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2016 Flashcards

1
Q

what is a BAT and how is it done?

A
  • BAT is a basophil activation test, which measures release of histamine from basophils when mixed with an allergen.
  • the most commonly used marker is CD63 to measure basophil activation
  • it is done by incubating an allergen and the patients serum and an activation buffer like IL-3, when the allergen binds and cross links IgE this leads to expression of CD63 and CD203
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2
Q

what are the most common way that basophils are activated in CSU?

A

Binding of Autoantibodies to the high affinity FCeRI receptor (IgE receptor)

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3
Q

name 4 features of photo toxic reactions

A
  1. requires a large amount of agent for eruption
  2. clinical appearance: sunburn, erythema, edema, bullae
  3. timing: erythroderma (mins to hrs) after sun exposure
  4. path: direct tissue injury
  5. incidence: high
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4
Q

name 4 features of photo allergic reactions

A
  1. path: immunogenic delayed type 4 hypersensitivity
  2. timing: onset of eruption is 24-48hrs after exposure
  3. incidence: low
  4. small amount of agent is required for rxn to occur
  5. clinical appearance: eczematous, vesicles, scaling, pruritic
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5
Q

what are lamellar bodies?

A
  • secretory organelles in the upper stratum of the skin layer
  • contain phospholipids, enzymes, cholesterol, B defensin 2, proteins and lipases
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6
Q

mutation in AD and the function of that gene

A
  • filaggrin mut

- mutation leads to decreased integrity of skin barrier, loss of hydration and infection inflammation

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7
Q

lab tests to order in EGPA

A
  1. CBC w smear for eosinophilia
  2. ANCA
  3. IgE
  4. CRP/ESR
  5. ?tissue biopsy
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8
Q

histological features of EGPA

A
  1. eos infiltrate in vessel
  2. perivascular necrotizing granulomas
  3. giant cell vasculitis
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9
Q

most common extra pulmonary manifestations of EGPA

A
  1. mononeuritis multiplex or polyneuropathy

2. allergic rhinitis

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10
Q

two phenotypes of nasal polyps

A
  1. eosinophilc

2. neutrophilic

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11
Q

in which type of CRS is TGF-b increased

A

CRSsNP

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12
Q

what is samters triad

A
  1. Nasal polyps
  2. Asthma
  3. Aspirin sensitivity
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13
Q

define CRS

A
  1. persistent symptoms fro > 12 weeks, 2 of which are
    - pain or pressure
    - obstruction
    - discharge
    - smell decreased
  2. evidence of inflammation on CT or rhinoscopy
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14
Q

what % of people with AR have conjunctivitis too

A

60%

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15
Q

treatment of mild to moderate rhino conjunctivitis

A

non pharma:

  • avoidance of triggers and allergens
  • HEPA filtres, vacuums, remove carpeting, remove animals, wash bedding

pharma

  • PO AH
  • INCS
  • topical AH eye drops with mast cell stabilizers PRN
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16
Q

3 y.o F with recurrent chest infections, normal CBC and IgGs. What two non invasive tests would you use?
what are three ddx relevant to this age?

A
  • CXR
  • sweat chloride
  • vaccine titres

ddx

  • CF
  • PCD
  • Asthma
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17
Q

what cytokine mediates IgA class switching in the gut?

A

CD40L and TGF-B

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18
Q

name of cells that uptake antigen into payer patches

A

M cells

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19
Q

4 situations in which Xolair is used

A
  1. severe allergic asthma
  2. CSU not responding to 2nd gen AH
  3. CRS w Nasal polyposis
  4. Idiopathic anaphylaxis
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20
Q

weight restrictions for Xolaire

3 indications for xolair in asthma

A

6-12: 20-150kg and IgE 30-1300
12 +: 30-150 kg and IgE 30-700

  1. uncontrolled asthma on ICS
  2. sensitization to an aeroallergen on SPT or sIgE
  3. exacerbation in the last year
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21
Q

4 RFs for OAS

A
  1. Pollen allergic
  2. high sIgE to pollens
  3. Allergic rhinitis
  4. Fhx of atopy
  5. living in are area with high prevalence of pollen
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22
Q

venom testing

  1. SPT dose
  2. ID dose
  3. min and max VIT dose
A
  1. 100 mcg/ml
  2. 1 mg/ml (can start with 0.001 mcg/ml, then 0.01 mcg/ml, then 0.01 mcg/ml)
  3. min 50 mcg/ml min and 100 mcg/ml max maintenance dose, however can go up to 200 mcg/mL if having breakthrough anaphylaxis to a sting
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23
Q

where does positive and neg selection occur in the thymus?

A

positive - cortex

negative - medulla

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24
Q

purpose of positive selection

A
  • to rescue thymocytes from apoptosis

- promotes survival of T cells and determining the spectrum of antigens that T cells can recognize

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25
Q

purpose of negative selection

A
  • this process prevents the survival of T cells that if were released into the periphery would cause auto immunity
26
Q

ddx for conjunctivitis

A
  1. VKC
  2. AKC
  3. Atopic KC
  4. Viral infection - adenovirus
  5. GPC
27
Q

indications to add LABA

A
  1. Step 3 GINA

2. Teen an use ICS/LABA PRN as step 1 or at step 2 can used maintenance and reliever ICS/LABA

28
Q

Patient has LLR to insect sting, whats your approach?

