Classification and Main Causes
The classification of excretory acidosis is based on the pathway through which the pathological loss of bases or retention of acids occurs. There are three main forms:
- Renal Excretory Acidosis
Develops when the kidneys lose the ability to adequately excrete acids or begin to excessively lose bases in the urine. As a result, acidic metabolic products accumulate in the bloodstream. The main causes include:
- Renal failure (global decline in organ function).
- Salt-losing nephritis.
- Intoxication with sulfonamides.
- Hypoxia of the renal tissue.
- Intestinal Excretory Acidosis
Normally, intestinal juice is extremely rich in bicarbonates. If the body begins to rapidly lose this secretion, an acute deficiency of bases arises. Typical examples of pathological conditions:
- Profuse diarrhea.
- Presence of a small bowel fistula.
- Open wounds of the small intestine.
- Hypersalivation Excretory Acidosis
Human saliva has a pronounced alkaline reaction. In conditions accompanied by excessive salivation and the loss of this fluid, the body is deprived of a significant pool of bases. This is characteristic of:
- Stomatitis of various etiologies.
- Poisoning (e.g., with nicotine or mercury preparations).
- Toxicosis of pregnancy.
- Severe helminthiases.
Immediate Compensatory Mechanisms
The body's compensatory reactions aim to eliminate the pH shift or reduce the severity of acidosis. Immediate mechanisms are implemented very quickly, but their main drawback is limited capacity.
- Activation of Buffer Systems: Extracellular buffers (bicarbonate and protein) and cellular systems (hemoglobin and phosphate) are instantly engaged.
- Respiratory Compensation: Hyperventilation develops. The body reflexively increases alveolar ventilation volumes to rapidly eliminate excess carbon dioxide (CO2) from the blood and reduce the acid load.
Long-Term Compensatory Mechanisms
These processes are activated much later, but they provide a profound and more sustained correction of the acid-base balance.
- Renal Mechanisms: Healthy kidneys enhance acidogenesis (active secretion of H+ ions), increase Na+ ion reabsorption, and increase the secretion of titratable acids (primarily in the form of NaH2PO4). Ammoniagenesis is also activated. Important: in renal excretory acidosis, ammoniagenesis is largely ineffective because the renal parenchyma itself is damaged.
- Metabolic Buffer Processes: Activation of the bicarbonate and phosphate exchange buffers occurs. Bone tissue is actively involved in this process, exchanging ions with the blood.
- Gastric Mechanisms: The gastric mucosa begins to intensely produce hydrochloric acid (HCl). This process physiologically removes free H+ protons from the systemic circulation.
- Hepatic Mechanisms: The liver increases the activity of its compensatory pathways, primarily by enhancing urea synthesis and initiating gluconeogenesis from lactate.