Copd Final 97-2003hiraa

8/4/2019 Copd Final 97-2003hiraa

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CasePresentation

By

House Officer

(CHK)

P-2


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HistoryM.Sajid , 60 years old , resident of Bihar colony Admitted through E.R on 21.7.2011

with C/O

Shortness of breathFever Since 3 days

Urinary Incontinence

H.O.P.CAccording to the pts attendent pt was alright 3 years back then he

developed shortnessOf breath on&off, pt was prescribed inhalers and oral medications but thecondition of the pt didnt improve. The shortness of breath increased three days back, pt can only walk few steps. Shortnessof breath aggrevates on exposure to dust, smoke and on lifting objects,shortness of breath is partly relieved by the use of Inhalers.

Pt has also comlpain of fever from 3 days which is high grade, intermittent,associated with cough which is productive, sputum is small in amount, white incolour.Fever is relived by taking Antipyretics.Pt has also C/O incontinence of urine and weakness for the last 3 days.


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Past history

Medical = H/O admission in hospital 3 years back for SOBSurgical = Not Significant.

Personal History

Sleep DisturbedApetite decreasedMicturation Incontinence

Bowel NormalAddiction Pan chewing ,smoking since 40-45 years.

Drug History

Pt has been taking Inhalers and oral medications for shorness of breath.

Socio-economic Status = Poor

General Physical Examination

Male pt of average height and built lying in bed, dysponic, concious oriented.


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Anemia -ve

Edema -ve

Dehydration -ve

Jaundice -ve

Lymph nodes Not palpable

Vitals

B.P 140/100 mm Hg

Pulse 120 b/min

Temp 98.6 F

R/R 30/min

System Examination

Chest: on Inspection: barrel shaped chest

No intercostal recession abserved.Pulsation visible in Epigastric region.

On palpation

Trachea central

AP diameter = Increased


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On Percussion: Hyperresonant note.

On Ausculation: Crepts heard Bilaterally all over the chest.

Abdomen: Soft, non- tender no visceromegaly.

CVS: S1 & S2 audible.

CNS: Intact.


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Test Result Unit

Hemoglobin (gm/dl) 12.90 Gm/dl

RBC Count 4.80 Mil.L

HCT 39.50 %

MCV 82.50 Fl

MCH 26.9 Pg

Total Leucocytes Count 24,900 Gm/dl

NEUTROPHILS 00 /L

LYMPHOCYTES 00 %

EOSINOPHILS 00 %

MONOCYTES 00 %

BASOPHILS 00 %

PLATELET COUNT 136,000 /L

HEMATOLOGY


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Test Result Unit

Electrolyte (Serum)

Sodium 137 mEq/L

Potassium 4.1 mEq/L

Chloride 90 mEq/L

Blood Urea Nitrogen 22 mg/dL

Creatinine 0.7 mg/dL

Sugar (Random) 164 mg/dL

BIOCHEMISTRY


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Test Result Unit

Arterial Blood Gas

Temp 37.0 CHb 15.0 g/dL

Flo2 21.0 %

PH 7.50

PCo2 44 mmHg

PO2 50 mmHg

SO2 88 %

HCO3 34 m.mol/L

ABE 10 m.mol/L

BIOCHEMISTRY


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Test Result Unit

Lipid Profile

Cholesterol 150 mg/dL

Triglycerides 106 mg/dL

HDL 50 mg/dL

LDL 78.8 mg/dL

BIOCHEMISTRY


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Test Result Unit

HbA1C 7 %

ESR (Westergren) 34 (mm 1st Hr)

Suger (Fasting) 69 mg/dL

BIOCHEMISTRY


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Test Requested Pt (Prothrombin Time)

Test 10.9 Seconds

Control 10.5 Seconds

INR 1.04

COAGULATION PROFILE


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ECG = Normal

Different diagnoses

COPD.

ASTHMA.


