Abo Flashcards
Is a destruction of the fetus and neonate by ab produced by the motter
Hdn and newborn
It is conditioned in which the life span of the fetal neonatal red cell is shortened due to
Maternal allo ab against red cell ag acquired from th father
Made from four polypeptide chain
Two light chain
Two identical heavy chain
Blood grouo ab can be classified as
Naturally occuring and immune ab
Cold and warm ab
Most immune abs are
Warm and can destroy red cell in vivo
Most natural abs are
Cold and wide thermal range like anti A and B
It is incomplete ab
Igg
Is a complete ab most naturally occuring ab
IgM
what are Ab of ABO system
Anti A, anti B, anti A1 and anti H
What are the Ab in ABO system that is naturally occurring and immune
Anti A and Anti B
Natural occurring in ab of rh system
Anti E
What is occassionally naturally occurring of Ab rh system
Anti D and anti C
This is mor immunogenic
D Ab
Most common in immune Abs is
anti E
After Anti D what is common cause of HDN
Anti c
Kell blood group system
Anti K
Kidd blood group system
Anti JKa
Are series of protein present in plasma as inactivate precursors
Complement
Complement activation involves and cause rapid destruction of red cell
Complemet
Complement activation involves 2 stages
Opsonization and lytic stage
Destruction depends on the amount of
Ab and complement
Coated rbc are removed by
Mononuclear phagocytic system
Less severe form
Mild anemia
Severe form
Icterus gravis neonatorum or kernicterus
Intrauterine death
Hydrops fetalis
Extravascular hemolysis of extramedullary erythropoiesis
Hepatic and cardiac failure
Oedematous ascites, bulky swollen and friable placenta
Pathophysiology
Hydrops fetalis
Hdn before birth
Anemia
Heart failure
Fetal death
Hdn after birth
Anemia Heart failure Build up of bilirubin Kernicterus Severe growth retardation Unconj bilirubin more than 18mgdl
Rh hdn ab against
Anti D less common anti c and anti E
Sensitization of mother occur
During gestation
At the time of birth
All subsequent offspring inheriting D Ag will be affected in case of
Anti D HDN
Factors affecting immunization and severity
Antigenic exposure
Host factors
Ab specificity
Influence pf abo group
Diagnosis cooperation bet
Pregnant women
Ob
Her spouse
Clin lab
Ab detection repeat testing required at
24 or 28 weeks first test neg
To detect clinically significant pf ab detection is
Igg ab which reacts at 37 deg
Recommended ob practice
Abo and rh testing History of prev pregnancy Ab detection Ab specificity Parental phenotype Amniocyte testing Ab titers
Ab titers difference of
2 dikution or score more than 10 is significant
Amniocentesis and cardiocentesis
Core of bilirubin
Spectrophotometric scan
Fetal blood sample can be tested
Increasing or unchange OD as pregnancy advance shows worsening of the fetal hem dse
Spectrophotometric scan indirect kethod
Fetal blood sample can be taken and tested for
Hb hct blood type and direct coombs test
Diagnosis and mgt
Intrauterine transfusion
Early delivery
Phototherapy
Newborn transfusion
Zone II or III
Intrauterine transfusion
Cardiocentesis blood sample hb less than 10g/dl
Ultrasound with evidence of hyrops
Intrauterine transfusion
New transfusion
Exchange transfusion
Effects of transfusion
Effects of transfusion
Removal of bilirubin
Removal of sensitized rbc and ab
Suppression of incompatible erythropoiesis
Selection of blood
Group O rbc
Rh neg units for rg neg case
Whole blood group O
Blood less than 7yoo
Prevention of active immunization
Administration of corresponding rbc ab which is Anti D
Use of high titer rh ig
Calculation of the dose
Kleuhauer test for fetal hb
What are predominant igm
Anti A and anti B
For practical purpose what group make high titer
Only group O individual make high titer IgG
Present ij the sera pf all individual whic rbc lack the corresponding Ag
Abo Ab
Two mechanism protect the fetus against
Anti A and anti B
Is the most time mild
Anemia
