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FRCPC > Allergy/Immunology > Flashcards

Allergy/Immunology Flashcards

1
Q

Name 4 functions of T cells

A

Delayed type hypersensitivity (type IV)

Cytotoxic host-defense functions

Immunoregulatory functions

Respond to MHC class I and class II APCs

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2
Q

What diseases can be associated with recurrent candida infection?

A

Diabetes mellitus
HIV infection
Patients treated with systemic or inhaled glucocorticoids Prolonged courses of antibiotics
CMCC

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3
Q

What is chronic mucocutaneous candidiasis?

A
  1. Recurrent Candida
    Persistent infections of the skin, nails and mucous membranes with candida species
    Disseminated infection RARE
  2. Autoimmunity
    - Cytopenias
  3. Endocrinopathies
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4
Q

What endocrine abnormalities can be associated with CMC?

A 
Hypoparathyroidism
Hypothyroidism
Addison's
T1DM
Gonadal dysfunction
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5
Q

What is the most common immunodeficiency causing recurrent meningococcal meningitis?

A

Late complement deficiency (C5, C6, C7, C8)

Susceptible to Neisseria meningococcal meningitis or extragenital gonococcal infection

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6
Q

What do C1-4 deficiencies typically present with?

A

Rheumatologic/lupus-like disorders

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7
Q

What is the most common complement deficiency?

A

C2

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8
Q

What diseases/infections are associated with C2 deficiency?

A 
SLE-like presentation
Recurrent pyogenic infections with encapsulated bacteria
HSP
RA
Dermatomyositis
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9
Q

What are the clinical features of Wiskott-Aldrich syndrome?

A

Eczema

Thrombocytopenia

Sinopulmonary infections, sepsis/meningitis, PJP, herpes

Watery diarrhea (can be bloody) and petechiae in the first few months of life

Impaired ability to make specific antibodies especially to polysaccharide antigen

Later manifestations: Autoimmunity, EBV-associated malignancies

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10
Q

What laboratory abnormalities do you see in Wiskott-Aldrich?

A

Thrombocytopenia
Low to normal IgG and IgM and high IgA and IgE
Impaired B-cell response to polysaccharide antigens

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11
Q

How is Wiskott-Aldrich inherited?

A

X-linked

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12
Q

What is the most cost effective screening test for T-cell defect?

A

Candida skin test

Intradermal skin testing with candida to evaluate delayed hypersensitivity

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13
Q

When does severe combined immunodeficiency typically present?

A

4-12 months of age, but can present earlier

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14
Q

What are the clinical features of SCID?

A 
Oral Thrush
Persistent/recurrent bacterial, fungal, viral infections
Chronic diarrhea
Pneumonitis
PCP infection
Disseminated CMV
FTT
Small thymus
Absent lymphoid tissue (except Omenn’s)
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15
Q

Name 2 SCID diseases

A

ADA deficiency (defect in purine metabolism)

Omenn’s syndrome (skin rash, HSM, short limbs, lymphadenopathy, eosinophilia, fever)

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16
Q

How do you treat SCID?

A

BMT

Peg-ADA

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17
Q

What is the immunologic abnormality in CVID?

A

Inability of B cells to differentiate into plasma cells capable of secreting Ig

Hypogammaglobulinemia

Normal number of B cells

Poor or absent response to immunizations (despite having normal number of B-cells)

Normal or near normal cellular immunity

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18
Q

What are the clinical features of CVID?

A

Recurrent Infections:

  • Sinopulmonary and chronic GI infections
  • H.influenzae, streptococcus pneumoniae, staph
  • Mycoplasma, enteroviruses, Giardia

Respiratory:

  • Bronchiectasis
  • Pulmonary fibrosis with granulomas

Allergic disease:
-Food allergy, eczema, urticaria, rhinitis

Gastrointestinal:

  • IBD picture - Diarrhea, weight loss, malabsorption
  • Giardia
  • Nodular lymphoid hyperplasia of the small bowel
  • Chronic pangastritis
  • FTT

Autoimmune disease

  • Autoimmune cytopenias
  • Evans syndrome

Granulomatous inflammation
-Lung, liver, spleen, skin

Malignancy

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19
Q

What laboratory features do you see in CVID?

A

Autoimmune cytopenias

Decreased serum immunoglobulins

Specific antibody titres decreased/absent

Impaired vaccine response

T-cell abnormalities in up to 50% of patients
(Reversed CD4/8 ratio, decreased function, restricted repertoire)

Usually normal number of B-cells

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20
Q

What types of infections are seen in X-linked agammaglobulinemia?

A 
Sinopulmonary
GI infection
Sepsis
Septic/non-infectious arthritis
Meningitis
PCP infection
S. pneumonia, Hib, enterovirus
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21
Q

What is the immunologic abnormality in X-linked agammaglobulinemia?