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Chronic Obstructive Pulmonary Disease


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Chronic Obstructive Pulmonary Disease

Gross pathologyof a lung showing centrilobular-typeemphysema characteristic of smoking. This close-up ofthe fixed, cut lung surface shows multiple cavities lined

by heavyblack carbon deposits.
http://en.wikipedia.org/wiki/Gross_pathologyhttp://en.wikipedia.org/wiki/Emphysemahttp://en.wikipedia.org/wiki/Fixation_(histology)http://en.wikipedia.org/wiki/Black_carbonhttp://en.wikipedia.org/wiki/Black_carbonhttp://en.wikipedia.org/wiki/Fixation_(histology)http://en.wikipedia.org/wiki/Emphysemahttp://en.wikipedia.org/wiki/Gross_pathology


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Introduction

Chronic obstructive pulmonary disease (COPD), also known aschronic obstructive lung disease (COLD), chronic obstructive

airway disease (COAD), chronic airflow limitation (CAL) andchronic obstructive respiratory disease (CORD), is the co-occurrence ofchronic bronchitis and emphysema, a pair ofcommonly co-existing diseases of the lungs in which the airways

become narrowed. This leads to a limitation of the flow of air to andfrom the lungs, causing shortness of breath.

COPD is caused by noxious particles or gas, most commonly fromtobacco smoking, which triggers an abnormal inflammatory

response in the lung. The inflammatory response in the largerairways is known as chronic bronchitis, which is diagnosed clinicallywhen people regularly cough up sputum. In the alveoli, theinflammatory response causes destruction of the tissues of the lung,

k h Th l f COPD i
http://en.wikipedia.org/wiki/Chronic_bronchitishttp://en.wikipedia.org/wiki/Emphysemahttp://en.wikipedia.org/wiki/Airwayshttp://en.wikipedia.org/wiki/Shortness_of_breathhttp://en.wikipedia.org/wiki/Tobacco_smokinghttp://en.wikipedia.org/wiki/Inflammatory_responsehttp://en.wikipedia.org/wiki/Inflammatory_responsehttp://en.wikipedia.org/wiki/Chronic_bronchitishttp://en.wikipedia.org/wiki/Sputumhttp://en.wikipedia.org/wiki/Alveolihttp://en.wikipedia.org/wiki/Alveolihttp://en.wikipedia.org/wiki/Sputumhttp://en.wikipedia.org/wiki/Chronic_bronchitishttp://en.wikipedia.org/wiki/Inflammatory_responsehttp://en.wikipedia.org/wiki/Inflammatory_responsehttp://en.wikipedia.org/wiki/Tobacco_smokinghttp://en.wikipedia.org/wiki/Shortness_of_breathhttp://en.wikipedia.org/wiki/Airwayshttp://en.wikipedia.org/wiki/Emphysemahttp://en.wikipedia.org/wiki/Chronic_bronchitishttp://en.wikipedia.org/wiki/Emphysemahttp://en.wikipedia.org/wiki/Emphysema


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a process known as emphysema. The natural course of COPD ischaracterized by occasional sudden worsenings of symptoms calledacute exacerbations, most of which are caused byinfections or airpollution.

The diagnosis of COPD requires lung function tests. Importantmanagement strategies are smoking cessation,vaccinations,rehabilitation, and drug therapy (often using inhalers). Somepatients go on to require long-term oxygen therapyor lung

transplantation.
http://en.wikipedia.org/wiki/Emphysemahttp://en.wikipedia.org/wiki/Infectionshttp://en.wikipedia.org/wiki/Air_pollutionhttp://en.wikipedia.org/wiki/Air_pollutionhttp://en.wikipedia.org/wiki/Medical_diagnosishttp://en.wikipedia.org/wiki/Lung_function_testshttp://en.wikipedia.org/wiki/Smoking_cessationhttp://en.wikipedia.org/wiki/Vaccinationhttp://en.wikipedia.org/wiki/Physical_medicine_and_rehabilitationhttp://en.wikipedia.org/wiki/Inhalerhttp://en.wikipedia.org/wiki/Oxygen_therapyhttp://en.wikipedia.org/wiki/Lung_transplantationhttp://en.wikipedia.org/wiki/Lung_transplantationhttp://en.wikipedia.org/wiki/Lung_transplantationhttp://en.wikipedia.org/wiki/Lung_transplantationhttp://en.wikipedia.org/wiki/Oxygen_therapyhttp://en.wikipedia.org/wiki/Oxygen_therapyhttp://en.wikipedia.org/wiki/Oxygen_therapyhttp://en.wikipedia.org/wiki/Inhalerhttp://en.wikipedia.org/wiki/Physical_medicine_and_rehabilitationhttp://en.wikipedia.org/wiki/Vaccinationhttp://en.wikipedia.org/wiki/Smoking_cessationhttp://en.wikipedia.org/wiki/Lung_function_testshttp://en.wikipedia.org/wiki/Medical_diagnosishttp://en.wikipedia.org/wiki/Air_pollutionhttp://en.wikipedia.org/wiki/Air_pollutionhttp://en.wikipedia.org/wiki/Infectionshttp://en.wikipedia.org/wiki/Emphysema


