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xB13W2 > THE NATURE OF AIRWAY OBSTRUCTION > Flashcards

THE NATURE OF AIRWAY OBSTRUCTION Flashcards

1
Q

what is asthma?

A

a hyperresponsiveness disorder that causes reversible airflow obstruction

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2
Q

what are the signs and symptoms of asthma?

A 
chest tighness
dyspnoea
difficulty breathing
wheezing
cough
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3
Q

what are some triggers of asthma?

A 
air pollution
cigarette smoke
dust
pet dander
cockroaches 
mold
pollen
medications such as aspirin and beta blockers
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4
Q

outline the steps of hypersensitisation of atopic asthma?

A

person is exposed to allergen
allergen is picked up by APC and presented to a T cell
T cell differentiates into Th2
Th2 releases IL4 to produce IgE and IL5 to activate eosinophils
IgE primes mast cells
when re-exposed to the allergen, IgE cross binds mast cells
this causes release of pro inflamamtory mediators to cause bronchoconstriction and eosinophil recruitement

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5
Q

what happens when we get chronic inflamamtion is asthma?

A

scarring
fibrosis
permenant narrowing of the airways

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6
Q

what is extrinsic asthma?

A

a type 1 hypersensitivity reaction triggered by extrinsic allergens
often affects indivisuald with atopic Fhx

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7
Q

what is intrinsic asthma?

A

non-immune

caused by viral infections, stress, exercise and smoking

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8
Q

why can NSAIDs trigger asthma?

A

as NSAIDs inhibit prostaglandin production which causes increased leukotriene production = smooth msucle contraction of airways

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9
Q

how do we diagnose asthma?

A

mainly from symptoms
then initiate treatment and assess response
can do spirometry , reversibility testing, mannitol challege testing, PEFR for 4 weeks
blood gases

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10
Q

what is reversibility testing?

A

spirometry is done without any inhaled therapy before test (have to be off short acting beta agonist for >4 hours and off long acting beta agonists for >15 hours).
You then administer a bronchodilator and repeat spirometry about 15 minutes later to see whether you have a significance improvement (FEV-1 increases by >12% indicates a significant difference)

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11
Q

what is the problem with reversibility testing?

A

asthma is episodic so you may find no response on some days

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12
Q

what is the mannitol challenege testing?

A

spurometry with inhaling increasiny concentrations of mannitol
at the point where FEV1 reduces by 15%, we consider this the concentration required to cause bronchial hyperresponsiveness to mannitol

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13
Q

how do we classify asthma?

A

with frequency of daytime and nighttime symptoms, FEV1 between exacerbation and the degree that asthma interferes with life

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14
Q

what is intermittent asthma?

A

<3 episodes of daytime symptoms in a week
<3 episodes of nightitime symptoms in a month
FEv1 >80% between exacerbations
no limitations

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15
Q

what is mild persistant asthma?

A

> 3 episodes of daytime symptoms in a week (but not every day)
3-4 episodes of nightitime symptoms in a month
FEv1 >80% between exacerbations
minor limitations

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16
Q

what is moderate perisstant asthma?

A

7 episodes of daytime symptoms in a week
1 or more episodes of nightitime symptoms in a week
FEv1 60-80% between exacerbations
moderate limitations

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17
Q

what is severe persistant asthma?

A

multiple episodes of daytime symptoms in a day
episodes of nightitime symptoms every night
FEv1 <60% between exacerbations
extreme limitations limitations

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18
Q

how do we treat intermittent asthma?

A

SABA as needed

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19
Q

how do we treat mild persistant asthma?

A

SABA as needed

daily low dose inhaled corticosteroid

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20
Q

how do we treat moderate persistant asthma?

A

SABA as needed
low dose inhaled corticosteroids daily
LABA

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21
Q

how do we treat severe persistant asthma?

A

SABA as needed
LABA
increased dose of inhaled corticosteroids

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22
Q

what happens if asthma isnt responsive to SABA, LABA or inhaled corticosteroids?

A

use systemic oral corticosteroids

23
Q

why are systemic oral corticosteroids left to the last resort?

A

because of their adverse systemic effects e.g. osteoporosis, cataracts, hyperglycaemia, adrenal supression, fat redistribution

24
Q

how do we characterise a life threatening asthma exacerbation?

A 
PEFR <25%
O2 sats <92
altered mental status
absence of wheezing
normal PaCO2
25
Q

how do we treat a near fatal asthma exacerbation?

A 
oxygen non-rebreater mask
SABA with nebulizer or metered dose inhaler
ipratropium bromide
oral or IV systemic corticosteoids
a
26
Q

at what PEFR can a patient go home?

