PBL -2 Case Scenario

Emilia Clarke –25/F gardener-designer and usually smokes 5-10

ciggs a day and marijuana on weekends and 1-2 glasses of beer,
had a diagnosis of Asthma and Allergic Rhinitis, past 3-4 months
she has been periodically coughing and feels tightness in her
chest. Hinderance in her daily life and causes her to wake up
from sleep as well coughing vigourously Past history is normal
with all vaccination up to date , signs of eczema and frequent
respiratory infection were persistent in childhood and diagnosis
of wheezy bronchitis was made also she had rhinorrhea and
some nasal obstruction , after systemic review all organ
systems were found to be normal also on futher assessment it
was seen that her peak flow recording was a bit decresed than
the normal values and Wheezing sounds were heard in both
lung fields during exhalation Also it was seen that her Tonsils
are slightly enlarged and mild swelling on nasal mucosa is found
and also she had a polyp in left nostril leading to more difficulty
in breathing. Her FEV was also a bit increased making her
eligible for Pulmonary Rehab. On complete assessment of her
condition she was given a prescription of Beclomethasone
(corticosteroid) and Salbutamol (Albuterol derivative and a beta
2 agonist) that relived her symptoms and she did not show to
the follow up.
LOBs
Q1:- Describe the anatomy and histology of normal airways (nose,
nasopharynx, oropharynx, trachea, bronchi & bronchioles ?
 Talking about the anatomy respiratory system is made up of the organs included in the
exchange of oxygen and carbon dioxide. And include Nose, Mouth, Throat(pharynx), Voice
Box(larynx), Wind Pipe(trachea), Large Airways(bronchi), Small Airway (Bronchioles). And Lungs
 The nose and nasal cavity form the main external opening for the respiratory system and are
the first section of the body’s airway, The mouth, also known as the oral cavity, is the secondary
external opening for the respiratory tract
 The pharynx, also known as the throat, is a muscular funnel that extends from the posterior end
of the nasal cavity to the superior end of the esophagus and larynx , The pharynx is divided into
3 regions: the nasopharynx, oropharynx, and laryngopharynx , The inhaled air descends into the
laryngopharynx, where it is diverted into the opening of the larynx by the epiglottis.
 The larynx, also known as the voice box, is a short section of the airway that connects the
laryngopharynx and the trachea , which is a 5-inch long tube made of C-shaped hyaline cartilage
rings lined with pseudostratified ciliated columnar epithelium
 At the inferior end of the trachea, the airway splits into left and right branches known as the
primary bronchi. The left and right bronchi run into each lung before branching off into smaller
secondary bronchi. The secondary bronchi carry air into the lobes of the lungs—2 in the left lung
and 3 in the right lung , The secondary bronchi in turn split into many smaller tertiary bronchi
within each lobe. Finally, the millions of tiny terminal bronchioles conduct air to the alveoli of
the lungs also The bronchi and bronchioles also use the mucus and cilia of their epithelial lining
to trap and move dust and other contaminants away from the lungs.
 The lungs are a pair of large, spongy organs found in the thorax lateral to the heart and superior
to the diaphragm. Each lung is surrounded by a pleural membrane that provides the lung with
space to expand as well as a negative pressure space relative to the body’s exterior. The
negative pressure allows the lungs to passively fill with air as they relax. The interior of the lungs
is made up of spongy tissues containing many capillaries and around 30 million tiny sacs known
as alveoli
 Also many accessory muscles are a part of respiration pathway small intercostal muscles that
assist the diaphragm with expanding and compressing the lungs
 Three major cell types are found in this region: ciliated, non-ciliated secretory cells, and
basal cells. Ciliated cells, each lined with 200 to 300 cilia, account for more than half of
all epithelial cells in the conducting airway.

Q2:- Revise the main accessory muscles of inspiration and of

expiration and explain their actions.
 The muscles of respiration are also called the 'breathing pump muscles', they form a complex
arrangement in the form of semi-rigid bellows around the lungs. All muscles that are attached
to the human rib cage have the inherent potential to cause a breathing action.
 The primary inspiratory muscles are the diaphragm and external intercostals. Relaxed normal
expiration is a passive process, happens because of the elastic recoil of the lungs and surface
tension. few muscles that help in forceful expiration and include the internal intercostals,
intercostalis intimi, subcostals and the abdominal muscles. The muscles of inspiration elevate
the ribs and sternum, and the muscles of expiration depress them.
 The accessory inspiratory muscles are the sternocleidomastoid, the scalenus anterior, medius,
and posterior, the pectoralis major and minor, the inferior fibres of serratus anterior and
latissimus dorsi, the serratus posterior superior may help in inspiration also the iliocostalis
cervicis
 The accessory expiratory muscles are the abdominal muscles: rectus abdominis, external
oblique, internal oblique, and transversus abdominis. .

