IS DAY 3 Flashcards

1
Q

T CELL DIFFERENTIATION (DDMA)

A

DOUBLE NEGATIVE STAGE
DOUBLE POSITIVE STAGE
MATURE T CELL
ACTIVATED T CELL

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2
Q

CD THAT APPPEARS DURING THE FIRST STAGE OF THE CELL DEVELOPMENT AND REMAINS PRESENT AS IDENTIFYING MARKER FOR T CELL

A

CD 2

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3
Q

STAGE IN T CELL DIFFRENTIATION THAT IS LACK OF CD 4 AND CD 8

A

DOUBLE NEGATIVE STAGE

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4
Q

STAGE IN T CELL DIFFRENTIATION EXPRESS BOTH CD 4 AND CD 8

A

DOUBLE POSITIVE STAGE

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5
Q

ALLOWS ONLYY THOSE CAN RECOGNIZE FOREIGN ANTIGEN BOUND TO MHC

A

POSITIVE SELCTION

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6
Q

STAGE IN T CELL DIFFRENTIATION EXPRESS ONLY ONE CD MARKER EITHER CD 4 OR CD 8

A

MATURE T CELL

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7
Q

CENTER OF ADAPTIVE IMMUNITY
RESPONSIBLE FOR DELAYED HYPERSENSITIVITY

A

CD 4 T HELPER CELL

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8
Q

RESPONSIBLE FOR CELL MEDIATED EFFECTOR MECHANISM

A

TH1

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9
Q

REGULATION OF AB PRODUCTION

A

TH2

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10
Q

KILLS INFECTED HOST INTRACELLULARLY

A

CD 8

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11
Q

MARKER OF CD 8

A

PERFORINS AND GRANZYMESS A-B

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12
Q

ASSESS THE ABILITY OF TC TO LYSE LABELED TARGET CELLS

A

LYMPHOLYSIS TESTS

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13
Q

FOR IMMUNE SUPPRESSION

A

CD 3, CD4, AND CD 25

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14
Q

T CELL IMMUNODEFICIENCY : THYMUS GLAND DEVELOP ABNORMALLY
PHARYNGEAL POUCH SYNDROME

A

DIGEORGE SYNDROME

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15
Q

ASSOCIATED TO ZINC DEFICIENCY

A

DIGEORGE SYNDROME

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16
Q

T CELL IMMUNODEFICIENCY
MOST LIKELY CONFUSED WITH AIDS IN PEDIATRIC PX

A

NEZELOF SYNDROME

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17
Q

T CELL IMMUNODEFICIENCY PATIENTS ARE ATHYMIC

A

NEZELOF SYNDROME

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18
Q

T CELL IMMUNODEFICIENCY AFFECT PURINE METABOLISM
CAN CONFUSED WITH NEONATAL HIV INFECTION

A

PURINE NUCLEOSIDE PHOSPHORYLASE DEFICIENCY

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19
Q

T CELL IMMUNODEFICIENCY T CELL SPECIFICALLY FAIL TO RECOGNIZE ONLY THE CANDIDA ANTIGEN

A

CHRONIC MUCOCUTANEOUS CANDIDIASIS

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20
Q

T CELL IMMUNODEFICIENCY
EFECT IN PROGRAMMED CELL DEATH
TNF RECEPTOR MUTATION
INCREASE DOUBLE NEG T CELL

A

AUTOIMMUNE LYMPHPROLIFERATIVE SYNDROME

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21
Q

STAGES IN B CELL DIFFERENTIATION PROPIMAP

A

PRO-B CELLS
PRE BCELLS
IMMATURE B CELLS
MATURE B CELLS
ACTIVATED B CELL
PLASMA CELLS
MEMORY CELLS

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22
Q

STAGE IN B-CELL DIFFERENTIATION WHERE REARRANGEMENT OF HEAVY CHAIN GENES (SUCCESSFUL)
EARLIEST B CELL PRECURSOR

A

PRO B CELL

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23
Q

STAGE IN B-CELL DIFFERENTIATION WHERE BEGINS HC SYNTHESIS OCCURS
SYNTHESIS OF N CHAIN IN THE CYTOPLASM
IG LIGHT CHAIN REARRANGED

A

PRE-B CELL

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24
Q

STAGE IN B-CELL DIFFERENTIATION WHERE APPEARANCE OF COMPLETE IGM

A

IMMATURE B CELL

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25
Q

RECEPTOR FOR A BREAKDOWN PRODUCT OF THE COMPLEMENT COMPONENT OF C3

A

CD 21

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26
Q

IMPORTANT FOR INTERACTION OF B CELLS WITH T CELLS

A

CD40

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27
Q

STAGE IN B-CELL DIFFERENTIATION WHERE IN THE SPLEEN IMATURE B CELL DEVELOP INTO MARGINAL ZONE B CELL

A

MATURE B CELL

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28
Q

PROLONGED THE LIFE SPAN OF MATURE B CELLS

A

IGD

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29
Q

THE SURFACE OF IG PROVIDE THE PRIMARY ACTIVATING SIGNAL TO B CELLS WHEN CONTACT WITH ANTIGEN TAKES PLACE

A

PRESENCE OF IGM AND IGD

30
Q

STAGE IN B-CELL DIFFERENTIATION WHERE ANTIGEN DEPENDENT
GIVES RISE TO PLASMA AND MEMORY CELL S

A

ACTIVATED B CELLS

31
Q

SPHERICAL AND ELLIPSOIDAL ECCENTRIC NUCLEUS
FX IS ANTIBODY PRODUCTION
NONDIVIDING

A

PLASMA CELL

32
Q

THEY ARE SIMILAR IN APPEARANCE TO UNSTIMUALTED B CELLS BUT TEHY REAINED INA N ACTIVATED STAET FOR MONTHS OR YEARS READY TO RESPOND TO THE INITIAL ANTIGEN

