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Core Conditions - Respiratory > Acute Asthma > Flashcards

Acute Asthma Flashcards

1
Q

What is asthma?

What are the common presenting features?

A

a chronic lung condition in which there is chronic inflammation of the airways, and hypersensitivity of the airways

symptoms include wheeze, cough, chest tightness and dyspnoea

it is often worse at night

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2
Q

What type of immune response is involved in asthma and how does this show on the lungs?

A

the immune response is CD4 mediated

the lungs will show an eosinophil infiltrate

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3
Q

What is the airflow obstruction like in asthma?

How is this different to in COPD?

A

airflow obstruction is varied over time and reversible

asthma exists where the obstruction is reversible by >15%

COPD exists where the obstruction is reversible by <15%

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4
Q

What are the typical characteristics of patients who fall into the grey area near the boundary between:

airway obstruction being reversible by >15% in asthma and <15% in COPD

and what is the usual diagnosis?

A
  • patients are typically in their 30s and early 40s
  • patients often have a history of smoking
  • as their airway obstruction is reversible, they are usually given a diagnosis of asthma
  • the actual diagnosis is more likely to be early stage COPD
  • this is not too significant as the treatment is very similar
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5
Q
A
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6
Q

What similar treatment is used in both COPD and asthma and why?

A

inhalers

COPD is irreversible, but patients often get symptomatic relief from inhalers

(although the only way to improve prognosis is to stop smoking and give long-term oxygen therapy)

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7
Q

What are the 3 main characteristics of asthma?

A

AIRFLOW LIMITATION:

  • usually reversible, either spontaneously, or with treatment

AIRWAY HYPER-RESPONSIVENESS:

  • occurs to a wide range of stimuli

INFLAMMATION OF THE BRONCHI:

  • with infiltration by eosinophils, mast cells and T cells
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8
Q

What other features are associated with inflammation of the bronchi in asthma?

A
  • infiltration by eosinophils, T cells and mast cells
  • associated plasma exudate
  • oedema
  • smooth muscle hypertrophy
  • mucus plugging
  • epithelial damage
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9
Q

What happens to asthma during viral infections?

A

asthma usually flares up with viral infections

this often causes a loud wheeze

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10
Q

What is the epidemiology of asthma like?

During what decade is prevalence highest and which gender is more likely to be affected?

A
  • increasing in incidence, particularly in Western countries
  • 10-20% of those in 2nd decade of life are affected (this is where prevalence is highest)
  • boys are more likely to be affected in childhood
  • girls are more likely to be affected after puberty
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11
Q

What % of individuals with childhood asthma will relapse in adulthood?

A

50% of those who have childhood asthma, but then “grow out of it” will relapse in adulthood

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12
Q

What are the 2 types of asthma?

A

INTRINSIC:

  • no causatory factor can be found (i.e. cryptogenic)

EXTRINSIC:

  • there is a definite external cause
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13
Q

At what age do people tend to be affected by intrinsic asthma?

What causes it?

A
  • it often starts in middle age
  • sometimes called late onset asthma
  • no trigger can be identified
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14
Q

Who is usually affected by extrinsic asthma?

What is it often accompanied by?

A
  • usually occurs in atopic individuals who have positive skin prick test results
  • causes 90% of childhood cases and 50% of adults with chronic asthma
  • often accompanied by eczema
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15
Q

How do non-atopic individuals tend to develop extrinsic asthma?

A

they develop asthma later in life via sensitisation

to e.g. occupational agents, aspirin,

or as a result of taking B-blockers for hypertension or angina

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16
Q

What is meant by sensitisation?

A

Encountering an allergen once is usually necessary to develop an allergy

sensitisation describes the process through which a person’s body becomes sensitive to a given allergen

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17
Q

What type of hypersensitivity reaction is involved in extrinsic asthma?

A
  • it involves a type I hypersensitivity reaction to inhaled allergens
  • there is also a delayed phase reaction ( type IV hypersensitivity ) which occurs hours to days after exposure
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18
Q

What is meant by atopy?

