Brainscape's Knowledge GenomeTM

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


See full index

Module 3 > Treatment Strategies of Allergic Disease > Flashcards

Treatment Strategies of Allergic Disease Flashcards

1
Q

Define allergic sensitisation

A

Process where B cells produce specific-antibodies against an allergen

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

Define atopy

A

Tendency to develop an exaggerated IgE response - often have a triad of: eczema (atopic dermatitis), Allergic rhinitis (hayfever) or allergic asthma

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

Outline the development of allergy towards an allergen

A

Allergen exposure

Sensitsation

Re-exposure

Allergic Inflammation

Acute or Chronic

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

Describe some ways in which sensitisation to an allergen can be affected

A
  1. Timing of exposure
    1. in utero
    2. Infancy
  2. Route of exposure
    1. Oral
    2. Cutaneous
  3. Dose of allergen
  4. Other
    1. Pollution
    2. Infection
    3. Diet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe ways in which allergic sensitisation can be prevented

A

Pregnant and breast-feeding mothers are adviced to be cautious with introduction of commonly allergenic food

HOWEVER,

needs updating:

  1. Du Toit, JACI, 2008
    1. _​_Study suggests early introduction of ellergen (peanut) leads to better toleration of the allergen
  2. LEAP study: Du Toit NEJM, 2015
    1. ​Early consumption rather than avoidance, effecitve at primary and secondary prevention of peanut allergy in at risk individuals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Outline the aims of the TRACE study

A

Aimed to identify the lowest dose of peanut allergen that allergic people can tolerate

Also looked at the effects of exercise and sleep deprivation on the induction of an allergic response

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

Describe the benefit and limitation of allergen avoidance to prevent an allergic reaction

A

Benefit: No allergen = no symptoms

Limitation: Not all foods are labelled sufficienty enough

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

Severe Asthma with Fungal Sensitisation (SAFS) is aspergillus sensitisation associated with imparied lung function (Fairs et al AJRCCM, 2010). This is treated with anti-fungals. Name an example, briefly descibe its MOA and describe how its effects may amplify other medications in asthmatics

A

Itraconazole

Cytochrome P450 inhibitor (inhibitis production of ergosterol)

Prednisolone metabolised by CP450, therefore, itraconazole can increase the effects of prednisolone by extending its half-life

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

Differentiate between an agonist and an inverse agonist

A

Agonist acts on a receptor to cause an effect.

Inverse agonist works on the same receptor but causes the opposite effet

E.g. Histamine receptors = Cetirizine (H1), Ranitidine (H2)

GABA receptors = BZD, hypnotics, BARBs

Beta-adrenergic receptors = propanolol

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

Outline the pathway for allergic iflammation

A

Early phase:

  1. Allergen binds IgE
  2. Binds to Mast cell (CD23/FcεI)
  3. Degranulation

Late phase:

  1. Allergen presented to T cells by dendritic cells
  2. Release of chemokines (eotaxin)
  3. Present to B cell -> affinity maturation
  4. IgE antibodies made
  5. Allergic inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe some immediate symptoms after allergen exposure

A

Urticaria (vasodilation)

Itching

Watery discharge

Nasal congestion

Bronchospasm

Anaphylaxis

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

Describe some late symptoms after allergen exposure

A

AHR

Nasal blockade

Loss of smell

Niphasic anaphylaxis

Nasal Hyperreactivity

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

Name the secretions of mast cells when activated by IgE-allergen complex

A

Histamine (main)

Eicosanoids (PGD2)

Tryptase

TNF-a, IL-33

Bradykinin

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

Describe the main effects of histamine

A

Vasodilation

↑vascular permeability

Smooth muscle contraction

Nerve-end stimulation

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

Describe the difference between first and second generation anti-histamines and give examples

A

1st = sedating: chlorphenamine - also have anti-muscarinic effects

2nd = non-sedating: cetirizine, loratidine

Sedating because they cross the blood brain barrrier

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

List some pharmacotherapy for allergies (7)

A

Anti-histamines

Lekotriene Antagonists

Mast Cell Stabilisers

Adrenline

Bronchodilators

Corticosteroids

Cell/Biologics Therapy

17
Q

Describe the mechanisms of Leukotriene antagonists (2) and give two examples of drugs

A
  1. 5-Lipoxygenase inhbitors
    1. Zileuton
      1. could cause hepatitis
  2. CystLT receptor antagonists
    1. Monetlukast

Heterogeneous response in patients (add-on therapy in asthma and 2nd line for allergic rhinitis)

18
Q

Describe the effects of Leukotrienes.

A

Smooth muscle contraction

Eosinophilic inflammation

Musuc prooduction

19
Q

Describe the pros and cons of mast cell stabilisers (sodium cromoglicate, INTAL)

Inhaled, eyedrops, intranasal

A

Pros: Well tolerated

Cons: short duration of action, needs frequent administration

20
Q

Name the dosage, route, and effects of adrenaline in anaphylaxis

A

Dosage

  • Adrenaline, 1 in 1,000, 0.5mg, i.m.
  • Cardiac rescucitatin: 1 in 10,000 i.v. 0.01mg/kg every 4 min

Effects

  • Vasoconstriction
  • ↑CO
  • bronchodilation
  • Inhibits mast cell degranulation
21
Q

Name three types of bronchodilators and describe their moa

A
  1. Beta-adrenoceptor agonists
    1. ↑adenylate cyclase -> ↑cAMP -> inhibition of Ca cytosolic influx -> SM relaxation
      1. Salbutamol, formoterol
  2. Methylxanthines
    1. Inhibit cAMP phosphodiesterases -> ↑cAMP
  3. Anti-cholinergics
    1. competitve inhibition of M3 receptors on bronchial SMCs
22
Q

Describe the mechanisms of action of glucocorticosteroids

A
  1. Trans-activation
    1. Binding to GRE to ↑transcription of anti-inflammatory genes (SLPI-I, annexin-1, IκB-α)
    2. Through ↑HDAC2?
  2. Trans-repression
    1. GC ↓HAT -> ↓Histone acetylation -> ↓pro-inflmmatory gene expression
23
Q

Describe the effects of GC on inflmmatory and structural cells

A
  1. Inflammatory Cells
    1. ↓Eos, mast cell, DC numbers
    2. ↓inflammatory cytokines
  2. Structural Cells
    1. ↓Cytokine mediators
    2. ↓vascular permeability
    3. ↓mucus secretion
    4. ↑B2-receptors in ASMC
24
Q

Describe the adverse effects of glucocorticosteroids

A
  1. Weight gain
  2. T2DM
  3. Muscle wasting
  4. Cataracts/glaucoma
  5. Immunosuppression
  6. Osteopenia/osteoporosis
  7. Skin (bruising, thining)
  8. Psychosis
  9. Suppression of HPA (instant wihdrawal leads to insufficiency as steroids inhibit adrenal production)

Module 3 (17 decks)

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