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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
COPD symptoms
``` Progressive breathlessness Persistent cough + sputum wheeze may be hypoxic frequent chest infections breathlessness on exertion ```
26
COPD mechanism
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
Exacerbation of COPD
Increased sputum production Increased sputum purulence dyspnea
28
Which organism most often cause infective COPD exacerbations
Haemophilus influenza
29
Diagnosis of COPD
``` History -smoking / family history of COPD Spirometry -FEV1/FVC < 0.7 -Post bronchodilator spirometry will show some improvements but still <0.7 ```
30
What may be the cause of COPD in patients that do not smoke
alpha-1 antitrypsin deficiency
31
Drug treatment of COPD
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
How can COPD lead to cor pulmonale
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
Management of COPD
Vaccination to prevent infective exacerbation | Smoking cessation
34
Examples of inhaled LABA
Salmeterol olodaterol formoterol
35
Examples of inhaled LAMA
Tiotropium Aclidinium Bromide Glycopyrronoium
36
Examples of SAMA
Ipratropium
37
LABA
Long acting beta agonist
38
LAMA
Long acting muscarinic antagonist
39
Mechanism of SABA and LABA
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
Side effect of LABA
Tremor Headache Palpitations
41
Why is olodaterol only administered once a day
bc it is an ultra LABA
42
SABA is administered
maximum 4 times a day
43
Why is ipratropium not ideal to use
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
SAMA binds to
M3 receptor
45
SAMA mechanism
Prevents bronchoconstriction by preventing ACh from binding to M3 receptors
46
Usage of corticosteroid
Anti-inflammatory effects and decrease immune response
47
Why do COPD patients have an increased risk of getting pneumonia when taking ICS
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
Long term consequence of COPD
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
Common side effect of inhaled corticosteroids
Oral candidiasis - oropharynx is erythematous and has white patches This is because steroids suppress the immune system
50
Common spirometry finding in asthma attacks
FEV1 / FVC lower than 70% FEV1 lower than normal FVC unchanged
51
Management of acute exacerbation of COPD
Inhaled SABA + SAMA oral prednisolone or IV hydrocortisone if severe Antibiotics if infective

Y1 Respiratory (4 decks)

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