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Respiratory > Asthma - Full summary > Flashcards

Asthma - Full summary Flashcards

1
Q

What is asthma?

A

Asthma is an episodic, chronic respiratory disorder, characterised by airway obstruction caused by inflammation and hyper-responsiveness of the bronchial smooth muscle

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2
Q

What are the 2 main classes of asthma?

A

Type II High (Atopic)
Type II Low (Non-atopic)

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3
Q

What are some common triggers of type II high asthma?

A

Pollen
Dust mites
Animal dander (FEL D1 proteins in cat saliva)

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4
Q

What are some common triggers of type II low asthma?

A

Cigarette smoke
Respiratory infection
Response to cold air
Emotional distress
Exercise

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5
Q

What 3 things make up the atopic triad?

A

Eczema
Allergic rhinitis
Asthma

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6
Q

What occurs in first contact to an allergen in type II high asthma?

A

The allergen stimulates the release of TSLP from the bronchial epithelium
This activates dendritic cells
This stimulates Th2 and B cells
Th2 cells release Interleukin 4, 5 and 14
This stimulates the release of IgE from B cells
Eosinophils and mast cells take up IgE

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7
Q

What occurs in second contact with an allergen in type II high asthma?

A

Eosinophils and mast cells release leukotrienes, cytokines and histamines
Mast cells also stimulate the production of arachidonic acid from membrane phospholipids, via the enzyme phospholipase A2
Arachidonic acid is then broken down into leukotrienes
This all causes bronchial smooth muscle inflammation and damages nerve fibres endings, increasing sensitivity of the bronchial smooth muscle

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8
Q

What are some changes that can occur to the bronchioles in chronic asthma?

A

Hyperplasia and hypertrophy of the smooth muscle
Pulmonary oedema
Increased mucus secretion
Sub-epithelial fibrosis, decreasing lung compliance

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9
Q

What occurs in aspirin sensitive asthma?

A

Both cyclooxygenase and 5-lipoxygenase breakdown arachidonic acid, COX into prostaglandins and lipoxygenase into leukotrienes
Aspirin blocks the enzyme cyclooxygenase, so more leukotrienes are produced
Leukotrienes stimulate increased mucus production, decreased mucus transport, damage to sensory nerve fibres (C-fibres) and increase contraction of airway smooth muscle

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10
Q

What are some symptoms and signs of asthma?

A

Intermittent episodes of:
- Dry cough
- Chest tightness
- Dyspnoea
- Diurnal variability
- Expiratory polyphonic wheeze
- Wheezing upon exhalation on auscultation
- Hyperressonance upon percussion
- Family history of atopic conditions

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11
Q

What is the name given to a severe asthma episode?

A

Status asthmaticus (Asthma attack)

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12
Q

What are some signs of a severe episode of asthma?

A

The patient may be unable to speak or can only use short phrases
They may be using accessory muscles during breathing

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13
Q

What are some examples of accessory muscles during breathing and what do they do?

A

Pectoralis major - Pull ribs up and outwards towards the humorous
Pectoralis minor - Pulls ribs 3-5 up towards the coracoid process of the scapula
Sternocleidomastoid - Pulls sternum and clavicle up towards the mastoid process of the temporal bone
Scalenus anterior, medius and posterior - Pulls rubs 1 and 2 up towards the cervical vertebrae

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14
Q

How can the severity of asthma be classified?

A

Using peak flow measurements
A peak flow metre is used 3 times and the highest measurement is used
The actual score is then divided by the normal score for that persons height, gender, weight and age, all multiplied by 100 to get a percentage normal value
Severity is the determined using the percentage:
>75% - Mild
50-75% - Moderate
33-50% - Severe
<33% - Life threatening

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15
Q

What are some red flag features that may be suggestive of conditions other than asthma?

A

Prominent systemic features - myalgia, fever, weight loss
Unexpected clinical findings - crackles, finger clubbing, cyanosis
Persistent, non-variale dyspnoea
Chronic sputum production
Unexplained restrictive spirometry
Chest X-ray shadowing

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16
Q

What are some conditions that can mimic asthma?