A

LLR is no longer and indication for VIT unless the following circumstances

  • frequent unavoidable exposure
  • unstable CV/resp disease
  • elevated serum tryptase
  • detrimental effect on QOL
29
Q

prognosis of milk allergy

A
  • 40% out grow by age 8, and 80% by age 16
30
Q

what % of children can tolerated BM and EG

31
Q

what is the heat labile component of milk

what is the heat stable component of milk

A
  • Bos d 4-6 (labile)

- Casein bos d 8 (stable)

32
Q

CMPA criteria to treat a family member

A
  1. emergency condition and no one else available
  2. minor condition and no one else available
  3. must not provide ongoing care
33
Q

1 requirement of physicians related to duty to themselves

A
  • participating in self regulation: includes seeking help from colleagues when needed, protect and enhance own health, lifelong learning
34
Q

2 criteria for determining costs for the non insured treatment

A
  • nature of the service provided

- patients ability to pay

35
Q

what are the options for TREGs that are negatively selected

A
  • apoptosis
  • cell anergy
  • becoming a treg
36
Q

What is AIRE?

A
  • AIRE is the autoimmune regulatory gene
  • it induces expression of self antigens which help in negative selection of T cells in central tolerance
  • lack of AIRE leads to auto reactive T cells in the periphery and multi organ AI (APECED)
37
Q

which cytokines are secreted by Tregs

A

IL-10

INF-b

38
Q

what is the phenotype of ADA SCID

39
Q

what is the phenotype in XL SCID

A

T- B+NK-

defect in IL-2

40
Q

What is the function of B cells in XLSCID?

A
  • they are present but not functional due to lack of stim from T cells and absent signalling from IL4 and IL21
41
Q

what is ADA and why does it cause SCID?

A
  • ADA is an enzyme found in cells that catalyzes the deamination of adenosine and deoxyadenosine
  • in ADA def you get a build up of metabolites which is toxic to lymphocytes
42
Q

why do patients with PJP and SCID get worse after transplant?

A
  • Immune reconstitution syndrome: a systemic inflammatory response that occurs after treatment is started, it is a paradoxical reaction
43
Q

name 2 polysaccharide vaccines

A
  • pneumococcal
  • hib

they require B cells to function and are used to assess the response to polysaccharide antigens

44
Q

name 2 protein vaccines

A
  • tetanus
  • diptheria

require both T and B cell functioning
evaluation ab mediated response to protein antigens

45
Q

what binds C1q hexamer?

A
  • IgM and IgG
46
Q

define desensitization

A

increase in reaction threshold to an allergen while receiving active therapy, often a temporary state which depends on continuous exposure

47
Q

define tolerance and give two features of it

A
  • state of not reacting to an allergen
  • the end goal of desensitization

features

  • movement away from Th2 response
  • permanent protection
  • non responsiveness of immune system to antigens
48
Q

what are adjuvants?

A
  • a compound or molecule incorporated with allergen/antigen to enhance immunogenicity
49
Q

why are adjuvants needed for pollen IT?

A
  • to increase immunogenicity without increasing allergenicity
50
Q

list 3 adjuvants in AIT

A
  1. CpG
  2. Aluminum hydroxide
  3. calcium phosphate
51
Q

what is the difference between protein and polysaccharide vaccine

A

Protein - B cell response T cell dependent, get formation of memory cells and isotype switching

Polysaccharide - B cell response is T cell independent, no isotype switching, limited memory

52
Q

Name lab tests in anaphylaxis and when to measure them

A

Serum total Tryptase - ideally 30-120 min from reaction, but up to 6 hours is still acceptable
Mature trypase - ideally 30-90 min from rxn
24 hr urine histamine - may be elevated in urine collected up to 24 hrs after symptom-onset
24 hr urine n - methylhistamine
24 hr urine prostaglandin

53
Q

Can pts with a sulfa allergy have latex

A

Yes.
Those with sulfonamide abx allergy are not at increased risk of reaction with non-abx sulfonamide. Exceptions include sulfasalazine, which is broken down into sulfapyridine which is similar to the structure in sulfonamide abx. Also possible dapsone.

54
Q

Differences between innate and adaptive immune system

A

Innate:

  • involves NK cells, neutrophils, monocytes and macrophages
  • uses receptors that recognize PAMPS (LPS, flagellin, nucleic acid)
  • non specific recognition
  • occurs minutes to hours
  • no memory is created

Adaptive - specific refined recognition

  • uses B and T cell receptors that recognize specific antigens on pathogens
  • uses CD4 and CD8 t cell
  • immunity is generated by recombination of VDJ regions and hyper variation
55
Q

what defines protection after pneumovax

A

There are 23 antigens in the pneumovax vaccine
>/= 1.3 ug/mL Ab titer, a normal person will have a 2 x increase in 70% of the serotypes assayed defines protection in >6, in under 6, this number is 50%.

56
Q

which vaccines cause a secretory IgA response

A
  1. rotavirus
  2. intranasal influenza
  3. oral polio
  4. oral typhoid
57
Q

RFs for RCM rxn

A

Female
Asthma
Previous rxn to RCM
Bblockers or cardiac comorbidity

58
Q

Mgmt of RCM hypersensitivity

A

Use different RCM than previous time - use non-ionic, hypo/iso-osmolar
Avoid RCM if possible
Medic-Alert bracelet
Can consider pre-medication prior to next procedure, although not strong evidence that it is effective:
Prednisone 50 mg 13, 7, and 1 hr prior
OAH 1 hour prior

59
Q

most common cause of CVID

A
  • idiopathic or unknown

- genetic mutations in NKKB1 and TACI

60
Q

non infectious complications of CVID

A
  1. ILD
  2. Malignancy
  3. Autoimmunity
  4. GI manifestations
  5. Splenomegaly

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