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ClassificationChronic bronchitis

Emphysema

Signs and symptomsEssentials of diagnosis include:

History of cigarette smoking.Chronic cough and sputum production (in chronic bronchitis).

DyspneaRhonchi, decreased intensity of breath sounds, and prolongedexpiration on physical examination.Airflow limitation on pulmonary function testing that is not fully

reversible and most often progressive.

O f h f O h f b h
http://en.wikipedia.org/wiki/Dyspneahttp://en.wikipedia.org/wiki/Dyspnea


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One of the most common symptoms of COPD is shortness of breath(dyspnea). People with COPD commonly describe this as: "Mybreathing requires effort," "I feel out of breath," or "I can't getenough air in".People with COPD typically first notice dyspnea

during vigorous exercise when the demands on the lungs aregreatest. Over the years, dyspnea tends to get gradually worse so thatit can occur during milder, everyday activities such as housework. Inthe advanced stages of COPD, dyspnea can become so bad that it

occurs during rest and is constantly present.

Other symptoms of COPD are a persistent cough, sputum or mucusproduction,wheezing, chest tightness, and tiredness.

P l i h d d ( ) COPD i d l
http://en.wikipedia.org/wiki/Dyspneahttp://en.wikipedia.org/wiki/Sputumhttp://en.wikipedia.org/wiki/Wheezinghttp://en.wikipedia.org/wiki/Wheezinghttp://en.wikipedia.org/wiki/Sputumhttp://en.wikipedia.org/wiki/Dyspnea


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People with advanced (very severe) COPD sometimes developrespiratory failure. When this happens, cyanosis, a bluishdiscoloration of the lips caused by a lack of oxygen in the blood, canoccur. An excess of carbon dioxide in the blood can cause

headaches, drowsiness or twitching (asterixis). A complication ofadvanced COPD is cor pulmonale, a strain on the heart due to theextra work required by the heart to pump blood through the affectedlungs. Symptoms of cor pulmonale are peripheral edema, seen as

swelling of the ankles and dyspnea.

Th f i f COPD h h l h k d
http://en.wikipedia.org/wiki/Respiratory_failurehttp://en.wikipedia.org/wiki/Cyanosishttp://en.wikipedia.org/wiki/Asterixishttp://en.wikipedia.org/wiki/Cor_pulmonalehttp://en.wikipedia.org/wiki/Peripheral_edemahttp://en.wikipedia.org/wiki/Peripheral_edemahttp://en.wikipedia.org/wiki/Cor_pulmonalehttp://en.wikipedia.org/wiki/Asterixishttp://en.wikipedia.org/wiki/Cyanosishttp://en.wikipedia.org/wiki/Respiratory_failurehttp://en.wikipedia.org/wiki/Medical_signhttp://en.wikipedia.org/wiki/Medical_sign


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There are a few signs of COPD that a healthcare worker may detectalthough they can be seen in other diseases. Some people haveCOPD and have none of these signs. Common signs are:

Tachypnea, a rapid breathing rate.

Wheezing sounds or crackles in the lungs heard through astethoscope.

Breathing out taking a longer time than breathing in.

Enlargement of the chest, particularly the front-to-back distance(hyperaeration).

Breathing through pursed lips.

