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Chronic Obstructive Pul monaryChronic Obstructive Pul monary

Disease (COPD)Disease (COPD)

M Farooq SaeedM Farooq Saeed

University of Health SciencesUniversity of Health Sciences

LahoreLahore
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ObjectivesObjectives

ll

Explain the importance of elastic recoil inExplain the importance of elastic recoil inkeeping respiratory bronchioles patent duringkeeping respiratory bronchioles patent duringexhalation.exhalation.

ll Explain how this relates to the classicExplain how this relates to the classic

definition of emphysema as "an abnormal,definition of emphysema as "an abnormal,permanent dilatation of part of all of thepermanent dilatation of part of all of theacinus, with destruction of alveolar walls."acinus, with destruction of alveolar walls."

ll Distinguish the two "classic" types ofDistinguish the two "classic" types ofemphysema, and mention their alleged causes.emphysema, and mention their alleged causes.

ll Tell what we think causes emphysema inTell what we think causes emphysema incigarette smokers and alphacigarette smokers and alpha--1 antitrypsin1 antitrypsindeficient patients.deficient patients.

ll Tell what a "pink puffer" looks like clinically,Tell what a "pink puffer" looks like clinically,and how emphysematous lungs look atand how emphysematous lungs look at

autopsy. Describe the complication of "bullousautopsy. Describe the complication of "bullousemphysema".

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Chronic Obstructive Pulmonary DiseaseChronic Obstructive Pulmonary Disease

(COPD)(COPD)

ll Also called chronic obstructi ve lungAlso called chronic obstructi ve lungdisease (COLD)disease (COLD)

ll Major cause of bed defining disabilityMajor cause of bed defining disability

ll Major symptom is dyspnea (shortness ofMajor symptom is dyspnea (shortness ofbreath)breath)

ll Usually due to cigarette smokingUsually due to cigarette smoking

ll Site of disease: bronchiSite of disease: bronchi --chronicchronic

bronchitis, bronchiectasis, asthma;bronchitis, bronchiectasis, asthma;ll BronchiolesBronchioles --bronchiolitisbronchiolitis

ll AciniAcini--emphysemaemphysema
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Obstructive airway diseaseObstructive airway disease:: Increase inIncrease in

resistance to airflow due to obstructi on at anyresistance to airflow due to obstructi on at anylevel; includes emphysema, chro nic bronchitis,level; includes emphysema, chro nic bronchitis,

bronchiectasis, asthma, tumor, foreign body;bronchiectasis, asthma, tumor, foreign body;

reduced maximal airflow rates (FEV1)reduced maximal airflow rates (FEV1)

Restrictive airway diseaseRestrictive airway disease:: ReducedReduced

expansion of lung parenchyma wi th decrease inexpansion of lung parenchyma wi th decrease in

total lung capacity; normal FEV1; due to chesttotal lung capacity; normal FEV1; due to chestwall disorders (pol io, obesity, pleural disease,wall disorders (pol io, obesity, pleural disease,

kyphoscoliosis), interstitial / infiltrative diseaseskyphoscoliosis), interstitial / infiltrative diseases

(ARDS, dust di seases, interstitial fibrosis)(ARDS, dust diseases, interstitial fibrosis)

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Obstructive Airway Disease:

Localised Mechanical

Tumors, Trauma, Foreign body collapse

Diffuse Distal airway diseases

COPD

chronicCOPD Definition:

Progressive irreversible airway obstruction with

destruction of parenchyma

Chronic Bronchitis

EmphysemaAsthma

Chronic Slowly progressive

Stable over several months

25% of smokers likely to develop COPD

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Chronic Bronchitis

Chronic bronchitis is a clinically definedsyndrome of chronic excessive mucus

production in the airwaysMucus is mainly produced by the bronchial

glands.

The pathologic hallmark of chronicbronchitis is mucous gl and enlargement.

