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Medicine year 1 semester 2 > Case 7- asthma > Flashcards

Case 7- asthma Flashcards

1
Q

Intrinsic asthma

A

Causative agent is unknown but may be associated with irritants or sensitisation to chemicals or biological products at work. Aspirin and beta blockers may induce asthma. Triggers include: exposure to chemical agents/drugs, exercise, respiratory infection or stress.

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2
Q

Extrinsic asthma

A

In atopic individuals with reactions to common allergens like dust mites, animal dander and pollens. More common in childhood where it is associated with eczema. Triggers include: allergens i.e. pollen, dust mites, animals, peanuts and eggs

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3
Q

Symptoms of asthma

A

Wheezing, shortness of breath and cough. Tends to be more severe at night or in the early morning

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4
Q

What causes an asthma attack

A

Normally a trigger such as exposure to dust, cold air or exercise

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5
Q

What causes the symptoms of asthma

A

Reversible airway obstruction, inflammation of airways, bronchial hyper-reactivity. Acute episodes of asthma can cause Hypoxaemia (abnormally low amounts of oxygen in the blood)

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6
Q

Pathophysiology of asthma

A

Asthma occurs due to a sustained inflammatory response. There is an infiltration of the airway wall with pro-inflammatory lymphocytes and mast cells which release cytokines and also eosinophils. This leads to swelling of the airway wall due to smooth muscle thickening or hypertrophy, a thickened basement membrane and the leaking of fluid from dilated blood vessels (oedema). This is associated with damaged epithelial cells, increased mucus production and bronchospasm which together may significantly reduce the airway lumen causing obstruction of movement of air.

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7
Q

The immediate phase of asthma

A

Begins within minutes of contact with the trigger and may last several hours, it mainly consists of shortness of breath and wheezing. It is when the mast cell degranulates leading to a bronchospasm

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8
Q

The late phase of asthma

A

Follows the immediate phase with sustained breathlessness and wheezing associated with an inflammatory response. It is when inflammatory cells like eosinophils release mediators. The late phase is a sustained inflammatory response

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9
Q

Asthma- irreversible remodelling

A

After years of repeated allergen exposure and exacerbation, there is remodelling of the airways

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10
Q

Irreversible remodelling- ciliated epithelial damage

A

Increases risk of secondary infections as it is easier for micro-organisms to get into the Lamina propria

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11
Q

Irreversible remodelling- mucus production

A

There is an increase in mucus production due to Goblet cell metaplasia, the epithelia cells undergo a differential change and turn into Goblet cells. There is also an increase in the number of mucus glands and the volume of mucus secreted by both the goblet cells and mucus glands.

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12
Q

Irreversible remodelling- basement membrane

A

In the inflammation and repair process, the ciliated epithelium undergoes fibrosis. This increases the thickness of the basement membrane

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13
Q

Irreversible remodelling- smooth muscle

A

Increase in airway smooth muscle, this can be due to Hyperplasia (increased number) or Hypertrophy (increased size). The smooth muscle is able to constrict the bronchiole even more.

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14
Q

Irreversible remodelling- immune cells

A

Immune cell infiltration causes an increase in Macrophages, Mast cells and Eosinophils. They get into the Lamina propria.

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15
Q

Irreversible remodelling- vascular changes

A

There is vasodilation and an increase in vascular permeability. This helps the Leukocytes get into the Lamina propria

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16
Q

Irreversible remodelling- chronic inflammation

A

Chronic inflammation- all the changes lead to a narrow airway and a decrease in bronchiole lumen diameter

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17
Q

Pathology of asthma

A

1) An allergen enters the bronchioles and damages the epithelial barrier
2) The allergen is phagocytosed, there is antigen presentation and activation of B cells
3) Mast cells are sensitised, secondary exposure to the allergen causes Mast cell degranulation
4) Histamine, Leukotrienes and Prostaglandins are releases

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18
Q

Risk factors for asthma

A
  • Family history of Atopy and genetics (6x)
  • Maternal smoking, can lead to epigenic changes in the foetus,
  • Bronchiolitis, especially if hospitalised.
  • Premature/low Birth rate
  • Urban environment
  • Early antibiotic exposure, remove commensal and pathogenic bacteria. Cant test out their immune system.
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19
Q

Protective factors for asthma

A

Vaginal birth, breast feeding, large number of siblings, daycare attendance and animal exposure. Increases the number of pathogens you will be exposed to so trains your immune system to respond appropriately.