A

the genetic tendency to develop allergic diseases, such as

  • allergic rhinitis
  • asthma
  • atopic dermatitis (eczema)

it is typically associated with heightened immune responses to common allergens

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19
Q

What is the difference between atopy and allergic disease?

A
  • Atopy is the tendency to produce an exaggerated IgE immune response to otherwise harmless environmental substances
  • allergic disease is defined as the clinical manifestations of the inappropriate IgE immune response
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20
Q

What genes tend to be involved in atopy?

A
  • the ADAM33 gene is associated with airway hyperresponsiveness and airway remodelling
  • the PHF11 gene is associated with increased IgE production
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21
Q

What is meant by the “hygiene hypothesis” that describes the development of atopy?

A

growing up in a “clean” environment in the early years of life can cause atopy

if you grow up in a “dirty” environment, and are exposed to various bacterial, fungal and viral proteins, this will direct the immune system away from recognising inert particles as allergens

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22
Q

How are asthma and allergic rhinitis similar?

What is rhinitis?

A

rhinitis is the inflammation of the mucosal lining of the URT, particularly affecting areas near the nose, thus causing a constant runny nose

the allergens for asthma are very similar to those that cause rhinitis

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23
Q

What is meant by “airway hyperresponsiveness”?

A

the predisposition of the airways of patients to narrow excessively in response to stimuli that would produce little or no effect in healthy individuals

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24
Q

What test is used to assess for airway hyperresponsiveness?

How is a positive diagnosis made?

A

BRONCHIAL PROVOCATION TEST

patient is asked to gradually inhale increasing amounts of methacholine or histamine

this will induce transient airflow limitation in 20% of the population - these exhibit airway hyperresponsiveness

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25
Q

What happens to the immune system when a patient with asthma is exposed to the antigen?

A

exposure to the antigen makes CD4+ T cells differentiate into T helper cells

these are Th2 type opposed to Th1

the Th2 helper cells begin to secrete IL-4 and IL-5

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26
Q

What are the roles of IL-4 and IL-5 that are released from Th2 type helper cells?

A
  • IL-4 will cause B cells to become plasma cells and begin secreting IgE
  • IL-5 will act on eosinophils and mast cells, making them reactive to the new antigen
  • other factors are also released that are chemotaxic for eosinophils
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27
Q

What happens to IgE after it is released by plasma cells?

What cell does it bind to?

A

the IgE binds to mast cells in the mucosa

!!! this initial exposure does NOT cause an allergic reaction !!!

the IgE sits on the mast cell surface, perhaps for years, waiting to come into contact with the antigen again

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28
Q

What happens once IgE on the surface of mast cells is re-exposed to the initial antigen?

A

upon re-exposure to the antigen, the mast cells are activated and will degranulate

this leads to the release of inflammatory mediators

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29
Q

Why do asthmatics have increased inflammatory responses to any antigens?

A

there are increased numbers of mast cells in both the airway secretion and the epithelial lining of the lung

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30
Q

What inflammatory mediators are involved in the initial asthma attack?

When does this occur?

A

initial asthma attack is mainly the result of histamine and prostaglandin

(as well as leukotrienes - particularly LTC4)

these are released by mast cells when they degranulate

this response occurs within minutes of initial exposure to the antigen

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31
Q

What are the actions of histamine in the initial asthma attack?

A

it causes…

  • smooth muscle contraction
  • increased bronchial secretions
  • increased vascular permeability
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32
Q

When does the late phase reaction occur in asthma?

What cell causes this?

A

the late phase reaction occurs several hours after the initial reaction

it is caused by the accumulation of eosinophils at the site

(there are also some neutrophils - but these are more numerous in COPD)

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33
Q

What is the main difference between the late phase reaction and the initial phase?

A
  • the late phase is a more sustained inflammation
  • the initial phase is more bronchoconstriction without as much underlying inflammation
34
Q

What is the difference in treatments for the initial phase and the late phase reaction?

