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Therapeutics > Asthma/ COPD > Flashcards

Asthma/ COPD Flashcards

1
Q

What is asthma?

A

Asthma is a chronic inflammatory condition of the airways

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2
Q

What is the typical origin of asthma?

A

Asthma is usually allergic in origin.

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3
Q

What are the characteristic features of asthma?

A

Asthma is characterized by hyper-reactive airways, bronchoconstriction in response to various triggers, and reversibility of airway obstruction.

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4
Q

How is reversibility of airway obstruction assessed in asthma?

A

Reversibility is assessed by an FEV1 increase of >12% or 200 mL 15-20 minutes following inhalation of 200-400 mcg of salbutamol, or a 20% improvement in peak expiratory flow (PEF) from baseline.

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5
Q

How is asthma clinically diagnosed in childhood?

A

In childhood, asthma is clinically diagnosed by the presence of chronic persistent or recurrent cough and/or wheeze that responds to a bronchodilator.

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6
Q

Normal bronchiole vs Asthmatic bronchiole

A

Normal Bronchiole
-Airway Lining: The lining of a normal bronchiole is smooth and unobstructed.
-Muscle Layer: The muscle layer around the bronchiole is relaxed, allowing easy airflow.
-Mucus Production: Normal levels of mucus are produced, which trap dust and other particles but do not block the airway.
-Inflammation: There is no significant inflammation in the airway.

Asthmatic Bronchiole
-Airway Lining: The lining of an asthmatic bronchiole is swollen and inflamed.
-Muscle Layer: The muscle layer around the bronchiole is constricted, which narrows the airway.
-Mucus Production: Excess mucus is produced, which can clog the already narrowed airway.
-Inflammation: Chronic inflammation is present, making the airway more sensitive and reactive to triggers like allergens, smoke, or cold air

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7
Q

What are the common symptoms of asthma?

A

The common symptoms of asthma include cough, wheeze, dyspnoea (shortness of breath), and chest tightness.

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8
Q

How do asthma symptoms typically vary?

A

Asthma symptoms show variability in their occurrence, such as changes between day and night, day to day, and seasonally.

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9
Q

What factors can precipitate asthma symptoms?

A

Asthma symptoms can be precipitated by a range of factors including environmental allergens, non-specific irritants, cold weather, and exercise.

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10
Q

What defines COPD?

A

COPD is defined by an abnormal inflammatory response of the lungs to irritants, resulting in partially reversible, progressive airflow limitation.

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11
Q

What are the pathological correlates of COPD?

A

The pathological correlates of COPD are chronic bronchitis and emphysema.

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12
Q

What criteria should be considered for diagnosing COPD?

A

Diagnosis of COPD should be considered in any patient with chronic progressive dyspnoea and/or chronic cough (with or without sputum production) who has a smoking history of more than 10 pack years and/or other risk factors for COPD.

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13
Q

How can early detection and intervention impact COPD?

A

Early detection and effective smoking cessation interventions can slow the decline in pulmonary function and may alter the natural history of COPD.

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14
Q

Type of COPD

A
  • chronic bronchiolitis
  • emphysema
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15
Q

Chronic bronchitis

A

Definition: Chronic bronchitis is a long-term inflammation of the bronchi (the large and medium-sized airways in the lungs), characterized by a persistent cough that produces mucus (sputum) for at least three months in two consecutive years.

Key Features:

-Inflammation: The lining of the bronchi becomes inflamed and swollen.
-Mucus Production: Increased production of mucus, which can clog the airways.
-Cough: Persistent, productive cough (producing mucus).
-Airway Obstruction: Narrowing and obstruction of the airways due to mucus buildup and inflammation.
-Symptoms: Chronic cough, mucus production, wheezing, shortness of breath, and chest discomfort.

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16
Q

Define emphysema

A

Definition: Emphysema is a chronic lung condition characterized by the destruction of the alveoli (air sacs) in the lungs, leading to reduced surface area for gas exchange and difficulty in breathing.