Q3:- Define asthma. Etiology, risk factors, symptoms, types, diagnostic

tests, treatment.
 Asthma :- Asthma is a condition in which your airways narrow and swell and may produce extra
mucus. This can make breathing difficult and trigger coughing, a whistling sound (wheezing)
when you breathe out and shortness of breath. For some people, asthma is a minor nuisance.
For others, it can be a major problem that interferes with daily activities and may lead to a life-
threatening asthma attack. Asthma can't be cured, but its symptoms can be controlled.
 Etiology and Risk Factors :-
1. probably due to a combination of environmental and inherited (genetic) factors.
2. Exposure to various irritants and substances that trigger allergies (allergens) can
trigger signs and symptoms of asthma , Airborne allergens, such as pollen, dust
mites, mold spores, pet dander ect also Various respiratory infections , Physical
Activity , Cold Air and Pollutants can be a cause.
3. Asthma can be triggred by various Beta 2 antagonists/Blockers and NSAIDS (as they
block cyclooxygenase pathway of Arachidonic Acid and indirectly enhancing the
Lipoxygenase one which would lead to increased Leukotriens that would promote
Bronchoconstriction)
4. Strong Emotions and stress can also be a predisposing factor
 RISK FACTORS:-
1. Having a blood relative with asthma, such as a parent or sibling
2. Having another allergic condition, such as atopic dermatitis — which causes red,
itchy skin — or hay fever — which causes a runny nose, congestion and itchy eyes
3. Being overweight , Smoker or even being exposed to Second hand/ Passive smoking
4. Also being exposed to occupational triggers like chemicals ect could be an important
risk factor.
 Symptoms:-
1. Asthma signs and symptoms include :- Dyspnea (shortness of breath) Chest Pain,
Wheezing while exhaling and Nocturnal difficulties , Coughing and wheezing may
be more aggravated by different kinds of viruses.
 Types:-
1. Exercise-induced asthma, which may be worse when the air is cold and dry
 2. Occupational asthma, triggered by workplace irritants such as chemical fumes,
gases or dust
3. Allergy-induced asthma, triggered by airborne substances, such as pollen, mold
spores, cockroach waste, or particles of skin and dried saliva shed by pets (pet
dander)
 Diagnostic Tests:- The two most common lung function tests used to diagnose asthma are
spirometry, exhaled nitric oxide and challenge tests
 Treatment :- There's currently no cure for asthma, but treatment can help control the
symptoms so you're able to live a normal, active life. Inhalers, which are devices that let you
breathe in medicine, are the main treatment. Tablets and other treatments may also be needed
if your asthma is severe. Therapies of Corticosteroids , Leukotriens Modifiers , Beta 2 Agonistics
drugs are helpful.

Q4:- Describe the pathological changes seen in the airways in asthma.

 During an asthma attack the muscle wall contracts and the lining of the airways becomes
swollen and inflamed. These changes cause a narrowing of the airways which is further
aggravated by an increase in secretions from the mucus membrane, which may actually
block the smaller airways. Which would lead to cough, wheeze and have troubled breathing.

Q5:- List the mechanisms that increase airway resistance in asthma

and explain how they relate to the pathological changes of the
airways.
 Bronchospasm, mucus plugging, and edema in the peripheral airways result in increased
airway resistance and obstruction. Air trapping results in lung hyperinflation,
ventilation/perfusion (V/Q) mismatch, and increased dead space(No Gas Exchange)
ventilation
 We can also define it as bronchoconstriction by airway muscle, obstruction of airflow by
intraluminal mucus, and inflammation and remodeling of the airway wall