A

Initial phase:

  • the main treatment is bronchodilators (B-adrenergics)
  • the late phase does not respond well to these

Late phase:

  • the main treatment is steroids (& other anti-inflammatories) to prevent the inflammation associated with this reaction
35
Q

In what types of patients is the late phase reaction more likely to occur?

What is an associated risk with this phase occurring?

A

it is more likely to occur in poorly controlled / chronic asthma where there is already a reasonable aggregation of eosinophils in the mucosa

in this phase, there may also be activation of platelets, which can lead to microthrombi in the lumen

36
Q

What are the 3 immediate main effects of bronchoconstriction and inflammation on lung function?

A
  • distal airway hyperinflation and collapse and reduced gaseous transfer to these regions
  • mucus plugging of the bronchi
    • occurs due to an increased number of goblet cells, which secrete more than normal goblet cells
  • bronchial inflammation
37
Q

What can be seen on the histology of mucus plugs from the bronchi of an asthmatic?

A

Curschmann’s spirals

these are bits of epithelium that have been shed

they are spiral-shaped and are found in the sputum of asthmatics

38
Q

What are Charcot-Leyden crystals?

A

crystals that are formed as a result of eosinophil aggregation

they are microscopic crystals composed of eosinophil protein galectin-10

39
Q

What happens to the bronchial basement membrane as a result of bronchoconstriction and inflammation?

Why is this significant?

A

there is thickening of the bronchial basement membrane

this occurs via the process of remodelling

the submucosa becomes thickened, meaning that when the smooth muscle does contract, there is excessive narrowing of the airway in response to contraction

40
Q

What are the effects of bronchoconstriction and inflammation on the lung epithelium?

A
  • epithelium loses many of its columnar ciliated cells
  • these are replaced with over-active mucous secreting cells
  • the mucosa also releases lots of inflammatory proteins
  • it is likely to get damaged in inflammatory processes, and this (along with the excess mucous production) increases risk of infection
41
Q

What are the effects of bronchoconstriction and inflammation on smooth muscle?

A
  • smooth muscle is hypertrophied
  • it undergoes changes which make it more likely to contract, and more likely to stay contracted for longer
42
Q

What are the stages involved in the pathology of an asthma attack?

A
  • excess mucous is produced
  • muscle bands constrict to narrow the airway
  • irritants which triggered the attack are stuck within the mucus
  • tissue within the bronchiole swells
43
Q

What are the effects of cold air and exercise on an asthmatic?

When does the asthma attack occur?

A
  • these both dry out the mucosa of the lung, which makes the lining hyperosmolar
  • this causes mast cells to release histamine & prostaglandins, causing inflammation
  • typically, the asthma attack does NOT occur during exercise, but afterwards
44
Q

How can atmospheric pollution influence asthma?

A

large amounts of dust, cigarette smoke, car fumes and other allergens can sometimes trigger asthma

ozone has also been known to be a trigger

45
Q

How can diet influence asthma?

A

high intake of fruit and vegetables is protective against asthma

this is probably due to the large amounts of anti-oxidants that they contain

genetic variations affecting antioxidant production can also affect severity of disease

46
Q

What is the role of the ADAM33 gene?

A

it is thought to be responsible for the release of factors by eosinophils, including:

  • major basic protein (MBP)
  • eosinophilic cationic protein (ECP)
47
Q

What are the roles of major basic protein (MBP) and eosinophilic cationic protein (ECP) released by eosinophils?

A

these factors can cause remodelling of the epithelium and stimulate growth of fibroblasts

this increases the amount of smooth muscle present

and makes the smooth muscle more likely to contract in response to the release of inflammatory factors

!!! this increases airway hyperresponsiveness !!!

48
Q

What usually stimulates bronchoconstriction?

What is the antagonist to this effect?

