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7/28/2019 Hemolytic Anemia II
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Acquired Hemolytic Anemia
Immune hemolytic anemiaNone-immune hemolytic anemia
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Allo -immune hemolytic anemia
Autoimmune hemolytic anemia
Drug induced immune hemolytic anemia
Immune hemolytic anemia
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Allo-immune hemolytic anemia
1. Incompatible ABO blood transfusion
Donor Blood
Goup A
Recipient
Group O
Agglutination
Hemolysis
(cells contain A antigen) (cells contain neither A or B antigen)
Plasma contains Anti-A and Anti-B
(iso-antibody)
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Clinical and Pathological effects
Rigor : loin pain.hemoglobinuria
jaudice (after 12 hours)
SHOCK maybe DEATH
Perhaps laterHemostatic failure, Renal failure maybe DEATH
Allo-immune hemolytic anemia
1. Incompatible ABO blood transfusion
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2. Incompatibilities with in the Rh blood group system
Incompatible blood transfusion
DONOR
(not previously transfused or pregnant)
Rh-ve (i.e. rbcs do not contain Rh antigen)
Plasma contains no Rh antibodies NO agglutination
Rh +ve
Later (months, years)Transfusion
of Rh +ve blood
to macrophage system for degradation
in usual way but Rh+ve cells
act as foreign antigens
Formation of
anti-Rh antibodies stimulated
Agglutination
and hemolysis
RECIPIENT
Allo-immune hemolytic anemia
(rbcs contain Rh antigen)
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Hemolytic Disease of the New born (HDN)
First Pregnancy Rh+ve fetus in Rh-ve mother-no antibodies present.
Healthy Baby
Fetal circulation
Placenta
UterusMaternal
circulation
Damaged
chorionic villus
Rh+ve
fetal rbcs
into mother
(Rh-ve)
maternal
blood sinus
Trophoblast
Gradual elimination
by macrophage system
Iso-immunisation
Anti-Rh antibodies
formed (IgG type)
2. Incompatibilities with in the Rh blood group system
Allo-immune hemolytic anemia
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Hemolytic Disease of the New born (HDN)
2. Incompatibilities with in the Rh blood group system
Allo-immune hemolytic anemia
Subsequent pregnancies
Maternal anti-Rh antibodies IgG type
Pass placental barrier
Enter fetal circulation and destroy fetal red cells
(agglutination and hemolysis)
Placenta
Uterus
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Hemolytic Disease of the New born (HDN)
2. Incompatibilities with in the Rh blood group system
Allo-immune hemolytic anemia
The effect are graded into 3 categories of severity:
1. Congenital hemolytic anemia
2. Icterus gravis neonatorum
3. Hydrops fetalis
severe anoxia in utero with cardiac failure and edema.
severe anemia and jaudice,
brain damage due to Kernicterus
mild anemia and jaundice
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Autoimmune Hemolytic Anemia (AIHA)
1. Warm autoimmune hemolytic anemia (WAIHA)
2. Cold autoimmune hemolytic anemia (cold AIHA)
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Autoimmune hemolytic anemia :Warm antibody type (WAIHA)
Reaction at normal temperature (37 C)
= Antibody usually IgG type
= Antigenic determinant
Cell membrane
modified
Cell becomes
microspherocytes
With consequences similar tohereditary spherocytosis-
early sequestration in spleen (RE)
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Autoimmune hemolytic anemia : Cold antibody type
Reaction at temperatures usually below 30 Cthey occur in peripheral circulation and in cold weather.
Antibody
combineswith RBC
Reactions
= Antigenic determinant
Agglutination
Clinically present as painfulhand and feet
Amboceptor effect
Ag/Ab activates complement
Acute intravascular hemolysis
usually of IgM type
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Raynauds phenomenon
manifested by marked pallorof the fingers, in the cold type
Peripheral blood film showing
a neutrophil/red cell rosette
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Drug-Induced Immune Hemolytic Anemia
1. Drug Adsorption Mechanism
Penicillins, Cephalosporin and Streptomycins
mechanism
First the drug is nonspecifically adsorbed to the patients red cellSecond the drug must be able to elicit an antibody response
+ Drug (Ag) AntibodyB-Lymphocyte
RBC
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Drug-Induced Immune Hemolytic Anemia
2. Immune Complex Mechanism : Innocent bystanderQuinidine and Phenacetin
Drug (Ag) Antibody
B-Lymphocyte
(IgG and/or IgM)
Extravascular
hemolysisIntravascular
hemolysis
RE Complement
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Drug-Induced Immune Hemolytic Anemia
3. Methyldopa-Induced (Autoimmune) Mechanism
methyldopa and related drugs (Aldomet, L-dopa):
treatment of hypertension
Drug (Ag) Antibody
B-Lymphocyte
Hemolysis
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Direct Coombs test
Indirect Coombs test
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None-immune hemolytic anemia
Red cell fragment syndrome
Microangiopathic hemolytic anemia
Macroangiopathic hemolytic anemia
March hemoglobinuria
Hypersplenism
Paroxymal Nocturnal Hemoglobinuria
the bone marrow produces red cells with defective cell
membrane which are particular sensitive to lysis by complement
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PNH : Acid lysis test. The affected red cells (on left) show
marked complement-dependent lysis in acidified fresh serum
at 37 C. Preheating the acidified serum inactivates complement,preventing lysis of the affected cells