C.O.P.

D
(Chronic Obstructive Pulmonary
Disorder)
Class Report by:
Austria
Chu
Lumapas
Mercader

What is COPD?
An umbrella term used to describe progressive
lung diseases including emphysema, chronic
bronchitis, refractory (non-reversable) asthma,
and some forms of bronchiectasis and is
characterized by increasing breathlessness
www.copdfoundation.org
chronic obstructive pulmonary disease,
involving constriction of the airways and
difficulty or discomfort in breathing.
-oxford dictionary

Common finding in COPD pt.

Common CXR finding

STAGES OF COPD
(symptoms, PFT, treatment)

Chronic Bronchitis
Krystel Lumapas

Overview
Chronic productive cough for at least
3 months a year for 2 consecutive
years
One of the first step towards chronic
lung disease
Also considered as an endstage
lung disease
BLUE BLOATER best describes this
kind of patient

Cause
Inhalation of irritants

Inflammation of tracheobronchial tree

Overtime..

-Increased mucus production

-Blocked or narrowed airway

As inflammation continues
Goblet & Epithelial cells hypertrophy
(Natural defense mechanism are blocked, the airways accumulate debris in
the respiratory tract)

Signs & Symptoms

History:

Long time smoker with frequent respiratory tract infections

Exertional dyspnea and/or worsening dyspnea that takes longer to subside
Productive cough
Substantial weight gain
Excessive expectoration

Inspection:

Copious gray/white/yellow sputum

May appear cyanotic with clubbing (severe cases)
Use of accessory muscles when breathing
Normal or barrel chested
Rhonchi and wheezes with prolonged expiration

Vital signs:
Tachypnea (due to hypoxia)

Diagnostic procedures
CHEST XRAY
-hyperinflation
-flattened diaphragm
-increased bronchovesicular markings

PFT
-increased RV
-decreased VC, FEF25-75, FEV1/FVC, FEV1
-Normal Cstat, Diffusing capacity

ABG ANALYSIS
-Increased/Normal PaCO2
-Decreased PaO2

CBC
-Increased HB
-Polycythemia (due to hypoxemia)

SPUTUM CULTURE
-microorganisms
-neutrophils

ECG
-arterial arrythmias
-Peaked P waves (II,III,AVF)
-RV hypertrophy (occasionally)

Treatment/Management
Smoking cessation
Avoiding air pollutants
Antibiotics
treat recurring infections
Bronchodilator therapy
Relieve bronchospasms and facilitate in mucus clearance
Adequate fluid intake
Promote hydration of secretions
Good bronchial hygiene
Effective cough methods should be thought
Chest physiotherapy, Nebulizer treatments
To loosen & mobilize secretions
Diuretics
To treat edema
Oxygen
Treat hypoxia

Emphysema
Matthew Chu

Overview
A long term progressive disease that
causes shortness of breath due to over
inflation of the alveoli.
It does not only affect the airways but it
also affects the blood flow.
Thin appearance
Increased CO2 retention
Also called Pink Puffers

Causes
The most dangerous cause is cigarette
smoking and it contributes to developing
emphysema in two ways:
Destroys lung tissue resulting to an
obstruction of airflow
Causes inflammation and irritation of
airways which adds to the obstruction
alpha 1 antitrypsin deficiency
Air pollution
Heredity
Old age

Symptoms
Shortness of breath is the most common
symptom
Cough with productive secretions and wheezing
Exercise tolerance (decreasing over time
especially if u are a smoker which is worse)
Patient is doing pursed lip breathing (emphysema
patients have trouble exhaling properly)
Barrel chest in x ray (resulted from air trapped in
airways due to obstruction)
SLOW DETERIORATION IS KEY AND MAY GO
UNNOTICED

Diagnosis
These tests serve to clarify the
extent of the disease and lung
function:
Chest x ray
Lung function tests
(ex. PFT)
Blood tests
(WBC count)

ABG

Treatment
Stop smoking
Bronchodilators
Albuterol (ventolin/proventil)
Ipratropium bromide (atrovent)
Methylxanthines (Theophylline)

Steroid medications
Antibiotics
Supplemental O2
NOTE: there is no cure to emphysema but there
are effective methods of treatment that can
slow the progression and allow for a normal life

Key Facts
Air sacs are destroyed in emphysema,
making it progressively difficult to breath.
Emphysema is usually accompanied by
chronic bronchitis, with almost-daily or
daily cough and phlegm.
Cigarette smoking is the major cause of
emphysema.
People with emphysema experience
shortness of breath with activities
It is not curable, but there are treatments
that can help you manage the disease

Definition

Refers to the abnormal, irreversible

dilation of the either the bronchi,
bronchioles or both. Caused by
destructive and inflammatory
changes in the airway walls

Bronchiectasis
Gabby Mercader

Major Anatomical
Patterns

Cylindrical
Bronchiectasis Regularly and uniformly
dilated
Varicose
Bronchiectasis Irregular pattern, with
alternating areas of
constriction and dilation
Cystic Bronchiectasis Progressive, distal
enlargement of the
airways, resulting in
saclike dilation

Cause

Local Bronchiectasis

Foreign body

Benign airway tumor (adenoma)

Bronchial compression by surrounding lymph nodes

Diffuse Bronchiectasis

Cystic fibrosis

Ciliary dyskinesia disorders

Hypogammaglobulinemia

AAT deficiency

Allergic bronchopulmonary aspergillosis

Rheumatoid arthritis

Serious lung infection

Clinical Manifestation

Hallmark of bronchiectasis is the chronic

production of large quantities of purulent sputum

Dyspnea is variable (depending on the

underlying disease)

Hemoptysis occurs frequently and is usually mild

Airway dilation in radiographic studies

Also may show cystic spaces and tram tracks

(thin parallel lines representing the airway walls)

Diagnostic Procedure/s

For bronchiectasis, CT is the diagnostic

standard.

