Formative Assessment Template

Change in anatomy and physiology:

Stroke is termed as sudden deficient within the neurological function, resulting in poor perfusion of oxygen within the brain. As stated by Li & Yang (2017), the brain is supplied anteriorly with a pair of internal carotid arteries and a pair of vertebral arteries posterior, residing within subarachnoid space. Thus, it is clear that there is a change at the cellular and tissue level of the body, leading to malfunction and change in human physiology.

Stroke within the posterior circulation may lead to vertigo, diplopia, and dysphagia. The stroke in the left anterior circulation results in aphasia and right haemi-paresis (Sommer, 2017). The change in anatomy is not limited to the brain; rather it affects the anatomy at the cellular and tissue levels.


Ischemic Stroke Pathophysiology

Cellular level

The complex pathophysiology of stroke is inclusive of energy failure, poor cell ion homeostasis and high levels of intracellular calcium. The increase in cytotoxicity at the cellular level causes a disruption of the brain-blood barrier (BBB). As influenced by Radak et al. (2017), disruption of BB activates the glial cells, accompanied by an outcome of leukocytes infiltration. These series of interrelated events can lead to ischemic necrosis. After the initial onset of cerebral ischemia, the core of the brain is subjected to reduced blood flow, gradually resulting in necrosis of the brain cells. Stroke severity is increased by BBB and may further worsen by predisposing factors such as systematic infection

Tissue or organ level

The necrotic core is guarded by a group of less effective tissue that is functionally counterproductive due to poor blood flow but continues to remain metabolically active (Anrather, 2017). The event of necrosis is marked by initial organelle and cellular swelling; leading to disruption of nuclear structure and associated cytoplasmic organelles (Chen, Ovbiagele & Feng, 2016). The region surrounding the ischemic core is termed as the ischemic penumbra, representing the area with scope for salvage, through the implementation of after stroke therapy. The tissue level of stroke can be supported by the evidence put forward by Park (2017), stating neurons within ischemic penumbra harbor the chance of apoptosis, only after several days or hours. Thus, the neurons around ischemic penumbra are recoverable for some time after the event of a stroke. Apoptosis results in DNA fragmentation, cross-linking of proteins, even the formation of apoptotic bodies. DNA fragmentation results in cell death which in result can help in approximating the injury faced by the stroke patient.

Body system

Citing an example from the muscular system, it can be easily stated that stroke affects one side of the brain. As stated by Radak et al. (2017), the left side of the brain controls the right side and vice versa. If one side is affected by stroke then the neurological signal cannot travel to the body muscles leading to muscle weakness and paralysis. Stroke often leads to respiratory damage-causing difficulty in swallowing, dysphagia.

FAST guidelines are used to detect possible changes (, 2020):

F (face): Uneven symmetry of the face

A (Arms): Unable to lift one or both arms due to muscle weakness

S (Speech): Slurred Speech

T (Time): Contact immediate medical help if the mentioned symptoms are noticed

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Reference list

Anrather, J. (2017). Pathophysiology of the Peripheral Immune Response in Acute Ischemic Stroke. Primer On Cerebrovascular Diseases, 139-145. doi: 10.1016/b978-0-12-803058-5.00028-x

Chen, R., Ovbiagele, B., & Feng, W. (2016). Diabetes and Stroke: Epidemiology, Pathophysiology, Pharmaceuticals and Outcomes. The American Journal Of The Medical Sciences, 351(4), 380-386. doi: 10.1016/j.amjms.2016.01.011

Li, Y., & Yang, G. Y. (2017). Pathophysiology of ischemic stroke. In Translational Research in Stroke (pp. 51-75). Springer, Singapore. Doi: 10.1007/978-981-10-5804-2_4 (2020) Recommendations | Stroke and transient ischaemic attack in over 16s: diagnosis and initial management | Guidance | NICE. Retrieved 22 January 2020, from

Park, J. (2017). Acute Ischemic Stroke. Springer Singapore.

Patel, R., & McMullen, P. (2020). Neuroprotection in the Treatment of Acute Ischemic Stroke. Retrieved 22 January 2020, from

Radak, D., Katsiki, N., Resanovic, I., Jovanovic, A., Sudar-Milovanovic, E., & Zafirovic, S. et al. (2017). Apoptosis and Acute Brain Ischemia in Ischemic Stroke. Current Vascular Pharmacology, 15(2), 115-122. doi: 10.2174/1570161115666161104095522

Sommer, C. J. (2017). Ischemic stroke: experimental models and reality. Acta neuropathologica, 133(2), 245-261. Doi: 10.1007/s00401-017-1667-0

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