Asthma Flashcards

1
Q

Characteristics of asthma

A

Asthma is a chonic inflammatory disorder of the airways characterised by airflow obstruction, airway hyperresponsiveness and bronchial inflammation.

Obstruction is often revesible, either spontaneously or with treatment.

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2
Q

How is asthma classified?

A

Categorised based on atopy

Extrinsic: immune reaction. Patients have positive skin-prick reactions to dustmites, animals, pollen and fungi.

Intrinsic: abnormal autonomic regulation of the airways. Often starts in middle age, may be due to occupation.

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3
Q

Pathogenesis of asthma

A

Inflammatory stimuli activate mast cells. Alveolar macrophages and epithelial cells which release inflammatory mediators (e.g. histamine) and recruit eosinophils.

Airway inflammation cause bronchoconstriction, increased vascular permeability and stimulation of mucus secretion.

In severe, chronic disease airway remodelling occurs. The airway wall becomes thickened due to hypertrophy of smooth muscle and oedema. Myofibroblasts increase collagen deposition which thickens the basement membrane and leads to fibrosis.

Mucus and exudate accumulates in the lumen forming a plug.

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4
Q

What signs might you detect on physical examination of an asthmatic patient?

A

Eczema

Wheeze

Tachycardia

Tachypnoea

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5
Q

Describe the tests used to assess the condition of a patient with asthma

A

Spirometry: FEV/FVC ratio is reduced. Residual volume may be increased. Patients show improvement of more than 15% with bronchodilators. Help determine if the cause is restrictive or obstructive.

Peak flow: used to assess airway obstruction. morning and evening measurements. Useful in long term assessment of variability. Morning dipping characteristically seen in poorly controlled asthma.

Bronchoprovocation test: use histamine or irritant to demonstrate bronchial hyperreactivity.

Immune tests: skin prick, IgE levels

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6
Q

Common clinical presentation of asthma

A

Wheeze

Dyspnoea

Cough

and sensation of tight chest.

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7
Q

Name four major precipitating factors for asthma attacks

A

cold air

allergens: moulds, dust, grass, pollen, pet hair

viral infection

exercise

Irritants: cigarrete smoke, perfume

occupation: wood, dust, latex

Atmospheric pollution

Drugs: NSAIDs, beta blockers

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8
Q

What findings might indicate poorly controlled asthma on examination

A

Patients with good control have a completely normal examination.

Patients with poor control may have expiratory wheeze as a result of turbuent airflow

Prolonged expiratory phase due to a delay in exhalation resulting from the airway narrowing

Increased use of short-acting reliever bronchodilators.

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9
Q

Describe the method used in spirometry

A

Measures airflow during a prolonged maximal blow. Measures the respiratory physiology.

Can measure flow (FEV1) with respect to time or lung volume (FVC).

FEV1 is affected in obstructed lung disease, which becomes progresively reduced as the airways narrow and flow decreases.

Reduction in FVC indicates a reduction in lung volume, and restrictive physiology.

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10
Q

What are the changes in seen in an arterial blood gas of an asthma attack?

A

The pO2 and pCO2 in a patient’s arterial blood suring an acute asthma attach changes depending on the severity.

In a mild attack pCO2 is low because the patient hyperventilates without bronchospasm affecting CO2 diffusion so CO2 is lost.

As the bronchospasm worsens, air trapping increases and the ability to ventilate the lungs worsens. pCO2 will be normal or raised which in these patients is a concern.

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11
Q

What are the groups of drugs used to treat asthma?

A

Bronchodilators:

B2 agonists. Can be short or long acting. Stimulate B2Rs in smooth muscle of the airway producing relaxation and bronchodilation. Used for acute management of symptoms. Given via inhaler. Long acting used for management of the disease

Methylxanthines: Inhibit breakdown of cAMP. Increase causes relaxation of airway smooth muscle. Used for acute management.

Anticholinergics: Short or long acting. Block vagal tone which bronchoconstrics smooth muscle. Given by inhalation in sever asthma attacks. Long acting used in management of asthma

Corticosteroids: Counteract airway inflammation. Preventative.

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12
Q

Side effects of long term oral corticosteroids

A

Oral candidiasis

hoarse voice

inhibits growth in children

osteoporosis

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13
Q

Non-drug management strageies in asthma

A

Avoid tigger factors

Family involvement in management of children

Patient education to improve compliance

Avoid smoking

Weight loss if obese

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14
Q

Action beta agnoists in asthma treatment

A

Relaxes airway smooth muscle

Inhibits mast cell, eosinophil and lymphocyte mediator release

Inhibits plasma leakage and oedema

Increased mucociliary clearance

Can be short (salbutamol, terbutaline) or long acting (salmeterol, formoterol)

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15
Q

Describe the events in the immediate phase on an asthma attack

A

In allergic asthma, there is a type 1 hypersensitivity reaction.

Initial exposure of the allergen to APCs leads to activation of Th2 cells. These activate B-cells to produce IgE which binds to receptors on mast cells. On re-exposure, the allergen binds to IgE and cross-links the receptors which activates mast cells.

Mast cells release histamine, leukotrienes and prostaglandinns. These promote vascular permability, bronchospasm and mucus production.

Chemokines released by mast cells attract eosinophils and monocytes.

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16
Q

What is the late phase of asthma and why does it occur?

A

The late phase response is due to a progressing inflammatory reaction.

Infiltration of Th2 cells, monocytes and eosinophils release leukotrienes, interleukins and pro-inflammatory proteins which cause damage and loss of the epithelium.

Loss of epithelium means irritant receptors are more accesible which contributes to hyperresponsiveness of the airway.

Continued inflammation and hyperresponsiveness causes bronchospasm, wheezing and coughing. FEV1 falls.

17
Q

Describe the changes that occur in chronic asthma

A

In chronic asthma patient remodelling of the airway occurs in response to inflammatory damage.

Growth factors released from the inflammatory cells act on smooth muscle cells to cause hypertrophy and hyperplasia. Goblet cell hyperplasia increase mucus secretions.

Epithelial damage increases hyperresponsiveness of the airway

Subepithelial fibrosis causes thickening of the basement membrane