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Allergy/Immunology Flashcards

1
Q

Best way to exclude antibody deficiency

A

check for specific antibodies to haemophilus, pneumococci and tetanus

Note: Immunoglobulins and subclasses can be normal in the setting of specific

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2
Q

Henoch-Schonlein Purpura is an immune complex type 2 hypersensitivity reaction T/F

A

False - type 3; not 2

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3
Q

What are some features of non IgE mediated food allergy?

A

Eczema
FTT
Irritability
Reflux

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4
Q

What lab is abnormal in hereditary angio edema C3 or C4?

A

C4 will be low

C3 is always normal

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5
Q

Post strep glomerulonephritis is what type of hypersensitivity?

A

Type III - immune complex deposition

Other Type III: SLE, serum sickness, reactive arthritis
Immune complex deposition

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6
Q

Example of a type I hypersensitivity reaction?

A

Anaphylaxis

Mediated by mast cells

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7
Q

Type II hypersensitivity reaction examples?

A

Autoimmune haemolytic anaemia

Rheumatic heart disease

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8
Q

What are type IV hypersensitivity reactions mediated by?

A

T cell

Examples: contact dermatitis, Mantoux test , GVHD, rheumatoid arthritis

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9
Q

Different reasons for patch vs skin prick testing?

A

Patch is for late phase reactions - contact dermatitis to latex for example , drug allergies
Skin prick is for IgE mediated immediate reactions

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10
Q

DiGeorge syndrome is assoc with what immuno abnormality?

A

Absent T cells

Note: may have normal serum immunoglobulins but low antibody responses.

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11
Q

Bruton’s disease is assoc with what immuno abnormality?

A

Absent mature B cells

This results in panhypogammaglobulinemia

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12
Q

Cow’s milk protein intolerance can manifest as anaphylaxis and shock T/F

A

T

Can also have other features of allergy without anyphylaxis

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13
Q

Rheumatoid arthritis is what type of hypersensitivity reaction?

A

Type IV

Note: as are contact dermatitis, Mantoux test , GVHD
Involves T cell antigens, delayed

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14
Q

What leukotrienes are involved in anaphlyaxis?

A

B4, C4, D4 and E4

NOT A4

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15
Q

In anaphylaxis what % of patients will have a repeat episode within 8 hours?

A

More than 20%

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16
Q

What is the prevalence of food allergies in westernised countries?

A

About 5%

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17
Q

What pneumococcal vaccine protects against more serotypes the conjugated or unconjugated?

A

Unconjugated (30-40 serotypes)

Note: conjugated is only 13 serotypes

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18
Q

What system is most commonly affected by IgE mediated cows’ milk protein allergy?

A

Skin

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19
Q

What system is most commonly affected by non IgE mediated cows’ milk protein allergy?

A

GI

Note: non IgE is delayed hypersensitivity

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20
Q

How is scombroid fish allergy mediated?

A

It is a histamine overdose - it occurs as a result of bacterial overgrowth producing the scombroid toxin.

Note: it is not IgE mediated and not a true allergy but an overdose as stated above

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21
Q

What is the inheritance of chronic granulomatous disease?

A

X linked

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22
Q

What are the typical organisms that cause infections in patient with chronic granulomatous disease?

A

Catalase positive

Remember as PLACESS for cats
Pseudomonas
Listeria
Aspergillus
Candida
E coli
S aureus 
Serratia
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23
Q

What cell type is deficient in chronic granulomatous disease? How does it typically present?

A

Phagocytes

Deep abscess, skin infections and pneumonia due to catalase + organisms. Can also present with colitis

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24
Q

How is cyclic neutropenia diagnosed?

How does it present?

A

Twice weekly full blood counts for 8 weeks (this is the only method to diagnosis!)

