Asthma Flashcards

1
Q

what is the definition of asthma?

A

Bronchial hyperresponsiveness
Asthma is a chronic inflammatory airway disease characterised by intermittent airway obstruction and hyper-reactivity. Many cellular components are involved in the asthmatic pathway, including mast cells, eosinophils, T lymphocytes, macrophages, neutrophils, and epithelial cells. On insult, in susceptible people, inflammation causes increased bronchial hyper-responsiveness and recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, which are usually associated with widespread but variable airway obstruction that is reversible either spontaneously or with treatment.

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2
Q

what is the epidemiology of asthma?

A

65% report severe (unable to speak)

Allergic = more common in childhood

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3
Q

what is the aetiology of asthma?

A

Allergic inflammation mediated by eosinophils
Eosinophilic asthma - 25% are atopic, igE mediated reactions tendency (only 50% will react), can be atopic or non-atopic, th2 high
Non-eosinophilic asthma - t helper 1 cells, th2 low
The genes associated with the disease include, but are not limited to, ADAM 33, dipeptidyl peptidase 10, PHD finger protein 11, prostanoid DP1 receptor, chromosome 12q, polymorphisms in tumour necrosis factor, and polymorphisms in the vitamin D receptor.
Patients’ genetic make-up may predispose them to hyper-responsiveness to environmental aetiological triggers. Those triggers include viral infections (e.g., rhinovirus, respiratory syncytial virus, human metapneumovirus, and influenza virus), bacterial infections (Mycoplasma pneumoniae or Chlamydia pneumoniae), allergen exposure (e.g., tree, grass, or weed pollen, fungi, or indoor allergens), occupational exposures (e.g., animal or chemical), food additives and chemicals (e.g., metabisulfites), irritants, or aspirin in predisposed people.
Many air pollutants have also been linked to increased asthma exacerbations. Strong emotions and reactions, such as laughter, can also precipitate attacks but often no clear aetiology can be identified.
Occupational asthma:
Animals, insects, fish, flour, enzymes, gases, fumes, smoke

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4
Q

what are the risk factors for asthma?

A

Family history
Allergens
Atopic history

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5
Q

what is the pathophysiology of asthma?

A

Airway increases in mass?
There are two major elements in the pathophysiology: inflammation and airway hyper-responsiveness (AHR). The large airways and the small airways with diameters <2 micrometres are the sites of inflammation and airway obstruction.
There are two major elements in the pathophysiology: inflammation and airway hyper-responsiveness (AHR). The large airways and the small airways with diameters <2 micrometres are the sites of inflammation and airway obstruction.
Airway inflammation occurs secondary to a complex interaction of inflammatory cells, mediators, and other cells and tissues in the airway. An initial trigger leads to the release of inflammatory mediators, which leads to the consequent activation and migration of other inflammatory cells. The inflammatory reaction is a T-helper type 2 (Th2) lymphocytic response. Th2 inflammation is characterised by the presence of CD4+ lymphocytes that secrete interleukin (IL)-4, IL-5, and IL-13, the chemokine eotaxin, tumour necrosis factor-alpha, and the leukotriene LTB4, a product of the lipoxygenase pathway, as well as mast cell tryptase. This Th2 response is important in the initiation and prolongation of the inflammatory cascade.
Other white blood cells involved are eosinophils, basophils and mast cells, macrophages, and invariant natural killer (NK) T cells, and in near-fatal exacerbations of asthma, neutrophils are important.

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6
Q

what are the key presentations of asthma?

A

Episodic wheeze
Cough
Breathlessness
Diurnal variation (worse at 3/4am) - nocturnal waking
Recent upper respiratory tract infection
Nasal polyposis
Provoking factors
Brittle disease - type 1 = chronic, type 2 = sudden dips

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7
Q

what are the first line and gold standard investigations for asthma?

A

FEV1/FVC - FEV₁/FVC <80% of predicted
Peak expiratory flow rate - flow rate as a comparison to patient’s personal best or normal values for height and gender
CXR - normal or hyper-inflated
FBC - normal or raised eosinophils and/or neutrophilia

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8
Q

what questions should be asked in an asthma history taking?

A

Assessment of severity:
Recent nocturnal waking, usual asthma symptoms, interference with day to day activities
Exacerbations:
A and E, GP, ICU
History:
Age of onset, childhood ventilation and respiratory disease (what was the birth like), unusual features (weight loss), any obvious causes (chlorine exposure)
Associated problems:
Eczema, hay fever, pets, nasal disease, food allergies, drug allergies, reflux disease
Check if taking beta blockers
Smoking history, asthma and eczema family history

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9
Q

what are the differential diagnoses for asthma?

A
CF
Chronic rhinosinusitis
Tracheomalacia 
Bronchiolitis
Bronchiectasis 
COPD - onset later, sputum production, winter symptoms, less variation - can overlap
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10
Q

how is asthma managed?

A

Infrequent symptoms:
Low-dose inhaled corticosteroid and formoterol as needed, add short acting beta agonist if needed
Troublesome most days:
Low dose inhaled corticosteroid and formoterol as maintenance and reliever therapy, add long acting beta agonist, add short acting beta agonist, add medium dose inhaled corticosteroid
Severe:
Medium dose inhaled corticosteroid and formoterol as maintenance and reliever, short course oral corticosteroids, high dose inhaled corticosteroid, SABA as needed, LABA, leukotriene receptor agonist, theophyllines, anticholinergics
Acute attack:
High flow oxygen. Emergency beta agonists, peak flow, oximetry, CXR for pneumothorax, treat with magnesium sulphate

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11
Q

how is asthma monitored?

A

Check drug compliance
Patients are recommended to self-monitor at home on a daily basis by checking and recording the peak expiratory flow rate (PEFR) using a PEFR metre.

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12
Q

what are the complications of asthma?

A

Severe exacerbation
Moderate exacerbation
Airway remodelling
Oral or esophageal candidiasis and dysphonia due to inhaled corticosteroids

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13
Q

what is the prognosis of asthma?

A

Worse - high number of drugs needed to treat, admission to ICU, A and E, attended to GP for steroids and antibiotics

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14
Q

how are acute asthma attacks classified?

A

Asses for - MODERATE (PEFR 50-75% best or predicted, Speech normal, RR < 25 / min, Pulse < 110 bpm), SEVERE (PEFR 33 - 50% best or predicted, Can’t complete sentences, RR > 25/min, Pulse > 110 bpm), or LIFE THREATENING ( PEFR < 33% best or predicted, Oxygen sats < 92%, Silent chest, cyanosis or feeble respiratory effort, Bradycardia, dysrhythmia or hypotension, Exhaustion, confusion or coma)

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15
Q

what is churg-strauss syndrome?

A

eosinophilic granulomatosis with polyangiitis: asthma, blood eosinophilis, paranasal sinusitis, mononeuritis multiplex, pANCA positive in 60^ of patients

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