Pathophysiology and Pharmacology: Ischemic Stroke Case Study Analysis

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This report provides an analysis of ischemic stroke, covering its pathophysiology and pharmacology based on a case study. It begins with an introduction to ischemic stroke, its prevalence, and risk factors such as atrial fibrillation and extracranial embolism. The report details the patient's presentation, including symptoms like right-sided facial drooping and gait issues, and links these to the underlying pathophysiology. It explores the cellular mechanisms involved, including cellular communication, and discusses the etiology and diagnostic investigations. Furthermore, the report examines the treatment modalities and prevention strategies for ischemic stroke, referencing relevant literature and research findings. It also discusses the importance of early diagnosis and the impact of age and genetics on stroke risk. The report concludes by summarizing the key elements of the case, highlighting the importance of understanding pathophysiology in clinical practice.
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Running head: PATHOPHYSIOLOGY AND PHARMACOLOGY
PATHOPHYSIOLOGY AND PHARMACOLOGY
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PATHOPHYSIOLOGY AND PHARMACOLOGY
Ischemic stroke is the most common stroke type representing about 85% of all strokes
(David, 2009). Recent years have witnessed increasing recognition and interests in stroke as a
significant public health problem (David, 2007, pp1). Right-sided facial drooping is a defect
caused by having extracranial embolism which has an important renal action that is central to
disorder bone metabolism with renal failure. PTH decreases proximal phosphate reabsorption by
diminishing the activity of the sodium phosphate cotransporter in the apical membrane (Helmut
& Rennker, 2007, p-318). Seward is a patient with atrial fibrillation with a history of
hypertension. He is reportedly to be in good condition. In Steward's case, an increase in renin
secretion (PTH) decrease caused the weakness in his arm. The ORG 10172 trial in actual stroke
treatment classification is commonly used to define the cause o ischemic stroke. Cardin embolic
stroke and dissections of cervical or cerebral are the most common etiologies of stroke (Turgut &
Lars, 2018). Other defects that Steward had included unconditional gait and dominant visual
gaze towards the left which is an eye movement disorder (Martinus).
Pathophysiology is the study of how the disease affects the functioning of the body. Risk
factors are factors that cause an increased risk of the illness (Sarah A., Justine R. & Vanessa T.).
In our patience case, the pathophysiology in the scenario includesright-sided facial drooping,
unconditional gait and dominant visual gaze towards the left which after a screening, he was
found to be diagnosed with ischemic stress caused by an extracranial embolism. Other onset
weakness includes numbness diplopia, dysarthria, vertigo and many more. All diseases involve
damage or injury to the cell which makes the cells to stop functioning correctly or death. Cellular
communication is one of the pathophysiology causing etiology. Different organs which include
tissues and cells must work together to form a fully functioning person. The working together of
the cells is called integration. This may be linked with Steward's case of right-sided facial
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PATHOPHYSIOLOGY AND PHARMACOLOGY
drooping (Sarah A., Justine R. & Vanessa T.). The stroke typically involves an absence of
functions. An example, our patient reported the loss of sight in an eye.
Recent years have witnessed increasing recognition and interest in stroke as a major
public health problem (Magdy S.). Imhota, the founder of Egyptian medicine, describes stroke in
one of the most ancient diseases in the world. By then, stroke treatment was rudimentary and
often nihilistic. Stroke victims might have been treated using maggots or leech to improve the
blood movement in the brain (Magdy S.). Despite the modern advances in the diagnosis and
treatment of cerebrovascular disease, stroke remains a significant cause of mortality and
morbidity worldwide (Rodney ). Stroke mortality rises rapidly with age. The increase in
mortality in the elderly is mainly a result of the steep rise in the incidence of stroke with age
(Sara T., Mathew F. & Peter M.). Research shows that the diagnosis of stroke can be accelerated
by age, where old people are likely to be affected. Two, studies of twins and families with stroke
suggest a genetic component to stroke risk (Andrew, Mathew & hunt 2012). Based on the
assumption that at list some of the dangers sporadic stroke is genetic, large numbers of studies
using different methodologies have been carried out in an attempt the genes involved. There are
only a few data relating to a family on stroke severity. Stroke prevention may be targeted at two
primary levers which include the mass approach for the population at large and the high-risk
approach for those in the population who are believed to be at great risk (Scott E. & Philip B.).
The essay has covered patient’s risk factors in relation to Steward's case. The scenario
has outlined the diagnosis, etiology and risk factors. Steward has atrial fibrillation which led to
him being diagnosed with ischemic stroke. On the risk factors, a brief description of the disease
is given. The essay has also described the pathophysiology causes in the clinical manifestation
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PATHOPHYSIOLOGY AND PHARMACOLOGY
where stewards brain is already affected. The last bit of the essay has justified the diagnostic
investigation and treatment.
Helmet, G., & Bradley, M., 2007. Renal pathophysiology: the essentials.
David, M. Greer. 2007. Acute ischemic stroke. Retrieved at www.wily.com/go/permision
Turgut, T., &Lars, T., 2018. Ischaemic stroke In youth. oxford
Martinus, N., an eye movement disorder. Junk publishers.Doi10/1007/978-94-009-3317-
0
Sarah A., Justine R. & Vanessa T, 2016.Pathophysiology &harmacology for nursing
students.
Andrew M, et al. (ed). 2012. Hemorrhagic and ischemic stroke.
Scott E., & Philip B., 2004. Prevention and treatment of ischemic stroke
Sara T., Mathew F. & Petre M, 2014. Cure and treatment of ischemic stroke.
Leonard S., 2011. Pathophysiology of heart disease.
Franklin H. & Jon C., 2010. Pathophysiology of blood disorders.
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