Brainscape's Knowledge GenomeTM

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


See full index

Human Diseases > 12.2 Allergy and anaphylaxis > Flashcards

12.2 Allergy and anaphylaxis Flashcards

1
Q

Define allergy.

A

Immune responses that are potentially harmful to the host but which are directed against external agents which are themselves not
harmful.
Symptoms and diseases not caused by the allergens themselves, but by the immunological reactions to them.

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

Define anaphylaxis.

A

A severe, life-threatening generalised hypersensitivity reaction.

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

What is a type 1 hypersensitivity reaction?

A
  • IgE mediated
  • Allergy
  • Atopy, anaphylaxis asthma

Every1 has an allergy

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

What is a type 2 hypersensitivity reaction?

A
  • IgM, IgG, complement
  • Cytotoxic, antibody dependent
  • Autoimmmune hemolytic anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is a type 3 hypersensitivity reaction?

A
  • IgG, complement
  • Immune complex disease
  • Serum sickness, SLE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is a type 4 hypersensitivity reaction?

A
  • Lymphocytes
  • Cell mediated
  • Delayed hypersensitivity, contact dermatitis, hypersensitivity in TB, chronic transplant rejection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the effector cells in IgE mediated reactions?

A
  • IgE = type 1
  • Mast cells and basophils
  • Produce 3 important classes of mediators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What mediators are produced by mast cells and basophils?

A
  • Vasoactive amines: histamine
  • Lipid mediators: prostaglandins, leukotrienes, PAF
  • Cytokines: TNF, IL-4, IL-5
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does IgE bind to mast cells?

A

Via. IgE Fc receptors (high affinity) on the mast cell surface

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

Where are mast cells predominantly found?

A
  • In the skin, respiratory and gut mucosa
  • Activation of mat cells via IgE binding = degranulation (histamine release)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Name the 5 things released by mast cells.

A

CLECT
- Cytokines: IL-4/3/5, TNF-alpha
- Lipid mediators: leukotrienes and PAF
- Enzymes: chymase and tryptase
- Chemokines:CCL3
- Toxic mediators: histamine and heparin

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

Where are histamine receptors found?

A

Histamine released from mast cells can bind to:
- H1 receptor
- H2 receptor
- H3 receptor
- H4 receptor

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

What is the role of the vasoactive amines (histamine) and lipid mediators (prostaglandins and leukotrienes) released by mast cells?

A
  • Cause the rapid vascular and smooth muscle reactions seen in immediate hypersensitivity
  • E.g. vasodilation, vascular leakage, oedema, bronchoconstriction, gut hypermotility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the role of the cytokines released by mast cells and Th2 cells in the late phase/delayed hypersensitivity reaction (4)?

A

Cytokines released by mast cells and Th2 cells mediate the late-phase reaction, which is an inflammatory reaction involving neutrophil and
eosinophil infiltration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is atopy?

A

The genetic predisposition to producing IgE following exposure to common environmental allergerns.
5-10% of the population show clinical features of 1 or more allergic disorders e.g. Asthma, hay fever.

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

What is the atopic triad?

A
17
Q

Describe atopy at a cellular level.

A
  • Atopy appears to be due to a predisposition toward a T-helper type 2 response
  • Th2 cells secrete large quantities of IL-) and IL-13, which promote the production of allergen-specific IgE by plasma cells
18
Q

Describe the features of the allergens that promote an IgE response.

A
  • Proteins, often proteases
  • Low doses
  • Low molecular weight
  • Stable
  • Highly soluble
  • Peptides which bind to MHC II
  • Mucosal presentation (usual site of parasite entry)
19
Q

What is sensitisation?

A
  • Sensitization refers to the production of allergen-specific IgE.
  • Sensitization to an allergen is not synonymous with being allergic to that allergen, because individuals may produce IgE to allergens in a
    given substance, but not develop symptoms upon exposure to that substance.
    It is unclear why some individuals demonstrate only sensitization while others have active allergic disease.
20
Q

Does sensitisation always lead to allergy?