Increased anteroposterior to lateral ratio of the chest (i.e. barrelchest).
http://en.wikipedia.org/wiki/Medical_signhttp://en.wikipedia.org/wiki/Tachypneahttp://en.wikipedia.org/wiki/Stethoscopehttp://en.wikipedia.org/wiki/Hyperaerationhttp://en.wikipedia.org/wiki/Barrel_chesthttp://en.wikipedia.org/wiki/Barrel_chesthttp://en.wikipedia.org/wiki/Barrel_chesthttp://en.wikipedia.org/wiki/Barrel_chesthttp://en.wikipedia.org/wiki/Hyperaerationhttp://en.wikipedia.org/wiki/Stethoscopehttp://en.wikipedia.org/wiki/Tachypneahttp://en.wikipedia.org/wiki/Medical_sign


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Cause

Intense and prolonged exposure to workplace dusts found in coalmining, gold mining, and the cotton textile industry and chemicalssuch as cadmium, isocyanates, and fumes fromwelding have beenimplicated in the development of airflow obstruction, even in

nonsmokers. Workers who smoke and are exposed to these particlesand gases are even more likely to develop COPD. Intense silica dustexposure causes silicosis, a restrictive lung disease distinct fromCOPD; however, less intense silica dust exposures have been linked

to a COPD-like condition. The effect of occupational pollutants onthe lungs appears to be substantially less important than the effectof cigarette smoking.

Occupational exposures
http://en.wikipedia.org/wiki/Coal_mininghttp://en.wikipedia.org/wiki/Coal_mininghttp://en.wikipedia.org/wiki/Gold_mininghttp://en.wikipedia.org/wiki/Cadmiumhttp://en.wikipedia.org/wiki/Isocyanateshttp://en.wikipedia.org/wiki/Weldinghttp://en.wikipedia.org/wiki/Silicahttp://en.wikipedia.org/wiki/Silicosishttp://en.wikipedia.org/wiki/Silicosishttp://en.wikipedia.org/wiki/Silicahttp://en.wikipedia.org/wiki/Weldinghttp://en.wikipedia.org/wiki/Isocyanateshttp://en.wikipedia.org/wiki/Cadmiumhttp://en.wikipedia.org/wiki/Gold_mininghttp://en.wikipedia.org/wiki/Coal_mininghttp://en.wikipedia.org/wiki/Coal_mining


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Air pollutionStudies of the industrial waste gas and COPD/asthma-aggravating

compound, sulfur dioxide, and the inverse relation to the presenceof the blue lichen Xanthoria (usually found abundantly in thecountryside, but never in towns or cities) have been seen to suggestcombustive industrial processes do not aid COPD sufferers. In manydeveloping countries, indoor air pollution from cooking fire smoke

(often using biomass fuels such as wood and animal dung) is acommon cause of COPD, especially in women.
http://en.wikipedia.org/wiki/Xanthoriahttp://en.wikipedia.org/wiki/Developing_countrieshttp://en.wikipedia.org/wiki/Biomass_fuelhttp://en.wikipedia.org/wiki/Biomass_fuelhttp://en.wikipedia.org/wiki/Developing_countrieshttp://en.wikipedia.org/wiki/Xanthoria


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Genetics

Some factor in addition to heavy smoke exposure is required for aperson to develop COPD. This factor is probably a geneticsusceptibility. COPD is more common among relatives of COPDpatients who smoke than unrelated smokers The genetic differencesthat make some peoples' lungs susceptible to the effects of tobaccosmoke are mostly unknown.Alpha 1-antitrypsin deficiencyis a

genetic condition that is responsible for about 2% of cases of COPD.In this condition, the body does not make enough of a protein, alpha1-antitrypsin. Alpha 1-antitrypsin protects the lungs from damagecaused byproteaseenzymes, such as elastase and trypsin, that can

be released as a result of an inf lammatory response to tobaccosmoke.
http://en.wikipedia.org/wiki/Genehttp://en.wikipedia.org/wiki/Alpha_1-antitrypsin_deficiencyhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsinhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsinhttp://en.wikipedia.org/wiki/Proteasehttp://en.wikipedia.org/wiki/Enzymeshttp://en.wikipedia.org/wiki/Elastasehttp://en.wikipedia.org/wiki/Trypsinhttp://en.wikipedia.org/wiki/Trypsinhttp://en.wikipedia.org/wiki/Elastasehttp://en.wikipedia.org/wiki/Enzymeshttp://en.wikipedia.org/wiki/Proteasehttp://en.wikipedia.org/wiki/Alpha_1-antitrypsinhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsinhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsinhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsinhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsin_deficiencyhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsin_deficiencyhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsin_deficiencyhttp://en.wikipedia.org/wiki/Gene


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Autoimmune disease

AutoimmunityThere is mounting evidence that there may be an autoimmunecomponent to COPD, triggered by lifelong smoking. Manyindividuals with COPD who have stopped smoking have activeinflammation in the lungs. The disease may continue to get worse

for many years after stopping smoking due to this ongoinginflammation. This sustained inflammation is thought to bemediated by autoantibodies and autoreactive T cells.