Key Features:

-Alveolar Damage: The walls between the air sacs are damaged, causing them to lose their elasticity and merge into larger air spaces.
-Reduced Gas Exchange: Less surface area for oxygen to enter the blood and for carbon dioxide to be expelled.
-Breathing Difficulty: Difficulty in exhaling fully, leading to air trapping in the lungs.
-Symptoms: Shortness of breath, particularly during physical activity, chronic cough, wheezing, and fatigue.

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17
Q

How chronic bronchitis and emphysema related to COPD

A

Chronic Bronchitis: Primarily affects the airways (bronchi) and involves inflammation and mucus production.

Emphysema: Primarily affects the alveoli and involves destruction of lung tissue and air trapping.

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18
Q

How do normal lungs appear in terms of airway structure?

A

In normal lungs, the airways are clear, bronchioles maintain their shape, and the alveoli (air sacs) are intact and numerous, facilitating effective gas exchange.

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19
Q

What changes occur in the lungs with COPD?

A

In COPD, the bronchioles lose their shape and become clogged with mucus, and the walls of the alveoli are destroyed, forming fewer, larger air sacs which impede gas exchange.

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20
Q

What are the key differences between normal alveoli and those affected by COPD?

A

Normal alveoli are numerous and intact, ensuring efficient gas exchange. In COPD, alveoli walls are destroyed, resulting in fewer, larger air sacs that reduce the efficiency of gas exchange.

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21
Q

How does COPD affect the bronchioles?

A

COPD causes the bronchioles to lose their shape and become clogged with mucus, leading to obstructed airflow.

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22
Q

Is a smoking history commonly associated with COPD or asthma?

A

A smoking history is nearly always associated with COPD, whereas it is only possibly associated with asthma.

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23
Q

Are symptoms under the age of 35 more common in COPD or asthma?

A

Symptoms under the age of 35 are rare in COPD but often occur in asthma.

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24
Q

Which condition commonly presents with a chronic productive cough between asthma and COPD?

A

A chronic productive cough is common in COPD and uncommon in asthma.

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25
Q

How does breathlessness present differently in COPD and asthma?

A

Breathlessness in COPD is persistent and progressive, while in asthma, it is variable.

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26
Q

Which condition is more likely to cause night-time waking with breathlessness and/or wheeze?

A

Night-time waking with breathlessness and/or wheeze is common in asthma and uncommon in COPD.

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27
Q

Are atopic symptoms and seasonal allergies more commonly associated with COPD or asthma?

A

Atopic symptoms and seasonal allergies are commonly associated with asthma and uncommon in COPD.

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28
Q

Which condition exhibits significant diurnal or day-to-day variability of symptoms?

A

Significant diurnal or day-to-day variability of symptoms is common in asthma and uncommon in COPD.

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29
Q

How do COPD and asthma respond to inhaled glucocorticoids?

A

Asthma shows a consistent favorable response to inhaled glucocorticoids, whereas the response in COPD is inconsistent.

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30
Q

Goals for management for asthma

A
  • Abolish symptoms and achieve a normal lifestyle
  • Optimize treatment and minimize medication adverse
    effects
  • Avoid causative and trigger factors
  • Restore normal/ best possible lung function
  • Reduce the risk of severe attacks
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31
Q

Intermittent asthma mild class I

A
  • Daytime symptoms - </= 2 per week

-Night symptoms- </= 1 per month

PEF >/= 80%

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32
Q

Chronic persistent asthma Mild Class II

A
  • Daytime symptoms - 3-4 per week

-Night symptoms- 2-4 per month

PEF >/= 80%

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33
Q

Chronic persistent asthma Moderate Class III

A
  • Daytime symptoms - >4 per week

-Night symptoms- >4 per month

PEF 60- 80%

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34
Q

Chronic persistent asthma Severe Class IV

A
  • Daytime symptoms - continuous

-Night symptoms- frequent

PEF : <60%

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35
Q

What are reliever medications in asthma therapy?

A

Reliever medications are short-acting bronchodilators with a rapid onset of action. They provide acute symptomatic relief by relaxing the muscles around the airways, allowing for easier breathing.

