ASSIGNMENT on HEALTH & HOMEOSTASIS


ASSESSMENT TASK 1 CLINICAL CASE SCENARIO ANALYSIS
1.Stroke is an acute neurological deficit due to a vascular lesion which persist for longer than 24 hours. It is characterized by loss of circulation to an area, resulting in a corresponding loss of neurological function. Also known as Cerebrovascular accident, can be focal or global (Sacco S, 2004).

Symptoms experienced by the patient: (reference: case study)
-severe headache,
-dizziness/giddiness
-nausea
-left arm and leg weakness
-vomiting, gradual onset of neurological signs
Sign experienced by the patient: (reference: case study)
-Reduced grip strength of the left hand
-Sleepy
-Respiratory distress

  1. In this case, the basal ganglia and cerebral lobes of the brain have been affected, thus making the patient to experience severe headache, dizziness, giddiness and nausea. The neurological system has been affected hence the patient experiences neurological deficits such as impaired consciousness, weakness in the left arm and leg weakness (Li, 2018).
  2. In this patient, the principle hazard factor causing intracerebral drain is hypertension due to resistance to hostile to hypertensive treatment. In an intracerebral discharge, draining happens legitimately into the mind parenchyma. The typical system is believed to be spillage from little intracerebral supply routes harmed by incessant hypertension (Prins M, 2013).
    Hypertension can cause stroke through various segments. High intraluminal weight will incite an expansive adjustment in endothelium and smooth muscle work in intracerebral gracefully courses. The extended load on the endothelium can assemble vulnerability over the blood-mind impediment and neighborhood or multifocal cerebrum oedema. Endothelial damage and altered platelet endothelium correspondence can provoke close by thrombi course of action and ischaemic wounds. Fibrinoid rot can cause lacunar infarcts through focal stenosis and obstructions (Wagner KR, 2004). Degenerative changes in smooth muscle cells and endothelium slant for intracerebral hemorrhages. Additionally, hypertension breathes life into the arteriosclerotic procedure, thusly improving the probability for cerebral injuries identified with stenosis and embolism starting from huge extracranial vessels, the aortic twist and from the heart (Sun J, 2016). Adaptable helper changes in the deterrent vessels, while having the useful result of diminishing the vessel divider pressure, have the negative aftereffect of extended periphery vascular restriction that may deal the security stream and improve the danger for ischaemic events in regards to scenes of hypotension or distal to a stenosis. The intracerebral channel has a tendency for explicit goals in the cerebrum, including the thalamus, putamen, cerebellum, and brainstem. Despite the zone of the cerebrum hurt by the release, the incorporating brain can be hurt by pressure conveyed by the mass effect of the hematoma. A general addition in intracranial weight may occur (Xi G, 1998).
    Cigarette smoking
    The patient in this case scenario has been smoking and this is a major risk factor for haemorrhagic stroke. Nicotine and carbon monoxide contribute to development of heart disease including hypertension and Atherosclerosis which damages the inner lining of the arteries with plaque which weaken arterial walls making them rupture easily. Continuous smoking can lead to severe hypertension leading too intracerebral hemorrhage.
    Hyperglycemia
    Hpyerglycemia is a well-recognized risk factor for Atherosclerosis and myocardial infarction, as well as microangiopathy affecting the brain. The patient has high blood glucose of 9mmol/L on admission. Hyperglycaemia may also augment brain injury by several mechanisms including tissue acidosis from anaerobic respiration and free radical formation and increased brain barrier. With disruption of the blood-brain barrier, red blood cells extravasate from the weakened capillary bed, leading to intracerebral hemorrhage (PubMed, 2011).

Lipidaemia.
Lipidaemia is elevation of plasma cholesterol, triglycerides or a low high-density lipoprotein that contributes to the development of Atherosclerosis. Causes can be primary or secondary. The main indication for dyslipidaemia treatment is prevention of Atherosclerotic cardiovascular disease, that include acute coronary syndromes and stroke. The patient in this case scenario is non-compliant with his lipidaemia medication hence predisposing himself to stroke (Kenneth R Feingold, 2020).

References
David S Liebeskind, M. F. (2019). Hemorrhagic Stroke.
Kenneth R Feingold, M. (2020). Approach to the Patient with Dyslipidemia.
Li, T. L. (2018). Quantitative proteomic analysis of intracerebral hemorrhage in rats with a focus on brain energy metabolism.
Prins M, G. T. (2013). The pathophysiology of traumatic brain injury at a glance. Disease Models & Mechanisms, 1307–1315.
PubMed, P. (2011). Molecular pathophysiology of cerebral hemorrhage: secondary brain injury. 1781-6.
Sacco S, M. C. (2004). Medical treatment of intracerebral hemorrhage. . Neurol Sci .
Sun J, J. G. (2016). The experimental study of increased ICP on cerebral hemorrhage rabbits with magnetic induction phase shift method. Iranian Journal of Medical Physics, 125–136.
Wagner KR, D. B. (2004). Hematoma removal, heme, and heme oxygenase following hemorrhagic stroke. 237–251.
Xi G, W. K.-M. (1998). Role of blood clot formation on early edema development after experimental intracerebral hemorrhage. 2580–2586.
Zhao, J. A. (2011). Molecular Pathophysiology of Cerebral Hemorrhage. Secondary Brain Injury.

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