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Anatomy of Neurovascular System

Wilma's cva (cerebrovascular accident) is identified as an ischemic stroke in this case study. According to sacco et al., 2013, the infarction of either brain, retina or spinal cord is the ischemic stroke. Stroke is a neurodegenerative condition marked by the obstruction of blood arteries. Within the brain, the blood flow is obstructed by the clot formation leading to clog in the arteries as well as blood vessels to rupture, causing blood haemorrhage.

A stroke is a rapid cerebrovascular event caused by insufficient blood flow to the brain. Understanding the neurovascular anatomy is essential for researching the clinical manifestations of a stroke. Two internal carotid arteries and two vertebral arteries controls the flow of blood to the brain. An abrupt drop in regional cerebral blood flow, which results in cell death, due to a shortage of blood and oxygen to the brain relates the ischemic stroke. This problem occurs when a blood artery in the neck or brain becomes obstructed.

Blood clot formation within a blood artery of the brain might cause a decrease in blood flow. The downstream brain tissue suffers from a lack of oxygen and nutrients due to the constriction of brain-supplying arteries. Wilma's blood vessel malfunction, which is caused by his hypertension and other factors, will restrict blood flow to the brain. Wilma's cva is most likely caused by hypertension, which was measured as 165/90 mmhg (normal range is 120/80 mmhg). Wilma's cva is caused by hypertension, which plays a role in the development of major artery atherosclerosis, which leads to ischemic stroke by thrombotic arterial occlusion. Hypertension causes blood vessels to leak, rupture, and damage, as well as blood clotting in the arteries, which prevents blood from being transfused to the brain, as in wilma's cva. Hypercholestemia could be another reason of wilma’s cva which is the deposition of the cholesterol on to the walls of the arteries and narrows the arteries. The atherosclerotic plaques formed in the arteries and arterioles of the brain can lead to occlusions and ischemic damage.

High blood pressure causes smooth muscle cell hypertrophy and re-modelling in the systemic and cerebral arteries, both of which are targeted at lowering arterial wall stress and protecting downstream microvessels. Smooth muscle cells undergo hypertrophy, hyperplasia, or rearrangement as a result of chronically high intra-luminal pressure and grow inward, encroaching into the artery lumen, resulting in narrowing of the vessel lumen, whether or not the wall thickness increases. Hypertension also causes arterial stiffness, which raises pulse pressure, which is a good predictor of stroke. Wilma's cva can be caused by a variety of factors. To begin with, hypertension places a great deal of stress on the endothelium, which is a key element in the formation of atheroma and subsequent atherosclerosis. Endothelial damage and altered blood cell endothelium interaction, on the other hand, can result in blood clots and ischemic lesions. Chronic hypertension also inhibits cerebral vasodilation and changes autoregulation, increasing the risk of ischemic stroke through compromising hemodynamics. Wilma's ischemic stroke may be caused by reduced vasodilator responses along with the limiting of increases in collateral blood flow

Causes of Stroke

1. Smoking - cigarette smoking has long been recognised as a risk factor for all types of stroke smoking raises the risk of stroke by raising blood pressure and lowering oxygen levels in the blood. It also makes the blood stickier, which increases the risk of blood clots forming. When you breathe cigarette smoke, carbon-monoxide (co) and nicotine penetrate your circulation. Nicotine is responsible for increasing blood pressure as well as the heart rate. On the other hand co decreases the blood oxygen levels. A stroke is more likely as a result of this. As a result of these circumstances, smokers are more likely to develop atherosclerosis, a condition in which arteries constrict and harden. This reduces blood flow and makes it more likely for blood clots to form leading to ischemic stroke.

2. Prediabetes: Prediabetes is a metabolic state that lies in-between the normal glucose metabolism and diabetes, with a high-risk of acquiring diabetes and cardiovascular disease in the future. Prediabetes is common in people having some insulin resistance. Resistance to insulin result in several cellular and metabolic changes which further c atherosclerosis, a high risk factor for stroke (jing et al., 2017).  Patients with prediabetes are more likely to develop cardiovascular and cerebrovascular disorders, such as ischemic stroke. Diabetes can cause a stroke through a number of different routes. In cerebral ischemia, acidosis is thought to be a key factor to neuronal damage. Glucose is the brain's sole energy source in both aerobic and anaerobic situations. Glycolysis is the sole mechanism capable of creating atp in excess under anaerobic conditions, such as brain ischemia, and lactate is the major result of glycolysis. Hyperglycemia can exacerbate ischemia outcomes by causing acidosis in ischemic brain tissues.