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36
Q

What are controller medications in asthma therapy?

A

Controller medications are drugs with anti-inflammatory and/or sustained bronchodilator actions. They are used to manage chronic symptoms and prevent asthma attacks by reducing inflammation and maintaining open airways over the long term.

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37
Q

What are some controller medications with anti-inflammatory action used to prevent asthma attacks?

A
  • Inhaled corticosteroids
  • Leukotriene modifiers
  • Oral corticosteroids

These medications help to reduce inflammation in the airways and prevent asthma attacks.

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38
Q

What are some controller medications that provide sustained bronchodilator action but have weak or unproven anti-inflammatory effects?

A
  • long acting B2 agonists
  • sustained release theophylline preparations

These medications help to maintain open airways over the long term but do not significantly address inflammation.

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39
Q

What are reliever medications used for quick relief of asthma symptoms and acute attacks?

A
  • short acting B2 agonists
  • anti cholinergic

These medications are used on an as-needed (PRN) basis to provide rapid symptom relief.

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40
Q

inhaled corticosteroids

A
  1. beclomethasone
  2. budesonide
  3. fluticasone
  4. ciclesonide
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41
Q

inhaled corticosteroids mechanism of action

A
  1. Suppressing Inflammation: ICS bind to glucocorticoid receptors in airway cells, which inhibits the production of inflammatory chemicals like cytokines and prostaglandins.
  2. Reducing Immune Response: They decrease the activity and migration of immune cells (e.g., macrophages, eosinophils) to the site of inflammation.
  3. Decreasing Mucus Production: By reducing inflammation, ICS help to lower mucus production and airway swelling.
  4. Preventing Airway Remodeling: Long-term use helps prevent structural changes in the airways that can occur with chronic inflammation.
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42
Q

Leukotriene modifiers

A
  1. Montelukast
  2. Zafirlukast
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43
Q
A

Blocking Leukotriene Receptors:

Leukotriene Receptor Antagonists (LTRAs), such as montelukast, zafirlukast, and pranlukast, block the action of leukotrienes by binding to leukotriene receptors (e.g., CysLT1) on the surface of cells. This prevents leukotrienes from binding to their receptors and exerting their inflammatory effects.

Effect: This action reduces bronchoconstriction, mucus production, and airway edema, helping to alleviate asthma symptoms and improve lung function.

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44
Q

Oral corticosteroids

A
  1. Prednisone
  2. Prednisolone
  3. Methylprednisone
  4. Methylprednisolone
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45
Q

mechanism of action of oral corticosteroids

A

Blocking Inflammatory Mediators: They inhibit the enzyme phospholipase A2, decreasing the production of inflammatory substances.

Suppressing the Immune Response: They lower the number and activity of white blood cells involved in inflammation.

Modulating Gene Expression: They bind to glucocorticoid receptors, altering the expression of genes to reduce inflammation.

Stabilizing Cell Membranes: They prevent the release of enzymes that can cause tissue damage.

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46
Q

Long acting B2 agonists

A
  1. Salmeterol
  2. Formoterol
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47
Q

Long acting beta 2 agonists (LABA)

A

Stimulating Beta-2 Receptors: They bind to beta-2 adrenergic receptors on the smooth muscle cells of the airways.

Relaxing Airway Muscles: This stimulation leads to the relaxation of bronchial smooth muscle, causing bronchodilation (opening of the airways).

Sustained Effect: LABAs have a longer duration of action compared to short-acting beta-2 agonists, providing extended bronchodilation and improving airflow over 12 to 24 hours.

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48
Q

Mechanism of action of sustained release theophylline preparations

A

Inhibiting Phosphodiesterase: Theophylline inhibits the enzyme phosphodiesterase, which leads to an increase in cyclic AMP (cAMP) levels in airway smooth muscle cells.

Bronchodilation: Elevated cAMP levels cause relaxation of bronchial smooth muscle, resulting in bronchodilation (widening of the airways).

