PHCP LEC WEEK 1: produces rhinorrhea, itching, sneezing,

and nasal obstruction.

THE RESPIRATORY SYSTEM
- A late-phase reaction may occur 4 to 8
hours after initial allergen exposure due
to cytokine release from mast cells and
thymus-derived helper lymphocytes.
- This inflammatory response causes
persistent chronic symptoms, including
nasal congestion.

ALLERGIC RHINITIS
- It involves inflammation of nasal mucous
membranes in sensitized individuals
when inhaled allergenic particles contact
mucous membranes and elicit a response
mediated by immunoglobulin E (IgE).
- Two types:
Manifestations
 Seasonal
 Clear rhinorrhea
 Persistent/perineal
 Sneezing
Pathophysiology  Nasal congestion
- Airborne allergens enter the nose during  Postnasal drip
inhalation and are processed by  Allergic conjunctivitis
lymphocytes, which produce antigen-  Pruritic eyes, ears, or nose
specific IgE, sensitizing genetically  Dark circles under the eyes (allergic
predisposed hosts to those agents. shiners) A transverse nasal crease caused
- On nasal re-exposure, IgE bound to mast by repeated rubbing of the nose
cells interacts with airborne allergens,  Adenoidal breathing
triggering release of inflammatory  Edematous nasal turbinates coated
mediators. with clear secretions
- An immediate reaction occurs within  Tearing
seconds to minutes, resulting in rapid  Periorbital swelling
release of preformed and newly
generated mediators from the arachidonic Diagnosis
acid cascade.  Medical history
- Mediators of immediate hypersensitivity  Careful description of symptoms
include histamine, leukotrienes,  Environmental factors and
prostaglandin, tryptase, and kinins. exposures Results of
- These mediators cause vasodilation, previous therapy
increased vascular permeability, and
production of nasal secretions. Histamine
  Use of medications - Previous
nasal injury or surgery – Family
history
 Microscopic examination of nasal
scrapings typically reveals
numerous eosinophils (WBC)
 Peripheral blood eosinophil count
may be elevated, but it is
nonspecific and has limited
usefulness.
 Allergy testing
 Determines whether rhinitis is
Non-pharmacologic Interventions
caused by immune response to
allergens.
 Immediate-type hypersensitivity
skin tests are commonly used
 Percutaneous testing is safer and
more generally accepted than
intradermal testing, which is
usually reserved for patients
requiring confirmation.
 The radioallergosorbent test
(RAST) can detect IgE antibodies in
the blood that are specific for a
given antigen, but it is less
sensitive than percutaneous tests.
Intervention
 Goals
 Minimize or prevent symptoms,
prevent long-term complications,
minimize or avoid medication side
effects, provide economical
therapy, and maintain normal
lifestyle.
Pharmacologic Interventions
 The most effective first-line drug
treatments are:
 Nasal corticosteroids with or
without oral or
nasal antihistamines
 Oral antihistamines plus oral
decongestants (eg,
a sympathomimetic such as
pseudoephedrine)
 Less effective alternatives include
 nasal mast cell stabilizers (eg,
cromolyn) given 3 or 4 times
a day,
 nasal H1 blocker azelastine 1 to 2
puffs twice a day, and
 nasal ipratropium 0.03% 2 puffs
every 4 to 6 hours, which relieves
rhinorrhea.
 Avoiding offending allergens
 Important but difficult to
accomplish, especially
for perennial allergens.
 Mold growth can be reduced by
keeping household humidity less
than 50% and removing obvious
growth with bleach or disinfectant.
 Removing pets from the home, if
feasible.
 Reducing exposure to dust mites
 Encasing bedding with
impermeable covers and washing
bed linens in hot water has little
benefit, except perhaps in
children.
 Prevent poor air quality in homes
 Avoiding wall-to-wall carpeting,
 Using moisture control to prevent
mold accumulation, and
 Controlling sources of pollution
such as cigarette smoke.
 On seasonal allergic rhinitis
 Keep windows closed and
minimize time spent outdoors
during pollen seasons.
 Filter masks can be worn while
gardening or mowing the lawn.