A

Lack of B cells, plasma cells (this is what differentiates it from CVID)
No immunoglobulin
Abnormal lymph tissue
BM shows arrest of B cell maturation

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22
Q

What is the most common mutation in X-linked agammaglobulinemia?

A

90 - 95% of patients with XLA have a BTK mutation

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23
Q

How do you treat X-linked agammaglobulinemia?

A

Ig replacement
Monitor for IgG levels
Aggressive antibiotic treatement of infections
PFTs

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24
Q

What are the clinical features of ataxia telangiectasia?

A

Progressive cerebellar ataxia

  • Earliest manifestation
  • Confined to wheelchair by 10-12 years of age

Telangectasias (eyes, ears)
-Appear at age 3-5

Recurrent sinopulmonary infections

Progressive pulmonary disease (multifactorial)

Increased risk of malignancy (mostly leukemia, lymphoma)

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25
Q

What are the immunologic abnormalities in ataxia telangiectasia?

A

50% - 80% have absent IgA
Reduced ability to make antibodies (esp to polysaccharide antigens)
Slightly decreased T-cell numbers (not usually clinically significant)
Decreased proliferations

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26
Q

What is the most common laboratory abnormality in ataxia telangiectasia?

A

Absent IgA

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27
Q

What 3 features are required to have GVHD?

A

Histocompatibility differences between the graft donor and recipient

Presence of immunocompetent cells in the graft that can respond to host antigens

Immunoincompetence of the host, preventing rejection

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28
Q

What is the time frame for acute GVHD?

A

14 (engraftment) to 100 days after transplantation

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29
Q

What are the clinical features of acute GVHD?

A

Skin
Liver
GI (diarrhea)

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30
Q

How do you treat acute GVHD?

A

Steroids
CSA
MTX

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31
Q

What is the timeframe for chronic GVHD?

A

3 to 15 months after transplantation and may last for years

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32
Q

What are the clinical features of chronic GVHD?

A

Progressive systemic sclerosis

Skin-mucous membranes may become dry

Hematologic-anemia thrombocytopenia, eosinophilia

GI-esophagus, small intestine (causing weight loss)

Liver-cholestatic liver disease

Lungs-restrictive pulmonary defects

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33
Q

How do you treat chronic GVHD?

A

Prednisone
CSA
Biologics

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34
Q

What is the inheritance pattern of CGD?

A

Majority x-linked

Some AR

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35
Q

How do you diagnose CGD?

A

NOBI is test of choice

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36
Q

How do you treat CGD?

A

Aggressive antibiotic therapy (itraconazole and septra prophylaxis)

BMT if not responding to therapy, sibling donor

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37
Q

What are the clinical features of CGD?

A 
Respiratory infections
Abscesses
Hepatomegaly
Suppurative lymphadenopathy
S. aureus, serratia, aspergillus, nocardia, burkholderia
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38
Q

Which component of penicillin is responsible for a) most allergies b) anaphylaxis?

A

a) Major determinant

b) Minor determinant

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39
Q

Name 5 types of penicillin reactions

A

Delayed maculopapular exanthems

Mucocutaneous syndromes such as Stevens-Johnson syndrome

Drug fever

Acute interstitial nephritis

Pulmonary infiltrates with eosinophilia

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40
Q

Can patients with egg allergy safely receive influenza vaccine?

A

Yes

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41
Q

How do you confirm milk allergy?

A

Milk challenge

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42
Q

In most cases, does allergic rhinitis persist through to adulthood?

A

Yes

43
Q

When do patients with allergic rhinitis typically develop symptoms?

A

Before age 20

44
Q

What are causes of perennial rhinitis?

A

Molds
Dust mite
Animal dander
Cockroach

45
Q

What is the best treatment for perennial allergic rhinitis?

A

Most important: Avoid allergens

  • Seal mattress/pillow in encasing,
  • Wash bedding/stuffed animals weekly in hot water,
  • Removal of carpets,
  • Removal of pets (this is the only way to get rid of dander)
  • HEPA filters lower airborne mold.
Oral antihistamines (if runny)
Nasal corticosteroids (if congested)
Immunotherapy
46
Q

What allergens cause non-IgE mediated anaphylaxis?

A

Cold

47
Q

How long should patients with anaphylaxis be observed?

A

12 hours

24 hours if severe respiratory distress, hypotension

48
Q

List 4 preventative recommendations for anaphylaxis

A
  • Educate about how to administer EpiPen, encourage to err on the side of caution
  • Keep EpiPen with child at all times (school, parent) with 2 doses available
  • Trigger avoidance!!
  • MedicAlert bracelets should be recommended
  • Referral to allergy re: testing, information, therapy
49
Q

When does biphasic reaction occur in anaphylaxis?

