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Immunology Block 4 > Secondary Immuno Def. > Flashcards

Secondary Immuno Def. Flashcards

1
Q

diagnosis of multiple myeloma depends on

A

10% of cells in bone marrow being plasma cells

monoclonal protein in serum/urine and end organ damage

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2
Q

MGUS may progress to

A

myeloma

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3
Q

IL-6 produced by

A

bone marrow stromal ells & by myeloma

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4
Q

what promotes survival by myeloma cells

A

IL-6

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5
Q

activation of osteoclasts is mediated by what chemokine

A

CCL3 & RANKL

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6
Q

CCL3 w/ RNKL stimualtes

A

development of osteoclasts & activation of osteoclasts

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7
Q

final phase of multiple myeloma is similar in presentation to

A

agammaglobulinemia

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8
Q

pts w/ multiple myeloma have increased susceptibility to

A

encapsulated infections esp. pneumococcus (strep pneumoniae)

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9
Q

pts with multiple myeloma have a lot of antibodies but they are

A

monoclonal

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10
Q

when does multiple myeloma present

A

later in life - 65-70

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11
Q

myeloma growing in bone and taking up marrow space, so what is often symptom of multiple myeloma

A

bone pain in lwoer back

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12
Q

defining feature of multiple myeloma is detection of

A

monoclonal band of Ig

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13
Q

upon electrophoresis what will you find in multiple myeloma

A

monoclonal paraprotein, often IgG and sometimes IgA

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14
Q

monoclonal protein band is sometiems called

A

paraprotein

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15
Q

where can monoclonal paraprotein be found

A

serum and urine

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16
Q

when multiple myeloma replaces bone marrow it produces

A

anemia and eventual bone marrow failure

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17
Q

activation of osteoclasts leads to

A

bone resorption

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18
Q

why is there hypercalcemia in multiple myeloma

A

b/c of the bone resportion

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19
Q

light chains are referred to as

A

bence jones proteins

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20
Q

bence jones proteins are

A

excess light chains

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21
Q

bence jones proteins are often what kind of chain

A

excess kappa chains

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22
Q

carpal tunnel is frequent in individuals of pts with

A

multiple myeloma

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23
Q

normal Ig production is decreased which is what gives rise to immunedeficiency in

A

multiple myeloma

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24
Q

monoclonal protiens are also called

A

paraproteins or M proteins

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25
Q

what are paraproteins

A

immunoglobulins produced by monoclonal plasma cells

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26
Q

in majority of cases paraprotein produced is

A

IgG

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27
Q

if not IgG paraprotein it will be

A

IgA paraprotein

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28
Q

bence jones proteins are usually what class of light chain

A

kappa

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29
Q

what test do you do to person if you suspect multiple myeloma

A

serum protein electropheresis

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30
Q

describe serum protein electropheresis

A

gamma goes toward negative electrode
gamma globulins contain all of the Igs (M, A, D, E, G)
you are interested in gamma globulin peak b/c that is where IgG and IgM will be

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31
Q

if somebody has protracted b cell stimluation what will you see in serum protein electropheresis

A

bigger band and darker spread out (pg 8)

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32
Q

somebody w/ multiple myeloma what will you see in serum protein electropheresis

A

monoclonal band b/c its not diffuse it is very tight and dark.

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33
Q

immunofixation electropheresis, describe

A

agarose gel electropheresis, get albumin stain toward positive and Ig toward negative eletrode
add antibodies to identify the bands

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34
Q

diffuse band is indicitive of

A

polyclonal

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35
Q

tight band is indicitive of

A

monoclonal

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36
Q

in multiple myeloma what happens to bone marrow

A

myeloma cells take over

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37
Q

review pg 10

A

10

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38
Q

what does presentation of multiple myeloma look like

A 
they will be older, 70 or so
plasma protein is elevated
high plasma protein
low white blood cell
much high IgG
serum electrophoresis - monoclonal protein
MRI: bone destruction
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39
Q