Anti-inflammatory Effects: Theophylline has mild anti-inflammatory effects, helping to reduce inflammation in the airways.

Sustained Release: The sustained-release formulation ensures a prolonged effect, maintaining bronchodilation over an extended period (up to 24 hours).

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49
Q

Short acting B2 agonists

A
  1. Salbutamol
  2. Fenoterol
  3. Terbutaline
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50
Q

Short acting B2 agonists mechanism of action

A

Stimulating Beta-2 Receptors: They bind to beta-2 adrenergic receptors on smooth muscle cells in the airways.

Relaxing Airway Muscles: This binding causes relaxation of the bronchial smooth muscle, leading to bronchodilation (widening of the airways).

Rapid Onset: SABAs have a quick onset of action, providing fast relief from acute asthma symptoms by opening the airways.

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51
Q

Anti- cholinergics

A

Ipratropium bromide

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52
Q

Mechanism of action of anti cholinergics

A

Blocking Muscarinic Receptors: They inhibit muscarinic acetylcholine receptors (specifically M3 receptors) on the smooth muscle cells of the airways.

Preventing Constriction: By blocking acetylcholine, which is a neurotransmitter that causes bronchoconstriction, anticholinergics prevent the contraction of bronchial smooth muscle.

Reducing Secretions: They also help reduce mucus production in the airways, which can contribute to airway obstruction.

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53
Q

What is the mainstay of chronic asthma management?

A

Inhaled corticosteroids are the mainstay of chronic asthma management. They help reduce inflammation and prevent asthma symptoms.

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54
Q

Why is a spacer device used with inhalers?

A

A spacer device is used with inhalers to improve medication delivery to the lungs and reduce the amount of medication that is deposited in the mouth and throat.

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55
Q

What reliever medication is commonly prescribed to all asthma patients?

A

Salbutamol is the common reliever medication prescribed to all asthma patients for quick relief of acute symptoms.

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56
Q

Why is checking inhaler technique important in asthma management?

A

Checking inhaler technique is important to ensure that the medication is being used correctly and effectively, which improves asthma control.

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57
Q

What is the starting dose for beclomethasone in asthma management?

A

The starting dose for beclomethasone is 200 mcg, taken 12 hourly.

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58
Q

What should be done if asthma is not controlled with the initial dose of beclomethasone?

A

If asthma is not controlled with 200 mcg of beclomethasone, increase the dose to 400 mcg, taken 12 hourly.

59
Q

What is the next step if asthma remains uncontrolled despite increasing beclomethasone?

A

If asthma is still not controlled, add a long-acting beta-2 agonist (LABA) such as Salmeterol in combination with Fluticasone (e.g., 50/250 mcg), taking 1 puff 12 hourly.

60
Q

What are the options if asthma remains uncontrolled after adding LABA?

A

If asthma remains uncontrolled, consider referral to a specialist and additional treatments such as leukotriene receptor antagonists, tiotropium bromide, or theophylline.

61
Q

How to access control of asthma

A
  • Daytime symptoms
  • Limitation of activities
  • Nocturnal symptoms/ awakening
  • Need for reliever medication
  • Lung function (PEF or FEV1)
  • Exacerbations
62
Q

Uncontrolled asthma

A
  • 3 or more features of partly controlled asthma in any week
  • An exacerbation in any week

Check adherence and inhaler technique
Step up control

63
Q

Partly controlled asthma

A
  • Daytime symptoms > twice a week
  • Any limitation of activity
  • Any nocturnal symptoms/ awakening
  • Need for reliever medication > twice/ week
  • Lung function < 80% predicted or personal best
  • </= exacerbation per year

Check adherence and inhaler technique
Step up control

64
Q

Controlled asthma

A
  • </= 2 daytime symptoms per week
  • No limitation of activity
  • No nocturnal symptoms/ awakenings
  • Reliever medication= twice/ week
  • Normal lung function
  • No exacerbations

Consider step down if controlled for 3 or more months

65
Q

inhaled formulations

A
  1. dry powder inhaler
  2. pressured metered dose inhaler
  3. nebuliser
66
Q

What are short-acting β2-agonists used for?

