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Step 1 > Immunology > Flashcards

Immunology Flashcards

1
Q

lymph node follicle function

A

B cell localisation and proliferation

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2
Q

follicles are found in

A

the outer cortex

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3
Q

types of follicles

A

primary - dense and dormant

secondary - pale germinal centre, active

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4
Q

closely packed lymphocytes and plasma cells

A

lymph node medulla

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5
Q

reticular cells + mpg

A

medullary lymphatics

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6
Q

lymph paracortex holds

A

T cells

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7
Q

function of paracortex

A

endothelial vessels letting T and B cells enter blood

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8
Q

mediastinal lymph nodes

A

trachea and oesophagus

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9
Q

lymph drainage for skin above umbilicus

A

axillary

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10
Q

para-aortic lymph node drainage

A

testes, ovaries, kidneys, uterus

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11
Q

superficial inguinal lymph nodes

A

anal canal below pectinate line, skin below umbilicus (not popliteal area), scrotum/ vulva

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12
Q

right lymphatic duct

A

right side of body above diaphragm

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13
Q

thoracic duct

A

everything that isn’t right lymphatic duct –> left subclavian&internal jugular

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14
Q

barrel hoop basement membrane

A

spleen

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15
Q

white pulp - T cells

A

periarteriolar lymphatic sheath

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16
Q

White pulp - B cells

A

follicles

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17
Q

Marginal zone of spleen

A

between white and red pulp

contains mpg + specialised B cells

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18
Q

where do antigen presenting cells present in the spleen?

A

marginal zone

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19
Q

Splenic dysfunction causes

A

decreased IgM, complement, C3b

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20
Q

Asplenic organism infection

A 
Encapsulates - Please SHINE my SKiS
Pseudomonas aeuriginosa
Strep pneumoniae
Haem flu B
N. meningitidis
E.coli
Salmonella
Klebsiella pneumoniae
Group B Strep
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21
Q

Where is the thymus derived from?

A

Third pharyngeal pouch

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22
Q

Types of T cell in the thymus

A

medulla - mature

cortex - immature

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23
Q

Hassall corpuscles are found in

A

the medulla of the thymus

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24
Q

what do hassall corpuscles contain?

A

epithelial reticular cells

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25
Q

myasthenia gravis neck lump

A

enlarged thymus

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26
Q

innate immunity secreted proteins

A

lysozyme, complement, CRP, defensins

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27
Q

TLR

A

toll like receptor used to recognise pathogens in innate immunity

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28
Q

e.g. of pathogen-associated molecular pattern and what recognises it

A

innate immunity e.g. LPS toxin

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29
Q

MHC encoded by

A

HLA genes

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30
Q

MHC I coded by

A

HLA - A, B, C

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31
Q

MHC II coded by

A

HLA - DP, DQ, DR

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32
Q

Where is MHC I expressed?

A

All nucleated cells

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33
Q

What does MHC I do?

A

presents to CD8 cytotoxic cells

viral/ cytosolic proteins (endogenous)

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34
Q

How do MHC I expressing cells load antigens?

A

in RER, delivered via TAP

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35
Q

B2-microglobulin

A

MHC I

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36
Q

What expresses MHC II?

A

APCs

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37
Q

What does MHC II do?

A

bacterial proteins (exogenously synthesised antigens)

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38
Q

HLA A3

A

Hemochromatosis

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39
Q

HLA B8

A

Addison’s disease, myasthenia gravis

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40
Q

HLA DQ2/8

A

Celiac disease

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41
Q

HLA DR2

A

MS, hay fever, SLE, Goodpasture syndrome

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42
Q

HLA DR3

A

SLE, DM-1, Grave’s, Hashimoto’s, Addison’s

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43
Q

HLA DR4

A

RA, DM-1, Addison

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44
Q

HLA DR5

A

Pernicious anaemia, Hashimoto’s

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45
Q

perforin + granzymes

A

NK cells

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46
Q

NK cells increased activity

A

IL-2, IL-12, INF-a, IFN-b

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47
Q

When do NK cells activate?

A

activation signal
No MHC-I molecules
antibody dependent

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48
Q

What does antibody-dependent cell-mediated cytotoxicity and how?