ASTHMA
- A chronic allergic disorder characterized
by episodes of severe breathing difficulty,
coughing, and wheezing using the air
passage to narrow & causes shortness of
breath.
- These episodes are usually reversible,
either spontaneous or with treatment.
- The inflammation is due to bronchia
hyper responsiveness to a variety of
stimuli
Pathophysiology
 Early phase allergic reaction
 Activation of IgE antibodies
 Rapid activation of airway mast cells
and macrophages
 Release of histamines and eicosanoids
 Induction of airway
smooth muscle constriction
 Mucous secretion
 Exudation of plasma in the
airway
 Plasma protein leakage
 Induces a thickened,
engorged, edematous
airway wall and
narrowing of the air
lumen.
 Late phase inflammatory reaction:
 Occurs 6-9 hours after allergen
provocation
 Involves the activation of eosinophils, T
lymphocytes, basophils, neutrophils and
macrophage
 EOSINOPHILS
 Migrates to the airways and release
inflammatory mediators (leukotrienes and
granule proteins) cytotoxic mediators and
cytokines
 T-lymphocytes
 Release cytokines from type 2 T-helper
cells that mediate allergic inflammation.(
IL-4, IL-5 and IL-13)
 Type 1- T-helper produces IL-2 and
Interferon gama that are essential for
cellular defense mechanism
 Mast Cell degranulation
 Release of histamine, eosinophil and
neutrophil chemotactic factors,
leukotriene C4, D4 and E4, prostaglandin
and platelet activating factors.
 Histamine is capable of inducing smooth
muscle constriction and bronchospasm
and may play a role in mucosal edema and
mucus secretion.
 Alveolar macrophages
 release a number of inflammatory
mediators including PAF and leukotrienes
B4, C4 and D4
 5 lipoxygenase pathway of arachidonic
acid metabolism
 Produce Cysteinyl leukotrienes C4, D4 and
E4
 Released during the inflammatory
process in the lungs and causes
bronchospasm, mucus secretion and
airway edema
 Bronchial epithelial cells
 Releases eicosanoids, peptidases, matrix
proteins, cytokines and nitric oxide
 Epithelial shedding results in heightened
airway responsiveness and may impair
mucocilliary transport
 Bronchial glands are increased in size,
goblet cells are increased in size and
number.
 Expectorated mucus from patients with
asthma are highly viscous.
CLINICAL PRESENTATION:
CHRONIC ASTHMA
 Characterized by episodic dyspnea with
wheezing
 Coughing particularly at night
 These often occurs during exercise
 Other signs:
 Expiratory wheezing on
auscultation
 Dry hacking cough
 Signs of atopy (Allergic rhinitis
or eczema)
Diagnosis: Chronic Asthma
 History of recurrent episodes of
coughing, wheezing and chest tightness.
SOB and confirmatory spirometry
 Family history
 Exercise or cold air precipitating dyspnea
may suggest asthma
 Spirometry demonstrates obstruction.
Forced expiratory volume in one second
with reversibility after bronchodilators (at
least 12 % improvement)
 If baseline spirometry is normal,
challenge testing with exercise,
histamine, or metacholine can be used
Allergens:
 Allergic reactions to some foods, such as
peanuts or shellfish
 Respiratory infections, such as the
common cold
 Physical activity (exercise-induced
asthma)
 Air pollutants and irritants, such as smoke
 Certain medications, including beta
blockers, aspirin, ibuprofen (Advil, Motrin,
others) and naproxen (Aleve)
 Strong emotions and stress
 Preservatives added to some types of
foods and beverages Gastroesophageal
reflux disease (GERD), a condition in
which stomach acids back up into your
throat
 Airborne allergens, such as pollen,
animal dander, mold, cockroaches
and dust mites
Factors that Increase Chances of Developing
Asthma
 Having a blood relative with asthma
Having another allergic condition, such as
atopic dermatitis or allergic rhinitis (hay
fever)
 Being overweight
 Being a smoker
 Exposure to secondhand smoke Having a
mother who smoked while pregnant
 Exposure to exhaust fumes or other types
of pollution
 Exposure to occupational triggers, such as
chemicals used in farming, hairdressing
and manufacturing
 Exposure to allergens, exposure to certain
germs or parasites, and having some types
of bacterial or viral infection
EXERCISE-INDUCED BRONCHOSPASM
- During vigorous exercise, pulmonary
functions (FEV1) in patients with asthma
increase during the first few minutes but
then begin to decrease after 6 to 8
minutes
- EIB is defined as a drop in FEV1 of greater
than 15% of. baseline (preexercise value).