A
  • bronchoconstriction occurs in response to direct parasympathetic stimulation
  • antagonism of this effect is produced by freely circulating adrenaline that acts upon B-receptors
49
Q

What type of drug is known to induce asthma attacks in patients and why?

A

BETA BLOCKERS

e.g. atenolol

these can induce asthma attacks as they prevent adrenaline from acting as an antagonist to the process of bronchoconstriction

50
Q

What medication is given to asthmatic patients to lessen the effects of bronchoconstriction?

A

BETA AGONISTS

e.g. salbutamol

these will stimulate the same receptors that adrenaline uses (B2) to cause bronchodilation

51
Q

What are the clinical features of intrinsic asthma?

A
  • wheezing attacks
  • periodic shortness of breath
  • symptoms often worse during the night
  • frequent cough
  • nocturnal cough alone can be a presenting feature
  • attacks precipitated by a very wide range of triggers
52
Q

What is the specific diagnostic test used to diagnose asthma?

A

there is no specific diagnostic test for asthma

the most useful test is the variability shown through twice daily measurements of peak expiratory flow (PEF)

53
Q

What is the most useful test in asthma?

How should it be performed?

A

PEAK EXPIRATORY FLOW (PEF)

  • patients should take 2 readings per day, to show the variability of the disease
  • in patients with suspected asthma, they should take 2 weeks of measurements whilst at work, and 2 weeks whilst at home to prove the cause of the disease
54
Q

How can spirometry be used to show the presence of asthma?

A

there should be demonstration of 15% improvement in FEV1 or PEF following the inhalation of a bronchodilator

55
Q

Why is spirometry not the gold standard test for asthma?

A

in some patients, it may not be possible to show reversibility through spirometry

e.g. those in remission or those with particularly severe chronic asthma

56
Q

How can nitrous oxide sometimes be used as a test for asthma?

A

for an unknown reason, levels of nitrous oxide are raised in the breath of those with asthma

57
Q

What test is usually used in children to diagnose asthma?

How is this performed?

A

EXERCISE TESTS

  • child runs on a treadmill for UP TO 6 minutes - enough to increase the heart rate to at least 160 bpm
  • peak flow is tested before and after
  • test every 15 minutes after running, looking for 15% improvement
  • negative test does not rule out asthma
58
Q

What test is used to identify hyper-responsiveness of the airway?

What type of patients is this good for?

A

histamine or metacholine bronchial provocation test

this indicates hyper-responsiveness which is found in most asthmatics

it is useful for diagnosing patients whose main/only symptom is cough

59
Q

How is the histamine or metacholine bronchial provocation test carried out?

A

the dose of the drug needed to produce a 20% drop in FEV1 is noted

patients with airway hyperresponsiveness require only a very small dose to acheive this

(<11 umol of metacholine)

this is dangerous and is only really done for research purposes

60
Q

What drugs are often trialled for children at first presentation for asthma?

A

corticosteroids

  • children are trialled on 20mg prednisolone for several days
  • or 30mg for up to 2 weeks in adults
  • the initial dose is a one-off
61
Q

How does trialling children (or adults) on corticosteroids assist in their diagnosis of asthma?

What are the other benefits to doing this?

A
  • corticosteroids will reduce their symptoms
  • it will also mean that they respond better to bronchodilators
  • if they respond to treatment, then you know it is asthma and you can start them on a normal management plan
  • this is just a bronchodilator (e.g. salbutamol) to begin with
62
Q

What is it important to do before and after the course of corticosteroids?

What result will suggest asthma in adults?

A
  • lung function must be measured immediately before and after the course of steroids
  • >15% improvement in FEV1 demonstrates the presence of asthma
63
Q

What type of blood / sputum test may be performed in someone with asthma?

A

blood / sputum tests are tested for high numbers of eosinophils

this helps to form the diagnosis, but is not diagnostic on its own

64
Q

Why is chest X-ray performed in patients with suspected asthma?

What will it look like?

