COPD Flashcards

1
Q

What causes COPD?

A

COPD is caused by long-term exposure to substances that can irritate and damage your lungs, such as smoking or certain types of fumes, dust and chemicals at work.

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2
Q

COPD primary cause and risk factors

A
Primarily caused by cigarette smoke
•Associated to active and passive smoking
•High risk of developing COPD with continued
long term smoking
•Other risk factors include:
•Occupational exposure
•Air pollution
•Genetic susceptibilities also have been
identified
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3
Q

Diagnosing COPD

A
•Based on history of smoking or exposure
to other noxious inhalation agents
•FEV1/FVC ratio of less than
70%
•Healthy ratio should be 80% or higher
•FEV1: forced expiratory volume in 1
second
•FVC: maximum amount of air that can be
forcibly exhaled in one breath
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4
Q

Emphysema

A

•is a lung condition that causes shortness of breath.

In people with emphysema, the air sacs in the lungs (alveoli) are damaged.

Over time, the inner walls of the air sacs weaken and rupture — creating larger air spaces instead of many small ones

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5
Q

Emphysema continued…

A

•Begins with destruction of alveolar septa
(alveoli, alveolar walls & alveolar capillaries)
•Tobacco smoke and pollution stimulate
inflammation which over time causes
alveolar destruction & loss of elasticity of the
bronchi.
•This eliminates portions of the pulmonary
capillary bed & increases the volume of air in
the alveoli

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6
Q

Destruction of Alveolar

A
Alveolar destruction
produces large air
spaces within the lung
tissue
• These areas are not
effective in gas
exchange due to loss of
respiratory membrane
where gases cross
between air and blood
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7
Q

Emphysema - Reduced gas exchange results in?

A
ventilation-perfusion mismatch
• Leads to hypoxaemia & hypercapnia
•Hypoxaemia: Low arterial blood oxygen levels
(PaO2)
•Normal PaO2: 80 – 100 mmHg
•Hypercapnia: Increased carbon dioxide in the
arterial blood
•Normal PaCO2: 35 – 45 mmHg
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8
Q

Pathophysiology of Emphysema

A
  1. Tobacco smoke/Air pollution
  2. Inflammation of the airway
  3. Infiltration of inflammatory cells & release of neutrophils,
    macrophages, lymphocytes, leukotrienes, interleukins
  4. Breakdown in lung elastic tissue
  5. Destruction of alveolar septa & loss of elasticity of bronchial
    walls
  6. Airway obstruction, Air trapping, loss of surface area for gas
    exchange
  7. Dyspnoea, Cough, Hypoxaemia, Hypercapnia
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9
Q

Manifestations of Emphysema

A
Dyspnoea
• initially on exertion & then on rest
•Wheezing
• may occur during exertion & exacerbations
•Minimal coughing
• Usually occurs in the morning
•No sputum
• or small amounts of mucous sputum
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10
Q

Manifestations of Emphysema contd.

A
Barrel chest
• alveoli over distended, air trapped, flattened
diaphragm
•Chest breather
•relying on intercostal & accessory muscles (ribs
become fixed in inspiratory position)
•Hypoxaemia & hypercapnia
•later in disease
•Weight loss & anorexia
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11
Q

Chronic Bronchitis

A

inflimmation and irritation of the bronchiol tubes

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12
Q

Chronic Bronchitis patho

A

•Inflammation caused by inspired irritants
•Infiltration of neutrophils, macrophages &
lymphocytes into the bronchial wall
•Continual bronchial inflammation causes
bronchial oedema & increases the size and
number of mucous glands & goblet cells in the
airway epithelium
•More mucous is produced & Ciliary function is
impaired

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13
Q

what is Chronic Bronchitis…

A

Thick, mucous is produced which
cannot be cleared due to impaired ciliary
function

•Increases the risk for infection and injury

•Infection exacerbations complicated by
bronchospasm, dyspnoea & productive
cough

