Ta'lim innovatsiyasi va integratsiyasi
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ISSN:3030-3621
PATHOLOGICAL PHYSIOLOGY OF POSTHEMORRHAGIC ANEMIA
Rakhimova Gulnoz Shamsiyevna
Bukhara State Medical Institute
https://orcid.org/0009-0003-5023-0656
Annotation.
Blood loss is a compleх of pathological disorders and
compensatory reactions directed against a decrease in the volume of circulating blood
and hypoxia caused by a decrease in the respiratory function of the blood.
Posthemorrhagic shock is a shock that occurs as a result of abundant acute blood loss.
A decrease in the volume of circulating blood, a drop in blood pressure, a violation of
microcirculation, disorders of the blood supply to vital organs (brain, heart, kidneys),
the development of hypoxia, acidosis and intoxication, "vicious circles" in the
pathogenesis leads to death. Post-hemorrhagic anemia-develops as a result of blood
loss.
Keywords:
blood vessels, posthemorrhagic anemia, hemoglobin, hematocrit,
blood pressure.
Introduction:
Acute post-hemorrhagic anemia occurs after rapid massive blood
loss when blood vessels are injured or damaged by a pathological process.
Chronic post-hemorrhagic anemia develops as a result of repeated blood loss
caused by damage to blood vessels in a number of diseases (dysmenorrhea, gastric
ulcer, hemorrhoids, etc.) and a violation of vascular-platelet and coagulation
hemostasis (hemorrhagic diathesis). The loss of iron with frequent bleeding gives this
anemia an iron deficiency character.
Etiology:
1) violation of the integrity of blood vessels when injured or affected by a
pathological process (atherosclerosis, tumor, tuberculosis);
2) increased permeability of the vascular wall (acute radiation sickness);
3) decrease in blood clotting (hemorrhagic diathesis).
A serious danger to human life is the loss of 50% of the volume of circulating
blood, fatal is the loss of blood over 60%.
Pathogenesis:
I. Initial stage. A decrease in the volume of circulating blood, a decrease in blood
pressure, hypoxia.
II. Compensatory stage. Activation of protective and compensatory reactions.
III. Terminal stage. The increase of pathological changes in the div up to a fatal
outcome.
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Protective and compensatory reactions in case of blood loss:
I. Centralization of blood circulation:
1) spasm of arterioles of the skin, muscles, organs of the digestive system;
2) opening of arteriovenous anastomoses of these organs and tissues as a result
of spasm of precapillary sphincters;
3) venoconstriction (contraction of the smooth muscles of the veins), an increase
in blood flow to the heart. These changes are based on the following mechanisms:
a) lowering of blood pressure - + excitation of baroreceptors - + activation of the
sympathoadrenal system -+ action of catecholamines on a-adrenoreceptors of smooth
muscles of arteries, arterioles, precapillary sphincters and veins;
b) a decrease in the volume of circulating blood and blood pressure - + excitation
of volumo-and baroreceptors - + activation of neurosecretory cells of the hypothalamus
that produce vasopressin -+ action on V1-receptors of vascular smooth muscles with
subsequent vasoconstriction;
c) decrease in the volume of circulating blood and activation of the
sympathoadrenal system - + release of renin by the cells of the juxtaglomerular
apparatus of the kidneys -+ activation of the renin-angiotensin system with the
formation of angiotensin II -+ spasm of the smooth muscles of blood vessels.
II. Increase in the volume of circulating blood:
1. The transfer of tissue fluid into the blood vessels. The Starling mechanism is
a decrease in the volume of circulating blood, a decrease in hydrostatic pressure in the
capillaries, a decrease in water filtration in the arterial part of the capillaries and an
increase in fluid reabsorption in the venous.
2. Increased reabsorption of water and sodium ions in the kidneys. Prevents the
loss of fluid in the urine:
a) the effect of vasopressin (antidiuretic hormone) on the V2-receptors of the
epithelium of the distal convoluted tubules and collecting tubes of the kidneys;
b) activation of the renin-angiotensin system, the release of aldosterone, which
increases the reabsorption of sodium in the distal convoluted tubules of nephrons;
c) activation of the sympathoadrenal system, redistribution of blood flow in the
nephron.
3. The output of blood from the depot into the bloodstream. Activation of the
sympathoadrenal system and the effect of catecholamines on the vessels of the liver,
spleen, subcutaneous fat.
III. Restoration of blood composition-from several days to 1-2 weeks after
bleeding. Circulatory (decrease in the volume of circulating blood) and hemic
(anemic) hypoxia of the kidneys, an increase in the number of renal erythropoietins, an
effect on erythropoietin-sensitive cells of class III of the red bone marrow, an increase
in young regenerative forms of red blood cells in peripheral blood.
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ISSN:3030-3621
Pathological changes in blood loss:
1. A decrease in the volume of circulating blood, a drop in blood pressure, shock.
2. Acute posthemorrhagic anemia.
3. Hypoxia. Initially, circulatory, and then hemic (anemic).
4. Non-gas acidosis. It is caused by hypoxia and the intake of lactic acid into the
blood.
5. Violation of the excretory function of the kidneys, acute renal failure, oligo -
and anuria, intoxication (azotemia), death.
Acute post-hemorrhagic anemia - there are three periods, each of which is
characterized by a certain picture of peripheral blood:
I. The first few hours after acute blood loss. During this period of time, the total
volume of blood decreases, as well as the total number of red blood cells in the div.
II. A period of time from several hours to several days after acute blood loss. As
a result of the transfer of fluid from the interstitial space to the blood vessels, blood
dilution (hemodilution) occurs. The number of red blood cells and hemoglobin
decreases, the hematocrit decreases. The color indicator remains unchanged
(normochromic anemia). Qualitative changes in red blood cells in the blood smear have
not yet been detected.
III. The time period is from several days to 1-2 weeks after acute blood loss. The
appearance of a large number of regenerative forms of red blood cells, which is
associated with increased erythropoiesis in the red bone marrow. Since young
immature red blood cells contain less hemoglobin compared to mature cells, the color
index decreases and anemia becomes hypochromic.
Chronic posthemorrhagic anemia - due to loss of iron with frequent bleeding,
signs of iron deficiency anemia develop: the concentration of hemoglobin and color
index decreases, degenerative forms of red blood cells appear in the blood smear
(micro-and poikilocytosis, hypochromia). The number of red blood cells and
hematocrit may remain unchanged.
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