Explanation for working with teaching material.

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PATHOLOGY OF THE RBC 2

Explanation for working with teaching material.

1. Examine the lecture information and guide.

2. Complete the table.

3. Give answers to the tests.

4. Give answers to situational tasks (analysis of blood).

5. Give an answer to one of the proposed variant  for the final control.

Addition to the lecture

Hemolytic disease of newborn

Definition. A condition in which fetus or neonate’s red blood cell (RBC) are destroyed by Immunoglobulin G (IgG) antibodies produced by mother. In some infants, it can be life-threatening.

· Rh incompatibility

· ABO incompatibility

The effect of a Rh negative mother on Rh positive fetal red blood cells occurs as a result of

- asymptomatic uterine hemorrhage during pregnancy,

- during pregnancy complicated by placental abruption,

- spontaneous or therapeutic abortion and toxemia,

- after cesarean section and ectopic pregnancy.

- amniocentesis procedures,

After the initial exposure to a foreign antigen, B-lymphocyte clones that recognize the RBC antigen are established. The maternal immune system initially produces antibodies of the immunoglobulin M (IgM), that do not cross the placenta, and later produces antibodies of the IgG1 and 3, that traverse the placental barrier.

IgG3 is more efficient in binding to reticuloendothelial cells and causing hemolysis.

After sensitization, maternal antibodies cross the placenta into fetal circulation and attach to Rh antigen on fetal RBCs, which form rosettes on macrophages in the reticuloendothelial system, especially in the spleen. These antibody-coated RBCs are lysed by lysosomal enzymes released by macrophages and natural killer lymphocytes.

Tissue hypoxia develops as fetal anemia becomes severe.

Hydrops fetalis occurs when fetal Hb deficit exceeds 70 g/L and starts as fetal ascites and evolves into pleural effusions and generalized edema.

The various mechanisms responsible for hydrops are: 1)hypoalbuminemia secondary to depressed liver function, 2)increased capillary permeability, 3)iron overload secondary to hemolysis, 4)and increased venous pressures due to poor cardiac function.

Prolonged hemolysis leads to severe anemia, which stimulates fetal erythropoiesis in the liver, spleen, bone marrow, and extramedullary sites, such as the skin and placenta. In severe cases, this can lead to displacement and destruction of hepatic parenchyma by erythroid cells, resulting in dysfunction and hypoproteinemia.

Destruction of RBCs releases heme that is converted to unconjugated bilirubin. Hyperbilirubinemia becomes apparent only in the delivered newborn because the placenta effectively metabolizes bilirubin.

Hemolysis associated with ABO incompatibility exclusively occurs in type-O mothers with fetuses who have type A or type B blood, although it has rarely been seen in type-A mothers with type-B infants with a high titer of IgG.

Hemolytic disease of the newborn is characterized by one or more of the following clinical presentations

· Enlarged liver or spleen

· Hydrops (fluid throughout the body's tissues, including in the spaces containing the lungs, heart, and abdominal organs), which can lead to heart failure from too much fluid

· Newborn jaundice

· Kernicterus or bilirubin encephalopathy results from high levels of unconjugated bilirubin in the fetus blood which is more than 20 mg/dL .

·   Because unconjugated bilirubin are lipid soluble and toxic , it can crosses the blood-brain barrier and it will penetrates neuronal and glial membrane thus cause neurotoxicity

·  Patients surviving kernicterus have severe permanent neurologic symptoms such as a) choreoathetosis b) spasticity c) muscular rigidity d) ataxia e) deafness f) mental retardation

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