COPD Flashcards

1
Q

What is the GOLD 2015 definition of COPD?

A

Chronic obstructive pulmonary disease (COPD) is a common and treatable disease, is characterised by persistent air flow limitation that is usually progressive and is enhanced with a chronic inflammatory response in the airways and the lung to noxious particles and gases.

Exacerbations and co-morbidities contribute to the overall severity in individual patients.

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2
Q

What are the histological features of COPD?

A

Thickened pulmonary arteriolar wall & narrowed lumen from chronic hypoxia

  • There are vascular changed in COPD due to hypoxic pulmonary vasoconstriction
  • COPD also leads to arterial remodelling, causing thickening of arterial walls
  • This leads to Pulmonary HTN + RV Hypertrophy in COPD pts

Connective tissue deposition
Inflammatory cells – predominantly neutrophils (Th1 response) vs eosinophils in asthma

Submucosal hyperplasia πŸ‘ͺ mucous hypersecretion πŸ‘ͺ chronic productive cough

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3
Q

What are the risk factors for acquiring COPD?

A
  • Tobacco smoke **
  • Smoke from home cooking: esp kerosene
  • Smoke from heating fuels
  • Occupational dusts and chemicals
  • Genetic factors (Ξ±1-anti-trypsin deficiency, MMP12 gene)
  • Ageing
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4
Q

What is the definition of chronic bronchitis?

A
  • Defined clinically as the presence of a chronic productive cough for 3 months during each of 2 consecutive years (other causes of cough being excluded)
  • Result of bronchial inflammation
  • Causing excessive mucous production + thickening of bronchial walls + narrowing of lumen πŸ‘ͺ obstruction to airflow
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5
Q

What is the definition of emphysema?

A
  • Defined pathologically as an abnormal, permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis
  • Air becomes trapped and with reduced SA πŸ‘ͺ air exchange becomes difficult
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6
Q

What are the symptoms of COPD?

A
  • Dyspnoea – progressive, persistent, worse w exercise
  • Chronic cough
    Chronic sputum production
  • Others: wheezing, chest tightness, cough syncope
  • History of exposure to risk factors
  • Family history of COPD

Post-bronchodilator FEV1/FVC <0.7 (ie. persistent limitation)

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7
Q

What are the physical examination findings in a patient with COPD?

A

Trachea

  • Central
  • Reduced cricosternal distance
  • Tracheal tug (due to stretching of the mediastinum by the low diaphragm)

Expansion

  • Reduced bilaterally
  • Hoover’s sign (inward movement of lower ribcage on inspiration – implying flat diaphragm from emphysematous changes)
  • Increased AP diameter πŸ‘ͺ sign of hyperinflation

Percussion

  • Normal or increased in emphysema
  • Loss of cardiac / liver dullness πŸ‘ͺ Sign of Hyperinflation

Auscultation

  • Reduced air entry (emphysema)
  • May have bilateral expiratory rhonchi – essentially low-pitched wheeze (rattling expiratory sounds resembling snoring; due to secretions/ narrowing of bronchi)

Vocal Resonance
- Normal

Other features

  • Nicotine stained fingers - Quiet heart sounds
  • Intercostal indrawing - Barrel Chest (not specific)
  • Pursed lip breathing
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8
Q

How do you assess severity of impairment of lung function in COPD patients?

A

GOLD 1

  • Mild severity
  • FEV1 >80% predicted
  • FEV1/ FVC < 0.7

GOLD 2

  • Moderate severity
  • FEV1 50%- 80% predicted
  • FEV1/ FVC < 0.7

GOLD 3

  • Mild severity
  • FEV1 30- 50% predicted
  • FEV1/ FVC < 0.7

GOLD 4

  • Mild severity
  • FEV1 < 30% predicted
  • FEV1/ FVC < 0.7
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9
Q

How do you assess the severity of symptoms in COPD patients?

