Classification and main causes
The classification of excretory acidosis is based on the pathway through which 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.
- Sulfonamide intoxication.
- 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 occurs. Typical examples of pathological conditions include:
- Profuse diarrhea.
- Presence of a small bowel fistula.
- Open wounds of the small intestine.
- Hypersalivatory 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 typical for:
- Stomatitis of various etiologies.
- Poisoning (e.g., with nicotine or mercury preparations).
- Toxicosis of pregnant women.
- Severe helminthiases.
Immediate compensatory mechanisms
The compensatory reactions of the body are aimed at eliminating the pH shift or reducing 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) as well as cellular systems (hemoglobin and phosphate) are instantly engaged.
- Respiratory compensation: Hyperventilation develops. The body reflexively increases alveolar ventilation volumes to excrete excess carbon dioxide (CO2) from the blood as quickly as possible and reduce the acid load.
Long-term compensatory mechanisms
These processes are activated much later, yet they provide a deep 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 (predominantly 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 intensively 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.
Briefly: answers to topical questions
What is the mechanism of bone tissue involvement in the compensation of excretory acidosis, and which ions does it release?
In bone tissue, activation of the bicarbonate and phosphate exchange buffers occurs. This involves the exchange of ions between bone tissue and blood to correct acidosis. However, the specific ions released from the bone tissue during this process are not specified in these sources.
How can you easily remember the three types of excretory acidosis? Remember the three fluids through which the body loses bases or retains acids: Urine (renal), Intestinal juice (intestinal), Saliva (hypersalivatory). Remember the acronym — UIS.
Class and exam questions
Why doesn't ammoniagenesis save the situation in renal acidosis?
Ammoniagenesis occurs directly in the kidneys. Since the organ parenchyma is initially damaged in renal excretory acidosis (e.g., in nephritis or hypoxia), this compensatory mechanism proves to be ineffective.
How does the stomach help combat acidosis?
The gastric mucosa compensatorily enhances the synthesis of hydrochloric acid (HCl). This process physiologically "removes" free hydrogen protons (H+) from the systemic circulation, thereby reducing the overall acidity of the blood.
Why can excessive salivation disrupt blood pH?
Saliva has a pronounced alkaline reaction. In hypersalivation (e.g., in toxicosis of pregnant women or poisoning) and the loss of saliva into the external environment, the body is deprived of important bases, which shifts the balance toward the acidic side.
What else to study on this topic
- Pathogenesis of salt-losing nephritis and its effect on the tubular apparatus
- Mechanisms of hemoglobin and phosphate cellular buffers
- Biochemistry of urea synthesis and gluconeogenesis in the liver during acidosis
- Ion exchange between bone tissue and blood during long-term compensation
- Effect of sulfonamides on the excretory function of the kidneys
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