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CLASSIFICATIONCLASSIFICATION

llChronic Simple BronchitisChronic Simple Bronchitis

ll

Chronic Obstructive BronchitisChronic Obstructive BronchitisllChronic Asthmatic BronchitisChronic Asthmatic Bronchitis

llConstrictive BronchiolitisConstrictive Bronchiolitis

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1.Smoking / pol lution - major cause.2.Acute & Chronic mucosal inflammation

3.The walls get thicker and this narro ws the

bronchial lumens.4.Lack of cilia - retention of secretions5.Increased mucous glands & viscid

mucous.6.Frequent secondary infections7.Inflammation retention infection

obstruction cycle.

PathogenesisPathogenesis

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ll The Reid indexThe Reid index , the ratio of the, the ratio of thebronchial mucous gland layer tobronchial mucous gland layer tobronchial wall thickness (frombronchial wall thickness (fromperichondrium to basementperichondrium to basement

membrane), serves as an indicatormembrane), serves as an indicatorof mucous gland hypertrophy.of mucous gland hypertrophy.

ll Approximate Reid index less thanApproximate Reid index less than0.36 to 0.550.36 to 0.55

ll In general, a Reid index of 0.4 orIn general, a Reid index of 0.4 orgreater is consistent w ith mucousgreater is consistent w ith mucousgland hypertrophy.gland hypertrophy.

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CHRONIC BRONCHITIS "smoker'sCHRONIC BRONCHITIS "smoker's

cough"cough"

ll The "classic chronic bronchitis patient" is aThe "classic chronic bronchitis patient" is a"blue bloater", with increased PaCO"blue bloater", with increased PaCO 22,,obese, edematous (cor pul monale),obese, edematous (cor pul monale),

cyanotic, producing purulent sputum.cyanotic, producing purulent sputum.

ll Distinguishing featureDistinguishing feature; acquired tolerance; acquired tolerancefor the hypercarbia that poor venti lationfor the hypercarbia that poor venti lation

(i.e., from emphysema) ul timately causes.(i.e., from emphysema) ul timately causes.

ll Unlike "pink puffers" (who retain theirUnlike "pink puffers" (who retain theirhypercarbic drive), these patients nohypercarbic drive), these patients nolonger really struggle to breathe, so longlonger really struggle to breathe, so longas they have adequate Oas they have adequate O22

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ll "Coarse breath sounds" / "coarse"Coarse breath sounds" / "coarse

rhonchi"rhonchi"ll Clubbing of fingersClubbing of fingers

ll Despite elaborate systems of testingDespite elaborate systems of testing

pulmonary function, the ultimatepulmonary function, the ultimatediagnosis of "COPD" is made on histor ydiagnosis of "COPD" is made on histor y

and physical exam.and physical exam.

ll This applies to most other dis eases too.This applies to most other dis eases too.
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COMPLICATIONSCOMPLICATIONS

ll Pulmonary hypertension super venesPulmonary hypertension super venes

earlier in "chronic bronchitis" patientsearlier in "chronic bronchitis" patients

than in emphysema patientsthan in emphysema patientsll At autopsy we find copious secretionsAt autopsy we find copious secretions

in the airways, even in the absence ofin the airways, even in the absence of

pneumonia.pneumonia.

ll The trachea itself may be almost filledThe trachea itself may be almost filled

with yellow slime (with yellow slime (slipperyslippery)) ..

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ll The chest cavity is opened at autopsy to reveal numerous large bThe chest cavity is opened at autopsy to reveal numerous large bullae apparent on the surface of the lungs in aullae apparent on the surface of the lungs in apatient dying with emphysema.Bullae are large dilated airspacespatient dying with emphysema.Bullae are large dilated airspaces that bulge out from beneath thethat bulge out from beneath the

pleura.Emphysema is characterized by a loss of lung parenchyma bpleura.Emphysema is characterized by a loss of lung parenchyma by destruction of alveoli so that there isy destruction of alveoli so that there is

permanent dilation of airspaces.permanent dilation of airspaces.

