Classification and Main Causes
There are three main forms of this pathology, depending on the specific route through which the body loses essential ions:
- Gastric. Occurs due to the loss of hydrochloric acid (HCl) along with gastric juice. The primary cause is profuse and repetitive vomiting. This condition is characteristic of hyperemesis gravidarum, pyloric stenosis, pylorospasm, and high intestinal obstruction.
- Enteric. Associated with increased excretion of potassium ions (K^+) along with alkaline intestinal contents. It develops with the abuse of laxatives or overly frequent enemas.
- Renal. Caused by enhanced excretion of chlorides, potassium, and protons (H^+) in the urine, alongside excessive reabsorption of bases. A typical cause is prolonged diuretic therapy.
Pathogenesis of Enteric Alkalosis
Potassium loss plays a key role in the development of the enteric form. The pathological chain of events unfolds as follows:
- Massive excretion of K^+ with feces leads to pronounced hypokalemia.
- The body attempts to compensate for the deficit: sodium ions (Na^+), which are alkaline, move from the extracellular fluid into the cells.
- This transport process occurs strictly in exchange for the efflux of intracellular potassium or protons (H^+).
- As a result, sodium accumulates inside the cells, and the loss of protons causes alkalosis—with the pH shift occurring both intracellularly and in the blood plasma.
How the Kidneys Exacerbate the Problem
Any significant fluid loss (repeated hemorrhage, vomiting, diarrhea, increased sweating) reduces the circulating blood volume. This leads to hypovolemia, which activates the renin-angiotensin-aldosterone system (RAAS).
RAAS activation leads to secondary hyperaldosteronism. Aldosterone prompts the renal tubules to actively reabsorb sodium into the blood while sharply increasing the secretion of H^+ and K^+ into the urine. Thus, an initially enteric or gastric alkalosis is subsequently potentiated (aggravated) by a secondary renal mechanism.
Mechanisms of Renal Alkalosis Induced by Diuretics
Diuretics cause renal alkalosis through several pathways simultaneously. The core principle is that increased renal sodium excretion is combined with bicarbonate retention. This is mediated by four mechanisms:
- Inhibition of sodium and water reabsorption. Tubular reabsorption of Na^+ and water is blocked. The relative concentration of alkaline bicarbonate anions increases in blood plasma (forming concentration alkalosis).
- Hypochloremic mechanism. Chloride (Cl^-) is actively excreted alongside sodium, leading to hypochloremia and the corresponding hypochloremic alkalosis.
- Cellular shift. Due to diuretic-induced hypokalemia, protons move from the extracellular fluid into cells (in exchange for potassium to compensate for its plasma deficit). Decreasing extracellular H^+ concentration deepens alkalosis.
- "Poorly reabsorbable anions" factor. Sulfates, nitrates, or penicillin metabolites may enter the glomerular filtrate via diet or medication. They are poorly reabsorbed in the proximal tubules. The accumulation of these anions in the primary urine demands enhanced cation excretion to maintain electroneutrality, which is accompanied by H^+ secretion and further pH deviation.