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Royal College Peds 2021 > ALLERGY & IMMUNOLOGY > Flashcards

ALLERGY & IMMUNOLOGY Flashcards

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1
Q

What are the 4 major categories of immunodeficiencies?

A
  1. Defective cell-mediated immunity
  2. Defective antibody-mediated immunity
  3. Defective phagocytosis
  4. Defective complement function
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2
Q

What are the infection susceptibilities with the following immunodeficiencies? What is your test for diagnosis?

  • humoral (antibody mediated)
  • cell mediated
  • phagocytes
  • complement
A
  1. Humoral:
    - deficiency in antibodies = infections start after 6 months when maternal antibodies start to wane
    - infections with encapsulated bacteria
    - test: immunoglobulin levels, immune titres (antibody response to vaccines)
  2. Cell mediated: difficulty with bacteria
    - fungal infections (especially aspergillus and candida)
    - unusually severe viral infections
    - pneumocystis, mycobacteria
    - test: lymphocyte count, T cell subsets (CD4, CD8)
  3. Phagocytes:
    - CATALASE POSITIVE organisms (staph, nocardia, serratia, aspergillus, salmonella)
    - abscesses, skin infection
    - poor wound healing
    - test: CBC + diff, looking at WBC differential
  4. Complement:
    - neisseria meningitidis and neisseria gonorrhea
    - sepsis with encapsulated bacteria
    - test: CH50 (total hemolytic component)
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3
Q

Which class of immunodeficiency is the most common primary immunodeficiency?

A

Antibody-mediated immunodeficiency (B-cell) - up to 50% of primary immunodeficiencies in kids

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4
Q

What are 2 potential complications of long-term IVIG treatment?

A
  1. Chronic lung disease (need PFTs q1yr)

2. Exposure to bloodborne pathogens

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5
Q

What is the pathogenesis of Bruton’s agammaglobulinemia?

  • pattern of inheritance?
  • at risk for which organisms?
  • clinical features?
  • diagnosis?
  • treatment? (3)
A

Pathogenesis: defective B cell production due to enzyme deficiency (tyrosine kinase)–> NO B CELLS = no antibodies (agammaglobulinemia)

  • X-linked = only affects males
  • at risk for: staph aureus, strep pneumo, H flu, pseudomonas, giardia, enterovirus

Clinical features:

  1. No lymphoid tissue! = small or absent tonsils & no palpable lymph nodes (that’s because you need B cells to have lymph tissue)
  2. Pyogenic bacterial infections of the resp tract, skin and joints (sinusitis, pneumonia, meningitis, etc.)
  3. Enterovirus infections are severe and can be fatal
  4. Risk of life threatening pseudomonas infections

Diagnosis:

  1. Immunoglobulin levels: will see low levels or completely absent
  2. Bone marrow with absence of B cells on flow cytometry

Treatment:

  1. IVIG replacement monthly
  2. Avoidance of live virus vaccines
  3. Follow PFTs and CT chests since patients are prone to develop bronchiectasis
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6
Q

What 5 organisms are most common causes of infection for patients with antibody-mediated (B cell) immunodeficiency?

A
  1. Staph aureus
  2. Strep pneumo
  3. H. flu
  4. Pseudomonas
  5. Giardia
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7
Q

What is the pathogenesis of common variable immunodeficiency (CVID)?

  • clinical features? (3)
  • pattern of inheritance?
  • treatment? (3)
A

Hypogammaglobulinemia with phenotypically NORMAL B cells that fail to mature appropriately into antibody-producing plasma cells
-no clear pattern of inheritance

Clinical features:

  1. recurrent bacterial infections (sinopulmonary, mycoplasma) and viral infections (enteroviruses) and parasitic infections (giardia)
  2. Autoimmune manifestations: inflammatory bowel disease like picture: diarrhea, weight loss, malabsorption, cytopenias
  3. Increased risk of malignancy: lymphoma and other malignancies

Treatment:

  1. IVIG replacement
  2. May require immunosuppressive treatment for rheumatologic disorders
  3. Monitor for malignancy!!
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8
Q

How do you differentiate between Bruton’s agammaglobulinemia and CVID?

