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BRS Allergy and Immunology Flashcards

1
Q

anaphylaxis is an ______ mediated reaction

A

IgE
antigen binds to IgE on the surface of mast cells and basophils –> release of potent mediators that affect vascular tone and bronchial reactivity

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2
Q

clinical features of anaphylaxis

A

pruritus, flushing, urticaria, angioedema
dyspnea and wheezing
N/V/D
cardiovascular sxs, mild hypotension to shock

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3
Q

how to tx anaphylaxis

A

epinephrine!!!

also systemic antihistamines, steroids, beta agonists

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4
Q

allergic rhinitis is an _____ mediated inflammatory response in the nasal mucosa to inhaled antigens

A

IgE

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5
Q

clinical signs of allergic rhinitis

A

allergic shiners
dennie’s lines- creases under the eyes 2/2 chronic edema
allergic salute

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6
Q

things associated with allergic rhinitis

A

otitis media
sinusitis
atopic dermatitis (eczema)
food or drug allergies

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7
Q

how to dx allergic rhinitis (besides H&P)

A
  • total IgE concentration is elevated
  • can do allergen skin testing- *D/C antihistamine 4-7 days prior to testing
  • nasal smear for cytology- look for > 10% eosinophils
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8
Q

how to tx allergic rhinitis

A
  • avoid allergens
  • drugs include
  • ->intranasal steroids (most effective)
  • ->first and second generation antihistamines
  • ->intranasal cromolyn sodium
  • ->decongestants for short period of time (insomnia, nervousness, rebound rhinitis)
  • immunotherapy
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9
Q

chronic inflammatory dermatitis- dry skin, lichenification (thickening of the skin), pruritus

A

eczema (atopic dermatitis)

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10
Q

eczema is worse in the _____ (summer/winter)

A

winter

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11
Q

skin findings of eczema

A

acute- erythema, weeping, crusting

chronic- lichenification, dry scaly skin, pigmentary changes (typically hyper pigmentation)

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12
Q

infantile form of eczema

A

truncal and facial areas, scalp, extensor surfaces

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13
Q

early childhood form of eczema

A

flexural surfaces, lichenification (hallmark of chronic scratching)

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14
Q

how to dx eczema

A

3/4 major criteria are needed

  1. pruritus
  2. personal or FHx of atopy
  3. typical morphology and distribution
  4. relapsing or chronic dermatitis
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15
Q

how to tx eczema

A

avoid triggers
low to medium potency topical steroids
antihistamines to avoid itching at bedtime
baths in lukewarm water, moisturize well

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16
Q

food allergy is an ____ mediated response to food antigens
most common foods:
exclusive breastfeeding for 6 months may ____ (increase/decrease food allergies)

A

IgE
egg, milk, peanut, soy, wheat, fish
decrease

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17
Q

how to dx food allergy

A

mostly by history

  • can do skin test
  • RAST tests identify serum IgE to specific food antigens
  • double blind placebo controlled food challenge is the definitive test
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18
Q

insect venom allergy is _____ mediated

how to tx?

A

IgE

tx with cold compresses, analgesics, antihistamines, systemic steroids, immunotherapy

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19
Q

circumscribed, raised, evanescent (vanishing) areas of edema that are almost always pruritic

A

urticaria (hives)

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20
Q

chronic urticaria lasts > _______
can be 2/2 malignancy and rheumatologic dzs
many ppl with chronic urticaria have ____ antibody to ____ receptor

A

6 months
T
IgG antibody to the IgE receptor

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21
Q

drug allergy is mediated by _____ or ______

most common drug allergies:

A

IgE or direct mast cell degranulation

PCN, sulfonamides, cephalosporins, AS, NSAIDs, narcotics

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22
Q 
phagocytic cells
NK cells
toll-like receptors
mannose binding protein
alternative pathway of complement
*these are all parts of the \_\_\_\_\_ immune system
A

innate

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23
Q

selective IgA deficiency is serum IgA levels < _____

this is the most common immune deficiency

A

7 mg/dL

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24
Q

sxs and signs of selective IgA deficiency

A

respiratory infections
GI infections
autoimmune and rheumatic disease
atopic diseases

