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- Epidemiology and risk factors
-
1. Epidemiology of COPD
- Dr. David Mannino
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2. COPD in never smokers
- Dr. Sundeep Salvi
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3. Genetics of chronic obstructive pulmonary disease (COPD)
- Prof. Martin Tobin
- Phenotypes of COPD
-
4. COPD and asthma: similarities and differences
- Prof. Peter Barnes
- Pathophysiology and mechanisms of COPD
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5. The pathology of chronic obstructive pulmonary disease
- Prof. James Hogg
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6. The continuum of COPD: a physiological perspective
- Prof. Denis O'Donnell
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7. Inflammatory and immune mechanisms in COPD
- Prof. Peter Barnes
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8. Mechanisms of COPD exacerbations and relation to exacerbation therapy
- Prof. Wisia Wedzicha
-
9. Protease-antiprotease balance
- Prof. Robert Stockley
- Therapy and management
-
10. Updates in chronic obstructive pulmonary disease (COPD)
- Dr. Omar S. Usmani
-
11. Long-acting bronchodilators in COPD
- Prof. Bart Celli
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12. Treatment of COPD exacerbations
- Prof. Antonio Anzueto
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13. Pulmonary rehabilitation: history, promise and problems
- Prof. Richard Casaburi
-
14. Lung volume reduction: advances in COPD
- Dr. Nick Hopkinson
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15. New pharmacological therapies for COPD
- Prof. Peter Barnes
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16. The Salford lung study in COPD
- Dr. Dave Leather
- COPD case studies
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17. COPD treatment case I: COPD with “bronchitis attacks”
- Dr. Janwillem Kocks
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18. COPD treatment case II: COPD with asthma as child
- Dr. Janwillem Kocks
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19. COPD treatment case III: COPD with pre-diabetes
- Dr. Janwillem Kocks
-
20. Tailoring care for advanced COPD
- Prof. Wissam Chatila
- Archived Lectures *These may not cover the latest advances in the field
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21. Alpha-1 antitrypsin deficiency: state of the art
- Dr. Jamie Stoller
-
22. Oxidative stress in COPD
- Prof. William MacNee
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23. Managing co-morbidity in COPD
- Dr. John Hurst
-
24. Clinical phenotypes of COPD
- Prof. Jørgen Vestbo
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25. Pulmonary rehabilitation: focusing on rehabilitative exercise
- Prof. Richard Casaburi
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26. Genetics of COPD
- Prof. Ian Hall
Printable Handouts
Navigable Slide Index
- Introduction
- Progressive airflow limitation in COPD
- Persistent inhalational injury
- Bronchus tree
- Composition of the airways
- Histology of a bronchial mucus gland
- Effect of small airway occlusion on survival
- Obstruction of small airways in COPD
- The anatomy of the lung lobule
- Number of generations to reach lobular branches
- Counting the small airways with an MDCT scan?
- MDCT scans from a lung cancer prevention trial
- Counting terminal bronchioles with microCT
- Cross sectional area of the terminal bronchioles
- How many terminal bronchioles in a human lung?
- MicroCT versus casts
- Terminal bronchioles and cross sectional area
- Bronchiolar loss and emphysematous destruction
- Bronchiolar destruction and thickened walls
- Wall V/SA ratio versus FEV1
- Small airway plugging in COPD
- Extent of inflammatory cell infiltrate versus FEV1
- Multi level sampling design
- Volume of inflammatory cell infiltrate vs. FEV1
- Summary
- Mucosal immune system
- Lymphoid follicles
- Airways with follicles
- Remodeling of the airway walls
- Airway remodeling
- Example of airway remodeling
- Thin slice and a bronchogram of a lung
- Centrilobular emphysema
- Gross anatomy versus radiology
- Isolated alveoli are collaterally ventilated
- Conclusion (1)
- Conclusion (2)
- Acknowledgements
Topics Covered
- Progressive airflow limitation in COPD
- Effect of small airway occlusion on survival
- Methods of assessing lung structure
- The role of the innate and adaptive immune systems in COPD
- Bronchiolar destruction
- Airway remodeling
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Hogg, J. (2013, January 31). The pathology of chronic obstructive pulmonary disease [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 21, 2024, from https://doi.org/10.69645/WOOP6320.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. James Hogg has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
A selection of talks on Respiratory Diseases
Transcript
Please wait while the transcript is being prepared...
0:00
This talk is on the
pathology of Chronic
Obstructive Lung Disease.
My name is Jim Hogg,
and I'm from
Vancouver in Canada.
0:10
This is from a famous study
conducted by Fletcher
and his associates
on London postmen,
where they followed a
group of people over the
course of six to seven
years and followed
the progression of their
forced expiratory volume
(FEV_1) in one second.
That refers to the
volume of air you
can blow out of your
lungs in one second,
you blow as hard and as
fast as you can and it's
a measurement of how well
you empty your lungs.
This indicates the GOLD
classification of the severity
of chronic obstructive
pulmonary disease (COPD).
It was named by a committee
that had the acronym,
GOLD for Global
Obstructive Lung Disease
and divided into four
categories of severity.
You can see from the top curves,
which are normal people
and non-smokers,
their FEV_1 declines with age.
That happens in everybody
and it is a function
of getting older.
The bottom one of
the three represents
what happens to most
people when they smoke,
and the middle curve represents
what happens to nonsmokers
if they've smoked for
a long period of time
and then stop for a
long period of time,
they go back towards
the normal decline.
Not absolutely the same,
but it's close to that.
Now, GOLD 1 is the mildest
form of the disease,
and at this level
of the disease,
that person doesn't really know
that there's anything wrong.
But you can see
this bottom curve,
which is the next step,
indicates that importantly,
many people don't get
to the very maximum
they should get to at age 25
when you're supposed to
be at your very best
because they've either
been born prematurely
or they've had a
childhood infection
that has done something
to their lungs.
Now, they become in
this group of what
we call the
susceptible minority,
who are usually smokers
but can be people
that have been exposed to
other things, other aerosols.
Most commonly of the others,
is in the developing world,
where people, mostly women,
are exposed to smoke
from cooking fires
and that is an enormous
factor in causing COPD.
There is this
susceptible minority
that have a rapid
decline in their FEV_1.
The real reason for
that is not known.
But the pathology is
such that we think that
they lose their airways at
a faster rate than normal
and that that causes this
rapid decline to occur.