COPD PART 1 Flashcards
What is the mucosa of the lining of the lungs made from?
Epithelium - Ciliated pseudostratified columnar epithelial cells
Goblet cell - makes mucus
Lamina propria
What are the 2 parts of the lamina propria?
BM
Loose connective tissue
What is the submucosa (found under mucosa) made from?
Smooth muscle
Connective tissue
Bronchial mucinous Glands
Underneath the submucosa is the cartilage (Bronchi only)
Definition of COPD: Chronic bronchitis
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.
Epidemiology of Bronchitis
Usually co-exists with emphysema, causing COPD.
RFs for Bronchitis
- Smoking
- Exposure to air pollutants e.g. sulfur and nitrogen dioxide
- Exposure to dust and silica
- Family history of chronic bronchitis
What do irritants and chemicals do to airways?
- 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.
Whatr do irritants stimulate hypertrophy and hyperplasia in?
mucinous glands in the main bronchi, as well as the goblet cells in the bronchioles, which increases mucus production in both locations.
What happens since the bronchioles are smaller?
even a slight increase in mucus can lead to airway obstruction, which contributes to the majority of the air trapping.
What does smoking do to the cilia?
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.
What do people people with chronic bronchitis often present with?
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.
Overall what happens in COPD bronchitis
airway narrowing due to hyperplasia, inflammation and oedema.
What happens to the FVC, FEV1, FEV1:FVC ration and TLC in COPD bronchitis?
- 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
Signs of COPD bronchitis
- 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
Symptoms of COPD bronchitis
- Productive cough
- Dyspnoea
- Signs of CO2retention
- Drowsy
- Asterixis
- Confusion
Management of COPD Bronchitis
- Smoking cessation
- Management of associated illnesses
- Antibiotics for infections
- Supplemental oxygen
- Bronchodilators
- Inhaled steroids
Complications of COPD bronchitis
- 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
What is COPD?
Chronic obstructive pulmonary disease (COPD) describes progressive and irreversible obstructive airway disease.
It is a combination of emphysema and chronic bronchitis.
Epidemiology of COPD
- 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
RFs for COPD
- 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
What is COPD a combination of?
Emphysema + Chronic Bronchitis
What is emphysema?
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
What is bronchitis?
involves increased mucus secretion secondary to ciliary dysfunction and increased goblet number and size → lung parenchymal destruction → impaired gas exchange
In COPD what happens to the lungs?
- 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
What is V/Q (ventilation perfusion) mismatch due to?
- damage and mucus plugging of smaller airways from the chronic inflammation
- rapid closure of smaller airways in expiration due to the loss of elastic support
What does V/Q mismatch lead to?
- 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.
What is the drive for respiration?
At first CO2
As patient becomes desensitised to CO2 - hypoxaemia becomes drive for respiration
What are exacererbations?
Worsening of patients lung function - beyond normal day to day variations leading to change in medication
Often triggered by infections
Signs of COPD
Barrel chest
Tachypnoea
Cyanosis
Tar staining fingers
Downward displacement of liver
Cor pulmonale
Symptoms of COPD
Dyspnoea
Wheeze
Productive Cough
Chest tightness
Weight loss
Primary investigations for COPD
- 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)**
Other investigations to consider?
ECG and Echo
ABG
CT chest
Serum alpha 1- antitrypsin
What is COPD characterised by
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).
Airflow obstruction numbers:
If FEV1/FVC ration < 0.7 you have airway/airflow obstruction
What is the inflammatory process and cell signalling drivign COPD?
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
Gold Grades and severity of Airflow Obstruction in COPD for FEV1 ratio (With FEV1/FVC ratio <0.7)
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
Factors in decline of patient with COPD
- Dyspnoea
- Depression + Anxiety
- Exercise limitation
- Disability
- Personality and environment
Egs of Acute exacerbation
- Breathlessness
- Sputum quantity
- Sputum colour
- Sputum thickness
- Fever
Clubbing and end inspiratory crackles are suggestive of
pulmonary fibrosis
wheezing and hyper resonance on auscultation is suggestive of
COPD
Typical signs and symptoms of pulmonary oedema
Shortness of breath
Pink frothy sputum
Tachypnoea
Decreased oxygen saturations
Raised jugular venous pressure (JVP)
pulmonary oedema on auscultation would show ?
Reduced breath sounds and/or coarse crackles are associated with pulmonary oedema.
