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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
Q

Nitroblue tetrazolium test is used to diagnosis?

A

Chronic granulomatous disease

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26
Q

Leukocyte adhesion molecule deficiency presents with delayed separation of umbilical cord, poor wound healing and recurrence abscesses T/F

A

F - patients are unable to form abscesses as neutrophils cannot leave blood vessels

Also have vasculitic skin lesions

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27
Q

T cell proliferation assay is useful in the diagnosis of cellular immune deficiencies. Examples?

A

DiGeorge
Wiskott- Aldrich
Combined immune deficiency

28
Q

Is hereditary angioedema autosomal dominant or recessive?

A

Autosomal dominant

29
Q

Is the oedema in hereditary angioedema pitting and or urticarial?

A

It is neither (non pitting, non urticarial)

Note: can be precipitated by pressure, stress, surgery or exercise

30
Q

Common features of hereditary angioedema?

A

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
Q

Patients with hypogammaglobulinaemia are especially prone to infections by which organism type?

A

Encapsulated - H. influenzas, meningococcus and strep pneumo

32
Q

Which immunoglobulin can activate complement via the alternative pathway?

33
Q

HyperIgE is associated with eosinophilia and thrombocytopenia T/F

A

F - associated with eosinophilia but not thrombocytopenia

Note: WAS is associated with thrombocytopenia. Both WAS and hyperIgE are assoc with eczema

34
Q

What is the typical triad of Wiskott-Aldrich syndrome?

A
  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
Q

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?

A

Fresh frozen plasma -as it contains C1 esterase inhibitor.

36
Q

What is the cause of hyper-acute rejection in organ transplant?

A

Pre-existing antibodies, happens within minutes to hours

37
Q

What is the cause of acute cellular rejection in organ transplant?

A

Lymphocytes than have been activated against donor antigens, commonly occurs in the first 6 months after transplant

38
Q

What is the allergy testing of choice?

A

Skin prick testing

39
Q

3 major complications of common variable immune deficiency?

A
  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
Q

Periodic fever syndrome is most likely to be associated with elevation in which Ig?

A

IgD

HyperIgD syndrome is associated with episodes of fever every 4-8 weeks and associated abdo pain, arthralgia, diarrhoea, emesis, lymphadenopathy and rash

41
Q

A patient with recurrent N meningitidis infections could have a primary immunodeficiency associated with what complement deficiency?

A

The lytic complement pathway ( c5 - c9)

42
Q

In a patient with SCID due to deficiency of adenosine deaminase what important cell function is impaired?

A

Purine salvage

43
Q

Long term mgmt of pt with anaphylactic peanut allergy?

A

Life long avoidance

NICE does not recommend oral immunotherapy

44
Q

What is omalizumab used for?

A

Allergic asthma and chronic urticaria (anti IgE monoclonal antibody)

45
Q

Abnormalities of the interferon gamma pathway will result in vulnerability to what type of infections?

A

Mycobacterial

46
Q

Patients with x linked agammaglobulinaemia present with recurrent bacterial and viral infections starting around 3-6 months of life T/F

A

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
Q

Contact dermatitis is mediated by?

A

T lymphocytes

48
Q

Kinins are proteins that attract phagocytes T/F

A

T

They also have role in pain, smooth muscle contraction, vasodilation and increasing the permeability of blood vessels

49
Q

Kinins perforate invading bacteria T/F

A

F

Complement perforates invading bacteria. Complement also stimulates histamine release and attracts neutrophils

50
Q

Complement stimulates histamine release and attracts phagocytes T/F

A

F - does stim histamine release but attracts neutrophils (not phagocytes)

51
Q

HyperIgE and HyperIgM are primarily a problem with what cells?

A

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
Q

Features of DRESS (drug reaction with eosinophilia and systemic symptoms)

A 
Pyrexia 
Arthralgia
Generalised lymphadenopathy 
Facial oedema
Rash: morbilliform or erythrodermic, often associated with pustules, papules, bullae or purpura
53
Q

Drugs associated with DRESS and typical time from exposure?

A 
AEDs such as phenytoin, carbamazepine, phenobarbitol
NSAIDs
Minocycline
Lithium
Fluoxetine

Usually 2-8 weeks but can be up to 12 weeks

54
Q

In a patient with early onset SLE and recurrent pyogenic infections what other deficiency should be suspected?

A

C2 complement deficiency

55
Q

Leukocyte adhesion deficiency Type 1 is associated with neutropenia T/F

A

F - it is associated with elevated neutrophils

56
Q

What is the mgmt of linear IgA bullous dermatosis?

A

If possible d/c the likely causative agent ( common is vancomycin)
If not possible treat with dapsone

57
Q

When does Bruton agammaglobulinaemia usually present?

Mgmt?

A

Around 4-6 months of age when transplacentally acquired IgG declines
Monthly IV immunoglobulin, no live vaccines

58
Q

Treatment of IgA deficiency?

A

There is no specific treatment, prophylactic antibiotics may be used in severe cases.

59
Q

Can children with a history of true anaphylaxis receive the flu vaccine?

A

Yes and they do not need to receive it in any particular setting/ receive any special monitoring

60
Q

Iodine allergy is a risk factor for radioiodine contrasts reaction T/F

A

F - note neither is shellfish allergy

RFs: female; asthma/atopy and CV disease

61
Q

Features of serum like sickness vs DRESS

A

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
Q

Partial albinism
Progressive neuro abnormalities
Recurrent pyogenic infections
Coag defects

What syndrome?

A

Chediak-Higashi

Note: Disease characterized by abnormal lyso- somes/granules in all cell types. Infections are mostly skin and respiratory tract

63
Q

Serum sickness can occur after initial exposure to a foreign substance and does not require a prior exposure T/F

64
Q

Patients with hyperIgM are particularly susceptible to what organism?

A

Pneumocystis

Cryptosporidium

65
Q

What is typical about the location of rash in a fixed drug eruption?

A

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
Q

Typical appearance of rash in fixed drug eruption

A

Well circumscribed, dusky, slightly oedematous. Central blistering often develops followed by desquamation, crusting and residual hyperpigmentation that may persist for months

67
Q

Patients with cyclic neutropenia are at risk of sepsis by Clostridium septicum. T/F

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