Q6:- Describe the putative roles of mast cells, eosinophils &

lymphocytes in an attack of allergic asthma, and the main mediators
they produce.
 Many cells and cellular elements play a role, in particular, mast cells, eosinophils, T lymphocytes,
macrophages, neutrophils, and epithelial cells.
 Like IgE molecules were found to have a strong affinity for tissue mast cells and basophils, and
when specific allergens combine with IgE antibody on these target cells, a noncytotoxic release
of a variety of potent chemical mediators was triggered. These observations identified IgE
antibodies as the cause of immediate allergic reactions which would signal bronchoactive
mediator to lead to bronchoconstriction.
 Also Mediators identified with the mast cell included preformed compounds like histamine and
eosinophil chemotactic factor of anaphylaxis (ECF-A) and others, such as slow-reacting
 substance of anaphylaxis (SRS-A), which was synthesized and released as a consequence of mast
cell activation by antigen- and cell-bound IgE antibody also had a potency to trigger Asthma
 Also leukotrienes produced while inflammation are very potent bronchoconstrictive signaling
molecules.
 Eosinophils have always been associated with asthma. Peripheral blood and tissue eosinophilia
are hallmark features of asthma—both allergic and nonallergic asthma. To be more specific MBP
(Major Basic Protein) is the key eosinophilic granule to induce asthma.
 And for lymphocytes Activated Th2 cell-mediated asthma is caused in part by the secretion of
interleukins e.g. IL-4, IL-5 and IL-13.

Q7:- Outline the immunological mechanisms involved in allergic

rhinitis and asthma.
 Allergic diseases like asthma and allergic rhinitis are characterized by a distinct type of
inflammatory response, driven by immunoglobulin E (IgE)-dependent mechanisms. In asthma
and allergic rhinitis, the inflammatory response is mediated by interaction of several immune
cells (monocytes, lymphocytes, and polymorphonuclear cells) and cellular chemical mediators.
 In asthma and allergic rhinitis, sensory nerves are sensitized, leading to clinical manifestations.
Sneezing and coughing are hypersensitivity responses of sensory nerves in allergic rhinitis and
asthma, respectively. Similarly, nasal congestion and discharge in allergic rhinitis are due to
vasodilatation that leads to plasma exudates as well as mucous secretion.
 The immunopathogenesis of allergic rhinitis and asthma involves a complex interplay between
the immune system and parenchymal cells of the lung, including the airway epithelium
 Inhaled allergens are phagocytosed by macrophages and dendritic cells (DCs) presented on
major histocompatibility complex (MHC) class II molecules and initiate the differentiation of Th2
cells and a humoral immune response. Following class switching, Ag-specific B cells secrete
immunoglobulin E which causes degranulation of mast cells.
 Cytokines, such as IL-4, IL-5, and IL-13, are produced by TH2 cells, mast cells, basophils, and type
2 innate lymphoid cells, as well as airway epithelial cells, and they trigger pathological events,
including airway wall remodeling, bronchial hyper responsiveness, and goblet cell metaplasia.

Q8:- Peak flow recording?

 Peak flow measurement is a quick test to measure air flowing out of the lungs. The
measurement is also called the peak expiratory flow rate (PEFR) or the peak expiratory flow
(PEF). Peak flow measurement is mostly done by people who have asthma.
 A peak flow test involves blowing as hard as you can into a small handheld device called a peak
flow meter
 Peak flow scores will vary depending on your age, your height and whether you’re a man or a
woman also it depends whether its day or night. The expected values are higher in younger
people, taller people and men.
 Normal adult peak flow scores range between around 400 and 700 litres per minute
  Flow rate lessens when the airways are blocked. If you notice a significant fall in your peak flow
speed, it may be caused by a flare-up in your lung disease. People with asthma may experience
low peak flow rates.

Q9:- Obstructive and restructive lung disease? Difference between

them
 While both types can cause shortness of breath, obstructive lung diseases (such as asthma and
chronic obstructive pulmonary disorder) cause more difficulty with exhaling air, while restrictive
lung diseases (such as pulmonary fibrosis) can cause problems by restricting a person's ability to
inhale air

Q10:- List the factors (including 2 classes of drugs) which commonly

trigger asthma attacks.
 The 2 major categories of Drugs that come to my my to correlate with Asthma and its
Exacrbation are NSAIDs like Aspirin and Beta 2 Antagonist like Propanolol and Metaprolol.
 As for Aspirin being a NSAID it blocks cyclooxygenase pathway of Arachidonic Acid and indirectly
enhances the Lipoxygenase one which would lead to increased Leukotriens that would promote
Bronchoconstriction extreme trigger.
 For Beta 2 Antagonist we must be clearly aware that one of the prominent function of Beta 2
Adrenergic receptor is Bronchodilation and when a beta antagonistst comes and blocks the Beta
2 receptor it causes heavy Bronchoconstrition which could also be Fatal