A

MEMORY CELLS

33
Q

B CELL SUBSET: CD 5, SELF RENEWING RESPOND TO MICROBIAL ATIGEN AND GENERATE AUTOANTIBODY

A

B1

34
Q

B CELL SUBSET: MOST COMMON, GREATER AG RECEPTOR DIVERSITY AND RESPONSE EFFECTIVELY TOO T CELLS

A

B2

35
Q

MOST COMMONLY ENCOUNTERED ANTIBODY AGAINST THE KELL BLOOD GROUP SYSTEM IS

A

ANTI-K1

36
Q

NOST ANTI-K APPEAR TO BE INDUCED BY ___ AND ___

A

PREGNANCY AND TRANSFUSION

37
Q

THE MOST RELIABLE METHOD OF DETECTION FOR KELL ANTIBODIES IS

A

INDIRECT ANTIGLOBULIN TEST

38
Q

CHARATERIZED BY BOTH HEMATOLOGICAL AND NEUROMSUCULAR ABNORMALITIES, TYPICALLY PRESENTS WITH AREFLEXIA, DYSTONIA, AND CHOREIFORM MOVEMENTS LATE IN LIFE

A

MCLEOD SYNDROME

39
Q

CAN ALSO BE ASSOCIATED WITH CHRONIC GRANULOMATOUS DISEASE

A

MCLEOD PHENOTYPE

40
Q

TRUE OR FALSE
MCLEOD SYNDROME IS EXCLUSIVE TO MALE ONLY

A

TRUE

41
Q

THIS BLOOD GROUP IS NOT INTRINSIC TO RBCS BUT ARE ON TYPE 1 GLYCOSPHINGOLIPIDS THAT ARE PASSIVELY ADSORBED ONTO THE RBC MEMBRANE FROM THE PALSMA

A

LEWIS

42
Q

AMORPHIC/ SILENT ALLELE OF LEWIS BLOOD

A

le gene

43
Q

_____ a causative agent of gastritis and ulcers binds to h, Leb and Ley antigen

A

h. pylori

44
Q

a _____ phenotype has been ;linked with higeher incidence of recurrent candida vaginitis and UTI

A

LEWIS NULL

45
Q

PHENOTYPE ASSOCIATED WITH AN INCREASED INCIDENCE OF HEART DISEASE

A

Le(a-b-)

46
Q

the epitope for the tumor marker CA19-9

A

Le (a-b-)

47
Q

this blood group phenotype is resistant to Plasmodium vivax and Plasmodium knowlesi

A

Fy (a-b-)

48
Q

Duffy antibody that is most commonly encountered antibody and associated with acute and delayed hdn

A

Anti-Fya

49
Q

Duffy antibody that is discovered in teh serum of Fy(a-b_) black child who was later died of leukemia

A

Anti-Fy5

50
Q

this null phenotype is found in filipino, japanese, indonesian, and chinese

A

Jk (a-b-)

51
Q

Kidd antibody that is most commonly encountered antibody

A

Anti-Jka

52
Q

Elevated i antigen is also observed on

A

Cord RBCs and Reticulocytes and in
Megalobalstic anemia
leukemia
Chronic hemolytic states

53
Q

I blood group antibody uncommon but has been reported in infectious mononucleosis

A

Anti-i

54
Q

I blood group antibody assocaited with cold autoimmune hemolytic anemia (CAIHA) and mycoplasma pneumonia

A

Anti-I

55
Q

testing for anti-I or anti-i antibodies is done at ______

A

4C using O group RBCS or cord RBCs

56
Q

Naturally occurring blood group antibodies

A

ABO, LEWIS, P1, MN, Lua

57
Q

CLINICALLY SIGNIFICANT blood group antibodies

A

ABO, Rh, Kell, DUFFY, Kidd, SsU

58
Q

warm antibodies blood group antibodies

A

Rh, kell, kidd, duffy

59
Q

Cold antibodies blood group antibodies

A

M, N P1

60
Q

blood group antibodies USUALLY REACT IN AHG

A

KELL KIDD DUFFY

61
Q

CAN REACT IN ANY PHASE OF TESTING blood group antibodies

A

LEWIS

62
Q

DETECTION ENHANCED BY ENZYME TREATMENT OF TEST CELLS blood group antibodies

A

RH, LEWIS, KIDD P1

63
Q

NOT DETECTED WITH ENZYME TREATMENT OF TEST CELLS

A

M,N, DUFFY

64
Q

ENHANCED BY ACIDIFICATION blood group antibodies

A

ANTI-M

65
Q

COMMON CAUSE OF DELAYED HTR blood group antibodies

A

KIDD

66
Q

ASSOCIATED WITH MYCOPLASMA PNEUMONIAE

A

ANTI-I

67
Q

ASSOCIATED WITH INFECTIOUS MONONUCLEOSIS

A

ANTI-i

68
Q

ASSOCIATED WITH PCH

A

ANTI-P

69
Q

associated with congenital cataracts

A

i adult phenotype

70
Q
A