 EIB is provoked more easily in cold,
dry air,
  and warm, humid air can blunt or
block it.
 Studies suggest a role of mastcell
degranulation
 There is increased plasma
histamine, leukotrienes,
prostglandins during EIB
 Notably, a refractory period of 3
hours happens after exercise.
 Wherein repeat exercise of the
same intensity will not produce
50% of the initial drop. 1. BETA2-ADRENERGIC AGONIST AGENTS
 Exercise-induced asthma - Beta, agonists relieve reversible
 which may be worse when the air bronchospasm by relaxing the smooth
is cold and dry muscles of the bronchi. Act as
 Occupational asthma bronchodilators and are used to treat
 triggered by workplace irritants bronchospasm in acute asthmatic episodes
such as chemical fumes, gases or and to prevent bronchospasm associated with
dust exercise-induced asthma or nocturnal
 Allergy-induced asthma asthma.
 triggered by particular allergens, Medication MOA Adverse Effects
such as pet dander, cockroaches or Albuterol Beta-2 - Tremor
pollen sulfate receptor - Nervousness
 FVC: Forced vital capacity is the volume of (Proventil HFA, agonist with in 2-6 years old
air that can forcibly be blown out after full Ventolin HFA, some beta-1 children
inspiration, measured in liters. ProAir HFA) activity - Insomnia in 6-
12 years old
 FVC is the most basic maneuver in
children
spirometry tests. receiving 4-12
 FEV1: Force Expiratory Volume per mg BID
second the volume of air that can forcibly Pirbuterol Beta-2 - Nervousness
be blown out in one second, after full (Maxair receptor - Restlessnes
inspiration. Autohaler) agonist with - Serum glucose
 Average values for FEV1 in healthy - Attractive some beta-1 increased
choice in activity - Serum
people depend mainly on sex
the potassium
and age, according to the diagram treatment decreased
at left. of acute - Trembling
 Values of between 80% and 120% symptoms
of the average value are in younger
considered normal. children
 FEV /FVC (FEV1%): the ratio of FEV, to Levalbuterol Beta-2 - tachycardia
(Xopenex receptor -hyperglycemia
FVC.
- Effective in agonist with – hypokalemia
 In healthy adults this should be smaller some beta-1 - Rhinitis
approximately 70-85% (declining doses and activity - Headache
with age) is reported
to have
 fewer permeability healing
adverse and suppressing
effects polymorphonucl
ear leukocyte
2. ANTICHOLINERGIC AGENT activity.
- Anticholinergic agents such as ipratropium Methyl- Decreases -Insomnia
may be added to beta, -agonist therapy for prednisolone inflammation by -Vertigo
acute exacerbations. (Solu reversing -Acne
Medrol, increased -Osteoporosis
Medication MOA Adverse Effects
Medrol) capillary -Delayed wound
Ipratropium - Anticholinergic - Bronchitis
permeability healing
(Atrovent) bronchodilator - Dyrsnes
and suppressing -Myopathy
- Inhibits - Cough
polymorphonucl
secretions from - Nausea
ear leukocyte
serous and
activity.
sexomucous
Prednisolone Decreases -Insomnia
glands lining the
(Pediapred, inflammation by -Vertigo
nasal mucosa.
