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Royal College Study > Allergy/Immunology > Flashcards

Allergy/Immunology Flashcards

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1
Q

Secondary Causes of PID

A

Meds (steroids, chemo, anti epileptics) Infections (HIV, TB etc), Structural (CF, indwelling catheter, impaired membrane integrity), Malignancy, Other (DM, renal insufficiency, protein losing enteropathy, malnutrition, asplenia)

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2
Q

T cell Defect age of onset

A

2-6 months

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3
Q

T cell typical bacteria

A

Gram + and -ve bacteria

Mycobacteria

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4
Q

T cell typical fungi

A

Candida, PJP

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5
Q

T cell defect sites of infection

A

sinopulmonary, GI, septicemia

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6
Q

T cell typical viruses

A

CMV, EBV, parainfluenza, adenovirus

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7
Q

Associated features of T cell defects

A

Omenn Syndrome, Disease post BCG or VZV vaccine

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8
Q

B cell typical age of onset

A

> 6 months after maternal immunoglobulin is gone. Up until adulthood

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9
Q

B cell typical bacteria

A

Encapsulated (streptococcus and haemophilus)

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10
Q

B cell Typical Viruses

A

Enterovirus

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11
Q

B cell Typical fungi/parasites

A

Giardia, cryptosporidium

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12
Q

B cell sites of infection

A

otitis media, sinusitis, pneumonia, arthritis, meningoencephalitis
SINOPULMONARY

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13
Q

B cell associated features

A

Autoimmunity, lymphoma

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14
Q

Phagocytic age of onset

A

Early onset

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15
Q

Phagocytic typical bacteria

A

staph, pseudomonas, serratia

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16
Q

Phagocytic typical viruses

A

none really

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17
Q

Phagocytic typical fungi/parasites

A

candida, aspergillus

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18
Q

Phagocytic Sites of Infection

A

Deep abscesses (liver, lungs), gingivitis, osteomyelitis, skin

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19
Q

Phagocytic Associated Features

A

Delayed cord separation, poor wound healing

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20
Q

Complement age of onset

A

Any

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21
Q

Complement typical bacteria

A

Pneumococcus and meningococcus

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22
Q

Complement Sites of infection

A

Septicemia, meningitis

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23
Q

Complement associated features

A

autoimmunity (can get a lupus like picture

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24
Q

Humoral Assessment: Number

A 
Quantitative Ig levels, albumin for secondary loss
Lymphocyte subsets (evaluates B cell numbers, CD 19 cells)- flow cytometry
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25
Q

Humoral Assessment: Function

A

Specific antibodies to vaccines the patient was exposed to

Isohemagglutinins (IgM antibody to blood group A and /or B)

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26
Q

Cellular Assessment: Number

A

Total Lymphocyte counts

Lymphocyte subsets to evaluate T cell numbers (CD4 and CD8). Flow cytometry

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27
Q

Cellular Assessment: Function

A

lymphocyte proliferation in response to mitogens and antigens
TRECs
T cell receipt Beta repertoire

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28
Q

Phagocytic Assessment: Number

A

Neutrophil Counts

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29
Q

Phagocytic Assessment: Function

A

NBT or NOBI (for CGD)

Measurement of adhesion markers: CD 11 and CD 18 (LAD)

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30
Q

Complement Assessment: Number

A

C1 esterase inhibitor (good for hereditary angioedema)

Specific complement levels

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31
Q

Complement Assessment: Function

A 
Total Hemolytic Complement (CH50)
Alternate Pathway (AH50)
C1 Esterase inhibitor function (for hereditary angioedema)
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32
Q

X Linked Agammaglobulinemia: pathophysiology

A

Mutation in Bruton Tyrosine Kinase
No B Lymphocytes in Blood: No lymph tissue, no immunoglobulin production
No lymph nodes or tonsils

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33
Q

XLA Age of onset

A

6-24 months (when maternal IgG disappears)

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34
Q

XLA Types of recurrent infections

A

otitis media, pneumonia, sinusitis, diarrhea, arthritis, meningitis, sepsis, skin infections
ENCAPSULATED BACTERIA (strep, haemophilus)
Enteroviral meningoencephalitis

