COPD Flashcards
What is the pathophysiology of COPD
Noxius fume -> lung inflammation (increased neutrophils, macrophages, and T cells (CD8)
Leads to oxidative stress
Impaired repair mechnaism
What are the inflammatory mediators in COPD
Leukotriene B4 - neutrophil and T cell chemoattractant
Chemostatic factors - IL 8 and growth related oncogene alpha; amplify pro-inflam responses
Pro-inflam cytokines e.g. alpha, IL-1beta, and IL6
GF: TGF-beta - fibrosis in airways
What occurs in oxidative stress
Inactivates anti-proteases
Stimulates mucus production
Amplifies inflammation by enhancing transcription factor activation
What does alpha1 antitrypsin cause
Genetic COPD
How is COPD inflammation different from asthma
Eosinophilic
What occurs in COPD airways
Hypertrophy and hyperplasia of bronchial submucosal glands
Increased number of goblet cells
Destruction of cilia - difficult to expectorate sputum
Narrowing of airways due to remodelling -> icnreased airways resistanced
What occurs in COPD lung parenchyma
Proteolytic enzymes destroy alveolar tissue
Elastin and collagen are destroyed - reduced elasticity and structural integrity of lungs
Compliance increases and elasticity decreases - loss of elastic recoil
Why is there expiratory flow limitation in COPD
Loss of elastic recoil, decreased gas exchange, hyperinflation, sputum production
What are the clinical features of COPD
Increased RR Accessory muscles use (trapezius, sternocleidomastoid) Wheeze Barrel chest Reduced breath sounds Asterixis Cyanosis Cor pulmonale
What are extrapulmonary features of COPD
Weight loss, muscle wasting, CV, cormorbidities, depression, osteoporosis
How to diagnose COPD
Chest X ray
Spirometry
How is severity measured for COPD
FEV1/FVC ratio post bronchodilator should be less than 0.7
%FEV1 predicted used to measure severity. Under 30 is severe
What causes low compliance
Lung fibrosis (high elastic resistance) -> increased lung recoil -> reduced FRC
What causes high lung compliance
Emphysema (tissue destruction) -> reduced recoil -> increased FRC
What happens to lungs in COPD
Hyper-inflation. FRC and RV increased. Gas trapping occurs during expiration
Why does gas trapping occur
Lower elastic recoil, increased airway obstruction -> positive airway pressure decreases more rapidly. EPP occurs in small airways -> px traps gas
Where is the normal equal pressure point
Trachea
What is expiratory flow limitation and why is this a problem in COPD
Flow ceases to increase with increasing expiratory effort. In COPD, this can occur in tidal breathing. Since max exp flow is reached during tidal breathing, minimum time for lung emptying is fixed
What occurs during exercise for COPD px
Resp rate increases –> EELV increases despite expiratory muscle activity–>inspiratory capacity and inspiratory reserve volume decreases. Air can’t be cleared fast enough
What happens when IRV lies within 0.5 of TLC
Tidal volume can’t increase anymore despite continue increases in contractile resp effort -> dyspnoea increases to intolerable levels -> exercise limitation
What is threshold load
Gas trapped in alveolar - so alveolar pressure is still positive at end of expiration. However, need positive pressure for inspiration
What is dynamic hyperinflation
Increase in end-expiratory lung volume (EELV) that may occur in patients with airflow limitation when minute ventilation increases
Why does functional diaphragm weakness occur in COPD
Hyperinflated lungs in COPD px, lungs have pushed down diaphragm
What is cor pulmonale
Abnormal enlargement of the right side of the heart
What does cor pulmonale lead to
Chronic hypoxia leads to chronic pulmonary vascular vasoconstriction to maintain V/Q matching to prevent shunting -> oedema and elevated JVP
What is an acute exacerbation of COPD
Acute worsening of respiratory
symptoms that result in additional therapy
What are the clinical features of acute exacerbation of COPD
Increased breathlessness
Increased cough and sputum production
Change in colour and/ or tenacity of sputum
Impaired daily activities
What is the treatment for mild COPD
Short acting bronchodilator
What is the treatment for moderate COPD
SABD + abx or corticosteroid
What is the treatment for severe COPD
Hospitalisation
What are the CV effects of CODP
Increased pulmonary arterial pressure
Decreased RV preload due to increased intravascular pressure
Increased LV afterload
What are the muscle morphological changes in COPD
Decreased T1 fibres
Decreased CSA for T1 and T2 fibres
Decreased myosin heavy chain I and oxidative enzyme activity
What muscle is used as a COPD biomarker
Quadriceps muscle strength
What occurs in peripheral muscles in COPD
Lower limb atrophy
Muscle weakness, increased susceptibility to fatigue, poor resistance of exercise
Reduce muscle metabolism
What happens to inspiratory muscles of COPD px
Increased elastic/threshold loading of inspiratory muscles - increased ventilator drive
Decrease PaO2, increased PaCO2, decreased pH
What happens when oxygen is overdone
Acidotic resp failure
When is ventilator support given
Resp acidosis (PaCo2>6kPa, pH<7.35). Signs of fatigue and increased work of breathing, persistent hypoxaemia
What benefits does ventilator support offer
Improves hypercapnia and acidosis, decreases RR and work of breathing
When is invasive ventilatory support used