Prelone, reversing -Acne
3. ANTICHOLINERGIC AGENT COMBINATIONS Orapred) increased -Osteoporosis
- Is used capillary -Delayed wound
(WITH BETA2-ADRENERGIC AGONIST)
for both permeability healing
Medication MOA Adverse Effects acute and suppressing -Myopathy
Ipratropium and Albuterol: - Bronchitis and polymorphonucl
albuterol Beta-2 - URT infection chronic ear leukocyte
(Combivent, adrenergic - Headache asthma activity
DuoNeb) bronchodilator -
- with little Nasopharyngitis 5. LONG-ACTING BETA2 AGONISTS
effect Ipratropium: - Long-acting bronchodilators are used for the
on cardiac Inhibits
preventive treatment of nocturnal asthma or
muscle secretions
contractility from serous exercise-induced asthmatic symptoms.
and Medication MOA Adverse Effects
seromucous Formoterol Long-acting -Viral infection
glands lining (Foradil, selective beta-2 -Bronchitis
the nasal Performist) agonist: Bronchial -Chest
mucosa. smooth muscle infection
relaxation -Dyspnea
4. CORTICOSTEROID, ORAL -Chest pain
- Frequent and repetitive use of beta, agonists Salmeterol Long-acting beta- -Headache
has been associated with beta receptor (Serevent) 2 agonist: By -Nasal
relaxing the congestion
subsensitivity and down-regulation; these
smooth muscles -Bronchitis
processes are reversed with corticosteroids.
of bronchioles -Influenza
- corticosteroids are administered to replace Arformoterol Long-acting -Back pain
deficient endogenous hormones (Brovana) beta2-agonist : -Chest pain
Medication MOA Adverse Effects Increased -Diarrhea
Prednisone It decreases -Insomnia intracellular cyclic -Dyspnea
(Deltasone, inflammation by -Vertigo AMP (adenosine
Orasone) reversing -Acne monophosphate)
increased -Osteoporosis levels cause
capillary -Delayed wound relaxation of
bronchial smooth
 muscle and Salmeterol/ Salmeterol: -Palpitations
inhibition of the fluticasone Long-acting beta -Dizziness
release of inhaled 2 agonist: By -headache
mediators of (Advair relaxing the -Hypokalemia
immediate smooth muscles -Candidiasis
hypersensitivity of bronchioles (oral)
from cells,
especially from Fluticasone:
mast cells. potent anti-
inflammatory
6. BETA2-AGONIST/CORTICOSTEROID activity: inhibits
COMBINATIONS multiple cell
- These combinations may decrease asthma types and
exacerbations when inhaled short-acting mediator
production or
- beta2 agonists and corticosteroids have
secretion
failed. involved in the
Medication MOA Adverse asthmatic
Effects response
Budesonide/ Budesonide: -Headache
formoterol inhibits multiple - 7. 5-LIPOXYGENASE INHIBITOR
(Symbicort) types of Nasopharyngiti - 5-lipoxygenase inhibitors act on leukotrienes
inflammatory s Medication MOA Adverse Effects
cells and -URI Zileuton - inhibits -Headache
decreasing the -Pain in throat leukotriene -Dyspepsia
production of -Stomach ache formation -generalized
cytokines and -Oral - Inhibitor of 5- pain
other mediators candidiasis lipoxygenase -nausea
involved in the
asthmatic
responses 8. METHYLXANTHINES
- These agents are used for long-term control
and prevention of symptoms, especially
Formoterol: nocturnal symptoms.
relieves Medication MOA Adverse Effects
bronchospasm by Theophylline directly relaxes -Tachycardia
relaxing the (Theo-24, smooth -Headache
smooth muscles Theochron, muscles of -Insomnia
of the Uniphyl) respiratory -Restlessness
bronchioles tract -Seizure
Mometasone Mometasone: -Headache -Diarrhea
and elicits local anti- - -Nausea
formoterol inflammatory Nasopharyngiti -Vomiting
(Dulera) effects to s
respiratory tract -Oral 9. MAST CELL STABILIZERS
candidiasis - These agents stabilize the mastcell
Formoterol: membrane, and inhibit the activation and
elicits bronchial release of mediators from eosinophils and
smooth muscle epithelial cells. They inhibit acute responses
relaxation.
to cold air, exercise, and sulfur dioxide.