Q11:- Describe the clinical features of nasal problems associated with

asthma (rhinitis, polyps).
 Many people who have asthma also have long-term (chronic) problems of the nose and sinuses.
These can include: Rhinitis. This is inflammation or swelling of the tissues in the nose caused by
 an allergen, such as pollen, dust, mould or flakes it is a common comorbidity of asthma that
contributes to asthma severity.
 A patient may get nasal polyps if they have chronic inflammation in their sinuses. People with
respiratory diseases such as asthma, allergic rhinitis and chronic sinusitis often have nasal
polyps. Symptoms of nasal polyps include: Runny or stuffed nose
 Larger growths or groups of nasal polyps can block your nasal passages or lead to breathing
problems, a lost sense of smell and frequent infections.

Q12:- Explain the clinical and physiological measures used to assess

the severity of asthma in adults presenting with an acute attack,
namely: pulse rate, respiratory rate, peak flow measurement and
arterial blood gas values.
 Pulse Rate :- Moderate acute asthma is characterized by an oxygen saturation level of 92% to
95%, a pulse of 100 to 125 beats per minute (in children older than 5 years) or 120 to 140 beats
per minute……… So to summarise it all up usually pulse rate is increased in Asthma.
 Respiratory rate :- When things are working normally, the amount of air we breathe in is about
the same as the amount of air we breathe out. But during an asthma attack, air gets trapped
inside the lungs making it harder and harder to breathe and thus increasing the Respiratory
rate making the patient prone to Tachypnea and Tachycardia , usually in asthmatic patients its
seen to be of 20 to 30 beats per minute.
 Peak Flow Measurement would be decreased as lungs wouldn’t be competent enough to
exhale out the complete amount of air.
 ABG values:- Initially Patients are prone to respiratory Alkalosis and later in severe asthma are
prone to Respiratory Acidosis. Eg;- Initial findings can be hypoxia and hypocarbia due to
hyperventilation. Leading to Alkalosis However, as the symptoms progress and air-
trapping gets worse, an ABG may show respiratory acidosis with hypercarbia

Q14:- Name a beta-2 adrenoceptor agonist, and explain how it

relieves an asthma attack.
 We must be clearly aware that one of the prominent function of Beta 2 Adrenergic receptor is
Bronchodilation which is very very beneficial in asthmatic patients as they are suffering from
bronchoconstriction and require immediate dilation of bronchus for proper ventilation So the
best beta 2 agonist drugs would be Albuterol , Terbutaline , Salmaterol and Formaterol that
would help by Sufficing the bronchodilation via receptor activation.

Q15:- Outline the mechanism by which glucocorticoids treat and

prevent attacks of asthma and allergic rhinitis.
 GLUCOCORTICOIDS are potent inhibitors of inflammatory processes and are widely used in the
treatment of asthma. The anti-inflammatory effects are mediated either by direct binding of the
 glucocorticoid/glucocorticoid receptor complex to glucocorticoid responsive elements in the
promoter region of genes, or by an interaction of this complex with other transcription factors.
 Treatment of asthmatic patients with inhaled glucocorticoids inhibits the bronchial inflammation
and simultaneously improves their lung function
 Inhaled glucocorticoids. IGCs are the main stay of asthma management. They were shown to
very consistently change many of the pathologic inflammatory features of asthma in the lung
airways. They lead to decrease cellular infiltrates including T-lymphocytes, mast cells,
eosinophils, and macrophages.
 To name a few Beclomethasone ,Fluticasone are a very good example

Q16:- Describe the unwanted effects of glucocorticoid treatment of

asthma.
 With an increase in the dose we could encounter ecchymosis, cushingoid features
(redistribution of body fat with truncal obesity, buffalo hump, and moon face) , parchment-like
skin, leg edema, and sleep disturbance.
 Also additionally we can see weight gain and glaucoma, depression, hypertension
 Long term use of glucocorticosteroids could influence the bones as well like it can cause
Osteoporosis in bones via extensive osteoclast function.
 Administration of glucocorticoids can suppress the hypothalamic-pituitary-adrenal (HPA) axis
decreasing the naturally happening corticotropin-releasing hormone (CRH) from the
hypothalamus
 Also it could lead to chronicity of various infections and many cardiovascular (fluid retention,
edema, weight gain, hypertension, and arrhythmias) as well as Dermatological effects (Acne,
mild hirsutism, facial erythema)