A

> 70%

27
Q

what are some lifestyle changes to help with asthma?

A

smoking cessation
weight loss in overweight patients
breathing exercises

28
Q

what is COPD?

A

a group of lung conditions that cause breathing difficulties. It includes chronic bronchitis and emphysema

29
Q

what are the symptoms of COPD?

A 
exertional breathlessness
cough
sputum production
wheezing
frequent chest infections
30
Q

what are the signs of COPD?

A

patient sitting up, pursed lip breathing, using accessory muscles
barrel chest
loss of weight
percussion shows hyperresonance

31
Q

outline how COPD can lead to cor pulmonate?

A

chronic hypoxemia causes hypoxic vasoconstriction which can cause pulmonary hypertension over time. This puts strain on the right side of the heart = failure

32
Q

what are the 2 main signs of cor pulmonale?

A

JVP distention
peripheral oedema
hepatomegaly

33
Q

whats the main risk factor for COPD?

A

smokng

34
Q

what are COPD exacerbations?

A

acute worsening of symptoms

35
Q

what are the 2 main types of COPD?

A

chronic bronchitis

emphysema

36
Q

what is chronic bronchitis?

A

inflammation of the airways which increases mucus production, causes smooth muscle hypertrophy, golblet cell hyperplasia, etc

37
Q

what are the symptoms of chronic bronchitis?

A

a continuous cough for >3 months a year for at least 2 consecutive years
phlegmy cough, wheeze, chest discomfort

38
Q

what is emphysema?

A

an inflammatory response leading to excess elastases being produced which causes excessive destruction of alveolar cell walls
this causes a loss in elastin so a loss in elastic recoil = alveoli colapse when we exhale. air becomes trapped in alveoli causing them to puff up, impairing gas exchange

39
Q

in people <45 who seeminly have COPD, what should you always consider?

A

alpha-1 antitrypsin deficiency

40
Q

what is alpha 1 antitrypsin deficiency?

A

an autosomal dominant disorder where alpha-1 antitrypsin isnt exported out of the liver so it cannot inhibit elastase. Elastase therefore accumulates in the lung parenchyma, causing damage
enzyme accumulates in liver so may get liver cirrhosis

41
Q

how do we diagnose COPD?

A

suspicion and relevant exposure
FEV1:FVC <70%
remeasure pulmonary function tests after giving an inhaled bronchodilator - results should be <12% change because its irreversible

42
Q

how do we treat COPD?

A 
smoking cessation
oxygen
broncodilators
corticosteroids
vaccines - dont want infections to trigger COPD excerbations
43
Q

when giving oxygen in COPD, why do we aim for sats of 88-92%?

A

because we want to maintain a level of hypoxaemia as this is stimulating the respiratory drive

44
Q

outline the differences between asthma and COPD?

A

COPD usually presents in >40s whilst asthma in childhood but can be any age
COPD is chronic and continuous whilst asthma varies with triggers
asthma patients will often have FHx of atopy
COPD patients will often have had exposure to cigarette smoke
changes are seen on an xray in COPD but not asthma

45
Q

what drives the inflamamtion in asthma?

A

eosinophils

46
Q

what drives the inflammation in COPD?

A

neutrophils

47
Q

what is bronchiectasis?

A

An obstructive lung disease caused by chronic inflammation leading to bronchi and bronchiole damage and dilation. This inflammation causes mucus plugs to form in the airways and obstruct airflow.

48
Q

what causes bronchiectasis?

A 
CF
severe pneumonia infection
COPD
asthma
whooping cough
TB
fungal infections
49
Q

outline the pathology of bronchiectasis?

A

chronic inflammation causes damage to ciliated epithelial cells and elastin fibres in airways. fibroblasts trying to repair the damage actually deposit more collagen, making the lungs less elastic and more stiff.
The stiff, mucus filled lungs make it diffiuclty for air to flow smoothly

50
Q

what are the symptoms of bronchiectasis?

A 
wheezing
coughing
SOB
foul smelling mucus
digital clubbing
51
Q

how do we treat bronchiectasis?

A

treat the recurrent pneumonias with antiboitics and remove excess mucus with percussion or postural drainage
remove any physical obstructions

52
Q

name some different types of asthma?

A 
allergic asthma
seasonal asthma
occupational asthma
non-allergic asthma
exercise-induced asthma
diffiuclt asthma
severe asthma
brittle asthma
53
Q

what are curshmanns spirals?

A

mucus plugs that block air exchange and prevent inhaled medications from reaching the site of inflamamtion
seen in asthma

54
Q

what are charcot leyden crystals?

A

crystals formed from the breakdown of eosinophils - seen in asthma

xB13W2 (7 decks)

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