A

Short-acting β2-agonists are the drugs of choice for the relief of bronchospasm during acute asthma exacerbations.

67
Q

What devices can be used to administer short-acting β2-agonists?

A

Short-acting β2-agonists can be administered using a metered dose inhaler with a spacer or a nebulizer.

68
Q

What does the frequency of short-acting β2-agonist use indicate?

A

The frequency of use is a measure of asthma control.

69
Q

Increased use of short acting B2 agonistis

A

Increased use indicates a deterioration in asthma control.

70
Q

When can short-acting β2-agonists be used as the sole therapy?

A

Short-acting β2-agonists may be used as the sole therapy for mild intermittent asthma

71
Q

How should short-acting β2-agonists be used in chronic persistent asthma?

A

In chronic persistent asthma, short-acting β2-agonists should only be used as needed and not as the primary treatment.

72
Q

Why are oral β2-agonists generally not recommended?

A

Oral β2-agonists have a slower onset of action and a higher risk of systemic side effects, making them less preferable for asthma management.

73
Q

What is a common anticholinergic used in asthma management?

A

Ipratropium bromide is a common anticholinergic used in asthma management.

74
Q

How do anticholinergics work in asthma?

A

Anticholinergics are antagonists of muscarinic receptors. They inhibit bronchoconstriction by blocking the action of acetylcholine, which reduces airway constriction.

75
Q

How does the effectiveness of anticholinergics compare to inhaled β2-agonists?

A

Anticholinergics are less effective as relievers in asthma compared to inhaled β2-agonists.

76
Q

What is the onset of action for anticholinergics like Ipratropium bromide?

A

The onset of action for anticholinergics is approximately 30 minutes

77
Q

How do anticholinergics interact with β2-agonists?

A

Anticholinergics have an additive effect with β2-agonists, meaning they can be used together to enhance bronchodilation.

78
Q

What is the role of inhaled corticosteroids in asthma management?

A

Inhaled corticosteroids are the cornerstone of asthma management, providing effective long-term control of asthma symptoms.

79
Q

How do inhaled corticosteroids work?

A

Inhaled corticosteroids bind to glucocorticoid receptors, alter gene expression, and produce an anti-inflammatory action, reducing inflammation in the airways.

80
Q

Do inhaled corticosteroids cure asthma?

A

No, inhaled corticosteroids do not cure asthma. If discontinued, asthma control typically deteriorates.

81
Q

Why do inhaled corticosteroids have fewer side-effects compared to systemic corticosteroids?

A

Inhaled corticosteroids target inflammation directly at the site of action (the airways), which results in fewer systemic side-effects.

82
Q

What are common side-effects of inhaled corticosteroids?

A

Common side-effects of inhaled corticosteroids include oropharyngeal candidiasis (thrush) and hoarseness.

83
Q

How to use a spray inhaler

A
  1. Take off the cap. Shake the inhaler
  2. Stand up. Breathe out
  3. Put the inhaler in your mouth or put it just in front of your mouth. As you start to breathe in, push down on the top of the inhaler and keep breathing slowly
  4. Hold you breath for 10 seconds. Breathe out
84
Q

What happens to aerosol medication when using an inhaler without a spacer?

A

Without a spacer, 90% of the aerosol medication is swallowed and absorbed in the gastrointestinal tract. This absorbed medication undergoes first-pass inactivation in the liver, potentially leading to systemic side effects. Only 10% of the medication reaches the lungs

85
Q

How does using a spacer with an inhaler impact medication delivery?

A

Using a spacer allows large particles to be deposited in the spacer chamber before inhalation. When inhaled, the aerosol is enriched with smaller particles that are more likely to reach and deposit in the small airways of the lungs.

86
Q

What are the benefits of using a spacer with an inhaler?

A

A spacer reduces the amount of medication swallowed, increases deposition in the lungs, and minimizes systemic side effects, leading to improved drug delivery to the target site.

87
Q

How does a spacer affect the deposition and absorption of aerosol medication?