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Other risk factors

A tendency to sudden airway constriction in response to inhaled

irritants, bronchial hyperresponsiveness, is a characteristic ofasthma. Many people with COPD also have this tendency. In COPD,the presence of bronchial hyperresponsiveness predicts a worsecourse of the disease. It is not known if bronchialhyperresponsiveness is a cause or a consequence of COPD. Other

risk factors such as repeated lung infection and possibly a diet highin cured meats (possibly due to the preservative sodium nitrite) maybe related to the development of COPD.
http://en.wikipedia.org/wiki/Infectionhttp://en.wikipedia.org/wiki/Sodium_nitritehttp://en.wikipedia.org/wiki/Sodium_nitritehttp://en.wikipedia.org/wiki/Infection


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Pathophysiology

It is not fully understood how tobacco smoke and other inhaledparticles damage the lungs to cause COPD. The most importantprocesses causing lung damage are:

Oxidative stress produced by the high concentrations offreeradicals in tobacco smoke.

Cytokine release due to inflammation as the body responds to

irritant particles such as tobacco smoke in the airway.

Tobacco smoke and free radicals impair the activity of antiproteaseenzymes such as alpha 1-antitrypsin, allowing protease enzymes todamage the lung.
http://en.wikipedia.org/wiki/Oxidative_stresshttp://en.wikipedia.org/wiki/Free_radicalshttp://en.wikipedia.org/wiki/Free_radicalshttp://en.wikipedia.org/wiki/Cytokinehttp://en.wikipedia.org/wiki/Inflammationhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsinhttp://en.wikipedia.org/wiki/Proteasehttp://en.wikipedia.org/wiki/Proteasehttp://en.wikipedia.org/wiki/Alpha_1-antitrypsinhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsinhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsinhttp://en.wikipedia.org/wiki/Inflammationhttp://en.wikipedia.org/wiki/Cytokinehttp://en.wikipedia.org/wiki/Free_radicalshttp://en.wikipedia.org/wiki/Free_radicalshttp://en.wikipedia.org/wiki/Oxidative_stress


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Diagnosis

Chest X-ray


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Spirometry

The diagnosis of COPD is confirmed byspirometry,a test thatmeasures the forced expiratory volume in one second (FEV

1

), whichis the greatest volume of air that can be breathed out in the firstsecond of a large breath. Spirometry also measures the forced vitalcapacity (FVC), which is the greatest volume of air that can bebreathed out in a whole large breath. Normally, at least 70% of the

FVC comes out in the first second (i.e. the FEV1/FVC ratio is >70%).A ratio less than normal defines the patient as having COPD. Morespecifically, the diagnosis of COPD is made when the FEV1/FVC ratiois


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Severity of COPD (GOLD scale) FEV1 % predicted

Mild (GOLD 1) 80

Moderate (GOLD 2) 5079

Severe (GOLD 3) 3049

Very severe (GOLD 4)


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Other testsOn chest x-ray, the classic signs of COPD are overexpanded lung(hyperinflation), a flattened diaphragm, increased retrosternalairspace, and bullae. It can be useful to help exclude other lungdiseases, such as pneumonia, pulmonary edema or a pneumothorax.Complete pulmonary function tests with measurements of lung

volumes and gas transfer may also show hyperinflation and can

discriminate between COPD with emphysema and COPD withoutemphysema. A high-resolution computed tomographyscan of thechest may show the distribution of emphysema throughout thelungs and can also be useful to exclude other lung diseases.

