Allergy and Immunology Flashcards

First Aid and NEJM Knowledge+

1
Q

Differentiate epidermal vs intradermal tests for allergen skin testing

A

Both are used to test for presence of allergen-specific IgE antibody

Epidermal skin test- some antigen extract put on skin then punctured into epidermis to see if IgE mediated response
-adequate for most things

Intradermal test of injected antigen into dermis for drug reactions
-use for venom and penicillin testing

Both should include histamine and saline controls, look for wheal and flare reaction 15-20 minutes after injection

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2
Q

What is RAST testing used for?

(a) What allergies can it not test for

A

RAST test = test serology for antigen-specific IgE (basically to see if there is an allergy)
Use when skin testing unavailable or not possible (ex: pt just took benadryl or would cause anaphylaxis)
-more for environmental and food allergens

However RAST alone is not adequate for venom (bee sting) or drug allergy (need intradermal skin test)

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3
Q

Candida and PPD purified antigens injected into skin- what is this a test of?

A

Both test for cell-mediated immunity

Lack of response to injection indicates inadequate cell-mediated immunity or anergy

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4
Q

Buzzword: otherwise healthy pt p/w recurrent neisseria meningitis

A

Recurrent neisserial infections c/w terminal complement deficiency (C5-C9 which makes the MAC complex)

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5
Q

What can be used as a screening test for the classic complement pathway?

A

CH50 can be used as a screening test for the classic complement pathway (triggered by immune complexes)
B/c all elements C1-C9 are needed to make normal CH50

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6
Q

Mnemonic for hypersensitivity type I-IV reactions

A

‘ACID’

Type I- anaphylactic
Type II- cytotoxic (antibodies directed at self cells)
type III- immune complex mediated
type IV- delayed hypersensitivity (T- cell mediated)

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7
Q

Describe the mechanism of type I hypersensitivity reaction

A

Type I = anaphylactic

Antigen exposure causes cross-linking of IgE on mast cells or basophils => release of histamine, leukotrienes, PGEs, and tryptase => symptoms

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8
Q

Give clinical examples of type II hypersensitivity

A

ACID- anaphylactic, cytotoxic (Ab mediated), immune complex, delayed hypersensitivity (T-cell)

Examples of antibody mediated hypersensitivity reaction:

  • drug-induced (ex: PCN) autoimmune hemolytic anemia
  • autoimmune thyroiditis
  • Goodpasture’s syndrome
  • ABO incompatibility
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9
Q

Describe the mechanism of type II hypersensitivity reaction

A

IgM or IgG antibodies produced that attack self- cell surface or tissue antigens

These IgM/G antibodies destroy cells by

  1. opsonization (coating for phagocytosis)
  2. complement-mediated lysis
  3. antibody-dependent cellular toxicity
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10
Q

Describe the mechanism of type III hypersensitivity reaction

A

‘ACID’: anaphylaxis, cytotoxic (auto-immunity), immune complex, delayed (T-cell)

Exposure to antigen in genetically predisposed individuals cause antigen-antibody complex formation, these immune complexes activate complement and neutrophil invasion => tissue inflammation

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11
Q

Prototypical type III hypersensitivity rxn

A

Serum sickness- where exposure to certain drugs (most frequently beta-lactam abx) causes symptoms 10-14 days after exposure due to immune complex deposition (causing inflammation and neutrophil invasion) into tissues

=>

rash
pruritus
arthralgia
fever
lymphadenopathy
malaise
hypotension
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12
Q

Most common type of type IV hypersensitivity rxn

A

Allergic contact dermatitis such as poison ivy (diagnosed by skin patch testing)

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13
Q

Describe the mechanism of type IV hypersensitivity reaction

A

Antigen (ex: poison ivy) directly activates already sensitized T cells (usually CD4+ cells)

CD4 activation => tissue inflammation 48-96 hrs after exposure

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14
Q

Best diagnostic test for allergic contact dermaitits

A

Allergen patch test- substance covered by adhesive x48 hrs- then watch for erythema, edema, vesiculation

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15
Q

Which to test for the following deficiencies

(a) Humoral immunity deficiency
(b) NK cell deficiency

A

(a) Test CD19 for B cell immunity

(b) Test CD16 and CD56 for natural killer cell immunity

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16
Q

19 y/oM w/ asthma- taking ICS BID and albuterol as needed

Persistent wheeze and cough day and night 2x per week

Next step in management?