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EmphysemaEmphysema

ll Emphysema is defined as "permanentEmphysema is defined as "permanentenlargement of airspaces accompaniedenlargement of airspaces accompanied

by destruction of alveolar walls andby destruction of alveolar walls and

capillary bed".capillary bed".

ll In pulmonary emphysema there is loss ofIn pulmonary emphysema there is loss of

alveolar septal tissue and correspondingalveolar septal tissue and corresponding

enlargement of airspaces.enlargement of airspaces.

ll Interstitial fibrosis is not seenInterstitial fibrosis is not seenhistologically, if present, is the result ofhistologically, if present, is the result of

additional lung injury due to some otheradditional lung injury due to some other

process.process.

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PathogenesisPathogenesis

ll The current concept of the of pulmonary e mphysema isThe current concept of the of pulmonary e mphysema isthat of athat of a proteaseprotease--antiproteaseantiprotease imbalance, with theimbalance, with theresultant enzymatic destruction of the lung structuralresultant enzymatic destruction of the lung structuralprotein,protein, elastinelastin

ll Cigarette smoke functions in several w ays as a mediatorCigarette smoke functions in several w ays as a mediatorof tissue destruction.of tissue destruction.

ll It stimulates pulmonar y inflammatory cells (It stimulates pulmonar y inflammatory cells (macrophagesmacrophagesand neutrophilsand neutrophils) to accumulate in the lung) to accumulate in the lung

ll Both macrophages and neutrophils release elastase,Both macrophages and neutrophils release elastase,although neutrophil elastase is considered to be morealthough neutrophil elastase is considered to be moreimportant in the degradation of lung elastin.important in the degradation of lung elastin.

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ll At the same time oxidants in cigaretteAt the same time oxidants in cigarette

smoke are thought to inhibit the activit ysmoke are thought to inhibit the activit y

of alphaof alpha--11--antitrypsin, the most importantantitrypsin, the most important

serum protease inhibitor.serum protease inhibitor.

ll There is additional evidence that theseThere is additional evidence that these

oxidants can directly injure lung tissueoxidants can directly injure lung tissue

as well as can impair elastin synthesis.as well as can impair elastin synthesis.

ll As alveolar septa are destroyed, lungAs alveolar septa are destroyed, lung

elastic recoil is reduced.elastic recoil is reduced.
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llElasticity & normal aging &Elasticity & normal aging &smoking.smoking.

llBoth emphysema and chronicBoth emphysema and chronic

bronchitis are most commonlybronchitis are most commonlycaused bycaused by cigarettecigarette smokingsmoking..

llMost smokers with one have theMost smokers with one have the

other, tooother, too

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Emphysema due to AEmphysema due to A--11--ATDATD

ll Genetic deficiencyGenetic deficiency

ll AlphaAlpha--11--antitrypsin (AAT) inhibits proteases, particularly elastase (whiantitrypsin (AAT) inhibits proteases, particularly elastase (whichchdigests lung tissue), which is secreted by neutrophils during indigests lung tissue), which is secreted by neutrophils during inflammationflammation

ll PiMM: normal phenotype; 90% of populationPiMM: normal phenotype; 90% of population

ll PiZZ: associated with AAT deficiency; 80% develop symptomaticPiZZ: associated with AAT deficiency; 80% develop symptomaticemphysema; occurs earlier and is more severe in smokersemphysema; occurs earlier and is more severe in smokers

ll Neutrophils are normally present in lung and alveolar space; wheNeutrophils are normally present in lung and alveolar space; whenn

stimulated, neutrophils and macrophages increase in number andstimulated, neutrophils and macrophages increase in number andrelease elastase and oxygen free radicals, which causes emphysemrelease elastase and oxygen free radicals, which causes emphysemaaunless counteracted by antiproteases such as AATunless counteracted by antiproteases such as AAT

ll Smokers have more neutrophils and macrophages in alveoli, tobaccSmokers have more neutrophils and macrophages in alveoli, tobaccoouse enhances release of elastase from neutrophils, enhances elasuse enhances release of elastase from neutrophils, enhances elastasetaseactivity, oxidants in tobacco smoke inhibit AATactivity, oxidants in tobacco smoke inhibit AAT