A blood sample taken from an artery, i.e.Arterial Blood Gas (ABG),can be tested for blood gas levels which may show low oxygen(hypoxaemia) and/or high carbon dioxide (respiratory acidosis if pHis also decreased). A blood sample taken from avein may show ahigh blood count (reactive polycythemia), a reaction to long-term

hypoxemia.
http://en.wikipedia.org/wiki/Chest_x-rayhttp://en.wikipedia.org/wiki/Hyperaerationhttp://en.wikipedia.org/wiki/Pneumoniahttp://en.wikipedia.org/wiki/Pulmonary_edemahttp://en.wikipedia.org/wiki/Pneumothoraxhttp://en.wikipedia.org/wiki/Computed_tomographyhttp://en.wikipedia.org/wiki/Arteryhttp://en.wikipedia.org/wiki/Arterial_Blood_Gashttp://en.wikipedia.org/wiki/Veinhttp://en.wikipedia.org/wiki/Veinhttp://en.wikipedia.org/wiki/Arterial_Blood_Gashttp://en.wikipedia.org/wiki/Arteryhttp://en.wikipedia.org/wiki/Computed_tomographyhttp://en.wikipedia.org/wiki/Pneumothoraxhttp://en.wikipedia.org/wiki/Pulmonary_edemahttp://en.wikipedia.org/wiki/Pneumoniahttp://en.wikipedia.org/wiki/Hyperaerationhttp://en.wikipedia.org/wiki/Chest_x-rayhttp://en.wikipedia.org/wiki/Chest_x-rayhttp://en.wikipedia.org/wiki/Chest_x-ray


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Management

Risk factor reduction

Smoking cessationSmoking cessation is one of the most important factors in slowingdown the progression of COPD. Once COPD has been diagnosed,stopping smoking slows down the rate of progression of the disease.

Even at a late stage of the disease, it can significantly reduce the rateof deterioration in lung function and delay the onset of disabilityand death. It is the only standard intervention that can improve therate of progression of COPD.

The chance of successfully stopping smoking can be greatlyimproved through social support, engagement in a smokingcessation programme and the use of drugs such as nicotinereplacement therapy, bupropion andvarenicline.
http://en.wikipedia.org/wiki/Nicotine_replacement_therapyhttp://en.wikipedia.org/wiki/Nicotine_replacement_therapyhttp://en.wikipedia.org/wiki/Bupropionhttp://en.wikipedia.org/wiki/Vareniclinehttp://en.wikipedia.org/wiki/Vareniclinehttp://en.wikipedia.org/wiki/Bupropionhttp://en.wikipedia.org/wiki/Nicotine_replacement_therapyhttp://en.wikipedia.org/wiki/Nicotine_replacement_therapy


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Bronchodilators

Bronchodilators are usually administered with an inhaler or via anebulizer.

There are two major types of bronchodilator, 2 agonists andanticholinergics. Anticholinergics appear to be superior to 2agonists in COPD. Anticholinergics reduce respiratory deaths while2 agonists have no effect on respiratory deaths. Each type may be

either long-acting (with an effect lasting 12 hours or more) or short-acting (with a rapid onset of effect that does not last as long).

i
http://en.wikipedia.org/wiki/Inhalerhttp://en.wikipedia.org/wiki/Nebulizerhttp://en.wikipedia.org/wiki/Nebulizerhttp://en.wikipedia.org/wiki/Inhaler


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2 agonists

2agonists stimulate 2receptors on airway smooth muscles,causing them to relax. There are several

2

agonists available.Salbutamol (common brand name: Ventolin) and terbutaline are

widely used short acting 2 agonists and provide rapid relief ofCOPD symptoms. Long acting 2 agonists (LABAs) such assalmeterol and formoterol are used as maintenance therapy and lead

to improved airflow, exercise capacity, and quality of life.
http://en.wikipedia.org/wiki/Receptor_(biochemistry)http://en.wikipedia.org/wiki/Salbutamolhttp://en.wikipedia.org/wiki/Terbutalinehttp://en.wikipedia.org/wiki/Salmeterolhttp://en.wikipedia.org/wiki/Formoterolhttp://en.wikipedia.org/wiki/Formoterolhttp://en.wikipedia.org/wiki/Salmeterolhttp://en.wikipedia.org/wiki/Terbutalinehttp://en.wikipedia.org/wiki/Salbutamolhttp://en.wikipedia.org/wiki/Receptor_(biochemistry)


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Anticholinergics

Anticholinergic drugs cause airway smooth muscles to relax by

blocking stimulation from cholinergic nerves. Ipratropium is themost widely prescribed short acting anticholinergic drug. Likeshort-acting 2 agonists, short-acting anticholinergics provide rapidrelief of COPD symptoms and a combination of the two iscommonly used for a greater bronchodilator effect. Tiotropium is

the most commonly prescribed long-acting anticholinergic drug inCOPD. It has more specificity for M3 muscarinic receptors, so mayhave fewer side effects than other anticholinergic drugs. Regular useis associated with improvements in airf low, exercise capacity, quality

of life and possibly a longer life. In January 2010, new researchshowed ipratropium used to treat COPD increased cardiovascularmorbidity. At the same time tiotropium was shown to be effective ineliminating the risk of all cause mortality, cardiovascular mortalityand cardiovascular events.