A

Given that they are both disorders of absent antibody production, will have similar infection susceptibilities. Thus, can differentiate by:

  1. Agammaglobulinemia: see only in males (X-linked), NO lymphoid tissue, NO B cells on bone marrow, see more enterovirus infection than with CVID
  2. CVID: see in both males and females, normal lymphoid tissue, normal B cells on bone marrow
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9
Q

What conditions are patients with CVID at increased risk for? (3)

A
  1. Lymphoma
  2. Autoimmune disorders
  3. Noncaseating granulomas of spleen, liver, lungs and skin
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10
Q

What is the most common immunodeficiency syndrome?

A

IgA deficiency

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11
Q

Which infections are patients with IgA deficiency at most risk, in general terms? (3)

A

IgA protects mucosal surfaces THUS are most susceptible to bacterial and viral infections involving mucosal surfaces such as:

  1. Respiratory tract
  2. Urinary tract
  3. GI tract
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12
Q

A patient receiving a blood transfusion post-trauma develops anaphylaxis. You have double-checked the blood product and it is correctly cross-matched to the patient. What diagnosis should you rule out?

A

Undiagnosed IgA deficiency = trace amounts of IgA in a blood product may trigger anaphylaxis in a patient who does not have IgA!

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13
Q

What is the diagnosis and treatment of IgA deficiency?

-minimum age at which IgA deficiency can be diagnosed?

A

Diagnosis: serum IgA levels < 10 mg/dL

  • cannot confirm diagnosis until at least 4 yo when IgA levels should reach adult levels
  • treatment: targeted treatment of associated infections (IVIG is not indicated since these patients make IgG normally)
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14
Q 
What is the pathogenesis of IgG subclass deficiency?
-at risk for what type of infections?
A

Occurs when the level of abs in one or more IgG subclasses (IgG1-4) is selectively decreased while total IgG levels are normal
-recurrent upper resp tract infections

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15
Q

What is the pathogenesis of Hyper IgM syndrome?

-inheritance pattern of most common form of Hyper IgM?

A

Failure of immunoglobulin isotype switching from IgM to IgG, IgA or IgE.

  • most commonly X-linked: defect in CD40 ligand gene thus, the T cell with CD40 ligand cannot bind to the B cell with CD40 receptor to trigger immunoglobulin isotype switching
  • **so in a way, you have both T cell and B cell dysfunction in X-linked Hyper IgM syndrome
  • thus patients have normal or high levels of IgM with low or absent levels of the other antibodies
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16
Q

What infections are patients with Hyper IgM syndrome at risk for?
-treatment for Hyper IgM syndrome?

A
  1. Sinopulmonary infections
  2. Opportunistic infections with PCP, cryptosporidium

Treatment: IVIG replacement

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17
Q

Which immunizations do not produce an antibody response in patients with IgG subclass deficiency?

A

Polysaccharide vaccines!

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18
Q

What infections are people with T cell immunodeficiencies at risk for? (3)

A
  1. Viral
  2. Fungal
  3. Intracellular infections

**disorders of T cell function also often result in B cell antibody production dysfunction because B cells need T cells to function properly = this is combined immunodeficiency

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19
Q

What is the only isolated congenital T–cell immunodeficiency?

A

DiGeorge syndrome = caused by thymic hypoplasia (thymus makes T cells)

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20
Q

What are the clinical manifestations of DiGeorge syndrome?

-diagnosis?

A

CATCH-22

  • Cardiac defects: TOF most common
  • Abnormal facies: low set ears, hypertelorism, hypoplastic mandible, bowing of upper lip
  • Thymic hypoplasia & T cell immunodeficiency
  • Cleft palate
  • Hypoparathyroidism with subsequent hypocalcemia

Diagnosis: genetic testing (FISH) for 22q11 deletion

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21
Q

What are lab results seen with combined immunodeficiency disorders? (3)

A
  1. Low lymphocyte count
  2. Low immunoglobulin levels
  3. Abnormal response to delayed type hypersensitivity testing (ie. TST)

***This reflects both B and T cell dysfunction since B cells depend on T cells to present antigens for antibody production

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22
Q

What is SCID?