A
  • CXR is used to exclude the possibility of pneumothorax, which can be a complication of asthma
  • CXR should be normal
  • in a particularly bad exacerbation, overinflation may be present
65
Q

Why might a skin prick test be performed in suspected asthma?

A

skin prick tests are performed on all newly diagnosed asthmatics to help find a cause

allergen provocation tests are also performed, but only in cases of occupational asthma

66
Q

What is the main advice given to patients for management of extrinsic factors that may trigger their asthma?

A

it is important to try and reduce the risk of a person coming into contact with a provocating factor

dust mite faeces is a major cause, so changing bedding regularly is a good way to manage this risk

67
Q

Which medication is an absolute contraindication in asthma?

A

beta blockers

patients should avoid taking beta blockers in any form

68
Q

Which group of medications are effective for treating asthma which patients are often scared to take?

A

asthma is a chronic inflammatory condition

patients are often scared, but should take anti-inflammatories, such as steroids

69
Q

What is the underlying treatment approach to asthma?

What is the main goal of treatment?

A
  • main goal is to achieve maximum control of symptoms with the fewest medications
  • the goal for optimal control is to have the patient as asymptomatic as possible with as normal PEF as possible
  • once a state of control is reached, an attempt should be made to reduce the doses of medications
70
Q

What do guidelines describe the management of asthma to be like?

A

Stepwise management of asthma

medication can be stepped up or stepped down the ladder based on the severity of the disease and adequacy of the control

71
Q

What generally indicates a need to step up the ladder in management of asthma control?

A

increasing use of a short-acting beta agonist (SABA)

or use >2 days a week for symptom relief

this generally indicates inadequate control and the need to step up treatment

72
Q

When is stepping down the ladder in the stepwise management of asthma recommended?

A

there should be regular assessments of the patient’s asthma

if the disease has been well controlled for at least 3 months, then the aim is to step down the treatment

73
Q

What is STEP 1 in the stepwise management of asthma?

What is PEFR in this step and what is treatment?

A

occasional symptoms - less frequent than daily

PEFR:

  • 100% predicted

Treatments:

  • PRN bronchodilators ( “2 puffs as required” )
  • these will deliver a dose of around 200ug
74
Q

What is STEP 2 in the stepwise approach to asthma management?

What is PEFR and what is treatment?

A

symptoms more than 3x a week

PEFR:

  • equal to or less than 80% predicted

Treatment:

  • low dose inhaled corticosteroid
  • start at 200-400ug but can be increased up to 800ug
  • OR sodium cromoglicate
75
Q

What is STEP 3 in the stepwise management of asthma?

What is PEFR and what is treatment?

A

severe symptoms

PEFR:

  • 50 - 80% predicted

Treatment:

  • add a long-acting B2 agonist
  • e.g. sertide and symbicort are combinations of LABAs and corticosteroids
76
Q

What is STEP 4 in the stepwise management of asthma?

What is PEFR and what is treatment?

A

severe symptoms not controlled by high dose corticosteroids

PEFR:

  • 50 - 80% predicted

Treatments:

  • give a higher dose corticosteroid - up to 2000ug
  • consider leukotriene receptor antagonist - such as montelukast
  • or theophyline
77
Q

What is STEP 5 in the stepwise approach to asthma management?

What is PEFR and what is treatment?

A

severe symptoms that are deteriorating

PEFR:

  • <50% predicted

Treatment:

  • add prednisolone 40mg daily
78
Q

What is STEP 6 in the stepwise approach to asthma management?

What is PEFR and what is treatment?

A

severe symptoms that are deteriorating despite prednisolone

PEFR:

  • <30% predicted

Treatment:

  • hospital admission
79
Q

How is step 1:

mild intermittent and exercise induced asthma

defined in terms of symptoms?

A
  • symptoms 2 times or less per week
  • asymptomatic and normal PEFR between attacks
  • attacks are brief with varying intensity
  • night-time symptoms 2 times or less per month
80
Q
A

Core Conditions - Respiratory (10 decks)

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