Waldenstrom’s Macrogobulinemia is characterized by

A

monoclonal IgM

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40
Q

Waldenstrom’s Macrogobulinemia when is onset

A

older 60-70

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41
Q

womeno r men more likely to get Waldenstrom’s Macrogobulinemia

A

men

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42
Q

what are symptoms of Waldenstrom’s Macrogobulinemia

A

fever, anemia, splenomegaly, weight loss, weakness, fatigue

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43
Q

cells in Waldenstrom’s Macrogobulinemia

A

plasmacitic lymphocytes - not quite plasma and not quite b cells

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44
Q

lots of IgM in Waldenstrom’s Macrogobulinemia leads to

A

hyperviscotiy of plasma - lots more protein and lots more high weight protein

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45
Q

how is Waldenstrom’s Macrogobulinemia treated

A

plasmapheresis and stem cell transplant

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46
Q

many of the symptoms in Waldenstrom’s Macrogobulinemia are due to

A

the increased viscosity of the plasma which will impair blood flow

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47
Q

HIV not only virus that can cause immunosuppression, what else can?

A

EBV
Measles
CMV

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48
Q

EBV how does it suppress imune system

A

binds IL-10 and can also make B cell to make IL-10 which suppresses CD8 anti-viral reactions

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49
Q

how does measles immunosuppress

A

inhibits production of IL-12 and prevents a Th1 response

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50
Q

how does CMV immunosuppress?

A

many other viruses can inhibit antigen processing pathways and prevent presentation of viral antigens

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51
Q

EBV, measles, CMB are all what kind of immunosuppression

A

transient

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52
Q

most individuals infected with HIV progress to

A

AIDS

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53
Q

CD4 is expressed where

A

surface of t cells, amcrophages, dendritic cells

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54
Q

HIV infects

A

CD4 cells, so t cells, macrophages, dendritic cells

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55
Q

HIV RNA is transcribe by viral reverse transcriptase into:

A

DNA that integrates into the host-cell genome.

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56
Q

replication of HIV occurs only when

A

t cells are activated

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57
Q

resting t cells will not allow what regarding HIV

A

HIV replication

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58
Q

dendritic cells take HIV to t cells and this causes

A

spread of HIV to lympho nodes and a reservoir for the HIV

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59
Q

during beginning of HIV it is actually

A

controlled by the immune system, it isn’t until loss of CD4 that virus gains control

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60
Q

destruction of immune function by HIV leads to

A

opportunistic infection

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61
Q

drugs that block HIV replication lead to decrease in

A

infectious virus and increase in CD4T cells

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62
Q

HIV is what kind of virus

A

RNA

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63
Q

HIV accumulates lots of what

A

mutations

64
Q

b/c HIV has so many mutations it allows them to become

A

drug resistant

65
Q

is there a vaccine against HIV

A

no

66
Q

HIV is what kind of virus

A

retrovirus

67
Q

what does HIV infect

A

CD4T ell and macrophage

68
Q

spike glycopotein of HIV is

A

gp120 head

stalk: gp41

69
Q

what is what allows HIV to bind to CD4

A

the head glycoprotein gp120

70
Q

what does gp120 in HIV bind to

A

CD4 co-recptor CCR5 or CXCR4

71
Q

what cells aquire HIV

A

dendritic cells

72
Q

what on DC bind to HIV

A

DC-SIGN

73
Q

what allows DC to pick up HIV

A

DC-SIGN

74
Q

once DC pick up HIV what do they do

A

take HIV to the lymph nodes

75
Q

what cell responsible for spreading HIV to CD4 T clls

A

DC

76
Q

first step in replication cycle of HIV

A

binding of the gp120 to CD4 and to chemockine receptor - this induces conformation change so it enter cell

77
Q

reverse transcriptase in HIV does what

A

conversion of viral RNA into double stranded cDNA then uses DNA to amke complementary starand and degrade the DNA

78
Q

how is HIV integrated into HIV

A

integrase that was packaged in the virus

79
Q

when is HIV activated

A

when T cell is activated

80
Q

if T cell with HIV is activated what happens

A

transcription and translation of the HIV

81
Q

after transcription and trnlsation what will HIV do

A

bud from the cell membrane

82
Q

gp120 initiall binds to

A

CD4

83
Q

following binding to CD4 of gp120 causes

A

conformational change

84
Q

after gp120 to CD4 what happens

A

conformation change that allows it to bind to CCR5 or CXCR4

85
Q

what part of HIV drives fusion

A

gp41

86
Q

HIV RNA is transcribed by

A

viral reverse transcriptase

87
Q

activity of reverse transcriptase:

A

Complementary DNA transcribed from RNA genome

RNase activity destroys RNA strand

Complementary DNA from DNA template

(RNA dependent DNA polymerase and DNA dependent DNA polymerase)

88
Q

what pH does HIV have fusion

A

neutral PH

89
Q

resting t cells are not ____ to HIV

A

permissive

90
Q

review pg 37

A

don’t have to memorize all that stuff just review env

91
Q

is HIV virus ever eliminated

A

no

92
Q

why is there elecation of CD4 t cells afte the first drop in untreated HIV infection

A

cytotoxic t cell response, but the CD4 will never go back up to the normal CD4 levels w/out drug treatment

93
Q

how long are ppl infected with HIV asymptomatic

A

10 years

94
Q

even though CD4 t cells increase w/ untreated HIV, eventually

A

they will slowly declinign and will enter to symptomatic phase and AIDS

95
Q

why can’t immune system clear HIV

A

b/c the CD4 T cells die due to the infection

96
Q

there is latent viral reservoir for HIV in

A

lympohid tissue

97
Q

evidence of exhaustion of what cells during HIV infection

A

cytotoxic t cells

98
Q

infected CD4 t cells die as a result of what in HIV

A

the budding

99
Q

b/c HIV induces fusion @ plasma membrane it can lead to formation f

A

syncytia

100
Q

syncytia in HIV, describe

A

uninfected CD4 t cells can aquire by fusing with the infected CD4 t cells

101
Q

can get exhaustion f CD8 cells and what cells in HIV

A

CD4 T cells

102
Q

what is the window period of HIV

A

high viral titers but will test negative for ELISA for HIV but pt is very infectious

103
Q

cell responsible for maintaing HIV virus at low level is

A

cytotoxic T cells

104
Q

what are constitutional symptoms of HIV

A

non descriptive, just like loss of eight, night sweats, etc. can appear with variety of infections

105
Q

in brain HIV can lead to formation of

A

syncitia

106
Q

how can you get formation of synctia in brain due to HIV

A

gp120 expressed on infected cell binds CD4 uninfected cell and they fuse

107
Q

what infections will pt with aids be vulnerable

A

things taht need Th1 and cell mediated immuniti. some fungi, virus

108
Q

review pg 47

A

47

109
Q

what is first test to see if somebody has HIV/AIDS

A

elisa

110
Q

if pt is positive in elisa for HIV/AIDS you will do

A

western blot

111
Q

what are you coating wells with in elisa for HIV

A

HIV antigen

112
Q

why are you coating wells w/ HIV antigen in elisa

A

if they are infected they will have antibodiy against HIV antigens

113
Q

in western blot for HIV you are looking for

A

body antibodies against it

114
Q

if pt has HIV specific antibody in elisa what will it look like

A

it will be colored

115
Q

describe western blot for HIV

A

virus and run it on gel to separate the viral proteins
transfer viral proteins onto membrane, they will bind to membrane
viral proteins separted from one another
if somebody has HIV they will have antibodies against more than one viral protein
have to have antibodies to at least 2 viral proteins
add serum to membrane

116
Q

western blot for HIV is

A

confirmatory -gives more info than elisa can

117
Q

review pg 49

A

49

118
Q

if you cannot determine if person is HIV pos or neg for HIV 1 and HIV2 you will do

A

nucleic acid test

119
Q

new elisa’s can detect HIV

A

much earlier

120
Q

how can you detect HIV earlier than 3rd generation immunoassay

A

4th generation that looks for actual viral detection or nucleic acid test

121
Q

goals of antiviral thearpy for HIV

A

supress HIV viral load
improve quality of life
preserve future therapeutic options
prevent HIV transmission

122
Q

when you suppress HIV load for HIV it allows

A

restoration of CD4

123
Q

the lower the level of HIV virus the less likely

A

they will transmit the virus

124
Q

how do antiretroviral drugs block virus entry of HIV

A

block CCR5
block fusion
inhibit gp41 fusion

125
Q

when HIV proteins are made there is polyprotein gp160 that has tobe

A

cleaved into gp120 and gp41

126
Q

how does antiretroviral drugs block HIV maturation

A

blocks the protease from cleaving gp160 into active gp120 and 41

127
Q

what are the classes of antiretroviral durgs

A

Nucleoside (and nucleotide) reverse transcriptase inhibitors (NRTIs)