 Medication MOA Adverse Effects Beclomethaso - Inhibits -infection of
Cromolyn Inhibits the -Diarrhea ne (QVAR, bronchoconstri mouth/pharynx
sodium release of -Headache Beclovent) ction with Candida
(Intal) histamine, -Nausea mechanisms albicans
leukotrienes, - causes direct
and other smooth
mediators muscle
from relaxation
sensitized - decrease the
mast cells number
exposed to and activity of
specific inflammatory
antigens. cells
Triamcinolone Glucocorticoid: -Pharyngitis
10. MONOCLONAL ANTIBODY inhaled anti- -Headache
- It is indicated for moderate-to-severe (Azmacort) inflammatory -Flu syndrome
persistent asthma in patients who react to Flunisolide Glucocorticoid: -Headache
perennial allergens, in whom symptoms are (Aerobid, anti- -URI
AeroSpan, inflammatory -Nausea
not controlled by inhaled corticosteroids.
Nasalide) -Sore throat
Medication MOA Adverse Effects -Nasal
Omalizumab Recombinant -Injection site congestion
(Xolair) humanized -Reactions
monoclonal -Viral infections 12. LEUKOTRIENE RECEPTOR ANTAGONIST
antibody; selec -URI - These are either 5-lipoxygenase inhibitors
tively binds to -Sinusitis
or leukotriene-receptor antagonists
IgE and -Headache
inhibits -Pharyngitis Medication MOA Adverse Effects
binding to IgE
Zafirlukast selective -Headache
receptors on
(Accolate) competitive -Abdominal pain
surface of
inhibitor -Infection
mast cells and
of LTD4 and -Nausea
basophils.
LTE4 -Diarrhea
receptors
11. CORTICOSTEROID, INHALANT
Montelukast Blocks binding -Headache
- Steroids are the most potent anti-
- of leukotriene -Abdominal pain
inflammatory agents. Inhaled forms are Advantages: D4 to its -Asthenia
topically active, poorly absorbed, and least chewable it receptor -Bronchitis
likely to cause adverse effects. has a once-a- -Cough
Medication MOA Adverse Effects day dosing It
Ciclesonide have a wide -Headache has no
(Alvesco) range of -Epistaxis significant
- is an aerosol effects on - adverse
inhaled multiple cell Nasopharyngitis effects.
corticosteroid types and -Ear pain
indicated for mediators
maintenance involved in
treatment of inflammation
asthma as
prophylactic
therapy
STEPWISE MX OF ASTHMA
 Step 1: Mild Intermittent asthma
 Inhaled short-acting B2-agonist as
required
 Step 2: Regular Preventer Therapy
 Add inhaled steroid 200-800ug/day
 Step 3: Add-on Therapy
 Add inhaled long acting B2 agonist. If
no response-stop LABA and give LTR
antagonist
 Step 4: Persistent Poor Control
 Consider trials of: increasing steroid
up to 2000 ug/day and add 4th drug:
LT antagonist, B2 agonist, and
Theophylline tablet
 Step 5: Use of oral steroids
 Use daily steroid tablet and refer to
specialist
Patient Education
 Avoid triggers by:
 Use your air conditioner
 Decontaminate your décor
 Prevent mold spores
 Reduce pet dander
 Clean regularly
 Cover your nose and mouth if it's
cold out.
 Stay healthy
 Get regular exercise.
 Maintain a healthy weight
 Eat fruits and vegetables - Control
heartburn and gastroesophageal
reflux disease (GERD
ALTERNATIVE MEDICINE
 Breathing techniques
 Yoga classes increase fitness and
reduce stress, which may help
with asthma as well.
 Acupuncture
 Relaxation techniques
 Techniques such as meditation,
biofeedback, hypnosis
and progressive muscle relaxation
may help with asthma by
reducing tension and stress.
 Herbal remedies
 may help improve asthma
symptoms LIKE: butterbur,
Indian frankincense, Pycnogenol.
 Omega-3 fatty acids
 Found in fish, flaxseed and other
foods, these healthy oils may
reduce the inflammation that
leads to asthma symptoms.
