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MindMap Gallery Primary aldosteronism (PA)

Primary aldosteronism (PA)

The mind map of primary aldosteronism (PA) is an increase in aldosterone secretion caused by adrenocortical lesions, leading to sodium retention and potassium excretion, expansion of body fluid volume, and inhibition of the renin-angiotensin system, manifesting as hypertension. and hypokalemia.

Edited at 2023-10-29 14:31:19

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Primary aldosteronism (PA)

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Outline

Primary aldosteronism (PA)

definition

Increased aldosterone secretion caused by adrenocortical lesions leads to sodium retention and potassium excretion, expansion of body fluid volume, and inhibition of the renin-angiotensin system, manifesting as hypertension and hypokalemia.

Cause classification

1. Aldosteronoma (Conn syndrome) [common]

More common, adenoma on one side, 1~2cm in diameter

The patient's plasma aldosterone concentration is parallel to plasma ACTH day and night, and has no obvious response to changes in plasma renin.

Mechanism: Aldosteronoma is regulated much more strongly by ACTH than by the RAAS system.

2. Idiopathic hyperaldosteronism [common]

Bilateral adrenal bulbar zone hyperplasia, a considerable part with nodules

Responsive to renin.

Mechanism: Teraldehyde has enhanced sensitivity to angiotensin II. Angiotensin-converting enzyme inhibitors can reduce aldosterone secretion in patients and improve hypertension and hypokalemia. A small number of nodular hyperplasia of aldehydes do not respond to renin.

3. Glucocorticoid-treatable aldosteronism (GRA)

Onset in teenagers, often hereditary in families

Adrenal glands show large and small nodular hyperplasia

Plasma aldosterone concentrations parallel the circadian rhythm of ACTH

mechanism

Normally, the aldosterone synthase gene is expressed in the zona glomerulosa of the adrenal gland and is regulated by angiotensin II; 11-β hydroxylase is expressed in the zona fasciculata and is regulated by ACTH.

In GRA, the 11β-hydroxylase gene is fused to the aldosterone and enzyme gene. This gene product has aldosterone synthase activity, is expressed in the zona fasciculata, and is regulated by ACTH but not angiotensin II.

4. Aldosterone cancer [rare]

The tumor is large in size, with a diameter >5cm. Hemorrhage and necrosis are often present on the cut surface. Calcification is common on CT or ultrasound.

Mechanism: Aldosterone cancer secretes large amounts of aldosterone, glucocorticoids, and androgens

5. Ectopic aldosterone-secreting adenoma or adenocarcinoma (extremely rare)

Pathogenesis

Excessive aldosterone → sodium retention, potassium excretion, extracellular fluid expansion, increased blood volume, and enhanced vascular response to norepinephrine → high blood pressure, hypokalemia → alkalosis → alkalosis leads to a decrease in Ca2, and aldosterone can also promote urinary magnesium After discharge, numbness of the extremities and tetany of the limbs may occur.

The "escape" phenomenon of mineralocorticoids: Under the action of a large amount of aldosterone, the extracellular fluid expands, causing a reaction in the body's natriuretic system. The renal tubules get rid of the influence of aldosterone, reduce sodium reabsorption, and increase the secretion of atrial natriuretic peptide, thus causing Sodium metabolism reaches a state of equilibrium.

clinical manifestations

1. High blood pressure

2. Neuromuscular dysfunction [low potassium]

①Myasthenia and periodic paralysis

② Numbness of extremities, twitching of hands and feet

3. Heart symptoms [low potassium]

Electrocardiogram shows hypokalemia pattern: T wave is low and flat

Arrhythmias: Supraventricular tachycardia is common, and ventricular fibrillation is the most severe form.

4. Kidney manifestations [low potassium]

①Chronic potassium loss leads to vacuolar degeneration of renal tubular epithelial cells and decreased concentrating function → polyuria and nocturia → thirst and polydipsia

② Often complicated by urinary tract infection

③Increase in urine protein and a small number of cases of decreased renal function

5. Others [low potassium]

During potassium deficiency, insulin release is reduced, its effect is weakened, and glucose tolerance may be impaired.

examine

Preliminary examination, qualitative diagnosis

1. Blood and urine biochemical tests [first choice]

①Hypokalemia: Generally 2~3mmol/L, even lower in severe cases

②Alkalemia

③ High urinary potassium: even when hypokalemia is more than 25mmol/24h

④ Hypernatremia (not particularly high due to escape phenomenon)

2. Aldosterone measurement

Aldosterone↑

3. Measurement of renin and angiotensin II

The base value decreases, sometimes below the measurable range

An increase in the blood aldosterone level and a decrease in the levels of renin and angiotensin II is characteristic of pro-aldehyde. A plasma aldosterone/plasma renin activity ratio >30 indicates the possibility of pro-aldehyde, and >50 is of diagnostic significance. The best test for detecting PA

4. Urine test

①Urine pH is neutral or alkaline

②Urine specific gravity: There may be hypotonic urine

③A few patients have proteinuria and decreased renal function

Further positioning and diagnosis

Mainly distinguish between aldosteronoma and special aldehyde [because these two are the most common]

1. Dynamic test

normal person

Bed resting, from 8 to 12 o'clock, plasma aldosterone, plasma ACTH and cortisol concentrations decreased consistently.

Standing, between 8 and 12 o'clock, plasma aldosterone rises because the rising effect of plasma aldosterone during standing exceeds the influence of ACTH.

Special aldehyde patients [high renin sensitivity]

When lying down, it is probably not much different from normal people.

From 8 to 12 o'clock, when standing upright, plasma aldosterone rises significantly and exceeds that of normal people (because plasma renin increases slightly after standing, and this type is more sensitive to angiotensin)

patients with aldosteronoma

In the supine position, plasma aldosterone and ACTH decrease in line with the rhythm

From 8 to 12 o'clock, in the standing position, plasma aldosterone does not rise but falls, because aldosteronoma is much more affected by ACTH than the renin-angiotensin system, so ACTH↓ and renin↑ are useless.

Imaging examination [Assist in identifying adrenal tumors and hyperplasia]

Large tumor size, >5cm in diameter → indicates adrenal cancer

Adrenal B-ultrasound

Aldosteronomas with a diameter >1.3cm can be detected

Adrenal CT, MRI

High-resolution CT: tumors <5mm in diameter (too small will not work)

Teraldehyde: CT reality is normal or bilaterally diffusely enlarged (a considerable part has nodules)

Aldosteronoma: MRI is more sensitive than CT in detecting aldosteronoma, but its specificity is lower.

treat

aldosteronoma

Surgical resection is the radical cure

Inoperable and special aldehydes

First choice: spironolactone

Sexual function decline after long-term use of spironolactone - triamterene, amiloride

Calcium antagonist (aldosterone synthesis requires the participation of calcium)

Teraldehyde patients - angiotensin-converting enzyme inhibitors

GRA - glucocorticoid