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COPD Flashcards

1
Q

What is the mucosa of the lining of the lungs made from?

A

Epithelium - Ciliated pseudostratified columnar epithelial cells
Goblet cell - makes mucus
Lamina propria

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2
Q

What are the 2 parts of the lamina propria?

A

BM
Loose connective tissue

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3
Q

What is the submucosa (found under mucosa) made from?

A

Smooth muscle
Connective tissue
Bronchial mucinous Glands

Underneath the submucosa is the cartilage (Bronchi only)

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4
Q

Definition of COPD: Chronic bronchitis

A

Bronchitis means inflammation of the bronchial tubes in the lung.

It is said to be chronic when it causes a productive cough for at least 3 months each year for 2 or more years.

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5
Q

Epidemiology of Bronchitis

A

Usually co-exists with emphysema, causing COPD.

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6
Q

RFs for Bronchitis

A
  • Smoking
  • Exposure to air pollutants e.g. sulfur and nitrogen dioxide
  • Exposure to dust and silica
  • Family history of chronic bronchitis
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7
Q

What do irritants and chemicals do to airways?

A
  • Infiltrate walls with inflammatory cells
  • epithelial layers becomes ulcerated + with time > columnar cells become squaumous epithelium
  • inflammation is followed by scarring and thickening of the walls, which narrows the small airways.
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8
Q

Whatr do irritants stimulate hypertrophy and hyperplasia in?

A

mucinous glands in the main bronchi, as well as the goblet cells in the bronchioles, which increases mucus production in both locations.

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9
Q

What happens since the bronchioles are smaller?

A

even a slight increase in mucus can lead to airway obstruction, which contributes to the majority of the air trapping.

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10
Q

What does smoking do to the cilia?

A

Makes it shorter and less mobile, making it harder to move mucus up and out of bronchioles. A cough is sometimes the only way to clear this mucus.

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11
Q

What do people people with chronic bronchitis often present with?

A

Hypoxemia + Hypercapnia

because the mucus plugs block airflow, causing high levels of CO2 and low levels of O2 in the lung so less O2 moves into blood and less CO2 moves out of blood.

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12
Q

Overall what happens in COPD bronchitis

A

airway narrowing due to hyperplasia, inflammation and oedema.

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13
Q

What happens to the FVC, FEV1, FEV1:FVC ration and TLC in COPD bronchitis?

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
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14
Q

Signs of COPD bronchitis

A
  • Wheeze: due to narrowing of the passageway available for air to move in and out
  • Crackles or rales: caused by the popping open of small airways
  • Cyanosis (blue bloaters): if there is buildup of CO2 in blood
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15
Q

Symptoms of COPD bronchitis

A
  • Productive cough
  • Dyspnoea
  • Signs of CO2retention
    • Drowsy
    • Asterixis
    • Confusion
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16
Q

Management of COPD Bronchitis

A
  • Smoking cessation
  • Management of associated illnesses
  • Antibiotics for infections
  • Supplemental oxygen
  • Bronchodilators
  • Inhaled steroids
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17
Q

Complications of COPD bronchitis

A
  • Cor pulmonale and right sided heart failure: vasoconstriction leads to pulmonary hypertension which affects the functioning of the right ventricle.
  • Lung infections: can develop behind the mucus plugs
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18
Q

What is COPD?

A

Chronic obstructive pulmonary disease (COPD) describes progressive and irreversible obstructive airway disease.

It is a combination of emphysema and chronic bronchitis.

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19
Q

What is COPD characterised by

A

persistent respiratory symptoms (such as breathlessness, cough, and sputum) and airflow obstruction (usually progressive and not fully reversible).

Results from chronic inflammation caused by exposure to noxious particles or gases (usually tobacco smoke but also from environmental and occupational exposures).

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20
Q

Epidemiology of COPD

A
  • There are 1.2 million people with COPD living in the UK
  • COPD is the fourth leading cause of death globally
  • Usually diagnosed >45 years
  • 28,600 deaths on average
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21
Q

RFs for COPD

A
  • Age:usually diagnosed after the age of 45
  • Tobacco smoking: the single greatest risk factor for COPD
  • Air pollution
  • Occupational exposure: such as dust, cadmium (in smelting), coal, cotton, cement and grain
  • Alpha-1 antitrypsin deficieny: younger patients present with features of COPD
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22
Q

Airflow obstruction numbers:

A

If FEV1/FVC ration < 0.7 you have airway/airflow obstruction

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23
Q

What is COPD a combination of?

A

Emphysema + Chronic Bronchitis

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24
Q

What is the inflammatory process and cell signalling drivign COPD?

A

factors driving inflammation (Autoimmunity, bacteria, particles) bind to cell surface receptor of immune cell (Macrophage, T cell, Neutrophil)

Activates intracellular signalling (NFkBeta and STAT3 pathway leading to the activation of:

Cytokines (TNFa, IL-1,IL-6)
ROS
Proteases - NE, MMPS

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25
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

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26
Q

What is bronchitis?