CHRONIC OBSTRUCTIVE PULMONARY
DISEASE (COPD)
- Airflow limitation that is NOT FULLY reversible
with bronchodilators
- Progressive and believed to reflect an
abnormal response of the lungs to noxious
particles or gasses
- Usually a consequence of prolonged habitual
smoking, but approximately 15% of cases
occur in non-smokers
- As compared to asthma, COPD is associated
with neutrophilic rather than eosinophilic
inflammation.
- Poorly responsive even to high dose inhaled
corticosteroids and is associated with
progressive, inexorable loss of pulmonary
function over time, especially with continuous
smoking
- Inhalation of toxic substance → activation of
immune system (neutrophils, macrophages,
CD8 lymphocyte) → Release of inflammatory
mediators (Tumor necrosis alpha, interleukin
8 and Leukotriene B) → pulmonary vascular
and airway changes.
- Oxidative stress and imbalance between
aggressive and protective defense systems in
the lungs (proteases and antiproteases)
- Smoking→ increase Oxidants→ promotes
inflammation → exacerbates Protease and
antiprotease imbalance, but inhibiting
antiprotease
CHRONIC BRONCHITIS
- Chronic bronchitis is associated with chronic
or recurrent excessive mucus secretion into
the bronchial tree with cough that is present
on most days for at least 3 months of the
year for at least 2 consecutive years.
- Mucosal gland hyperplacia
- Airway structural changes via atrophy,
hyperplacia, inflammation, bronchial wall
thickening.
- Decrease ventilation + Increase Cardiac
output → hypoxemia and polycythemia →
hypercapnia and respiratory acidosis
→ pulmonary artery vasoconstriction cor
pulmunare
- "Blue bloaters"
EMPHYSEMA
- Permanent enlargement of the airspaces
distal to the terminal bronchioles 
decreased alveolar spaces available for gas
exchange → 1. loss of alveoli walls →
Decreased elastic recoil → airway limitation.
- loss of alveoli wall decreased alveoli structure
airway narrowing.
- Noxious stimuli → activation of inflammation
( neutrophils, macrophages, lymphocytes) →
release of chemotactic factors and pro
inflammatory cytokines that amplify
inflammation and growth factors that
promotes structural changes.
- Pink puffers
- Inflammation → oxidative stress ( from
smoke and inflammatory cells)and protease
production ( from inflammatory and epithelial
cells) → proetase-antiprotease imbalance→
destruction of elastin and structural elements
→ emphysema
- Two Types:
 Centriancinar: emphysema
associated with smoking and
typically most severe in the upper
lobe
 Panancinar: involves central
alveioli, distal and terminal
bronchioles. Typically most severe
in the lower lungs. Common in
patients with HOMOZYGOUS
ALPHA 1 ANTITRYPSIN
Pathophysiology - INFLAMMATION
- The actions of these cells and mediators
are complementary and redundant,
leading to the widespread destructive
changes.
- The stimulus for activation of
inflammatory cells and mediators is an
exposure to noxious particles and gas
through inhalation
- The most common etiologic factor is
exposure to environmental tobacco
smoke
Pathophysiology - OXIDANTS
- Increases in markers (e.g., hydrogen
peroxide and nitric oxide) of oxidants are
seen in the epithelial lining fluid of COPD
patients.
- Cigarette smoke increases oxidants_that
damage various proteins and lipids.
- It leads to cell and tissue damage.
Pathophysiology - AAT DEFICIENCY
- AAT is α1-antitrypsin
- AAT is responsible for inhibiting several
protease enzymes, including neutrophil
elastase.
- In the presence of unopposed activity,
elastase attacks elastin, a major
component of alveolar walls.
Pathophysiology – DIFFERENT WITH ASTHMA
- The inflammatory cells that predominate
differ between the two conditions, with
neutrophils playing a major role in COPD
and eosinophils and mast cells in asthma.