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Anatomic Classification ofAnatomic Classification of

EmphysemaEmphysema

ll Emphysema can be classifiedEmphysema can be classified

anatomically into four subtypes:anatomically into four subtypes:

ll Centriacinar (centrilobular)Centriacinar (centrilobular)

ll Panacinar (panlobular)Panacinar (panlobular)

ll Paracicatricial (irregular)Paracicatricial (irregular)ll Paraseptal (distal acinar)Paraseptal (distal acinar)

ll OthersOthers

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ll Frequently there is a mixture of typesFrequently there is a mixture of types

within the same lung. There is nowithin the same lung. There is noevidence at present to suggest thatevidence at present to suggest thatone subtype evolves into another.one subtype evolves into another.

ll The factors which lead to each of theseThe factors which lead to each of theseanatomic forms of emphysema ar eanatomic forms of emphysema ar eunclear.unclear.

ll Each type has its own clinical correlatesEach type has its own clinical correlatesand should be considered as a distinctand should be considered as a distinctentity.entity.

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Centriacinar Emph ysemaCentriacinar Emph ysema

95% of emphysema cases95% of emphysema cases

ll Causes signif icant airflow obstruction,Causes signif icant airflow obstruction,ll Affects central part of acini, sparingAffects central part of acini, sparing

distal alveoli.distal alveoli.

ll Worse in upper lobes, particularly apicesWorse in upper lobes, particularly apices

ll Men more proneMen more prone

ll Walls are anthracotic with parabronchialWalls are anthracotic with parabronchial

inflammationinflammation

ll

Seen in heavy smokers, coal workerSeen in heavy smokers, coal workerpneumoconiosispneumoconiosis

ll Clinically significant at age 40+ in smokers,Clinically significant at age 40+ in smokers,

although ventilatory deficits seen earlieralthough ventilatory deficits seen earlier

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Panlobular EmphysemaPanlobular Emphysema

ll 5% of cases5% of cases

ll Acini uniformly enlarged fromAcini uniformly enlarged fromrespiratory bronchiole to terminalrespiratory bronchiole to terminal

alveolialveolill Usually lower lungsUsually lower lungs

ll More common in women below 40More common in women below 40yearsyears

ll Associated with AAssociated with A--1AT deficiency1AT deficiency

ll Lungs usuallyLungs usually voluminousvoluminous
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Paraseptal (Distal Acinar) EmphysemaParaseptal (Distal Acinar) Emphysema

Involve the distal periphery of the acinusInvolve the distal periphery of the acinusadjacent to pleura, interlobular septa oradjacent to pleura, interlobular septa or

bronchovascular bundles.bronchovascular bundles.

Minor clinically ; RareMinor clinically ; RareEmphysema is next to pleuraEmphysema is next to pleura

Near areas of fibrosis, scarring or atelectasisNear areas of fibrosis, scarring or atelectasis

Multiple continuous airspaces affectedMultiple continuous airspaces affected

May be source of spontaneous pneumothoraxMay be source of spontaneous pneumothorax

in young adultsin young adults

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Senile emphysemaSenile emphysema

::

Due to ageDue to age--relatedrelated

alterations in internal geometryalterations in internal geometryof alveoli leading to larger alveolarof alveoli leading to larger alveolar

ducts, smaller alveoli, but no lossducts, smaller alveoli, but no loss

of elastic tissue or destruction ofof elastic tissue or destruction oflung substancelung substance

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Paracicatricial emphysemaParacicatricial emphysema

ll

Dilated airspaces are of ten seen on the edge ofDilated airspaces are of ten seen on the edge ofpulmonary scars. This form of emphysema bearspulmonary scars. This form of emphysema bearsno uniform relationship to the acinus & is someno uniform relationship to the acinus & is some --times called " irregular" emphysema.times called " irregular" emphysema.

