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Flashcards in Abo Deck (131)
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1
Q

Is a destruction of the fetus and neonate by ab produced by the motter

A

Hdn and newborn

2
Q

It is conditioned in which the life span of the fetal neonatal red cell is shortened due to

A

Maternal allo ab against red cell ag acquired from th father

3
Q

Made from four polypeptide chain

A

Two light chain

Two identical heavy chain

4
Q

Blood grouo ab can be classified as

A

Naturally occuring and immune ab

Cold and warm ab

5
Q

Most immune abs are

A

Warm and can destroy red cell in vivo

6
Q

Most natural abs are

A

Cold and wide thermal range like anti A and B

7
Q

It is incomplete ab

A

Igg

8
Q

Is a complete ab most naturally occuring ab

A

IgM

9
Q

what are Ab of ABO system

A

Anti A, anti B, anti A1 and anti H

10
Q

What are the Ab in ABO system that is naturally occurring and immune

A

Anti A and Anti B

11
Q

Natural occurring in ab of rh system

A

Anti E

12
Q

What is occassionally naturally occurring of Ab rh system

A

Anti D and anti C

13
Q

This is mor immunogenic

A

D Ab

14
Q

Most common in immune Abs is

A

anti E

15
Q

After Anti D what is common cause of HDN

A

Anti c

16
Q

Kell blood group system

A

Anti K

17
Q

Kidd blood group system

A

Anti JKa

18
Q

Are series of protein present in plasma as inactivate precursors

A

Complement

19
Q

Complement activation involves and cause rapid destruction of red cell

A

Complemet

20
Q

Complement activation involves 2 stages

A

Opsonization and lytic stage

21
Q

Destruction depends on the amount of

A

Ab and complement

22
Q

Coated rbc are removed by

A

Mononuclear phagocytic system

23
Q

Less severe form

A

Mild anemia

24
Q

Severe form

A

Icterus gravis neonatorum or kernicterus

25
Q

Intrauterine death

A

Hydrops fetalis
Extravascular hemolysis of extramedullary erythropoiesis
Hepatic and cardiac failure

26
Q

Oedematous ascites, bulky swollen and friable placenta

Pathophysiology

A

Hydrops fetalis

27
Q

Hdn before birth

A

Anemia
Heart failure
Fetal death

28
Q

Hdn after birth

A
Anemia
Heart failure
Build up of bilirubin
Kernicterus
Severe growth retardation
Unconj bilirubin more than 18mgdl
29
Q

Rh hdn ab against

A

Anti D less common anti c and anti E

30
Q

Sensitization of mother occur

A

During gestation

At the time of birth

31
Q

All subsequent offspring inheriting D Ag will be affected in case of

A

Anti D HDN

32
Q

Factors affecting immunization and severity

A

Antigenic exposure
Host factors
Ab specificity
Influence pf abo group

33
Q

Diagnosis cooperation bet

A

Pregnant women
Ob
Her spouse
Clin lab

34
Q

Ab detection repeat testing required at

A

24 or 28 weeks first test neg

35
Q

To detect clinically significant pf ab detection is

A

Igg ab which reacts at 37 deg

36
Q

Recommended ob practice

A
Abo and rh testing
History of prev pregnancy
Ab detection
Ab specificity
Parental phenotype
Amniocyte testing
Ab titers
37
Q

Ab titers difference of

A

2 dikution or score more than 10 is significant

38
Q

Amniocentesis and cardiocentesis

A

Core of bilirubin
Spectrophotometric scan
Fetal blood sample can be tested

39
Q

Increasing or unchange OD as pregnancy advance shows worsening of the fetal hem dse

A

Spectrophotometric scan indirect kethod

40
Q

Fetal blood sample can be taken and tested for

A

Hb hct blood type and direct coombs test

41
Q

Diagnosis and mgt

A

Intrauterine transfusion
Early delivery
Phototherapy
Newborn transfusion

42
Q

Zone II or III

A

Intrauterine transfusion

43
Q

Cardiocentesis blood sample hb less than 10g/dl

Ultrasound with evidence of hyrops

A

Intrauterine transfusion

44
Q

New transfusion

A

Exchange transfusion

Effects of transfusion

45
Q

Effects of transfusion

A

Removal of bilirubin
Removal of sensitized rbc and ab
Suppression of incompatible erythropoiesis

46
Q

Selection of blood

A

Group O rbc
Rh neg units for rg neg case
Whole blood group O
Blood less than 7yoo

47
Q

Prevention of active immunization

A

Administration of corresponding rbc ab which is Anti D

Use of high titer rh ig

48
Q

Calculation of the dose

A

Kleuhauer test for fetal hb

49
Q

What are predominant igm

A

Anti A and anti B

50
Q

For practical purpose what group make high titer

A

Only group O individual make high titer IgG

51
Q

Present ij the sera pf all individual whic rbc lack the corresponding Ag

A

Abo Ab

52
Q

Two mechanism protect the fetus against

A

Anti A and anti B

53
Q

Is the most time mild

A

Anemia

54
Q

May be seen in the 1st preg

A

Abo hdn

55
Q

Characteristics of abo hdn

A

Microsoherocytes

56
Q

Bilirubin peak

A

1-3 days after birth

57
Q

Soluble and found in saliva and plasma

A

Lewis system

58
Q

Known as plasma Ag

A

Lewis system

59
Q

Secondarilu absorbed to red cell

A

A serum Ag

60
Q

It priduces Lea

A

Le gene

61
Q

Secretor changed the Lea to

A

Leb

62
Q

May also modify the A Ag

A

Le

63
Q

Is not true blood Ag

A

Lewis Ag

64
Q

The expression f the Lewis Ag is influences by the presence of

A

Hh and Sese gene

65
Q

determines secretor status

A

Se gene

66
Q

It is a gene that produces the ability to secrete water soluble blood group soecific substances in the tissue