- Mediators of the inflammation also differ
 Chronic Obstructive Pulmonary Disease (COPD)

Features of Inflammation in Chronic Obstructive Signs and Symptoms

Pulmonary Disease (COPD) Compared with  Cough: usually worse in the morning
Asthma  Breathlessness: MOST SIGNIFICANT
COPD ASTHMA
SYMPTOM
Cells Neutrophils Eosinophils
- Large - Small increase  If FEV1 has decreased by 50%, the patient
increase in macrophages may experience breathlessness even with
in macropahge - Increase in minimal exertion.
s CD4+ TH,  Wheezing: may occur particularly
- Increase in lymphocytes during exertion and airflow obstruction
CD8+ - Activation of
exacerbation
T lymphocytes mast cells
Mediators LTB4 LTD4 Systemic manifestation
IL-8 IL-4, IL-5
 Decrease fat free mass
TNF-α (Plus many
others)  Impaired systemic muscle function
Consequences - Squamous - Fragile  Increase risk of osteoporosis:
metaplasia of epithelium  Smoking increases level of cortisol
Epithelium - Thickening of which increases bone breakdown
- Parenchymal basement and impedes calcitonin which
destruction membrane helps in bone formation.
Response - Mucus - Mucus
 Anemia: may be due to decreased
to treatment metaplasia metaplasia
- Glandular - Glandular absorption of iron.
enlargement enlargement  Depression: may be due to nicotine effect
- -  Pulmonary hypertension
Glucocorticost Glucocorticoster  Cor pulmunare
eroids have oids inhibit
variable effect variable effect CLINICAL PRESENTATION
IL, interleukin; LT, leukotriene; TH, T-helper; TNF,
tumor necrosis factor. Diagnostic Tests
 Spirometry with reversibility testing
 used to measure FEV1 (Force
expiratory volume in second)
 Radiograph of chest
 Arterial blood gas (not routine)
Features of Chronic Obstructive Pulmonary Physical Examination
Disease Exacerbation  Fever
 Symptoms  Wheezing, decreased breath sound
 Increased sputum volume
 Acutely worsening dyspnea Diagnostic Tests
 Chest tightness  Sputum sample for Gram stain and culture
 Presence of purulent sputum  Chest radiograph to evaluate for new
 Increased need for bronchodilators infiltrates
 Malaise, fatigue
Desired Outcomes
 Decreased exercise tolerance
Others include:
 Cor pulmunare
 Prevent disease progression
EMPHYSEMA "PINK PUFFER"  Relieve symptoms
 Increase CO2 Retention (Pink)  Improve exercise tolerance
 Minimal Cyanosis  Improve overall health status
 Purse Lip Breathing  Prevent and treat exacerbations
 Dyspnea  Prevent and treat complications
 Hyperresonance on Chest Percussion  Reduce morbidity and mortality
 Orthopneic
General Approach to Treatment
 Barrel Chest
The clinician should address four primary
 Exertional Dyspnea
components of management:
 Prolonged Expiratory Time
 Assess and monitor the condition;
 Speaks in Short Jerky Sentences
 Avoidance of or reduced exposure to risk
 Anxious
factors;
 Use of Accessory Muscles to Breathe
 Manage stable disease;
 Thin Appearance
 Treat exacerbations.
CHRONIC BRONCHITIS “BLUE BLOATER”
Treatment
 Airway Flow Problem  Stage 0: at risk
 Color Dusky to Cyanotic  Cough and sputum
 Recurrent Cough & high Sputum  Normal FEV1
Production  Treatment:
 Hypoxia o Smoking cessation
 Hypercapnia (high pCO2) o Reduce indoor pollution
 Respiratory Acidosis o Reduce occupational
 High Hemoglobin exposure
 High Respiratory Rate o Yearly flu vaccine.
