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COPD - Coggle Diagram
COPD
COPD - Chronic Obstructive Pulmonary Disease
- SPECTRUM of Emphysema & CB
- COPD has mixed features of both
- UNCOMMON
- Isolated emphysema and pure chronic bronchitis are relatively uncommon;
- Most patients have combination of both
- Having one is a risk factor for the other
Epidemiology
- Prevalence 1/20 MA - 5% prevalence among middle-aged (>45yo) population
- 5th Leading cause for Mortality - 5th leading cause of death
RISK FACTORS
- MODIFIABLE
- Inhalation of Chronic Irritants
- Pollution
- Tobacco Smoking
- Severe Childhood Pneumonia
- NON-MODIFIABLE
- Age
- Family History
Differentiating Clinical Findings suggestive of COPD
- May have concurrent asthma
- SoB - Breathlessness and Wheeze
- Smoking Hx or Occupationl Hx - Seek for evidence of smoking or history of chronic irritation
- EMPHYSEMA = Seek Family history - Their are genetic polymorphisms associated with hereditary emphysema
Chronic Bronchitis (Blue Bloater)
- Clinically Definition (1);
- Cough + productive sputum
- On most days
- For three months of the year
- For two consecutive years
- Susepectible to seasonal infection
- Clinical Definition (2)
- Irreversibly reduced FEV
- Below 80% - Reduced Ratio of FEV/FVC to less than 80% of what is expected
Clinical Features
Blue Bloater
- Blue - becomes desensitised to hypercapnic state and respiratory drive depreciates = hypoxic blue
- Bloater - secondary to compromised pulmonary vasculature, they develop cor pulmonale and see to bloat
-
Clinical Correlations and Complications
- HYPERSECRETION - of mucous in dilated airways
- IMPAIRED Mucocilliary Clearance - there are two mechanisms which mediate this change
- Smoking impairs action of mucocilliary escalator
- Irritation leads to diminished number of cilliated cells
- Environment conducive to Infection - increased mucin, impaired clearance and airway dilatation
- Compromised Gas Exchange - increased distance across which diffusion must occur
- Oxygen transfer is more severely impacted (since O2 has reduced H20 permeability
- Disordered Gas Transfer impacts pulmonary blood flow - perfusion regulated by gas partial pressures
Cor Pulmonale - RHF
- Disorder gas transfer and impacted perfusion
- Obliteration of vascular supply/routes causes pulmonary Hypertension
- Reduced cross-sectional SA
- Unchanged volume of Blood
- Increased Blood Pressure
Squamous Metaplasia
- Cilliated columnar epithelium to squamous in response to chronic irritant
- DYSPLASIA - Possible progression to dysplasia =malignancy
- Abnromal gene expression increases the likelihood of undergoing a mutation
Increase in Acute Infective Episodes
- Haemophilus Influenzae is a common culprit
- Superimposed infective exacerbations are a secondary concern
Secondary Fibrosis of bronchiole lumen
- Fibroblasts proliferate in inadequate attempts at healing
Chronic Hypoxia = Secondary Polycythaemia
- Increased blood viscosity, a diathetic cause of systemic hypertension
AetioPathogensis
Micro-pathology observed in Chronic Bronchitis reflects the efforts made by the body to maintain homeostasis when exposed to chronic irritation
0. Exposure to Chronic Irritant
1. Hypertrophy of Mucous Glands and Hypersecretion of Mucin
- Increased mucin production in an effort to protect epithelium from irritant
- Hypersecretion w/o eosinophils - not a hypersensitivity reaction as seen in Asthma
2. Hyperplasia and Expansion of Goblet Cells
- Goblet cells occupy greater portion of epithelium
- Goblet cells extend into terminal bronchioles
3. Replacement of Ciliated Cells
- Goblet cell hyperplasia and glandular hypertrophy replace cilliateed cells
- Impaired Mucocilliary Escalator
- This reduces number of cilliated cells operating the mucocilliary escalator
- Additionally, tobacco smoke also impairs the efficacy of mucocilliary clearance
- 1 more item...