  1. Left side hemiplegia: Hemiplegia is a disorder in which one side of the body's lower jaw, arm, and leg muscles are paralysed. The most common cause of hemiplegia is stroke, which damages the corticospinal connections in one hemisphere of the brain. The corticospinal tracts run from the lower spinal cord to the cerebral cortex. The lack of oxygen causes damage to the brain tissue and nerves in the case of an ischemic stroke. Wilma's ischemic stroke is thought to produce right middle cerebral artery syndromes, according to research (meschia & brott, 2017). The function of the middle cerebral artery will be affected if blood clotting prevents blood and oxygen from reaching the brain. The middle cerebral artery, which is the principal branch of the circulation central carotid artery in the lateral cerebral cortex, is the most commonly damaged artery in stroke syndrome. Right middle cerebral artery syndromes frequently induce left-sided hemiplegia, while wilma's ischemic stroke causes obstruction of the middle cerebral artery.  The lateral part of the human body includes motor and sensory functions affecting the upper extremity, and is notably relevant for wilma's characteristic presentation of contralateral hemiparesis involving the entire left side of his body. In cerebral artery syndromes, symptoms of the upper extremities typically predominate.
  2. Expressive dysphasia: Dysarthria is a common and long-lasting complication of stroke that can occur in a variety of places. The mca (middle cerebral artery)  is the most frequently affected artery in stroke. A large percentage of the lateral surface of the brain, as well as a portion of the basal ganglia and the internal capsule, is supplied by four segments (m1, m2, m3, and m4). The m1 (horizontal) section supplies the basal ganglia, which is important in motor control, motor learning, executive function, and emotions. The insula, superior temporal lobe, parietal lobe, and infero-lateral frontal lobe are all supplied by the m2 (sylvian) segment. The lateral cerebral cortex is involved in the mca distribution. This corresponds to the traditional symptoms of contra-lateral hemiparesis, facial and upper-extremity sensory loss.

1. Apixaban - apixaban is a direct oral anticoagulant that reduces thrombin production and thrombus progression by inhibiting free and clot-bound factors. Apixaban is helpful for preventing ischemic stroke in cardiovascular systems because it may specifically block xa agent in both free and bound forms, preventing thrombus formation. Because wilma has a history of hypertension, health care practitioners will prescribe apixaban to wilma to lower the risk of ischemic stroke relapse. Apixaban absorption begins in the small intestine and gradually decreases in efficiency as it travels through the gastrointestinal tract. Apixaban will be absorbed throughout the gastrointestinal tract during the absorption process, with the distal small bowel and ascending colon accounting for roughly 55 percent of apixaban absorption. Apixaban binds to plasma protein and is transported throughout the body in about 87 percent of cases. Apixaban is mostly metabolised in the liver and gut, with approximately a quarter of orally administered apixaban being recovered as metabolites in urine and faeces.  Apixaban is generally expelled in faeces and is removed in both urine and faeces. A tiny amount of apixaban can also be secreted through the bile. Renal excretion accounts for around a quarter of the overall excretion rate. Apixaban can be eliminated through biliary excretion and bowel opening. Hypotension or hypertension, dizziness, vertigo, headache, and stomach discomfort are all side-effects of apixaban. Anticoagulant or anti-platelet supplements or medications are contraindicated.