 Exertional Dyspnea  Stage 1: Mild COPD
 Higher Incidence in Smokers  Cough, sputum
 Digital Clubbing  Little or no dyspnea
 Cardiac Enlargement  Mild symptoms
 Use of Accessory Muscles to Breathe *  No abnormal signs FEV1: Greater
Leads to Right-Sided Heart Failure: than or equal to 80%
Bilateral Pedal Edema, high JVD  Treatment:
o PRN: beta 2 agonists
 o Pulmonary rehabilitation o Consider surgical treatment
 Stage 2: Moderate COPD and bullectomy
 Cough, sputum - Dyspnea on
Treatment
moderate exertion
 Oral N-acetylcysteine
 Continuous intermittent symptoms
 With antioxidant and mucokinetic
 FEV1: 50-79%
property
 Treatment:
 May elicit bronchospasm: if so:
o For intermittent symptoms:
o Inhalant therapy of NAC +
beta 2 agonists
Bronchodilator
o For continuous symptoms:
 Oxygen therapy
tiotropium inhalation, 1 cap
 Continuous flow nasal canula
daily, mucokinetic agent ( add
 Vaccine
long acting b2 agonist if
 Pneumococcal vaccine for patient
unresponsive to thiotropium
>60 years old with FEV1 of <40%
alone
 Influenza virus vaccine for all COPD
o Pulmonary rehabilitation
patients
 Stage 3: Severe COPD
 AAT: al-antitrypsi
 Cough, sputum
 Prolantin, Zemaria, aralast: derived
 Dyspnea on mild exertion
from donor blood
 Lung hyperinflation
 Bullectomy: via midline
 wheezing
sternotomy or video assisted
 FEV1: 30-49%
thoracoscopy
 Treatment:
 Bupropion
o For intermittent symptoms:
 A drug used as an antidepressant.
beta 2 agonists
 Can markedly reduce nicotine
o For continuous symptoms:
cravings.
thiotropium inhalation, 1
 Though associated with an
cap daily, mucokinetic agent
increased risk for seizures
( add long acting b2
 Varenicline
agonistif unresponsive
 a new agent became available to
to thiotropium alone
assist in tobacco cessation
o For frequent exacerbations:
attempts.
( more than 4 times a year)
 a nicotine acetylcholine receptor
add inhaled steroids and
partial agonist that has shown
LABA
benefit in tobacco cessation.
o Pulmonary rehabilitation
 Varenicline relieves physical
 Stage 4: Very Severe COPD
withdrawal symptoms and reduces
 Dyspnea even at rest
the rewarding properties of
 Chronic respiratory failure
nicotine.
 FEV1: < 30%
 Treatment: NONPHARMACOLOGIC THERAPY
o Treatment is the same with  Smoking Cessation
stage three but added with:  Pulmonary Rehabilitation
o Long term oxygen therapy
at home
  Exercise training with pulmonary
Rehabilitation

 Immunizations
 Due to increased risk for infection
and thus exacerbations; also
influenza could further decrease
lung immunity leading to
secondary bacterial pneumonia
 Long-Term Oxygen Therapy
 For those with Chronic Hypoxemia
 Classification of Asthma Severity ≥ 12 years of age
Components of Severity Persistent
Intermittent Mild Moderate Severe
Symptoms ≤ 2 days/week > 2 days/week Daily Throughout
but not daily the day
Night time > 1/week but Often 7x/week
Impairment awakenings ≤ 2x/month 3-4x/month not nightly
Short-acting β2- > 2 days/week Daily Several times
Normal agonist use for but not daily, per day
FEV1 /FVC symptom ≤ 2 days/week and not more
8-19 85% control (not than 1x on any
20-39 80% prevention of day
40-59 75% EIB)
60-80 70% Interference None Minor Some Extremely
with normal limitation limitation limited
activity
Long Function  Normal FEV,  FEV1 >  FEV1 >  FEV1 < 60%
between 80% 60% but < predicted
Exacerbations predicted 80%  FEV1 /FVC
 FEV, > 80%  FEV1 /FVC predicted reduced
predicted normal  FEV1 /FVC >5%
 FEV1 /FVC reduced
normal 5%
Exacerbations
requiring oral 0-1/ year ≥ 2/year
systemic Consider severity and interval since last exacerbation. Frequency and
Risk corticosteroids severity may fluctuate over time for patients in any severity category.

Relative annual risk of exacerbations may be related to FEV

Step 1 Step 2 Step 3 Step 4 or 5

Recommended Step for Initiating And consider short course of

Treatment oral systemic corticostreroids
In 2-6 weeks, evaluate level of asthma control that is achieved and
adjust therapy accordingly.