Hd newborn
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Transcript of Hd newborn
UNIVERSIDAD AUTÓNOMA DE GUERRERO
UNIDAD ACÁDEMICA FACULTAD DE MEDICINA
Mendoza McGinnis Gema Itzel
Villagómez Vélez Julio Andrés
Arzeta Serrano Laura Gabriela
Hernández Barrera Mario
ENGLISH CLASS: HEMOLYTIC DISEASE OF NEWBORN
EQUIPO FISIOLOGÍA.
Objectives
The student is expected to learn about clinical symptoms, diagnosis, and treatment for hemolytic newborn disease.
Reinforce everything learned in physiology class by applying a case study.
Participate in a group dynamic to simplify the learning experience.
Antibodies - Anticuerpos Shortened - acortado Ocurring - ocurriendo Ag Glutination - Glutinacion antigenico Inmunogenic - Inmunogenico Involves - Involucrar
Phagocytic - Fagocitico Binding - Fristloorn - Microspheocytes - Microfeoscitos.
Hemolytic disease of the new born and fetus (HDN) is a destruction of the red blood
cells (RBCs) of the fetus and neonate by antibodies produced by the mother
It is a condition in which the life span of the fetal/neonatal red cells is shortened due to
maternal allo-antibodies against red cell antigens acquired from the father
Antibodies
Five classes of antibodies IgM IgG IgA IgD IgE
Blood groups specific antibodies are IgG IgM and rarely IgA
Blood group antibodies
Blood group antibodies can be classified as Naturally occurring and immune antibodies
Depending on presensitization
Complete and incomplete antibodies Depends on agglutination of saline suspended
red cells IgM is complete antibody; most naturally
occurring antibodies are complete and of IgM class
IgG is incomplete antibody
Antibodies of ABO system
Anti- A
Anti- B
Anti- A1
Anti- H
Antibodies of Rh system
Naturally occurring Anti- E Occasionally anti-D and anti Cw
Immune antibodies D antibodies are more immunogenic Other are anti c, E, e, C. Most common is anti- E After anti- D, anti- c is the common cause of HDN
(The vast majority of Rh antibodies are IgG and do not fix complement)
Complement
Complements are series of proteins, present in plasma as an inactive precursors
When activated and react sequentially with each other they mediate destruction of cells and bacteria
Complement activation involves two stages Opsonization Lytic stage
Complement
Antibodies can fix complement and cause rapid destruction of red cells
Destruction depends on the amount of antibody and complement
In ABO- incompatible transfusion no surviving A or B red cells can be seen after 1 hour of transfusion
Why? Remember naturally occurring Abs. are IgM and fix
complement mediating the hemolysis
Disease mechanism - HDN
There is destruction of the RBCs of the fetus by antibodies produced by mother
If the fetal red cells contains the corresponding antigen, then binding of antibody will occur to red cells
Coated RBCs are removed by mononuclear phagocytic system
Conjugatedbilirubin
Unconjugatedbilirubin
Neonatalliver is immature and
unable to handle bilirubin
Coated red blood cellare hemolysed in
spleen
Clinical features Less severe form
Mild anemia
Severe forms Icterus gravis neonatorum (Kernicterus)
Intrauterine death Hydrops fetalis
Oedematous, ascites, bulky swollen & friable placenta
Pathophysiology Extravascular hemolysis with extramedullary
erythropoiesis Hepatic and cardiac failure
Hemolytic disease of newborn HDNBOFORE BIRTH Anemia (destruction of red cells) Heart failure Fetal death
AFTER BIRTH Anemia (destruction of red cells) Heart failure Build up of bilirubin Kernicterus Severe growth retardation
Rh HEMOLYTIC DISEASE OF NEWBORN
Antibodies against Anti-D and less commonly anti-c, anti-E
Mother is the case of anti-D is Rh -ve (negative)
Firstborn infant is usually unaffected Sensitization of mother occurs
During gestation At the time of birth
All subsequent offspring inheriting D-antigen will be affected in case of anti-D HDN
Pathogenesis
Fetomaternal Hemorrhage
Maternal Antibodies formed against Paternally derived antigens
During subsequent pregnancy, placental passage of maternal IgG antibodies
Maternal antibody attaches to fetal red blood cells
Fetal red blood cell hemolysis
Factors affecting immunization and severity
Antigenic exposure
Host factors
Antibody specificity
Influence of ABO group ABO-incompatible Rh- positive cells will be hemolysed
before Rh antigen can be recognized by the mother’s immune system
Diagnosis and Management Cooperation between
Pregnant patient
Obstetrician
Her spouse
Clinical laboratory
Diagnosis and Management contd.
Intrauterine transfusion Zone II or III Cordocentesis blood sample Hb less than 10g/dl Ultrasound evidence of hydrops
Early delivery Phototherapy Newborn transfusion
Exchange transfusion Effects of transfusion
Removal of bilirubin Removal of sensitized RBCs, and antibodies Suppression of incompatible erythropoiesis
Mechanism of action
Administered antibodies will bind the fetal Rh- positive cells
Spleen captured these cells by Fc-receptors
Suppressor T cell response is stimulated
Spleen remove anti-D coated red cells prior to contact with antigen presenting cells “antigen deviation”
ABO HEMOLYTIC DISEASE OF NEW BORN
For practical purpose, only group O individuals make high titres IgG
Anti-A and anti-B are predominantly IgM
ABO antibodies are present in the sera of all individuals whose RBCs lack the corresponding antigens
ABO HDN contd. Signs and symptoms
Two mechanism protects the fetus against anti-A and anti-B Relative weak A and B antigens o fetal red cells Widespread distribution of A & B antigen in fetal tissue diverting
antibodies away from fetal RBCs Anemia is most of the time mild ABO- HDN may be seen in the first pregnancy
Laboratory findings Differ from Rh- HDN; microspherocytes are characteristic of ABO-
HDN Bilirubin peak is later; 1- 3 days after birth Collection of cord blood and testing eluates form red cells will
reveal anti-A or anti-B
Treatment Group O donor blood for exchange transfusion which is rarely
required