Anemia

True, false, and latent anemia

In clinical practice, true pathology must be strictly differentiated from conditions where only the hemoglobin concentration per unit volume changes, but not its total amount in the body.

• Hydremia (pseudo-anemia). The essence of this condition is an increase in the liquid part of the blood (plasma), which leads to hemodilution (blood thinning). The total count of erythrocytes and hemoglobin remains normal, but their concentration per unit volume drops, creating a formal laboratory picture of the disease. Most often, this is due to a massive infusion of plasma, serum, or other liquids into the vascular bed.
• Latent anemia. This is the reverse situation, occurring against the background of severe dehydration (intensive sweating, profuse diarrhea, untamable vomiting) without adequate fluid volume replacement. Hemoconcentration (thickening of the blood) develops. Due to plasma loss, the hemoglobin concentration per unit volume may appear normal or even elevated. In reality, the total hemoglobin content in the body is reduced, but this deficit is masked by hemoconcentration.

Classification

The pathology can act as an independent nosological form (for example, classical iron deficiency anemia) or, which is much more common, be merely a symptom of other pathological processes.

Basic principles of systematization:

1. According to origin, primary forms caused by congenital genetic alterations (hereditary) and secondary forms acquired during life (symptomatic) are distinguished.
2. According to the leading developmental mechanism:
3. Posthemorrhagic — arise as a result of blood loss.
4. Hemolytic — develop due to the destruction of erythrocytes.
5. Dyserythropoietic — associated with impaired erythropoiesis.
6. According to the type of hematopoiesis, the process can be normoblastic (normal type preserved) or pathological — megaloblastic.

Acute posthemorrhagic anemia

The acute form occurs with massive bleeding from damaged large vessels or heart cavities. By its characteristics, it is normochromic normocytic hyperregeneratory.

Risk factors include severe trauma, extensive surgical interventions, gastrointestinal bleeding, and complications in labor. Acquired or congenital disorders of the blood hemostatic potential often serve as a predisposing background.

The severity of the clinical picture directly depends on the volume of lost blood, the rate of bleeding, and its source. General signs include pallor of the mucous membranes and skin, shortness of breath, tachycardia, and a drop in venous and arterial pressure. An important specific marker of acute bleeding is a progressive feeling of dryness in the mouth.

Important nuance: changes in the body are staged in nature. In the early period (first hours and days), the stage of reflex vascular compensation is activated. Blood actively flows from depots into the bloodstream, forming normovolemic hypovolemia (normocytic hypovolemia). At the same time, there is an equivalent decrease in plasma and formed elements. Because of this, hemoglobin concentration and hematocrit may remain normal or decrease only slightly, completely failing to reflect the real severity of the condition at the moment.

Mechanisms of hemolysis

Hemolytic forms are caused by premature destruction of erythrocytes. This process can follow two main scenarios:

• Intracellular hemolysis. It occurs predominantly with the participation of macrophages of the spleen and, to a lesser extent, the liver. The mechanism is triggered when erythrocyte membrane defects appear. The cells lose their deformability (plasticity), due to which they cannot circulate freely and are retained in the cords of Billroth of the red pulp of the spleen, where they are phagocytosed by macrophages. Clinically, this is manifested by enlargement of the spleen (splenomegaly) and liver (hepatomegaly).
• Intravascular hemolysis. Occurs directly in the blood plasma. Causes can include autoimmune and allogeneic reactions, exposure to exogenous cytotoxic agents, or mechanical damage to erythrocytes in capillaries (e.g., by platelet microaggregates or fibrin strands). The main laboratory markers of this condition are hemoglobinemia (appearance of free hemoglobin in plasma) and a sharp decrease in the concentration of haptoglobin (the protein that binds this free hemoglobin).

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Compensation stages in acute posthemorrhagic anemia (apart from the early period).
• The role of congenital hemostasis disorders as a risk factor for massive bleeding.
• Mechanisms of loss of erythrocyte plasticity in intracellular hemolysis.
• Exogenous cytotoxic agents causing intravascular hemolysis.
• Features of the megaloblastic type of hematopoiesis in dyserythropoietic anemias.

Other topics in "Chapter 21. Typical Pathology Forms of the Blood System"

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