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obstructive lung disease Flashcards

1
Q

define asthma

A

Lung problem characterised by chronic inflammation which causes structural changes which leads to reversible airflow limitations

heterogenous condition that affects children and adults

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2
Q

what are risk factors for asthma?

A

dust, mould, tobacco smoke, chemicals, animals, pollen, air pollution, medicines, physical exercise, cold air, stress, viruses

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3
Q

how does chronic asthma impact airways?

A

o Thickening of the basement membrane
o Airway smooth muscle hypertrophy (increase in volume)
o Leukocyte infiltration
o Goblet cell hyperplasia (increase in numbers)
o Mucus hypersecretion  leads to cough in people with asthma

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4
Q

why do people with asthma have a cough?

A

mucus hypersecretion

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5
Q

explain how eosinophilic asthma occurs

A
  • Inhaled allergens cause cross linking of surface bound IgE on mast cells
  • mast cells release several bronchoconstrictor mediators e.g. histamine
  • Dendritic cells present the allergen as an antigen to Th2 cells and activate them
  • Th2 activation leads to release of inflammatory mediators
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6
Q

in eosinophilic asthma, what inflammatory mediators are released and what do they do?

A
  • IL-4, IL-13 –> stimulate B cells to synthesise more IgE
  • IL-5  eosinophil activation
  • IL-9  mast cell proliferation
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7
Q

what are the symptoms of asthma

A

• Cough, breathing difficulty, chest pain, shortness of breath, allergens, feeling tired

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8
Q

define wheezing

A

a continuous, high pitched musical sound coming from the chest

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9
Q

what is an asthma diagnosis based on?

A
  • based on previous + current medical history + lung function tests
  • episodic nature of symptoms e.g. asthma attacks instead of symptoms alone
  • Looking for patients who present with; wheeze, cough, breathlessness, chest tightness
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10
Q

in a clinical assessment of someone with the symptoms of asthma, what things are you looking for to make a diagnosis?

A

o Recurrent episodes of symptoms
o Symptom variability
o Absence of symptoms of alternate diagnosis
o Recorded observation of wheeze
o Personal history of atopy
o Historical record of variable PEF or FEV1

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11
Q

what is PEF?

A

peak expiratory flow

maximal flow rate

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12
Q

describe the normal curve in a flow-volume graph

A

initial exhalation is rapid and fast. Breathe out until they hit the residual volume and can’t breathe out anymore.

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13
Q

what FEV1/FVC ratio does someone with asthma or COPD have?

A

<70%

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14
Q

what spirometry result would increase the probability of asthma?

A

Obstructive spirometry with positive bronchodilator reversibility increases the probability of asthma

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15
Q

what are the 3 main demographics that affect asthma and why?

A

age, gender and height

o Taller you are, the greater your lung capacity
o As you get older, your lung function declines
o Post-puberty, males have larger lung capacities than women
o Ethnicity also has an effect

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16
Q

what is the result of a positive BD reversibility test in adults?

A

Adults: FEV1 improvement ≥12% and ≥200 ml as a positive test

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17
Q

what is the result of a positive BD reversibility test in children?

A

FEV1 improvement ≥12% as a positive test

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18
Q

how many attempts should be done with PEF?

A

3

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19
Q

what is PEF used for?

A

Best used to provide an estimate of variability of airflow from multiple measurements made over at least 2 weeks

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20
Q

what PEF result increases the likelihood of asthma?

A

> 20%

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21
Q

what risk factors cause a greatly increased risk of asthma?

A
  • a history of previous asthma attacks

- persistent asthma symptoms

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22
Q

what risk factors cause moderately increased risk of asthma?

A
  • suboptimal drug regimen
  • comorbid atopic/allergic disease
  • low-income family
  • vitamin d deficiency
23
Q

what risk factors cause slightly increased risk of asthma?

A

younger age
exposure to environmental tobacco smoke
obesity
low parental education

24
Q

what risk factors cause no increased risk of asthma?

A

gender

urban residence

25
Q

what are the goals of pharmacotherapy?

A 
o	No daytime symptoms
o	No night-time awakening due to asthma
o	No need for rescue medication
o	No asthma attacks
o	No limitations on daily activity
o	Normal lung function
o	Minimal drug side effects
26
Q

what is rescue medication and when is it used?

A

inhaled short-acting β2 agonist as short-term reliever therapy for all patients with symptomatic asthma

used when there’s a sudden onset of breathlessness

27
Q

when should rescue medication be reviewed?

A

if its being used more than 3x a week

28
Q

what is first line therapy for asthma?

A

Low-dose Inhaled corticosteroids (ICS) - smokers/ex-smokers may require higher doses

29
Q

what is add on therapy for asthma?

A

Long acting B2 agonists
• Consider combined maintenance and reliever therapy (SMART/MART) in adult patients who have a history of asthma attacks on medium dose ICS or ICS/LABA

30
Q

what are additional controller therapies for asthma?