ll

It is probably, in part, the result of traction onIt is probably, in part, the result of traction onsurrounding lung tissue by the contractingsurrounding lung tissue by the contractingfibrous scar.fibrous scar.

ll Usually, paracicatricial emphysema is an inci dentalUsually, paracicatricial emphysema is an inci dental

finding without clinical signif icance. However, infinding without clinical signif icance. However, inseverely scarred lungs associated with granulomatousseverely scarred lungs associated with granulomatousdisorders such as tuberculosis, extensive paracicatricialdisorders such as tuberculosis, extensive paracicatricialemphysema can produce airf low obstruction.emphysema can produce airf low obstruction.

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Obstructive emphysema

Due to tumor, foreign body or congenitallobar over inflation

(infants, perhaps due to hypoplasia ofbronchial cart ilage; associated with other)cardiopulmonary anomalies

Due to ball-valve effect with inhalation viacollaterals (pores of Kohn, canals of Lambert)

Compress normal lung, may be life-threatening

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Interstitial emphysemaInterstitial emphysemaAir into connective tissue stroma ofAir into connective tissue stroma of

lung, mediastinum or subcutaneouslung, mediastinum or subcutaneous

tissue, due to alveolar tears, chesttissue, due to alveolar tears, chest

wounds, coughing, whooping coughwounds, coughing, whooping cough

Compensatory emphysemaCompensatory emphysema

Response to loss of l ung elsewhere,Response to loss of l ung elsewhere,

such as postsuch as post --lobectomylobectomy

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Bullous emphysemaBullous emphysema

ll Produces airProduces air --filled blebs (called "bullaefilled blebs (called " bullae

if >1 cm) containing little or no lung tissueif >1 cm) containing little or no lung tissue

located immediately adjacent to the viscerallocated immediately adjacent to the visceral

pleura.pleura.

ll Usually at the apicesUsually at the apices

ll Sometimes at the sites of old TBSometimes at the sites of old TB scars.scars.

ll Most cases probably r esult from common emphysema,Most cases probably r esult from common emphysema,

with the inelastic lung "collapsing under its own wei ght";with the inelastic lung "collapsing under its own wei ght";

the upper lobes have more contact more tobacco smokethe upper lobes have more contact more tobacco smoke

because they are better ventilated.because they are better ventilated.

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The blebs may be removed s urgically,The blebs may be removed s urgically,

with improvement in the "pink puffer"'swith improvement in the "pink puffer"'spuffing.puffing.

Blebs are also prone to rupture, causingBlebs are also prone to rupture, causing

pneumothorax and sudden deathpneumothorax and sudden death

Iatrogenic disease: "IPPB breathingIatrogenic disease: "IPPB breathing

treatments" are irrational therapy fortreatments" are irrational therapy foruncomplicated emphysema, and killuncomplicated emphysema, and kill

patients by blowing out blebspatients by blowing out blebs

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Pulmonary Vascular ChangesPulmonary Vascular Changes

ll The small pulmonary arteries and arteriolesThe small pulmonary arteries and arterioles

in emphysema show increased medial smoothin emphysema show increased medial smoothmuscle, abnormal muscle which has extendedmuscle, abnormal muscle which has extended

into normally noninto normally non--muscular arteries & longitudinalmuscular arteries & longitudinal

muscle bundles in the intima.muscle bundles in the intima.

ll The strongest stimulus for this arterialThe strongest stimulus for this arterial

muscularization in emphysema appearsmuscularization in emphysema appears

to be chronic hypoxia.to be chronic hypoxia.

ll The net effect of the increased mural musculatureThe net effect of the increased mural musculature

is to compromise vascular lumens and possiblyis to compromise vascular lumens and possibly

increase vascular tone.increase vascular tone.

