obstructive lung disease Flashcards

(54 cards)

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
what are the goals of pharmacotherapy?
``` 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
what is rescue medication and when is it used?
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
when should rescue medication be reviewed?
if its being used more than 3x a week
28
what is first line therapy for asthma?
Low-dose Inhaled corticosteroids (ICS) - smokers/ex-smokers may require higher doses
29
what is add on therapy for asthma?
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
what are additional controller therapies for asthma?
consider increasing ICS to medium dose or adding LTRA (Leukotriene receptor antagonist). If no response to LABA consider stopping LABA
31
what should you do if a patient doesnt respond well to controller therapies for asthma?
refer to specialist care
32
what devices can be used for asthma?
aerosol dry powder inhaler spacers
33
what is an aerosol?
metred dose inhaler (MDI). Pressurised container which you press down on to release the drug - Inhale slow and steady
34
how do you inhale with a dry powder inhaler?
inhale quick and deep
35
what are corticosteroids?
Broad spectrum anti-inflammatory drugs
36
what are the 2 mechanisms of action of corticosteroids?
* 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
how does acetylcholine affect the bronchi?
Acetylcholine maintains the bronchomotor tone --> leads to constriction
38
how do beta-2-agonists work?
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
what drugs are used in combination therapy?
Beta 2 agonists and ICS
40
what effect do LABAs have on ICS?
• LABA increase the inflammatory effects of corticosteroids; o Increase GR translocation o Increase GRE binding o Increase anti-inflammatory effect
41
what effect do corticosteroids have on LABA?
``` • 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
how many people have COPD worldwide?
65 million people worldwide
43
define COPD
chronic inflammation which causes airflow limitation
44
what history do people with COPD present with?
History of persistent respiratory symptoms (e.g. dyspnoea (shortness of breath), cough &/or sputum production)
45
describe how risk factors lead to persistent airflow limitation in COPD?
Smoking, pollutants and genetic factors drive chronic inflammation --> small airway disorders --> emphysema --> systemic effects --> persistent airflow limitation and clinical signs
46
name COPD risk factors
* 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
describe how cellular and molecular inflammation occur with COPD?
* 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
how is steroid response in asthma and COPD?
Asthma (good) vs COPD (poor)
49
what are the clinical signs and symptoms of COPD?
``` • Shortness of breath • Chronic cough • Phlegm • Wheezing • Chest tightness • Respiratory infection - dyspnea that's progressive over time, characteristically worse with exercise, persistentw ```
50
how do you diagnose COPD?
* 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
how is FEV1/FVC affected in COPD?
Decreased
52
what are the pharmacotherapy goals in COPD?
o Reduce symptoms o Reduce frequency & severity of exacerbations o Improve health status & Quality of Life o Improve exercise tolerance
53
what are the 2 classes of bronchodilators?
* Long acting muscarinic antagonists (LAMA) – M3 muscarinic receptor antagonists * Long acting beta 2 agonists (LABA) – beta 2 receptor agonists
54
how do muscarinic antagonists work?
block the binding of acetylcholine (ACh) to M3 muscarinic receptor, thereby inhibiting smooth muscle cell contraction