A

Occurs in approximately 15 to 30% of cases within 4 to 8 hours

50
Q

What is Radioallergosorbent Test

(RAST)?

A

In vitro test looking at specific IgE to specific allergens

51
Q

What are the benefits of RAST over skin testing?

A

Do not need to discontinue antihistamines/immunosuppressants
Can be used as an adjunct to skin testing to determine safety for oral challenge
No risk of anaphylaxis

Disadvantages:
Low PPV
Not as sensitive as SPT
False positives associated with hyper IgE states

52
Q

What are the benefits of skin testing over RAST?

A

More sensitive
Higher PPV (less false positives)
Preferred testing for food allergies

53
Q

What are the indications for immunotherapy?

A
  • Allergic rhinoconjunctivitis(seasonal or perennial)
  • Asthma triggered by allergen exposures
  • Insect venom sensitivity
54
Q

What is the non-immunologic differential for recurrent infections?

A
  • Cystic fibrosis
  • GERD with aspiration
  • Diabetes
  • Sickle cell
  • HIV
  • Nephrotic syndrome
  • Malignancy
55
Q

Name 5 categories of primary immunodeficiencies

A 
Humoural
Combined
Cell-mediated
Complement
Phagocytic
56
Q

What are red flags for primary immunodeficiency?

A
  1. ≥1 systemic bacterial infections (sepsis, meningitis)
  2. ≥2 serious respiratory or documented bacterial infections within 1 year (cellulitis, abscesses, draining otitis media, pneumonia, lymphadenitis)
  3. Serious infections occurring at unusual sites (liver, brain abscess)
  4. Infections with unusual/opportunistic pathogens (Pneumocystis jiroveci, Aspergillus, Serratia marcescens, Nocardia, Burkholderia cepacia)
  5. Infections with common childhood pathogens but of unusual severity
  6. FTT
  7. Chronic diarrhea
  8. Persistent infections after receiving live vaccines
  9. Chronic oral or cutaneous candida infections
57
Q

Name 5 antibody defect immunodeficiencies

A 
X-linked agammaglobulinemia
CVID
Transient hypogamaglobulinemia of infancy
HyperIgM syndrome
IgA deficiency
58
Q

Name 2 cell-mediated immunodeficiencies

A

DiGeorge

CMC

59
Q

Name 4 combined immunodeficiencies

A

SCID
Wiskott Aldrich
Ataxia Telangectasiae
X-linked lymphoproliferative disease

60
Q

Name 2 phagocytic defect immunodeficiencies

A

CGD

Leukocyte adhesion deficiency

61
Q

How do you test for humoral immunity?

A

CBC, differential (WBC, lymphocyte count)

Quantitative tests:
Quantitative immunoglobulins (IgG, IgA, IgM)
Lymphocyte immunophenotyping (CD19, CD20)

Qualitative tests:
Specific antibody titres (tetanus IgG (pre and post booster), measles IgG, rubella IgG, mumps IgG): tests protein antigen response

Pneumococcal IgG (pre/post vaccine): tests polysaccharide antigen response

Isohemagluttanin (Anti-A, Anti-B titres): tests IgM and polysaccharide response

62
Q

How do you treat CVID?

A

IVIg replacement therapy 400-600mg/kg Q3-4 weeks
Avoid live vaccines
Do not usually give routine vaccinations, but this is debated

63
Q

After what age can you assess polysaccharide responses?

A

2 years of age

64
Q

What should you do if you need to give blood products to a patient with selective IgA deficiency?

A

Should measure IgA level and if <0.1 need IgA depleted blood products or triple washed blood products, medic alert bracelet

65
Q

How would you work up cell-mediated immunity (T cell)?

A

CBC, differential

Quantity:
Lymphocyte immunophenotyping (CD2, CD3, CD4, CD8)
Function:
Mitogen stimulation (incubate T cells with phytohemagluttinin and they should rapidly divide)
Intradermal skin testing with heat-killed candida (older test, no longer used)
66
Q

What is the immune defect in DiGeorge?

A

T cell numbers, mitogen response may be low

Usually does not result in clinically significant immunodeficiency

Usually grow out of it

Delay live vaccines until T cell numbers/mitogen response improves

67
Q

What should patients with T cell problems be advised?

A

No live vaccines
CMV negative, irradiated blood products
If exposed to chickenpox, may need VZIg
Medicalert

68
Q

How do you treat CMCC?

A

Supportive care

Antifungals

69
Q

What is the immunologic defect in CMCC?

A

Impaired mitogen response to candida specifically

Normal immunophenotyping

70
Q

Should you breastfeed a baby with SCID?

A

No
Mom can pass maternal lymphocytes that baby could engraft (also CMV risk)
Needs to be pumped and irradiated

71
Q

What are the clinical features of Omenn’s syndrome?

