ALS Lecture 5 - The Nature of Airways Obstructions DONE Flashcards
airway obstruction
blockage of any part of airway
common obstructive airway diseases (3)
asthma, COPD, bronchiectasis
to diagnose airflow obstruction we must use
spirometry
label the spirometry diagram (A)
done
FEV1
forced expiratory capacity in 1 second (amount of air blown out in 1sec)
FVC
forced vital capacity, total amount of air you can blow out
FEV1:FVC ratio should be
> 70%
FEV1:FVC ratio <70% =
diagnosed obstruction
if FEV1 and FVC are symmetrically decreased (ratio is still normal) then =
diagnosed restriction
label the diagrams of mechanisms of airflow obstructions (B)
done
3 mechanisms of airflow obstruction
mucus, constricted smooth muscle, supporting structure damage
increased secretions/mucus in airways obstruction
cough may clear
constricted smooth muscle obstruction
asthma, bronchitis
supporting structure damage obstruction
alveoli collapse in emphysema
bronchial hyper reactivity is a measure of airway
‘twitchiness’
the ‘twitchier’ the airways, the
harder to control
asthmatic airways are very
sensitive
label the flowchart (C)
done
bronchial hyperactivity can be assessed with a
bronchial challenge test
most often used products in bronchial challenge test (2)
methacholine, histamine
chemicals used in bronchial challenge test trigger a bronchospasm in normal individuals but people with _____ ___ ______ have a ____ ____
bronchial hyper responsiveness, lower threshold
bronchial hyper responsiveness is usually found in (2)
asthma, COPD
PC20 =
point where FEV1 drops by 20%
lower PC20 =
worse asthma
look at the diagrams of bronchial challenge testing (D)
done
asthma is usually characterised by (3)
reversible airflow obstruction, chronic airway inflammation, increased airway responsiveness
chronic airway inflammation is mostly
eosinophilic
asthma is commonly divided into 2 types
atopic (extrinsic), non-allergic (intrinsic
atopic/extrinsic asthma is characterised by symptoms that are triggered by an
allergic reaction
non-allergic/intrinsic asthma is triggered by factors not related to
allergens
how many children get asthma?
1/6
how many children grow out of asthma?
50%
variable airflow obstruction
> 50% increase of FEV1 following bronchodilator use
2 types of T lymphocytes in asthma
T helper 1, T helper 2
T helper 1 promote cell immunity by (2)
IgG production, gamma interferon
T helper 2 promote immunity by (3)
enhancing mast cells and eosinophils, IgE synthesis
in asthma there is more __ activity than __
more Th2 than Th1
label the diagram of asthma (E)
done
mechanism of atopic asthma (7 steps)
- APC present antigen to T cell
- Th2 cells produce IL-4, IL-5, IL-13
- interleukins signal B cells to produce IgE
- IgE recognises allergen, binds to mast cells in airway
- with antigen, IgE causes mast cell degranulation
- degranulation of mast cells release inflammatory mediators like histamine, leukotrienes that promote bronchospasm
- cytokines attract eosinophils (more inflammation)
IL-4 in asthma
stimulates IgE production
IL-5 in asthma
activates recruited eosinophils
IL-13 in asthma
activates mucus secretion, promotes IgE
4 main asthma phenotypes
atopic, non-allergic, obesity, persistent airflow limitation
atopic asthma (3)
childhood, eosinophils, identifiable triggers
non-allergic asthma (2)
eosinophilic, neutrophilic?
persistent airflow limitation asthma (2)
fixed obstruction or incompletely reverses
asthma and obesity (2)
prominent respiratory symptoms, little evidence of eosinophils
asthma triggers (6)
pets, dust, mould, pollen, occupational, food
atopy pathophysiology (4 steps)
- first allergen exposure, IgE antibodies bind to mast cells and basophils
- same allergen reenters, attaches to IgE
- mast cells and basophils release histamines
- more smooth muscle contraction and mucus
objective evidence of atopy (3)
total IgE blood, specific IgE to aeroallergens (RAST) blood, skin prick
acute asthma airway changes (5)
smooth muscle contraction, mucus, plasma leak, oedema, sensory nerve activation
chronic asthma airway changes (2)
subepithelial fibrosis, smooth muscle hypertrophy
diagnosis of asthma (3)
variable airway narrowing, bronchodilator reversibility study, peak flow
look at the diagram of asthma flow chart (F)
done
PEFR monitoring (2)
depends on meter, effort
reversibility testing (2)
pre- and post- bronchodilator spirometry
when is reversibility testing considered positive?