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20
Q

Airway hyper-responsiveness

A

Often induced with asthma. Involves exaggerated bronchoconstriction and breathlessness. It is a combination of both hypersensitivity to a stimulus and a larger response then expected. You are more susceptible in asthma due to the damaged epithelia exposed nerves

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21
Q

Hypersensitivity

A

A normal response but at lower levels of stimulus

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22
Q

Hyperreactivity

A

An exaggerated response at normal doses of the stimulus.

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23
Q

Types of asthma

A

Atopic or non-atopic

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24
Q

Non-atopic asthma triggers

A

Exercise, smoking, emotions, the cold, a viral infection

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25
Q

Atopic asthma exposure

A

Environmental exposures to allergens (i.e. pollen, pets, mold). Irritant dusts, vapour and fumes (i.e. perfume, smoke). Medication (NSAIDs, B-blockers). Atmospheric pollution and occupational sensitisers.

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26
Q

Why do NSAID’s cause asthma

A

They block the effects of Prostglandins. Leukotrienes are released instead causing an immune response

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27
Q

Why do beta blockers cause asthma?

A

They block beta adrenergic receptors which are responsible for bronchodilation, this causes bronchoconstriction

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28
Q

How does physical exercise and cold air induce asthma

A

1) There is an increase in ventilation and air flow through your mouth.
2) This causes respiratory induced water loss from the respiratory cells. This is due to the difference in temp between the external air and your mouth.
3) This causes an increase in intracellular osmolarity.
4) This will cause an influx of intracellular Ca+, activating a signalling cascade leading to the activation of Phospholipase.
5) This causes the Mast cell to degranulate releasing Histamine leading to bronchoconstriction and increased Mucus production.
6) Prostoglandin and Leukotrienes are also released which are inflammatory mediators leading to immune cell recruitment.

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29
Q

What inhaler should you take before exercise

A

The blue preventative inhaler which is a beta-2 Adrenergic agonist- Salbutamol

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30
Q

Lung sensitizer

A

Something which increases a persons pre-disposition to develop a lung disease

31
Q

Occupational lung sensitizers

A

People who work in these jobs are more likely to develop a lung disease. Normally due to long term exposure but can be from a single hazardous agent.

32
Q

How to prevent occupational lung diseases

A

With Hypoallergic materials and chemicals, PPE and ventilation

33
Q

Cause of asthma in a farmer

A

Allergens from animals and insects. Will also affect lab workers

34
Q

Cause of asthma in health care workers

A

Latex, antibioitics

35
Q

Cause of asthma metal refining

A

Complex salts of platinum

36
Q

How can the immediate phase of an asthma attack be treated?

A

This can be treated with beta2- adrenoceptor agonists, CysLT-receptor antagonists and theophylline. Cysteinyl LT1 receptor antagonists are a type of leukotriene receptor antagonists.

37
Q

How can you treat the late phase of an asthma attack?

A

Glucocorticoids- the lowest effective dose should be used to avoid adverse effects

38
Q

The aims of pharmacological interventions in asthma

A

Abolish symptoms, restore normal or best possible lung function, reduce the risk of severe attacks, enable normal growth to occur in children and minimise absence from school or treatment.

39
Q

Prevention and asthma

A

Education about managing treatment is important, especially to the family and school. Avoiding coming into contact with triggers is advised.

