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III > COPD > Flashcards

COPD Flashcards

1
Q

What can COPD lead to?

A

May led to pulmonary hypertension, cynosis, hypoxia, right heart failure.

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2
Q

What is the defining criteria for COPD?

A

Progressive airflow limitation that is not fully reversible.
(Associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarily cigarette smoke)

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3
Q

What does COPD include?

A

Chronic bronichitis: productive cough present over years. Excessive sputum production.

Emphysema: alveolar wall destruction, irreversible enlargement of the terminal air spaces.

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4
Q

Who is a blue bloater?

A

Chronic bronchitis. overweight, cyanotic, elevated hemoglobin, peripheral edema, rhonchi and wheezing.

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5
Q

Who is a pink puffer?

A

Emphysema: permanent enlargement and destruction or airspaces distal to the terminal bronchiole.

Older and thin, severe dyspnea, quiet chest, X-ray: hyperinflation with flattened diaphragms.

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6
Q

Risk factors for COPD:

A 
Tobacco Smoke
Urban pollution
Industrial pollution 
Textile dust
Biomass fuels
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7
Q

How does COPD progress?

A

Stage I: Asymptomatic
Stage II: Progressive dyspnoea
Stage III: Systemic disease, comorbidities.
Stage IV: respiratory failure, death.

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8
Q

How does the sputum differ between COPD and Asthma patients?

A

COPD: Neutrophil-rich sputum
Asthma: Eosinophilic rich.

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9
Q

Marked-hyper-responsiveness is associated with

A

Ashtma. Limited = COPD.

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10
Q

Reduced airflow which is very variable and has a diurnal variation is associated with:

A

Asthma. No variation = COPD.

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11
Q

Lymphocytes found in COPD are predominantly of what type?

A

TH1 and TC1

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12
Q

Lymphocytes found in Asthma are predominantly:

A

TH2

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13
Q

What is the Dutch hypothesis?

A

Asthma + Chronic bronchitis + Emphysema all overlap.

A: reversible airflow limitation
B: fixed obstruction, persistent sputum.
E: destruction of alveolar septa.

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14
Q

Neutrophil-rich sputum is associated with:

A

COPD

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15
Q

Fibrosis that is ______ is found in COPD.

A

Peribronchiolar,

Subepithelial is Asthma.

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16
Q

Eosinophilic sputum is associated with:

A

Asthma

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17
Q

How does excessive airway mucus occur in COPD?

A

Increased production: inflammatory cells, oxidative stress, viral infection, bacterial infection.

Reduced elimination: poor ciliary clearance, airway occlusion, reduced PEF, resp muscle weakness.

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18
Q

What are the three main mechanisms of airflow reduction in COPD?

A

Occlusion of airways by mucus.
Thickened airway walls
Loss of elasticity due to emphysema.

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19
Q

Leukocyte infiltration in COPD takes the form of:

A

Macrophages and CD8+ T cells.

Neutrophils in infection.

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20
Q

Chemoattractants found in COPD include:

A

IL-8 and LTB4

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21
Q

What are the consequences of the inflammation in COPD?

A

Epithelial damage: decreased ciliary cell function, increased mucus secretion from goblet cells.
Mucus cell hyperplasia - more cells, increased bronchial permeability –> airway oedema and protein exudation.

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22
Q

What is a cough?

A

Motor reflex in response to sensing chemicals, particulates and airway excessive mucus.

23
Q

How can a cough be suppressed?

A

High dose opioids are effective,
OTC limited efficacy.
Most of the soothing benefit is from the sugar causing increased salivation.

24
Q

What is emphysema?

A

Permanent enlargement of airspaces distal to the terminal bronchiole: destruction of the alveolar walls.

“Proteinase-antiproteinase hypothesis”

25
Q

Decreased levels of what are seen in some emphysema patients?

A

Decreased serum alpha 1 antitrypsin.

26
Q

IL-8 and LTB4

A

Chemoattractants

27
Q

Lung elastases such as____, _____ and ______ are derived from neutrophils and macrophages.

A

Cathepsins,
Proteinase 3
Gelatinase

They degrade elastin, basement membrane and connective tissue.

Increased levels after smoking.
Strongly implicated in emphysema.