May be seen in the 1st preg
Abo hdn
Characteristics of abo hdn
Microsoherocytes
Bilirubin peak
1-3 days after birth
Soluble and found in saliva and plasma
Lewis system
Known as plasma Ag
Lewis system
Secondarilu absorbed to red cell
A serum Ag
It priduces Lea
Le gene
Secretor changed the Lea to
Leb
May also modify the A Ag
Le
Is not true blood Ag
Lewis Ag
The expression f the Lewis Ag is influences by the presence of
Hh and Sese gene
determines secretor status
Se gene
It is a gene that produces the ability to secrete water soluble blood group soecific substances in the tissue
Se gene
Produces the ability to secrete H ag
H gene
The basic matrix of the ABO system
H Ag
The lewis Ag is inheried by twi gene
Le and le
Converts a precursor materila to Lea substance
Lewis positive Le gene
Cannot convert a precursor katerial to Lea substance
The lewis negative le gene
Lewis gene is located at
Chrom 19
Changes in lewis phenotype occur in the ff situation
Preg
Cancer
Alcoholic cirrhosis
Viral and parasitic infection
Le Se
Le a- Leb+
Le se
Lea+ Leb-
lele
Lea- Leb-
le se
Lea- Leb- Lec+
le Se
Lea- Leb- Led+
Present in secretors
Le (a-b+)
Present in non secretors
Le (a+b-)
Usually found in secretors
Le (a-b-)
This individual will not produced any individual
lele / Le(a-b-)
A person who inherits atleast one Le gene and one Se gene will be
Leb positive
With Le gene and Se gene will be Leb positive
Le (a-b+)
A person atleast one Lea gene and Sese gene will be
Le (a+b-)
Constrils ABH secretors but has no conrol in Le secretor
Se
Newborn borns
Le a-b-
2 weeks to 6 months
Lea+
Then 1
Le a+b+
Then 2
Le a-b+
Igm in nature, cold reactive, naturally occurring
Lewis Ab
May cause HTR
Lea
Most commonly found Ab
Anti Lea
Best room atemp or below some at ICT and enzymes
Anti Lea
Some in vitro hemolysis
Lewis Ab
Often found with anti-Lea
Anti Leb
Most react at room temp or below
Anti Leb
Two types of anti Leb
Anti LebH and anti LebL
Rare cause of HTR
Anti Leb
Are found in individuals who hae never been transfused or received other antigenic stimuli
Lewis Ab
Not known to cause cause of two reasons
Lewis Ab
Two reasons why lewis ab not cause hdn
Most infants do not take up the lewis soluble ag from plasma top the rc by birth
Lewis ab are invariably Ig, in forms too large to cross plcenta
Reacts with both Lea and Leb as single Ab
Anti Lex
It is found in adukts
I Ag
Infants are rich in
i Ag
Ag can neutralized by
Human milk
Varies in strength in adult cell
I Ag
Can be found in saliva, human milk, lympho and plasma
I substance or I blood group
Usually reacts at room temp, sakine or beliw
Anti I
Often attaches conplement
Anti I
Doesnt care about hemolysis unless reacts at
37 deg anti I
Can be found in almost all sera in low titers, titer increase during some dse amswer 3 dse
Anti I viral infect, syphilis, atypical pneumonia
Rare Ab occur in pt with infectious mononucleosi , cirrhosis p, myeloid leukiemia, reticulosis
Anti i
Receptor for parvovirus B 19
P ag
P ag can be ass with
Pyelonephritis, e coli, strep sinus, shigella dysenterias, vibrio cholerae, vibrio parahaemolyticus
May attach complement
Anti P1
Rarely a problem with transfusion
Anti P1
Easily inhibited by P1 substance
Anti P1
Found in sera from pk individual an igm hemolytic Ab that is clin significant
Anti P
Anti P found as an
IgG biphasic Ab in paroxysmal cold hemoglobinuria
IgG biphasic Ab in paroxysmal cold hemoglobinuria
Donath lansteiner Ab
Has only been found as part of other Ab in p blood group
Anti pk
Found in p individual fromerly callled anti TJ
Anti P+P1+Pk
Anti TJ ass with
Early abortion
Ass with african amrican population
Duffy null Fy a-b- phenotype
Appear to privide protection in p vivax
Fya-b-
Do not store well in saline suspension
Fya and Fyb Ag
Usually AHG reaction IgG
Anti Fya and Fyb
Destroyed by enzymes
Anti Fya and Fyb
Is an Ab made by duffy null phenotype
Anti Fy3
Cause of HTR and HDN
Anti Fya and Anti Fyb
