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55 Cards in this Set
- Front
- Back
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Hemolytic disease of the newborn
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blood group incompatibility with mom and baby. mom has an IgG antibody and baby has the antigen from dad
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extramedullary hematopoiesis
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increased RBC production outside the bone marrow to compensate for RBC destruction
(spleen, liver) |
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erythroblastosis fetalis
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premature release of many NRBCs into the fetal circulation may occur
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hydrops fetalis
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fetus develops a generalized edema when the RBC production cannot compensate for RBC destruction
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kernicterus
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free bilirubin is deposited in the basal ganglia and in the lipid rich tissue of the central nervous system.
results in permanent irreversible damage to the CNS |
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primary sensitization
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first child
mother will begin to produce antibodies but it will not affect the baby |
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secondary (anamnestic) response
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second pregnancy or transfusion
characterized by increasing titres causes HDN |
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elution is the most useful for
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-most useful in diagnosing an ABO HDN
-confirms HDN or when the cause is unknown (ie. DAT-pos & Ab screen-neg = suspect ABO HDN) |
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phototherapy
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treatment for slight jaundice
expose baby to blue-violet or yellow-green light (420-475nm) this wavelength decomposes the bilirubin to a non toxic product(photobilirubin) which is excreted rapidly by the liver into the bile in an unconjugated form |
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antenatal
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prenatal period
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significant titre
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16-32
changes two or more tubes (maternal Ab) -rising titre may indicate HDN or mom is being sensitized to produce an Ab |
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amniocentesis and when it is preformed
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-aspirate of amniotic fluid
-usually preformed on women with a history of previously affected babies even if the baby is stable, with significant titres(>16) or a significant rise in titre |
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liley graph
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difference between optical density at 450nm baseline is plotted
-bottom zone(zone1)- baby is unaffected or mildly unaffected -mid zone(zone2)- mild to moderately affected, monitor baby -top zone(zone3)- fetus is severly affected if it is before 32 weeks interuterine transfusion may be given, after 32 weeks exchange transfusion after birth |
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L/S ratio (lecithin/sphengomyelin) and PG (phosphatidylglycerol)
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tests done on the amniotic fluid to evaluate lung maturity
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intrauterine transfusion
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preformed between 20-34 weeks gestation
donor blood must be: -Group O (neg unless know babies Rh group) and*compatible with maternal serum -<7 days old -packed RBC(Hct=0.75-0.80L/L) -irradiated (to get rid of Tcells to prevent graft vs. host) -CMV negative |
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perform on cord bloods
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ABO- forward only
Rh- including weak D DAT- [HDN-weak pos (ABO), Pos (Rh)] |
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objectives of an exchange transfusion
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-remove babies sensitized cells
-lower serum bilirubin concentration -provide O2-carrying RBCs which are compatible with circulating maternal Ab -reduce the level of unbound maternal Ab -suppress RBC production |
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exchange transfusion criteria
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rbc must lack the offending antigens
less than one week old reconstituted with FFP or 5%albumin to a hct of 0.40-0.40L/L irradiated CMV neg compatible with moms serum Do not necessarily have to be Rh neg, it can be the same as the baby. if mom and baby are same blood group can use that ABO group |
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HPA-1A
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human platelet antigen-1A
old term for the antigen involved in baby thrombocytopenia |
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Platelet transfusion in HDN
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-platelet Abs in the mother can cause thrombocytopenia in the baby
-antigen involved is usually HPA-1A. the Ab crosses the placenta causing thrombocytopenia in the baby |
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RhIg
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Rh immunoglobulin
Win Rho |
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when to give win Rho
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cannot be given if mother already has circulating anti-D
Rh neg women -at 28 weeks gestation -following a birth of a Rh pos baby or unknown -following amniocentesis, abortion, ectopic pregnancy, stillbirth or miscarriage -following a transfusion of Rh pos platelets, granulocytes or RBCs |
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fetal maternal hemorrhage (FMH)
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a single dose of 300ug RhIg covers up to 30 mL of fetal blood therefore all non-immunized Rh neg women who have delivered a Rh pos baby should be screened for this.
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rosette test
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-screening test not used often
-detect Rh pos fetal red cells in circulation of a Rh negative mom -qualitative test used to detect FMH greater than 30mL |
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rosette test procedure
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mom 4% + anti-D (incubate)
-anti-D will sensitize any Rh pos (fetal) cells present add Rh pos (R2R2) indicator cells -indicator cells will form a rosette around the sensitized Rh positive cells microscopically (>7 in 5 feilds=pos) |
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kleihauer betke acid elution stain
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-test is a quantitation of fetal RBCs in maternal blood
- used to determine the amount fo Rh immune globulin the mother should recieve to prevent her from producing anti-D |
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kleihauer betke principle
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fetal hgb is resistant to acid elution (adult isnt). when a fixed thin blood smear is exposed to an acid buffer the adult RBCs lose their Hgb.
