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COPD Flashcards

1
Q

What is the pathophysiology of COPD

A

Noxius fume -> lung inflammation (increased neutrophils, macrophages, and T cells (CD8)
Leads to oxidative stress
Impaired repair mechnaism

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2
Q

What are the inflammatory mediators in COPD

A

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

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3
Q

What occurs in oxidative stress

A

Inactivates anti-proteases
Stimulates mucus production
Amplifies inflammation by enhancing transcription factor activation

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4
Q

What does alpha1 antitrypsin cause

A

Genetic COPD

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5
Q

How is COPD inflammation different from asthma

A

Eosinophilic

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6
Q

What occurs in COPD airways

A

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

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7
Q

What occurs in COPD lung parenchyma

A

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

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8
Q

Why is there expiratory flow limitation in COPD

A

Loss of elastic recoil, decreased gas exchange, hyperinflation, sputum production

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9
Q

What are the clinical features of COPD

A 
Increased RR
Accessory muscles use (trapezius, sternocleidomastoid)
Wheeze
Barrel chest
Reduced breath sounds
Asterixis
Cyanosis
Cor pulmonale
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10
Q

What are extrapulmonary features of COPD

A

Weight loss, muscle wasting, CV, cormorbidities, depression, osteoporosis

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11
Q

How to diagnose COPD

A

Chest X ray

Spirometry

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12
Q

How is severity measured for COPD

A

FEV1/FVC ratio post bronchodilator should be less than 0.7

%FEV1 predicted used to measure severity. Under 30 is severe

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13
Q

What causes low compliance

A

Lung fibrosis (high elastic resistance) -> increased lung recoil -> reduced FRC

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14
Q

What causes high lung compliance

A

Emphysema (tissue destruction) -> reduced recoil -> increased FRC

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15
Q

What happens to lungs in COPD

A

Hyper-inflation. FRC and RV increased. Gas trapping occurs during expiration

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16
Q

Why does gas trapping occur

A

Lower elastic recoil, increased airway obstruction -> positive airway pressure decreases more rapidly. EPP occurs in small airways -> px traps gas

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17
Q

Where is the normal equal pressure point

A

Trachea

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18
Q

What is expiratory flow limitation and why is this a problem in COPD

A

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

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19
Q

What occurs during exercise for COPD px

A

Resp rate increases –> EELV increases despite expiratory muscle activity–>inspiratory capacity and inspiratory reserve volume decreases. Air can’t be cleared fast enough

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20
Q

What happens when IRV lies within 0.5 of TLC

A

Tidal volume can’t increase anymore despite continue increases in contractile resp effort -> dyspnoea increases to intolerable levels -> exercise limitation

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21
Q

What is threshold load

A

Gas trapped in alveolar - so alveolar pressure is still positive at end of expiration. However, need positive pressure for inspiration

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22
Q

What is dynamic hyperinflation

A

Increase in end-expiratory lung volume (EELV) that may occur in patients with airflow limitation when minute ventilation increases

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23
Q

Why does functional diaphragm weakness occur in COPD

A

Hyperinflated lungs in COPD px, lungs have pushed down diaphragm

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24
Q

What is cor pulmonale

A

Abnormal enlargement of the right side of the heart

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25
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
26
What is an acute exacerbation of COPD
Acute worsening of respiratory | symptoms that result in additional therapy
27
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
28
What is the treatment for mild COPD
Short acting bronchodilator
29
What is the treatment for moderate COPD
SABD + abx or corticosteroid
30
What is the treatment for severe COPD
Hospitalisation
31
What are the CV effects of CODP
Increased pulmonary arterial pressure Decreased RV preload due to increased intravascular pressure Increased LV afterload
32
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
33
What muscle is used as a COPD biomarker
Quadriceps muscle strength
34
What occurs in peripheral muscles in COPD
Lower limb atrophy Muscle weakness, increased susceptibility to fatigue, poor resistance of exercise Reduce muscle metabolism
35
What happens to inspiratory muscles of COPD px
Increased elastic/threshold loading of inspiratory muscles - increased ventilator drive Decrease PaO2, increased PaCO2, decreased pH
36
What happens when oxygen is overdone
Acidotic resp failure
37
When is ventilator support given
Resp acidosis (PaCo2>6kPa, pH<7.35). Signs of fatigue and increased work of breathing, persistent hypoxaemia
38
What benefits does ventilator support offer
Improves hypercapnia and acidosis, decreases RR and work of breathing
39
When is invasive ventilatory support used
``` Unable to tolerate NIV/NIV failure Post cardioresp arrest Reduced consciousness Haemodynamic instability Life threatening hypoxaemia Aspiration/vomiting ```
40
What is the only treatment that improves mortality in COPD
Stopping smoking
41
What is used to monitor smoking cessation
CO monitoring | Give varenicline + support
42
What are bronchodilator effects
``` Alter smooth muscle tone, reduce dynamic hyperinflation, improve exercise performance B2 agonists (stimulate B adrenergic receptors, increase cAMP) ```
43
What are examples of SDBD
Salbutamol, terbutaline
44
What are long acting bronchodilators
Forometrol, salmeterol - improve FEV1, lung volumes, dyspnoea, health status Indactero - improves dyspnoea, health status, exacerbation rate
45
What is pulmonary rehab
26 hours with resp team Muscle strengthing: education, effective post hospitalisation episode for COPD Highest treatment value
46
What are side effects of b2 agonists
Increase HR, arrhythmias, hypokalaemia
47
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
48
Why are combination LAMA/LABA used
Increase bronchodilation with lower risk of SE - increase FEV1 and reduce symptoms
49
When are corticosteroids prescribed
Px has 2-3 exacerbations each year
50
How are corticosteroids prescribed
ICS plus LABA improves FEV1, health status, and reduce exacaerbation frequency
51
What are the SE of ICS
Increased risk of TB, bone fracture, skin thinning, cataract, diabetes
52
What long term macrolide ab therapies are used
Azithromycin or erthyromycin reduces exacerbation frequency
53
What are surgical treatment options
Emphysema and sig hyperinflation - interventional bronchosoopy Large bulla - surgical bullectomy Severe COPD - lung transplantation
54
What's target oxygen for acute px
over 94
55
What's target oxygen for px at risk of hypercapnia resp failure
88-92 (Not used in COPD px with high bicarb)
56
What is domicillary oxygen
Admin of oxygen at concentration at higher than than those in room
57
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
58
What is ambulatory oxygen therapy
O2 delivered by equipment carried by px. Consider in px in LTOT, evidence of exercise desats,
59
Who is contraindicated for O2 therapy
SaO2 below 92% | Smokers
60
What are the two main underlying pathologies in COPD
Chronic Bronchitis and Emphysema
61
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
62
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
63
What happens to airways in chronic bronchitis
No reversible obstruction. Peribronchiolar fibrosis and airway obstruction
64
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
65
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
66
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.
67
Why are emphysematous more prone to collpase
Degradation of elastin fibre tethering
68
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
69
What is centriolobular emphysema
Expansion of alveolar unit proximal to terminal alveolus; chronic emphysema relating to chronic smoker
70
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
71
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
72
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
73
What is the treatment for COPD
Short acting BD->Long acting BD->inhaled glucocorticoid steroids->long term O2
74
How is lung aging accelerated in COPD
Excessive telomere shortening in COPD px, decreased telomere length used as a marker for cellular turnover

Supporting Life (14 decks)

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