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Respiratory > Allergy in the Lung > Flashcards

Allergy in the Lung Flashcards

1
Q

What is the term for failure to breathe out?

A

Ventilatory failure

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2
Q

Why is lung compensation an issue?

A

Because you can lose up to 70% of the capacity of your lungs without noticing or getting symptoms

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3
Q

How does the narrow inlet/exhaust make the lung vulnerble?

A

Because it is so narrow, it is easily occluded.

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4
Q

How does the enormous reserve surface area make the lung vulnerable?

A

Pathology is advanced before clinical deterioration is detected
- lost lung can’t be replaced like the liver

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5
Q

What is an allergy?

A

An immune system mediate intolerance.

  • requires exposure to a trigger
  • memory is a characteristic clinical feature
  • dependent on which arm of the immune system
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6
Q

Allergies have two possible clinical reactions, what are they?

A

Acute and very sudden

Slow and progressive

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7
Q

What happens to lung tissue in a chronic allergy?

A

Tissue remodelling

  • acute inflammation
  • repair
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8
Q

What is the most common allergy of the airways?

A

Asthma

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9
Q

What is the most common allergy of the parenchyma?

A

Extrinsic allergic alveolitis

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10
Q

Which airways are not susceptible to intra-thoracic pressure?

A

Upper/Extra Thoracic airways

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11
Q

Give an example of extra-thoracic disease.

A

Laryngeal oedema

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12
Q

Which airways are susceptible to intra-thoracic pressure?

A

Bronchi

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13
Q

What are the clinical consequences of bronchial disease?

A

Medium to small airways have flaccid walls that aren’t protected by cartilage to hold them open

  • narrowing occurs during the expiatory phase (causes wheeze)
  • Impairs muco-ciliary clearance (sputum build up)
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14
Q

What are the three types of definitions of asthma?

A

Clinical
Physiological
Pathological

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15
Q

What is the clinical definition of asthma?

A 
Appropriate symptoms with signs
- wheeze, cough, yellow/clear sputum 
- breathlessness, exercise intolerant
Episodic, triggered, variable (paroxysmal)
- exercise, cats, chemicals
- diurnal 
Responds to asthma therapies
- 20% of asthma cases don't respond to treatment
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16
Q

What is the physiological definition of asthma?

A

Reversible airflow obstruction - spirometry before and after a nebuliser
Variable airflow obstruction
Airways are hyper-responsive
- histamine causes airway narrowing at lower concentrations in asthmatics

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17
Q

What inflammatory cells would you expect to find in an asthmatic airway?

A

Neutrophils
Macrophages
Eosinophils
Lymphocytes

18
Q

What are the inflammatory phenotypes of asthma?

A

Neutrophillic (61% neutrophils)
Eosinophilic (3% eosinophils)
Paucigranulocytic
Mixed

19
Q

What is the pathophysiological definition of asthma?

A

Inflammation of the airways - has an inflammatory phenotype

20
Q

Why does airway smooth muscle hypertrophy occur in asthmatic airways?

A

Remodelling occurs in the airways due to inflammation

  • the body is trying to regrow the lung (isn’t possible)
  • enters a cycle or repair and regrowth, leading to increased muscle in the airway wall
21
Q

Why is hypertrophy of smooth muscle in the airways bad?

A

This decreases the size of the lumen of the airways - compression

22
Q

What are the most important factors to consider when making a diagnosis of asthma?

A

Appropriate clinical history
Clinical signs at the times of symptoms
Supportive physiological tests

23
Q

How can the causative allergen be found in asthma cases?

A

Scratch the patients skin with various common allergens and see which has a reaction

24
Q

Briefly describe how an allergen can cause eosinophilic asthma?

A

The pathogen binds to IgE antibodies

  • the body recognises this as a pathogen and the mast cell is activated, producing histamine and cytokines
  • histamine activates smooth muscle and causes inflammation
  • this is when the airway becomes swollen and narrow
  • cytokines attract eosinophils to the area and also drive inflammation and remodelling
25
Q

What is corticosteriod responsive disease?

A

A disease which is commonly found in asthma airways and if stimulated, will drive an asthma phenotype
- stimulated by late allergic reactions and viral infections

26
Q

Which cytokines stimulate eosinophil release from bone?

A

Chemokines

  • IL-5
  • IL-13
  • TSLP
27
Q

Which cytokines stimulate airway remodelling in asthmatic airways?

A

TNF alpha
TGF beta
VEGF
IL-13

28
Q

What happens during airway remodelling?

A

Angiogenesis
Epithelial cell damage
Fibrosis
Smooth muscle hypertrophy

29
Q

What established therapies are available that target specific pathologies within asthma?

A

Anti-IgE biological therapy
Corticosteriods - affects mast cells and smooth muscle
Anti-leukotriene receptor drugs - affects macrophages and smooth muscle
Bronchodilators - affect smooth muscle and autonomic nerves controlling bronchial closing

30
Q

What future therapies are available that target specific pathologies within asthma?

A

Immunotherapy
Biological therapes
- TNF, IL-5, IL-13
Thermoplasty

31
Q

How allergy of the parenchyma different from asthma?

A

T-mediated inflammatory pathway that causes IgG production in the lung

  • delayed allergic response
  • 4/6 hours after the exposure
  • may last for several days
  • chronic exposure leads to fibrosis
32
Q

What are the signs and symptoms of extrinsic allergic alveolitis?

A 
Wheeze 
Cough
Fever
Chills
Headache 
Myalgia
Malaise 
Fatigue 
Lung consolidation
Immune complex disease
33
Q

What is the pathology of extrinsic allergic alveolitis?

A

Thickening of the spetae and filling of the alveolus with fluid

  • fibrosis
  • peribronchial granulomas
  • honeycombing
34
Q

How can EAA be identified?

A 
Low oxygen levels
Normal carbon dioxide levels 
- hypoxaemia 
- meaured by CO gas transfer
Chest X-Ray
- air space shadowing
35
Q

What can happen in there is chronic exposure to an antigen that causes EAA?

A

Fibrosis
- interstitial scarring from chronic tissue remodelling/reapir pathways
Emphysema
- interstitial destruction from neutrophilic enzyme release

36
Q

What ventilation/perfusion problems occur in EAA?

A

Reduced oxygen levels
Normal carbon dioxide levels
- emphysema (reduced surface area)
- pulmonary fibrosis (thicker membrane to travel through)

37
Q

How does EAA effect spirometry?

A

Pulmonary fibrosis is a resitrictive lung defect
- flow/volume loop shows reduced lung capacity and reduced flow during exhalation and inspiration (no change in the size of airspaces)

38
Q

Describe acute extrinsic allergic alveolitis.

A

Acute illness is due to type 3 reaction

- serum sickness or immune complex disease

39
Q

Describe sub-acute extrinsic allergic alveolitis.

A

Sub-acute can take days to weeks

  • type IV T-cell mediated reaction
  • like chronic dermatitis of lung
40
Q

Describe chronic extrinsic allergic alveolitis.

A

Fibrosis and Emphysema

- final pathway of all chronic inflammatory conditions

41
Q

How is extrinsic allergic alveolitis managed?

A

Allergy - avoid the trigger
Inflammation is controlled with corticosteriods
- neutrophils are modestly steriod responsive
- cytotoxics
Oxygen supplementation

Respiratory (12 decks)

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