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Year 3 - Clinical Science and Professionalism > The Allergic Lung > Flashcards

The Allergic Lung Flashcards

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1
Q

What are the clinical features of asthma

A
  1. Acute attacks of shortness of breath
    - Acute airway obstruction
    - Contraction of smooth muscle
  2. Excessive mucus secretion
  3. Airway Inflammation
  4. Bronchial Hyper-responsiveness
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2
Q

What are the external triggers of asthma

A
  • Allergens
  • Chemical Irritants
  • Dust, smoke
  • Cigarette smoke exposure
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3
Q

What are the internal triggers of asthma

A
  • Cold
  • Post Exercise
  • Post coughing
  • Post laughter
  • Viral colds
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4
Q

Describe the phases of an asthma attack

A

Early phase bronchospasm

  • initial decrease in FEV1 in bronchospasm
  • everything gets better again

Late phase inflammation
- after several hours there is then worsening of FEV1

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5
Q

the more severe the asthma the ..

A

worse and quicker the response

- shown in bronchial hyper-responsiveness

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6
Q

What are the cellular features of the immune response

A
  • Mast cells increase
  • Eosinophils increase
  • Lymphocytes increase
  • Th1/Th2 imbalance
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7
Q

What does the epithelium in asthma look like

A
  • Goblet Cell hyperplasia
  • Thick basement membrane
  • Cellular infiltrate +++ with both neutrophils and eosinophils in the airway
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8
Q

describe the pathogensis of asthma

A
  • IgE antibodies play a vital role
  • IgE synthesis takes place when inhaled allergens encounter dendritic cells
  • dendritic cells then migrate to lymph nodes
  • dendritic cells present antigen to T and B cells
  • B cells switch to produce IgE
  • after synthesis IgE is released and circulates in the blood
  • binds to high affinity IgE receptors on mast cells
  • Binds to low affinity receptors on lymphocytes, eosinophils, platelets and macrophages
  • unclear if low affinity binding activates cells
  • molecular bridging FceRI (e stands for epillson) occurs when allergen interacts with receptor bound IgE causing activation
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9
Q

Describe how B cells switch to produce IgE in asthma

A

First signal
• IL4, IL13 (receptors share common alpha chain and common STAT-6 transduction pathway)

Second signal
• CD14 on B cells binds to ligand on T cells

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10
Q

What is the early response of IgE in asthma

A
  • bronchospasm
  • edema
  • airflow obstruction
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11
Q

What is the late response of IgE in asthma

A
  • airway inflammation
  • airway obstruction
  • airway hyperresponsiveness
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12
Q

What is omalizumab

A

IgE monoclonal antibody - binds to free IgE in the blood and membrane bound IgE on the surface of B lymphocytes but not onto IgE on mast cells or dendritic cells
- designed to treat people with severe persistant asthma and those who require significant amounts of oral corticosteroids

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13
Q

What are the benefits of omalizumab

A
  • reduction in days of symptoms
  • reduces the number of exacerbations
  • need for inhaled glucocortocoid steroids
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14
Q

What happens when you have an inhaled allergen

A

Causes acute obstruction
- via histamine and leukotrienes
- constrict smooth muscle
resident inflammatory cells and recruited cells in the late phase

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15
Q

Where do eosinophils originate from

A
  • the bone marrow
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16
Q

What regulates eosinophils

A

IL-3, IL-5

17
Q

What causes terminal differentiation of eosinophils

A

GM-CSF and IL-5

18
Q

what do eosinophils do

A

• Contain proteins that damage airway epithelium, increased BHR
• Rich source of of leukotrienes
- migrate to where they are

19
Q

what therapy can be used to target eosinophils

A

Anti IL-5 therapy

20
Q

Name an anti IL-5 therapy

A

Reslizumab - used for severe eosinophilic asthma

21
Q

What is the role of prostaglandin in asthma

A
  • they act on dendritic cells, bronchial vessel, TH2 cells, eosinophils and airway smooth muscle cell
22
Q

What are prostaglandins produced from

A
  • produced from mast cells
23
Q

Name a prostaglandin inhibitor

A
  • Fevipiprant - prostaglandin D2 receptor 2 antagonists
24
Q

What does a bronchial biopsy show

A
  • Increased IL-4 and IL-5 mRNA (even in non-atopic subjects)
  • High GATA-3 mRNA (transcription factor confined to Th2) in asthmatics - suggests there is a TH1/TH2 imbalance in patients with asthma
25
Q

Describe how TH2 causes asthma

A

TH2

  • T cells interact with B cells causing production of IgE causing asthma
  • TH2 response is produced - for IL-4 B cell is activated then through IL-5 eosinophil is activate d
  • these cause histamine, leukotrienes, prostaglandins, cytokines, and basic proteins and enzymes to become activated
  • this leads to allergic asthma
26
Q

what do TH1 cells do

A

promote protective immunity

27
Q

What are the factors that favour TH1 phenotype

A
  • presence of older sibilings
  • early exposure to day care
  • tuberculosis, measles, or Hep A infection
  • rural environment
28
Q

What are the factors that favour TH2 phenotypes

A
  • widespread use of antibiotics
  • wester lifestyle
  • urban environment
  • diet
  • sensitisation to house dust mites and cockroaches
29
Q

Why does asthma persist

A

• Aberrant structure

Airway remodelling
• Thickened airway walls
• Increased submucosal tissue
• Increased smooth muscle

Compromised repair
• ”chronic wound”

30
Q

What is atopy

A
  • predisposition to IgE and thus allergic disorders
31
Q

what type of hypersenstivity is anaphylactic shock

A

Type I - IgE mediated hypersenstiivty reaction

32
Q

What are the symptoms of anaphylactic shock

A
  • capillary leak
  • wheeze
  • cyanosis
  • oedeam
  • urticaria
33
Q

What are the signs and symptoms of anaphylactic shock

A
  • itching
  • sweating
  • diarrhoea
  • vomitting
  • erythema
  • urticaria
  • oedema
  • wheeze, larygenal obstrunction
  • cyanosis
  • tachycardia
  • hypotension
34
Q

What is the management of anaphylaxis

A
  • Secure airway - give 100% of oxygen
  • give adrenaline IM 0.5mg (0.5ml of 1:10000) = repeat every 5 minutes if needed
  • secure IV access
  • ## chlorphenamine 10mg IV and hydrocortisone 200mg IV
35
Q

What can you measure to see if you have had anaphylaxis

A

serum tryptase - 1-6 hours after suspected anaphylaxis

Year 3 - Clinical Science and Professionalism (32 decks)

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