40
Q

Newly diagnosed asthma treatment

A

Newly diagnosed patients may use a short acting beta-2-agonist (SABA) when they need to relieve symptoms, they may also consider a low dose inhaled Corticosteroid (ICS) to control the frequency of asthma episodes.

41
Q

The initial add on therapy for asthma

A

Adding a long acting beta2-agonists (LABA)

42
Q

Second add on therapy for asthma

A

1) Consider increasing ICS to the medium dose
or
2) Adding a Leukotriene receptor antagonist (LTRA)
If there is no response to LABA consider stopping it

43
Q

Highest step for asthma treatment

A

Refer the patient to specialist care, maybe use an oral corticosteroid

44
Q

Uncontrolled asthma

A

Asthma that has an impact on a persons life and restricts their normal activities

45
Q

Thresholds to define uncontrolled asthma

A

3 or more days a week with symptoms or 3 or more days a week with required use of a SABA or symptomatic relief or 1 or more nights a week with awakening due to asthma.

46
Q

Mechanism of action of bronchodilators

A

They stop membrane bound phospholipids from entering the arachidonic acid metabolism pathway, which produces lots of signalling molecules

47
Q

Mechanism of action of Corticosteroids (bronchodilator)

A

Blocks the enzyme Phospholipase A2 which makes Arachidonic acid. It also blocks the enzyme Cyclooxygenase from producing Prostaglandins. This inhibits the production of pro-inflammatory mediators and the bronchoconstrictor prostaglandin

48
Q

Mechanism of action of Leukotriene antagonists and 5-lipoxygenase inhibitor

A

It blocks the production of Leukotrienes from Arachidonic acid, using the enzyme 5-lipoxygenase, blocking its inflammatory and bronchoconstrictor effect.

49
Q

Classification of asthma treatment

A

Drugs used to treat asthma may be classified as Relievers or Preventers/controllers (Mathylxanthines are both)

50
Q

Asthma treatment- relievers

A

Beta 2 adrenoreceptor agonists, Methylxanthines and Anticholingerics.

51
Q

Asthma treatment- Preventers/controllers

A

Anti-inflammatory agents, corticosteroids and leukotriene receptor antagonists.

52
Q

Metered dose inhalers

A

They use a compressed gas (freon) which propels a fixed dose of a drug. There needs to be coordination between inhalation and activation of the device to ensure the drug passes down the respiratory tract to the target

53
Q

Drug powder inhaler

A

The act of inhalation creates turbulent flow which scatters the drug powder moving down the respiratory tract

54
Q

Nebulisers

A

Can be used at hospitals and at home. They use compressed gas to create a mist of drug particles permitting deep penetration down the respiratory tract

55
Q

Asthma treatment- beta 2 agonists

A

Cause relaxation of airway smooth muscle by increasing cAMP through activation of Gs protein coupled receptors, they act as a physiological antagonist to bronchoconstrictor mediators. BRONCHODILATOR. Can be given via IV in life threatening situations.

56
Q

Short-acting beta2 agonists SABA

A

Salbutamol, terbutaline- commonly used as needed for infrequent episodes and also for acute exacerbation. Maximum effect is 30 min but lasts 3-5 hours.

57
Q

Longer acting beta 2 agonists LABA

A

Salmeterol, formoterol- these drugs are used for regular twice daily administration, they have a slow onset so are not used for an acute episode. Last for 12 hours and are used in addition to corticosteroids. Side effects are minimised with delivery via inhalation, you may get muscle tremors at high doses as well as tachycardia and a risk of cardiac dysrhythmia.

58
Q

Leukotriene receptor antagonists

A

Examples include montelukast, zarfirlukast. These drugs block the Cysteinyl LT1 receptor located on the respiratory mucosa reducing the infiltration of inflammatory cells. This reduces exercise-induced asthma, the response to inhaled allergens and reduces the acute response to aspirin in sensitive patients. It can be administered orally 1-2 times daily and undergo extensive metabolism and biliary excretion. LTRA’s are often used in combination with steroids if a patient does not respond to beta2 agonists.