A

COPD
Hypersensitivity pneumonitis
Inducible Laryngeal Obstruction (ICO)
Allergic Broncho-Pulmonary Aspergillosis
Dysfunctional breathing
Bronchiolitis
Gastroesophageal reflux disease
Churg-Strauss syndrome

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17
Q

What is hypersensitivity pneumonitis?

A

A type III and IV hypersensitivity reaction to an air-born allergen

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18
Q

What is Inducible Laryngeal Obstruction?

A

A condition that results in the adduction of the vocal cords together, resulting in stridor (loud inspiration) and wheezing (Loud expiration)
Patients will often complain of something being stuck in their throat

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19
Q

What are some common triggers of Inducible Laryngeal Obstruction?

A

Strong smells
Cold air
Smoking
Exercise

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20
Q

What is Allergic broncho-pulmonary aspergillosis?

A

An allergic response to aspergillum fungus in the lungs, causing mucus plugging and proximal bronchiectasis
It presents with wheezing and high serum levels of IgE and eosinophils

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21
Q

How is allergic broncho-pulmonary aspergillosis usually treated?

A

Using steroids and possible Itraconazole (Anti-fungal)

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22
Q

How does bronchiolitis usually present?

A

It usually presents in children under 2 years old, with asthma like symptoms following an upper respiratory infection

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23
Q

How does gastroesophageal reflux disease differ from asthma?

A

Though Gastroesophageal reflux disease can cause a chronic cough and wheezing, it often occurs in obese adults who will respond well to proton pump inhibitors

24
Q

What is Churg-Strauss syndrome?

A

A small vessel vasculitis that, like asthma, is associated with wheezing and eosinophilia, however, unlike asthma, it also causes skin purpura and peripheral neuropathy

25
Q

How is asthma diagnosed in a symptomatic patient?

A

PFTs are used
In asthma, both FEV1 and FVC are reduced, however, FEV1 is reduced more,
This means that the FER is usually <70% expected
Asthma is reversible so PFTs are performed again after a dose of a SABA
This should cause a >12% increase in FEV1 if it is asthma

26
Q

How can asthma be diagnosed in an asymptomatic patient?

A

Challenge testing can be performed in which metacholine, a muscarinic acetylcholine agonist, is given, which causes bronchoconstriction
In a healthy patient, this bronchoconstriction will be negligible, however, in an asthmatic patient, it will bring on symptoms and cause a decrease in PFTs

27
Q

What are some tests that can be performed in asthma?

A

PFTs
FeNO
Serum IgE measurement
Blood eosinophil count
Skin-prick testing

28
Q

What happens in Skin-prick testing?

A

Skin is injected with known allergens to test for immune over-reaction
However, this only tests for atopic conditions, not only asthma

29
Q

What are the 2 forms of asthma treatment?

A

Relievers
Preventers

30
Q

What is the first line reliever treatment for asthma?

A

Short Acting ß-Agonists (SABA)
This is given as a reliever for use when required, with a maximum dose per day of 4x2 puffs (800mg)

31
Q

What is the first line preventer treatment for use when relievers are not controlling the condition fully?

A

An Inhaled CorticoSteroid (ICS)

32
Q

What is the second line preventer treatment for use in asthma, which an ICS is not controlling the condition?

A

Long Acting ß-Agonist

33
Q

What are some drugs that can be added to a SABA, ICS, LABA treatment regime in those whose asthma is not being controlled?

A

Long Acting Muscarinic Antagonist (LAMA)
Cysteinyl Leukotriene-1 receptor antagonist
Methylxanthine

34
Q

What is the final stage of management for asthma, when no other treatment options have worked?

A

5 days regiment of oral steroids (40mg per day)
Biologics

35
Q

What is meant by Maintenance and Reliever Therapy (MART)?

A

The combination of a LABA with an ICS, to be used twice per day as both a reliever and preventer

36
Q

What are the 2 main types of steroid?