A

No. Sensitisation won’t always lead to allergy. But people who have allergies would have had sensitisation initially.

21
Q

Describe type 2 hypersensitivity reactions.

A

Antibody mediated. Cytotoxic.
IgG and IgM antibodies specific for cell surface or ECM antigens cause tissue injury (often organ specific) by:
- Activating the complement system
- Recruiting inflammatory cells
- And interfering with normal cellular function e.g. antibody mediated stimulation of the thyroid stimulating hormone receptor => Grave’s disease (hyperthyroidism)

22
Q

Describe type 3 hypersensitivity reactions.

A

Immune complex mediated.
- Immune complexes form (Ag-Ab)
- These immune complexes may deposit in the BV walls in various tissues, causing inflammation, thrombosis and tissue injury
- E.g. lupus, rheumatoid arthritis

23
Q

Describe type 4 hypersensitivty reaction.

A

T-cell mediated
Delayed type reaction
- Tissue injury due to T lymphocytes that induce inflammation or directly kill target cells
- T-helper cells secrete cytokines that promote inflammation and acitvate leukocytes, mainly neutrophils and macrophages
- Cytotoxic T cells also contribute to tissue injury in some diseases
- Reaction 24 to 48 hours after antigen challenge in a previously sensitised individual
- E.g. contact dermatitis

24
Q

How can allergies be treated?

A
  • Avoidance
  • Drugs: antihistamines, inhalers, topical steroids, adrenaline (emergency)
  • Desensitisation: currently only available for aeroallergens and venoms
25
Q

What should you consider if a patient reports an allergy?

A
  • Ask where the diagnosis has come from
  • Clarify if any investigations have been performed
26
Q

How are allergies diagnosed?

A
  • History: timing of exposure and symptoms, what were the symptoms, what tx
  • Investigations: skin prick tests, specific IgEs, challenge testing, tryptase (taken at time 0, 2 and 24 hours)
27
Q

How do drug allergies occur?

A
  • Drug allergies are adverse reactions whereby antibodies and/or activated T-cells are directed against the drugs or against one of its metabolites.
  • Drug reactions can occur via any of the Type I to IV hypersensitivity reactions.
  • Anaphylactic reactions (due to mast cell activation) are of rapid onset and
    life threatening
  • The management is to avoid those drugs to which the patient reacts
28
Q

What are the clinical presentations of drug hypersensitivity reactions?

A

Immediate DHR:
- Urticaria (hives)
- Angiodema
- Rhinitis
- Bronchospasm
- GI symptoms: nausea, vomiting, diarrhoea
- Anaphylaxis

Non-immediate DHR:
- Late occuring or delayed urticaria
- Vasculitis
- Blistering diseases
- Maculopapular eruptions

29
Q

What type of LA reactions are there?

A
  • Rare, but in most cases reaction is due to intravascular injection
  • Reactions to amide LA are very rare
  • Reactions to ester type LAs e.g. benzocaine, are more likely to produce allergic reactions as they are metabolised by PABA which is an allergenic compound
30
Q

What should you do if you suspect a pt has an LA allergy?

A
  • Refer for evaluation by an allergist or dermatologist because most don’t have a true LA allergy
  • Challenge testing is possible
  • Idenify a safe LA alternative for future tx
31
Q

Describe what type of reaction latex allergy is.

A
  • Reactions to latex can be mediated by Type I hypersensitivity and by Type IV delayed hypersensitivity
  • Where latex allergy is present care should be taken to avoid exposure of the patient to latex
32
Q

What is anaphylaxis?

A

Anaphylaxis is an acute, potentially life-threatening, multisystem syndrome caused by the sudden release of mast cell mediators into
the systemic circulation.

33
Q

What is the long treatment of anaphylaxis?

A
  • Identify precipitant
  • Avoid precipitant
  • Adrenaline auto-injectors
  • Medic-alert pendant/bracelet
  • To whom it may concern letter

Human Diseases (47 decks)

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