A

Se gene

67
Q

Produces the ability to secrete H ag

A

H gene

68
Q

The basic matrix of the ABO system

A

H Ag

69
Q

The lewis Ag is inheried by twi gene

A

Le and le

70
Q

Converts a precursor materila to Lea substance

A

Lewis positive Le gene

71
Q

Cannot convert a precursor katerial to Lea substance

A

The lewis negative le gene

72
Q

Lewis gene is located at

A

Chrom 19

73
Q

Changes in lewis phenotype occur in the ff situation

A

Preg
Cancer
Alcoholic cirrhosis
Viral and parasitic infection

74
Q

Le Se

A

Le a- Leb+

75
Q

Le se

A

Lea+ Leb-

76
Q

lele

A

Lea- Leb-

77
Q

le se

A

Lea- Leb- Lec+

78
Q

le Se

A

Lea- Leb- Led+

79
Q

Present in secretors

A

Le (a-b+)

80
Q

Present in non secretors

A

Le (a+b-)

81
Q

Usually found in secretors

A

Le (a-b-)

82
Q

This individual will not produced any individual

A

lele / Le(a-b-)

83
Q

A person who inherits atleast one Le gene and one Se gene will be

A

Leb positive

84
Q

With Le gene and Se gene will be Leb positive

A

Le (a-b+)

85
Q

A person atleast one Lea gene and Sese gene will be

A

Le (a+b-)

86
Q

Constrils ABH secretors but has no conrol in Le secretor

A

Se

87
Q

Newborn borns

A

Le a-b-

88
Q

2 weeks to 6 months

A

Lea+

89
Q

Then 1

A

Le a+b+

90
Q

Then 2

A

Le a-b+

91
Q

Igm in nature, cold reactive, naturally occurring

A

Lewis Ab

92
Q

May cause HTR

A

Lea

93
Q

Most commonly found Ab

A

Anti Lea

94
Q

Best room atemp or below some at ICT and enzymes

A

Anti Lea

95
Q

Some in vitro hemolysis

A

Lewis Ab

96
Q

Often found with anti-Lea

A

Anti Leb

97
Q

Most react at room temp or below

A

Anti Leb

98
Q

Two types of anti Leb

A

Anti LebH and anti LebL

99
Q

Rare cause of HTR

A

Anti Leb

100
Q

Are found in individuals who hae never been transfused or received other antigenic stimuli

A

Lewis Ab

101
Q

Not known to cause cause of two reasons

A

Lewis Ab

102
Q

Two reasons why lewis ab not cause hdn

A

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

103
Q

Reacts with both Lea and Leb as single Ab

A

Anti Lex

104
Q

It is found in adukts

A

I Ag

105
Q

Infants are rich in

A

i Ag

106
Q

Ag can neutralized by

A

Human milk

107
Q

Varies in strength in adult cell

A

I Ag

108
Q

Can be found in saliva, human milk, lympho and plasma

A

I substance or I blood group

109
Q

Usually reacts at room temp, sakine or beliw

A

Anti I

110
Q

Often attaches conplement

A

Anti I

111
Q

Doesnt care about hemolysis unless reacts at

A

37 deg anti I

112
Q

Can be found in almost all sera in low titers, titer increase during some dse amswer 3 dse

A

Anti I viral infect, syphilis, atypical pneumonia

113
Q

Rare Ab occur in pt with infectious mononucleosi , cirrhosis p, myeloid leukiemia, reticulosis

A

Anti i

114
Q

Receptor for parvovirus B 19

A

P ag

115
Q

P ag can be ass with

A

Pyelonephritis, e coli, strep sinus, shigella dysenterias, vibrio cholerae, vibrio parahaemolyticus

116
Q

May attach complement

A

Anti P1

117
Q

Rarely a problem with transfusion

A

Anti P1

118
Q

Easily inhibited by P1 substance

A

Anti P1

119
Q

Found in sera from pk individual an igm hemolytic Ab that is clin significant

A

Anti P

120
Q

Anti P found as an

A

IgG biphasic Ab in paroxysmal cold hemoglobinuria

121
Q

IgG biphasic Ab in paroxysmal cold hemoglobinuria

A

Donath lansteiner Ab

122
Q

Has only been found as part of other Ab in p blood group

A

Anti pk

123
Q

Found in p individual fromerly callled anti TJ

A

Anti P+P1+Pk

124
Q

Anti TJ ass with

A

Early abortion

125
Q

Ass with african amrican population

A

Duffy null Fy a-b- phenotype

126
Q

Appear to privide protection in p vivax

A

Fya-b-

127
Q

Do not store well in saline suspension

A

Fya and Fyb Ag

128
Q

Usually AHG reaction IgG

A

Anti Fya and Fyb

129
Q

Destroyed by enzymes

A

Anti Fya and Fyb

130
Q

Is an Ab made by duffy null phenotype

A

Anti Fy3

131
Q

Cause of HTR and HDN

A

Anti Fya and Anti Fyb