The diagnosis for bronchiectasis is

established when the diameter of the
bronchus exceeds the diameter of the
adjacent pulmonary artery branch

Because reversible airway changes

consistent with bronchiectasis can follow
pneumonia, CT should be deferred for 6 to
8 weeks after pneumonia resolves, when a
diagnosis of bronchiectasis can be made

 ABG
Significant hypoxemia may be present

CHEST XRAY
May show some cystic spaces with recognizable air-fluid levels
Honeycomb appearnace
(due to fibrosis of emphysematous area)

BRONCHOGRPAHY
Most definitive test for diagnosing bronchiectasis

Illustrates size and appearance of the tracheobronchial tree

Management

Antibiotics and Bronchopulmonary hygiene are the mainstays of

bronchiectasis management.

Sputum cultures may be helpful in guiding antibiotic choice

Secretions can be cleared by chest physiotherapy (with postural

drainage, cough maneuvers, and humidification)

Inhaled bronchodilators may be helpful in some patients when they also

have airflow obstruction

Inhaled hyperosmolar substances may help in clearing secretions

Dry powder mannitol improves tracheobronchial clearance in patients

with bronchiectasis, cystic fibrosis, asthmatics, and normal subjects

For cases complicated by massive hemoptysis, embolization of the

bleeding bronchial artery may be helpful

Surgery is done for patients with localized disease who develop massive
hemoptysis or who are severely symptomatic despite appropriate
medical therapy

ASTHMA
Jack Austria

 Chronic inflammatory disorder of

the airway causing
hyperresponsiveness
Widespread, variable, and
reversible airway obstruction
An asthmatic starts with a
propensity for asthma
6%: (-) asthma in family
30%: if one parent is asthmatic/
allergic
70%: if both parents are asthmatic

2 KINDS OF ASTHMA
EXTRINSIC
Also known as bronchial asthma
Common in children and an allergic type
Pathophysiology:
Bronchiole spams then mucosal swelling which develops to
narrowing of airways, an increase in thick secretions
IgE mediated (causes airway hypersensitivity and
bronchoconstriction)

INTRINSIC
Bronchoconstricion is caused by an imbalance in the ANS
(parasympathetic system is overactive, sympathetic is
underactive)
Mostly seen in adults

ASTHMA CLASSIFICATION

In asthma, there is:

1. Bronchoconstriction
-hyperreactive airway
2. Inflammation
3. Mucus over-production

Triggers

Viral infection
Allergies (pets, pollens)
Food and food additive
Exercise
Irritants including smoke
Medication
Weather
Strong emotion
Hormonal
Gastroesophageal reflux

Asthma

Cough
Wheeze
Chest tightness
Shortness of breath
"Halak"
Episodic
Nocturnal
Seasonal
After exercise

Diagnostic procedures
PFT
During attack:
Decreased VC, FVC, flow rates
Increased FRC, TLC, RV (due to airtrapping)

ABG
Hypoxemia (severity depends on the severity of attack)
Hypercapnia (if attack is severe)

SPUTUM CULTURE
Presence of eosinophils (extrinsic asthma)

CHEST XRAY
Hyperinflation
Increased A-P diameter
Areas of atelectasis

Acute exacerbation :
Temporary worsening of symptoms
Form part of the natural history of
the disease
Failure of ongoing long-term therapy

STATUS ASTHMATICUS
an acute exacerbation of asthma that remains unresponsive to
initial treatment with bronchodilators
life-threatening form of asthma
can vary from a mild form to a severe form with bronchospasm,
airway inflammation, and mucus plugging that can cause
difficulty breathing, carbon dioxide retention, hypoxemia, and
respiratory failure
The primary signs & symptoms of asthma are:

cough, dyspnea, and wheezing

Management goals for status asthmaticus are

(1) to reverse airway obstruction rapidly through the aggressive use of beta2agonist agents and early use of corticosteroids
(2) to correct hypoxemia by monitoring and administering supplemental oxygen
(3) to prevent or treat complications such as pneumothorax and respiratory
arrest.

Exam findings that signify severe respiratory function

compromise include:
Retractions
Prolonged expiratory phase
Pulsus paradoxus
Evidence of cyanosis/hypoxemia - PaO2 less than
60mmHg
Change in consciousness
Hypercapnia - PaCO2 greater than 40mmHg in presence
of dyspnea and wheezing
Metabolic acidosis
FEV1 or PEFR (peak expiratory flow rate) less than 20%
predicted with little or no response to acute therapy

Management

Management
Treatment : Acute Attack
Rescue
1. B2 agonist drugs
> Salbutamol

> Terbutaline

> Procaterol
Inhaled is better
> faster onset of action
> lesser side effects

B2 agonist drugs

> Initially: give every 15 minutes

for 3 doses or continuously until
relief
> Then give every 4-6 hours as
needed

Steriod
oral or parenteral better than inhaled
ex. Oral : prednisone.prednislone

dexamethasone

Parenteral: hydrocortisone,

methylprednisolone

> usually started when in acute attack

Prednisone is a pro-drug and is converted
to prednisolone
Therefore, use prednisolone as onset of
action is faster

Treatment: Maintenance controller

Needed because of the chronic inflammation

Goal: A normal life as possible
Inhaled is better than oral
Inhaled steroid
> budesonide
>fluticasone
Anti-leukotriene antagonist
> montelukast

Devices:

Small volume nebulizer

Dry powder inhaler
Metered dose inhaler
Diskus
Turbohaler