A

NK cells activated by CD16 binding the Fc of I

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49
Q

CD4 cells

A

help B cells make antibodies, produce cyokines

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50
Q

CD8 cells

A

kill virus infected cells

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51
Q

autoimmune polyendocrine syndrome-1

A

AIRE deficiency

doesn’t apoptose autoimmune reacting T cells

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52
Q

Th1 cells secrete

A

IFN-y

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53
Q

What do Th1 cells do?

A

activate mpg, and Tk cells

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54
Q

Th1 differentiation

A

INF-y, IL-12

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55
Q

Th1 inhibition

A

IL- 4, 10

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56
Q

Th2 cells secrete

A

IL-4, 5, 10, 13

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57
Q

What do Th2 cells do?

A

recruit eosinophils for parasites, promotes IgE from B cells

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58
Q

Differentiation of Th2 cells

A

IL-4

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59
Q

Inhibition of Th2 cells

A

IFN-y

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60
Q

What is factor released by antigen presenting cells?

A

IL-12

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61
Q

Mpg stimulated by

A

IFN-y

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62
Q

Regulatory T cells

A

supress CD4+8

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63
Q

Regulatory T cells express

A

CD3, 4, 25, FOXP3

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64
Q

Regulatory T cells produce

A

IL-10, TGF-B

anti-inflammatory

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65
Q

antigen presenting cells

A

B cell, mpg, dendritic cells

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66
Q

naive t-cell acitvation by

A

dendritic cell

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67
Q

proliferation of T cells

A

CD28, B7 (CD80/86)

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68
Q

Class switching relies on

A

CD40 on Th hells (CD4)

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69
Q

variable Ig region

A

Fab

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70
Q

Fc region

A

fixed

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71
Q

Heavy chain

A

Fc and Fab regions

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72
Q

Light chain

A

Fab only

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73
Q

Fc region of IgM and IgG

A

fix complement

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74
Q

What determines the Ig isotype?

A

Fc region

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75
Q

VJ

A

light chain

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76
Q

V(D)J

A

heavy chain

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77
Q

how does antibody diversity happen?

A

random addition of nucleotides to DNA during recombination

Uses terminal deoxynucleotidyl transferase

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78
Q

where do B cells undergo isotype switching?

A

germinal centre of lymph node

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79
Q

what is isotype switching mediated by?

A

cytokines and CD40L

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80
Q

IgG

A 
secondary response to antigen
serum
fixes complement
crosses placenta
opsonizes bacteria
neutralises bacterial toxins and viruses
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81
Q

IgA

A

dimer (with J chain)
prevents bacteria/virus attachment to mucous membranes
Peyer’s patches produce, released in secretions
most produced antibody

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82
Q

IgM

A

primary response to antigen
fixes complement
does not cross placenta (mummy only)
pentomer (J chain)

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83
Q

IgD

A

surface of many B cells and in serum

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84
Q

IgE

A

mast cells + basophils
cross links when exposed to allergen
type I hypersensitivity (histamine)
low concentration in serum

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85
Q

what has to be present to allow for presenting?

A

peptide components

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86
Q

e.g. of bacteria with no peptide components

A

gram -ve bacteria

can’t be presented

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87
Q

Upragulated in the acute phase

A 
inFlammation Fuels A High Concentration
Ferritin
Fibrinogen
Amyloid A
Hepcidin
CRP
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88
Q

Hepcidin

A

decreases iron absorbtion, release from mpg –> anaemia of chronic disease

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89
Q

Classic complement pathway activation

A

IgG or IgM anigen-antibody complex

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90
Q

Lectin complement pathway activation

A

mannose/ sugar

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91
Q

Alternative complement pathway activation

A

spontaneous and microbial surfaces

92
Q

C3a, 4a, 5a

A

anaphylaxis

93
Q

C5a

A

neutrophil chemotaxis

94
Q

what do opsonins do? what are they?

A

C3b, IgG

enhance phagocytosis, help clear immune complexes

95
Q

what helps inhibit complement activation on self cells?