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14
Q

Pathophysiology of Chronic Bronchitis

A
  1. Tobacco smoke/Air pollution
  2. Inflammation of the airways
  3. Infiltration of inflammatory cells & release of neutrophils,
    macrophages, lymphocytes, leukotrienes, interleukins
  4. Continuous bronchial irritation & inflammation
  5. Bronchial oedema, hypersecretion of mucous, bacteria
    buildup of airways
  6. Airway obstruction, air trapping, loss of surface area for gas
    exchange
  7. Dyspnoea, cough, hypoxaemia, hypercapnia
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15
Q

Chronic Bronchitis - Effects

A

Initially affects only the larger bronchi
• Eventually all airways are involved
•As airways become narrowed, expiratory airway
obstruction results
•Airways collapse, gas is trapped in the lungs
•Ventilation-perfusion mismatch occurs
•Hypoventilation, Hypoxaemia & hypercapnia

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16
Q

Manifestations of Chronic

Bronchitis

A
Earliest symptoms:
Frequent productive cough during winter
Frequent respiratory infections
Bronchospasm can occur at end of intense bout of coughing
Cough usually exacerbated by respiratory irritants or cold air
Dyspnoea on exertion
History of smoking is almost always present
Normal weight
Ruddy appearance
Intermittent wheezing
Cyanosis
Chronic hypoventilation
17
Q
Comparison- Emphysema
• Onset 50 - 75yrs
• Below average BMI
• Marked weight loss
• Severe dyspnoea
• Negligible cough
• Common wheeze
• Cyanosis uncommon
• Scanty mucoid sputum
• RTI occasional
• Barrel chest classic
A
Chronic Bronchitis
• Onset 40 - 45yrs
• Above average BMI
• No weight loss
• Mild dyspnoea
• Productive cough
• Intermittent wheeze
• Cyanosis common
• Copious purulent sputum
• RTI common
• Barrel chest occasionally
18
Q

Risk Factors for COPD

A
• Exposure to tobacco
smoke (80%)
• Passive smoking
•Occupational exposure
•Air pollution
•Genetic abnormalities
19
Q

COPD

Cigarette Smoking

A

Approx. 4000 chemicals & gases are
inhaled into lungs when smoking

•More than 60 carcinogens have been
isolated from cigarette smoke

•Cyanide, formaldehyde, ammonia.
Nicotine acts as a stimulant to the
sympathetic nervous system resulting in:
•Increased HR
•Increased peripheral vasoconstriction
•Increased BP & cardiac workload
20
Q

Cigarette Smoking effects

on the respiratory system

A

•Hyperplasia of goblet cells (increase in number) which
results in increased mucous production.

  • Reduction of airway diameter
  • Decrease and loss of ciliary activity
  • Destruction of alveolar walls
  • Production of mucous
  • Increased difficulty in clearing secretions
21
Q

Oxygen Therapy

A
Used to treat hypoxaemia
•Goals:
•Reduce work of breathing
•Maintain PaO2 / SaO2 ˃ 90%
•Reduce workload of heart
• Long-term O2 therapy improves:
• Survival
• Exercise capacity
• Cognitive performance
• Sleep
22
Q

Oxygen Therapy continued…

A

• CO2 & O2 two chemoreceptors that control the drive to
breathe
• Normally ↑ CO2 is the major stimulant
• Over time COPD patients develop a tolerance for high CO2
levels
• Respiratory centre loses its sensitivity to elevated CO2 levels

23
Q

Oxygen Therapy…

A

• O2 therapy must be administered (as prescribed and at appropriate
low flow rate initially)
• Failure to administer O2 therapy will cause death by hypoxia
• Critical to start O2 at low flow rates
• Arterial blood gas (AGB’s) used as a guide to determine the flow rate
for administration
• Assess patients mental status & vital signs

24
Q

Pharmacology for COPD

A
  • Bronchodilators: β2- adrenergic agonists
  • Short acting
  • Salbutamol (Ventolin)
  • Terbutaline (Bricanyl)
  • Ipratropium bromide (Atrovent)
  • Long acting
  • Salmeterol (corticosteroid + bronchodilator)