Symptoms of Stroke

2. Amlodipine – it is a dihydrothiophene calcium antagonist and a cardiovascular hypotensive drug that prevents calcium ion transmembrane insertion into vascular smooth muscle and myocardium. A branch artery vasodilator that operates directly on vascular smooth muscle might produce local vasoconstriction and a rise in blood pressure. Amlodipine binds to both dihydropyridine and non-dihydropyridine binding sites. Amlodipine's role is to prevent angina by reducing after load due to its vasodilation and antihypertensive effects. Because the heart does not have to work as hard to pump blood into the systemic circulation, myocardial oxygen demand will be reduced at any degree of exercise. Wilma is given amlodipine because she has hypertension, which is a risk factor for ischemic stroke. Wilma's blood pressure can be lowered to prevent a repeat of her ischemic stroke. Amlodipine is absorbed slowly and nearly completely through the intestinal system, increasing in plasma six to twelve hours after oral administration. Amlodipine travels throughout the body via binding to proteins and acting directly on vascular smooth muscle, causing peripheral vasodilation. In vascular smooth muscle and myocardium, amlodipine stops calcium ions from binding to calmodulin. Amlodipine is broken down into inactive metabolites in the liver, the bulk of which are excreted in the urine. The majority of circulating amlodipine binds to plasma proteins, according to studies. In both phases, amlodipine will be removed from the plasma, and a little amount of amlodipine will be excreted unchanged in the urine. Amlodipine has a bioavailability of 64 percent to 90 percent, and its bioavailability is unaffected by the presence of meals. Headache, dizziness, hypotension, asthenia, and arrhythmia are some of the side-effects of amlodipine. Patients who have a known hypersensitivity to amlodipine or its components should avoid taking it.

3. Perindopril - perindopril is a prodrug that is hydrolyzed in the body to produce perindoprilat, an ace inhibitor. Perindopril causes dose-dependent ace inhibition, resulting in lower plasma angiotensin ii levels, decreased vasoconstriction, higher plasma renin activity, and lower aldosterone secretion after oral treatment. Diuresis and natriuresis are caused by the action on aldosterone. The amount of ace inhibition obtained by a particular dose tends to decrease over time. 4 to 6 hours after drug delivery, pharmacodynamic effects are at their peak. Perindopril reduces systolic and diastolic blood pressure while having no effect on heart rate or the typical diurnal variation in blood pressure (khashaba et al., 2021).Perindopril has a 75 percent absolute bioavailability when taken by mouth. Perindoprilat has a high bioavailability, having a 25 percent mean bioavailability. Perindoprilat accumulates 1.5 to 2 times after repeated once-daily perindopril injection, reaching steady-state plasma concentrations in 3 to 6 days. Only 10–20% of circulating perindopril is linked to plasma proteins, whereas 60% of the active metabolite is. Perindopril is extensively metabolised, with only 12% of medications taken remaining unaltered in urine. Hydrolysis, glucuronidation, and dehydration/cyclization processes have resulted in the identification of six metabolites. Perindoprilat is eliminated from the bloodstream in a multiphase process. Perindoprilat is entirely cleared through the kidneys.

Before a drug reaches the site of action or systemic circulation, it is digested in a specific area in the body, lowering the concentration and efficiency of the active agent. Before being disseminated into the general circulation, drugs ingested from the gi tract pass through the portal circulation and pass through the liver. They go through first-pass metabolism in the liver and may be heavily processed before reaching the bloodstream. When a medicine is taken orally, its bioavailability refers to how well it is absorbed into the systemic circulation. The "First pass effect" Refers to the reduction in total medication delivery to the systemic circulation. The bioavailability of apixaban is roughly 50 %, which causes inadequate absorption and first-pass metabolism in the gut and liver (leal et al., 2021).

References

Jing j, pan y, zhao x, et al. Insulin resistance and prognosis of nondiabetic patients with ischemic stroke: The across-china study (abnormal glucose regulation in patients with acute stroke across china). Stroke 2017;48:887-893.

Khashaba, p. Y., mohamed, h. A., & shahin, r. Y. (2021). Analysis of angiotensin converting enzyme inhibitors and antagonists. Sphinx journal of pharmaceutical and medical sciences, 1(1), 1-41.

Leal rato, m., diógenes, m. J., & sebastião, a. (2021). Pharmacodynamics and pharmacokinetics of stroke therapy. In precision medicine in stroke (pp. 41-69). Springer, cham.

Sacco, r. L., kasner, s. E., broderick, j. P., caplan, l. R., connors, j. J., culebras, a., ... & vinters, h. V. (2013). An updated definition of stroke for the 21st century: A statement for healthcare professionals from the american heart association/american stroke association. Stroke, 44(7), 2064-2089.

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