Q13:- Describe and explain the abnormalities of arterial blood gases

commonly seen in an asthma attack.
 Initially Patients are prone to respiratory Alkalosis and later in severe asthma are prone to
Respiratory Acidosis. Eg;- Initial findings can be hypoxia and hypocarbia due to hyperventilation.
Leading to Alkalosis However, as the symptoms progress and air-trapping gets worse, an ABG
may show respiratory acidosis with hypercarbia
Q17:- Distinguish between drugs that relieve asthma attacks and
those that prevent them.
 Asthma is a condition that cannot be cured and that’s for sure but we have 2 options that are to
either relieve the symptoms when they happen or prevent the condition from exacerbating
before an attack, So to describe it more we have the Relievers and the Preventers
 So for Relievers they open the lungs by relaxing airway muscles. Often called rescue
medications, they can ease worsening symptoms or stop an asthma attack in progress. They
begin working within minutes and are effective for four to six hours , Such kind of quick relief
medications involve Abuterol and Levalbuterol also for some time Ipratropium , a short acting
bronchodilator can also be prescribed which is a cholinergic antagonist and is usually used in
Emphysema and chronic bronchitis. Sometime some oral corticosteroids may also be very
helpful like Predinisone and Methylpredinisone but due to excessive side effects are avoided
usually.
 And then for Long Term Asthma Control medications which usually prevent severe asthmatic
attacks we have Inhaled Corticosteroids , These anti-inflammatory drugs are the most effective
and commonly used long-term control medications for asthma. They reduce swelling and
tightening in your airways. Examples include Fluticasone , Beclomethasone , Mometasone ect.
 Then we can have Leukotriene Modifiers These medications block the effects of leukotrienes,
immune system chemicals that cause asthma symptoms.. Examples include Montelukast ,
Zafirlukast ect.
 Then we have one more type that is Long acting Beta Agonist (LABAs) and example for it is
Salmaterol.
 We also have one more drug called as Theophylline this bronchodilator is taken daily in a pill
form to treat mild asthma. Theophylline (Theo-24, others) relaxes the airways and decreases the
lungs' response to irritants

Q18:- List the main routes by which drugs are given to asthmatic
patients (inhaled/nebulized, oral, intravenous) and outline
advantages and disadvantages of each.
 Oral drug administration is simple, but, until recently, oral asthma therapy has primarily consisted
of sustained-release theophylline and glucocorticoids. Theophylline has a narrow therapeutic
index, necessitating regular monitoring of serum drug concentrations, and long term oral
glucocorticoid therapy is associated with potentially serious adverse events including osteoporosis
with bone fracture.
 Same rules imply to intravenous drug administration only difference is The intravenous route is
indicated in cases of non-rapid improvement in patients' receiving inhaled treatment. And drugs
given via an IV are usually Corticosteroids
 Inhaled/Nebulized – Advantages and Disadvantages (Explain the same for Q- Revise the use of
inhalers focusing more on advantages)

Q19:- Explain to a patient how to use two different sorts of inhaler.

 There are various kind of inhalers that can be used according to both doctor and patients
preference and Commonly used 3 main kind of inhalers that I would like to describe are METERED
DOSE INHALER , DRY POWDER INHALER and SOFT MIST INHALER and the processes to administer
these vary from one other but can be easily maintained by patient once taught properly.

 METERED DOSE INHALER :- Remove the cap and hold the inhaler in an upright position.
 If your doctor recommends that you use a spacer, then you may do so. A spacer protects
your throat from irritation when you inhale the medication.
 Stand or sit up straight and shake the inhaler.
 Press the inhaler to release the medicine and start breathing slowly. Breathe in slowly for 3-5
seconds.
 Repeat puffs as advised by your doctor. Wait for at least a minute before you take your
second puff.
 DRY POWDER INHALER :-
 Remove the inhaler cap, if there is one.
 Add a dose of medicine as instructed by your doctor.
 Hold the inhaler away from your mouth while you breathe out. It is important to remember to
not breathe out into the inhaler as this can blow some of the powder medicine out of the
inhaler.
 Place the inhaler’s mouthpiece in your mouth. Inhale quickly and through your mouth for 2 or
3 seconds. After you have inhaled the powder, take the inhaler out of your mouth.
 Hold your breath for 10 seconds and let the medicine settle in your lungs. Follow these steps
when you take a second dose
 SOFT MIST INHALER :-
 Remove the inhaler cap, if there is one.
  Add a dose of medicine as instructed by your doctor.
 Hold the inhaler away from your mouth while you breathe out. It is important to remember
to not breathe out into the inhaler as this can blow some of the powder medicine out of the
inhaler.
 Place the inhaler’s mouthpiece in your mouth. Inhale quickly and through your mouth for 2
or 3 seconds. After you have inhaled the powder, take the inhaler out of your mouth.
 Hold your breath for 10 seconds and let the medicine settle in your lungs. Follow these
steps when you take a second dose