Cyclical fevers, mouth ulcers and bacterial infections

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25
Nitroblue tetrazolium test is used to diagnosis?
Chronic granulomatous disease
26
Leukocyte adhesion molecule deficiency presents with delayed separation of umbilical cord, poor wound healing and recurrence abscesses T/F
F - patients are unable to form abscesses as neutrophils cannot leave blood vessels Also have vasculitic skin lesions
27
T cell proliferation assay is useful in the diagnosis of cellular immune deficiencies. Examples?
DiGeorge Wiskott- Aldrich Combined immune deficiency
28
Is hereditary angioedema autosomal dominant or recessive?
Autosomal dominant
29
Is the oedema in hereditary angioedema pitting and or urticarial?
It is neither (non pitting, non urticarial) Note: can be precipitated by pressure, stress, surgery or exercise
30
Common features of hereditary angioedema?
Can mimic acute abdomen, recurrent abdominal pain, diarrhoea and emesis Recurrent episodes of angioedema mainly effect the face limb and genitals Can have laryngeal oedema - change in voice, secretions and stridor which is life threatening Family history
31
Patients with hypogammaglobulinaemia are especially prone to infections by which organism type?
Encapsulated - H. influenzas, meningococcus and strep pneumo
32
Which immunoglobulin can activate complement via the alternative pathway?
IgA
33
HyperIgE is associated with eosinophilia and thrombocytopenia T/F
F - associated with eosinophilia but not thrombocytopenia Note: WAS is associated with thrombocytopenia. Both WAS and hyperIgE are assoc with eczema
34
What is the typical triad of Wiskott-Aldrich syndrome?
1. Recurrent bacterial sinupulmonary infections 2. Eczema 3. Bleeding diathesis caused by thrombocytopenia and plt dysfunction Note: Will also have increased IgA and decreased IgM. Platelets are small. Contrast with Bernard-Soulier in which they are large
35
A patient with known hereditary angio-oedema presents to the ED with stridor, there is no C1 esterase inhibitor available for a few hours. What can be used while waiting?
Fresh frozen plasma -as it contains C1 esterase inhibitor.
36
What is the cause of hyper-acute rejection in organ transplant?
Pre-existing antibodies, happens within minutes to hours
37
What is the cause of acute cellular rejection in organ transplant?
Lymphocytes than have been activated against donor antigens, commonly occurs in the first 6 months after transplant
38
What is the allergy testing of choice?
Skin prick testing
39
3 major complications of common variable immune deficiency?
1. Bronchiectasis 2. Malignancy (esp B cell lymphoma) 3. AI disease (up to 20%) Note: AI diseases are diagnosed clinically as may not produce autoantibodies. Often also have GI issues - malabs; chronic diarrhoea, IBD
40
Periodic fever syndrome is most likely to be associated with elevation in which Ig?
IgD HyperIgD syndrome is associated with episodes of fever every 4-8 weeks and associated abdo pain, arthralgia, diarrhoea, emesis, lymphadenopathy and rash
41
A patient with recurrent N meningitidis infections could have a primary immunodeficiency associated with what complement deficiency?
The lytic complement pathway ( c5 - c9)
42
In a patient with SCID due to deficiency of adenosine deaminase what important cell function is impaired?
Purine salvage
43
Long term mgmt of pt with anaphylactic peanut allergy?
Life long avoidance NICE does not recommend oral immunotherapy
44
What is omalizumab used for?
Allergic asthma and chronic urticaria (anti IgE monoclonal antibody)
45
Abnormalities of the interferon gamma pathway will result in vulnerability to what type of infections?
Mycobacterial
46
Patients with x linked agammaglobulinaemia present with recurrent bacterial and viral infections starting around 3-6 months of life T/F
F - recurrent bacterial infections. 3-6 months is correct as that is when maternal IgG decreased Note: CVID and SCID will have bacterial and viral infections
47
Contact dermatitis is mediated by?
T lymphocytes
48
Kinins are proteins that attract phagocytes T/F
T They also have role in pain, smooth muscle contraction, vasodilation and increasing the permeability of blood vessels
49
Kinins perforate invading bacteria T/F
F Complement perforates invading bacteria. Complement also stimulates histamine release and attracts neutrophils
50
Complement stimulates histamine release and attracts phagocytes T/F
F - does stim histamine release but attracts neutrophils (not phagocytes)
51
HyperIgE and HyperIgM are primarily a problem with what cells?
IgE : Neutrophils - they fail to adhere to the endothelium and enter tissues. IgM : T cells - failure of T cell activation and Ig isotope switching
52
Features of DRESS (drug reaction with eosinophilia and systemic symptoms)
``` Pyrexia Arthralgia Generalised lymphadenopathy Facial oedema Rash: morbilliform or erythrodermic, often associated with pustules, papules, bullae or purpura ```
53
Drugs associated with DRESS and typical time from exposure?
``` AEDs such as phenytoin, carbamazepine, phenobarbitol NSAIDs Minocycline Lithium Fluoxetine ``` Usually 2-8 weeks but can be up to 12 weeks
54
In a patient with early onset SLE and recurrent pyogenic infections what other deficiency should be suspected?
C2 complement deficiency
55
Leukocyte adhesion deficiency Type 1 is associated with neutropenia T/F
F - it is associated with elevated neutrophils
56
What is the mgmt of linear IgA bullous dermatosis?
If possible d/c the likely causative agent ( common is vancomycin) If not possible treat with dapsone
57
When does Bruton agammaglobulinaemia usually present? | Mgmt?
Around 4-6 months of age when transplacentally acquired IgG declines Monthly IV immunoglobulin, no live vaccines
58
Treatment of IgA deficiency?
There is no specific treatment, prophylactic antibiotics may be used in severe cases.
59
Can children with a history of true anaphylaxis receive the flu vaccine?
Yes and they do not need to receive it in any particular setting/ receive any special monitoring
60
Iodine allergy is a risk factor for radioiodine contrasts reaction T/F
F - note neither is shellfish allergy RFs: female; asthma/atopy and CV disease
61
Features of serum like sickness vs DRESS
Serum sickness: 7 -14 days; rash is urticarial and red; does not involve internal organs DRESS: 1 - 8 weeks: rash can also be urticarial and red but also pustular; can involve internal organs. Often have elevated transaminases, eosinophilia and atypical lymphocytes Note: both have fever and lymphadenopathy
62
Partial albinism Progressive neuro abnormalities Recurrent pyogenic infections Coag defects What syndrome?
Chediak-Higashi Note: Disease characterized by abnormal lyso- somes/granules in all cell types. Infections are mostly skin and respiratory tract
63
Serum sickness can occur after initial exposure to a foreign substance and does not require a prior exposure T/F
T
64
Patients with hyperIgM are particularly susceptible to what organism?
Pneumocystis | Cryptosporidium
65
What is typical about the location of rash in a fixed drug eruption?
Characteristically recurs in the same locations upon reexposure to the offending drug. Note: typical location is hands, trunk, genital. Sometimes perioral/lips. Initial lesions do not appear for a week or more after drug ingestion but subsequent time occurs within HOURS.
66
Typical appearance of rash in fixed drug eruption
Well circumscribed, dusky, slightly oedematous. Central blistering often develops followed by desquamation, crusting and residual hyperpigmentation that may persist for months
67
Patients with cyclic neutropenia are at risk of sepsis by Clostridium septicum. T/F
True

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