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Disease
Dr. Khalid Al-Mobaireek
King Khalid University
Hospital
Obstructive airway Disease:
Obstructive diseases are worse during expiration in the thoracic
cavity
During inspiration, we have negative pleural pressure leading to airway
expansion, and with expiration the opposite happens leading to
narrowing of the airways. Therefore, obstructive diseases are worse on
expiration.
Reversible = Asthma
Irreversible: Bronchiectasis because the membrane is destroyed
therefore the obstruction is permanent. They present with
productive cough with high amount of sputum that are more in the
morning with clubbing (indicating pus formation).
very important to know if its localized or systemic (diffuse)
Localized: very important to know if its localized or
systemic.
Anatomical defect
Airway: Internal, External,
Parenchymal
Examples: foreign body, a lymph node compressing the airway
or vascular problem compressing a segment, or a systemic
disease starting as local.
Diffuse:
Aspiration
Muco-ciliary clearance:
primary ciliary dyskinesia (PCD) is an autosomal recessive disease
where the ciliary function (clearance of mucous) is impaired and
do not have good coordination, with normal mucous secretions.
They are at increased risk of bronchiectasis. 50% have
kartegners syndrome.
CF very thick and sticky secretions,, cilia and cough can not clear it
out its the worse than PCD
Immune deficiency because of recurrent infections.
Post-infectious: Pertussis, TB, adenovirus..
Swallowing difficulties: Neuromuscular disease, GERD, and
congenital defects e.g. palate diseases or congenital defect in
the cartilage, T-E fistula. These can cause aspiration leading to
bilateral bronchiectasis.
Congenital bronchiatasis born with abnormal cartilage.
Bronchiectasis:
CT is the diagnostic method of choice, characteristic
finding is signet ring appearance. Normally each
bronchus is accompanied by a vessel and shouldnt
exceed the vessel diameter. In bronchiectasis, the
diameter of the bronchus is larger than that of the
vessel. Tram line appearance (two airways running in
parallel lines) in cross section.
Definition of Asthma
A chronic inflammatory disorder of the airways
Many cells and cellular elements play a role
Chronic inflammation is associated with airway
hyper-responsiveness to minor stimuli that leads
to recurrent episodes of wheezing,
breathlessness, chest tightness, and coughing
Widespread, variable, and often reversible airflow
limitation recurrent disease.
The commonest chronic disease in children.
Bronchospasm
Edema, Mucus
Hyper-responsiveness
INFLAMMATION!!!
(hallmark)
Asthma Inflammation: Cells and
Mediators
INSP
EXP
Air trapping leads to enlargement of the alveoli, if these ruptured the air
will leak leading to pneumothorax and air under the skin (sub-cutaneous
emphysema).
There will be V/Q mismatch because the blood coming to the lung is not
being oxygenized due to obstruction.
Burden of Asthma
Jeddah 13%
Abha 17%
Factors that Influence Asthma
Development and Expression
Host Factors Environmental Factors
Genetic Indoor allergens are biological
Molds
Cockroaches:
More than
Daytime symptoms None (2 or less / week)
twice / week
Exacerbation
(requirement of systemic None One or more / year 1 in any week
steroids)
REDUCE
LEVEL OF CONTROL TREATMENT OF ACTION
maintain and find lowest
controlled controlling step
consider stepping up to
partly controlled gain control
INCREASE
uncontrolled step up until controlled
REDUCE INCREASE
TREATMENT STEPS
STEP STEP STEP STEP STEP
1 2 3 4 5
Treatment objectives
Achieve and maintain control of symptoms
Maintain normal activity levels, including exercise
Maintain pulmonary function as close to normal levels as
possible
Prevent asthma exacerbations
Avoid adverse effects from asthma medications
Prevent asthma mortality
Non-steroidal anti-
inflammatory
Weak action on Early and
late phases
Slow onset of action
If no response in 6 weeks
change to ICS
Side effects: Irritation
Inhaled Corticosteroids
Effective in most cases
Safe especially at low doses
The anti-inflammatory of choice in
asthma ( drug of choice coz they
are broad spectrum so they target
many cells and mediators)
Laitinen LA
Inhaled Steroids
Side Effects
No systemic side effects with inhaled steroids , candida infection may
occur.
Growth: No significant effect at low to moderate doses.
Bones: not important
HPA axis: No serious clinical effect (high doses)
Alteration of glucose and lipid metabolism: Clinical significant is
unclear (high doses)
Cataract: No increase risk
Skin: Purpura, easily bruising, dermal thinning
Local side effects
Assessment: History
Symptoms
Previous attacks
Prior therapy
Triggers
Physical examination:
Signs of airway obstruction:
Fragmented speech
Unable to tolerate recumbent position prefer
to sit in order to use accessory muscles.
Expiration > 4 seconds
Tachycardia, tachypnea and hypotension
Use of accessory muscles
Pulsus paradoxus > 10 mmHg
Silent hyper=inflated chest
Air leak
Wheezing is a poor sign of obstruction.
Physical examination:
Signs of tissue hypoxia:
Cyanosis
Cardiac arrhythmia and hypotension
(due to increase in thoracic pressure
causing a decrease in venous return
and consequently hypotension).
Restlessness, confusion, drowsiness
and obtundation
Physical examination:
Signs of Respiratory muscles
fatigue:
Increase respiratory rate
Respiratory alterans (alteration
between thoracic and abdominal
muscles during inspiration)
Abdominal paradox (inward movement
of the abdomen during inspiration)
Investigations:
Investigations do not help in acute
asthma, and blood gases are rarely done
except in severe cases
Peak expiratory flow rate ONLY IN FEW CASES
Pulse oximetry
ABG ( its very painful)
Only done in
CXR severe cases
CBC will show leukocytosis because its
an inflammation.
Oxygen
Hypoxemia is common
It worsens airway hyperreactivity
Monitor saturation
Inhaled 2 agonist
Every 20 minutes in the
first hour ( 6-8 puffs )
Assess after each nebulizer
-better than nebulizer
because its more
localized, less side
effects and faster onset
of action.
Steroids
Do not wait for inhaled B2 agonist
response, start immediately on
suspicion with oral steroids because it
takes 3-4 hours to work.
If not responding to the agonist
If severe in the beginning
If on PO prednisolone or high dose
inhaled steroids.
Previous severe attacks
Ipratropium Bromide
Anticholinergic is not routinely used
Anti-cholinergic
For severe cases
Along with 2 agonist
Response to the first hour
wait and observe for 1-2 hours
and if he didnt respond then
admit
Good POOR
Discharge Admit
Partial
Keep for 1-2 hours
Admit
Discharge
Follow up
Give inhaled 2 agonist
Steroids
When to come back?
Turbohaler came in the last osce.