Chronic bronchitis, emphysema and COPD Flashcards

1
Q

What is the definition of bronchitis?

A

The inflammation of mucus membranes in the bronchial passages. This can either be acute (lasting from one to three weeks) or chronic (lasting at least 3 months of the year, 2 years in a row).

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2
Q

How is chronic bronchitis clinically defined?

A

Clinically defined as a productive cough (sputum) most days in at least 3 consecutive months for two or more consecutive years, without other underlying disease

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3
Q

What tends to cause chronic bronchitis?

A

Overexposure to lung irritants (e.g. tobacco exposure)

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4
Q

What is the pathophysiology of chronic bronchitis?

A

Due to sustained inflammation, physiological and functional changes occur which result in mucus hyper secretion (hypertrophy of mucus-secreting glands and hyperplasia of goblet cells). The combination of inflammation of the airways and mucus hypersecretion leads to obstruction to airflow through narrowing of the airways and excessive mucus.

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5
Q

What pathological findings do you see in chronic bronchitis?

A

Large airways

  • Mucous gland hypertrophy/hyperplasia
  • Goblet cell (secrete mucins) hyperplasia
  • Inflammation and fibrosis

Small airways

  • Goblet cell appearance - Goblet cells are not normally found in the smaller airways.
  • Inflammation and fibrosis.
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6
Q

What is emphysema?

A

A permanent increase in size of airspaces distal to the terminal bronchiole beyond their normal capacity. This arises either from dilatation or from destruction of the walls of the airspaces without obvious fibrosis.

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7
Q

How does emphysema occur?

A

It arises from destruction of alveoli beyond the terminal bronchiole. The alveoli (with their elastic fibres) hold the bronchiole open, similar to the way tent ropes hold up an awning. Destruction of the alveoli results in loss of elastic support, meaning the bronchioles become progressively collapsible, especially on expiration.

In severe cases, entire acini are lost, and large bullae form in the lung parenchyma.

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8
Q

How is emphysema classified pathologically?

A
  • Centriacinar
  • Panacinar
  • Periacinar
  • Irregular
  • Bullous
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9
Q

What is centriacinar emphysema?

A

Distension and damage is concentrated around the respiratory bronchioles, while more distal alveolar ducts and alveoli remain intact.

Very common; severe cases associated with limited airflow. It begins with bronchiolar dilatation, and then alveolar tissue loss.

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10
Q

What is panacinar emphysema?

A

Damage and distension affects the whole acinus (portion of the lung distal to a terminal bronchiole). This results in severe airflow and V/Q mismatch.

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11
Q

What deficiency is panacinar emphysema associated with?

A

Alpha-1 antitrypsin deficiency

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12
Q

What is periacinar emphysema?

A

Enlarged air spaces along the edge of the acinar unit, but only where it abuts against fixed structures such as pleura and vessels.

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13
Q

What are emphysematous bullae?

A

These are emphysematous space becomes greater than 1cm

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14
Q

How does smoking cause emphysema?

A

Chemicals in tobacco smoke cause an imbalance in the protease-antiprotease control system. Cigarette smoke encourages neutrophils to infiltrate the airways. It’s also thought to inhibit alpha1-antitrypsin activity.

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15
Q

What contributes to the development of emphysema?

A
  • Smoking
  • Ageing
  • Alpha1-antitrypsin deficiency
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16
Q

What is cor pulmonale?

A

Hypertrophy of the Right Ventricle resulting from disease affecting the function and/or the structure of the lung (Chronic lung disease which leads to chronic hypoxaemia).

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17
Q

How does cor pulmonale occur?

A

Chronic lung disease which leads to chronic hypoxaemia. This in turn causes vasoconstriction to occur across the entirety of the lung, increasing overall vascular pressure. This creates back pressure against the action of the heart, causing it to work harder, which causes the right ventricle to hypertrophy.

This can lead to cardiac failure as the heart begins to dilate.

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18
Q

If you saw this in someone with chronic lung diseasae, what might you suspect is happening?

A

Development of cor pulmonale

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19
Q

What blood changes may you see in someone with chronic hypoxaemia?

A

Polycythaemia

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20
Q

If you saw cor pulmonale on X-ray, what different causes would you think of?

A
  • COPD
  • Hypoventilation syndromes - scoliosis, neuromuscular disease, obesity
  • ILD
  • Long term high altitude exposure
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21
Q

Why do individuals get fluid overload in cor pulmonale?

A

Hypoxia is sensed by kidneys and carotid bodies, which increases sympathetic activity and renal vasoconstriction. Sympathetic activation (plus other mechanisms) leads to renal retention of salt and water. In the context of chronic hypoxia, vasculature becomes more permeable, which leads to fluid extravasation.

