Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pediatrics > BRS Allergy and Immunology > Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

clinical features of anaphylaxis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how to tx anaphylaxis

A

epinephrine!!!

also systemic antihistamines, steroids, beta agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

clinical signs of allergic rhinitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

things associated with allergic rhinitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

eczema (atopic dermatitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

eczema is worse in the _____ (summer/winter)

A

winter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

skin findings of eczema

A

acute- erythema, weeping, crusting

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

infantile form of eczema

A

truncal and facial areas, scalp, extensor surfaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

early childhood form of eczema

A

flexural surfaces, lichenification (hallmark of chronic scratching)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

insect venom allergy is _____ mediated

how to tx?

A

IgE

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

urticaria (hives)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

selective IgA deficiency is serum IgA levels < _____

this is the most common immune deficiency

A

7 mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

sxs and signs of selective IgA deficiency

A

respiratory infections
GI infections
autoimmune and rheumatic disease
atopic diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

how to tx IgA deficiency

A

just manage the infections and other stuff

you cannot replace IgA

26
Q

hypogammaglobulinemia

-normal numbers of B and T cells but variable degrees of T cell dysfunction

A

common variable immunodeficiency

27
Q

clinical features of common variable immunodeficiency

A

respiratory infections- Hflu, Moraxella, strep pneumo
GI infections
autoimmune disorders
increased risk of malignancy

28
Q

how to dx common variable immunodeficiency

A
  • decreased serum immunoglobulin concentrations

- measure titers generated in response to childhood immunizations- this will show diminished antibody function

29
Q

how to tx common variable immunodeficiency

A

monthly IVIG
manage infections with abx
manage GI issues with nutritional support

30
Q

profoundly defective T cell and B cell function

A

SCID

31
Q

2 types of SCID

A
  1. X linked SCID- 50% of all cases, caused by deficiency of common gamma chain of receptor for cytokines
  2. autosomal recessive SCID
32
Q

increased infection within first few months of life with common pathogens and opportunistic infections (candida, PCP)

  • chronic diarrhea
  • FTT
A

SCID

33
Q

how to dx SCID

A
  • persistent lymphopenia (<1500)
  • flow cytometry shows decreased # of T cells
  • severe hypogammaglobulinemia
  • T cell responses to mitogens and antigens are depressed
34
Q

how to tx SCID

A

monthly IVIG
PCP ppx with bacterium
bone marrow transplant can be curative
-if getting blood products, they should be irradiated to prevent GVHD

35
Q

combined immunodeficiency, cerebellar ataxia, oculocutaneous telangiectasias, predisposition to malignancy
what is it, how inherited, what chromosome

A

ataxia telangiectasia
autosomal recessive
long arm of chromosome 11

36
Q

how does the immunodeficiency in ataxia telangiectasia usually manifest

A

chronic sinopulmonary infections

37
Q

course of ataxia in ataxia telangiectasia

A

progressive.. many are wheelchair bound by teen years

38
Q

where do you see telangiectasias in ataxia telangiectasia

A

first on the bulbar conjunctiva then later on on exposed skin and areas of trauma

39
Q

how to dx ataxia telangiectasia

A
  • 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
Q

how to tx ataxia telangiectasia

A

tx neuro complications
abx for infections
monitor for malignancies
avoid ionizing radiation- 2/2 faulty DNA repair mechanisms

41
Q

what is digeorge syndrome

A 
CATCH-22
cardiac defects
abnormal facies
thymic hypoplasia
cleft palate
hypocalcemia
2/2 deletion on chromosome 22q11
42
Q

X linked disorder

combined immunodeficiency, eczema, congenital thrombocytopenia with small defective plts

A

wiskott-aldrich syndrome

43
Q

with wiskott-aldrich syndrome, what infections are you susceptible to?

A

encapsulated organisms- strep pneumo, h flu

44
Q

how to dx wiskott-aldrich syndrome

A

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
Q

how to tx wiskott-aldrich syndrome

A
  • 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
Q

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

A

Bruton’s (X-linked) agammaglobulinemia

  • BTK gene mutation
  • high risk for encapsulated bacteria, staph aureus, and chronic enteroviral infection
47
Q

how to dx bruton’s agammaglobulinemia

A

low immunoglobulin levels in general
no B cells
T cells are fine
mutations in the BTK gene

48
Q

how to tx bruton’s agammaglobulinemia

A

monthly IVIG

49
Q

defective neutrophil oxidative metabolism 2/2 issues with the NADPH system –> problems with intracellular killing of catalos-positive bacteria and some fungi

A

chronic granulomatous disease

50
Q

increased susceptibility to infections, esp to forming abscesses

A

chronic granulomatous disease

51
Q

how to dx chronic granulomatous dz

A

NBT test
flow cytometry
-they both demonstrate defective neutrophil oxidative burst

52
Q

how to tx chronic granulomatous dz

A
  • drain abscesses
  • ppx with bacterium, itraconazole, and interferon-gamma
  • BMT is curative
53
Q

decreased neutrophil chemotaxis, cyclic neutropenia, pancreatic exocrine insufficiency –> recurrent soft tissue infection, chronic diarrhea, FTT

A

AR disorder

schwachman-diamond syndrome

54
Q

neutropenia and thrombocytopenia, giant lysosomal granules in neutrophils, issues with neutrophil/monocytes/NK cell function –> staph aureus infection, partial oculocutaneous albinism

A

chediak-higashi syndrome

55
Q

most complement deficiencies are inherited in an ____ way

A

AR

56
Q

deficiency early components of the classic complement pathway (_____) are associated with ______

A

C1q, C2, C4

autoimmune diseases

57
Q

deficiency late components of the classic complement pathway (______) are associated with ________

A

C5, C6, C8

disseminated meningococcal and gonococcal infections

58
Q

deficiency of ______ causes angioedema

A

C1 esterase inhibitor

59
Q

what does a normal CH50 mean for complement deficiency?

A

all components of the classic pathway are present and functional

60
Q

how to manage complement deficiency

A
  • monitor for infections and autoimmune diseases

- fibrinolysis inhibitors and attenuated androgens for angioedema

61
Q

adenosine deaminase deficiency is a form of _____

A

SCID

Pediatrics (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions