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Haematology > CLASP Immunology > Flashcards

CLASP Immunology Flashcards

1
Q

Where do allergen-specific B cells encounter the allergen?

A

primary follicles of secondary lymphoid follicles

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2
Q

What MHC molecule do B cells present peptides in?

A

MHC-II

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3
Q

What is the function of IL-4 secreted by Th2 cells?

A

triggers class switching in activated B cells

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4
Q

What are the functions of IL13 and IL5 produced by Th2 cells?

A

promote recruitment, activation and survival of eosinophils

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5
Q

What substances do mast cells/eosinophils release?

A

histamine; tryptase and heparin

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6
Q

What pro-inflammatory cytokines do mast cells/ eosinophils produce?

A

TNFa and IL4

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7
Q

What position should you put a patient with anaphylaxis in?

A

lie patient flat and raise legs

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8
Q

What is the dose of adrenaline given for anaphylaxis?

A

IM dose of 1:1000 (500mcg)

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9
Q

When does type III hypersensitivity reactions occur?

A

excess of antigen causes immune complexes

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10
Q

What is the difference in antigen between type 2 and type 3 hypersensitivity?

A

type 2: bound to cell surface; type 3: soluble antigen

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11
Q

What is the function of C3a in type 3 reactions?

A

mediates induction of granule release from mast cells

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12
Q

What is the function of C5a in type 3 reactions?

A

recruitment of neutrophils in to the tissue

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13
Q

What are the 3 killing mechanisms of neutrophils?

A

phagocytosis; degranulation and NETs

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14
Q

What chemical is involved in phagocytosis?

A

superoxide hydrogen peroxide

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15
Q

What chemicals are invovled in degranulation?

A

lysozyme; NADPH oxidase; myeloperoxidase

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16
Q

What are NETs

A

neutrophils extracellular traps which are structures of DNA that kill and tap microbes

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17
Q

What type of T cells are invovled in the initial steps of type 4 reactions?

A

CD4 Th1 cells

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18
Q

What cytokine do CD4 Th1 cells release in type 4 reactions?

A

IFN gamma

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19
Q

What is the fcuntion of IFNgamma?

A

enhance macrophage activity and promote further inflammation and recruitement of other cells eg CD8

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20
Q

How do cytotoxic T cells destroy cells?

A

peptide/MHC-I manner

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21
Q

What type of drugs can cause false positives in skin prick testing?

A

monoamine oxidase inhibitors and TCAs

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22
Q

What are the typical signs of small vessel vasculitis?

A

purpura; vesiculobullous lesions; urticaria; glomerulonephritis; alveolar haemorrhage; cutaneous extravascular necrotising granulomas; splinter haemorrhages; scleritis/episcleritis/uveitis

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23
Q

What are the typical signs of medium vessel vasculitis?

A

cutanoeous nodules; ulcers; livedo reticularis; digital gangrene; mononeuritis mutliplex; microaneuryms

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24
Q

What are the typical signs of large vessel vasculitis?

A

limb claudication; asymmetric BPS; absence of pulses; bruit; aortic dilatation

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25
Q

Give examples of large vessel vascultides?

A

takayasu arteritis; GCA

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26
Q

Give example of medium vessel vasculitis?

A

PAN; kawasaki

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27
Q

Give examples of vasculitis type 3 hypersensitiity?

A

SLE; PAN

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28
Q

Give examples of vasculitis which are type 4 hypersensitibity?

A

GCA; takayasu

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29
Q

Where does inflammation in the vessels in takayasu start?

A

in the adventitia and moves toward intima

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30
Q

What are the immunological features of steroid use?

A

lymphocytopenia; neutrophilia; secondary immunodeficiency

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31
Q

What are the endocrine features of steroid use?

A

DM; HT; increased appetitie and weight gain; adrenal cortex suppression

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32
Q

What are the skin/soft tissue features of steroid use?

A

cushingoid appearance; abdominal striae; acne; hirsutism; oedema; increased risk of skin cancer

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33
Q

What are the neuro features of steroid use?

A

neuropathy; pseudomotor cerebri/ IIH

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34
Q

What are the ophthalmic features of steroid use?

A

cataracts; narrow-angle glaucoma

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35
Q

What are the MSK features of steroid use?

A

oseopenia; AVN; myopathy

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36
Q

What are teh CVS features of steroid use?

A

HT

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37
Q

What type of hypersensitiity is cryoglobulinaemiac vasculitis?

A

type 3

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38
Q

What mediates the damage in cryoglobulinaemic vascultiis?

A

complemetn

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39
Q

What is the function of RF in RA?

A

predicts extra-articular features

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40
Q

What are the psychiatryic effects of acute steroid use?

A

insomnia; agitation; depression/anxiety; psychosis

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41
Q

What are the GI effects of actue steroid use?

A

GI haemorrhage

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42
Q

how do steroids cause GI haemorrhage?

A

inhibit phospholipase A2 which converts cell membrane phsopholipis into arachidonic acid- reduced LTs and PGs

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43
Q

What activates complement in the classical pathway?