  • inheritance patterns?
  • mean age of presentation?
A

Severe combined immunodeficiency = severe T cell dysfunction and resultant B cell dysfunction

  • interitance: autosomal recessive (usually ADA = adenosine deaminase deficiency) and X-linked forms
  • present by 6 months of age with SEVERE immunodeficiency
  • most children die of infection during the first 2 years of life without intervention
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23
Q

What are clinical manifestations of SCID? (7)

A
  1. FTT
  2. Chronic diarrhea
  3. Chronic candidiasis
  4. Severe bacterial infection within 1st month of life
  5. Infection with opportunistic organisms: PCP, cryptosporidium
  6. Eczema (possibly from GVHD from engraftment of maternal lymphocytes)
  7. Absent thymus/lymph nodes/tonsils
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24
Q

What condition are patients with SCID at increased risk for developing?

A

Graft versus host disease: from engrafted maternal T cells or from blood transfusions
-THUS, should always be given irradiated blood products

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25
Q

What is the treatment for SCID?

A
  1. Bone marrow transplant is curative
    - until BMT can occur, need to give IVIG replacement and PCP prophylaxis and avoid transfusions, no live vaccines

***Enzyme replacement therapy for patients with ADA deficiency can work BUT is not as good as BMT

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26
Q

How do you diagnose Ataxia Telangiectasia?

-findings on bloodwork

A
  1. Bloodwork:
    - normal IgM and IgG levels but DECREASED IgA and IgG2
    - increased serum AFP****
  2. Definitive diagnosis with gene testing of ATM gene (ataxia-telangiectasia mutated) = DNA repair enzyme
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27
Q

Which organisms are considered “catalase positive”? (5 groups)

A
  1. Staph aureus
  2. Gram negative enteric bacteria: E coli, klebsiella, enterobacter, serratia, salmonella
  3. Fungi: aspergillus, candida
  4. Nocardia
  5. Burkholderia
28
Q

What are clinical features of chronic granulomatous disease? (3)

  • pathogenesis?
  • inheritance pattern?
  • Diagnosis (2 tests)?
  • treatment?
A

CGD:

  1. Recurrent abscesses in lymph nodes, skin, liver, spleen and lungs
  2. FTT
  3. Granulomas in resp/GI/GU tracts
    - Pathogenesis: neutrophils lack oxidative burst that is needed for destruction of catalase positive bacteria and fungi
    - inheritance pattern: 2/3s are X linked, 1/3 are AR
    - diagnosis: nitroblue tetrazolium test or DHR-123 (flow cytometry test)
    - treatment: lifelong prophylaxis with septra (because of high risk of staph aureus infections), gamma interferon in severe cases, bone marrow transplant
29
Q

What are the clinical features of Hyper IgE recurrent infection syndrome?

  • inheritance pattern?
  • diagnosis?
  • treatment?
A

Clinical features (due to abnormal neutrophil migration):

  1. Coarse facial features
  2. Eczema
  3. Recurrent “cold boils” = no pain, heat or redness (most caused by staph aureus) and resp infections
    - Inheritance pattern: AD
    - Diagnosis: IgE > 20000 (not diagnostic)
    - Treatment: antistaph antimicrobial prophylaxis (Septra)
30
Q

What are the clinical features of Chediak-Higashi syndrome?

  • inheritance pattern?
  • diagnosis?
  • treatment?
A

Clinical features (due to impaired natural kill cell function and chemotaxis):

  1. Oculocutaneous albinism
  2. Recurrent skin and resp tract infections
  3. Almost all develop proliferative lymphoma like illness (typically fatal)
    - inheritance: AR
    - diagnosis: giant granules seen in neutrophils, eosinophils, granulocytes
    - treatment: BMT
31
Q

Which immunodeficiency is associated with delayed seperation of umbilical stump?

