Clinical Case Conference Report on Exacerbation of COPD

Clinical Case Conference Report 1
CLINICAL CASE CONFERENCE REPORT
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Clinical Case Conference Report 2
Introduction
Patient’s brief account
The patient is a 71-years old woman called Mrs. Sue Thompson. The physician has
diagnosed her with Exacerbation of COPD. She is of an Australian origin and hails from the
south.
Physiological, social, and economic background
Mrs. Thompson is married and lives together with her husband and their children. She
has two biological sons and one foster son. She is a former office worker and a bank cleaner.
Furthermore, she likes sewing and her husband have been unwell recently. The patient has been
doing most of the housework although the sons and daughter-in-law have been helping her. All
her family members are supportive. She does not take alcohol but is an ex-smoker.
Presenting complaints and reasons for admission
Sue reported to the health facility with numerous complaints. She was suffering from
hypertension, Type 2 diabetes, and COPD. Furthermore, the patient had depression and mini-
stroke (TIA). She is also allergic to latex, amoxicillin, and erythromycin. The doctor admitted
her after diagnosing Exacerbation of COPD.
Past Medical History
She has had an ectopic pregnancy and reflex sympathetic dystrophy. Furthermore, the
patient has a history of recurrent depression and rotator cuff pathology. Mrs. Thompson has a
past surgical history of reduction mammoplasty in 2001. In 2002, she passed through incisional
Hernia repair. She also underwent nonalcoholic steatohepatitis and CARB in 2003 and 2007
respectively. Additionally, she had cataract removal and IOL implant on the right in 2016.
Family History

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The patient’s mother had breast cancer. The other relations had IHD and muscular
degradation. There is also a history of diabetes.
Patient’s Observation
The patient has been frequently comes out of bed; thereby, having miserable nights. She
also pants and has sarcotic lung disease. Furthermore, she has additional breathing problems.
Current Medication: ATROVENT UDV Neb solution and AZAPIN tablet.
Current Diagnosis: Exacerbation of COPD.
Anatomy/pathophysiology of Exacerbation of COPD
Epidemiology
Fourteen percent of Australians above the age of forty have COPD (Kelly et al., 2018).
The figures elevate in individuals above the age of seventy. Thirty percent of those people have
the disease, and Mrs. Thompson happens to be one of them. Seven percent of the affected
individuals above the age of forty have chronic COPD with signs and symptoms. However, a
quarter of the affected individuals are unaware of the infection. Recent research has ranked the
disease as the second cause admissions in Australian hospitals (Meszaros et al., 2015).
Furthermore, the disease ranks third in the mortality list after cancer, heart disease, and stroke.
Australian lung foundation states that over seven hundred thousand individuals have the disease.
Anatomy and physiology
Exacerbation of COPD affects the circulatory and respiratory systems. The disease
affects the lung thereby limiting its ability to carry out gaseous exchange (Qing et al., 2018). The
human body contains a trachea and a pair of lungs. The trachea is responsible for oxygen
inhalation and carbon dioxide expulsion. During inhalation, atmospheric air passes through the

Clinical Case Conference Report 4
nose where it gets filtered of harmful materials. The mucous in the nasal cavity aids in air
filtration. The clean air moves to the lungs from the nose via the trachea.
The epiglottis prevents the entry of unwanted materials in the windpipe. The air then
moves to the bronchi from the trachea and eventually reaches the lungs. Afterward, the filtered
air runs into the bronchioles and finally into the air sacks. The alveoli enable oxygen to diffuse
into the capillaries. Moreover, the air sacs can uptake carbon dioxide and exhale the gas at a later
stage. The diaphragm lies below the lungs on the right side, and it separates the lungs from other
body organs.
Additionally, the organ aids in inhalation and expiration. Intercostal muscles also help the
diaphragm in the breathing process (Broussard, Hall, and Levitzky, 2014). Exacerbation of
COPD interferes with the normal breathing and blood circulation.
Pathogenesis
COPD limits the flow of expiratory generation during inspiration and expiration. The
disease occurs due to the limitation of the time that the lung needs to empty its contents. Severe
inflammation of the airwaves prevents the patients from having a flawless breath. Furthermore,
the elevation of the lymphocytes and macrophages in the walls of the airwaves decrease the
lumen of passage. Air pollution is the primary cause of severe airwave inflammation.
Furthermore, bacterial and viral infections also inflame the air channels. The
inflammation alters the cellular pattern during exacerbations. The condition worsens due to an
elevation in the number of neutrophils and eosinophils.
Inflammatory mediators are also responsible for the narrowing of the air channels. The
mediators include RANTES, chemokines, and cytokines (Kato, and Hanaoka, 2017). An increase
in the level of inflammation interferes with the functions of the lungs. Furthermore, the health of