Water-electrolyte metabolism disorders

Water imbalance and edema classification

Changes in body fluid volume follow two main scenarios: hypohydration (water excretion prevails over intake, resulting in exicosis) and hyperhydration (positive water balance).

If fluid accumulates excessively in tissues or cavities, edema develops. Depending on prevalence, edema is divided into localized (a single limb or organ) and generalized. Depending on the localization, special terms are used in pathomorphology:

• Anasarca — infiltration of fluid into the intercellular spaces of the skin and subcutaneous tissue.
• Dropsy — accumulation of transudate in body cavities. Includes ascites (abdominal cavity), hydrothorax (pleural cavity), and hydropericardium (pericardial cavity).

By distribution level, edema can be extracellular (most common) and intracellular. The latter is extremely dangerous: due to fluctuations in osmotic or oncotic pressure, the cell swells, which can lead to the rupture of its membrane (cytolemme) and death.

Pathogenesis of edema: three main factors

The mechanism of fluid retention in tissues depends on the leading pathogenetic factor:

1. Hydrodynamic (mechanical) factor. Occurs when hydrostatic pressure rises in the venous section of the capillary. Fluid cannot be reabsorbed back into the vascular bed. A clear example is heart failure. With left ventricular weakness, pulmonary edema develops; with right ventricular failure, pressures in the systemic veins rise, producing generalized "congestive" edema.
2. Lymphogenic factor. Associated with a mechanical obstacle to lymph outflow (thrombi, parasites, cancer emboli, scars) or dynamic insufficiency when too much lymph is formed (during starvation). Prolonged lymph stagnation stimulates irreversible fibrotic changes, leading to organ deformation (elephantiasis).
3. Oncotic factor. Based on blood hypo-onchia — a drop in the concentration of proteins (exclusively albumins) in the plasma. Blood loses its ability to retain water, filtration pressure rises, and fluid rushes into tissues. This is the initial mechanism in nephrotic (protein lost in urine), hepatic (impaired synthesis), and nutritional edema. Such edema is generalized and rapidly appears where tissue pressure is low — in loose connective tissue.

Sodium metabolism disorders

Sodium determines the plasma osmotic pressure and the volume of extracellular fluid.

• Hyponatremia occurs in aldosterone deficiency (hypocorticism), kidney diseases, heavy sweating, severe diarrhea, or hemodilution (blood dilution). A drop in plasma osmotic pressure causes water to move inside cells, causing them to swell. Patients complain of muscle weakness, drop in blood pressure, sensory disturbances, and GI dysfunction.
• Hypernatremia is a consequence of aldosterone excess (Conn's syndrome) or excessive intake of hypertonic solutions. Cells lose water, and the circulating blood volume increases. Vascular sensitivity to adrenaline and angiotensin II rises, leading to arterial hypertension, convulsions, and increased neuromuscular excitability.

Potassium and copper metabolism disorders

Potassium is critically important for normal tissue excitability.

• Hypokalemia sharply reduces neuromuscular excitability. General adynamia, muscular hypotonia develop, and reflexes are depressed. Smooth muscle atonia (meteorism, bladder weakness), vomiting, and cardiac arrhythmias are characteristic.
• Hyperkalemia often accompanies renal failure, endocrinopathies, massive tissue breakdown (shock, hemolysis, protein and glycogen destruction), and metabolic acidosis. It causes bradycardia, arterial hypotension, painful spastic GI contractions, and characteristic ECG changes (tented T wave).

A genetic disorder worth noting separately is Wilson-Konovalov disease (hepatolenticular degeneration). This is an autosomal recessive pathology. Due to a defect in copper excretion into bile and reduced ceruloplasmin production, the toxic metal is deposited in target organs: hepatocytes and the basal ganglia of the brain. About 1% of healthy people are hidden heterozygous carriers.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Mechanisms of cardiac edema development in right- and left-ventricular failure
• Dynamic lymphatic insufficiency: causes and consequences
• The role of vascular wall permeability in the formation of oncotic edema
• Pathogenesis of cellular edema in hyponatremia
• Mechanism of potassium ion efflux from cells in metabolic acidosis

Other topics in the section "Morphology of Metabolic Disorders — Dystrophies"

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