A

Fc portion of antiobdy

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44
Q

Which type of antibody is best at activating complement?

A

IgM- pentamer

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45
Q

Which antibodies can activate complemetn?

A

IgM and IgG

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46
Q

What complemetn binds to the Fc region of hte heavy hcain?

A

C1

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47
Q

What is C4b2a known as?

A

C3 convertase

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48
Q

What part of C1 binds to antibody?

A

C1q

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49
Q

What must happen for C1q to become firmly fixed?

A

cross link at least 2 antibody molecules before firmly fixed

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50
Q

What does the binding of C1q cause?

A

activation og C1r which activates C1s

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51
Q

What is the function of C1qrs?

A

cleaves C4 into C4a and C4b; and C2 into C2a and C2b

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52
Q

What is C4bC2aC3b known as

A

C5 convertase

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53
Q

What happens in the alternate pathway?

A

bacterial, fungal and viral cells surfaces bind C3 and factor B

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54
Q

What is the C3 and factor B cleaved by?

A

factor D

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55
Q

What does cleavage by factor D procue?

A

C3bBb

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56
Q

What is the function of C3bBb?

A

C3 convertase

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57
Q

What initiates the lectin pathway?

A

mannose-binding lectin to bacterial surface

58
Q

What does binding of MBL to a pathogen result in?

A

association og 2 serin proteases MASP-1 and MASP-2

59
Q

What does the activation of the MASPs restul in?

A

cleave of C4 and C2

60
Q

What forms MAC?

A

C5b which activates C6-C9

61
Q

What are isohaemoagglutins?

A

natural IgM antibodies to group antigens A and/or B

62
Q

When would expect specific antibodies to protein antigens?

A

within 2 weeks

63
Q

When would youexpect an antibody response to polysaccharide antigen?

64
Q

What is the difference in onset between congenital antibody deficiencies and congential cellular immunodeficinesi?

A

antibody- onset 7-9 months usually (3-18 months); first months of life for cellular

65
Q

What is the function of RAG-1 and RAG-2 ?

A

first cleavage step in somatic recombination of immunoglobulin genes

66
Q

What condiiton have Rag mutations?

67
Q

What is the most severe form of SCID?

A

reticular dysgenesis

68
Q

What name is Kostamnn syndrome also known as?

A

severe congential neutropenia

69
Q

What is the inheritance of kostmann syndrome?

70
Q

What side effects is granulocyte colony stimulating factor implicated in?

A

AML; myelodysplastic syndrome

71
Q

What is the most common genetic cause of CGD?

A

x-linked deficinecy of NADPH oxidase

72
Q

What is the test fo CGD?

A

nitroblue tetrozolium test- a dye sensitive to hydrogen peroxide

73
Q

What is the second commonest cause of pancreatic exocrine insufficnecy?

A

schwachman-diamond syndrome

74
Q

What is the inheritance of cyclic neutropenia?

75
Q

What is the most common form of neutropenia seen in young children?

A

primary autoimmune neutropenia

76
Q

What is the mutation in XLA?

A

brutons tyrosine kinase?

77
Q

What does the mutations in BTK cause?

A

block in B cell maturation

78
Q

What is the cause of hyper-IgM?

A

B cell inability for class switching

79
Q

What type of infections are seen with antibody deficiency?

A

encapsulated bacteria

80
Q

How can leukocyte adhesion deficiency present with?

A

severe gingivostomatitis and dental erosion

81
Q

What producd by macrophages stimualtes the liverto produce acute phase proteins?

A

TNFa; IL1 and IL6

82
Q

What causes leukocyte adhesion deficiency?

A

mutation in leucocyte integrins

83
Q

What are the 3 groups of moelcules which interact to cause adhesion and transmigration?

A

leukocyte integrins; endothelial intercellular adhesion molecules and glycosaminoglycans or selectins

84
Q

What molceules are involved in firm adhesion?

A

integrins and ICAMs

85
Q

What is dariers sign?

A

urticaria after stroking or rubbing affected skin

86
Q

What conditions cause dariers sign?

A

systemic mastocytosis; urticaria pigmentosa

87
Q

What natibody is reduced with CVID?

88
Q

What drugs have been implicated in the development of CVID?

A

anti-rhuematic and anticonvulsants (phenytoin)

89
Q

What are B cels in CVID not able to do?

A

form memory B cells and mature plasma cells

90
Q

What causes digeorge syndrome?

A

failure of pharyngeal pouches 3 and 4 to differentiate into thymus and parathyroid glands

91
Q

what is IgG2?

A

sublass of IgG that is produced in reposnse to polysacchraide antigen by B cells in the spleen without T cells

92
Q

What other antibiotic classes wre pencillin allergy patients often also allergic to?

A

cephalosporin and carbapenems

93
Q

What chemokines are invovled in chemotaxis?

A

IL8; TNFy and C5a

94
Q

Give examples of encapsulated bacteria?

A

strep. pneumo; h. influenzae

95
Q

What other type of infections are patients with antibody deficiency more likely to get?

A

infectious diarrhoea

96
Q

How is the definitive diagnosis of CGD made?