A

Is on meds for mild persistent (ICS and SABA PRN) but now meets criteria for moderate persistent (given more than 2 nights a month) =>

Increase to medium dose ICS
Add LABA

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17
Q

Use of methacholine challenge in diagnosing asthma

A

Methacoline challenge alone is not diagnostic for asthma- negative test rules out asthma (sensitive) but not very specific (positive test can be from other things)

So sensitive but not specific

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18
Q

Numeric datapoint useful in helping when to use systemic corticosteroids in asthma exacerbation

A

Consider systemic ‘roids when PEF (peak expiratory flow) remains under 80% of personal best after albuterol

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19
Q

Which asthma related med, when used as mono therapy, is associated w/ asthma-related deaths

A

LABA (salmeterolol, formoterol) mono therapy associated w/ asthma-related death => hence why always used in combo w/ ICS

ex: symbicort = budesonde (ICS) + formoterol (LABA)

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20
Q

Distinguish mild persistent and moderate persistent asthma

A

Mild persistent: more than 2 days per week but less than 1 time/day or more than 2 nights per month
PEF is still 80 or above

While moderate persistent is daily symptoms or more than one night per week, PEF 60-80%

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21
Q

For asthma treatment

(a) When to add LABA
(b) When to add ICS

A

Asthma step up treatment

(a) Add LABA when moving from mild persistent (2 days a week, 2 or fewer nights per month) to moderate persistent (every day or more than 2 nights/month)

22
Q

Define mild intermittent asthma

(a) Tx

A

Symptoms 2 or fewer days per week, 2 or fewer nights per month

(a) SABA PRN, doesn’t require daily meds

23
Q

Mechanism of drug

(a) Ipratropium
(b) Formoterol
(c) Salmeterolol
(d) Tiotropium

A

(a) Anticholinergic
(b) LABA
(c) LABA
(d) LAMA

24
Q

Name the typical

(a) SABA
(b) LABA
(c) ICS
(d) LAMA

A

(a) SABA- albuterol, levalbuterol
(b) LABA- formoterol, salmeterolol
(c) ICS- budesonide, fluticasone, mometasone
(d) LAMA- tiotropium

25
Q

Advair vs. Symbicort

A

Both ICS/LAMA combos

Adair = fluticasone + salmeterol

Symbicort = budesonide + formoterol

26
Q

Most effective treatment for allergic rhinitis

(a) Only tx that modifies long-term course of disease

A

Intranasal corticosteroids

(a) Allergen immunotherapy which dampens the response to allergens

27
Q

What is hypersensitivity pneumonitis?

(a) Symptoms of acute vs. chronic disease

A

Hypersensitivity pneumonitis = complex immune reaction to repeated inhalation exposure to a variety of organic dusts

(a) Acute easily confused w/ viral/bacterial PNA as acute onset (6-12 hrs of exposure) of fever, SOB, cough

While chronic- gradual onset of dyspnea, productive cough, fatigue, weight loss

28
Q

53 y/oM p/w acute cough, SOB, fever a few hours after getting out of his hot tub.
CXR w/ interstitial infiltrates
CT w/ centrilobular nodules and GGOs

(a) Most likely dx
(b) Tx

A

(a) Acute hypersensitivity pneumonitis to MAC
Immune reaction to inhalation exposure to organic dust

(b) Tx- PO steroids w/ taper

29
Q

PFTs findings of hypersensitivity pneumonitis

(a) Acute
(b) Chronic

A

PFTs in HP: DLCO reduced in both acute and chronic

(a) Mainly restrictive
(b) Mixed restrictive and obstructive pattern

30
Q

Contrast CT chest findings in acute vs. chronic hypersensitivity pneumonitis

A

Acute- diffuse GGOs c/w pneumonitis

Chronic- patchy GGOs with centrilobular nodules, traction bronchiectasis, honeycombing

31
Q

Prototypical causes of HP

A
  1. Farmer’s lung due to moldy hay

2. Bird/pigeon breeder lung from bird feces

32
Q

Treatment of HP

A

HP tx- it’s an immune reaction to inhalation of organic dusts => tx w/ steroids!

PO prednisone 40-80mg daily then taper once see clinical improvement

33
Q

Poorly controlled asthmatic p/w wheezing, bronchial breath sounds
CXR w/ new infiltrates
Serum IgE 2000

(a) Most likely dx
(b) Tx

A

(a) ABPA = allergic bronchopulmonary aspergillosis = immunologic reaction to antigens of aspergillus in the bronchial tree
(b) Steroids

34
Q

4 diagnostic criteria for ABPA

A
  1. presence of asthma
    • immediate kin tests to aspergillus
  2. Elevated Serum IgE (over 1,000)
  3. Elevated aspergillus IgG or IgM
35
Q

18 y/oM p/w recurrent abdominal pain, episodes self-resolve slowly and are associated w/ b/l arm swelling

