Allergy/immunology Flashcards

1
Q

Resolution food allergy

A

Cows milk 85% by 8
Egg 70%
Peanut 20%
Fish 3%

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2
Q

Venom allergic reaction risk next event anaphylactic

A

10%

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3
Q

Drug urticaria

A

Last 6-12h and in 0.3%

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4
Q

Percent of infants with food allergy

A

10%

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5
Q

Anaphylaxis to egg and influenza vaccine

A

Do in hospital with 1/10th of dose

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6
Q

Adrenaline for anaphylaxis

A

1;1,000 / 0.3-0.5mg

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7
Q

Primary immunodeficiency presenting with recurrent sinopulm infections

A

CVID, XLA, transient hypogammaglobulinemia of infancy, complement def

Tx with ivig 4 weekly or subcutaneous ig weekly (300-600mg/kg/month) aim for igG 7-8g/L (doesn’t correct igA def)

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8
Q

XL hypogammaglobulinaemia caused by

A

Present at 6-8m when maternal levels fall
Bruton kinase def with absent B cells and low immunoglobulins (all)
No LN (lymphoid hypoplasia)
No tonsils
Poor response to vaccine

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9
Q

CVID clinically

A

Low IgG and decrease in IgA or IgM
Poor antibody response to vaccine

Ddx transient

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10
Q

SCID presentation

A

Broad infections, FTT, persistent diarrhoea, by 3m, no thymic shadow on cxr, total lymphocytes < 2.5
Fatal by 1 year
T and B cell failure
1/50,000 (45% XL)

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11
Q

XL hyper IgM syndrome presentation

A

40% pneumocystis jiroveci, cryptosporidium
T cell defect
CD40 ligand is the affected protein (can’t class switch)
Immunoglobulin Tx
Pcp prophylaxis
With BMT 70% survival

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12
Q

CGD signs and treatment

A

Defect in NADPH dep oxidase pathway

Signs:
Adenopathy, HSM, gingivitis, stomitis, abscess, diarrhoea, colitis
Raised Igs (Kell sratis in XL)
Catalase positive organisms

Dx: nitroblue tetrazolium test

Tx: Cotrimox and itraconazole prophylaxis
BMT

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13
Q

Leukocyte adhesion def 1 presentation

A

Most common with <1% normal expression CD18, delay cord, high leuks (WCC over 15)
Destructive gingivitis
Severe necrotising bacterial infections
BMT curative

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14
Q

C3 action

A

Half life 60 microsecond, opsonisation, solubilises immune complexes, enhances killing via MAC, potential humoral response

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15
Q

Which cytokines causes T cell proliferation

A

IL2

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16
Q

Digeorge Tx for immunodeficiency

A

BMT, thymic transplant curative

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17
Q

Selective IgA def clinically

A

1/700 Caucasian
Sporadic
Asymptomatic
Occ Resp and Gi infections

Anaphylaxis to blood products cos contain IgA
Assoc autoimmune disorders

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18
Q

IL-1 - 6 rolls

A

Hot T-bone sTEAk

IL-1 HOT (fever)made by macrophages causes fever, lymphocyte proliferation
IL-2 stimulates T cells (secreted by T)
IL-3 stimulatess bone marrow (secreted by T)
IL-4 induces Th2 and stimulates IgE production
IL-5 stimulates IgA production (proliferates eosinophils) Th2
IL-6 regulates CRP

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19
Q

Half life neutrophils

A

6 h

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20
Q

Symptoms of langerhans cell histocytosis

A

Common symptoms of LCH in children are recurrent rash, diabetes insipidus (24%) and
bone lesions (lytic usually scalp)
Seborrhaic dermatitis

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21
Q

SCID specific tests

A

ƒLymphocyte phenotype (i.e. numbers of T cells/subsets, B cells)
ƒ Lymphocyte proliferation responses (i.e. lymphocyte function)

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22
Q

Which IL causes T cell proliferation

A

2

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23
Q

Milk and egg allergy percent tolerate it baked

A

> 75%

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24
Q

Will next allergic reaction be worse

A

It’s a myth

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25
Q

Cow’s milk resolution age and percent

A

85% by age 8

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26
Q

Serum sickness reaction is a type 1-4?

A

Type III hypersensitivity reaction (immune complex mediated)

Also retaliated to autoimmune conditions

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27
Q

Steven johnsons syndrome and chronic renal transplant rejection are what type of hypersensitivity reaction

A

Type IV delayed type when sensitised Th1 cells activat and release cytokines and bind causing increase in macrophages and cytotoxic T cells

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28
Q

Type 1 and 2 hypersensitivity reactions are? Which illnesses

A

1: immediate IgE in anaphylaxis or hay fever
2: antibody mediated in haemolytic anaemia of newborn or graves

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29
Q

Double row of teeth with what syndrome

A

Hyper IgE

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30
Q

Hyper IgE triad

A

Abscesses, increased IgE and pneumatocoele pneumonia

31
Q

Immune cell important in transplant rejection

A

T cell (t for transplant)

32
Q

If brother allergic to peanuts sibling risk

A

5-10%

33
Q

Anaphylaxis to penicillin risk with cephalosporins

A

<5% (likely less than 1%)

34
Q

Serum sickness triad (eg adter thymoglobulin)

A

Rash (urticaria)
Migratory poly arthritis (joints)
Fever

35
Q

Half life of serum IgM

A

7 days

36
Q

Cows milk allergy 80% outgrow by

A

16

Milk too allergen then egg second

37
Q

IgE receptors mostly on

A

Mast cells

(Th2 cell sends IL3/4/5/9 to mast and eosinophils

38
Q

What cell produced antibodies

A

B cell

T cell CD4 (MHC II) and CD8 (MHC I)

39
Q

Mutation in NBN

Microcephalic immune def and increased cancer risk in

A

Nijmegen breakage syndrome

40
Q

Eye telegectasia and ataxia and risk infection

Test and dx?