A

male or female with abnormal NBT or respiratory burst in activated neutrophils who has mutations or family history

97
Q

Where are the mutations in CGD found?

A

NADPH oxdase copmlex

98
Q

What are the 2 types of genetic mutation found with CGD?

A

X-linked and AR

99
Q

What is the difference in X-linked and AR forms of CGD?

A

X-CGD is majority of patients and present earlier and have more severe disease

100
Q

What are the symptoms of X-CGD?

A

failure to thrive; severe bacterial and fungal infections

101
Q

What is the differential diagnosis of CGD?

A

LAD; sarcoid; hyper-IgE syndrome

102
Q

How are neutrophils activated?

A

binding of bacterialor fungal frgamnets to Fc, complement or PRRs, particle is internalised and cell activated

103
Q

Where are the ROS and toxins found in the neutrophil?

104
Q

What is the function of hte H ion produced by the NADPH oxidase complex?

A

acidification in phagosome speeds up breakdown

105
Q

What is the respiratory burst?

A

increase in O2 consumption during production of microbicidal oxygen metabolites

106
Q

The respiratory burst occurs in which cells/

A

neutrophils and macrophages

107
Q

What is SCID?

A

adaptive immune responses do not occur due to lack of T cells and impaired B function

108
Q

How is the diagnosis of SCID made?

A

male/female patient less than 2 years with <20% CD3 T cells and absolute lymphocyte count <300

109
Q

What are the common presenting illnesses in SCID?

A

PCP; significant bacterial infections and disseminated BCG infection

110
Q

What are the symptoms of SCID?

A

failure to thrive, persisten diarrhoea; resp symptoms and/or thrush in first 2-7 months

111
Q

What is the prognosis of SCID?

A

fatal in first 2 years without treatment

112
Q

What infections are seen with complement deficiency?

A

> 1 episode of invasive mengococcal infection or other neisserial bacterial

113
Q

What are the main tests of complement system activity?

A

CH50 and AP50

114
Q

What does the CH50 test asses?

A

classical complement pathway

115
Q

What would result in an abnormal CH50 test?

A

deficiencies of C1-C9 or consumption of complement due to immune complexes

116
Q

What is the function of the AP50 test?

A

alternative pathway

117
Q

What is the MAC formed by?

A

C5b and C6-9

118
Q

What complement components are invovled in inflammation?

A

C5a and C3a

119
Q

What complement is an opsonin?

120
Q

Which complement is invovled in immune complex solubilisation?

121
Q

What are teh 2 main categories of complement problems?

A

disorders invovling inhibitors of complement system; activators of complement system

122
Q

What conditions are invovled with problem of inhibitors of complement?

A

hereditary angioedema; haemolytic -uraemic syndrome

123
Q

What is the diagnosis of LAD made with?

A

decreased intensity of expression of CD18 on neutrophils

124
Q

What gene encodes CD18?

A

beta2 integrin gene

125
Q

What are the features of LAD?

A

recurrent/persistent bacterial.fungal infections; leukocytosis; delayed separation of the umbilical cord; and/or defetive wound healing; periodonitis

126
Q

Which types of infection are particularly problematic with LAD?

A

staphylococcus; gram negative enteric bacteria nad fungal infections

127
Q

What is the diagnosis of XLA made with?

A

male patient with low levels of CD19+ B cells and mutation of BTK gene

128
Q

What are the common organisms in XLA?

A

strep pneumo and h.influenza

129
Q

When is the diagnosis of CVID usually made?

A

third of fourth decade

130
Q

What are the usual presenting features of CVID?

A

reucrrent infections invovling the ears; nasal sinuses; bronchi and lungs

131
Q

what does both low CH50 and AP50 suggest?

A

problem in terminal MAC pathway

132
Q

What is the function of immunoglobulin replacement therapy?

A

reduce freq of infections and risk of lung damage

133
Q

What is hypogammaglobulinaemia defined as?

A

value is less than 2 SD below age-adjusted normal

134
Q

what is the diagnosis of CVID?

A

low IgG with low IgA and/or IgM as well as defective antibody repsone to vaccine; exlusion of other PIDs

135
Q

What are the treatment options for LAD?

A

prophylactic antibiotics; haematopoeitic stem cell transplant

136
Q

What are the treatment optiosn for CGD?

A

prophylactic antibiotics/anti-fungals; IFNgamma; steroids

137
Q

What ILs and TNF can contribute to cachexia and fever?

A

IL1 and TNFa (cockexia- alpha is balls and 1 is shaft)

138
Q

What IL is involved in T cell activation?

A

Il2- 2 cell activation

139
Q

What IL is the bone marrow stimulant?

A

IL3- 3-some if you wanna bone

140
Q

what is the eosinophil activator?

A

IL5- 5 fingers on the hand, and hand looks like eosinophil-2 lobes

141
Q

What is the neutrophil chemotactic agne?

A

IL8- on side looks like infinity (most infinite WBC)

142
Q

What is the granuloma activator?

A

IFN-gamma (activates macrophages to make granulomas) G for granuloma

Haematology (29 decks)

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