Final Copd Mam Somo

8/4/2019 Final Copd Mam Somo

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Overview Currently, COPD is the fourth leading cause of

mortality and the 12th leading cause of disability.

However, by the year 2020 it is estimatedthat COPD will be the third leading cause ofdeath and the forth leading cause of disability(Sin, McAlister, Man. Et al., 2003).

People with COPD commonly becomesymptomatic during the middle adult years, andthe incidence of the disease increases with age.


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Predisposing Factor

-increases mucusproduction in thelungs andparalyzes the cilia

-too much mucusclogs the gasexchangefunction of your

air sacs -Smoking can

interfer in yourability to cough

effectively


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PATHOPYSIOLOGY In COPD, the airflow limitation is both

progressive and associated with an abnormal

inflammatory response of the lungs to noxiousparticles or gases. The inflammatory responseoccurs throughout the airways, parenchyma, andpulmonary vasculature. Because of the chronic

inflammation and the bodys attempts to repair it,narrowing occurs in the small peripheral airways.


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. Over time, this injury-and-repair process causesscar tissue formation and narrowing of the airway

lumen. Airflow obstruction may also be caused byparenchymal destruction, as is seen withemphysema, a disease of the alveoli or gasexchange units.


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What COPD is: The deadly combo In the vast majority of patients, COPD refers to a

combination of a chronic bronchitis and

emphysema. Most COPD patients have bothconditions, although one maybe more advancethan the other.


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CHRONIC BRONCHITIS a chronic inflammation of the bronchi

(medium-size airways) in the lungs. It is

generally considered one of the two formsof (COPD).It is defined clinically as apersistent cough that produces sputum(phlegm) and mucus, for at least threemonths in two consecutive years.


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-an increasednumber andincreased size of the

goblet cells andmucous glands of theairway.

-BLUE BLOATERS


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Narrow opening

Excess mucus

Inflamed airwaywith significantswelling.


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Sympotms include chronic coughing and throatclearing, increased mucus and shortness of

breath.

To meet the clinical definition of chronicbronchitis you must cough up mucus most days

for atleast 3months for two consecutive years.


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Pathophysiology

smoking/pollution

continued irritation of lungpassages

inflammation

excessive mucusproduction

narrowing of the

bronchi

Chronic

Bronchitis


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EMPHYSEMA

characterized by loss of elasticity(increased pulmonary compliance) of thelung tissue caused by destruction ofstructures feeding the alveoli.


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EMPHYSEMA -takes time to

develop, 9 out of 10people diagnosed

with it are 45 yearsold and up

- characterized byloss of elasticity

(increasedpulmonarycompliance) of thelung tissue caused bydestruction ofstructures feeding


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This causes thesmall airways to

collapse duringforced exhalation,as alveolarcollapsibility has

decreased.


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Pathophysiology

Smoking/Pollutants

Attraction of inflammation cells

Release of

elastaseinhibition of alpha 1-antitrypsin

inherited alpha 1-antitrypsindeficiency

destruction of

elastic fibers

Emphysema


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Emphysema Chronic BronchitisAge 40-50 30-40

Clinical Findings

Barrel Chest Often dramatic infrequent

Wt. loss Maybe absent in early

disease

Maybe present

Shortness of

Breathing

Maybe frequent Maybe present,

predominant early

symptomsBreath Sound

Wheezing Absent Variable

Rhonchi Absent Often prominent

Sputum Often absent, maybepresent in late course Frequent earlymanifestation

Blood Gasses Relatively normal until

late process

Hypercapnia and

Hypoxemia is present

Cor Pulmonale Only in advance cases Frequent


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ASSESSMENTHISTORY

Health perception-health management Greater than normal shortness of breath, with

inability to control symptoms with prescribed ornon prescribed therapies.

Increased fatigue and inability to cope with crisis

Increasing anxiety and panic

Increasing difficulty expectorating sputum


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Nutritional-metabolic pattern

Anorexia Inability to eat and digest without shortness ofbreath

Nausea, possibly associated with medications Bloating, especially after eating foods known

cause flatulence

Difficulty maintaining adequate fluid intake (atleast 8 oz/240ml glasses per day).


