Acute Asthma Flashcards
(80 cards)
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
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
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%
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
5
Q
A
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)
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
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
9
Q
What happens to asthma during viral infections?
A
asthma usually flares up with viral infections
this often causes a loud wheeze
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
25
What happens to the immune system when a patient with asthma is exposed to the antigen?
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_**
26
What are the roles of IL-4 and IL-5 that are released from Th2 type helper cells?
* **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
27
What happens to IgE after it is released by plasma cells?
What cell does it bind to?
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
28
What happens once IgE on the surface of mast cells is re-exposed to the initial antigen?
upon re-exposure to the antigen, the mast cells are **activated** and will **_degranulate_**
this leads to the release of **inflammatory mediators**
29
Why do asthmatics have increased inflammatory responses to any antigens?
there are **_increased numbers of mast cells_** in both the **airway secretion** and the **epithelial lining** of the lung
30
What inflammatory mediators are involved in the initial asthma attack?
When does this occur?
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
31
What are the actions of histamine in the initial asthma attack?
it causes...
* **smooth muscle contraction**
* increased **bronchial secretions**
* increased **vascular permeability**
32
When does the late phase reaction occur in asthma?
What cell causes this?
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)
33
What is the main difference between the late phase reaction and the initial phase?
* the **late phase** is a more **_sustained inflammation_**
* the **initial phase** is more **_bronchoconstriction_** without as much underlying inflammation
34
What is the difference in treatments for the initial phase and the late phase reaction?
**_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
In what types of patients is the late phase reaction more likely to occur?
What is an associated risk with this phase occurring?
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
What are the 3 immediate main effects of bronchoconstriction and inflammation on lung function?
* **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
What can be seen on the histology of mucus plugs from the bronchi of an asthmatic?
**_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
What are Charcot-Leyden crystals?
crystals that are formed as a result of **eosinophil aggregation**
they are microscopic crystals composed of **eosinophil protein _galectin-10_**
39
What happens to the bronchial basement membrane as a result of bronchoconstriction and inflammation?
Why is this significant?
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
What are the effects of bronchoconstriction and inflammation on the lung epithelium?
* 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
What are the effects of bronchoconstriction and inflammation on smooth muscle?
* smooth muscle is **_hypertrophied_**
* it undergoes changes which make it **more likely to contract**, and more likely to **stay contracted for longer**
42
What are the stages involved in the pathology of an asthma attack?
* 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
What are the effects of cold air and exercise on an asthmatic?
When does the asthma attack occur?
* 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
How can atmospheric pollution influence asthma?
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
How can diet influence asthma?
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
What is the role of the ADAM33 gene?
it is thought to be responsible for the **_release of factors by eosinophils_**, including:
* **major basic protein** (MBP)
* **eosinophilic cationic protein** (ECP)
47
What are the roles of major basic protein (MBP) and eosinophilic cationic protein (ECP) released by eosinophils?
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
What usually stimulates bronchoconstriction?
What is the antagonist to this effect?
* bronchoconstriction occurs in response to **direct _parasympathetic_ stimulation**
* antagonism of this effect is produced by **freely circulating _adrenaline_** that acts upon **B-receptors**
49
What type of drug is known to induce asthma attacks in patients and why?
**_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
What medication is given to asthmatic patients to lessen the effects of bronchoconstriction?
**_BETA AGONISTS_**
e.g. salbutamol
these will stimulate the same receptors that adrenaline uses (B2) to cause **bronchodilation**
51
What are the clinical features of intrinsic asthma?
* 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
What is the specific diagnostic test used to diagnose asthma?
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
What is the most useful test in asthma?
How should it be performed?
**_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
How can spirometry be used to show the presence of asthma?
there should be demonstration of **_15% improvement_** in **FEV1** or **PEF** following the **_inhalation of a bronchodilator_**
55
Why is spirometry not the gold standard test for asthma?
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
How can nitrous oxide sometimes be used as a test for asthma?
for an unknown reason, levels of nitrous oxide are raised in the breath of those with asthma
57
What test is usually used in children to diagnose asthma?
How is this performed?
**_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
What test is used to identify hyper-responsiveness of the airway?
What type of patients is this good for?
**_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
How is the histamine or metacholine bronchial provocation test carried out?
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
What drugs are often trialled for children at first presentation for asthma?
**_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
How does trialling children (or adults) on corticosteroids assist in their diagnosis of asthma?
What are the other benefits to doing this?
* 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
What is it important to do before and after the course of corticosteroids?
What result will suggest asthma in adults?
* **_lung function_** must be measured **immediately before and after** the course of steroids
* **_\>15% improvement in FEV1_** demonstrates the presence of asthma
63
What type of blood / sputum test may be performed in someone with asthma?
blood / sputum tests are tested for **_high numbers of eosinophils_**
this helps to form the diagnosis, but is not diagnostic on its own
64
Why is chest X-ray performed in patients with suspected asthma?
What will it look like?
* 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
Why might a skin prick test be performed in suspected asthma?
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
What is the main advice given to patients for management of extrinsic factors that may trigger their asthma?
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
Which medication is an absolute contraindication in asthma?
**_beta blockers_**
patients should avoid taking beta blockers in any form
68
Which group of medications are effective for treating asthma which patients are often scared to take?
asthma is a **chronic _inflammatory_ condition**
patients are often scared, but should take **_anti-inflammatories_**, such as **steroids**
69
What is the underlying treatment approach to asthma?
What is the main goal of treatment?
* 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
What do guidelines describe the management of asthma to be like?
**_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
What generally indicates a need to step up the ladder in management of asthma control?
**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
When is stepping down the ladder in the stepwise management of asthma recommended?
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
What is STEP 1 in the stepwise management of asthma?
What is PEFR in this step and what is treatment?
**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
What is STEP 2 in the stepwise approach to asthma management?
What is PEFR and what is treatment?
**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
What is STEP 3 in the stepwise management of asthma?
What is PEFR and what is treatment?
**_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
What is STEP 4 in the stepwise management of asthma?
What is PEFR and what is treatment?
**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
What is STEP 5 in the stepwise approach to asthma management?
What is PEFR and what is treatment?
**severe symptoms that are _deteriorating_**
**PEFR:**
* \<50% predicted
**Treatment:**
* add **_prednisolone 40mg daily_**
78
What is STEP 6 in the stepwise approach to asthma management?
What is PEFR and what is treatment?
**severe symptoms that are _deteriorating despite prednisolone_**
**PEFR:**
* \<30% predicted
**Treatment:**
* hospital admission
79
How is step 1:
**mild intermittent and exercise induced asthma**
defined in terms of symptoms?
* 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