A

Symptoms: COPD Assessment Test (CAT)

  • <10 low impact of symptoms
  • β‰₯10 high level of symptoms, requires comprehensive assessment of symptoms
  • Cat is similar to mMRC but also includes sputum etc

Breathlessness: mMRC breathlessness scale
- mMRC β‰₯2 significant impact of life

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10
Q

What are the investigations to be conducted in COPD patients?

A

Lung Function Test – FVC, FEV1, FVC/FEV1 ratio

CXR

  • Hyperinflation (>6 anterior ribs above diaphragm in mid clavicular line);
  • Flat hemidiaphragm; coarsened airways;
  • Narrowed mediastinum (long thin heart)
  • Decreased peripheral vascular markings;
  • Large central pulmonary arteries due to hypoxic pulmonary vasoC
  • Right heart hypertrophy

CT thorax HR (high resolution) for emphysematous changes

Lung volume and diffusion capacity: increased TLC (total lung capacity), reduce DLCO

Oximetry and ABG analysis

  • If FEV1 <35%, underlying respiratory failure
  • Do ABGs if SpO2 <92%

Ξ±1 anti-trypsin deficiency – age <45 (YOUNG) and lower lobe emphysema

  • Suspect homozygous of A1AT deficiency if A1AT level <15-20% normal range
  • We always want to screen and Dx these patients!
  • Because this is potentially reversible + consider transplant – because criteria for lung transplant is to STOP SMOKING!

Exercise tests – objective assessment of exercise impairment (e.g. 6-minute walk test, shuttled walk test)

Composite scores – BODE score (BMI, obstruction, dyspnoea, exercise). Survival prediction.

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11
Q

What is the differential diagnosis of COPD?

A
  • Asthma
  • CCF/cor pulmonale/LV failure
  • Bronchiectasis
  • TB
  • Obliterative bronchiolitis
  • Diffuse pan bronchiolitis
  • Pneumonia
  • Pneumothorax
  • Pulmonary embolism
  • Tumour
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12
Q

What is non pharmacological management of COPD?

A

Smoking cessation *most effective way to stop decline of lung function

  • Nicotine replacement e.g. nicotine gum, inhaler, sublingual tablet, nasal spray, transdermal patch, lozenges
  • Bupropion (SSRI)
  • Varenicline (nicotinic receptor partial agonist)
  • Nortriptyline (TCA)
  • Counselling and/or CBT

Vaccination

  • Important because most exacerbations caused by viral infection
  • Pneumococcal (Hib/Strep pneumoniae/pertussis), Influenza
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13
Q

What is the pharmacological management of COPD?

A

GOLD A:

  • Low risk, less symptoms
  • ANY Bronchodilator (SABA / LABA / SAMA / LAMA)
  • If ineffective, consider switching to other inhalers

GOLD B:

  • Low risk, more symptoms
  • LABA / LAMA
  • If a LAMA is started, SAMA (including nebulisations) should be stopped.
  • Patients with persistent breathlessness should be escalated to a LABA/LAMA combination

GOLD C:

  • High risk, less symptoms
  • LAMA as first line treatment
  • If further exacerbations, consider LABA + LAMA OR LABA + ICS

GOLD D:

  • High risk, more symptoms
  • LAMA + LABA (preferred)
  • OR LABA + ICS
  • if further exacerbation: LAMA + LABA+ ICS
  • consider adding macrolides
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14
Q

When is long term oxygen therapy indicated in COPD patients?

A

Long term oxygen therapy is indicated in patients with severe COPD who are in chronic respiratory failure [blood oxygen saturation (SpO2) ≀ 88%].

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15
Q

What are the causes of acute exacerbations of COPD?