fetal cells will appear bright pink and refractile. adult cells will appear as pale ghost cells |
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kleihaur betke calculations
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(oil immersion, 2000 cells)
#fetal cells / 2000 (total cells counted) x 100 volume of fetomaternal hemorrhage %fetal cells x 50 = mls RhIg needed volume of FMH / 30 = vials needed |
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immune hemolysis
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RBC destruction mediated by an antibody causing immune hemolytic anemia
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what is autoimmune hemolytic anemias (AIHA)
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immune system is no longer able to identify self from non-self
ususally the cause is unknown but can also be due to other diseases or drugs |
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alloimmune hemolytic anemia
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HDN
Hemolytic transfusion reaction |
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autoimmune hemolytic anemia
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warm autoimmune hemolytic anemia (WAIHA)-70%
cold hemagglutinin disease (CHD)-16% paroxysmal cold hemoglobinuria (PCH)-2% drug induced immune hemolytic anemia-12% |
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intravascular hemolysis
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destruction of RBCs within circulation
In the vein |
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extravascular hemolysis
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desruction of RBCs once removed from circulation
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diseases associated with AIHA
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systematic lupus erythematosis (associated with secondary WAIHA)
infectious mononucleosis (with secondary CHD) |
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drugs associated with positive DAT
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cephalosporins
penicillins |
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cold hemagglutinin disease
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primary- idiopathic disease
secondary- disease in association with lymphoproliferative disorders (lymphomas) or infectious diseases (IM, mycoplasma pneumonia(anti-I)) IgM-most are due to anti-I rarer- autoanti-i (Infectious mono) and autoanti-P Warm and wash cells to remove excess complement |
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Cold autoantibody DAT
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positive with polyspecific AHG and C3, neg with anti-IgG
IgG is not detected because it is a unique protein that elutes from RBC membrane at warmer temperature |
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paroxysmal cold hemoglobinuria
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acute illness (seen in young kids)after a bacterial or viral infection
usually IgG (biphasic) specificity usually anti-P(donath- landsteiner) rarer- anti-i intravascular hemolysis |
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warm auto antibodies
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primary disease (idiopathic) or secondary to other diseases
usually IgG subclasses (Most destructive)IgG3, IgG1, IgG2, IgG4(little hemolysis) no cure treatment is steriods, splenectomy(site of RBC destruction), cytotoxic/immunosuppressive drugs(last resort) extravascular hemolysis |
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WAIHA more severe than CHD
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because autoantibodies reacts best at body temperature
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C3b, IgG3, IgG1
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sensitize cells in warm autoantibody conditions
macrophages have receptors for them IgG3= most destructive |
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warm autoantibody DAT
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most cases positive
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chloroquin diphosphate
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elution reagent
used to remove IgG from the RBC with little damage to the cell membrane may weaken the expression of Rh and other antigen |
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drug induced hemolytic anemia
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drug adsorption
immune complex mechanism membrane modification autoantibody formation |
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drug induced autoantibodies
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positive DAT, hemolytic anemia does not usually occur
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drug adsorption
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the drug acts as a hapten and the RBC is the protein carrier
the drug binds to the patient's RBC membrane drug-RBC complex can stimulate antibody formation IgG Ab's are produced AC, DAT pos (IgG) if hemolysis it is extravascular Antibody screen- neg causes-intravenous penicillins, cephalosporins |
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immune complex mechanism
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drug causes a production of antibodies. the drug and IgM or IgG antibody to the drug form immune complexes in the plasma. immune complexes attach non specifically to RBCs and activate complement
intravascular hemolysis "innocent bystander" causes are quinidine, sulfonamides, antihistamines, quinine, phenacetin DAT, AC positive antibody screen negative eluate non-reactive |
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membrane modification mechanism
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drug that causes a modification to the RBC membrane. altered membrane adsorbes serum protein non-specifically (including IgG or complement)
no evidence of hemolysis causes -cephalosporins DAT pos(IgG and complement) antibody screen- negative eluate non reactive |
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autoantibody formation
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most common cause of drug related positive DAT.
drug causes production of IgG, warm reaction Abs that recognize RBC Ags. Abs react with intrinsic red cell Ags and are autoAbs caused by alpha-methyldopa extravascular hemolysis AC, Ab screen positive eluate reactive May take 6mo. to 2yrs. for DAT to revert to negative |
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eluate control
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last wash- should not react just saline
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Needed for hemolytic disease of the newborn to occur
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IgG
maternal antibodies |
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interuterine transfusion
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group O negative
unless you know the Rh type and lack any maternal antibodies (compatible with mom) |
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warm and cold autoantibodies -enzymes
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enhanced
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Positive DAT
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autoimmune antibody
hemolytic disease of the newborn hemolytic transfusion reaction warm/cold autoantibody |
