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Respiratory System > Lecture 8.1: COPD > Flashcards

Lecture 8.1: COPD Flashcards

1
Q

What is the long form of COPD?

A

Chronic Obstructive Pulmonary Disease

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2
Q

What is COPD?

A
  • The name for a group of lung
    conditions that cause breathing
    difficulties
  • It includes: emphysema (damage to
    the air sacs in the lungs), chronic
    bronchitis (long-term inflammation of
    the airways)
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3
Q

What is COPD predominantly caused by?

A

Smoking

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4
Q

What is COPD characterised by (NICE)?

A
  • COPD is characterised by airflow
    obstruction
  • The airflow obstruction is usually
    progressive
  • Not fully reversible
  • Does not change markedly over
    several months
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5
Q

How many people in the UK are living with COPD?

A

1.2 million

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6
Q

Risk Factors for COPD (7)

A
  • Smoking
  • Coal Mining/Mining of any kind really
  • Asbestos Exposure
  • People with Asthma
  • Exposure to fumes from burning fuel
  • Occupational exposure to dusts and
    chemicals
  • Genetics
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7
Q

Causes of COPD (4)

A
  • Vast majority in HICs due to smoking
  • Alpha-1 anti-trypsin deficiency
  • Occupational exposure (e.g. coal dust)
  • Pollution (including indoor smoke
    pollution)
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8
Q

What percentage of Smokers get COPD?

A

15%

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9
Q

What is Emphysema?

A
  • A pathological process in which there is
    destruction of the terminal bronchioles
    and distal airspaces
  • Leads to loss of alveolar surface area
  • Spaces get bigger to form bullae
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10
Q

Why do small airways collapse in Emphysema?

A
  • Spaces get bigger to form bullae
  • Destruction of tissues removes
    ‘scaffolding’ support of small airways,
    which tend to collapse
  • Leads to airflow obstruction
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11
Q

What is Pulmonary Compliance?

A

A measure of the lung expandability

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12
Q

What is the Equation of Pulmonary Compliance?

A

Compliance = Δvolume/Δpleural pressure

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13
Q

What is the effect of loss of tissue in Emphysema?

A
  • Loss of tissue increases compliance
  • Lung recoil reduced so lungs have
    higher resting expiratory level
  • Hyperinflation
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14
Q

Centrilobular/Centriacinar Emphysema

A
  • Primarily the upper lobes
  • Occurs with loss of the respiratory
    bronchioles in the proximal portion of
    the acinus
  • With sparing of distal alveoli
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15
Q

Panlobular/Panacinar Emphysema

A
  • Involves all lung fields
  • Particularly the bases
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16
Q

What is Chronic Bronchitis?

A

A daily productive cough that lasts for 3 months of the year and for at least 2 years in a row

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17
Q

Pathophysiology of Chronic Bronchitis

A
  • Chronic mucus hypersecretion
  • Mucus hyper secretion caused by
    inflammation in larger airways
  • Leads to chronic productive cough and
    frequent infections
  • Get re-modelling and narrowing of
    airways
18
Q

Symptoms of COPD (5)

A
  • Cough
  • Sputum Production
  • Progressive Breathlessness
  • Dyspnoea
  • Increasingly frequent exacerbations
19
Q

MRC Dyspnoea Score (5 Grades)

A
  • Grade 1: not troubled except in hard
    exercise
  • Grade 2: short of breath when hurrying
    or walking up slight hill
  • Grade 3: walks slower than
    contemporaries on level ground
    because of breathlessness
  • Grade 4: stops for breath after walking
    100m or so
  • Grade 5: too breathless to leave the
    house, or breathless on dressing and
    undressing
20
Q

Signs of COPD (10)

A
  • ‘Purse Lip’ Breathing
  • Increases pressure within airways to
    delay closure
  • Tachypnoea
  • Use of accessory muscles
  • Hyperinflation (harder to breath)
  • May have wheeze or quiet breath sounds
  • Cyanosis
  • Carbon dioxide retention
  • Right heart failure (cor pulmonale)
21
Q

Investigations for COPD

A
  • Spirometry
  • Chest X-Ray
  • High Resolution CT
  • ABGs (to assess respiratory failure)
  • Alpha-1 anti trypsin assay for younger patients
22
Q

How is Airflow Obstruction Staged?