A

Leukocyte adhesion deficiency (type 1)

32
Q

What are clinical features of complement deficiencies? (3)

  • diagnosis?
  • inheritance pattern?
A
  1. Increased infection (pyogenic bacterial infections, encapsulated bacteria)
  2. Angioedema
  3. Autoimmune disorders (ie. glomerulonephritis
    - diagnosis: CH50 assay
    - inheritance: AR
33
Q

Which immunodeficiency results in increased risk of meningococcus infections?

A

Complement deficiency (late complement deficiency C5-C9)

34
Q

An infant presents to you with steatorrhea, pancytopenia, FTT and recurrent infections. What is your diagnosis?

A

Shwachman-Diamond syndrome

35
Q

What is a RAST test?

-comparison to skin testing?

A

RAST = serum test that quantifies IgE level for a given antigen

  • The suspected allergen is bound to an insoluble material and the patient’s serum is added. If the serum contains antibodies to the allergen, those antibodies will bind to the allergen. Radiolabeled anti-human IgE antibody is added where it binds to those IgE antibodies already bound to the insoluble material. The unbound anti-human IgE antibodies are washed away. The amount of radioactivity is proportional to the serum IgE for the allergen
  • compared to skin testing, RAST is less sensitive but is safer and not influenced by skin disease or medications (antihistamines)
36
Q

What is the definition of acute articaria?

A

< 6 weeks duration

37
Q

What is cold urticaria?

-diagnosis?

A

Total body exposure to cold water results in extensive vasodilation, hypotension and death

  • diagnosis: place an ice cube on the patient’s body x 10-15 minutes. If hives develop with rewarming the chilled area, diagnosis made.
  • warn patients NOT to swim or submerge themselves in cold water
38
Q

What is an anaphylactoid reaction?

  • common triggers?
  • treatment?
A

Non-IgE mediated; instead they involve direct degranulation of mast cells

  • common triggers: IV contrast material, opioids
  • treatment: similar to anaphylaxis treatment
39
Q

What is serum sickness?

  • clinical manifestations?
  • diagnosis?
  • treatment?
A

Immune complex-mediated disease that begins 1-3 wks after an allergic exposure (ie. medication)

  • antigen-antibody immune complexes deposit in small vessels and cause vasculitis
  • clinical manifestations:
    1. Appear unwell
    2. Fever
    3. Rash
    4. Arthralgias/myalgias
    5. Abdominal cramping
    6. Diarrhea
  • diagnosis: depressed C3 and C4 levels, peripheral blood smear with increased number of plasma cells, skin biopsy of lesion with immune complex formation
  • treatment: mild = NSAIDs/antihistamines. Severe = steroids x 7-10 d, plasmapheresis
40
Q

A patient presents to you in anaphylaxis after 1st time eating peanut butter. Mom asks you how this is possible. What is your explanation?

A

In order to mount an allergic reaction, your body has to be previously exposed to the allergen in order for your body to have mounted antibodies to it (IgE).
-if a child has an allergic reaction the “first” time they’ve eaten something, they’ve definitely been exposed to it before often without parents knowing (ie. hidden in other foods) OR through maternal breast milk

41
Q

What is immunotherapy?

-indication?

A

Gradual introduction of increasing amounts of allergen to decrease sensitization

  • consider in patients with insect venom sensitivity who have had anaphylaxis due to insect bite
  • NOT effective for food allergies
42
Q

What is the atopic march?

A

Typical sequence of IgE antibody development and disease evolution in allergic patients
-Food allergies (early infancy) –> eczema (late infancy) –> asthma (early childhood) –> allergic rhinitis (late childhood)

43
Q

In which immunodeficiency do you see bony abnormalities?