This, combined with increased fluid volume, presents clinically as increased JVP and ankle oedema. These features are not due to impaired cardiac output

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22
Q

What is Chronic obstructive pulmonary disease?

A

Chronic obstructive pulmonary disease (COPD) is a chronic, slowly progressive disorder characterised by airflow obstruction that does not change markedly over several months. Most of the lung function impairment is fixed, although some reversibility can be produced by bronchodilator (or other) therapy

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23
Q

What are thought to be the causes of COPD?

A
  • Smoking (85-95%)
  • Chronic asthma
  • Air pollution
  • Occupation
  • Alpha1-antitrypsin deficiency
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24
Q

What is the general pathology of COPD?

A
  • Mucus gland hyperplasia
  • Chronic inflammation and fibrosis
  • Emphysema
  • Thickened pulmonary arteriolar wall and remodelling
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25
Q

What are symptoms of COPD?

A
  • Dyspnoea - exertional
  • Chronic cough - may be productive
  • Decreased exercise tolerance
  • Wheeze
  • Chest tightness
  • Peripheral oedema
  • Orthopnoea
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26
Q

What colour is the sputum produced by someone with COPD?

A

Clear or mucoid

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27
Q

What signs may you see in someone with COPD?

A
  • Cyanosis
  • Asterixis - CO2 retention
  • Barrel chest
  • Decreased chest expansion
  • Tachypnoea
  • Pursed lip breathing
  • Quiet breath sounds +/- wheeze
  • Quiet heart sounds - due to lung hyperinflation
  • Signs of cor pulmonale
  • Paradoxical breathing
  • Tracheal tug
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28
Q

What might you see in someone with COPD that uses ß2 agonist?

A

Fine tremor

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29
Q

What are signs of Cor pulmonale?

A
  • Increased JVP
  • Hepatomegaly
  • Ascites
  • Ankle oedema
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30
Q

What are signs of chronic CO2 retention?

A
  • Warm peripheries
  • Plethoric conjunctivae
  • Bounding pulse
  • Possible Asterixis
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31
Q

What is pursed lip breathing?

A

A breathing practice, often taught, which includes a long, slow expiration against pursed lips.

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32
Q

What is the mechanism behind pursed lip breathing?

A

Pursing the lips allows the patient to breathe against resistance, thus maintaining a slow exhalation back pressure within the lungs. This helps keep bronchioles and small airways open for much-needed oxygen exchange. As such, it allows deeper breathing and improved V/Q matching

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33
Q

What is barrel chest?

A

A ratio of anteroposterior (AP) to lateral chest diameter of greater than 0.9. The normal AP diameter should be less than the lateral diameter and the ratio of AP to lateral should lie between 0.70 and 0.75.

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34
Q

What is the mechanism behind the development of a barrell chest?

A

Considered to be due to over-activity of the scalene and sternocleidomastoid muscles, which lift the upper ribs and sternum. With time, this overuse causes remodelling of the chest.

In chronic obstructive pulmonary disease, there is a chronic airflow limitation that results in increased end-expiratory volumes and chronic hyperinflation.

Chronic hyperinflation reduces airway resistance and improves elastic recoil at the expense of higher lung volumes. Over time this leads to chest wall remodelling and barrel chest abnormality.

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35
Q

What is the mechanism behind patients with COPD experiencing orthopnoea?

A

Increased inspiratory effort owing to intrinsic PEEP and increased airways resistance in the supine position is proposed to contribute to orthopnoea in COPD. As a result of higher end-expiratory pressures, more work is required to take in air on inspiration.

Dynamic flow limitation is exacerbated by lying flat, as is tidal breathing. It thus may contribute to hyperinflation, intrinsic PEEP, inspiratory work and the development of orthopnoea.

36
Q

What is the mechanism behind paradoxical breathing seen in those with COPD?

A

As the diaphragm tires, accessory muscles assume a larger role in breathing. In an effort to overcome airway obstruction, the accessory muscles produce greater negative intrathoracic pressure on inspiration. This negative pressure sucks the chest inwards on inspiration (particularly in children with compliant chest walls).

This negative pressure may also pull the diaphragm upwards, causing the abdomen to move inwards instead of out on inspiration

37
Q

What is the mechanism behind tracheal tug in COPD?

A

Campbell’s Sign

This is downward displacement of the thyroid cartilage during inspiration.

Patients in respiratory distress have increased work of breathing and the movements of the chest wall, muscles and diaphragm are transmitted along the trachea, pulling it rhythmically downwards.

https://studentconsult.inkling.com/read/dennis-mechanisms-clinical-signs-2nd/chapter-2/9780729542371-0009

38
Q

If you suspected someone had COPD, how would you investigate them?