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35
Q

XLA Diagnosis

A

Absent B cells (<2% of lymphocytes)
Absent IgG, IgA, IgM
Absent antibodies to vaccines
Genetic confirmation of BTK mutation

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36
Q

Management of XLA

A

Antibiotics for active infections
IVIg for life
Follow PFTs and CT: at risk for bronchiectasis

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37
Q

CVID Age of Onset

A

1st decade of life, 3rd decade of life

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38
Q

CVID Clinical features

A

Recurrent Infections, Autoimmunity, Malignacy

Presence of lymph tissue normal or enlarged

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39
Q

CVID Infections

A 
Recurrent sinopulmonary infections (encapsulated bacteria)- bronchiectasis and fibrosis in lungs
GI Infections (Giardia and campylobacter)
Atypical Bacteria (Mycoplasma, Ureaplasma joint infections)
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40
Q

CVID types of AI/Inflammatory processes occur in what % of patients

A 
20-25% patients
Cytopenias
GI (IBD, pan gastritis, small bowel nodule lymphoid hyperplasia), 
Arthritis
Granulomas (lung, liver, spleen, skin)
Thyroiditis
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41
Q

Is CVID at risk of malignancy?

A 
Yes
Increased lymphoreticular and gastric malignancies 
15% in aldutgood
Non Hodgkin's lymphoma
Gastric Carcinomas
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42
Q

CVID Lab

A

Decreased Serum IgG (normal or reduced IgA0
Normal or low numbers of B cells
Decreased/absent antibodies to vaccines
Low Isohemagglutinins

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43
Q

Management of CVID

A

Antibiotics to treat infections
IgG replacement for life ( DOES NOT DECREASE AI OR MALIGNANCY)
PFTs and Chest CTs

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44
Q

SCID Pathophysiology

A

Defective Tcell and B cell function

Mutation in common gamma chain of IL-2 receptor on X chromosome (X LINKED)

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45
Q

SCID age of onset

A

2-6 months

die in infancy without treatment

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46
Q

SCID Clinical Features

A

Persistent, recurrent, sever, opportunistic infections
Bacterial, fungal, viral, sinopulmonary, oral thrush, chronic diarrhea
FTT
Absent Lymph Nodes and Tonsils
Absent thymus

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47
Q

Diagnosis of SCID

A

Lymphopenia
Severely reduced T cell Numbers
B and NK cell numbers can be low, normal, or elevated
Low or absent T cell function (in vitro lymphocyte proliferation in response to mitogens and antigens(
Absent antibodies to vaccines

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48
Q

Management of SCID

A

IVIg
PJP Prophylaxis
Blood products should be CMV -ve and irradiated
No breast feeding if mother is CMV +ve
Avoid Live vaccines
Strict isolation
New immune system ASAP: HSCT. Gene therapy for some cases (ADA deficiency)

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49
Q

Wiskott Aldrich Syndrome Triad

A

Thrombocytopenia, Eczema, Recurrent Pyogenic Infections (encapsulated organisms)
Can also have autoimmunity
Increased risk of malignancy as well

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50
Q

Diagnosis of WAS

A 
Thrombocytopenia (small too), lymphopenia
Variable IgG
High IgA
Low IgM
High IgE
Poor antibody responses to some vaccines
Decreased T cell function
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51
Q

Management of WAS

A

IVIg
PJP prophylaxis
HSCT
Monitor for AI and malignancy

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52
Q

Ataxia Telangiectasia mode of inheritance

A

AR

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53
Q

Ataxia Telangiectasia clinical features

A

Ataxia (starts as a toddler)
Progressive Neurodegeneration
Telangiectasia (face, conjunctiva, ear lobes)
Immune deficiency (only in 2/3, not as severe)
25% develop malignancy especially LYMPHOMA
Abnormal DNA repair…should avoid Xray and CT

54
Q

Ataxia Telangiectasia type of malignancy

A

LYMPHOMA

55
Q

Ataxia Telangiectasia Diagnostic Labs

A 
Increased Alpha Fetoprotein
Decreased T cell numbers
Low or normal IgG
Absent IgA
Sometimes elevated IgM
Decreased T cell function 
Can have poor antibody response to some vaccines
56
Q

Ataxia Telangiectasia Management

A 
Supportive (HSCT doesn't fix neuro problems)
Avoid Ionizing radiation
IVIg for those with humoral deficiencies
Genetic counselling (ATM increased risk of breast cancer)
57
Q

DiGeorge Syndrome clinical features

A 
CATCH-22
Cardiac Defects (interrupted aortic arch)
Abnormal Facial Features
Thymic Hypoplasia
Cleft Palate and midline abnormalities
Hypocalcemia
22q11 deletion

Also FTT, DD, Psychiatric issues

58
Q

DiGeorge Syndrome Lab Features

A

Mildly reduced CD4 and CD8
Hypocalcemia
Normal or mildly reduced T cell function
May (rare) have poor response to vaccines

59
Q

DiGeorge Syndrome Management

A

Usually only have mild T cell deficiency which improves with age.
Some have complete DiGeorge- severe T cell deficiency
Blood products should be CMV -ve and irradiated
Should not have live vaccines until immune competence is demonstrated
Screen parents too

60
Q

Chronic Granulomatous Disease Genetics

A

Phagocytic Defect
Defect in NADPH oxidase
65% are X linked (others are AR)

61
Q

CGD organisms

A 
Susceptible to catalase positive pathogens
S. Aureus
Aspergillus
Nocardia
Serratia Marcesscens
Burkholderia Cepacia
Salmonella
62
Q

CGD Clinical Features

A

Recurrent bacterial and fungal infections (suppurative adenines, pneumonia, abscess, osteo, sepsis)
Abscesses and granulomas (in organs)
Inflammation (IBD)

63
Q

CGD Lab features

A

Normal or increased neutrophil numbers

Abnormal NOBI or NBT

64
Q

CGD Management

A

Antibiotics for infection
Antibacterial and Antifungal prophylaxis (septa and itraconazole)
Anti-inflammatory treatments if needed
HSCT

65
Q

Hyper IgE Syndrome (Job Syndrome) Clinical features

A

AD mutation STAT3
Recurrent Abscesses in the skin, lungs (cold boils)
Mucocutneous Candidiasis
Eczema
Facial Features (deep set eyes, prominent forehead, broad nasal bridge, bulbous nose, coarse skin)
Delayed shedding of teeth
Bone fractures, scoliosis, joint hyperlaxity

66
Q

Lab features HyperIGE

A

VERY high IgE >20 000
Eosinophilia
Normal IgG, IgA, IgM
Function: poor antibody response to vaccines

67
Q

Management of Hyper IgE

A

Treat Infections

Anti Staph prophylaxis (septra)

68
Q

Leukocyte Adhesion Defects Pathophysiology

A

AR

Deficiency in adhesion molecules (abnormal neutrophil migration and penetration into tissue)

69
Q

LAD Clinical features

A

Delayed Separation of umbilical cord (>4 weeks)
Staph infections in 1st year of life (dental, gingivitis, intestinal)
NO PUS FORMATION

70
Q

LAD Lab Findings

A

Neutrophilia

Absent surface adhesion molecules CD11 and CD 18

71
Q

LAD Management

A

Antibiotic treatment and prophylaxis

HSCT

72
Q

Complement Deficiencies Characteristics

A

Severe, recurrent or invasive infections with encapsulated bacteria
Defects in C1-C4: Rheumatic Diseases
Defects in C5-C9: Disseminated Neisseria Infections, meningitis

73
Q

Management of Complement Deficiencies

A

Antibiotic Prophylaxis

Immunizations (meningococcal and pneumococcal)

74
Q

Lab Features of Complement Deficiencies

A

C3 C4 usually normal
Other complement levels more useful
Abnormal CH 50 (function)
AH 50 (alternate pathway function)

75
Q

PJP prophylaxis is needed in what type of immune deficiency

A

Cell mediated (T cell)

76
Q

Does Transient hypogammaglobulinemia need treatment?