A

involves increased mucus secretion secondary to ciliary dysfunction and increased goblet number and size → lung parenchymal destruction → impaired gas exchange

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27
Q

In COPD what happens to the lungs?

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
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28
Q

What is V/Q (ventilation perfusion) mismatch due to?

A
  • damage and mucus plugging of smaller airways from the chronic inflammation
  • rapid closure of smaller airways in expiration owing to the loss of elastic support
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29
Q

What does V/Q mismatch lead to?

A

fall in PaO2 and increased respiration.

Usually PaCO2 is unaffected until patient’s are unable to maintain their respiratory efforts.

Buildup of CO2 leads to cyanosis.

30
Q

What is the drive for respiration?

A

At first CO2
As patient becomes desensitised to CO2 - hypoxaemia becomes drive for respiration

31
Q

What are exacererbations?

A

Worsening of patients lung function - beyond normal day to day variations leading to change in medication
Often triggered by infections

32
Q

Egs of Acute exacerbation

A

Breathlessness
Sputum quantity
Sputum colour
Sputum thickness
Fever

33
Q

Gold Grades and severity of Airflow Obstruction in COPD for FEV1 ratio (With FEV1/FVC ratio <0.7)

A

Gold 1 (Mild) - FEV1 >_ 80% predicted
Gold 2 (Moderate) - 50%<_ FEV1 < 80% predicted
Gold 3 severe - 30%<_ FEV1< 50% predicted
Gold 4 (V.Severe) - FEV1< 30% precited

34
Q

Signs of COPD

A

Barrel chest
Tachypnoea
Cyanosis
Tar staining fingers
Downward displacement of liver
Cor pulmonale

35
Q

Symptoms of COPD

A

Dyspnoea
Wheeze
Productive Cough
Chest tightness
Weight loss

36
Q

Factors in decline of patient with COPD

A

Dyspnoea
Depression + Anxiety
Exercise limitation
Disability
Personality and environment

37
Q

Primary investigations for COPD

A
  • Spirometry and bronchodilator reversibility (BDR): FEV1/FVC<0.70; bronchodilator will not reverse symptoms.
  • Chest X-ray: flattened diaphragm, hyperinflation and bullae. Should also be performed to see if there is evidence of lung cancer.
  • FBC: COPD causes chronic hypoxia which may result in secondary polycythaemia; also required to determine if eosinophilia is present.
  • Calculate body mass index (BMI): as a baseline to later assess weight loss (e.g. cancer or severe COPD) or weight gain (e.g. steroids)
  • ECG
  • Sputum culture
  • ABG
  • ** Inflammatory markers (calcitonin)**
38
Q

Other investigations to consider?

A

ECG and Echo
ABG
CT chest
Serum alpha 1- antitrypsin

39
Q

Classification for COPD

A

Look it up

40
Q

Differential Diagnosis for COPD

A

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

41
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
42
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

43
Q

What have none of the existing medications for COPD done?

A

Shown conclusively to modify long term decline in lung function

44
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
45
Q

Initial Management according to NICE for COPD

A

SABA/SAMA - inhaler

46
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
47
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

48
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

49
Q

Against use of ICS with long-acting bronchodilators

A

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

50
Q

Management of COPD exacerbation

A

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

▶ Systemic corticosteroids
▶ Antibiotics if signs of infection

51
Q

Additional therapies

A

Nebulisers
Theophylline
Surgery
Oral mucolytic therapy
Phosphodiesterase -4 inhibitors

52
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

53
Q

Complications of COPD

A

Pulmonary Hypertension
Cor pulmonale
Pneumothorax
Respiratory failure
Exacerbation
Secondry polycythaemia

54
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.

55
Q

RFs for COPD emphysema

A

Smoking
Emphysema usually co -exists whith chronic bronchitis

56
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 and elastin in the walls prevents the lungs from collapsing inwards in a low pressure environment. This allows air to be exhaled out.

57
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.

58
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.
59
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.

60
Q

Types of emphysema

A

Centriacinar
Panacinar
Paraseptal
Irregular

61
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.

62
Q

Pacinar 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

63
Q

Paraseptal emphysema

A

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

64
Q

Irregular emphysema

A

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

65
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
66
Q

Signs of emphysema

A

Breathing with pursed lips
Barrel shaped chest
Downward displacement of liver
Cardiac dullness

67
Q

Symptoms of emphysema

A
  • Dyspnoea
  • Cough: could be productive
  • Weight loss: due to energy expenditure while breathing
  • Signs of CO2retention
    • Drowsy
    • Asterixis
    • Confusion
68
Q

Management for emphysema

A
  • Smoking cessation
  • Supplemental oxygen
  • Bronchodilators
  • Inhaled steroids
  • Antibiotics: for secondary infections
69
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
70
Q

Management of COPD exacerbation

A

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

▶ Systemic corticosteroids
▶ Antibiotics if signs of infection

Respiratory (21 decks)

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