A

AFP

Ataxia telegectasia

41
Q
Which of the following immunoglobulins fix complement when they bind to antigen? 
A. Only IgG. 
B. IgG and IgA. 
C. IgG, IgA and IgM. 
D. IgG and IgM. 
E. Only IgM.
A

D

42
Q

IL-5 role

A

acts as a growth and differentiation factor for both B cells and eosinophils

43
Q

Interleukin 1 (IL-1) is primarily produced by

A

Mast cells

44
Q

CVID risk of what infections

A

Encapsulated bacteria such as S pneumoniae, S pyogenes, and H influenzae are the most common pathogens.

45
Q

Moderate reaction to bee likelihood of anaphylaxis next time

A

10%

30-60% if previous anaphylaxis

46
Q

Food allergy afftcys what percent NZ infants

A

10% (5% overall)

47
Q

Present with recurrent sinopulmonary infections DDx

A

CVID
XLA
THI

48
Q

A type 2 helper T lymphocyte (Th2 cell) differs most from a type 1 helper T lymphocyte (Th1 cell) in which one
of the following?
A. Production of interleukin 3 (IL-3).
B. Production of interleukin 5 (IL-5).
C. Responsiveness to antigen presented by macrophages.
D. Surface expression of CD4.
E. Surface expression of major histocompatibility complex (MHC) class II molecules.

A

B

All IL starting with T and F secreted by T cells (Th1 secretes IFN gamma)

49
Q
Which one of the following major immunoglobulin classes in the human fixes the alternate complement 
pathway? 
A. IgA. 
B. IgD. 
C. IgE. 
D. IgG. 
E. IgM.
A

A

50
Q

FcER1 receptor is on what cell

A

Mast cell derived from CD4 haematopoetic progenitor cell

51
Q

CGD catalase positive organisms are

A

CGD Catalase-positive organisms: PLACESS for CATs

Pseudomonas, Listeria, Aspergillus, Candida, E-coli, S. aureus, Serratia

52
Q

Interferon one and two and TNF alpha

A
Interferons: 
Type I (alpha and beta): 
o Antiviral agents mainly produced by fibroblasts and 
monocytes. Inhibit viral RNA and DNA production, 
increase expression of MHC1 leading to enhanced lysis 
by cytotoxic T lymphocytes. 
o Antiproliferative function. 
Type II (gamma): 
o Gamma interferon activates macrophage and 
neutrophil intracellular killing, stimulates NK cells and 
enhances T cell responses by increasing MHCII 
expression. 
 TNFAlpha: increases phagocyte funct
53
Q

What cell in terminal centres predominate

A

B cells

54
Q

Half life igG

A

1 month

55
Q

What is in a mast cell graunule

A

histamine, various cytokines (such as tumour necrosis factor (TNF), IL-4) and mast cell-specific proteases (such as chymases, tryptases and carboxypeptidase A3 (CPA3) chondroitin, heparin

56
Q

Measles exposure (5 days prior and after onset rash) prophylaxis for 1 year old? Pregnant woman?

A

Can consider MMR in infant over 6m but need a second booster 4 weeks laster

immunocompromised or immune-deficient people
susceptible pregnant women
immune-competent infants aged under 6 months where there is no evidence of maternal immunity (presence of maternal antibody, or documentation of two MMR doses or previous history of measles infection) immune-competent children aged between 6 and 15 months, who are outside the 72-hour exposure window for MMR vaccine.

57
Q

Half life IgA IgM and IgE

A

5-7 days M and A

IgE 3 days

58
Q

Complement for chemotaxsis

A

C5a

59
Q

What protects complement cascade from inactivation

A

Properdin

60
Q

Initially all immature T cells (CD3) become CD4 or 8 what do these both do?

A

CD 4 are T helper cells which bind to MHC2 on APC and activate B cells to make immunoglobulins, activate macrophages

CD8 cells are NK cells and bind MHC1-Ag and kill viral infected and tumour cells

61
Q

Half life neutrophils

A

6 hours

62
Q

Complement pathway how does it work? What does a and b do

A

C1-4 classical
Usual cascade if known antigen
C3 randomly splits on own if unknown antigen
Then C5 joins C6,7,8,9 to form MAC (membrane attack complex)
A parts signal allergy like response and b parts bind proteins

63
Q

HPV and Hep B what type of vaccine?

A

Recombinant

HPV types 6, 11, 16, 18, 31, 33, 45, 52 and 58.

64
Q

Pneumococcus vaccine type

A

Conjugated

65
Q

Dihydrorhodamine (DHR) flow cytometric analysis is used to evaluate

A

granulocyte oxidative bursts and is the test of choice for the diagnosis of chronic granulomatous disease (CGD)

66
Q

12-24 month old with low albumin, protein losing enteropathy and microcytic anaemia possible cause?

A

Cow milk protein induced

67
Q

IL 7-18 rolls?

A

Maturation is Key at 21st for All Party Games

IL-7: maturation from marrow 
IL-8: chemotaxsis neutrophils
IL-10: decrease IL-2
IL-12: make Th1
IL-13: allergy 
IL-17: pro inflammatory
IL-18: IFgamna production
68
Q

Name the antigen or sending cells with MHC class two molecules?

A

B cells
Macrophages
Monocytes

69
Q

SCID screening from

A

No detected TREC T cell receptor excision circle

70
Q

STAT3 mutation in

A

Hyper IgE

71
Q

FoxP3 affected in

A

IPEX

72
Q

Adult range IgA IgG complements and IgM

A

IgM and complement 12m
IgG 5y
IgA adolescent

73
Q

Most common complement deficiency

A

2