COPD PART 2 Flashcards

1
Q

General management for COPD

A
  • Smoking cessation: offer nicotine replacement, varenicline or bupropion
  • Pulmonary rehabilitation: for patients who are self-perceived as functionally disabled by COPD (e.g. MRC grade ≥3)
  • Vaccinations: one-offpneumococcaland annualinfluenza
  • Good diet and exercise: esp if obese
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2
Q

Key pharmacological management for COPD

A
  • SABA:short-acting beta2-agonist (e.g. salbutamol)
  • SAMA: short-acting muscarinic antagonist (ipratropium)
  • LABA: long-acting beta-agonist (e.g. salmeterol)
  • LAMA: long-acting muscarinic antagonist (e.g. tiotropium)
  • ICS: inhaled corticosteroid (e.g. beclometasone)
  • Combination inhaler (Some or all LABA/LAMA ICS)
  • Mucolytics (carbocisteine_
  • Systemic corticosteroids (prednisolone)
  • Azithromyocin
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3
Q

Initial Management according to NICE for COPD

A

SABA/SAMA - inhaler

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4
Q

Management if symptoms persist according to NICE

A

If there are no features of asthma: LABA + LAMA - long acting bronchodilators - improve lung function, dyspnoea, exacerbations

If there are features of asthma: LABA + ICS

  • If symptoms still persist: LABA + LAMA + ICS
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5
Q

Additional therapies

A

Nebulisers
Theophylline
Surgery
Oral mucolytic therapy
Phosphodiesterase -4 inhibitors

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6
Q

Complications of COPD

A
  • Pulmonary Hypertension
  • Cor pulmonale
  • Pneumothorax
  • Respiratory failure
  • Exacerbation
  • Secondry polycythaemia
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7
Q

What is COPD emphysema?

A

alveolar air sacs become damaged or destroyed.

alveoli permanently enlarge and lose elasticity, and as a result, individuals typically have difficulty with exhaling, which depends heavily on the ability of lungs to recoil.

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8
Q

RFs for COPD emphysema

A

Smoking
Emphysema usually co -exists whith chronic bronchitis

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9
Q

What happens in normal airflow?

A

oxygen flows out of the alveoli and into the blood while carbon dioxide makes the reverse commute.

  • Normally, there is a low pressure environment in the airways
  • elastin in the walls prevents the lungs from collapsing inwards in a low pressure environment
  • allows air to be exhaled out
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10
Q

What happens when lung tissue is exposed to irritants (smoke)

A

Triggers inflammatory reaction

Inflammatory reactions attract various immune cells which release inflammatory chemicals as well as proteases e.g. elastases and collagenases.

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11
Q

What happens in emphysema?

A

elastin is lost which causes collapse.
This results in:

  • Air-trapping distal to the point of collapse
  • The lungs becoming more compliant - when air is inhaled, the lungs easily expand and hold onto that air.
  • Breakdown of the thin alveolar walls - septa. This reduces the surface area for gas exchange.
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12
Q

Over time what happens in emphysema

A

Over time, as more and more lung tissue is affected, emphysema can lead to hypoxemia.

This leads to hypoxic vasoconstriction to navigate blood flow away from damaged lung tissue.

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13
Q

Types of emphysema

A
  • Centriacinar
  • Panacinar
  • Paraseptal
  • Irregular
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14
Q

Centriacinar empyhsema

A

most common pattern. Only damages the central or proximal alveoli of the acinus. It also typically affects the upper lobes of the lungs. This is usually due to smoking.

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15
Q

Panacinar emphysema

A
  • entire acinus is uniformly affected and typically affects the lower lobes of the lungs.
  • Often associated with alpha-1 antitrypsin deficiency.
  • Alpha-1 antitrypsin is a protease inhibitor and protects collagen and elastin. Without it, the proteases are able to break down the alveolar walls
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16
Q

Paraseptal emphysema

A

distal alveoli of the acinus are most affected. Typically affects the lung tissue on the periphery of the lobules.

17
Q

Irregular emphysema

A

scarring and damage that affects the lung parenchyma
patchily, independent of acinar structure

18
Q

COPD lab results

A
  • FVC (max air exhaled in one breath): lowered
  • FEV1 (first second of air breathed out in a single breath): lowered, more than the FVC
  • FEV1:FVC ratio: lowered
  • TLC (total lung capacity): increased due to air trapping
19
Q

Signs of emphysema

A
  • Breathing with pursed lips
  • Barrel shaped chest
  • Downward displacement of liver
  • Cardiac dullness
20
Q

Symptoms of emphysema

A
  • Dyspnoea
  • Cough: could be productive
  • Weight loss: due to energy expenditure while breathing
  • Signs of CO2retention
    • Drowsy
    • Asterixis
    • Confusion
21
Q

Management for emphysema

A
  • Smoking cessation
  • Supplemental oxygen
  • Bronchodilators
  • Inhaled steroids
  • Antibiotics: for secondary infections
22
Q

Complications of emphysema

A
  • Pneumothorax: the distal enlarged alveoli in paraseptal emphysema can rupture and cause a pneumothorax.
  • Cor pulmonale and right-sided heart failure: extensive vasoconstriction causes pulmonary hypertension and puts pressure on right ventricle
23
Q

Differential Diagnosis for COPD

A

▶ Heart failure
▶ Pulmonary embolus
▶ Pneumonia
▶ Lung cancer
▶ Asthma
▶ Bronchiectasis
▶MI
▶ Pneumothorax
▶ Cardiac arrythmia

24
Q

What has the greatest capacity to influence COPD?

A

Smoking cessation - healthcare providers should tell people to quit
Pharmacotherapy and nicotine replacement help with long term smoking abstinence rates
Need regular activity and remain active

25
Q

What have none of the existing medications for COPD done?

A

Shown conclusively to modify long term decline in lung function

26
Q

When should you add ICS to long acting bronchodilators (Strongly favours)

A

Strongly favours use - History of hospitalisations for exacerbations of COPD, 2 or more moderate exacer of COPD per year, blood eosinophils more than 300cells/uL
History of or concomitant asthma

27
Q

What factors favor use of ICS in long acting bronchodilators? (Mildly favors)

A

1 moderate exacerbation of COPD per year
Blood eosinophils 100 to < 300 cell /uL

28
Q

Against use of ICS with long-acting bronchodilators

A

Repeated pneumonia events
Blood eosinophils < 100cells/ uL
History of mycobacterial infection

29
Q

Management of COPD exacerbation

A

Bronchodilators
▶ Salbutamol (SABA)
▶ +/- Ipratropium (SAMA)

▶ Systemic corticosteroids
▶ Antibiotics if signs of infection

30
Q

When should you use non-invasive ventilation?

A

▶ Respiratory acidosis
▶ Hypercapnia
▶ Hypoxaemia despite oxygen

Improves respiratory acidosis, decreases respiratory rate, severity of dyspnoea, complications and length of hospital stay.
Decreases mortality and needs for intubation

31
Q

What is emphysema?

A

involves loss of alveolar integrity due to an imbalance between proteases and protease inhibitors (e.g. alpha-1 antitrypsin) triggered by chronic inflammation, such as smoking, which causes elastin breakdown