A

Infectious (60-80%) *

  • Haemophilus influenzae
  • Streptococcus pneumoniae
  • Moraxella catarrhalis
  • **Viruses (influenza and parainfluenza viruses, rhinoviruses, coronaviruses)
  • Pseudomonas aeruginosa (investigate for underlying bronchiectasis)
  • Opportunistic gram-negative species
  • Staphylococcus aureus
  • Chlamydophila pneumonia
  • Mycoplasma pneumoniae
  • Legionella pneumophilia

Non-infectious (20-40%)

  • Heart failure
  • Pulmonary embolism
  • Non-pulmonary infections
  • Pneumothorax
  • Pneumonia

Precipitating and environmental factors

  • Cold air
  • Air pollution
  • Allergens
  • Tobacco smoking
  • Non-adherence to respiratory medication
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16
Q

What is the ddx to acute COPD exacerbation?

A
  • Asthma
  • Pulmonary Oedema
  • Upper respiratory tract obstruction
  • Pulmonary emboli
  • Anaphylaxis
  • Pneumothorax
  • Infection
17
Q

What is the Anthonisen Criteria for Infective COPD exacerbation?

A

+ve if 2/3

  • Increased dyspnoea
  • Increased sputum production
  • Increased purulence of sputum
18
Q

What is the management of COPD exacerbation?

A
  1. Secure airway via RSI and ETT insertion if imminent respiratory arrest
  2. Provide supplemental O2 – aim SpO2 88-92%
    - Should not aim for >92% because in chronic COPD –> O2 serves as a bronchodilator and will cause shunting of blood to poorly functioning alveoli!
    - Worsens V/Q mismatch and tips patient into Type 2 respiratory failure
  3. Nebulised Salbutamol (SABA) + ipratropium (SAMA) every 20min for 1 hour (3 cycles)
  4. Oral Prednisolone OR IV hydrocortisone
  5. Empirical Antibiotics
    - Criteria to initiate antibiotics: 2/3 of Anthonisen Criteria
    - Augmentin + Clarithromycin (TTSH) for 5-7/7
19
Q

What is the pressure settings of the ventilation used in type 1 respiratory failure ?

A

Positive End-Expiratory Pressure (PEEP)

  • Pressure imposed at the end of expiration: this ensures alveoli remain patent
  • Improves oxygenation
  • Used in type I respiratory failure
  • Alternatives: CPAP, EPAP
20
Q

What is the pressure settings of the ventilation used in type 2 respiratory failure ?

A

Bi-level Positive Airway Pressure (biPAP)

  • Has pressure both during inspiration and expiration
  • Inspiratory pressure: increases alveolar ventilation; reduces work of inhalation
  • Expiratory pressure: prevents airway collapse during exhalation, prolonging expiration and increases elimination of CO2; opens up small airways improving ventilation
  • Overall effect: improves tidal volume and minute ventilation
21
Q

What are the indications for non invasive ventilation?

A
  • Acute Pulmonary Edema
  • Acute exacerbation of COPD
  • Acute pneumonia in immunocompromised patient
  • NM abnormalities eg: MG
  • OSA

Indications at least one of the following:

  • 7.25≀ pH ≀7.35 and/or PaCO2 >6kPa (>45mmHg)
  • severe dyspnoea with clinical signs suggestive of respiratory muscles fatigue, use of respiratory accessory muscles, paradoxical movement of abdomen or retraction of inter-costal spaces
22
Q

What are the benefits and complications of non invasive ventilation?

A

Complications: pneumothorax, aspiration in patients with reduced consciousness, GI distension and perforation

Benefits: ↓ mortality, ↓ need for intubation, ↓ length of hospitalisation

23
Q

What is the indications for MEchanical ventilation?

A
  • If NIV fails
  • pH<7.25 (higher risk of failure)
  • Respiratory arrest, somnolence, severe
  • Hemodynamic instability
  • Massive aspiration /persistent vomiting
  • Persistent inability to clear respi secretions
  • Severe arrhythmia
24
Q

What are the indications for ICU admission?

A
  • Severe dyspnoea that response inadequately after initial emergency therapy
  • Changes in mental state (confusion, lethargy, coma)
  • Persistent or worsening hypoxaemia (PaO2 <5.3kPa/40mmHg) and/or severe or worsening respiratory acidosis (pH <7.25)
  • Need for mechanical ventilation
  • Haemodynamic instability – need for vasopressors