L 50. COPD Flashcards

1
Q

What is COPD?

A

An inflammatory disease of the airways in response to an exposure to a particle or gas.

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2
Q

Is airflow obstruction reversible in COPD?

A

It is a progressive disease, so some can be reversed but not all.

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3
Q

2 main components of the COPD disease

A
  1. Chronic bronchitis (mucus producing cough most days for 2 years or more)
  2. Emphysema (damage and destruction of alveolar cells causing shortness of breath)
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4
Q

How is COPD gotten? (lol)

A

Genetics + environment

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5
Q

What environ factors help to get COPD?

A

Smoking and pollution (e.g air particulates)

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6
Q

In lower income countries, … factors had a greater impact than … factors

A

In lower income countries, environmental factors had a greater impact than behavioural factors.
(e.g bad air is worse than smoking)

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7
Q

COPD risk factors

A

Environment: occupational (farming, textiles, industry) and pollution (inside and outside home)

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8
Q

What is the trend with NZ smoking rates?

A

Trending downwards (less people smoking)

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9
Q

Risk factors for smoking x6

A

Media, social influences, friends/parents who smoke, low self esteem, taking part in risk activities, access and affordability.

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10
Q

What is the overall prevalence of COPD?

A

0.95%

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11
Q

COPD epidemiology x4

A
  • Prevalence increases with age
  • Rates higher for women <65 and men >65
  • Higher mortality rates for elderly men
  • Hospitalisation and mortality rates increase with increasing deprivation.
  • Highest hospitalisation in māori and pacifika
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12
Q

Barriers identified for COPD management

A
  • Access to care
  • Inattention to culturally accepted practises
  • Sporadic/poor quality care
  • Inadequate provision of health care ifnormation
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13
Q

How to address inequities for COPD care

A
  • Audits of care providing
  • Systematic approach to health literacy and COPD education for whānau
  • Providers need to support staff to develop Cultural safety skills to engage with māori and their whānau (about COPD)
  • Assess patients using a māori model of health
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14
Q

Pathogenesis of COPD

A

Production of inflammatory mediators and oxidants by airway epithelium and macrophages
Accumulation of immune cells (more macrophages, neutrophils, CD4 and CD8 cells)

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15
Q

What type of CD4 cells are involved in COPD pathogenesis?

A

Th1 cells

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16
Q

What role do macrophages play in COPD pathogenesis? x3

A

Macrophages release:

  • Proteases (cause tissue destruction, mucus hypersecretion)
  • TGF beta (fibroblasts to release CTGF - connective tissue growth factor)
  • Oxidants (goblet cell hyperplasia, decrease in HDAC2 gene causing steroid resistance)
17
Q

What role do neutrophils play in COPD pathogenesis? x2

A
  • An increase in number of neutrophils correlates with a decline in airway function
  • Neutrophils also release proteases
18
Q

What role do CD8 cells play in COPD pathogenesis?

A

They kill alveolar cells (directly or by inducing apotosis)

19
Q

What role do Th1 and Th17 cells play in COPD pathogenesis?

A

Th1 and Th17 are pro-inflammatory.

20
Q

Requirements to get COPD

A

An inappropriate inflammatory response to noxious airway irritants in genetically susceptible individuals.

21
Q

Define noxious

A

Toxic, harmful

22
Q

How does smoking impact COPD pathogenesis?

A

Cigarette smoking impairs innate immune responses, therefore increasing susceptibility to infection (along with other methods of damaging health)

23
Q

What is the deal with eosinophils and COPD pathogenesis

A

15-40% of cases are based on Th2 biased eosinophilic inflammation.
COPD is usually more neutrophils and Th1 based, but there is a small subset that is Th2

24
Q

Exacerbations of COPD can be triggered by…

A

Symptoms of exacerbations
Triggers: infection, pollutants
Symptoms: worsening symptoms overall, often increased airway inflammation

25
Q

Features of COPD x4

A
  • Early changes in airways (fibrosis and vascular smooth muscle proliferation)
  • Air trapping, dyspnoea, FEV1 decline, irreversible destruction.
  • Enhanced parasympathetic activity causing hyperresponsiveness to irritants. (DRUG TARGET)
  • Gas exchange abnormalities, pulmonary hypertension.
26
Q

What is fibrosis?

A

Formation/thickening of scar tissue, usually as a result of injury.

27
Q

What is dyspnoea?

A

Breathlessness

28
Q

What are some other impacts of COPD?

A

Accelerated ageing, Cachexia, increased CVD risk, osteoporosis, depression and anxiety

29
Q

Define cachexia?

A

Weakness and wasting of the body due to severe chronic illness

30
Q

What % of COPD patients have comorbidities?

A

94% have at least 1 comorbidity.

31
Q

How is COPD diagnosed? x3

A

Symptoms (cough, sputum or dyspnoea)
Pulmonary function testing
Imaging (e.g chest x-ray)

32
Q

Management of COPD … x5

A
Smoking cessation
Pharmacological options
Nutrition and exercise
Pulmonary rehabilitation!!!! (physio)
Surgery
33
Q

Asthma vs COPD

A

There may be differences, it can also be considered as a continuum. Stupid 2 slides.