A
  • Mild airflow obstruction: FEV1.0 50-80%
    predicted
  • Moderate airflow obstruction: FEV1.0 30-49%
    predicted
  • Severe airflow obstruction: FEV1.0 <30%
    predicted
23
Q

Pathophysiology of Emyphsema

A
  • Parenchymal destruction
  • Matched V/Q defect
  • Mild hypoxia
  • Cachexia
24
Q

Pathophysiology of Chronic Bronchitis

A
  • Airway inflammation
  • V/Q mismatch
  • Severe hypoxia and hypercapnia
  • Pulmonary hypertension and cor pulmonale
25
Q

Cor Pulmonale

A

What is abnormal enlargement of the right side of the heart as a result of disease of the lungs or the pulmonary blood vessels

26
Q

2 Types of Management of COPD

A
  • Stable disease management
  • Management of exacerbations
27
Q

Stable COPD Management (10)

A
  • Smoking cessation support
  • Pulmonary rehabilitation
  • Bronchodilators
  • Anti-muscarinics
  • Steroids
  • Mucolytics
  • Diet
  • Influenza vaccination
  • Long term oxygen therapy in advanced disease
  • Lung volume reduction if appropriate
28
Q

Drug Therapy for COPD: Bronchodilators

A
  • A type of medication that make breathing easier
    by relaxing the muscles in the lungs and
    widening the airways (bronchi)
  • Beta-2 agonists (eg salbutamol)
  • May help with emphysema even if there is no
    improvement in FEV1
29
Q

Adverse Effects of Beta-2 Agonists (5)

A
  • Tachycardia
  • Tremor
  • Anxiety
  • Palpitations
  • Hypokalaemia
30
Q

Drug Therapy for COPD: Steroids

A
  • Steroids help reduce inflammation
31
Q

Drug Therapy for COPD: Mucolytics

A
  • Mucolytics help clear mucus
  • Carbocysteine
32
Q

Drug Therapy for COPD: Anti-Muscarinics

A
  • Also known as anticholinergic agents
  • Are effective bronchodilators used in the
    treatment of chronic obstructive pulmonary
    disease (COPD)
  • Used to alleviate dyspnea and improve
    exercise tolerance
33
Q

Adverse Effects of Anti-Muscarinics

A
  • Dry Mouth
  • Upper Respiratory Tract Infection
  • Nausea
  • Pharyngitis
  • Supraventricular Tachycardia
  • Atrial Fibrillation
  • Urinary Difficulty/Retetention
  • Constipation
34
Q

What is the Effect of Anti-Muscarinics on the Urinary System

A
  • Decreasing the motility of smooth muscle cells
    in the urinary tract and increasing the tone of
    the sphincters controlling urination
  • They do this by inhibiting parasympathetic.
    stimulation of the myenteric and submucosal
    neural plexuses
  • Anticholinergic agent that blocks the activity of
    the muscarinic acetylcholine receptor
35
Q

Adverse Effects of Corticosteroids (10)

A
  • Thin Skin
  • Bruising
  • Cataracts
  • Adrenal Insufficiency
  • Osteoporosis
  • Diabetes
  • Increased Weight
  • Mental Disturbance
  • GI Symptoms
  • Proximal Myopath
36
Q

Managing Acute Exacerbations (6)

A
  • Aim for oxygen saturation 88-92% with.
    controlled oxygen therapy
  • Use nebulised bronchodilators
  • Oral/sometimes IV steroids
  • Antibiotics if suspect infection
  • Consider IV Aminophylline
  • If ABGs do not improve consider ventilator
37
Q

Long Term Oxygen Therapy

A
  • Help to stop long term hypoxia leading to
    renal and cardiac damage
  • Continuous oxygen for at least 16 hours each
    day
  • Offered if arterial pO2 consistently below
    7.3kPa
  • Patients must be non-smokers
  • Patients must not be retaining high levels of
    carbon dioxide
  • Balance with loss of independence
38
Q

Endobronchial Valves

A
  • A small one-way valve, which may be
    implanted in an airway feeding the lung or
    part of lung
  • The valve allows air to be breathed out of the
    section of lung supplied
  • Prevents air from being breathed in
  • This leaves the rest of the lung to expand
    more normally and avoid air-trapping
39
Q

Pulmonary Rehabilitation Encourages…?

A

6-12 week supervised MDT programme of:
* Exercise supervised and unsupervised at home
* Diet
* Disease education

40
Q

Why can’t we give too much oxygen to COPD patients?

A
  • Normal oxygen threshold is reduced in COPD patients
  • Giving them O2 increases saturation in lungs enough
    that their body breaths less
  • This means less CO2 is blown off
  • This could leads to hypercapnia which can be very
    dangerous

Respiratory System (19 decks)

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