Brainscape's Knowledge GenomeTM

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


See full index

Clinical Pathology > Allergy > Flashcards

Allergy Flashcards

1
Q

What is hypersensitivity?

A

Undesirable, damaging, discomfort-producing and sometimes fatal reactions produced by the normal immune system (directed against innocuous antigens) in a pre-sensitized (immune) host.

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

What is the immunopathogenesis of type II (cytotoxic) hypersensitivity?

A

IgG/IgM Ab response against combined self/foreign antigen at the cell surface- complement activation/phagocytosis/ADCC.

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

What are the clinical features of type II hypersensitivity?

A
  • Onset minutes to hours

- Cell lysis and necrosis

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

What is a common antigen that stimulates type II reactions?

A

Penicillin.

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

What diseases are associated with type II hypersensitivity?

A
  • Erythroblastosis fetalis,

- Goodpasture’s nephritis

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

What is the immunopathogenesis of type III (immune complex) hypersensitivity?

A

IgG/IgM Ab against soluble antigen- immune complex deposition.

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

What are the clinical features of type III hypersensitivity?

A
  • Onset 3-8h

- Vasculitis

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

What is type III hypersensitivity traditionally associated with?

A

Serum sickness

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

What is the immunopathology of type IV (delayed) hypersensitivity?

A

Antigen specific T-cell mediated cytotoxicity

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

What are the clinical features of type IV hypersensitivity?

A
  • Delayed onset 48-72h

- Erythema induration

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

Which antigens are commonly associated with type IV hypersensitivity?

A
  • Metals-e.g nickel
  • (tuberculin reaction)
  • Poison ivy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What disease is commonly associated with type IV hypersensitivity?

A

Contact dermatitis

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

What is the hygiene hypothesis?

A
  • Stimulation by microbes is protective
  • Epidemiological data – Increase in Allergy
  • Animal Models – T1DM, EAE, Asthma
  • Increased atopy (Asthma) after anti-parasitic Rx
  • Prevention of autoimmunity (Crohn’s) by infections
  • Pro-biotics in pregnant women
  • Mechanism – Th1 Th2 deviation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the genetic influences on the immune response?

A
  • Polygenic diseases
  • Cytokine gene cluster IL3,5,9,13
  • IL12R; IL4R
  • FceRI
  • IFNg; TNF
  • NOT sufficient for disease
  • ONLY susceptibility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are allergens?

A
  • Antigens that initiate an IgE-mediated response

- First encounter results in innate & IgM response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What happens to the allergen during a conventional immune response?

A
  • Allergen requires processing
  • Presentation to T cells & cytokine release
  • Results in delineation of T-helper subsets into different types
17
Q

What is the immunopathology of type I hypersensitivity (allergic)?

A

IgE Ab mediated mast cell and basophil degranulation- release of preformed and de novo synthesized inflammatory mediators

18
Q

What are the clinical features of type I hypersensitivity?

A
  • Fast onset (15-30 min)

- Wheal and flare

19
Q

What cells are involved in the late phase response?

A
  • Eosinophils

- Central role for Th2 T cell

20
Q

What is the role of the Th2 cell?

A
  • Multiple cytokine release.
    • epithelial cell damage
    • airway remodelling
    • survival and activation of eosinophils
    • bronchial hyperreactivity
21
Q

What is the atopic triad?

A

asthma
rhinitis
eczema

22
Q

What are the features of rhinitis?

A
  • ALLERGIC/NON-ALLERGIC
  • ALLERGIC - PERENNIAL or SEASONAL
  • Blocked nose, runny nose - often with eye symptoms
  • House dust mite, animal danders, pollens
  • Treatment – Antihistamines & Nasal steroids
23
Q

What are the features of asthma?

A
  • Disease of INFLAMMATION and HYPER-REACTIVITY of small airways
  • In childhood - AERO-ALLERGIC stimuli - HOUSE DUST MITE key pathogenic importance
  • IMMEDIATE symptoms are IgE-mediated
  • DAMAGE TO AIRWAYS due to LATE PHASE RESPONSE
  • DAMAGED AIRWAYS ARE HYPER-REACTIVE to non-allergic stimuli e.g. fumes
24
Q

What are the features of atopic dermatitis?

A
  • DERMATITIS – MANY DIFFERENT TYPES
  • ATOPIC CONTACT - ALLERGIC/NON-ALLERGIC
  • CLINICALLY - Intense itching, blistering/weeping, cracking of skin
  • HOUSE DUST MITE now thought to be MAJOR TRIGGER in atopic disease
  • Topical Steroids and moisturisers
25
Q

What is anaphylaxis?

A

An acute, potentially life-threatening, IgE mediated systemic hypersensitivity reaction.

26
Q

What are the diagnostic tests used in the diagnosis of allergy?

A
  • History
  • Specific IgE (>0.35 KuA/L)
  • Skin prick test (>3mm wheal) SPT Video
  • Intra-dermal test
  • Oral challenge test – Gold standard
  • Basophil activation test
  • Component resolved diagnostics
27
Q

What are the advantages and disadvantages of using specific IgE?

A

Safe but false positives and negatives.

28
Q

What are the advantages and disadvantages of using the skin prick test?

A
  • Quick
  • Patient satisfaction
  • False negatives
  • False positives
  • Antihistamines
  • Slight risk
29
Q

What symptomatic treatment can be given for allergies?

A

Antihistamines, Steroids, Adrenaline

30
Q

What kind of allergies is immunotherapy good for?

A
  • Life threatening reactions to Wasp & Bee sting
  • Severe Hay fever
  • Animal dander allergy
31
Q

What kind of allergies is immunotherapy not good for?

A
  • Multiple allergies
  • Food allergy
  • Allergic rashes – Eczema, Urticaria
32
Q

What are the various mechnisms behind immunotherapy?

A
  • Ratio of Th1 cytokines to Th2 cytokines is increased following specific immunotherapy (SIT)
  • Functional regulatory T cells are induced.
  • Production of IL-10 by monocytes, macrophages, B cells and T cells is increased.
  • Expression of TGF is increased and, together with IL-10, TGF might contribute to regulatory T-cell function and immunoglobulin class switching to IgA, IgG1 and IgG4. These immunoglobulins compete with IgE for allergen binding, decreasing the allergen capture and presentation that is facilitated by IgE in complex with the high-affinity receptor for IgE (FcRI) or the low-affinity receptor for IgE (FcRII).
  • SIT reduces number of mast cells and ability of mast cells to release mediators.
  • Recruitment of eosinophils and neutrophils to sites of allergen exposure is also reduced.
33
Q

What are the major food allergens?

A
  • Water soluble glycoproteins 10 - 60 kd
  • COW’S MILK
  • EGG
  • LEGUMES - PEANUT; SOYBEAN; TREE NUTS
  • FISH
  • CRUSTACEANS / MOLLUSCS
  • CEREAL GRAINS
34
Q

What are the potential clinical features of adverse food reactions?

A
  • Gastrointestinal
    • vomiting, diarrhoea, oral symptoms
  • Respiratory (upper & lower)
    • rhinitis, bronchospasm
  • Cutaneous
    • urticaria, angioedema
    • role of food in atopic dermatitis unclear
  • Anaphylaxis

Clinical Pathology (65 decks)

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