A

consider increasing ICS to medium dose or adding LTRA (Leukotriene receptor antagonist). If no response to LABA consider stopping LABA

31
Q

what should you do if a patient doesnt respond well to controller therapies for asthma?

A

refer to specialist care

32
Q

what devices can be used for asthma?

A

aerosol
dry powder inhaler
spacers

33
Q

what is an aerosol?

A

metred dose inhaler (MDI). Pressurised container which you press down on to release the drug - Inhale slow and steady

34
Q

how do you inhale with a dry powder inhaler?

A

inhale quick and deep

35
Q

what are corticosteroids?

A

Broad spectrum anti-inflammatory drugs

36
Q

what are the 2 mechanisms of action of corticosteroids?

A
  • 1st mechanism; Translocates from cytoplasm into the nucleus where it can bind GRE (glucocorticoid response element)  increases expression of anti-inflammatory genes
  • 2nd mechanism; corticosteroid can recruit transcriptional machinery which dampens expression of pro-inflammatory chemicals e.g. CXCL8, IL-6, TNF-a. or other genes important in the recruitment of these chemicals
37
Q

how does acetylcholine affect the bronchi?

A

Acetylcholine maintains the bronchomotor tone –> leads to constriction

38
Q

how do beta-2-agonists work?

A

Beta2-adrenergic receptor agonists bind to beta2-adrenergic receptor → A cascade of signal transduction events = airway smooth muscle relaxation
o AC converts ATP to cAMP
o cAMP converts PK to PKA  relaxation

39
Q

what drugs are used in combination therapy?

A

Beta 2 agonists and ICS

40
Q

what effect do LABAs have on ICS?

A

• LABA increase the inflammatory effects of corticosteroids;
o Increase GR translocation
o Increase GRE binding
o Increase anti-inflammatory effect

41
Q

what effect do corticosteroids have on LABA?

A 
• Corticosteroids increase LABA effect;
o	Increase B2-receptor expression
o	Increase B2 receptor coupling
o	Decreases down-regulation of B2 receptors
o	Also prevention of B-agonist tolerance
42
Q

how many people have COPD worldwide?

A

65 million people worldwide

43
Q

define COPD

A

chronic inflammation which causes airflow limitation

44
Q

what history do people with COPD present with?

A

History of persistent respiratory symptoms (e.g. dyspnoea (shortness of breath), cough &/or sputum production)

45
Q

describe how risk factors lead to persistent airflow limitation in COPD?

A

Smoking, pollutants and genetic factors drive chronic inflammation –> small airway disorders –> emphysema –> systemic effects –> persistent airflow limitation and clinical signs

46
Q

name COPD risk factors

A
  • Smoking, passive smoking and smoke from crackers  biggest risk factor
  • Genetic reasons (alpha-1-antitrypsin deficiency)
  • Occupational dust and chemicals
  • Indoor smoke from wood, coal, cow dungs, crop residues used for cooking
  • Frequent lung infections as a child
47
Q

describe how cellular and molecular inflammation occur with COPD?

A
  • Cigarette smoke irritates + activates epithelial cells + macrophages –> inflammatory mediators
  • Macrophages release CXCL8 (chemokine) –> attracts neutrophils
  • Epithelial cells release CXCL9 & CXCL10 (chemokines) attracts TH1 cells and type 1 cytotoxic T (TC1) cells
  • TC1 & neutrophils → Proteases (e.g. metalloproteinase 9 (MMP9) = elastin degradation
  • Neutrophil elastase = mucus hypersecretion.
  • Epithelial cells & macrophages → transforming growth factor-β (TGFβ) = stimulates fibroblast proliferation = fibrosis in the small airways
48
Q

how is steroid response in asthma and COPD?

A

Asthma (good) vs COPD (poor)

49
Q

what are the clinical signs and symptoms of COPD?

A 
• Shortness of breath
• Chronic cough
• Phlegm
• Wheezing
• Chest tightness
• Respiratory infection
- dyspnea that's progressive over time, characteristically worse with exercise, persistentw
50
Q

how do you diagnose COPD?

A
  • Use previous and current medical history and lung function tests
  • Consider COPD & perform spirometry, if any of the below are present + Age > 40 yrs
  • Spirometry is essential for COPD diagnosis
51
Q

how is FEV1/FVC affected in COPD?

A

Decreased

52
Q

what are the pharmacotherapy goals in COPD?

A

o Reduce symptoms
o Reduce frequency & severity of exacerbations
o Improve health status & Quality of Life
o Improve exercise tolerance

53
Q

what are the 2 classes of bronchodilators?

A
  • Long acting muscarinic antagonists (LAMA) – M3 muscarinic receptor antagonists
  • Long acting beta 2 agonists (LABA) – beta 2 receptor agonists
54
Q

how do muscarinic antagonists work?

A

block the binding of acetylcholine (ACh) to M3 muscarinic receptor, thereby inhibiting smooth muscle cell contraction

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