Case Study on Copd

Three days prior to consult, the patient’s condition further declined – having experienced dyspepsia on moderate exertion, associated with worsening cough and increased sputum production from -2 tablespoons to approximately 1-2 cups dally. ETC cough medication was taken, offering temporary relief of cough.

Three hours prior to consult, the patient complained of severe dyspepsia associated with occasions, hence sought medical advice. Patient had no medical history of Cancer, Asthma, Hypertensive Heart Disease, CHEF, CAD, or DTV. Patient had no known allergies.

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Surgical or trauma history was unremarkable. Personal history revealed that he lived alone but received 4 hours of paid caregiver assistance for his ODL/Dials daily, history of 60 pack-year smoking ND still smoked up to this time. Family history was unremarkable.

Review of systems was pertinent for worsening dyspepsia, chronic cough productive of copious sputum, and generalized weakness. No chest pain, edema, fever, or cache reported. Physical Examination On physical examination, vital signs revealed: BP= 120/70 meg; HER=90/min; OR=32/ min; Temp=37. OFF; 02 sat = 85% in room air.

Inspection showed a well-groomed, medium-built man, looked appropriate for his age, In corporeality’s distress as manifested by pursed-lip breathing and use of some accessory respiratory muscles or breathing, with barrel chest, cyanic finger nails, and had weak cough productive of copious, thick, yellowish sputum. Pulmonary findings revealed presence of tactile premises over both lung fields, hypertension’s on percussion on both anterior and posterior lung fields, and presence of rancho on bilateral lung fields.

No crackles or wheezes were noted.

His CB values were all normal except for HCI and Hag – BUMP values were all normal. FIVE = 0. 63. Differential Diagnoses 1) COOP VOLVO -Translators spectrometry revealed post a. Rule in: Patient presents with dyspepsia, chronic productive cough, hypertension’s on chest percussion, rancho on bilateral lung fields, radiological findings of hyperinflation and prominent bronchial markings; history of smoking; Bag’s suggestive of compensated respiratory acidosis; spectrometry revealed irreversible airflow obstruction.

B. Rule out: none 2) Asthma c. Rule in: Patient presents with dyspepsia and chronic cough d.

Rule out: Patient has no personal or family history of asthma or allergy, no wheezing observed; cough is usually non-productive in Asthma; onset of asthma is usually early in life; in Asthma, airflow obstruction is reversible following short-acting bronchiolar retirement 3) CHEF e. Rule in: Patient presents with dyspepsia, chronic cough f.

Rule out: Patient did not have edema, crackles, radiological findings of infiltrates; normal heart size; No history of hypertensive heart disease 4) Tuberculosis g. Rule in: Patient presents with dyspepsia and chronic cough h.

Rule out: Patient did not have fever, or radiological findings of pulmonary infiltrates, cavitations, or Hilary lymphocyte’s 5) Pneumonia I. Rule in: Patient presents with dyspepsia and cough J. Rule out: Patient did not have fever, or radiological findings of pulmonary infiltrates Final Diagnosis COOP Discussion Definition Chronic Obstructive Pulmonary Disease (COOP), a common preventable and treatable disease, is characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gales.

Prevalence COOP is currently the third leading cause of death in the United States. Fifteen million Americans report that they have been diagnosed with COOP. More than 50% of adults with low pulmonary function were not aware that they had COOP; therefore the actual number may be higher: Risk Factors Cigarette smoking is the best-studied factor that increases the risk of developing COPED. However, among people with similar smoking history, not all will develop COOP possibly due to variations in their genetic predisposition to the disease.

The best documented genetic risk factor is a severe hereditary deficiency of alpha-I antiperspirants.

Single genes such as the gene encoding matrix interpretations 12 (MUMMY) have also been related to decline in lung functions. Pathologically an a Clinical Molestations The following Figure is a summary of the Pathologically Mechanisms and Clinical manifestations for COPED, 8, 9, 10 as applied to the case presented. Genetic predisposition? Inhalation of Cigarette smoke (60 pack-years) Figure 1.