Copd Exacerbation

I will analyse the prevalence of the condition and what the potential causes may be. My interests have been directed to pre hospital care and community lead treatment packages, which are potentially available to the patient, as this is the acute environment, which I will have contact with in my employment as a paramedic. The initial reading was to understand COPD as a chronic condition, what is COPD? and its prevalence in the population. The (World health organisation, 2000), states that one in four deaths in the world are caused by COPD. In 2010 (Vos T Flaxman etal, 2012), says globally there were approximately 329 million, which is 4.8% of the population who are affected by this chronic condition, In the UK (NICE, 2010), have estimated that 3 million people suffer from COPD, with more yet to be diagnosed. This information about the amount of people living with this condition was surprising, as I little knowledge of its existence. During the early 1960’s (Timothy Q. Howes, 2005), says the term COPD had been designated as a single term unifying all the chronic respiratory diseases. Since then the term COPD, has been sub divided in to three umbrella areas, Bronchitis, Emphysema and Chronic asthma, which are separate conditions, which I have been previously aware of as their individual conditions. The 58 year old patient who we visited,

It was concluded that mr chari had Exacerbations of COPD which is defined as a sustained worsening of the above copd symptoms from the usual stable state that is beyond normal day-to-day variations, and is acute in onset. Commonly reported symptoms are worsening breathlessness, cough, increased sputum production and change in sputum colour.

EH is a 68-year-old male who comes into the clinic complaining of a fever with a temperature of 103 °F. He has had a cough for the last three days that is producing some thick green brown mucous. The MD feels he most likely has bacterial pneumonia. He also has a history of having rheumatoid arthritis, and being immune compromised as he is on an immunosuppressant methotrexate. He has noted that over the last year he has lost weight unintentionally and feels he is underweight.

D.Z., a 65-year-old man, is admitted to a medical floor for exacerbation of his chronic obstructive pulmonary disease (COPD; emphysema). He has a past medical history of hypertension, which has been well controlled by Enalapril (Vasotec) for the past 6 years. He has had pneumonia yearly for the past 3 years, and has been a 2-pack-a-day smoker for 38 years. He appears as a cachectic man who is experiencing difficulty breathing at rest. He reports cough productive of thick yellow-green sputum. D.Z. seems irritable and anxious; he complains of sleeping poorly and states that lately feels tired most of the time. His vital signs (VS) are 162/84, 124, 36, 102 F, SaO2 88%. His admitting diagnosis is an acute

I was well versed with the patient’s medical history and current treatment, as I was the Long Call IM PGY – II Resident who supervised the medical intern when this patient was being downgraded from the ICU to the medical floor on 5/20/17 (and even suggested to the medical intern to add in her notes that the patient would benefit from statins, ACE inhibition and Spironolactone given CAD, CVA and HFrEF (LVEF < 35%.) The medical team subsequently started the patient on Atorvastatin 40 MG PO QHS, Lisinopril 10 MG PO QD and Spironolactone 12.5 MG PO QD.

Shortness of breath and wheezing are classical signs of COPD. The first part of the essay is discussed on pathophysiology of COPD. Another part is going to be informing on the pharmacology aspect of treating the disease. Nutrition also plays as a critical component of relieving the symptoms of the disease or aiding the work of medication. One of the signs that COPD can be established as a primary cause of illness is by receiving lab report on Arterial Blood Gases ABG.

All over the world, chronic obstructive pulmonary disease (COPD) is a very significant and prevalent cause of morbidity and mortality, and it is increasing with time (Hurd, 2000; Pauwels, 2000; Petty, 2000). Due to the factor of COPD being an underdiagnosed and undertreated disease, the epidemiology (Pauwels, Rabe, 2004) is about 60 to 85 % with mild or moderate COPD remaining undiagnosed (Miravitlles et al., 2009; Hvidsten et al., 2010).