A
  • Bedside - PFTs, ECG
  • Bloods - FBC, TFTs, Alpha1-antitrypsin
  • Imaging - CXR
  • Sputum culture
  • Consider ECHO if cor pulmonale suspected
39
Q

What may you see on spirometry in someone with COPD?

A
  • < 80% predicted FEV1
  • FEV1/FVC ratio <70%
40
Q

How would you classify the degree of airflow obstruction based on FEV1 in someone with COPD?

A
  • >/= 80% - Mild
  • 50-79% - Moderate
  • 30-49% - Severe
  • <30% - Very Severe
41
Q

What symptoms might someone with moderate airflow obstruction have if it was caused by COPD?

A
  • Cough
  • SOB with moderate exertion
42
Q

What symptoms might someone with severe airflow obstruction have if it was caused by COPD?

A
  • SOB with mild exertion
  • Cough +/- sputum
43
Q

What symptoms might someone have with very severe air flow obstruction caused by COPD?

A
  • SOBOE
  • Wheeze
  • Cough +/- sputum
  • Signs of cor pulmonale
44
Q

When looking at lung volumes, what might you see in someone with COPD?

A

Evidence of gas trapping

  • Increased RV
  • Increased TLC
  • RV/TLC > 30%
45
Q

When looking at gas transfer, what might you see in someone with COPD?

A

Decreased TCO and KCO

This indicates impaired gas transfer

46
Q

Why is gas transfer impaired in someone with COPD?

A

Interstitial parenchymal destruction leads to impaired diffusion

47
Q

If you were investigating someone for suspected COPD, what would you find by doing bronchodilator/minimal coritcosteroid reversibility testing?

A

Minimal revesibility - Significant response indicates asthma

48
Q

When looking at a CXR of someone with COPD, what might you see?

A
  • Hyperinflation (> 7 posterior ribs)
  • Flattened diaphragm
  • Lucent lung fields
  • Bullae - especially in apices
  • Prominent pulmonary vessels - if pulmonary HTN
  • Decreased peripheral vascular markings
49
Q

What might you see in the FBC in someone with COPD?

A
  • Anaemia
  • Secondary polycythaemia
50
Q

What might you see on an ECG in someone with COPD?

A

Signs of cor pulmonale

  • Right axis deviaton
  • Peaked P waves - atrial hypertrophy
  • Shift in transition point towards V5/V6
51
Q

If you used blood gases to as part of you investigation of someone with COPD, what might you find?

A
  • Normal
  • Decreased PaO2 = Type I respiratory Failure
  • Decreased PaO2, increased PaCO2 = Type II respiratory failure
52
Q

What is the diagnosis of COPD based on?

A
  • History of smoking
  • Progressive dyspnoea
  • Evidence of irreversible airflow obstruction on spirometry
53
Q

How does COPD differ symptomatically from asthma?

A
  • Chronic productive cough - not in asthma
  • Breathlessness progressive and persistent - asthma is variable
54
Q

If someone was said to have grade 1 dyspnoea based on the MRC grading scale, what would this mean?

A

Not troubled by breathlessness except for on strenuous exertion

55
Q

If someone was said to have grade 2 dyspnoea based on the MRC grading scale, what would this mean?

A

Short of breath when hurrying or walking up hill

56
Q

If someone was said to have grade 3 dyspnoea based on the MRC grading scale, what would this mean?

A

Walks slower than others on level ground due to breathlessness or has to stop to catch breath when walking at own pace

57
Q

If someone was said to have grade 4 dyspnoea based on the MRC grading scale, what would this mean?

A

Stops for breath after walking about 100 m or after a few minutes on level ground

58
Q

If someone was said to have grade 5 dyspnoea based on the MRC grading scale, what would this mean?

A

Too breathless to leave the house, or breathless when dressing/undressing

59
Q

What non-pharmocological measures could you employ when treating someone with COPD?

A
  • Smoking cessation
  • Vaccinations
  • Pulmonary rehabilitation
  • Nutritional advice
  • Psychological support
60
Q

What is involved in pulmonary rehabilitation?

A
  • Graded exercise to improve lower limb muscle function
  • Breathing techniques
  • Education
61
Q

What medications would initially prescribe someone who had been diagnosed with COPD?

A

SABA or SAMA

62
Q

In patients who remain symptomatic after being started on a SABA/SAMA, what would you do before considering which treatment to start them on?

A

Assess their FEV1

63
Q

If someone was on a SABA/SAMA for COPD remained symptomatic after starting initial treatment, and they had an FEV1 of <50%, what treatment would you give them?

