Tobacco and Chronic Obstructive Pulmonary Disease

A major problem still on the rise

By Allan R. Handysides, M.B., Ch.B. FRCPc, FRCSc, FACOG.. Director, GC Health Ministries Department

COPD

C hronic O bstructive P ulmonary D isease

An

airway flow disease A very common problem2

Tobacco and COPD

COPD

Chronic Bronchitis Emphysema

These two are the most common diagnoses given to patients
Tobacco and COPD

Prevalence

Affects 16,000,000 Americans Males more than Females Whites more than Blacks History of Low Birth Weight

Tobacco and COPD

Death Dealing Disorder

COPD = 4th leading cause of death in the USA The only disease in the top 10 diseases still showing an increasing rise in mortality rates
Tobacco and COPD

Pathology of COPD

Small and large airway narrowing caused by

Epithelial thickening Increased mucus cells Hyperplasia Fibrosis Mucus plugs
Tobacco and COPD

Air-flow regulation
Bronchiolar diameter Elastic recoil of the lung Collapsibility of the lung ( lesser factor )

Tobacco and COPD

Tobacco Smoke

Potentiates the effects of Air Pollution in general and in some work places, such as plastics factories Potentiates the effects of infection
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Tobacco and COPD

Emphysema

Alters the inflation baseline Which alters the Residual volume and the functional residual volume by increasing them In fact the total lung capacity is increased
Tobacco and COPD

Impaired Gas Exchanges

The VQ (ventilation/perfusion) ratio altered in chronic bronchitis/emphysema (COPD) Ventilation altered by both Perfusion altered in emphysema so that the ratio may look more normal as the emphysema progresses 10
Tobacco and COPD

Respiratory center response

Pink Puffers increase the ventilatory rate = dyspnoeic but normal gases

Blue Bloaters have rising CO2 and falling O2 but less respiratory effort
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Pulmonary Hypertension
Loss of vascular bed Hypoxemic effect on the pulmonary vasculature Hypoxemia leads to increased erythrocytosis and increased viscosity of the blood Carboxyhemoglobin increases 12 respiratory drive

Tobacco and COPD

Flow through pipes!

REMEMBER
The one inch pipe serves one house The two inch pipe serves sixteen houses

THIS PROBLEM IS ONE OF NARROWED AIRWAYS

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The wheeze

Inspiration
Expiration

Widens the airway

narrows the airway

WHEEZING IS WORSE DURING EXPIRATION AND MAY BE THE FIRST SIGN OF AIRWAY NARROWING
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THE DISEASE PROCESS

Largely an inflammatory process

Resulting from increased activity of oxidants combined with decreased activity of antioxidants

OXIDATIVE

STRESS

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Tobacco smoke
High

concentrations of oxygen free radicals including

Superoxides hydrogen peroxide hyperchlorous acid
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Tobacco smoke

Independent source of Ferrous molecules which stimulates eosinophils and alveolar macrophages to form highly active hydroxyl radicals from oxygen and hydrogen peroxide
O2 O2
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Tissue Damage

Smoke also inhibits the action of alpha 1 antitrypsin an elastase inhibitor which (elastase) in company with the free radicals set about damaging tissue Alpha 1 antitrypsin usually inhibits the activity of elastase which degrades elastin( the collagen giving elasticity to the lung)
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Antitrypsin inhibition

Effected through Tobacco smoke oxidants Neutrophils Type II alveolar pneumocytes

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Cellular changes
Smoking

leads to increased numbers of

CD8 cells Eosinophils Macrophages Mast cells
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Transforming Growth Factor B

This factor(TGFB) is related to fibrogenesis , which is needed in tissue repair. Patients with COPD have twofold increases in this factor which strongly correlates in a negative fashion with the Forced Expiratory volume 1 second FEV1 The factor is produced in Macrophages and Mast cells
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FEV1
F orced E xpiratory V olume 1 second
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Pathways to a reduced FEV1

Impaired childhood lung growth and development leads to a lower peak and a normal decline from this capacity Normal early growth but premature peak then a normal decline from this level Normal peak but accelerated decline from the peak
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90%
90%

of COPD patients are current or former smokers

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Tobacco Smoke

Inhibits ciliary action Inhibits the function of alveolar macrophages Leads to hypertrophy and hyperplasia of the mucus secreting cells Inhibits anti-proteases and encourages the release of proteases from leukocytes Increases airway resistance 25
Tobacco and COPD

Genotype factors

Only 15% of smokers get COPD Twin studies suggest an underlying genetic predisposition may also be at work
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Alpha 1 anti-trypsin deficiency

394 amino acid chain it is a serine protease inhibitor produced in the liver and it counteracts the neutrophil elastase 1 in 2000-7000 Caucasians are deficient in the enzyme such deficiency leads to emphysema of the pan-acinar variety

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Secondary Effects

Renal dysfunctions Weight loss Muscular wasting Osteoporosis

all complicating factors in COPD

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Tobacco and COPD

The Christians Response?

Prevention

where

possible!

Compassion always
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These are broken, hurting, frightened, people, children of our heavenly Father who loves them as he loves us all.
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Tobacco and COPD

THE END

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