTH

Front 2

Primary aldosteronism:
Symptoms
Lab values (general)
Affected ions and hormones

Why isn't there hypernatremia?

Back 2

Primary aldosteronism = autonomous aldosterone excess

Increased Na+ retention (HTN, suppressed renin, but no hypernatremia (usually) bc water being retained, this under control of ADH, a separate system)
Increased K+ excretion (hypokalemia--most patients are normokalemic bc K+ is intracellular not extracellular)

Front 3

When would you consider screening someone for primary aldosteronism?

Back 3

3 HTN drugs and BP not under control

HTN and hyperkalemia

HTN at a young age

Front 4

Primary aldosteronism:
Causes
Which are unilateral/bilateral?

Back 4

Aldosterone producing adenoma (UNILATERAL)
Bilateral adrenal hyperplasia (BILATERAL)

RARE:
unilateral hyperplasia (UNILATERAL)
aldosterone producing carcinoma (UNILATERAL)
glucocorticoid remediable aldosteronism (BILATERAL)

Front 5

Idiopathic hyperaldosteronism AKA

Back 5

Bilateral adrenal hyperplasia (2/3 of cases of PA)

Front 6

Glucocorticoid-remediable aldosteronism:
Cause
Lab findings

Back 6

aldosterone synthase, 11-OHase (glucocorticoid production) sit near each other on chromosome

can get cross-over between genes so that thing that promotes 11-OHase (ACTH) will activate aldosterone synthase

Results in hybrid steroids (measurable: 18-oxocortisol, 18-hydroxycortisol)

Front 7

Screening tests for Primary Aldosteronism
Requirements prior to screening?
Confirmatory testing?

Back 7

Aldosterone/Plasma Renin Activity ratio will be elevated
(Must discontinue any diuretics or licorice products; NSAIDs, HTN drugs; except verapamil and alpha-1 antagonists FOR ONE MONTH)

False positives due to low-renin essential hypertension (non-identifiable cause)

Confirm:
Load with salt
Normal persons will suppress aldosterone
If aldosterone is elevated-->primary aldosteronism

Front 8

Patient has confirmed primary aldosteronism.
Next steps?

Back 8

ADRENAL CT:
If unilateral nodule >1cm and under 40-->adrenalectomy

If normal or b/l abnormalities <1 cm OR over 40-->Adrenal Vein Sampling
If after sampling-->Lateralization (compare L and R veins)-->Unilateral adrenalectomy

If no lateralization-->Screen for GRA (hybrid steroids)

(Imaging correlates with diagnosis in under 50% of patients)

Front 9

Spironolactone:
Mechanism
Use
AE's

Back 9

Aldosterone receptor ANTAGONIST
USE: BILATERAL ADRENAL HYPERPLASIA (or if pt not eligible for sx)

AE: gynecomastia in men--antagonizes androgen receptors! hyperkalemia
If gynecomastia, try EPLERENONE (won't antagonize androgen receptors like spironolactone does, but $$$)

Front 10

Glucocorticoid-Remediable Aldosteronism:
Treatment
AE's

Back 10

Dexamethasone qHS (Suppress AM surge of ACTH), and normal renin-angiotensin system controls resumes

AE:
HPA axis suppression, secondary adrenal insufficiency

Front 11

Syndrome of Apparent Mineralocorticoid Excess:
Cause

Back 11

Defect in HSD2
Cortisol not inactivated to cortisone and binds mineralocorticoid receptor

Front 12

Glucocorticoid resistance:
Mechanism
Affected hormones

Back 12

Defect in glucocorticoid receptor resulting in compensatory increases in ACTH and cortisol
HSD2 overwhelmed and cortisol binds MR

Front 13

CAH of the 17-OHase variety can result in excess ______ due to ________.

Relevance?

Back 13

CAH can result in excess DOC due to defective 17-OHase

DOC has mineralocorticoid activity