A

Glucocorticoids
Mineralocorticoids

37
Q

Which type of steroid is used in the treatment of asthma?

A

Inhaled glucocorticoid steroids

38
Q

Where are steroid hormones produced naturally in the body?

A

In the adrenal cortex

39
Q

What are the functions of glucocorticoids, useful in the treatment of asthma?

A

They are anti-inflammatory and immune suppressors

40
Q

How do glucocorticoid steroids work?

A

They are lipophilic molecules and so enter cells via diffusion
In the cytoplasm, they combine with glucocorticoid receptors, which dissociate inhibitory heat shock proteins from the receptor (e.g. HSP90)
The now activated receptor translocates to the nucleus, aided by importing proteins
Here, the activated receptor monomers combine to form homodimers, which bind to glucocorticoid response elements (GRE) in the promotor regions of some genes
They can switch genes on and off
This is because they can cause expression of genes for histone acetyltransferases or histone deacetylases, which can modify the structure of chromatin

41
Q

What are some examples of corticosteroids?

A

Prednisolone
Beclometasone
Budesonide
Mometasone
Fluticasone

42
Q

What are the risks of inhaled corticosteroids?

A

They can increase the risk of oral Candida albicans infection due to local immunosuppression in the oropharynx
They can also increase the risk of pneumonia

43
Q

What is a muscle related side effect of glucocorticoid steroids?

A

Myopathies

44
Q

What are some bone related side effects of glucocorticoid steroids?

A

Osteoporosis
Aseptic necrosis of the femur

45
Q

What is a skin related side effect of glucocorticoid steroids?

A

Skin thinning

46
Q

What are some systemic side effects of glucocorticoid steroids?

A

Hyperglycaemia
Weight gain
Fluid retention
Cushingoid appearance (fatty deposits in the face, making it more round)
HPA insufficiency
Hypertension

47
Q

What are some psychiatric side effects of glucocorticoid steroids?

A

Neuropsychiatric disorders such as mania, depression and steroid psychosis

48
Q

What are some eye related side effects of glucocorticoid steroids?

A

Cataracts
Glaucoma

49
Q

What is a gastrointestinal side effect of glucocorticoid steroids?

A

Increased stomach acid production, leading to reflux

50
Q

How are cysteinyl leukotrienes formed?

A

Cell membrane phospholipids ate converted to arachidonic acid by the enzyme phospholipase A2
Arachidonic acid can then be broken down into leukotriene A4by the 6-lipoxygenase enzyme
LTA4 is then converted into either LTC4 or LTB4
LTC4 then becomes LTD4 and then LTE4
LTC4, D4 and E4 are the cytseinyl leukotrienes

51
Q

What are some effects of cysteine leukotrienes?

A

They cause oedema, increased mucus production, decreased mucus transport, eosinophil influx and damage to sensory nerve fibres (C-fibres) increasing bronchoconstriction

52
Q

What is an example of a cysteinyl leukotriene receptor antagonist?

A

Monteleukast

53
Q

What are some examples of methylxanthines?

A

Theophylline
IV aminophylline

54
Q

How should you take a metred dose (Standard spray) inhaler?

A

Shake for 5 seconds
Remove cap and check hole is clear
Breath normally and upon breathing out, place inhaler in mouth
Press down on the bottle upon breathing in
Hold breath for 10 seconds
Breath out slowly

55
Q

How should you take a metered dose inhaler with a spacer?

A

Shake for 5 seconds
Remove cap and check hole is clear
Attach the inhaler to the spacer
Seal mouth around spacer device
Press the bottle down
Take 5 normal breaths through the mouth
The device will whistle if breathing too quickly

56
Q

How should you take a dry powder inhaler (Circular or bullet shape)?

A

Load the device (Pull down lever on circular, twist end on bullet)
Breath out fully
Seal lips around the mouthpiece
Breath in quickly and forcefully
Hold breath for 10 seconds
Breath out slowly

Respiratory (23 decks)

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