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Activity-exercise pattern Shortness of breath with even minimal exertion

or when performing activities of daily living

Shortness of breath and panic controlled withbreathing techniques

Sleep-rest pattern


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PSYCHOSOCIAL

Cognitive-perceptual pattern Fluctuating compliance with therapeutic regimen

Role-relationship pattern

Multiple role changes, resulting in depression,isolation and increased dependence

Difficulty verbalizing feelings because emotionsintensify shortness of breath


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Sexuality-reproductive pattern

Complex interpersonal role changes with spouseor partner, with decreased desire for andfrequency of sexual activity because of actual orpotential shortness of breath.


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Coping-stress tolerance pattern

Difficulty expressing either positive or negativeemotions because of shortness of breath

Fluctuating behaviour

Value-belief pattern

Ambivalence about resuscitative measures thatmay be necessary during hospital stay but maynot ultimately improve quality of life


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PHYSICAL

General Appearance Apprehension and anxiety; maintenance of

upright tense posture

Tendency to panic easily if activity is requested

Cachexia (emphysema); plethora (chronicbronchitis)

Cardiovascular


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Pulmonary

Accentuated accessory neck muscles Barrel chest hyperinflation

Decreased breath sounds bilaterally

Prolonged expiratory phase Productive cough: tapioca-like plugs or copious

amounts of sputum

Gurgles if secretions are copious; crackles if heart


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Neurologic

Anxiety Restlessness with hypoxemia

Lethargy and sleepiness with increased partialpressure of carbon dioxide levels

Integumentary

Skin that discolours (mottling and cyanosis)easily during coughing spells, strenuous activity,or episodes of acute shortness of breath


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DIAGNOSIS Spirometry- used to evaluate airflow obstruction,which is determined by the ration FEV1 to force

vital capacity (FVC) Broncodilator Testing- peformed to rule out the

diagnosis of asthma.

Arterial blood gas (ABG) measurements- assessbaseline oxygentation and gas exchange and isimportant in advance COPD.

Theopylline level- normal is 10 to 15ug/ml; maybe elevated if the atient has ad usted


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Alpha1-antitrypsin assay- uncommon; performedto determine alpha1 antitrypsin deficiency in

young patients with suspected emphysema Other tests- white blood cell count,

hematocritand serum electrolytes levels are

performed according to suspected causes. Chest X-ray- shows hyperinflation, with flattening

of the diaphragm caused by air trapping in thechest, that may worsen during exacerbation; may

also show infiltrates, depending on exacerbation


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TREATMENT

The goals of COPD treatment are: 1) to prevent further deterioration in lung

function, 2) to alleviate symptoms,

3) to improve performance of daily activities andquality of life.

The treatment strategies include

1) quitting cigarette smoking,


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PROBLEM LIST Impaired Gas Exchange related to airway

narrowing secondary to mucus secretions and

inflammation Ineffective airway clearance related to excessive

secretions

Nutritional deficit related to shortness of breathduring and after meals and adverse reactions tomedication.

Ineffective cardiopulmonary tissue perfusionrelated to im aired ventilation secondar to


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UPDATES Patients With COPD Have Higher Risk of

Shingles, Study Finds

ScienceDaily (Feb. 23, 2011) Patients withchronic obstructive pulmonary disease (COPD)are at greater risk of shingles compared with the

general population, according to a studypublished in CMAJ(Canadian MedicalAssociation Journal). The risk is greatest forpatients taking oral steroids to treat COPD.

Shingles, or herpes zoster, is a reactivation of the


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People with a compromised immune system areat greater risk of developing shingles although it

has not been previously studied in patients withCOPD.

There is increasing evidence that COPD is an

autoimmune disease. "Given that variousimmune-mediated diseases, such as rheumatoidarthritis and inflammatory bowel disease, havebeen reported to be associated with an increased

risk of herpes zoster, it is reasonable toh othesize that immune d sre ulation found in


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This study, using data from the TaiwanLongitudinal Health Insurance Database,

included 8486 patients with COPD and 33 944subjects from the comparison cohort. Of the totalsample of 42 430 patients, 1080 had incident ofherpes zoster during the follow-up period. There

were 321 cases of shingles identified in the COPDcohort, 16.4 per 1000 person years, and 759 casesin the comparison cohort, 8.8 per 1000 personyears.


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"Our cohort study demonstrated that patientswith COPD are at an increased risk of developing

herpes zoster compared with the generalpopulation, after controlling for other herpeszoster risk factors," write the authors. "The risk ofherpes zoster associated with COPD is greater for

patients with inhaled or oral corticosteroidstherapy than patients without."

The authors conclude it is possible that "increased

disease severity further contributes to theincreased risk of her es zoster associated with


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Final Copd Mam Somo

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