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ll The pulmonary capillary bed isThe pulmonary capillary bed is

extensively destroyed along withextensively destroyed along withalveoli in emphysema.alveoli in emphysema.

ll Anatomic right ventricul ar hypertrophyAnatomic right ventricul ar hypertrophyis regularly seen in patients withis regularly seen in patients with

severe (high grade) emphysemasevere (high grade) emphysema

(either panacinar or centriacinar) and(either panacinar or centriacinar) andunusual in those with minimalunusual in those with minimal

emphysemaemphysema

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Clinical PictureClinical Picture

llNo symptoms until 1/3 of func tionalNo symptoms until 1/3 of func tionalcapacity is lostcapacity is lost

llThe only consistent finding on phys icalThe only consistent finding on phys ical

exam is slowing of forced expirationexam is slowing of forced expirationllShortness of breath, coughing,Shortness of breath, coughing,wheezing, weight losswheezing, weight loss

llBarrel chest, pursed li ps, dyspneic,Barrel chest, pursed li ps, dyspneic,tachypneic, thintachypneic, thin

llThe classic "emphysema" patient is aThe classic "emphysema" patient is a

"pink puffer", with normal Pa"pink puffer", with normal Pa--COCO22

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COMPLICATIONSCOMPLICATIONS

ll Exacerbations and death often follow infectionExacerbations and death often follow infectionwithwith S. pneumS. pneum ororH. influenH. influen

ll Death may also result from cor pulmonale or fromDeath may also result from cor pulmonale or fromapnea brought about by breathing oxygenapnea brought about by breathing oxygen

(remember, hypercarbia no longer stimulates(remember, hypercarbia no longer stimulatesrespiration in these patients.)respiration in these patients.)

ll May cause secondary pulmonary vascularMay cause secondary pulmonary vascularhypertension, cor pulmonale, congestive hearthypertension, cor pulmonale, congestive heartfailure, death due to respiratory acidosis andfailure, death due to respiratory acidosis and

coma, pneumothoraxcoma, pneumothoraxll Best to assess based on morphometry, not lungBest to assess based on morphometry, not lung

function datafunction data

ll At autopsy, the lungs are hyperinflated andAt autopsy, the lungs are hyperinflated andrelatively bloodlessrelatively bloodless

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Blue BloaterBlue Bloaterll Mild dyspnoea, lateMild dyspnoea, late

ll Infections commonInfections common

ll CorCor--pulmonalepulmonale

ll Increased resistanceIncreased resistance

ll

Prominent BV, largeProminent BV, largeheartheart

ll Infrequent wt lossInfrequent wt loss

ll Sputum & RonchiSputum & Ronchi

MaximalMaximalll CyanosisCyanosis

ll Normal ABGNormal ABG

ll Episodic, recurrentEpisodic, recurrent

Pink PufferPink Pufferll Dyspnoea severe, earlyDyspnoea severe, early

ll OccassionalOccassional

ll Rare, lateRare, late

ll Mild increaseMild increase

ll Hyperinflation smallHyperinflation smallheartheart

ll Severe wt lossSevere wt loss

ll Sputum & RonchiSputum & Ronchi

MinimalMinimalll Severe HypoxemiaSevere Hypoxemia

ll Prognosis, terminalPrognosis, terminal

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Smokers PathologySmokers Pathologyll Tobacco pigment in the lungs (brow n stuff)Tobacco pigment in the lungs (brow n stuff)

ll Carbon pigment in the lungs "anthracosisCarbon pigment in the lungs "anthracosis

ll Loss of ciliary motilityLoss of ciliary motility

ll Goblet cell proliferation in remaining columnarGoblet cell proliferation in remaining columnar

epitheliumepitheliumll Hypertrophy and hyperplasia of mucous glandsHypertrophy and hyperplasia of mucous glands

ll Thickening of the respirator y epithelialThickening of the respirator y epithelialbasement membrane ("subepithelial collagenbasement membrane ("subepithelial collagen

deposition")deposition")ll Increased numbers of pol ys in the lungs, 4XIncreased numbers of pol ys in the lungs, 4X

ll Increased numbers of alveolar macrophagesIncreased numbers of alveolar macrophages(x6 or so)(x6 or so)