A

DAF (CD55)

C1 esterase

96
Q

C1 esterase inhibitor deficiency

A

hereditary angioedema - unregulated kallikrein activation

don’t use ACE inhibitors

97
Q

C3 deficiency

A

increase risk of sinus and resp infections, type III hypersensitivity

98
Q

C5-9 deficiencies

A

increases susceptibility to neisseria bacteremia

99
Q

DAF deficiency

A

complement mediated lysis of RBCs (PNH)

100
Q

IL stimulation pneumonic

A 
Hot T-Bone stEAK
1 - fever
2 - T cells
3 - bone marrow
4 - IgE
5 - IgA
6 - aKute phase proteins
101
Q

IL-1

A

fever, acute inflammation, osteoclasts, recruit WBC

102
Q

IL-6

A

fever, acute phase proteins

103
Q

IL-12

A

NK cells, Th1

104
Q

TNF-a

A

spetic shock, activates endothelium, WBC recruitment, vascular leak

105
Q

Mpgs secrete

A

IL-1, 6, 8, 12, TNF-a

106
Q

Secreted by T cells

A

IL-2, 3

107
Q

IL-3

A

bone marrow stem cells

108
Q

IL-4

A

T –> Th2, B cell growth, IgE –> IgG

109
Q

IL-5

A

B cell growth, –> IgA, eosinophils

110
Q

IL-10

A

anti-inflammatory, decreases MHC II + Th1, inhibits mpg, dentritic cells

111
Q

Interferons

A

interfere with viruses

112
Q

T cell receptors which are co-receptors for HIV

A

CXCR4/CCR5

113
Q

regulatory T cell cell surface proteins

A

CD4, CD25

114
Q

B cell surface proteins

A

CD19, 20, 21, 40

115
Q

Receptor for EBV

A

CD21 on B cells

116
Q

Mpg surface proteins

A

CD14, 40, CCR5, MHC II, B7, Fc, C3b

117
Q

NK cells surface proteins

A

CD16, Cd56

118
Q

Haematopoietic stem cell surface protein

A

CD34

119
Q

anergic

A

can’t be activated

120
Q

bacterial toxin superantigens

A

cross link, no need for costimulation

121
Q

how do endotoxins activate mpgs?

A

TLR4/CD14 binding

122
Q

passive vaccination

A

To Be Healed Very Rapidly

Tetanus, botulinum, HBV, Varicella, Rabies

123
Q

live attenuated vaccines

A

BCG, MMR, influenza, polio, varicella, yellow fever

124
Q

live attenuated vaccine response

A

cellular and humoral

125
Q

inactivated/ killed vaccine response

A

humoral response

126
Q

inactivated/killed vaccines

A

RIP Always

Rabies, Influenza, Polio (salk), hepA

127
Q

hypersensitivities

A

ACID

Anaphylaxis, cytotoxic, immune complex, delayed

128
Q

type I

A

free antigen cross links IgE

129
Q

IgE reaction type I

A

vasoactive amine release

130
Q

delayed anaphylactic response

A

arachidonic acid metabolites

131
Q

type II reaction

A

IgM, IgG bind to fixed antigen

shouldn’t bind

132
Q

type III

A

IgG activates complement, neutrophils release lysosomal enzymes

133
Q

type III associated with

A

SLE, PAN, strep glomerulonephritis, serum sickness

134
Q

serum sickness

A

type III

antibodies to forein proteins are produced, deposited in membranes and fix complement –> tissue damage

135
Q

Arthus reaction

A

type III, immune complex formation in skin

136
Q

Type IV

A

delayed T cell mediated, release cytokines

137
Q

e.g. type IV

A

contact dermatitis, GVHD, MS

138
Q

transfusion, urticaria, pruitus, wheeze, fever

A

allergic reaction
I hypersensitivity against plasma proteins
antihistamine

139
Q

transfusion, fever, headache, chills, flushing

A

febrile nonhemolytic transfusion reaction

II hypersensitivity, host antibodies against donor HLA antigens and WBCs

140
Q

transfusion, fever, hypotension, tachypnea, tachy, flank pain, hemoglobinuria, jaundice