FEV1 increases by 200mls
gold standard in asthma diagnosis testing
sputum eosinophilia
treatment for asthma that works in most people (2)
corticosteroids, bronchodilators
if an asthmatic is highly atopic (too much IgE we can use drugs such as (1)
Omalizumab
in asthma we can also use IL-5 blockers such as (1)
Mepoluzimab
label the flow chart of asthma medications (G)
done
reasons patient may not be getting better with asthma treatment (3)
poor compliance, poor technique, misdiagnosis
COPD is characterised by (3)
slow progression, air trapping, airflow limitation
main risk factor for COPD
smoking
label the FEV1 COPD diagram (H)
done
types of COPD (2)
chronic bronchitis, emphysema
obstructive bronchitis
small airway disease
emphysema
breakdown of lung tissue
chronic bronchitis involves (5)
mucus gland hypertrophy, smooth muscle hypertrophy, goblet cell hyperplasia, inflammatory cell infiltrate, excess mucus
in chronic bronchitis inflammatory cell infiltrates are
lymphocytes, neutrophils
emphysema involves (3)
enlargement of airspace distal to terminal bronchiole, fibrosis, wall destruction
2 major types of emphysema
centrilobular, panlobular
centrilobular emphysema (3)
upper lobes, proximal acinus of bronchiole, spared distal alveoli
panlobular emphysema (2)
all lung fields, loss of all portions from bronchiole to alveoli
label the diagram of emphysema types (I)
done
on emphysema scans, lung destruction is more marked in
upper zones
emphysema CT scans show (2)
emphysematous bulla, squashes normal lung
look at scans of emphysema (J)
done
lebel the diagram of the normal airway and airway in emphysema (K)
done
how does emphysema cause airflow obstruction (2 steps)
- alveolar pressure = pleural pressure + elastic recoil
2. reduced pressure and traction in emphysema
label the flow chart of vicious cycle of inactivity and symptoms (L)
done
COPD and inactivity (3 steps)
- airflow obstruction worsened by exacerbations
- air trapping
- hyperinflation, breathlessness
- limited activity = less fitness = less muscle
- increased breathing rate
causes of COPD (6)
smoking, drugs, chronic asthma, occupations, familial, passive smoking
diagnosis of COPD
FEV1:FVC doesn’t improve by 20% with bronchodilator
2 phenotypes in COPD patients
blue bloaters, pink puffers
blue bloater has predominantly
bronchitis
blue bloaters symptoms (5)
sputum, oedematous ankles, cyanosed, overweight, sleep apnoea
blue bloaters go into ______ ____ early on in natural history of disease
ventilatory failure
pink puffer has predominantly
emphysema
pink puffer symptoms (3)
thin, pursed lip breathing, accessory muscle use
look at the Fletcher-Peto plot and label it (M)
done
fill in the table of asthma and COPD (N)
done
label the venn diagram of COPD and asthma (O)
done
label the diagram of flow through the airway (P)
done
resistance =
inversely proportional to radius4
airflow obstruction can cause hypoxia due to (2)
ventilation perfusion mismatch, poorly ventilated alveoli due to bronchial narrowing
pulmonary hypertension is a bad sign in
COPD
pulmonary hypertension is improved by
long term O2 therapy
consequence of pulmonary hypertension
cor pulmonale
cor pulmonale
right sided heart failure, usually due to chronic lung disease
bronchiectasis is a disease in which there is a permanent
enlargement of parts of airways
most common cause of bronchiectasis
cystic fibrosis
symptoms of bronchiectasis (3)
bronchial dilation, recurrent infection, chronic purulent sputum
other causes of bronchiectasis (5)
immunodeficiency, rheumatoid arthritis, colitis, post-measles, idiopathic
bronchiectasis CT scan of lungs
signet ring sign, dilated bronchiole
