Asthma Flashcards

1
Q

What is the definition of asthma?

A

Chronic inflammatory disorder of airways characterised by bronchial hyperactivity to stimuli which leads to airways obstruction (can be irreversible)

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2
Q

What changes occur in the bronchioles in someone with asthma?

A

SM contraction
SM hypertrophy= thickening of walls
BM membrane thickening
Mucous and exudate in lumen

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3
Q

What are the 3 main causes of airway obstruction in asthma?

A

Inflammatory cell infiltration by TH cells, lymphocytes, eosinophils and mast cells
Mucus hypersecretion and mucus plug formation
SM contraction

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4
Q

What changes occur microscopically in asthma?

A

Desquamated epithelial cells
Eosinophil membranes
Infiltration of inflammatory cells i.e. CD4 lymphocytes

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5
Q

How is the hygiene hypothesis related to asthma?

A

Early life exposure to bacterial endotoxins switches off allergic response
I.e. lack of early exposure can lead to increase risk of developing asthma

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6
Q

What are the main factors leading to the development of asthma?

A

Environmental
-asthma after 12= likely environmental cause

Genetic:

  • Asthma before 12= genetic link
  • FH has important role in asthma
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7
Q

What is the trilogy of conditions referred to as atopy?

A

Allergic rhionitis
Asthma
Eczema

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8
Q

What are the 2 types of triggers for asthma? Give examples of each.

A

Inducers= enhance inflammatory response

  • allergens
  • viral infection
  • occupational exposure
  • animal fur
  • dust
  • mould
  • aerosols

Provokers= activate bronchospasm

  • exercise
  • cold air
  • stress
  • aspirin
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9
Q

What are the classic presenting symptoms? What are the characteristics of these symptoms?

A

Episodic breathlessness (SOB)
Cough
Wheezing
Chest tightness

Variable and intermittent
Diurnal variation= worse at night
Associated with triggers

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10
Q

What are clinical signs to look out for on examination?

A

Wheeze= polyphonic and expiratory

Hyperinflation (associate with longstanding or poorly controlled asthma)
-pronounced pectoral and SCM muscles due to increased use of accessory muscles for breathing

No wheeze and silent chest= life-threatening asthma

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11
Q

How is the wheeze for asthma different from that associated with tracheal/subglottic stenosis?

A

Asthma

  • polyphonic= due to multiple small airways being affected
  • expiratory

Tracheal stenosis:

  • monophonic= single tone due to narrowing of large airway
  • inspiratory
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12
Q

What are the components required for diagnosis of asthma?

A
Day to day peak flow variability 
Asthma symptoms 
Airway hyperresponsiveness 
Reversibility of airway obstruction 
i.e. >15% increase in FEV1 after single dose of SABA or several weeks of steroids
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13
Q

How is a peak flow used to support the diagnosis of asthma?

A

Diurnal variation

-20% variation in PEF for >3/7 days

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14
Q

How can spirometry be used to support a diagnosis of asthma?

A

Can show an obstructive pattern i.e. decrease forced expiratory volume in 1 second (FEV1)

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15
Q

What are the possible differentials for asthma?

A

Upper airway obstruction
-can cause wheeze BUT it is monophonic

COPD
-irreversible

Tracheal tumour

GORD
-micro aspiration of acid= can cause inflammatory response in airways

Interstitial lung diease

HF

Pulmonary hypertension

Chronic thromboembolic disease

Bronchiectasis

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16
Q

What are the non-pharmacological managements of asthma?

A

Smoking cessation
Weight reduction in obesity
Allergen avoidance in sensitised individuals

17
Q

How is asthma managed pharmacologically? What are the different classifications of drugs and their basic mechanism?

A

Step wise approach (most appropriate TX for severity) to gain early control

Selective Beta-2 agonist= RELIEVER (blue inhaler)
Eg= salbutamol + terbutaline
Mech= bronchodilation

Inhaled corticosteroids= PREVENTER (brown inhaler)
Eg= Beclometason + Fluticason + Budesonide
Mech= acts as anti-inflammatory

Long-acting beta-2 agonist= LABARs
Eg= Salmeterol + Foromoterol
Mech= used in combo with steroids on step 3 of asthma management

Leukotrienes receptor antagonist= ADD ON to inhaled steroids
Eg= Montelukast
Mech= target leukotrienes as a prophylaxis for asthma

Xantaine derivatives= ADD ON to relieve acute bronchospasm
Eg= IV aminophyline (specialist use only)
Mech= non-selective phosphodiesterase inhibitors to interfer with bronchial SM

Long acting antimuscarinics= LAMAs
Eg= Tiotropium
Mech= bronchodilators in severe asthma

18
Q

What are the 3 different levels of severity of acute severe asthma?

A

Moderate:

  • increasing symptoms
  • PEFR 50-75% of predicted or best

Severe: (any one of)

  • PEFR 33-50%
  • RR> 25
  • HR>110
  • inability to complete sentence in one breath

Life threatening:

  • PEFR <33%
  • Sats <92%
  • PaO2 <8kPA
  • cyanosis
  • silent chest
  • bradycardia
  • hypotension
  • exhasution
  • confused
  • coma
I.e CHEST
C= cyanosis 
H= hypotension 
E= exhaustion 
S- silent chest 
T- tachy/Brady/arrhythmia
19
Q

Why is it important to look at changes in CO2 levels in someone with severe asthma?

A

Severe asthma= CO2 normally low due to hyperventilation

Rising= life-threatening attack

Normal= patient is tiring i.e. unable to breath enough

20
Q

How is a patient with acute severe asthma managed?

A

Sit upright
High flow oxygen via non-rebreath mask
Salbutamol (5mg) + ipratropium (0.5mg) nebs
Steroids= 100mg IV hydrocortisone or 40mg PO prednisolone
Inhaled ipratropium bromide (SAMA) 500mg every 4-6 hrs via O2 driven neb
MgSO4= 2g IV
Inform ITU as may need to be intubated
Monitor ECG
-due to salbutamol increased HR

21
Q

Once a patient with severe acute asthma is stabilised, what can be done to monitor them?

A

PEFR every 15-30 mins

SpO2 maintained above 92%

ABG (if initial CO2 normal or high)

Oral prednilosone 15mg 1x day for 5 days

Neb salbutamol every 5 hrs

22
Q

What are the signs of asthma on CXR?

A

Hyper expansion with flattened hemi-diaphragms

23
Q

What are the possible adverse effects of using a high dose nebuliser SABA?

A

Tremor
tachycardia due to cross reaction with B1 receptor in heart
Decreased K+ due to action on Na+/K+ ATPase causing increased uptake of K+ by cells

24
Q

What are the possible adverse affects of using inhaled corticosteroids?

A
Oral candidiasis (oral thrush)
-can be due to poor technique and lack of use of spacer 

Osteoporosis

Growth suppression

25
Q

What are the common reasons for poor response to asthma treatment?

A

Non-adherence

  • poor understanding
  • trouble managing polypharmacy
  • stress
  • complicated regiment

Poor technique

Presence of inducers

Wrong diagnosis