A

A spacer increases the amount of medication that reaches the lungs by allowing more small particles to be inhaled and reduces the amount of medication swallowed and absorbed in the gastrointestinal tract

88
Q

How do long-acting β2-agonists cause bronchodilation?

A

Long-acting β2-agonists bind to beta-2 receptors, stimulate adenylyl cyclase, and increase cyclic AMP (cAMP) levels, leading to bronchodilation

89
Q

Do long-acting β2-agonists have anti-inflammatory effects?

A

No, long-acting β2-agonists do not have anti-inflammatory effects. They are used to provide sustained bronchodilation.

90
Q

Can long-acting β2-agonists be used as monotherapy for asthma?

A

No, long-acting β2-agonists should never be used as monotherapy for asthma. They should be used as add-on therapy to inhaled glucocorticosteroids

91
Q

How are long-acting β2-agonists typically administered?

A

Long-acting β2-agonists are typically administered via inhalation.

92
Q

What are common side effects of long-acting β2-agonists?

A

Common side effects of long-acting β2-agonists may include tremor and palpitations.

93
Q

What triggers the release of arachidonic acid from cell membranes?

A

Arachidonic acid is released from cell membranes in response to stimuli such as allergens, infections, or other factors.

94
Q

What products are formed in the cyclooxygenase pathway of arachidonic acid metabolism?

A

The cyclooxygenase pathway produces thromboxane (TX) and prostaglandins (PG), which are involved in inflammation and bronchoconstriction

95
Q

What does the 5-lipoxygenase (5-LO) pathway convert arachidonic acid into?

A

The 5-lipoxygenase pathway converts arachidonic acid into leukotriene (LT) A4.

96
Q

What are the different leukotrienes produced from LTA4, and their roles?

A

From LTA4, leukotrienes are further converted into:

LTB4: Involved in neutrophil chemotaxis and mucus production.

LTC4, LTD4, LTE4: Involved in allergy, bronchoconstriction, and mucus production.

97
Q

What are some examples of cysteinyl leukotriene receptor antagonists and their action?

A

Examples of cysteinyl leukotriene receptor antagonists include Montelukast, Zafirlukast, and Pranlukast. They block the effects of cysteinyl leukotrienes (LTC4, LTD4, LTE4) in the airways, reducing bronchoconstriction, mucus production, and inflammation.

98
Q

Why are leukotriene receptor antagonists significant in asthma and COPD management?

A

Leukotriene receptor antagonists are significant because they help manage asthma and COPD by targeting the inflammatory processes and reducing bronchoconstriction and mucus production.

99
Q

Are leukotriene receptor antagonists effective as monotherapy for asthma?

A

No, leukotriene receptor antagonists are not effective as monotherapy for asthma.

100
Q

How do leukotriene receptor antagonists compare to long-acting β2-agonists when added to corticosteroids?

A

Leukotriene receptor antagonists are less effective than long-acting β2-agonists when added to corticosteroids.

101
Q

When are leukotriene receptor antagonists useful as add-on therapy

A

Leukotriene receptor antagonists are useful as add-on therapy when symptoms persist despite being on corticosteroids and long-acting β2-agonists, or if the patient cannot tolerate long-acting β2-agonists.

102
Q

Do all patients respond to leukotriene receptor antagonists?

A

No, not all patients respond to leukotriene receptor antagonists.

103
Q

What should be done if there is no improvement with leukotriene receptor antagonists after 4 weeks?

A

If there is no improvement after 4 weeks, leukotriene receptor antagonists should be withdrawn

104
Q

What are the side effects of leukotriene receptor antagonists?

A

Leukotriene receptor antagonists have very few side effects.

105
Q

What is the mechanism of action of theophylline?

A

Theophylline works by non-selectively inhibiting phosphodiesterases, which may result in bronchodilation and an anti-inflammatory effect by inhibiting the release of mediators.

106
Q
A
107
Q

How does theophylline’s mode of action complement other bronchodilators?

