Asthma Flashcards
Summarise asthma
Patients with asthma present with recurrent episodes of shortness of breath, chest tightness, wheezing, or coughing.
Examination typically demonstrates an expiratory wheeze; however, in severe asthma there is poor air entry and the chest is silent.
Treatment is step-wise, based on symptoms. Patients may need to monitor their peak expiratory flow daily and should be aware of the warning signs of a severe attack.
Some patients may develop progressive, irreversible obstructive lung disease.
Define asthma
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
Describe the epidemiology of asthma
The prevalence of asthma worldwide is variable. Countries with the lowest prevalence in adults include China and Vietnam, whereas Australia and Sweden have the highest.[2] The global burden is reported to be 300 million people, potentially increasing to 400 million by 2025.[3]
As of 2018, asthma affects about 25 million people in the US, with an overall prevalence of 7.7%.[4] There were 109,000 hospital inpatient stays, 1.2 million emergency department visits, and 7.3 million physician office visits for adults with asthma in the US in 2018.[4] The death rate for asthma was highest among black people in the US in 2018.[4] Despite the improved understanding of pathophysiology and treatment methods, asthma continues to be undertreated.
Describe the aetiology of asthma
Asthma is a complex disease with underlying multi-gene association interacting with environmental exposure.[5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20]
The genes associated with the disease include, but are not limited to, ADAM 33,[6][21][22][23][24][25][26] dipeptidyl peptidase 10,[27][28] PHD finger protein 11,[27][28] prostanoid DP1 receptor,[27][28] chromosome 12q,[29] and polymorphisms in tumour necrosis factor (TNF).[30][31]
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.[16]
Many air pollutants have also been linked to increased asthma exacerbations.[32] Strong emotions and reactions, such as laughter, can also precipitate attacks[33] but often no clear aetiology can be identified.
Describe the two major elements of the pathophysiology of asthma
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.[34][35]
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 (TNF)-alpha,[36] 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.
Describe some Other WBCs involved in asthma
Other WBCs involved are eosinophils, basophils and mast cells, macrophages, and invariant natural killer (NK) T cells,[37] and in near-fatal or status asthmaticus, neutrophils are important.[17] These cells move to the airway, causing changes in the epithelium, airway tone, and related autonomic neural control and hyper-secretion of mucus, mucociliary function alteration and increased smooth muscle responsiveness. Pathological studies of fatal asthma show severe hyper-inflation and mucous plugging with the mucus-containing mucins (proteins that are present in the blood).[17] Tissue biopsies show the deposition of eosinophil granular proteins throughout the lung tissue and damage of the epithelium mediated by those proteins. Denudation of the basal layer by epithelial cell sloughing produces clumps of cells in the sputum referred to as Creola bodies. There is also sub-basement membrane deposition of collagen often referred to as thickened basement membrane, which is considered another hallmark
Describe the products of the inflammatory response in asthmatics
Products of the inflammatory response induce smooth muscle contraction and consequent AHR. There appear to be at least two different kinds of AHR: a baseline fixed and an episodic variable element.[38] The underlying fixed AHR is possibly related to airway remodelling, whereas the variable AHR reflects the action of the inflammatory mediators, and they are distinguished by direct and indirect bronchial challenges, respectively. Finally, airway smooth muscle in asthmatic people is increased in mass, probably as a result of hypertrophy and hyperplasia, which in vitro studies display as having increased contractility
Describe a typical case history for asthmatics
A 25-year-old woman presents with shortness of breath. She reported that in secondary school, she occasionally had shortness of breath and would wheeze after running. She experiences the same symptoms when she visits her friend who has a cat. Her symptoms have progressively worsened over the past year and are now a constant occurrence. She also finds herself wheezing when waking from sleep approximately twice a week.
Describe some other presentations of asthma
Asthma commonly presents in children, but may present in otherwise healthy middle-aged individuals. Symptoms may start as a non-productive cough, chest tightness, shortness of breath, or wheezing, either spontaneously or on exposure to trigger factors. When the cough is productive, it is associated with clear and sometimes stringy sputum. Frequently, the patient is a non-smoker and will often have an atopic history, such as childhood eczema. In people with nasal polyps, examination of the lung is usually normal.
Exercise-induced symptoms may occur in around 50% to 65% of people with asthma. The concept of the ‘cough-variant asthma’ syndrome was popularised in the mid-1980s and it has become an all-embracing label for the symptom of recurrent cough. This has resulted in overdiagnosis of asthma and inappropriate therapy. ‘Cough-variant’ asthma is rare and its existence is now questioned.
Describe key features in the history of asthmatics
Recurrent episodes of dyspnoea, chest tightness, wheezing, or coughing typically occur.
The patient’s medical history may help to identify allergen exposures that worsen the asthma: for example, episodes may be exacerbated by exposure to irritants such as tobacco smoke or fumes from chemicals, such as bleach. Attacks may occur seasonally or upon exposure to cats in allergic patients. Exercise can also make the symptoms worse.
More severely asthmatic people have night-time symptoms, waking them up from sleep. In severe exacerbations, patients are continuously short of breath and may use accessory muscles of respiration.
Describe the physical examination in asthmatics
The examination may be normal in patients with bronchial asthma. Examination of the nasal passages may reveal nasal polyposis or nasal congestion. Chest auscultation may reveal expiratory wheezes.
With more severe asthma, the wheezes may be audible without the use of a stethoscope. In patients with severe exacerbations, the lung examination may be silent.
What tests should be done on patients presenting with asthma for the first time
For patients presenting for the first time, chest x-ray, full blood count, and differential are indicated in the initial work-up, to exclude other pathologies. For patients presenting with an acute exacerbation, these may also be performed if complicating factors are suspected from history and exam.
International guidelines from the Global Initiative for Asthma (GINA) state that characteristic symptoms together with confirmed variable expiratory airflow limitation are required to make a diagnosis of asthma. GINA defines confirmed variable expiratory airflow limitation as documented excessive variability in lung function plus documented expiratory airflow limitation
Describe the tests that show airflow limitation
Pulmonary function testing (PFT), including forced expiratory volume at 1 second (FEV₁) and forced vital capacity (FVC), are used to demonstrate airflow limitation. Adults without airflow limitation normally have an FEV₁/FVC ratio of >0.75 to 0.80.