(a) Most likely Dx

A

Think hereditary angioedema- abdominal pain 2/2 gut edema, 2/2 C1-INH (complement 1 inhibitor) deficiency

36
Q

Hereditary angioedema

(a) Typical presenting features
(b) Diagnostic test
(b) Tx

A

(a) Recurrent abdominal pain 2/2 gut edema
(b) Serum C1-INH (C1 inhibitor) levels, should be low
(c) Tx by replacing C1-INH typically w/ concentrate or FFP

37
Q

Distinguish angioedema associated w/ anaphylaxis from hereditary angioedema

(a) Clinical features
(b) Response to tx

A

Angioedema seen in anaphylaxis

(a) Typical edema in airway, associated w/ urticarial hives.
(b) Responds to epinephrine

Hereditary angioedema

(a) Not always hives, involves more of face (eyes, tongue)
(b) Doesn’t respond to epi, need FFP or C1-INH concentrate

38
Q

Location of atopic dermatitis vs. psoriasis

A

Atopic dermatitis on flexor surfaces (popliteal fossa, antecubital fossa)

While psoriasis is typically on extensor surfaces- back of elbow, front of knee

39
Q

Treatment for eczema

A
  • Skin emollients/lotions- keep it hydrated
  • then topical corticosteroids
  • can use topical antihistamines for the pruritus
  • for severe can use tacrolimus (immunosuppressant)
40
Q

2 drugs aside from epi to give in anaphylaxis

A

Anaphylaxis

  • epi
  • benadryl
  • systemic steroids to blunt delayed phase of reaction
41
Q

Dose of epi used in anaphylaxis vs PEA arrest

A

Epipen = .3mg (.3ml of 1:1,000)

Epi push in code = 1 mg q3-5 minutes

42
Q

Differentiate ‘allergic’ reaction to PCN vs. vanc/radiocontrast

A

Anaphylactic reaction to PCN, bee sting, peanuts = IgE mediated
No use of pre-medication

AnaphylacTOID reaction = clinically indistinguishable, but this is non-IgE mediated
Pretreatment can avoid reaction

43
Q

Lab test to confirm type I-IV drug hypersensitivities

A

‘ACID’

Type I = anaphylactic- skin testing, RAST testing, serum tryptase

Type II = cellular (Ab)- direct/indirect Coomb’s test for drug-induced autoimmune hemolytic anemia

Type III = Immune complex- tissue biopsy w/ stains, ESR/CRP, complement levels

Type IV = Delayed hypersensitivity- allergic contact dermatitis- allergen patch test

44
Q

Explain how rubbing/stroking hyper pigmented skin in pt w/ mastocytosis causes pruritis

A

Mastocytosis = kit (tyrosine kinase) mutation causing overabundance of mast cells, cutaneous regions w/ too many mast cells that release vasoactive substances with mechanical disruption

So pigmented macular skin rash that urticates (starts itching) when stroked is typical of mastocytosis

45
Q

IgA deficiency

(a) Screen for what other complications
(b) Tx

A

(a) Monitor for lymphoproliferative diseases and celiac disease

For unknown reasons ppl w/ IgA deficiency are 10-20 times more likely to develop autoimmune response to gluten

(b) Tx- vaccinations and abx as needed

46
Q

Differentiate treatment for CVID and IgA deficiency

A

CVID- tx w/ monthly IVIG
then same as IgA deficiency: vaccines and antibiotics for treatment/ppx as needed

IgA deficiency- vaccines and antibiotics as needed IVIG contraindicated due to risk of anti-IgA IgE antibody

47
Q

Lab tests to distinguish CVID from IGA deficiency

A

CVID- low levels of IgG (diagnostic below 500 mg/dl), usually with also low IgA and IgM but doesn’t have to be

IgA deficiency- absent IgA (under 7 mg/dl? w/ normal IgG and IgM

48
Q

Most common primary immunodeficiency

A

IgA deficiency: 1 in 500 ppl

49
Q

Other etiology of hypogammaglobulinemia that must be ruled out before diagnosing CVID

A

Other causes of protein loss: nephrotic syndrome, protein-losing enteropathy, meds, lymphopenia

50
Q

Special transfusion needs for its w/ IgA deficiency

A

Washed blood products- ‘wash’ the product of plasma to get rid of all antibodies
Given risk of anaphylaxis due to exposure to IgA (b/c ppl w/ deficiency presumed to have anti-IgA)

Expect IgA deficiency in pt who gets blood transfusion and develops anaphylaxis within seconds to minutes

51
Q

Typical clinical presentation of primary immunodeficiency

A

Recurrent sinopulmonary infections (sinus infection, otitis media, pneumonias), typically presents in 20-30s