(C.O.P.D) Ch.Bronchitis Emphysema

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(C.O.P.D) (C.O.P.D) Ch.Bronchitis Ch.Bronchitis Emphysema Emphysema AISHA M SIDDIQUI AISHA M SIDDIQUI

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(C.O.P.D) Ch.Bronchitis Emphysema. AISHA M SIDDIQUI. C.O.P.D. Pathology Pathophysiology Types Clinical features Acute complications Chronic complications Investigations Differential diagnosis Treatment References. Ch.Bronchitis. Normal mechanism of cough. - PowerPoint PPT Presentation

Transcript of (C.O.P.D) Ch.Bronchitis Emphysema

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(C.O.P.D) (C.O.P.D) Ch.Bronchitis Ch.Bronchitis Emphysema Emphysema

AISHA M SIDDIQUIAISHA M SIDDIQUI

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C.O.P.DC.O.P.D PathologyPathology PathophysiologyPathophysiology TypesTypes Clinical featuresClinical features Acute complicationsAcute complications Chronic complicationsChronic complications InvestigationsInvestigations Differential diagnosisDifferential diagnosis TreatmentTreatment ReferencesReferences

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Ch.BronchitisCh.Bronchitis

Normal mechanism of cough.Normal mechanism of cough.

Ch.irritation>>>>ch.bronchitisCh.irritation>>>>ch.bronchitis

Smoking, industries & pollution.Smoking, industries & pollution.

Mortality ^ with infectionMortality ^ with infection

More in winter & autumnMore in winter & autumn

More in low socioeconomic class.More in low socioeconomic class.

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EmphysemaEmphysema

Pathology:Pathology:

Enlarged air spaces distal to Enlarged air spaces distal to terminal bronchioles with terminal bronchioles with destruction to the walls.destruction to the walls.

Centrilobular(U.Z)>>>>>BullaeCentrilobular(U.Z)>>>>>Bullae

Panacinar(L.Z)----Panacinar(L.Z)---->>>>>>>>

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EmphysemaEmphysema

Pathogenesis:Pathogenesis:

Smoking,air Smoking,air pollution,infection,Intrinsic.pollution,infection,Intrinsic.

- Alpha 1 Antitrypsin def: inhibits - Alpha 1 Antitrypsin def: inhibits proteolytic enzymes released from proteolytic enzymes released from macrophages and neutrophils.macrophages and neutrophils.

Increases in smokers Increases in smokers

Basal segments.Basal segments.

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EmphysemaEmphysema Pathophysiology:Pathophysiology: Airway dis.(narrowing)>>>limitation of air Airway dis.(narrowing)>>>limitation of air

flow>>> poorly ventillated.flow>>> poorly ventillated. VENTILLATION PERFUION MISMATCHVENTILLATION PERFUION MISMATCH Extensive dis.>>>Resp. Failure(type 2)Extensive dis.>>>Resp. Failure(type 2) ELASTIC RECOIL OF THE LUNG LOSTELASTIC RECOIL OF THE LUNG LOST Expansion of lung >>> increase T.L.CExpansion of lung >>> increase T.L.C Earlier closure of airways >>> inc. R.V (air Earlier closure of airways >>> inc. R.V (air

trapping)trapping) Reduction of surface area for gas Reduction of surface area for gas

exchange>>>decrease in transfer factor.exchange>>>decrease in transfer factor.

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TYPESTYPES

Blue bloatersBlue bloaters Pink puffersPink puffers

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Clinical FeaturesClinical Features

BreathlessnessBreathlessness Insidiuos onsetInsidiuos onset Increase graduallyIncrease gradually Irritation of Irritation of

mucosa>>>mucous>>>cough>>mucosa>>>mucous>>>cough>>> bronchoconstriction.> bronchoconstriction.

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Clinical FeaturesClinical Features

Physical signs:Physical signs: Mild- Moderate >>> No abnormalityMild- Moderate >>> No abnormality Tachypnea.Tachypnea. Prolonged expiration, pursed lips.Prolonged expiration, pursed lips. Xssory ms. Of resp.Xssory ms. Of resp. Posture; mechanical advantage.Posture; mechanical advantage. Chest:Chest:

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ComplicationsComplications

CHRONIC: Type 2 resp. failure.CHRONIC: Type 2 resp. failure.

Polycythemia.Polycythemia.

Corpulmonale.Corpulmonale. ACUTE: Infections.ACUTE: Infections.

L.V.F.L.V.F.

P.E.P.E.

Pneumothorax.Pneumothorax.

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Differential DiagnosisDifferential Diagnosis

CHRONIC BRONCHITIS: B.asthmaCHRONIC BRONCHITIS: B.asthma

BronchiectasisBronchiectasis

Ch.sinusitisCh.sinusitis

AspirationAspiration

T.B/ NeoplasmT.B/ Neoplasm EMPHYSEMA: C.O.P.D/ B.asthmaEMPHYSEMA: C.O.P.D/ B.asthma

Obstructive/ RestrictiveObstructive/ Restrictive

Large airways obstruc/ smallLarge airways obstruc/ small

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InvestigationsInvestigations

C.X.R/C.TC.X.R/C.T

Bld. GasesBld. Gases

Pulm. Function tests: FEV1/ FVCPulm. Function tests: FEV1/ FVC

PEFRPEFR

DL coDL co

SputumSputum

ECGECG

CBCCBC

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TreatmentTreatment

STOP SmokingSTOP Smoking Domociliary O2 therapy: 15 hrs. 2L 28%Domociliary O2 therapy: 15 hrs. 2L 28% Bronchodilators: B2 agonistsBronchodilators: B2 agonists Anticholinergics Anticholinergics

(Ipratropium Bromide)(Ipratropium Bromide) Methylxanthines?Methylxanthines? Corticosteroids: Acute exacerbationsCorticosteroids: Acute exacerbations Stable dis.?Stable dis.? InhalersInhalers

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TreatmentTreatment

Antibiotics: FEV1<50%, More strong Antibiotics: FEV1<50%, More strong A/BA/B

DiureticsDiuretics VasodilatorsVasodilators Chest physiotherapyChest physiotherapy N.I.V: C.P.A.PN.I.V: C.P.A.P VenesectionVenesection VaccinationsVaccinations

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ReferencesReferences

Scientific American Medicine 9/01Scientific American Medicine 9/01 NEJM : June 26, 2003. Vol. 348(26)NEJM : June 26, 2003. Vol. 348(26) NEJM : June 24, 2004. Vol. 350(26)NEJM : June 24, 2004. Vol. 350(26) DavidsonDavidson’’s Principles and Practice s Principles and Practice

of Medicineof Medicine Uptodate 2008Uptodate 2008

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BRONCHIAL ASTHMABRONCHIAL ASTHMA

DefinitionDefinition Cardinal pathophysiological features:Cardinal pathophysiological features: Airflow limitation (reversible)Airflow limitation (reversible) Airway hyperresponsivenessAirway hyperresponsiveness Airway inflammationAirway inflammation Types and aetiologyTypes and aetiology Clinical featuresClinical features InvestigationsInvestigations ManagementManagement