Brainscape's Knowledge GenomeTM

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


See full index

Studying > Allergy and Immunology > Flashcards

Allergy and Immunology Flashcards

1
Q

Role for IV epi in anaphylaxis

A
  • after repeated doses of IM epi
  • persistent hypotension despite fluid resuscitation wtih 20mL/kg of NS

concentration 0.1mg/mL (1:10,000)

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

Biphasic reaction

A
  • most are in first 4-6 hrs (range 1-72 hrs)

- higher risk if delayed epi, more than 1 epi doses, more severe sx (b-agonist given, wide pulse pressure)

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

25kg epipen

A

0.3mg IM

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

Skin prick testing pros:

A
  • results within 15 minutes
  • more sensitive
  • high negative predictive value
  • cost effective
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Skin prick testing cons:

A
  • false positives
  • affected by use of antihistamines and corticosteroids
  • low risk of having a systemic reaction
  • cannot perform if skin disease at testing site (e.g. eczema)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

High risk for food allergy (CPS)

A
  • personal history of atopy

- first degree relative with an allergic condition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Food protein induced proctitis onset

A

2-8 weeks of age

by age 9 months, 95% tolerate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Food protein induced enterocolitis syndrome onset and features

A

1-4 weeks after intro of the food
- vomiting 1-3hrs after ingestion
- hypotension in 15%
(generally resolve by 3 yrs)

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

Test to look for systemic mastocytosis

A

serum tryptase

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

Cross-reactivity between penicillin and cephalosporins

A

2%

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

Erythema multiforme

A
  • target lesions
  • +/- mucosal membrane
  • cna be infections OR medications
  • tx with topical corticosteroids, antihistamines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

SJS/TEN onset and features

A

1-3 weeks of drug exposure

  • fever, sore throat
  • mucus membranes
  • blistering lesions with skin detachment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

DRESS onset and features

A

1-8 weeks of drug exposure

- rash, eosinophilia, hepatic dysfunction, fever, facial angioedema, lymphadenopahty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Serum sickness onset and features

A

1-3 weeks of drug exposure

  • rash, arthralgia, arthritis, renal disease, fever
  • low complement
  • e.g. ATG, monoclonal antibodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Serum sickness -like

A

1-3 weeks of drug exposure

  • rash, fever, arthralgia, arthritis
  • NO renal disease
  • normal complement
  • e.g. cefaclor, penicillin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Treatment for SJS/TEN

A
  • discontinue med
  • supportive therapy
  • steroids + IVIG = controversial
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Treatment for DRESS

A
  • discontinue med

- steroids if severe

18
Q

Treatment for serum sickness

A
  • discontinue meds
  • NSAIDS, analgesics
  • steroids, PLEX if severe
19
Q

Treatment for serum-sickness-like

A
  • discontinue med
  • NSAIDS, analgesics
  • steroids if severe
20
Q

Hereditary angioedema

  • genetics
  • test
  • triggers
A
  • autosomal dominant
  • C1 esterase inhibitor (will be low)
  • triggers by trauma, infection, estrogen
21
Q

Treatment allergic rhinitis

A
  1. allergen avoidance
  2. 2nd gen oral antihistamines (cetirizine, loratadine)
  3. intranasal steroids
  4. leukotriene receptor antagonist
  5. immunotherapy
22
Q

Humoral deficiencies (B-cell)

A
  • X linked agammaglobulinemia

- common variable immunodeficiency

23
Q

Combined immunodeficiencies (T and B cell)

A
  • SCID
  • Wiskott-Aldrich
  • ataxia - telangiectasia
  • DiGeorge
24
Q

Phagocyte defects

A
  • CGD

- leukocyte adhesion deficiency

25
Q

B-cell immunodeficiency features

A

> 6 months

  • encapsulated, enterovirus, giardia,
  • AOM, sinopulmonary, arthitis, meningoencephalitis
26
Q

Phagocytic immunodeficiency features

A
  • early onset
  • staph, pseudomonas, serratia
  • abscesses, gingivitis, osteomyelitis, skin
27
Q

Complement immunodeficiency features

A
  • any age
  • pneumococcus, meningococcus
  • septicemia, meningitis
28
Q

10 warning signs of PID

A
  1. 2+ serious sinus infections /yr
  2. 2+ months on abx
  3. 2+ pneumonias /yr
  4. 2+ deep seated infections (e.g. septicemia)
  5. 4+ AOM/yr
  6. recurrent deep skin or organ abscesses
  7. persistent thrush or fungal infection
  8. FTT
  9. need for IV abx
  10. family history of PID
29
Q

Humoral (B-cell) assessment

A

Quantitative: IgG, IgA, IgM, IgE, lymphocyte subsets (CD19+cells) by flow cytometry
Qualitative: specific antibodies e.g. diphtheria, tetanus, measles, mumps, rubella, varicella titres, isohemagglutinins,

30
Q

Cellular assessment (T-cells)

A

Quantitative: total lymphocyte counts, lymphocyte subsets by flow cytometry
Qualitative: in vitro lymphocyte proliferation in response to mitogens and antigens, enzyme levels, TRECs, Vbeta

31
Q

Phagocytic assessment

A

Quantitative: Neutrophil counts
Qualitative: neutrophil oxidative burst index (or nitroblue test) , measumrent of adhesion markers (for LAD)

32
Q

Complement assessment

A

Quantitative: C1 esterase inhibitor levels, specfici complement levels
Qualitative: CH50, AH50, C1 esterase inhibitor fxn (for HAE)

33
Q

SCID

A
  • presents 2-6 months
  • most common = X-linked SCID
  • die in infancy unless treated
  • severe, recurrent, persistent opportunistic infections and failure to thrive
34
Q

Ataxia telangiectasia features

A
  • AR
  • ataxia (cerebellar) starts as toddler and progresses
  • progressive neurodegenerations
  • telangiectasia (appear at 4-5 yrs)
  • immune deficiency
  • abnormal DNA repair
  • 25% develop malignancy (esp lymphoma)
35
Q

Ataxia Telangiectasia screen test

A
  • increase alpha fetoprotein

- absent IgA in 80%

36
Q

CGD susceptibilities

A

Catalase positive pathogens:

- s. aureus, aspergillus, serratia, nocardia, brukhorderia, salmonella

37
Q

HyperIgE features

A

AD

  • recurrent abscesses (cold boils)
  • scoliosis, fractures,
  • eczema
  • dealyed shedding of teeth
  • facial features
38
Q

complement infection susceptibilities

A
  • neisseria
39
Q

4 types hypersensitivity reaction

A

Type I = IgE (<2hrs)
Type II = cytotoxic e.g. anemia, thrombocytopenia (10hrs to weeks)
Type III = immune complex e.g. serum sickness (1-3 weeks)
Type IV = T-cell mediated e.g. SJS (2-14 days)

40
Q

When is penicillin drug challenge contraindicated?

A

If history is consistent with anaphylaxis or systemic, non-immediate immune reaction e.g. serum sickness, SJS, dRESS or drug-induced hemolytic anemia

41
Q

Stinging allergy and tryptase

A
  • baseline level of tryptase if hx severe anaphylaxis
  • high levels means higher risk for systemic reactions and higher failure rate to VIT
  • > 20ng/mL may indicate comorbid systemic mastocytosis
42
Q

IgE reactions to stinging insects

A
  1. large local reactions - no epipen
  2. systemic reaction - carry epipen
    (exception = urticaria alone, low risk for anaphylaxis)

Studying (25 decks)

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