A

No! Usually self resolves

77
Q

Hyper IgM type of immunodeficiency

A

Combined Immunodeficiency

78
Q

Hyper IgM Clinical features

A

Infections (bacterial in 1st year of life, opportunistic as well)
Autoimmunity
Liver Disease (sclerosis cholangitis, chronic hepatitis)
Malignancy (lymphoma)

79
Q

Lab Features of Hyper IgM

A 
High IgM
Low IgG
Low IgA
Normal T and B cells
50% have neutropenia
Poor antibody response to vaccines
80
Q

Hyper IgM management

A

Immunoglobulin replacement therapy
PJP prophylaxis
HSCT (for immune deficiency and to prevent malignancy)

81
Q

Cartilage Hair Hypoplasia

A 
Short limbed dwarfism
combined immune deficiency
Short pudgy hands, hyper extensible joints, sparse hair
Hirschsprung disease
Immune: SCID to near normal
Increased frequency of malignancy

Management: immunoglobulin replacement to HSCT

82
Q

IRAK 4 Deficiency

A

recurrent, sever, invasive infections

Normal B and T, phagocyte and complement function

83
Q

Chronic Mucocutaneous Candidiasis features

A

Persistent candida infection in the skin, nails and mucous membranes
Endocrine Autoimmunity
APCED

84
Q

Hereditary Angioedema

A

Recurrent episodes of swelling to face, extremities and internal organs
No urticaria, pain, heat or itch
Deficiency in C1 esterase inhibitor (AD). Low C4 levels

85
Q

Hereditary Angioedema Management

A

Concentrates of C1 inhibitor infusions during attacks

Androgens for prophylaxis as well

86
Q

ALPS

A

Autoimmune cytopenias
Lymphoproliferation
Increased malignancy

Management with immune suppression

87
Q

Lab findings of ALPS

A

Anemia, Neutropenia, and/or thrombocytopenia
Elevated IgG
Elevated % of T cells not expressing CD4 or CD 8
Elevated B12 levels
Normal antibody responses to vaccines
Normal T cell function

88
Q

IPEX

A

Immune Dysregulation
Polyendocrinopathy (IDDM)
Enteropathy
X linked

89
Q

Epinephrine should be given via what route for anaphylaxis

A

IM

90
Q

Dose of epinephrine for anaphylaxis

A

0.01mg/kg IM max dose 0.5mg

91
Q

How often can you repeat epi for anaphylaxis

A

every 5-15 minutes

92
Q

Why don’t we give SC epi for anaphylaxis

A

Local vasoconstriction may inhibit absorption

93
Q

When do we give IV epi for anaphylaxis

A

After 3 doses of IM epi

Persistent hypotension despite fluid resuscitation

94
Q

In patients who are on Beta Blockers and are not responding to epi in anaphylaxis…what can you give them?

A

Glucagon
Has inotropic and chronotropic effects…not mediated through beta receptors
IV bolus

95
Q

Second line agents in anaphylaxis (5)

A 
Salbutamol
Nebulized Epinephrine
H1 Antagonist (antihistamines)
H2 Antagonists (ranitidine)
Corticosteroids
96
Q

When do most biphasic reactions occur?

A

Within first 4-6 hours

5-20% of patients with anphylaxis

97
Q

What increases your risk of a biphasic reaction?

A

Delayed epinephrine
More than one dose of epi
Severe symptoms at presentation

98
Q

Anaphylaxis teaching

A

Epi pen
Anaphylaxis Action Plan
Medical Identification Device
Consider 3 day course of antihistamines and corticosteroids
Avoidance of trigger if obvious from history
Referral to Allergist

99
Q

Most common causes of anaphylaxis

A

Food, venom, medication

100
Q

Skin prick testing advantages

A

Fast
More sensitive than serum specific IgE
High negative predictive value
Cost Effective

101
Q

SPT disadvantages

A

False Positives
Affected by use of antihistamines and steroids
Risk of systemic reaction
Can not perform if skin site affected

102
Q

Serum Specific IgE testing pros (RAST)

A

Not affected by antihistamines, steroids, montelukast
No risk of systemic reaction
Can be performed if skin disease

103
Q

Serum Specific IgE testing cons (RAST)

A

False positives if elevated total IgE
Less sensitive compared to SPT
More expensive

104
Q

Management of Food Allergy

A 
Avoid trigger
OIT 
Epi auto injector
Anaphylaxis Action Plan 
Medical Identification Device
105
Q

Who is at high risk of a food allergy?

