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Supporting Life > COPD > Flashcards

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
Q

What does cor pulmonale lead to

A

Chronic hypoxia leads to chronic pulmonary vascular vasoconstriction to maintain V/Q matching to prevent shunting -> oedema and elevated JVP

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26
Q

What is an acute exacerbation of COPD

A

Acute worsening of respiratory

symptoms that result in additional therapy

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27
Q

What are the clinical features of acute exacerbation of COPD

A

Increased breathlessness
Increased cough and sputum production
Change in colour and/ or tenacity of sputum
Impaired daily activities

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28
Q

What is the treatment for mild COPD

A

Short acting bronchodilator

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29
Q

What is the treatment for moderate COPD

A

SABD + abx or corticosteroid

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30
Q

What is the treatment for severe COPD

A

Hospitalisation

31
Q

What are the CV effects of CODP

A

Increased pulmonary arterial pressure
Decreased RV preload due to increased intravascular pressure
Increased LV afterload

32
Q

What are the muscle morphological changes in COPD

A

Decreased T1 fibres
Decreased CSA for T1 and T2 fibres
Decreased myosin heavy chain I and oxidative enzyme activity

33
Q

What muscle is used as a COPD biomarker

A

Quadriceps muscle strength

34
Q

What occurs in peripheral muscles in COPD

A

Lower limb atrophy
Muscle weakness, increased susceptibility to fatigue, poor resistance of exercise
Reduce muscle metabolism

35
Q

What happens to inspiratory muscles of COPD px

A

Increased elastic/threshold loading of inspiratory muscles - increased ventilator drive
Decrease PaO2, increased PaCO2, decreased pH

36
Q

What happens when oxygen is overdone

A

Acidotic resp failure

37
Q

When is ventilator support given

A

Resp acidosis (PaCo2>6kPa, pH<7.35). Signs of fatigue and increased work of breathing, persistent hypoxaemia

38
Q

What benefits does ventilator support offer

A

Improves hypercapnia and acidosis, decreases RR and work of breathing

39
Q

When is invasive ventilatory support used

A 
Unable to tolerate NIV/NIV failure
Post cardioresp arrest
Reduced consciousness
Haemodynamic instability
Life threatening hypoxaemia
Aspiration/vomiting
40
Q

What is the only treatment that improves mortality in COPD

A

Stopping smoking

41
Q

What is used to monitor smoking cessation

A

CO monitoring

Give varenicline + support

42
Q

What are bronchodilator effects

A 
Alter smooth muscle tone, reduce dynamic hyperinflation, improve exercise performance
B2 agonists (stimulate B adrenergic receptors, increase cAMP)
43
Q

What are examples of SDBD

A

Salbutamol, terbutaline

44
Q

What are long acting bronchodilators

A

Forometrol, salmeterol - improve FEV1, lung volumes, dyspnoea, health status
Indactero - improves dyspnoea, health status, exacerbation rate

45
Q

What is pulmonary rehab

A

26 hours with resp team
Muscle strengthing: education, effective post hospitalisation episode for COPD
Highest treatment value

46
Q

What are side effects of b2 agonists

A

Increase HR, arrhythmias, hypokalaemia

47
Q

What anti-muscarinics are given for CODP

A

Long acting - 12 or 24 more cost effective
Tiotropium: improves symptoms, health status, effectiveness of PR
No effect on lung function decline

48
Q

Why are combination LAMA/LABA used

A

Increase bronchodilation with lower risk of SE - increase FEV1 and reduce symptoms

49
Q

When are corticosteroids prescribed

A

Px has 2-3 exacerbations each year

50
Q

How are corticosteroids prescribed

A

ICS plus LABA improves FEV1, health status, and reduce exacaerbation frequency

51
Q

What are the SE of ICS

A

Increased risk of TB, bone fracture, skin thinning, cataract, diabetes

52
Q

What long term macrolide ab therapies are used

A

Azithromycin or erthyromycin reduces exacerbation frequency

53
Q

What are surgical treatment options

A

Emphysema and sig hyperinflation - interventional bronchosoopy
Large bulla - surgical bullectomy
Severe COPD - lung transplantation

54
Q

What’s target oxygen for acute px

A

over 94

55
Q

What’s target oxygen for px at risk of hypercapnia resp failure

A

88-92 (Not used in COPD px with high bicarb)

56
Q

What is domicillary oxygen

A

Admin of oxygen at concentration at higher than than those in room

57
Q

What is LTOT

A

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
Q

What is ambulatory oxygen therapy

A

O2 delivered by equipment carried by px. Consider in px in LTOT, evidence of exercise desats,

59
Q

Who is contraindicated for O2 therapy

A

SaO2 below 92%

Smokers

60
Q

What are the two main underlying pathologies in COPD

A

Chronic Bronchitis and Emphysema

61
Q

Define chronic bronchitis

A

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
Q

What happens with chronic irritation in bronchitis

A

Defensive increase in mucus production->increase in goblet cells. Loss of stratified cells -> squamous metaplasia (loss of cilia) but no BM thickening

63
Q

What happens to airways in chronic bronchitis

A

No reversible obstruction. Peribronchiolar fibrosis and airway obstruction

64
Q

How does smoking amplify lung inflammation

A

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
Q

Describe oxidative stress mechanism in chronic bronchitis

A

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
Q

What is emphysema

A

Damage to the alveolar units of lung distal to the terminal bronchiole that deliver oxygen into the lung and remove the CO2.

67
Q

Why are emphysematous more prone to collpase

A

Degradation of elastin fibre tethering

68
Q

What is destruction of pulmonary capillary bed cause

A

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
Q

What is centriolobular emphysema

A

Expansion of alveolar unit proximal to terminal alveolus; chronic emphysema relating to chronic smoker

70
Q

What is panacinar emphysema

A

Destruction of entire unit; emphysema with alpha 1 antitrypsin deficiency and exposure. More diffuse destructive pattern. Can cause rupture -> formation of bullous airspaces

71
Q

How does emphysema impair resp function

A

Diminished alveolar surface area for gas exchange

Loss of elastic recoil and support of small airways leading to tendency to collapse with obstruction

72
Q

What are systemic manifestations of COPD

A

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
Q

What is the treatment for COPD

A

Short acting BD->Long acting BD->inhaled glucocorticoid steroids->long term O2

74
Q

How is lung aging accelerated in COPD

A

Excessive telomere shortening in COPD px, decreased telomere length used as a marker for cellular turnover

Supporting Life (14 decks)

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