A

Erythroderma
Lymphadenopathy
HSM
Abnormal T cell clones (many T cells, but they are proliferations of a few clones!)

72
Q

How do you test for a phagocytic defect?

A

CBC, diff
NOBI
(Nitrozolium blue test is the old test)
Measurement of adhesion markers (CD11, CD 15, CD 18-leukocyte adhesion deficiency)

73
Q

How do you test for complement deficiency?

A

C3, C4
CH50, AH50
C1 esterase inhibitor (herediatry angioedema)

74
Q

What is the immunologic abnormality in CGD?

A

Normal number of neutrophils, migration and adhesion

But do not burst when stimulated

Can’t kill catalase-positive bacteria (Staph, Serratia,Aspergillus, Cepacia, Nocardia, Salmonella, BCG)

75
Q

What vaccines should patients with complement deficiencies receive?

A

Pneumococcal

Meningococcal

76
Q

What is the cross-reactivity between penicillins and cephalosporins?

A

1-2%

77
Q

What advice do you give for high risk infant (first degree relative with atopy) re: prevention of allergy?

A

Exclusive breastfeeding for at least 6 months

Partially/extensively hydrolyzed formulas for those who cannot breastfeed

No evidence of delayed introduction beyond 4-6 months (eggs, peanut, milk)

78
Q

What is the most common food allergen in children?

A

Cow’s milk

79
Q

What percentage of children outgrow peanut allergies?

A

20%

80
Q

What foods can you introduce to children with egg/milk allergy to decrease time to tolerability?

A

Baked egg and milk (70-80% of allergic children will tolerate it)

81
Q

What are the 3 types of non-IgE mediated food protein allergy?

A

FPIES
FFIAP
FPE

82
Q

What is the age of onset for FPIES?

A

1 day to 1 year

83
Q

What is the age of onset for FFIAP?

A

Days to 6 months

84
Q

What is the age of onset for FPE?

A

Up to 2 years

85
Q

What are the food allergens implicated in FPIES?

A

CM, rice, soy, oat, egg (and many others)

86
Q

What are the food allergens implicated in FFIAP?

A

CM, soy, wheat, egg

87
Q

What are the food allergens implicated in FPE?

A

CM, soy, wheat, egg

88
Q

What are the symptoms of FPIES?

A

Mostly vomiting, persistent diarrhea, bloody stool, shock, FTT

89
Q

What are the symptoms of FFIAP?

A

Bloody stools, mild diarrhea

90
Q

What are the symptoms of FPE?

A

Mostly diarrhea, some vomiting

Can look like post-infectious

91
Q

What are the laboratory findings of FPIES?

A 
Anemia
Hypoalbuminemia
Leukocytosis
Thrombocytosis
?Methemoglobinemia
?Acidemia
92
Q

What are the laboratory findings of FFIAP?

A

Rarely Hb, low albumin

93
Q

What are the laboratory findings of FPE?

A

Anemia, hypoalbuminemia

94
Q

What are the main differences between FPIES, FFIAP, and FPE?

A

FPIES is most severe and most likely transition to IgE allergy. Vomiting is prominent. Abnormal bloodwork.

FPE is mild. Diarrhea is prominent symptom.

FFIAP minimal blood in the stool, but appear well. Usually better by 12 months.

95
Q

What do you use to treat dietary protein enterocolitis?

A

Extensively hydrolyzed formula (not SOY)

96
Q

When do you rechallenge in dietary protein enterocolitis?

A

12 months

97
Q

What is the natural history of FPIES, FFIAP, and FPE?

A

FPIES-resolve by age 3-5
FFIAP-resolves by 12 months
FPE-resolves by 24-36 months

98
Q

Do patients with FPIES transition to IgE mediated cow’s milk allergy?

A

Yes, 35% do

99
Q

What test can you do for allergic rhinitis to determine the allergen?

A

Skin test

100
Q

What are the 3 WHO definitions of anaphylaxis?

A

1) Skin/mucosa involvement
- Pruritus
- Flushing
- Angioedema
- Hives

AND EITHER
A) Respiratory 
-Dyspnea
-Wheezing
-Stridor
-Hypoxemia

B) Hypotension/end-organ

  • Collapse
  • Syncope
  • Incontinence

2) 2 of respiratory, skin, GI, hypotension in a patient exposed to known allergen
3) Hypotension after known allergen

101
Q

When can you do skin testing after anaphylaxis?

A

6 weeks after

102
Q

What allergens cause direct mast cell activation?

A

Physical factors (cold, heat, exercise, sunlight)
Ethanol
Medications (opoids)

103
Q

What are patients with selective IgA deficiency at risk for (List 2 things)?

A
  • Increased risk of autoimmune diseases, malignancy, and malabsorption
  • Risk of anaphylaxis to blood products due to presence of IgA antibodies

FRCPC (27 decks)

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