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PA20320 > COPD > Flashcards

COPD Flashcards

1
Q

What is COPD?

A

Chronic obstructive airway disease

  • progressive airflow limitation that isn’t completely reversible
  • associated with inflammation due to noxious gases
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2
Q

What is Chronic bronchitis?

A

Chronic bronchitis is a productive cough present over years and associated with excessive mucous production

Symptoms present as:

  • overweight
  • cyanosis
  • increased haemoglobin
  • peripheral oedema
  • rhonchi and wheezing
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3
Q

What is emphysema?

A

Emphysema is associated with alveolar wall destruction resulting in a reduction in the surface areas of the lung

Symptoms present as:

  • in older men
  • skinny
  • SOB
  • Quiet chest
  • Hyperinflation
  • Flattened diaphragm
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4
Q

Risk factors that cause COPD?

A 
Smoking 
Urban pollution 
Textile dust 
Industrial pollution 
Biomass
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5
Q

COPD vs Asthma

A

COPD has neutrophil rich sputum as opposed to eosinophil rich sputum

There is little variation in air flow

There is limited hyper-responsiveness

The t cells involved are Th1 and Tc1 cells (no Th2)

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6
Q

How are the airways obstructed in COPD?

A

Airways blocked by mucus

Airway walls are thickened due to:

  • cell infiltrate
  • thickened smooth muscle
  • peribronchial fibrosis

Loss of elasticity due to emphysema

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7
Q

What is the cause of the mucus hypersecretion?

A

Mucous glands are enlarged
Goblet cell hyperplasia (lots of them) and metaplasia
Mucus production is controlled by neuronal impulses and inflammatory mediators
There is increased production but reduced clearance

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8
Q

Regulation of mucus production

A

Inhaled irritants stimulate sensory nerve
Signal sent to CNS via vagus nerve and signal sent back through cholinergic nerve
ACh released by nerve and acts on M3 receptor on mucus releasing cell

Local nerves release neuropeptides which act on NK1 receptors

Adrenaline suppresses mucus production

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9
Q

Inflammation in COPD

A

Leukocytes (macrophages and CD8+ cytotoxic cells) are sent in to clear up irritants

Elevated CD8+ counts indicate both this mechanism and also increased susceptibility to infection due to extra mucus

Neutrophils will release proteases that damage cells as well as IL-8 and LTB4 which attracts more leukocytes

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10
Q

Consequences of inflammation in COPD

A

Epithelium damaged:
cilia damaged: less mucus clearance
muscle hyperplasia
increased bronchial permeability

Increased stimulation of sensory nerves:
neurogenic inflammation
stimulates cough

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11
Q

What causes a cough?

A

A motor reflex initiated by irritants, chemicals and excessive mucus in the airway

Nerves are sensitised by inflammatory mediators

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12
Q

Treatments for a cough

A

High dose opioids effective
-OTC opioids are pretty ineffective, it does however cause the release of endogenous opioids which can suppress cough

The sugar in products can increase salivation which can also soothing cough

Placebo effect is pretty significant in cough suppression: can still be suppressed by opioid antagonists (naloxone)

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13
Q

Emphysema

A

Destruction of alveolar walls

Smoking can cause imbalance of protease/antiprotease where protease becomes higher

alpha1 anti-trypsin deficiency can exacerbate effects of COPD

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14
Q

What is elastase?

A

Protease most common in alveolar wall destruction

Comes neutrophils/macrophages

Degrades elastin, basement membrane and connective tissue in the airways

Levels of elastase increase after smoking

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15
Q

What are metallo proteinases?

A

Proteinases released by neutrophils and monocytes (collagenase is one example)

Inhibited by TIMP

TIMP decreased in emphysema and metallo proteinases are increased

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16
Q

Cytokines in COPD

A

TNF and IL-8 are increased in COPD

TNF increases mucin secretion and elastase production

17
Q

Bronchodilators in COPD treatment

A

Since bronchoconstriction is not the biggest cause of constriction in COPD it’s effect is limited

18
Q

How do muscarinic antagonists help?

A

Reduces parasympathetic stimulation of mucus secretion of mucus

Mucus associated with reduction in FEV and hospitilisations

eg. Ipratropium, Tiotropium and Aclidinium

19
Q

Corticosteriods in COPD

A

I.V corticosteroids help in acute exacerbations

Steroids in maintenence have limited effect (but still help a little) on neutrophil counts, cytokine levels or proteases

20
Q

PDE inhibitors

A

PDE 3/4 inhibition leads to bronchodilation
PDE 4 inhibition leads to reduced chemotaxis, granule release, respiratory release and TNFalpha release

Roflumilast is a PDE 4 selective inhibitor

21
Q

Acute exacerbations of COPD

A

Usually involve infection of some sort
Bacerial; H. Influenza, S. Pneumoniae,
Viral: Rhinovirus, influenza, parainfluenza and coronavirus

22
Q

What are Serpins?

A

Serine protease inhibitors

They are inactivated by oxidative stress

23
Q

Protease inhibitors and antioxidants

A

alpha1 antitrypsin augmentation therapy can be used in patients who have a deficiency

Elastase inhibitors have not been great in trials

Anti oxidants have limited evidence for efficacy
-includes: Vit C/E, Omega 3 etc

24
Q

Alondroate: How can it be used in COPD?

A

A bisphosphonate that acts by killing osteoclasts which are similar to macrophages

Could be used as an inhaled powder to kill macrophages in the airways

Shown to reduce symptoms of emphysema: alveolar enlargement, TNF production, macrophage production

25
Q

Alternative treatments for COPD

A

High % O2

Physiotherapy

Mucolytics; N-acetyl cysteine breaks disulphide bonds in mucin
DNAse
Not useful in COPD but effective in CF

26
Q

Why don’t ICS work in COPD?

A

Oxidative stress results in reduced steroid sensitivity

Steroids inhibit neutrophil apoptosis which are causative of COPD
Smoking reduces binding of glucocorticoids to the glucocorticoid receptor

27
Q

What is histone acetylation?

A

Histone acetyltransferase (HAT) unpacks chromatin and allows RNA polymerase to bind to DNA
Allows for increased binding of transcription factors
This enhances inflammatory gene expression

Histone deacetylase (HDAC) does the exact opposite

  • it wraps the DNA tightly on the nucleosome surface
  • steroids inactivate HAT hence increasing amounts of HAT reduce sensitivity to steroids
28
Q

How does smoking/irritants effect histone acetylation?

A

Infammatory stimulation increases HAT
Oxidative stress reduces HDAC

Mechanism for this might be inactivation via peroxynitrate made by reaction of NO with cigarette smoke and superoxide anions (O2-)
The peroxynitrate nitrates the tyrosine residue on HDAC2 blocking enzyme activity and marking it for destruction via protease

Combined effect of these increases inflammation

PA20320 (15 decks)

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