C i id
http://en.wikipedia.org/wiki/Cholinergichttp://en.wikipedia.org/wiki/Ipratropiumhttp://en.wikipedia.org/wiki/Tiotropiumhttp://en.wikipedia.org/wiki/Morbidityhttp://en.wikipedia.org/wiki/Morbidityhttp://en.wikipedia.org/wiki/Tiotropiumhttp://en.wikipedia.org/wiki/Ipratropiumhttp://en.wikipedia.org/wiki/Cholinergic


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Corticosteroids

Corticosteroids act to reduce the inflammation in the airways, in

theory reducing lung damage and airway narrowing caused byinflammation. Unlike bronchodilators, they do not act directly onthe airway smooth muscle and do not provide immediate relief ofsymptoms. Some of the more common corticosteroids in use areprednisolone, fluticasone, budesonide, mometasone, and

beclomethasone. Corticosteroids are used in tablet or inhaled formto treat and prevent acute exacerbations of COPD. Well-inhaledcorticosteroids (ICS) have not been shown to be of benefit forpeople with mild COPD, however, they have been shown to decrease

acute exacerbations in those with either moderate or severe COPD.They however have no effect on overall one-year mortality and areassociated with increased rates of pneumonia.

O h di i
http://en.wikipedia.org/wiki/Prednisolonehttp://en.wikipedia.org/wiki/Fluticasonehttp://en.wikipedia.org/wiki/Budesonidehttp://en.wikipedia.org/wiki/Mometasone_furoatehttp://en.wikipedia.org/wiki/Beclomethasonehttp://en.wikipedia.org/wiki/Beclomethasonehttp://en.wikipedia.org/wiki/Mometasone_furoatehttp://en.wikipedia.org/wiki/Budesonidehttp://en.wikipedia.org/wiki/Fluticasonehttp://en.wikipedia.org/wiki/Prednisolone


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Other medication

Theophylline.

Phosphodiesterase.

Roflumilast.

Cilomilast.

S l t l
http://en.wikipedia.org/wiki/Theophyllinehttp://en.wikipedia.org/wiki/Phosphodiesterasehttp://en.wikipedia.org/wiki/Roflumilasthttp://en.wikipedia.org/wiki/Cilomilasthttp://en.wikipedia.org/wiki/Cilomilasthttp://en.wikipedia.org/wiki/Roflumilasthttp://en.wikipedia.org/wiki/Phosphodiesterasehttp://en.wikipedia.org/wiki/Theophylline


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Supplemental oxygen

l h bili i


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Pulmonary rehabilitation

Pulmonary rehabilitation is a program of exercise, diseasemanagement and counselling coordinated to benefit the individual.Pulmonary rehabilitation has been shown to improve shortness ofbreath and exercise capacity. It has also been shown to improve thesense of control a patient has over their disease as well as theiremotions.

Surgery

Bulla.

Lung volume reduction surgery.

Lung transplantation.

P i
http://en.wikipedia.org/wiki/Pulmonary_rehabilitationhttp://en.wikipedia.org/wiki/Bullahttp://en.wikipedia.org/wiki/Lung_volume_reduction_surgeryhttp://en.wikipedia.org/wiki/Lung_transplantationhttp://en.wikipedia.org/wiki/Lung_transplantationhttp://en.wikipedia.org/wiki/Lung_volume_reduction_surgeryhttp://en.wikipedia.org/wiki/Bullahttp://en.wikipedia.org/wiki/Pulmonary_rehabilitation


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Prognosis

COPD usually gradually gets worse over time and can lead to death.The rate at which it gets worse varies between individuals. The

factors that predict a poorer prognosis are:

Severe airflow obstruction (low FEV1).Poor exercise capacity.

Shortness of breath.Significantly underweight or overweight.Complications like respiratory failure or cor pulmonale.Continued smoking.Frequent acute exacerbations.


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THANK YOU

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Copd Final 97-2003hiraa