Q20:- Outline ways in which adherence with asthma treatment might

be achieved.
 Adherence to the Asthma treatment is very helpful in obtaining a proper treatment , Basically it
means to sticking to the treatment without any negligence.
 There can be various ways where adherence could be promoted and advised and these methods can
be limited to self and also can be related to the surroundings and people around us
 For Example , Using shared-decision making with the patient and extended family as part of the
initial discussion of asthma diagnosis and management and continued at each follow-up visit has
been shown to improve adherence to taking the prescribed medications.
 Also some more ways are:- Educate patients about what to expect. ...Nurture relationships with
patients. ...Team up with prescribers. ...Engage the staff. ...Learn about and use available
technologies. ...Help patients customize their support tools. ...Schedule appointments. ...Synchronize
medications,

Q21:- Demonstrate an ability to perform peak flow monitoring and

spirometry on a patient.
 A peak flow meter is used for the procedure to assess the function of lungs.

 Sit or stand up straight. Whichever you choose, make sure you do it this way each time.
 Make sure the red marker is at the bottom of the meter.
 Take a deep breath, filling your lungs completely.
 Place the mouthpiece in your mouth. Close your lips tightly on the peak flow meter’s
mouthpiece.
 Blast the air out as hard and as fast as possible in a single blow.
 Write down the number by the red marker on the meter.
 Put the red marker back at the bottom of the peak flow meter and repeat these steps three
times.
 The highest of these three readings is your daily peak flow.
 Write down the highest of the three readings on a sheet of paper, calendar or in your asthma
diary.
 Record any symptoms you are having, like wheezing, chest tightness, shortness of breath or
coughing and if you’ve taken your rescue/emergency medication.
  Spirometry is a standard test doctors use to measure how well your lungs are functioning. The
test works by measuring airflow into and out of your lungs. To take a spirometry test, you sit and
breathe into a small machine called a spirometer. This medical device records the amount of air
you breathe in and out as well as the speed of your breath. Doctors use spirometry tests
to diagnose these conditions:
 COPD

 asthma

 restrictive lung disease, such as interstitial pulmonary fibrosis

 other disorders affecting lung function

 Also we have to keep in mind that while performing this test :-

 Wear loose clothing.

 If you smoke, avoid smoking for at least 1 hour before the test.

 If you drink alcohol, avoid consuming it for at least 4 hours before the test.

 Avoid eating or drinking for at least 2 hours before the test.

 Avoid heavy physical effort or exercise for at least 30 minutes before the test.

 Check with a healthcare professional about whether you should avoid are any medications, such
as inhalers, before the test, since they may interfere with the accuracy of the results.

A spirometry test usually takes about 15 minutes and generally happens in your doctor’s office. In some
cases when more in-depth tests are necessary, it may take place at a respiratory laboratory.

Here’s what happens during a spirometry procedure:

1. You’ll sit in a chair in an exam room at your doctor’s office. The doctor or a nurse will place a clip
on your nose to keep both nostrils closed. They’ll also place a cup-like breathing mask around
your mouth.

2. Your doctor or nurse will next instruct you to take a deep breath in, hold your breath for a few
seconds, and then exhale as hard as you can into the breathing mask .
 3. You’ll repeat this test at least three times to make sure that your results are consistent,
especially if there is a lot of variation between your test results. They’ll take the highest value
from three close test readings and use it as your final result. Your entire appointment should last
about 30 to 90 minutes.

If you have evidence of a breathing disorder, your doctor might then give you an inhaled medication
known as a bronchodilator to open up your lungs after the first round of tests. They’ll then ask you to
wait 15 minutes before doing another set of measurements. Afterward, your doctor will compare the
results of the two measurements to see whether the bronchodilator helped increase your airflow.

Q22:- Demonstrate an ability to interpret lung function tests.