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🌱來自: Pathogenesis: Generation and Maintenance of Metabolic Alkalosis A Brief Pathophysiologic Review

Metabolic Alkalosis—Source of Excess HCO3−

Usually metabolic alkalosis indicates an accumulation of “excess” HCO3−. The source of excess HCO3− can be exogenous, endogenous, or both. Exogenous sources are Na+ or K+ HCO3− salts or salts of precursors (organic anions such as lactate, acetate or citrate, which generate HCO3− when completely oxidized). These salts can be ingested/absorbed or infused (Table 1).

The two potential endogenous sources of large amounts of HCO3− are (1) the stomach and (2) the kidneys. Net endogenous HCO3− generation requires H+ removal from the body. HCO3− is generated when HCl is secreted into gastric lumen, but net HCO3− accumulation in the ECF requires the HCl to be lost externally, usually as a result of vomiting and/or suction (see section on gastric alkalosis).

Normally, kidney H+ excretion into the urine (as NH4+ and/or titratable acid) generates HCO3− to replace the quantity decomposed by nonvolatile H+ derived from dietary intake and metabolism and any HCO3− lost in alkaline stool. To the extent kidney HCO3− generation exceeds this requirement, “excess” HCO3−is generated. This generally occurs when the following conditions coexist: (1) the kidney tubules/ducts beyond the early distal tubule are avidly reabsorbing Na+ (for example, aldosterone activity is high), and (2) the delivery of salt and volume to these sites is relatively large.

Clinical examples of kidney bicarbonate overproduction are:

1. Primary hyperaldosteronism (especially when a high-salt diet is ingested) and other mimics of primary hyperaldosteronism (Table 2).

2. Loop and/or thiazide diuretics and several inherited syndromes that have diuretic like manifestations (i.e., Bartter and Gitelman syndromes).

3. The infusion of Na+ salts of poorly absorbed anions (PO4, SO4, penicillin, etc.) if distal tubule Na+ reabsorption is stimulated by mineralocorticoids and/or volume contraction (19,20).

Another endogenous source of HCO3− is the movement of K+ from within cells into the ECF. In response to hypokalemia, K+ exit is partially balanced by movement of H+ into cells and this generates ECF HCO3− (21,22). ECF [HCO3−] can also increase when the ECF volume contracts around a fixed quantity of HCO3− (23) (see section on gastric alkalosis).

Explain by ChatGPT

• Exogenous sources of metabolic alkalosis : (sodium and potassium bicarbonate salts, or organic anion precursors);
• Endogenous sources of metabolic alkalosis : (stomach and kidneys);
• Primary hyperaldosteronism : (a condition where aldosterone activity is high, leading to increased sodium reabsorption in the kidney tubules);
• Loop and thiazide diuretics : (drugs that increase urine output and can lead to metabolic alkalosis);
• Hypokalemia : (low potassium levels in the blood, which can lead to HCO3- accumulation in the ECF)

窩的英文不太好，只好請估🐶

• 代謝性鹼中毒的外源性來源：（碳酸氫鈉和碳酸氫鉀鹽，或有機陰離子前體）；
• 代謝性鹼中毒的內源性來源：（胃和腎）；
• 原發性醛固酮增多症：（醛固酮活性高，導致腎小管鈉重吸收增加的情況）；
• 袢利尿劑和噻嗪類利尿劑：（增加尿量並可導致代謝性鹼中毒的藥物）；
• 低鉀血症：（血液中鉀含量低，可導致 ECF 中 HCO3- 積累）