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Emphysema - (Pink Puffer)
- Pathological Definition
- Small Airway Ectasia - Permanent Pathological dilatation of airways distal to terminal bronchiole
- Vessel Destruction - airway walls damaged
- Lost Elastic Recoil - Damaged parenchyma diminishes elastic recoil (lowered FEV) whilst increasing compliance
- Air Trapping and Obstruction - air becomes trapped within the small airways and obstructs exhalation
- No interstitial fibrosis
Aetiology
Two Scenarios
- ACCUMULATION of neutrophils and macrophages in respiratory bronchioles
- GENETIC predisposition
Primary Emphysema
Genetic Predisposition - LESS COMMON
Caused by an ⍺1-antitrypsin deficiency
- Role of ⍺1-antitrypsin - antiprotease that counteracts the effects of protease enzymes, which are capable of breaking down elastin fibres
- Homozygous form
- (10% of normal ⍺1-antitrypsin levels)
- Heterozygous form
- (60% of normal ⍺1-antitrypsin levels)
Heterozygous ⍺1-antitrypsin deficiency
- 60% Production - Production of ⍺1-antitrypsin is 60% of normal levels
Asymptomatic
- Enough of this protease to look after your body
- Yet not enough - if one is exposed to environmental pollutants or has a smoking habit
May be asymptomatic but develop emphysema much earlier if exposed to
environmental pollutants
Homozygous ⍺1-antitrypsin deficiency
- Production of ⍺1-antitrypsin is 10% of normal levels
Two genetic variants exist for homozygous ⍺1-antitrypsin deficiency
- Z variant - the defective ⍺1-antitrypsin enzyme is unable to be transported out of synthesising cell
- ⍺1-antitrypsin accumulates and is cytotoxic
- S Variant - ⍺1-antitrypsin enzyme has increased susceptibility to degradation
- Patients are more likely to be asymptomatic
Z has more marked effects than S variant
Z Variant - Symptomatic with Emphysema and Cirrhosis
- Hepatic Production/Accumulation leads to Cirrhosis -hepatocytes synthesis ⍺1-antitrypsin
- Cells are unable to export the enzyme and it accumulates in the liver.
- Accumulation is cytotoxic and triggers hepatitis and subsequent cirrhosis
- Pulmonary Deprivation leads to Emphysema - pulmonary parenchyma is exposed without the anti-protease.
- Excessive protease activity destroys connective tissue and increases compliance of lung whilst disrupting elastance
Secondary Emphysema
Accumulation of Leukocytes
- Accumulation because of;
- Smoking
- Air Pollution
- Industrial Exposure
Smoking inhibits ⍺1-antitrypsin and other anti-proteases
- Protease activity >>> than anti-protease activity
Inflammation
- Destruction of Connective Tissue - since protease activity predominates
-
Clinical Features
Pink Puffers
- Puffer - expends considerable effort maintaining arterial oxygen saturation
- Pink - adequate oxygen saturation
Represent the extremes of disease composition which more commonly presents along a spectrum as opposed to a binary
Signs & Symptoms
-
Progressive Dyspnoea
- Severe dyspnoea once more than 1/3 of lung is affected
-
-
- Hyper-Resonance - Chest is hyper-resonant because of increased residual volume
-
Complications (PRR)
- Since Emphysema and Chronic Bronchitis occur concurrently, they share similar complications
Respiratory Failure
- Hypercapnia leads to respiratory acidosis => Carbon Dioxide narcosis => coma
Cor-pulmonalae w/ Bullous Emphysema
Right-sided heart Failure due to increased vascular resistance in the arterial vessels of the pulmonary circuit.
- Destruction of the lung parenchyma caused by Emphysema reduces X-sectional area through which the blood may travel.
- The same volume of blood is needing to be pushed through fewer functional blood vessels.
- This increases resistance and leads to pulmonary hypertension and this can cause RHF
Pneumothorax
- Rupturing of Subpleural bullae - in the event of bullae rupture pneumothorax may result
Macroscopic Features
- PSH - Pale spngy and hyperinflated lungs
- Emphysematous Bullae - blisters signifying damaged alveoli and trapped air
- Anthracosis - air pollution, infection
PSH, Anthracosis and Bullae
Physical Examination
- Increased Respiratory Rate
- Pursed-lips breathing
- Cyanosis/Rubor
- Tripoding
- Hoover's Sign - inward movement of lower ribs on inspiration - usually these should move outward
- Tracheal tug
- Hyperresonance on percussion
- Reduced vocal resonance on auscultation
Diagnostic Investigation
- Spirometry - Irreversibly reduced FEV
- Below 80% - Reduced Ratio of FEV/FVC to less than 80%
- I.e. you aren't able to expire forcefully the expected 80% of your functional vital capacity within 1 second
- CXR
COPD MANAGEMENT
NON-PHARMACOLOGICAL
- Support Smoking Cessation
- Encourage Vaccine uptake - reduce the risk of superimposing infection
- Manage Co-morbidities - CVS, anxiety, depression etc
- Optimise Function - encourage physical exercise, adequate nutrition and develop a written management plan
COPD MANAGEMENT
PHARMACOLOGICAL
- SABA or SAMA - short acting beta-adrenergic agonists or short acting muscarinic antagonists
- LABA or LAMA - add long acting agents
- Consider ICS - consider anti-inflammatory agent
Confirm that they know proper technique and importance of adherence
Treat symptoms and prevent exacerbations-