A

SCID with ADA deficiency = autosomal recessive

-50% of children have bony abnormalities in ADA-deficient SCID

44
Q

What are clinical features of Heiner’s syndrome?

A
  1. Pulmonary hemosiderosis (due to recurrent bleeding into the lungs)
  2. GI bleeding
  3. Iron deficiency anemia
  4. FTT
    * **results from severe CMPA
45
Q

Patients with spina bifida are at increased risk for anaphylaxis on exposure to which agent?

A

Latex

46
Q

What is the best screening test for T-cell defect?

A

Candida skin test

47
Q

Which immunologic conditions can cause elevated IgE levels? (3)

A
  1. DiGeorge
  2. IgA deficiency
  3. Wiskott-Aldrich
48
Q

What are the indications for IVIG? (11)

A
  1. Humoral or combined immunodeficiency with low or absent levels of IgG
  2. Kawasaki
  3. B cell chronic leukemia
  4. HIV
  5. ITP
  6. GBS
  7. Chronic inflammatory demyelinating polyradiculopathy
  8. Graves Ophthalmopathy
  9. CMV-induced pneumonia in solid organ transplants
  10. TEN
  11. Prophylaxis of infection post BMT
49
Q

A male patient presents with a liver abscess. What condition should you exclude?

A

CGD

50
Q

A child has received IVIG for treatment of Kawasaki. How long do you have to wait before giving immunizations to ensure effective immune response?

  • high dose?
  • low dose?
A 
11 mo (if high dose IVIG)
8 mo (if low dose IVIG)
51
Q

What is the classic triad of ataxia-telangiectasia?

-treatment?

A
  1. Progressive ataxia
  2. B and T cell deficiency
  3. Telangiectasia not present at birth
    - treatment: supportive since bone marrow transplant is not possible (not tolerated well)
52
Q

What is the inheritance pattern of hereditary angioedema?

  • what is the deficiency?
  • clinical features?
A

Autosomal dominant

  • C1 esterase deficiency
  • complement system is activated and cannot deactivate itself
  • clinical features:
    1. Angioedema (non-pitting): self-resolves within 3 days
    2. No pruritis/erythema/pain
    3. Abdo pain = can be secondary to angioedema of bowel
    4. Hoarseness and stridor due to airway edema
53
Q

What are the triggers for angioedema episodes in hereitary angioedema? (5)

A
  1. Medications: OCP
  2. Pregnancy
  3. Stress
  4. Infection
  5. Menstruation

Aka being a lady

54
Q

What is the treatment of hereditary angioedema?

A
  1. Concentrate of C1 esterase inhibitor

2. Danazol: androgen

55
Q

What is the treatment for chronic urticaria?

A

First line: H1 antihistamine
If no result: add H2 antihistamine
If no result: then add PO steroids on alternating days

56
Q

A patient who is post-cardiac transplant and is on immunosuppressive therapy develops fever, weight loss, fatigue and an enlarging lymph node. What is the most likely diagnosis?

  • what is the most likely cause?
  • treatment?
A

Post-transplant lymphoproliferative disease = occurs as result of immunosuppression in patients who have undergone solid organ or allogeneic stem cell transplantation

  • 90-95% are associated with EBV proliferation in B cells due to suppressed T cells by immunosuppressants
  • this is a MALIGNANT condition! (20% of all patients)
  • treatment: reduction of immunosuppression, rituximab, chemotherapy, and radiation therapy
57
Q

In the following cases, list what you would expect to see for serum IgG, IgA, IgM, T-cell function and parathyroid function?

