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Y1 Respiratory > Asthma and COPD > Flashcards

Asthma and COPD Flashcards

1
Q

What should be prescribed to asthmatic patients even if they are not experiencing symptoms

A 
Inhaled SABA (for acute relief when needed)
Inhaled corticosteroids
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2
Q

Symptoms of Asthma

A

Wheeze
Cough
dyspnea
Chest tightness

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3
Q

What are symptoms of asthma like

A

Intermittent; worse at night and when it’s cold

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4
Q

Type 1 hypersensitivity Mechanism

A
  1. Sensitization - first encounter of allergen

2. Allergic stage - re-encounter of allergen

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5
Q

Sensitization stage of type 1 hypersensitivity

A
  1. Neutrophils phagocytose and break down the proteins of the pathogen into small peptides and present it on MHC II molecules
  2. Specific CD4+ T cells become activated and differentiated into TH2 and TFH
  3. B cell bind to the antigen and TFH binds to the B cell, which fully activates the B cell
  4. TH2 cell release IL-4 and IL-13 to stimulate B cell to differentiate into plasma cells that produce IgE
  5. B cell proliferates and differentiates into plasma cells that produce IgM and IgE (mainly IgE)
  6. TH2 also release IL-5 to cause eosinophilia
  7. Allergen is cleared, remaining IgE binds to Fc receptors of mast cells and basophils
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6
Q

Allergic stage of type 1 hypersensitivity

A
  1. Re-encounter of allergen
  2. Allergen binds to IgE on mast cells and basophils, causing them to degranulate and release histamine and leukotriene
  3. Histamine and leukotrine both cause inflammatory response
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7
Q

In asthma, histamine causes

A

Bronchoconstriction
Mucous production
Mucosal oedema

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8
Q

In asthma, leukotrine causes

A

Attract eosinophils
Mucous production
Bronchoconstriction
Increase vascular permeability

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9
Q

Type 1 hypersensitivity features

A

eosinophilia

involvement of IgE

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10
Q

Treatment of asthma

A

Inhaled SABA for acute relief when needed
Inhaled corticosteroids as prophylaxis
Inhaled corticosteroid + inhaled LABA (if ICS is ineffective in controlling asthma attacks)
Increase dosage of ICS before adding leukotriene modifier
Omalizumab if still inadequately controlled

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11
Q

Drug treatment for acute asthma attacks

A

Inhaled SABA
Inhaled SABA + SAMA
oral prednisolone for severe attacks
Consider oxygen if hypoxic

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12
Q

Chronic inflammation of asthma attacks can cause

A

Remodeling of the airways

  1. smooth muscle hypertrophy
  2. collagen deposits
  3. thickening of basement membrane
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13
Q

Diagnosis of asthma

A

History - pets / family history of atopy
Spirometry - FEV1/FVC < 75%
Peak flow rate - less than 50-75% than expected
If suspect asthma, prescribe the patient 6months of inhaled corticosteroids. Measure the peak flow rate or spirometry before and after the drug treatment. If there is improvement, confirm diagnosis

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14
Q

Management of asthma

A

Remove pets (allergen)
Weight loss if needed
stop drugs such as NSAID /beta blockers

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15
Q

Triggers of asthma

A 
Allergen
Drugs (NSAID; aspirin /beta blockers) 
Alcohol 
Exercise
Smoking
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16
Q

SABA

A

short acting beta agonists

acts on beta 2 receptors, causing bronchodilation

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17
Q

Examples of SABA

A

salbutamol
Albuterol
Terbutaline

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18
Q

Side effects of SABA

A 
tremor (most common) 
tachycardia 
dry mouth
cardiac dysrhythmia 
hypokalaemia
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19
Q

Uses of SABA

A

Acute relief for asthma attacks and COPD

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20
Q

Examples of inhaled corticosteroid

A

Beclomethasone dipropriate

fluticasone

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21
Q

Example of oral corticosteroid

A

prednisolone

methylprednisolone

22
Q

COPD includes

A

chronic bronchitis

emphysema

23
Q

chronic bronchitis

A

Excess mucus secretion
Mucociliary dysfunction
Bronchoconstriction
smooth muscle hypertrophy

24
Q

Emphysema

A

destruction of alveolar attachments - these kept bronchioles patent
destruction of alveolar epithelium - reduce gas exchange
-alveolar sacs become larger -> reduce SA

25
Q

COPD symptoms

A 
Progressive breathlessness
Persistent cough + sputum 
wheeze
may be hypoxic
frequent chest infections 
breathlessness on exertion
26
Q

COPD mechanism

A
  1. Breathe in noxious gas / pollutants
  2. Activates macrophages which then secretes cytokines to attract neutrophils
  3. Neutrophils degranulate to release proteins
    - elastase
    - caspase
    - matrix metlloproteinase
  4. these proteins cause destruction of the alveolar wall and mucous hypersecretion
27
Q

Exacerbation of COPD

A

Increased sputum production
Increased sputum purulence
dyspnea

28
Q

Which organism most often cause infective COPD exacerbations

A

Haemophilus influenza

29
Q

Diagnosis of COPD

A 
History
-smoking / family history of COPD 
Spirometry
-FEV1/FVC < 0.7 
-Post bronchodilator spirometry will show some improvements but still <0.7
30
Q

What may be the cause of COPD in patients that do not smoke

A

alpha-1 antitrypsin deficiency

31
Q

Drug treatment of COPD

A

Inhaled SABA or SABA + SAMA for relief of symptoms
Inhaled LABA + ICS for prophylaxis in patients that have asthmatic features
Inhaled LABA + LAMA for prophylaxis in patients that do not have asthma
Inhaled LABA + LAMA + ICS if still not controlled well
Oral carbocisteine (mucolytic) = easier to cough up mucus to ensure airway clearance

32
Q

How can COPD lead to cor pulmonale

A
  1. Progressive airflow obstruction can lead to V/Q mismatch
  2. Lack of O2 causes vasoconstriction in pulmonary vessels
  3. This can cause pulmonary hypertension and increased vascular resistance
  4. This means that the left ventricle needs to pump harder to push blood into the lungs
  5. Overtime, it causes left ventricular hypertrophy and eventually cardiac failure
33
Q

Management of COPD

A

Vaccination to prevent infective exacerbation

Smoking cessation

34
Q

Examples of inhaled LABA

A

Salmeterol
olodaterol
formoterol

35
Q

Examples of inhaled LAMA

A

Tiotropium
Aclidinium Bromide
Glycopyrronoium

36
Q

Examples of SAMA

A

Ipratropium

37
Q

LABA

A

Long acting beta agonist

38
Q

LAMA

A

Long acting muscarinic antagonist

39
Q

Mechanism of SABA and LABA

A
  1. Beta 2 agonist binds to Beta 2 receptor on airway muscles
  2. This causes the B2 receptor to attach to G proteins
  3. GDP is exchanged for GTP
  4. Gas + GTP detaches and moves to interact w adenylyl cyclase
  5. adenylyl cyclase converts ATP to cAMP
  6. cAMP phosphorylates PKE
  7. PKE inhibits myosin light chain kinase and stimulates myosin phosphatase to cause bronchodilation
40
Q

Side effect of LABA

A

Tremor
Headache
Palpitations

41
Q

Why is olodaterol only administered once a day

A

bc it is an ultra LABA

42
Q

SABA is administered

A

maximum 4 times a day

43
Q

Why is ipratropium not ideal to use

A

Because it is a non-selective muscarinic receptor antagonist

It can bind to M2 receptors on postganglionic neurone which can stimulate mroe secretion of ACh

44
Q

SAMA binds to

A

M3 receptor

45
Q

SAMA mechanism

A

Prevents bronchoconstriction by preventing ACh from binding to M3 receptors

46
Q

Usage of corticosteroid

A

Anti-inflammatory effects and decrease immune response

47
Q

Why do COPD patients have an increased risk of getting pneumonia when taking ICS

A

COPD predisposes patients to chest infections due to dysfunction of mucociliary escalator (chronic bronchitis). corticosteroids reduces immune response hence patients are more likely to catch pneumonia.

48
Q

Long term consequence of COPD

A

Lack of O2 causes vasocontriction in pulmonary vessels, causing pulmonary hypertension
This makes it harder for right ventricle to pump blood into lungs
Overtime, right ventricle hypertrophy occurs and eventually right heart failure (cor pulmonale)
This can lead to congestion of blood in systemic venous system
leading to pleural transudate

49
Q

Common side effect of inhaled corticosteroids

A

Oral candidiasis - oropharynx is erythematous and has white patches
This is because steroids suppress the immune system

50
Q

Common spirometry finding in asthma attacks

A

FEV1 / FVC lower than 70%
FEV1 lower than normal
FVC unchanged

51
Q

Management of acute exacerbation of COPD

A

Inhaled SABA + SAMA
oral prednisolone or IV hydrocortisone if severe
Antibiotics if infective

Y1 Respiratory (4 decks)

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