The World Health Organization (WHO) (2006A) defines COPD as a disease state characterized by airflow limitation that is not wholly reversible. The airflow limitation is usually both progressive and associated with abnormal inflammatory response of the lungs to noxious particles or gases. John's chronic bronchitis is defined, clinically, as the presence of a chronic productive cough for 3 months in each of 2 successive years, provided other causes of chronic cough have been ruled out. (Mannino, 2003). The British lung Foundation (BLF) (2005) announces that chronic bronchitis is the inflammation and eventual scarring of the lining of the bronchial tubes which is the explanation for John's dyspnea. The BLF (2005) believe that when the bronchi become inflamed less air is able to flow to and from the lungs and once the bronchial tubes have been irritated over a long period of time, excessive mucus is produced. This increased sputum results from an increase in the size and number of goblet cells (Jeffery, 2001) resulting in John's excessive mucus production. The lining of the bronchial tubes becomes thickened and an irritating cough develops, (Waugh & Grant 2004) which is an additional symptoms that john is experiencing.

Chronic Obstructive Pulmonary Disease, also known as COPD, is the third leading cause of death in the United States. COPD includes extensive lungs diseases such as emphysema, non-reversible asthma, specific forms of bronchiectasis, and chronic bronchitis. This disease restricts the flow of air in and out of the lungs. Ways in which these limitations may occur include the loss of elasticity in the air sacs and throughout the airways, the destruction of the walls between air sacs, the inflammation or thickening of airway walls, or the overproduction of mucus in airways which can lead to blockage. Throughout this paper I am going to explain the main causes, symptoms, diagnosis, and ways to reduce COPD.

Rod ahs returned six months since the last appointment. Up until a month ago, Rod has been quite stable. During that time, he has been aware of increased breathlessness, but no real cough or fevers. He does not recall any upper respiratory tract infective symptoms. He had three days of prednisolone a few weeks ago without any improvement and a couple of days ago completed ten days of ciprofloxacin and feels slightly better.

Burt, L., & Corbridge, S. (2013). COPD exacerbations. AJN The American Journal of Nursing, 113(2), 34-43. Doi: 10.1097/01.NAJ.0000426688.96330.60

Defіnіtіon of COPD The Global Іnіtіatіve for Obѕtrustіve Lung Dіѕeaѕe (GOLD) Guіdelіneѕ defіne COPD, chronic progreѕѕіve dіѕeaѕe, even after admіnіѕtratіon of Broncodіlatorѕ but not full reverѕіble aіrway obѕtructіon іѕ charasterіzed. The aіrway obѕtructіon іѕ cauѕed but mіxture of obѕtrustіve causes bronshіtіѕ and bronchial іnјuruy and іѕ an abnormal inflammatory with the lungs associated with harmful particles. Symptoms of COPD are chronic and progressive dyspnea, cough and sputum production. The diagnosis of COPD and backup is done in addition to the clinical diagnosis of the Spirometry. It should be assumed that COPD when the forced post bronchodilator force expiratory volume (FEV1) less than 80% of the

Asthma is one of the main differential diagnosis in COPD exacerbation because of the similarities in the presenting symptoms. The patient complains of a cough and shortness of breath. These are typically seen in asthma but asthma will be ruled out because the cardinal signs that include; wheezing, an intermittent sensation of chest tightness, non-productive cough and a possible trigger such as exposure to allergens (Jo & Laurie, 2014) were not noted in the patient’s H&P or in the health assessment.

The patient is a 70-year-old gentleman who presents to the ED complaining of productive cough with yellow sputum over the past 2-3 days gradually getting worse associated with shortness of breath and some subjective fevers aggravated on exertion with no definitely relieving factors. The patient is known to be Losartan and Simvastatin. There is a question of a diabetes history. The patient presents with no white count, afebrile. The chest x-ray report is not available at the time of this dictation. However, the patient is described as being in some mild respiratory distress with wheezing over the entire lung fields. The patient is started on respiratory treatments, as well as intravenous is in the ED and placed acutely inpatient in the

"The common clinical features among the case-patients included a prodromial illness of fever, chills, and myalgia. The prodrome was followed by dyspnea, cough, throbocytopenia, severe hemodynamic instability, neutrophilid with immature forms, atypical lymphocytes, elevated serum levels of lactate dehydrogenase. There was a high mortality rate, approximately eighty percent in the initial group of patients, the chest x-ray examinations revealed a diffuse, interstitial infiltrate that resembled that observed in patients with adult respiratory distress syndrome (ARDS), which is a common pattern in patients