Unable to tolerate NIV/NIV failure Post cardioresp arrest Reduced consciousness Haemodynamic instability Life threatening hypoxaemia Aspiration/vomiting
What is the only treatment that improves mortality in COPD
Stopping smoking
What is used to monitor smoking cessation
CO monitoring
Give varenicline + support
What are bronchodilator effects
Alter smooth muscle tone, reduce dynamic hyperinflation, improve exercise performance B2 agonists (stimulate B adrenergic receptors, increase cAMP)
What are examples of SDBD
Salbutamol, terbutaline
What are long acting bronchodilators
Forometrol, salmeterol - improve FEV1, lung volumes, dyspnoea, health status
Indactero - improves dyspnoea, health status, exacerbation rate
What is pulmonary rehab
26 hours with resp team
Muscle strengthing: education, effective post hospitalisation episode for COPD
Highest treatment value
What are side effects of b2 agonists
Increase HR, arrhythmias, hypokalaemia
What anti-muscarinics are given for CODP
Long acting - 12 or 24 more cost effective
Tiotropium: improves symptoms, health status, effectiveness of PR
No effect on lung function decline
Why are combination LAMA/LABA used
Increase bronchodilation with lower risk of SE - increase FEV1 and reduce symptoms
When are corticosteroids prescribed
Px has 2-3 exacerbations each year
How are corticosteroids prescribed
ICS plus LABA improves FEV1, health status, and reduce exacaerbation frequency
What are the SE of ICS
Increased risk of TB, bone fracture, skin thinning, cataract, diabetes
What long term macrolide ab therapies are used
Azithromycin or erthyromycin reduces exacerbation frequency
What are surgical treatment options
Emphysema and sig hyperinflation - interventional bronchosoopy
Large bulla - surgical bullectomy
Severe COPD - lung transplantation
What’s target oxygen for acute px
over 94
What’s target oxygen for px at risk of hypercapnia resp failure
88-92 (Not used in COPD px with high bicarb)
What is domicillary oxygen
Admin of oxygen at concentration at higher than than those in room
What is LTOT
Long term oxygen therapy - over 15 hours a day
Arterial blood gas when patient is stable and optimised
• Titration of oxygen flow rate to PaO2 >8kPa
• Check no hypercapnia
• Prescribe and send HOOF to Oxygen Company
• Patient education
• CO reading and discussion re smoking
• Home risk assessment
• Ongoing review
What is ambulatory oxygen therapy
O2 delivered by equipment carried by px. Consider in px in LTOT, evidence of exercise desats,
Who is contraindicated for O2 therapy
SaO2 below 92%
Smokers
What are the two main underlying pathologies in COPD
Chronic Bronchitis and Emphysema
Define chronic bronchitis
Chronic inflammation and excess mucus production. Presence of productive cough, with intermittent dyspnoea. Frequent and recurrent pulmonary infections. Progressive cardiac/resp failure. Use of accessory muscles to aid resp
What happens with chronic irritation in bronchitis
Defensive increase in mucus production->increase in goblet cells. Loss of stratified cells -> squamous metaplasia (loss of cilia) but no BM thickening
What happens to airways in chronic bronchitis
No reversible obstruction. Peribronchiolar fibrosis and airway obstruction
How does smoking amplify lung inflammation
Trigger macrophages to produce inflammatory cytokines which increase recruitment of cytokines and CD lymphocytes to cause more damage
Degranulation of neutrophils release proteases - contribute to destruction of cell wall and stimulate mucus secretion
Myofibroblast -> fibroblast, causing small level fibrosis
Describe oxidative stress mechanism in chronic bronchitis
Activation of nuclear factor-kB->TNFa->Interleuki-8->Neutrophil recruitment
Decrease in antiproteases (a-antitrypsin)
Increase mucus secretion
Isoprostanes: enforce oedmatous response for plasma leak and bronchoconstriction
What is emphysema
Damage to the alveolar units of lung distal to the terminal bronchiole that deliver oxygen into the lung and remove the CO2.
Why are emphysematous more prone to collpase
Degradation of elastin fibre tethering
What is destruction of pulmonary capillary bed cause
Increase in inflammatory cells: macrophages, CD8+ lymphocytes. Chronic cough with late onset of non-productive cough. Occasional mucopurulent relapses. Eventual cachexia and resp failure
What is centriolobular emphysema
Expansion of alveolar unit proximal to terminal alveolus; chronic emphysema relating to chronic smoker
What is panacinar emphysema
Destruction of entire unit; emphysema with alpha 1 antitrypsin deficiency and exposure. More diffuse destructive pattern. Can cause rupture -> formation of bullous airspaces
How does emphysema impair resp function
Diminished alveolar surface area for gas exchange
Loss of elastic recoil and support of small airways leading to tendency to collapse with obstruction
What are systemic manifestations of COPD
Gradient of inflam mediators that are able to move down concentration gradient:
IL-6, IL-1b, TNFa-> muslce cachexia
Ischaemic heart disease, cardiac failure (esp cor pulmonale), osteoporosis, diabetes, anaemia, depression
What is the treatment for COPD
Short acting BD->Long acting BD->inhaled glucocorticoid steroids->long term O2
How is lung aging accelerated in COPD
Excessive telomere shortening in COPD px, decreased telomere length used as a marker for cellular turnover