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25
how to tx IgA deficiency
just manage the infections and other stuff | you cannot replace IgA
26
hypogammaglobulinemia | -normal numbers of B and T cells but variable degrees of T cell dysfunction
common variable immunodeficiency
27
clinical features of common variable immunodeficiency
respiratory infections- Hflu, Moraxella, strep pneumo GI infections autoimmune disorders increased risk of malignancy
28
how to dx common variable immunodeficiency
- decreased serum immunoglobulin concentrations | - measure titers generated in response to childhood immunizations- this will show diminished antibody function
29
how to tx common variable immunodeficiency
monthly IVIG manage infections with abx manage GI issues with nutritional support
30
profoundly defective T cell and B cell function
SCID
31
2 types of SCID
1. X linked SCID- 50% of all cases, caused by deficiency of common gamma chain of receptor for cytokines 2. autosomal recessive SCID
32
increased infection within first few months of life with common pathogens and opportunistic infections (candida, PCP) - chronic diarrhea - FTT
SCID
33
how to dx SCID
- persistent lymphopenia (<1500) - flow cytometry shows decreased # of T cells - severe hypogammaglobulinemia - T cell responses to mitogens and antigens are depressed
34
how to tx SCID
monthly IVIG PCP ppx with bacterium bone marrow transplant can be curative -if getting blood products, they should be irradiated to prevent GVHD
35
combined immunodeficiency, cerebellar ataxia, oculocutaneous telangiectasias, predisposition to malignancy what is it, how inherited, what chromosome
ataxia telangiectasia autosomal recessive long arm of chromosome 11
36
how does the immunodeficiency in ataxia telangiectasia usually manifest
chronic sinopulmonary infections
37
course of ataxia in ataxia telangiectasia
progressive.. many are wheelchair bound by teen years
38
where do you see telangiectasias in ataxia telangiectasia
first on the bulbar conjunctiva then later on on exposed skin and areas of trauma
39
how to dx ataxia telangiectasia
- quantitative measurement of serum immunoglobulins- deficient IgE or IgA - skin test anergy and diminished T cell proliferation to mitogens on evaluation of T cell function
40
how to tx ataxia telangiectasia
tx neuro complications abx for infections monitor for malignancies avoid ionizing radiation- 2/2 faulty DNA repair mechanisms
41
what is digeorge syndrome
``` CATCH-22 cardiac defects abnormal facies thymic hypoplasia cleft palate hypocalcemia 2/2 deletion on chromosome 22q11 ```
42
X linked disorder | combined immunodeficiency, eczema, congenital thrombocytopenia with small defective plts
wiskott-aldrich syndrome
43
with wiskott-aldrich syndrome, what infections are you susceptible to?
encapsulated organisms- strep pneumo, h flu
44
how to dx wiskott-aldrich syndrome
CBC- thrombocytopenia with small defective plts Ab response to polysaccharide antigens is defective cellular immune function is defective, anergy is present, antigen- specific cytotoxic T cells don't develop
45
how to tx wiskott-aldrich syndrome
- HLA-matched BMT is preferred - IVIG for hypogammaglobulinemia - splenectomy cures the low plts but you must give ppx abx or IVIG regularly after splenectomy
46
severe hypogammaglobulinemia with paucity of mature B cells but normal T cell number and function what is it, what is it caused by, what does it put you at risk for
Bruton's (X-linked) agammaglobulinemia - BTK gene mutation - high risk for encapsulated bacteria, staph aureus, and chronic enteroviral infection
47
how to dx bruton's agammaglobulinemia
low immunoglobulin levels in general no B cells T cells are fine mutations in the BTK gene
48
how to tx bruton's agammaglobulinemia
monthly IVIG
49
defective neutrophil oxidative metabolism 2/2 issues with the NADPH system --> problems with intracellular killing of catalos-positive bacteria and some fungi
chronic granulomatous disease
50
increased susceptibility to infections, esp to forming abscesses
chronic granulomatous disease
51
how to dx chronic granulomatous dz
NBT test flow cytometry -they both demonstrate defective neutrophil oxidative burst
52
how to tx chronic granulomatous dz
- drain abscesses - ppx with bacterium, itraconazole, and interferon-gamma - BMT is curative
53
decreased neutrophil chemotaxis, cyclic neutropenia, pancreatic exocrine insufficiency --> recurrent soft tissue infection, chronic diarrhea, FTT
AR disorder | schwachman-diamond syndrome
54
neutropenia and thrombocytopenia, giant lysosomal granules in neutrophils, issues with neutrophil/monocytes/NK cell function --> staph aureus infection, partial oculocutaneous albinism
chediak-higashi syndrome
55
most complement deficiencies are inherited in an ____ way
AR
56
deficiency early components of the classic complement pathway (_____) are associated with ______
C1q, C2, C4 | autoimmune diseases
57
deficiency late components of the classic complement pathway (______) are associated with ________
C5, C6, C8 | disseminated meningococcal and gonococcal infections
58
deficiency of ______ causes angioedema
C1 esterase inhibitor
59
what does a normal CH50 mean for complement deficiency?
all components of the classic pathway are present and functional
60
how to manage complement deficiency
- monitor for infections and autoimmune diseases | - fibrinolysis inhibitors and attenuated androgens for angioedema
61
adenosine deaminase deficiency is a form of _____
SCID

Pediatrics (14 decks)

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