A

Having a first degree relative with an allergic condition (asthma, eczema, allergies)

106
Q

How to prevent food allergy in children

A

No dietary restrictions during pregnancy or breastfeeding
Exclusively breastfed for 6 months
Hydrolyzed formula if infant not breastfed
Don’t delay introduction of allergenic foods
Regular ingestion of newly introduced foods

107
Q

Who gets food protein proctitis

A

Exclusively breastfed infants ages 2-8 weeks

Cow’s milk protein, eggs, soy, corn

108
Q

Clinical features of food protein proctitis

A

Blood tinged stools

Otherwise healthy

109
Q

Management and diagnosis of food protein proctitis

A

Skin testing and IgE not helpful
Eliminate food from moms diet or extensively hydrolyzed formula
By 9 months 95% will tolerate food

110
Q

Food protein induced enterocolitis syndrome (FPIES) onset

A

1-4 weeks after introduction of food

111
Q

FPIES trigger foods

A 
CMPA
Soy
grains
rice
meat
poultry
egg
potato
legumes
112
Q

FPIES S/Sx

A

Repetitive vomiting 1-3 hours after ingesting food
hypotension
relieved by 3 years usually

113
Q

FPIES diagnosis

A

Skin testing and serum IgE not helpful

Eliminate offending agent

114
Q

Venom Allergy 3 types of reactions

A 
Local reaction (erythema, swelling, pruritus. immediate onset, resolves in a day)
Large Local Reactions (localized erythema, swelling >15cm. Develops 12-48 hours after sting and resolves in 5-10 days)
Systemic Reaction (anaphylaxis, generalized cutaneous symptoms beyond the site of the sting)
115
Q

Management of venom allergy

A

If local reaction: testing not indicated
Anaphylaxis: Epi pen, all require testing, Immunotherapy
Generalized cutaneous reactions (<16 no testing. >16 yo testing if high risk)

116
Q

What is the cross reactivity between penicillins and cephalosporins?

A

2%

117
Q

Urticaria/Angioedema onset

A

Minutes to Days after exposure
Resolves 1-2 days after stopping medication
Treat with antihistamines

118
Q

Exanthemous Eruption onset

A

Days to 2 weeks after drug exposure
Diffuse fine macule and papule
Resolves 5-14 days after stopping medication

119
Q

Fixed Drug Eruption features

A 
Hyperpigmented plaques
Same site wth re exposure
Discontinue the medication
Topical steroids and antihistamines
Steroids if really severe
120
Q

Erythema Multiforme Features

A 
Target Lesions
Mucosal membrane involvement 
Stop meds
Topical steroids, antihistamines
Steroids for severe cases
121
Q

SJS/TEN features

A

1-3 weeks after drug exposure
Fever, sore throat
Blistering lesions and skin detachment (<10% SJS, >30% TEN)
Mucus membrane
Discontinue med and supportive treatment
Systemic corticosteroids and IVIG controversial

122
Q

Drug rash with eosinophilia features

A

Onset 1-8 weeks after drug exposure
Rash, Eosinophilia, hepatic dysfunction, fever, facial angioedema, LAD
stop meds
steroids if bad

123
Q

Serum Sickness

A 
1-3 weeks after drug exposure
Rash, arthralgia, renal disease, fever
LOW COMPLEMENT
Stop med, NSAIDs, analgesia
Steroids or plasmapheresis for severe cases
124
Q

Serum Sickness- LIKE

A 
1-3 weeks after drug exposure
No renal disease
NORMAL COMPLEMENT
Stop med, NSAIDs, analgesia
Steroids for severe cases
125
Q

Can you have flu vaccine if allergic to eggs?

A

Yes

126
Q

Egg allergic patients…can they receive all vaccines?

A

MMR: receive as a single dose
Inactivated Influenza Vaccine: single dose normal monitoring
Live Attenuated Influenza Vaccine: single dose normal monitoring
Yellow fever: NEEDS SKIN TESTING BEFORE!

127
Q

Chronic Urticaria Treatment

A

2nd gen antihistamine

second line: increase dose 4 fold
third line: add montelukast or cyclosporin or omalizumab
short course of steroids

128
Q

Hereditary Angioedema Inheritance

A

AD

129
Q

Hereditary Angioedema Pathphys

A

C1 esterase inhibitor deficiency/dysfunction

130
Q

Allergic Rhinitis Treatment

A 
Allergen Avoidance
Second gen antihistamine
Intranasal corticosteroids
LTRA
Immunotherapy

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