A

Theophylline’s mechanism of action is complementary to other bronchodilators, providing additional bronchodilation and anti-inflammatory effects

108
Q

When is theophylline used in asthma management?

A

Theophylline is only used as add-on therapy in asthma management, not as a primary treatment.

109
Q

What are the potential side effects of theophylline, and why is its therapeutic index a concern?

A

Theophylline has a narrow therapeutic index, which means there is a high potential for side effects. These include gastrointestinal symptoms (nausea and vomiting), cardiac arrhythmias, and central nervous system symptoms (tremor, confusion, seizures).

110
Q

When are oral corticosteroids typically used in asthma management?

A

Oral corticosteroids are used for a short course after an acute exacerbation and in cases of severe and poorly-controlled asthma.

111
Q

What are some significant side effects of oral corticosteroids?

A

Oral corticosteroids carry a risk of significant side effects including:

-HPA Axis Suppression: Adrenal atrophy and inadequate stress response.

-Cardiovascular Issues: Hypertension, fluid and electrolyte disturbances.

-Metabolic Effects: Hyperglycemia, diabetogenic, dyslipidemia.

-Musculoskeletal Problems: Muscle weakness, osteoporosis, osteonecrosis.

-Gastrointestinal Issues: Peptic ulcer disease.

-Eye Problems: Cataracts.

-Growth Issues: Growth retardation in children.

-Psychiatric Effects: Euphoria, behavioral changes, depression.

112
Q

What are some long-term risks associated with oral corticosteroid use?

A

Long-term use of oral corticosteroids can lead to Cushing’s syndrome, and contribute to various metabolic and musculoskeletal problems, as well as psychiatric effects.

113
Q

What is the initial step in managing acute severe asthma?

A

Administer oxygen by face mask to ensure adequate oxygenation.

114
Q

How should beta2-agonists be administered in acute severe asthma?

A

Beta2-agonists can be administered via a metered dose inhaler (MDI) with a spacer or by nebulizer.

115
Q

: What type of corticosteroids should be used early in the management of acute severe asthma?

A

Early systemic corticosteroids, such as oral prednisone or intravenous corticosteroids, should be used.

116
Q

When should ipratropium bromide be considered in acute severe asthma management?

A

Ipratropium bromide should be considered if the response to salbutamol is poor.

117
Q

What role does intravenous magnesium sulfate play in the treatment of acute severe asthma?

A

Intravenous magnesium sulfate can be used in acute severe asthma to help relax the bronchial muscles and improve breathing.

118
Q

When might intubation and ventilation be necessary in acute severe asthma?

A

Intubation and ventilation may be necessary if the patient has severe respiratory failure or is unable to maintain adequate oxygenation and ventilation despite other treatments.

119
Q

Why should intravenous aminophylline be avoided in the management of acute severe asthma?

A

Intravenous aminophylline should be avoided due to its increased risk of adverse effects, such as vomiting and dysrhythmias, and because it does not improve bronchodilation or outcomes.

120
Q

What are the concerns with using intravenous beta2 stimulants in acute severe asthma?

A

Intravenous beta2 stimulants can have adverse effects and are generally not recommended for acute severe asthma management.

121
Q

What medication is typically prescribed at discharge for managing asthma?

A

Discharge usually includes a course of oral prednisone for 7 to 14 days to help manage inflammation and control symptoms.

122
Q

What should patient education cover when discharging someone with asthma?

A

Patient education should include:

-Chronic Nature of Disease: Understanding that asthma is a long-term condition.
-Drug Education: Information on both relievers and controllers, and how to use a spacer.
-Correct Techniques: Proper inhaler and spacer techniques.
-Monitoring Peak-Flow: How to monitor peak-flow readings and interpret them.
-Warning Signs: Recognizing warning signs of worsening asthma.
-Triggers and Avoidance Plans: Identifying triggers and strategies to avoid them.