A

acute hemolytic transfusion reaction

type II - ABO issue or extravascular hemolysis

141
Q

Anti ACh

A

Myasthenia rgavis

142
Q

Anti-basement membrane

A

Goodpasture’s

143
Q

Anticentromere

A

Scleroderma

144
Q

Anti-desmoglein

A

pemphigus vulgaris

145
Q

anti-smith

A

SLE

146
Q

Anti-glutamic acid decarboxylase

A

DM-1

147
Q

antihemidesmosome

A

bullous pemphigoid

148
Q

anti-histone

A

drug induced lupus

149
Q

anti-Jo-1, anti-SRP, anti-Mi-2

A

polymyositis, dermatomyositis

150
Q

antimicrosomal, antithyroglobulin

A

hashimoto’s

151
Q

anti-mt

A

primary biliary cirrhosis

152
Q

antiphospholipase A2 R

A

primary membranous nephropathy

153
Q

anti-Scl-70

A

scleroderma

154
Q

anti-smooth muscle

A

autoimmune hepatitis 1

155
Q

Anti-SSA/ SSB =

linked with

A

Ro, La

Sjogren’s

156
Q

Anti-U1 RNP

A

mixed CTD

157
Q

voltage gated Ca channel antibodies

A

Lambert-Eaton

158
Q

anti-CCP

A

RA

159
Q

BTK gene
is
defect
causes

A

tyrosine kinase gene
X linked (Bruton) a-y-globulinaemia
no mature B cells

160
Q

recurrnet bacterial and enteroviral infections after 6 months, decreased Ig, absent tonsils

A

a-y-globulinaemia

161
Q

most comon primary immunodeficiency

A

selective IgA deficiency

162
Q

airway and GI infection, atopy, anaphylaxis to IgA

A

selective IgA deficiency

163
Q

defect in B cell differentiation

A

common variable immunodeficiency

164
Q

immunodeficiency in 20-30s

A

common variable immunodeficiency

165
Q

decreased plasma cells, decreased Ig, autoimmune disease, 25yrs

A

common variable immunodeficiency

166
Q

tetany, recurrent odd infections, heart defects

A

DiGeorge

don’t develop 3rd and 4th pharyngeal pouches

167
Q

decreased INF-y, bacterial and fungal infections, had BCG vaccine recently

A

IL-12 receptor deficiency

168
Q

coarse facies, cold abscesses, retained primary teeth, eczema

A

autosomal dominant hyper-IgE syndrome

Job syndrome

169
Q

Job syndrome

A

Th17 deficiency - STAT3 mutation

170
Q

no thymic shadow

A

severe combined immunodeficiency - SCID

IL-2R chain

171
Q

failure to thrive, diarrhoea, thrush, recurrent infection

A

SCID

172
Q

Defect in ATM gene causes, called

A

can’t repair DNA breaks

Ataxia-telangiectasia

173
Q

ataxia, spider angioma, IgA deficiency

A

ataxia-telangectasia

174
Q

raised AFP, low IgA, G, E, lymphopenia, cerebellar atrophy

A

ataxia-telangectasia

175
Q

defective CD40L, causes, called

A

Low IgG, A, E
Normal/ High IgM
pyogenic infection
Hyper-IgM syndrome

176
Q

WAS gene defect - issue, called

A

T cells cannot recognise actin cytoskeleton

Wiskott-Aldrich

177
Q

thrombocytopenia, eczema, recurrent infection, high IgE, IgA

A

Wiskott-Aldrich

178
Q

defect in LFA-1 integrin

A

leukocyte adhesion deficiency

179
Q

recurrent bacterial skin and mucosal infection, absent pus, impaired wound healing
called
what about neutrophils?

A

Leukocyte adhesion deficiency

Lots of neutrophils, not at infection site

180
Q

LYST defect, called, causes

A

Chediak-Higashi

microtubule dysfunction

181
Q

recurrent pyogenic infection from stap and strep, albinism, peripheral neuropathy, neurodegeneration
will see
called

A

giant granulocytes, pancytopenia, coagulation defect

Chediak-Higashi

182
Q

defect of NADPH oxidase

A

chronic granulomatous disease

can’t kill phagocytosed catalase positive material

183
Q

increased susceptibility to catalse positive organisms

A

chronic granulomatous disease

184
Q

abnormal dihydrorhodamine test

A

chronic granulomatous disease

185
Q

catalase positive organisms

A

Nocardia, Pseudomonas, Listeria, Aspergillus, Candida, E coli, Staph, serriatia, B cepacia, H pylori

