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(Edited) Respiratory System > S8) COPD > Flashcards

S8) COPD Flashcards

1
Q

What is Chronic Obstructive Pulmonary Disease?

A

- COPD is a disease state which encompasses both emphysema and chronic bronchitis and is characterised by airflow limitation that is not fully reversible

  • Airflow limitation is progressive and associated with an abnormal inflammatory response of lungs to noxious particles/gases
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2
Q

What is emphysema?

A

Emphysema is a long-term, progressive disease of the lungs that primarily causes shortness of breath due to over-inflation of the alveoli

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3
Q

What is chronic bronchitis?

A

Chronic bronchitis is a chronic obstructive pulmonary disease involving a productive cough due to inflamed bronchial tubes and the overproduction of mucus

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4
Q

Describe the aetiology of COPD

A
  • Tobacco smoking (90% of cases)
  • Air pollution
  • Occupational exposure
  • Alpha-1 antitrypsin deficiency (rare)
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5
Q

Briefly, describe the pathophysiology of COPD

A
  • The host response to inhaled cigarette smoke and other noxious substances causes a chronic inflammatory process and oxidative injury
  • This affects central and peripheral airways, lung parenchyma, alveoli, and pulmonary vasculature
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6
Q

Describe 6 pathological changes which occur in COPD

A
  • Enlargement of mucus-secreting glands
  • Increased number of goblet cells
  • Ciliary dysfunction
  • Breakdown of elastin
  • Larger air spaces → reduced gas exchange
  • Vascular changes → pulmonary hypertension
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7
Q

What is the final pathological outcome of emphysema?

A
  • Elastin breakdown
  • Loss of alveolar integrity
  • Loss of elastic recoil
  • Permanent destructive enlargement of alveolar air spaces
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8
Q

What is the final pathological outcome of chronic bronchitis?

A
  • Inflammatory changes due to irritant (e.g. smoke) - similar to asthma but no IgE activity
  • Chronic cough for at least 3 months (productive)
  • Excessive mucus secretion (mucus glands & goblet cells)
  • Impaired removal of the sections (ciliary dysfunction)
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9
Q

Provide 3 reasons as to why the pathological changes in COPD lead to increased airway resistance

A
  • Luminal obstruction of airways by secretions
  • Narrowing of small bronchioles due to elastin break down (loss of radial traction)
  • Decreased elastic recoil leads to reduced expiratory force (air trapping)
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10
Q

In 5 steps, explain how pathological changes in COPD lead to pulmonary hypertension and right heart failure

A

⇒ Airway narrowing and destruction of lung parenchyma

⇒ Progressive hypoxia

⇒ Pulmonary vasoconstriction

⇒ Vascular smooth muscle thickening

⇒ Pulmonary hypertension (& right heart failure)

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11
Q

Identify 2 symptoms of COPD

A
  • Cough (morning, productive)
  • Breathlessness (initially on exertion, but progresses)
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12
Q

Identify and describe 5 signs of COPD

A
  • Tachypnoea – compensate for hypoxia and hypoventilation
  • Barrel chest – hyperinflation and air trapping due to incomplete expiration
  • Hyper-resonance on percussion – hyperinflation and air trapping
  • Reduced air entry – loss of lung elasticity and lung tissue breakdown
  • Wheezing
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13
Q

Identify and describe 3 late signs of COPD

A
  • Central cyanosis – respiratory failure
  • Flapping tremors – CO2 retention (hypercapnia)
  • Signs of right-sided heart failure (distended neck veins, hepatomegaly, ankle oedema) – pulmonary hypertension
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14
Q

Identify and describe 4 investigations for COPD

A
  • Spirometry – obstructive pattern with FEV1/FVC ratio <70%, limited reversibility following treatment with bronchodilators
  • Chest X-ray – hyper-inflated and hyperlucent lungs, flattened diaphragm, increased antero-posterior diameter of the chest
  • Pulse oximetry and/or ABG analysis – assess for hypoxia and hypercapnia
  • Alpha-1 antitrypsin level – atypical COPD (young patients and non-smokers)
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15
Q

Describe the conservative management of COPD

A
  • Smoking cessation
  • Patient education
  • Pneumococcal vaccination
  • Monitor patient weight, nutrition status and physical activity
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16
Q

Describe the specific management (pharmacological and surgical) of COPD

A
  • Bronchodilators
  • Inhaled corticosteroid
  • Pulmonary rehabilitation (exercise, disease education, nutritional advice)
  • Low dose oxygen therapy (long term – 16 hours per day)
  • Surgery (removal of large bullae, lung volume reduction, lung transplant)
17
Q

What is the acute exacerbation of COPD?

A

Acute exacerbation of COPD is an event characterised by a change in the patient’s baseline dyspnoea, cough, and/or sputum that is beyond normal day-to-day variations and is acute in onset

18
Q

How do patients with acute infectious exacerbations present?

A
  • Severe breathlessness
  • Fever
  • Chest pain
19
Q

What are some complications of COPD?

A
  • Recurrent pneumonia
  • Pneumothorax
  • Respiratory failure
  • Right sided heart failure
20
Q

Describe the management for the acute exacerbation of COPD

A
  • Pulse oximetry and ABG analysis (hypoxia and hypercapnia)
  • Antibiotics (Haemophillus influenzae, Strep pneumoniae)
  • Nebulised bronchodilators (SABA + SAMA (ipratropium))
  • Oral steroids
  • Low dose oxygen therapy (24-28%) if O2 < 92%
21
Q

Distinguish between asthma and COPD in terms of the following factors:

  • Family history
  • Atopy
  • Diurnal symptoms
  • Spirometry
A
22
Q

How does Alpha 1 antitrypsin deficiency cause emphysema and COPD?

A
  • Malformed or absent alpha 1 antitrypsin protein
  • Autosomal recessive
  • Function of protein is to balance elastase and protease in presence of inflammation
  • In absence elastase can breakdown elastin leading to destructin of alveolar walls → emphysema
23
Q

How do you get air trapping in emphysema?

A
  • During inhalation alveolus is able to expand with force (due to no elastic fibres)
  • Narrowed bronchioles due to loss of elasticity (during inhalation)
  • During exhalation: lack of recoil system and narrowed bronchioles causes air to become trapped → hard to breath out
24
Q

Why do we give patients with COPD very controlled amountws of oxygen and aim for a lower range of saturation?

A
  • In COPD, prelonged high CO2 that cant be corrected by hyperventilation → HCO3- released to balance pH
  • Chronic high CO2 but pH normal → brian wont detect changes in CO2 → lost this mechanism for driving respiraiton
  • Peripheral chemoreceptors less sensitive, require O2 to drop v low for hypoxia to drive respiration
  • If you overcorrect the oxygen you could remove hypoxic drive and respiration → RR can plummet

(Edited) Respiratory System (19 decks)

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