123
Q

Preventative measures

A
  • Avoid exposure to personal and second-hand tobacco smoke
  • Avoid contact with furry animals
  • Reduce pollen exposure
  • Reduce exposure to house dust mite
  • Avoid irritants (dust and fumes)
  • Avoid food and beverages containing preservatives
  • Avoid beta blockers, NSAIDS and aspirin
124
Q

What should be considered if asthma is poorly controlled?

A

Consider if the diagnosis might be wrong, as conditions like heart failure, COPD, gastro-oesophageal reflux disease, or foreign body aspiration (in kids) can mimic asthma symptoms

125
Q

What should be checked if asthma remains poorly controlled despite treatment?

A
  • Poor adherence
  • Confusion about when to use controller and reliever drugs
  • Concomitant medications such as aspirin, NSAIDS & β-blockers that
    aggravate asthma
  • Inhaler Technique
  • Exposure to trigger factors
  • Rhinitis or sinusitis
126
Q

Treatment of COPD- goals

A
  1. Recognition of disease (early diagnosis and staging of severity)
  2. Prevention of disease progression (including smoking cessation)
  3. Alleviation of brethlessness and improvement in effort tolerance (treatment of airflow obstruction)
  4. Pulmonary rehabilitation and education 9improving quality of life)
  5. Prevention and treatment of exacerbations
  6. Prevention and treatment of complications
  7. Reduction in mortality
127
Q

Stage 1 COPD

A

Mild COPD

Airflow limitation FEV1>= 80% of predicted symptoms of chronic cough and sputum production

128
Q

Stage 2 COPD

A

Moderate COPD

Worsening airflow limitation 50% <= FEV1 <= 80% predicted with SOB on exertion with cough and sputum production

129
Q

Stage 3 COPD

A

Severe COPD

Further worsening airflow limitation 30% ,= FEV1 <= 50% predicted with SOB, decreased exercise capacity and fatigue

130
Q

Stage 4 COPD

A

Very severe COPD

Airflow limitation FEV1< 30%; or FEV1<= 50% in respiratory failure (PaO2 < 8kPa) and/ or presence of cor pumonale

131
Q

What is the initial medication for managing chronic COPD?

A

The initial medication is a short-acting β2-agonist, such as salbutamol, used with a spacer

132
Q

What should be done if there is no response to short-acting β2-agonists?

A

If there is no response, switch to a long-acting β2-agonist (LABA), such as formoterol or salmeterol.

133
Q

What is the treatment approach for COPD patients with frequent exacerbations (≥2 per year)?

A

For frequent exacerbations, replace the LABA with a LABA + inhaled corticosteroid (ICS) combination.

134
Q

What should be added if COPD remains inadequately controlled?

A

Add slow-release theophylline, typically 200 mg at night, if control remains inadequate

135
Q

Are oral corticosteroids recommended for stable COPD?

A

No, oral corticosteroids are not recommended for stable COPD.

136
Q

What are the signs of an acute exacerbation of COPD?

A

Signs of an acute exacerbation include worsening dyspnoea, increased cough, increased sputum production or purulence, and an increase in symptom variability

137
Q

What should be done before treating an acute exacerbation of COPD?

A

Exclude other potential causes such as cardiac failure, pulmonary embolism, or pneumonia.

138
Q

What is the first-line treatment for an acute exacerbation of COPD?

A

The first-line treatment is nebulized salbutamol.

139
Q

When should ipratropium bromide be added during an acute exacerbation?

A

Add ipratropium bromide if there is a poor response to nebulized salbutamol.

140
Q

What corticosteroid treatment should be started for an acute COPD exacerbation?

A

Start prednisone; use hydrocortisone if oral therapy cannot be taken.

141
Q

What should be prescribed at discharge for an acute exacerbation of COPD?

A

Discharge with prednisone 40 mg for 5 days.

142
Q

What antibiotic should be prescribed for an acute exacerbation of COPD?

A

Prescribe amoxicillin 500 mg every 8 hours for 5 days.

143
Q

What should be done if the patient has had recent exposure to amoxicillin?

A

If there has been recent exposure to amoxicillin, prescribe amoxicillin + clavulanic acid for 5 days.

Therapeutics (15 decks)

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