Nonnucleoside reverse transcriptase inhibitors (NNRTIs)
Protease inhibitors (PIs)
Integrase inhibitors (IIs)
CCR5 antagonists
Fusion inhibitors target gp41
128
Q

what is HAART stand for

A

highly active anti-retroviral therapy

129
Q

what is in HAART

A

HAART = 2 NRTIs + a PI/NNRTI/II

pg 55

130
Q

use of multiple inhibitors for HIV means that

A

less likely the HIV will mutate and avoid suppresion

131
Q

regardless of CD40 t cell number in HIV you will

A

go on hard treatment of HIV

132
Q

whyat has been the issue with HIV vaccine development

A

Rapid generation of HIV variants.

Vaccines to elicit neutralizing antibodies fail to protect against the diverse HIV subtypes and quasi-species.

Vaccines designed to elicit CTL responses fail to provide protection.

Difficult to generate neutralizing antibodies in vivo.

133
Q

clinical presentation of omenn syndrome?

A

completel block: SCID
usually not complete block, present with SCID but there are some t and b cells. oligoclonal, elevated IgE
eosinophilia

134
Q

phenotype of DiGeorge syndrome?

A

thymus affected
complete will have thymic aplasia (rare)
usually thymic hypoplasia

135
Q

x linked proliferative syndrome clinical presentation?

A

fulminant EBV infection

136
Q

Wiskott-aldrich syndrome clinical presentation?

A

classic triad: small plaetlets and thrombocytopenia, severe eczema, recurrent pyogenic infections

137
Q

ataxia telangiectasia clinical presentation?

A

ataxia
recurrent infections largely lung and thymic
increase alpha fetoprotein
sometime decreased IgA (not understood)

138
Q

multiple myeloma clincal presentation?

A

back/bone pain
deposition of light chains
recurrent infections, renal failure

139
Q

serum abnormaility of multiple myeoloma

A

monolonal spike IgG

140
Q

waldernstrom’s macroglobulinemia clinical presentation

A

no bone pain or renal failure

141
Q

waldernstrom’s macroglobulinemia serum?

A

monoclonal spike IgM

plasma hyperviscosity

142
Q

receptor for HIV?

A

CD4

143
Q

coreceptor for HIV?

A

CCR5 or CXCR4

144
Q

non-permissive and permissive host cells for HIV

A

activated T celsl are permissive

resting are non permissive

145
Q

window period for HIV

A

period b/w when person infected and when they have antibodies/serum positive
can have high viral titers but screen as serumnegative

146
Q

agglutination reaction done for what two things

A

ABO blood typing

Rheumatoid factor test (it is IgM antibody specific for Fc portion of IgG)

147
Q

indirect and direct coombs test does what

A

if mom has antibody against recess G antigen

148
Q

what coombs test would you do to test mom for the recess b antigen

A

indirect

149
Q

in antibody excess or antigen excess do not get formation of

A

precipitant - cannot form lattice structure

150
Q

when antibody binds to antigen at zone of equivalence they will

A

percipitate in gel

151
Q

describe ouchterlony analysis

A

poke holes
if they are specific they will precipitate
will form line of perciptate in gel called percipitate line
antibody defuses out from well

review on pg 67

152
Q

line of identity says

A

what is coming out of the wells is the same

153
Q

line of non identity says

A

what is coming out of wells is not the same

154
Q

line of partial identity

A

they share epitopes but not exactly the same

155
Q

spur is line of

A

partial identity - antigens share an epitope

156
Q

Immunoelectrophoresis describe

A

add serum in two wells from testing individual and control
albumin goes towards positive electrode
Ig go toward negative electrode
in central part add anti-serum against human serum and allow it to diffuse out
when antibodies (antihuman serum) meets components in serum they are reactive against they will form percipient lines

157
Q

what is one of initial test to see if someone has XLA

A

Immunoelectrophoresis

Immunology Block 4 (10 decks)

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