A
  • Try LABA with ICS in an inhaler combination
  • Offer LAMA in place of SAMA
64
Q

If someone was on a SABA/SAMA for COPD remained symptomatic after starting initial treatment, and they had an FEV1 of >/=50%, what treatment would you give them?

A

LABA or LAMA

65
Q

If somone with COPD with an FEV1 <50% who was being treated with LABA + ICS, what would be your next step?

A

LAMA + LABA + ICS

66
Q

If somone with COPD with an FEV1 >50% who was being treated with LABA + ICS, what would be your next step?

A

LABA + LAMA + ICS

67
Q

When should inhaled steroids be prescribed in COPD?

A

All patients with a FEV1 < 60% predicted, who have had two or more exacerbations per year requiring treatment with antibiotics or oral steroids

68
Q

When would you consider starting someone on long-term oxygen therapy?

A

PaO2 <7.3 kPa

Or

PaO2 7.3 - 8 kPa, plus any of:

  • 2o polycythaemia
  • Peripheral oedema
  • PHT
  • Nocturnal hypoxia

Use for a minimum of 15 hrs per day - low flow (2-4 L/min)

69
Q

What vaccinations would you give someone with COPD?

A
  • Influenza
  • Penumococcal
70
Q

What mucolytics could you give someone with a productive cough?

A
  • Carbocisteine
  • Mecysteine Hydrochloride
71
Q

What are complications of COPD?

A
  • Acute exacerbation
  • Micro-nutrient deficiency/Weight loss/muscle atrophy - hypermetabolic state
  • Polycythaemia
  • PHT
  • Cor Pulmonale
  • Depression
  • Pneumothorax
72
Q

What is alpha1-antitryspin?

A

Glycoprotein protease inhibitor produced by the liver. It is secreted into the blood stream where it is transported to the lungs, where it opposes neutrophil elastase

73
Q

What is the following sign and what does it suggest?

A

Dahl’s Dign/Tripod position

This sign is seen in long-term, chronic respiratory illness. It is caused by patients spending long periods of time in the tripod position (i.e. with elbows resting on the epidermis of the thighs), resulting in hyperpigmented, hyperkeratotic plaques.

It is most commonly associated with COPD

74
Q

What is the type of V/Q mismatch which occurs in chronic bronchitis?

A

Pulmonary Shunting

75
Q

What is a blue bloater?

A

Patients with predominantly chornic bronchitic COPD

76
Q

What causes blue bloaters to be blue?

A

V/Q mismatch seen (shunting - normal perfusion, decreased ventilation) leads to hypoxaemia and hypercapnia, causing respiratory acidosis and 2o polycythaemia. These contribute to cyanosis (BLUE).

77
Q

What causes blue bloaters to be bloated?

A

Pulmonary vasculature vasoconstricts to divert flow to better ventilated areas, but in chornic bornchitis this can happen to such a degree that it causes pulmonary hypertension. This causes back pressure into the right side of the heart (RHF - cor pulmonale, increased JVP, peripheral oedema), and decreased LV output. This decreases circulating volume, activation of the RAAS system, and subsequent fluid retention.

78
Q

What type of respiratory failure occurs in COPD?

A

Type II - hypoxaemia and hypercapnia - respiratory acidosis results

79
Q

What is a pink puffer?

A

Those with predominantly ephysemic COPD

80
Q

Why do pink puffers puff?

A

To create back pressure into the alveoli to keep them open during expiration, as they are more prone to collapsing due to elastase breakdown

81
Q

Why are pink puffers pink?

A

They have less hypoxaemia than blue bloaters, therefore do not struggle with cyanosis

82
Q

Why might pink puffers have increased TLC?

A

Due to gas trapping caused by emphysemic pathology

83
Q

Why can those with COPD become cachexic?

A

This occurs in severe disease - combination of oxidative stress, increasingly anaerobic metabolism and inflammation increases energy expenditure in relation to intake, which favours catabolism and thus weight loss

84
Q

What type of V/Q mismatch occurs in emphysema (pink puffers)?

A

Both V and Q decrease - Global V/Q deficit

85
Q

What factors contribute to the sensation of dyspnoea in COPD?

A
  • Hypoxaemia - stimulate peripheral chemoreceptors -> increases ventilatory drive
  • Hypercapnia - directly cause ‘air hunger’ but also increased central ventilatory drive (to blow off carbon dioxide)
  • Increased airways resistance and hyperinflation - increased the load the respiratory muscles must work against, thereby stimulating muscle receptors.
  • Deconditioning via increased lactic acidosis - further contribute to dyspnoea.