28
Q

Why can a lack of liver produced a1 anti-trypsin be a problem?

A

a1 anti-trypsin is an elastase inhibitor.

High levels of elastase = emphysema.

29
Q

TIMPS

A

Tissue inhibitors of metalloproteinase.

30
Q

Elastase is produced by:

A

Neutrophils, macrophages.

31
Q

Metallo-proteinases are produced by:

A

Monocytes, neutrophils.

32
Q

Increased levels of which cytokines are found in COPD sputum compared with smoking or non-smoking controls?

A

IL-8
TNF

TNF increases mucin secretion, and elastase production.

33
Q

Why can high levels of TNF cause emphysema?

A

TNF increases mucin secretion, and elastase production.

34
Q

What do macrophages release that can cause fibrosis?

A

Fibroblast growth factors.

TGFB and EGF.

35
Q

What is Aclidinium?

A

Muscarinic antagonist with a fast M2 off time.

DPI

36
Q

Why are bronchodilators not of much use in COPD?

A

Bronchoconstriction is not a major cause of airway obstruction.

37
Q

Why is tiotropium of pharmacokinetic advantage?

A

M3 selective agent, less effect on M2 so negative feedback is preserved and ACh release is suppressed.

38
Q

What actions does ACh have when bound to:

a) M3
b) M2

A 
M3 = bronchoconstrictive actions
M2 = negative feedback, preventing its own release
39
Q

What can occur if M2 ACh release negative feedback is inhibited by non-selective muscarinic agents such as ipratropium?

A

Non-specific muscarinic antagonists block both M2 and M3 so remove negative feedback via blocking M2 and thus sufficient ACh can be released as to overcome the M3 block.

40
Q

Neurokinin antagonists and agents inhibiting sensory fibre activation are showing some efficacy in preventing what?

A

Mucus secretion in COPD.

Hypersecretion is associated with decline in FEV1 and hospitalisation.

41
Q

Are corticosteroids of use in COPD treatment?

A

Some benefit of IV for acute exacerbations.

Limited evidence of benefit from inhaled steroids for maintenance.

42
Q

Rofulimast is what?

A

PDE IV selective phosphodiesterase inhibitor.

PDE IV is present in leukocytes.

inhibitors prevent chemotaxis, granule release etc.
TNFa release prevented.

43
Q

PDE III and IV inhibition leads to what?

A

Bronchodilation.

44
Q

Bacterial infections caused by: _________ or _________ can be found in to ___ of stable COPD patients.

A

H.influenzae
S. Pneumoniae
50%

45
Q

Viral infection in COPD is associated with acute exacerbation of symptoms and is predominantly caused by _______. __________. ________ and ________

A

Rhinovirus
Influenza
Parainfluenza
Coronavirus

46
Q

Which antibiotic apparently has beneficial actions unrelated to antibiotic activity such as alveolar protection in smoke injury?

A

Clarithromycin, macrolide.

47
Q

________ may be useful as a novel therapy in COPD. Normally used in the treatment of osteoporosis.

A

Alondronate
Inhaled bisphosphonates.
Inhibit experimental emphysema.

48
Q

What effect do statins have on COPD management?

A

No benefits shown on lung function in randomised prospective trials.

49
Q

What is N-acetyl cysteine?

A

Breaks disulphide bonds in mucin, Mucolytics.
DNAse (Dornase Alpha)
No evidence on mucus removal in COPD but beneficial in asthma,

50
Q

Why do bronchodilators work well in COPD?

A

The occlusion is not due to bronchoconstriction but due to tissue remodeling and secretion.

51
Q

Why are anti-inflammatory glucocorticoids not useful in COPD usually?

A

Oxidative stress results in decreased steroid sensitivity - impaired glucocorticoid receptor function.

Neutrophil apoptosis is inhibited by glucocorticoids.

52
Q

What role does HAT play in gene expression?

A

Histone acetyltransferase acetylates histones:
unpacks chromatin and allows RNA polymerase binding to DNA.
Co-operates and amplifies NFKB action.

53
Q

What role does HDAC play in gene expression?

A

Histone Deacetylase (HDAC) represses inflammatory gene expression.

54
Q

Theophylline has what effect on HDAC?

A

Promotes its activity hence repressing gene expression.

III (24 decks)

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