  • 5 yo boy, who after 3 months of age, developed recurrent OM, pneumonia, diarrhea, sinusitis, often with simultaneous infections at 2 or more disparate sites
  • a distinctive appearing 8 mo old boy with interrupted aortic arch, hypocalcemia, cleft palate
  • 1 yo boy with severe eczema, recurrent middle ear infections, lymphopenia, thrombocytopenia
  • 9 yo with eczema like rash and recurrent severe staph infections
  • 4 mo with FTT, chronic diarrhea, variety of rashes, recurrent serious bacterial, fungal, viral infections
A
  • 5 yo boy: hypogammaglobulinemia: low IgG, IgA, IgM, normal T cell function, normal parathyroid function
  • 8 mo boy: DiGeorge syndrome = normal immunoglobulins, decreased T cell function, decreased parathyroid function
  • 1 yo boy: Wiskott Aldrich = Normal IgG, High IgA, Low IgM, decreased T cell function, normal parathyroid function

9 yo: Joe-Buckley syndrome = disorder of phagocytic chemotaxis associated with hypergammaglobulin E, eczema like rash and recurrent severe staphylococcal infections = normal IgG, IgM, IgA, high IgE, normal T cell function, normal parathyroid function

4 mo: SCID = low IgG/IgA/IgM, decreased T cell function, normal parathyroid function

58
Q

What are the levels of immunoglobulins seen in Wiskott-Aldrich syndrome? (IgM, IgA, IgE)

A
  1. Increased IgA and IgE

2. Decreased IgM

59
Q

What is the most common type of primary immunodeficiency?

A

By far: humoral deficiencies (65%)

-then combined (15%), then phagocytic (10%), then complement and cellular (5% each)

60
Q

What are the 10 warning signs of primary immunodeficiency?

A
  1. 4 or more new ear infections within 1 year
  2. Two or more serious sinus infections within 1 year
  3. Two or more months on abx with little effect
  4. Two or more pneumonias within 1 year
  5. FTT
  6. Recurrent deep skin or organ abscesses
  7. Persistent thrush in mouth or fungal infection on skin
  8. Need for IV abx to clear infxns
  9. Two or more deep seated infections including septicemia
  10. Family history of immunodeficiency
61
Q

What are tests to order for suspected humoral deficiency?

  • cellular deficiency?
  • phagocytic assessment?
  • complement assessment?
A
  • Humoral deficiency:
    1. Immunoglobulins
    2. Titres to vaccines (usually will show no response to prior vaccines)
  • Cellular deficiency:
    1. CBC to look at lymphocytes
    2. Intradermal skin testing with candida = will see no urticaria
    3. Thymic biopsy
  • Phagocytic assessment:
    1. Nitroblue tetrazolium
    2. Neutrophil oxidative burse index
  • Complement assessment:
    1. CH50
    2. C1 esterase inhibitor levels
62
Q

An 11 mo female has recurrent viral infections following cardiac surgery. She has FTT and abnormal facial features. CD4+ t cells are 800 cells/ml (normal is >1500). IgG is slightly low. What is your move appropriate immunological management?

a. Delay live vaccines until T cells are evaluted
b. immunoglobulin replacement therapy
c. prophylactic abx
d. bmt

A

Answer: A
This is DiGeorge!
-ONLY give .live viral vaccines when immune competence has been demonstrated! ie. when T cells are evaluated and found to be at normal levels (normal = >1500)

63
Q

What are the clinical features of autoimmune lymphoproliferative syndrome?
-management?

A

ALPS = autoimmune cytopenias, lymphoproliferation in spleen, lymph nodes,

  • see elevated % of T cells not expressing CD4 or CD8
  • increased risk of malignancy
  • management: immune suppression
64
Q

What are the clinical features of IPEX?

-treatment?

A
  • immune dysregulation, poly-endocrinopathy, enteropathy, X-linked disorder! (IPEX)
  • see severe colitis, cytopenias, polyendocrinopathy (usually neonatal insulin dependent diabetes), seen in males
  • treatment: immunosuppression and BMT
65
Q

A 1 yo male has persistent bloody diarrhea, eczema and insulin dependent diabetes mellitus. Normal CBC, IgA, IgG, IgM, elevated IgE. Normal CD4+, T cell and CD8+ T cell numbers and function. What is your diagnosis?

A

IPEX! Immune dysregulation, polyendocrinopathy, enteropathy, x linked

Royal College Peds 2021 (55 decks)

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