59
Q

Side effects of Leukotriene receptor antagonists

A

Abdominal pain, thirst and headache

60
Q

Methylxanthines

A

They are phosphodiesterase inhibitors preventing the breakdown of cAMP in cells causing smooth muscle relaxation. Can be administered via IV for treatment of severe acute asthma. The drug may be administered as a 2nd line drug treatment in addition to steroids in patients who respond poorly to beta2 agonists. Narrow therapeutic window. Adverse effects can be significant and include cardiac dysrhythmias, seizures, tremor, positive inotropic/chronotropic actions on the heart and insomnia.

61
Q

Methylxanthines example

A

Theophylline which causes bronchodilation and a reduction in the late phase effects of asthma

62
Q

Examples of antimuscarinic drugs

A

Ipratropium (derived from atropine) and tiotropium

63
Q

Antimuscarinic drugs

A

Are muscarinic (M3) receptor antagonists which cause bronchodilation and reduce mucus secretion. They can be used in addition to beta 2 agonists and steroids but they are mostly used to treat COPD. They increase mucociliary clearance. Administered by inhalation (3-4 times daily) and are highly absorbed via the respiratory epithelium with ~8% bioavailability. If these drugs are taken orally bioavailability drops to 2%. Onset is 30-60 minutes and lasts 4-6 hours. Side effects include dry mouth, gastrointestinal motility disorder(constipation), tachycardia and nausea

64
Q

Examples of inhaled corticosteroids ICS

A

Beclomethasone, budesonide

65
Q

When to use inhaled corticosteroid ICS

A

Not bronchodilators but a preventative form of medication , can take weeks till they achieve their full effect. They are administered via metered dose or dry powder inhalers.

66
Q

Mechanism of action of inhaled corticosteroid ICS

A
  • Reduced transcription and decreased formation of pro-inflammatory cytokines, Th2 cytokines.
  • Reduced activation of eosinophils.
  • Reduced production of IgE.
  • Reduced production of leukotrienes and PAF
  • Inhibition of the cyclooxygenase pathway,
  • Possible upregulation of beta 2 receptor expression.
67
Q

Side effects of oral corticosteroid ICS

A

Prolonged use can lead to suppression of the immune response to infection, Crushing’s syndrome, Osteoporosis, Hyperglycaemia, Muscle wasting and inhibition of growth in children. So, its use is limited to a short time.

68
Q

How oral corticosteroids produce their effect

A

The steroid is bound to albumin and corticosteroid binding-globulin (CBG) in the plasma and is in its inactive form. The steroid then enters the target cell by diffusion across the cell membrane where it binds to its intracellular steroid receptor in the cytosol before migrating to the nucleus where it interacts with DNA, modifying gene transcription and protein synthesis. Last 2-8 hours. Have anti-inflammatory, immunosuppressive and metabolic action.

69
Q

How to treat a severe asthma attack

A

Oxygen (> 60%), Nebulised salbutamol and IV hydrocortisone followed by oral prednisolone. Other drugs may also be considered if the patient does not improve including: Nebulised ipratropium and IV salbutamol or theophylline (or aminophylline).

70
Q

Sensitivity

A

Of all the people who have the disease it the percentage who are picked up on the test (true positives). Quantifies the avoidance of false negatives

71
Q

Specificity

A

Of all those who do not have the disease, % who are correctly undetected by the test (false positives). The true negative rate

72
Q

Positive predictive value (PPV)

A

Of all the people who test positive, its the percentage who actually have the disease

73
Q

The cardinal symptoms of respiratory disease

A
  • Chest pain
  • Wheeze/cough
  • Sputum (colour/amount)
  • Odema
  • Fever/general malaise
  • Haemoptysis
  • Breathlessness
  • Pain

Medicine year 1 semester 2 (61 decks)

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