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ll Impaired ability of alveolarImpaired ability of alveolar

macrophage to function usefullymacrophage to function usefullyll Increased neutro and macro elastaseIncreased neutro and macro elastase

production and releaseproduction and release

ll Impaired ability of alveolarImpaired ability of alveolarmacrophage to function usefullymacrophage to function usefully

ll Squamous metaplasia of respiratorySquamous metaplasia of respiratory

epitheliumepitheliumll Loss of elasticity of alveolar wallsLoss of elasticity of alveolar walls

ll Eventual destruction of alveolar wallsEventual destruction of alveolar walls

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ll Smokers have a greater number ofSmokers have a greater number ofneutrophils and macrophages in their alveoli.neutrophils and macrophages in their alveoli.

ll Smoking irritates alveolar macrophages,Smoking irritates alveolar macrophages,which in turn release neutrophil chemotacticwhich in turn release neutrophil chemotacticfactors, such as interleukin 8, thus recruitingfactors, such as interleukin 8, thus recruitingneutrophils.neutrophils.

ll Nicotine is chemotactic for neutrophilsNicotine is chemotactic for neutrophilsll Activate the alternative complement pathwayActivate the alternative complement pathway

ll Proteases, particularly elastase, are secretedProteases, particularly elastase, are secreted

by these neutrophils and macrophagesby these neutrophils and macrophages

ll Proteases are enzymes that are capable ofProteases are enzymes that are capable ofdigesting lung tissue and these chemicals aredigesting lung tissue and these chemicals areresponsible for the damage seen inresponsible for the damage seen inemphysema.emphysema.
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llOxidants and free radicals in smokeOxidants and free radicals in smoke

also inhibit the alphaalso inhibit the alpha --11--antitrypsinantitrypsincirculating in the lung that protectscirculating in the lung that protectsalveoli from proteases.alveoli from proteases.

llChronic irritation by smoke also canChronic irritation by smoke also canlead to chronic bronchitis with excesslead to chronic bronchitis with excessproduction of mucus.production of mucus.

ll Smoke interferes with the ciliary actionSmoke interferes with the ciliary action

of the respiratory epithelium and theof the respiratory epithelium and themucus cannot be cleared. Thismucus cannot be cleared. Thispredisposes the smoker to secondarypredisposes the smoker to secondary

and repeated infectionsand repeated infections
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DiagnosisDiagnosis

ll HistoryHistoryll Physical ExaminationPhysical Examination

ll Radiological ExaminationRadiological Examination

ll

Laboratory Examination of sputum, bloodLaboratory Examination of sputum, bloodll Pulmonary Func Tests:Pulmonary Func Tests:

Inc Expiratory PhaseInc Expiratory Phase

Mismatch Ventilation PerfusionMismatch Ventilation Perfusion

Inc FVCInc FVC Dec FEVDec FEV11

Inc RVInc RV

Inc TLCInc TLC

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3 Investigations:

Spirometry (FEV1/VC), PaO2, PCO2.

3 gradesMild 69-80 FEV1 cough, exertional

dysp.

Mod 40-60 FEV1 - + Wheeze, cough,sputum.

Sev - < 40 FEV1 - + Right Heart Failure.

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TREATMENTTREATMENT

Palliative Non Pharmacol ogical Therapy:Palliative Non Pharmacol ogical Therapy:ll Counselling and preventionCounselling and prevention

ll Check sputumCheck sputum

ll Feed modificationFeed modification

ll Breathing ExercisesBreathing Exercises

Pharmacological Therapy:Pharmacological Therapy:ll Bronchodilators (Bronchodilators ( adrenergic, anticholinergic)adrenergic, anticholinergic)

ll TheophyllineTheophylline

ll Corticosteroids ?Corticosteroids ?

ll OO22 Therapy (1Therapy (1--2 Lit/min; PO2 Lit/min; PO2=2= 5555--65 mm Hg)65 mm Hg)

ll SurgerySurgery

Date post:	07-Apr-2018
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