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Asthma and COPD


Asthma in Greek=Panting

Characterized by: Chronic inflammation leading to an increase in responsiveness of tracheo-

bronchial tree to a variety of stimuli causing smooth muscle contraction and narrowing of airway.

-Expiration is more difficult that inspiration

-3% of population have Asthma

-Males have it more than females

-It is common in those who are younger than 30 yrs

Asthma: It is a chronic-episodic in nature with exacerbation it develops at any age


-Exposure to Allergensynthesis of IgE these bind with the mast cells in the airway of the
mucosa and triggers the release of mediators of anaphylaxis

-Antihistamines are not used in treatment because there are other substances that are released
other than histamines.

-Leukotrien Antagonists are used because Leukotriens cause bronchospasm and they are more

-There is cytokine release and IL4, IL5 which are inflammatory mediators. That’s why we use
anti-inflammatory drugs

Mediators of anaphylaxis cause:

-Contraction of airway smooth muscle cells

-Infiltration of inflammatory cells

-Edema, Mucus hyper secretion

For the treatment:

-Contractionwe use B agonists

-Inflammation we use anti-inflammatory mediators (steroids)

Etiology and types:

1-Extrinisic Asthma:

-Immune mechanism plays a role

-There is increase in IgE level

-Positive Family history

2- intrinsic Asthma:

-No immune response

-No IgE

-No family history

Asthma management:

Intrinsic asthma:

A-Management of patient with education of the patient

b-Assess and monitor the severity of the diseases

FEV1 VERY Important investigation

APDFAnti-platelet derived factor

ABG Increase in arterial blood gases

In acute stage: PO2 decrease and PCO2 decrease


Low PO2, LOW CO2Not in resp. failure

Once there is an increase in PCO2 then this is an indication that there is a risk of respiratory

c-Establish management plan for managing the exacerbation

d- Regular follow up

For each patient management must be individualized

Anti-Asthma Agents

1- B2 AgonistSalbutamol, (Long acting), Formetrol (long acting)

2- Corticosteroid Hydrocortisone-Methylprednisolone

3- Leukotrien anatagonist Montelaukast

4- Anticholenergic drug Ipratropium,butamol

5- Methylxanthine Theophylline, aminophylline


Acute Asthma:

Initial assessment which includes, history, physical examination, PEF, FEV1

Most important is FEV1this is an indicator of the severity of the disease

Initial ttt is bronchodilator.

There are 2 ways of giving a drug to a lung:

a- Inhalation (you should train the patient on how to use it)

b- Nebulizer

Nebulizervaporized drug which is dissolved in O2

Advantages of Nebulizer:

1- Hydration: It helps to liquefy the mucous lugs

2- No need to train the patient

3-Drug reaches the site where it is required

4-Systemic effects of the drug are low

So in severe cases it is best to use a nebulizer rather than inhaler.

If the response is good, observe the patient for one hour and if he is stable discharge and send
him home. If the response is not good, this indicates respiratory failure and admit to ICU

Diagnosis of severe Asthma is based on:

Severe asthmatic attack will not respond to B2 agonistB2 receptor becomes insensitive to B2

There will be wheezing for a day and patient will go into respiratory failure

Chronic asthma:

Treatments used: Beta 2 agonists, Cortiosteroids, Leukotrien antagonists

Patients will have: reduced FEV1 and inflammation so they will have a certain degree of
constriction at all times

Beclomethasone and Bedasonide are the inhaled steroids which are used. They are NOT given
alone, they are given along with B2 agonists.

The steroids are give because of chronic inflammation.

If the patient still doesn’t improve, Leukotrien Antagonist are added Montelaukast cannot be
used alone. It is added to B2 agonist or inhaled corticosteroids

-if patient has difficulty in breathing we give him systemic steroids but this has more systemic
Side effects

-Long term therapy is with B2 agonists.

Acute severe Asthma management:

Hallmark signs:


-marked respiratory effort


-Severe limitation in airflow




-Prevention by ttt of acute attack early

-Identify patients

-Intensive care



-Intubate in ICU

NOTE: old text books say that you must not give them more than 28% O2, but now we know
that you can give them as much O2 as they require.

-The patients have LOW PO2 and INCREASE in PCO2 (normally 35-40 yrs of age)

-If the patient is OVER-BREATHING there is a loss of fluid so he gets dehydrated

We must hydrate the patient and Hydration helps hydrate the tracheobronchial tree


1- Corticosteroids (Hydrocortisone given by IV to re-sensitize B2 receptors to B2 agonists. So

now e can use salbutamol

2- We give sulbutamol as nebulizer

3- Antibiotics: Macrolide antibiotic AZITHROMYCIN is the drug of choice because

a- Long half life only one drug per day is needed for 3 days duration and even if you stop the
medication, the blood level will still be high so it will be good for many micro-organisms

b-It is good for respiratory organisms

After the Attack:

No medications are to be given if the patient is free of symptoms. If he has some degree of
bronchoconstriction, give Beta agonists.


Definition + Definition of chronic bronchitis + Definition of emphysema

Risk factors



-Occupation: Silicosis, Pneumoconiosis

-Infection (esp. measles in childhood)

-Familial and genetic factors


-Complete education of patient

-Removal of risk factors

E.g cessations of smoking, and removal of environment factors, annual vaccination

-Vaccination of patient

NOTE: In winter respiratory tract infections make the disease very severe so annual vaccination
must be given against hemophyllus influenza b

-Antibiotics of choice: Ampicillin-Amoxicillin-Augmentinused to treat hemophillus,

pnemococcus, streptococcus

-Bronchodilators: Beta 2 agonists

-If the sputum has lots of eosinophils, add steroids to their treatment

-Broncho-pulmonary drainage: You must drain the patient’s secretions.

NOTE: in these patients it is the hypoxia that drives the respiratory center because their bodies
get used to the increase in CO2 and unlike normal people it is no longer a stimulus for breathing.
So the hypoxia is what drives the respiratory center and If they are given more than 30% O2,
their respiratory center will stop.

From the note books of: Afrah Sait

Bashayer Al-Dossary

Eman Bakhashwain