186
Q

hyperacute transplant rejection

A

thrombosis of graft vessels

187
Q

acute transplant rejection

A

Tk cells, IV hypersensitivity

188
Q

Chronic transplant rejection

A

Th cells, II and IV hypersensitivity

189
Q

Cyclosporine, tacrolimas

A

calcineurin inhibitor, prevents IL-2 transcription

190
Q

cyclosporine use

A

transplant rejection prophylaxis, psoriasis, RA

191
Q

cyclosporine s.e.

A

nephrotoxicity, htn, hyperlipidaemia, neurotoxicity, gingival hyperplasia, hirsuitism

192
Q

Binds FK506

A

tacrolimus, sirolimus

193
Q

use tacrolimus

A

transplant rejection prophylaxis

194
Q

tacrolimus s.e.

A

diabetes, nephrotoxicity, htn, hyperlipidaemia

195
Q

sirolimus =

A

rapamycin

196
Q

sirolumis use, s.e

A

kidney transplant rejection prophylaxis

pancytopenia, insulin resistance, hyperlipidaemia

197
Q

daclizumab, basiliximab

A

block IL-2R

198
Q

use daclizumab, basiliximab, s.e.

A

kidney transplant rejection prophylaxis

edema, htn, tremor

199
Q

azathioprine

A

inhibits lymphocyte proliferation by blocking necleotide synthesis

200
Q

use azathioprine, s.e.

A

transplant rejection, RA, Crohn’s, glomerulonephritis, autoimmune conditions
leukopenia, anemia, thrombocytopenia

201
Q

c.e. azathioprine

A

allopurinol (both degraded by xanthine oxidase)

202
Q

mycophenolate mofetil

A

inhibits IMP dehydrogenase - prevents B and T cell synthesis

203
Q

use mycophenolate mofetil, s.e.

A

transplant rejection, lupus nephritis

GI, pancytopenia, htn, hypergylcaemia, CMV infection

204
Q

corticosteroids action

A

inhibit NF-kB

decrease cytokine transcription

205
Q

aldesleukin
is
for

A

IL-2
RCC
met. melanoma

206
Q

filgrastim
is
for

A

G-CSF

recovery of bone marrow

207
Q

Sargramostim
is
for

A

GM-CSF

Recovery of bone marrow

208
Q

IFN-a use

A

chronic hep B and C, Kaposi sarcoma, malignant melanoma

209
Q

IFN-y use

A

chronic granulomatous disease

210
Q

Romiplostim, eltrombopag
is
use

A

thrombopoetin receptor agonist

thrombocytopenia

211
Q

oprelvekin
is
use

A

IL-11

thrombocytopenia

212
Q

Alemtuzumab, for

A

CD52

CLL, MS

213
Q

Bevacizumab, for

A

VEGF

Colorectal ca, RCC

214
Q

Cetuximab, for

A

EGFR

IV colorectal ca., head and neck ca

215
Q

Rituximab, for

A

CD20

B cell lymphoma, CLL, RA, ITP

216
Q

Trastuzumab

A

HER-2

217
Q

Adalimumab, certolizumab, infliximab, use

A

soluble TNF-a

IBD, RA, AS, psoriasis

218
Q

eculizumab, use

A

complement C5 protein

PNH

219
Q

Natalizumab use

A

a4-integrin

MS, Crohn’s

220
Q

Natulizumab + JC virus

A

PML risk

221
Q

denosumab

A

RANKL, OP

222
Q

omalizumab, use

A

IgE, allergic asthma

223
Q

palivizumab, for

A

RSV F protein

RSV prophylaxis

224
Q

Ranibizumab, bevacizumab

for

A

VEGF

Neovascular age-realted macular degeneration

225
Q

N-acetylcyctine

A

given in pcm overdose, precursor to GSG (glutathione)

226
Q

What is oxidative burst?

A

the method of producing free radicals to kill phagocytosed material

227
Q

What is decreased in hyper IgE syndrome?

A

decreased TNF-y

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