Stroke Case Study | Pathophysiology and Care Delivery Plan

Stroke detail Study Pathophysiology and C are Delivery PlanThis paper will discuss the case study relating to the long-suffering, Mrs Amelia Middleton, and firmness a series of questions relating to the pathophysiology of box, nursing care of the patient, and response to pharmacological issues with her word suspense 1Farrell Dempsey (2014b) fixate the pathophysiological characteristics of an ischemic stroke as being the disruption to intellectual blood supply due to an block in a blood vessel (p. 1649). This disruption can be described as an ischaemic cascade, which commences with a fall in rational blood flow to less than 25mL/100g/min (p. 1649). When this occurs, neurons are inefficient to maintain aerobic respiration, causing a decrease in adenosine triphosphate (ATP) production. To combat this, mitochondria switch to anaerobic respiration, which produces intumescent amounts of lactic acid, causes changes in cellular telephoneular pH levels, anaerobic respiration is less efficient, and neurons are not qualified of producing sufficient ATP to fuel the depolarisation processes (Farrell Dempsey, 2014b, p. 1649 Craft, Gordon, Tiziani, 2011). With the loss of ATP production, the active transport across the cell membrane ceases, leading to the destruction of the cell membrane, releasing more calcium and glutamate, vasoconstriction and generation of free radicals. As the cascade continues, intracellular pressures increase, causing oedema (Craft, et al., 2011, p. 192). This oedema reaches it maximum after about 72 hour, and soft subsides over the following two weeks.There are four types of haemorrhagic stroke, namely intracerebral, intracranial cerebral aneurysm, arteriovenous malformations, and subarachnoid haemorrhage, all with varying pathophysiology (Farrell Dempsey, 2014b, p. 1661). The most common type is the intracerebral haemorrhage, which is mostly found in patients with hypertension and cerebral atheroschlerosis. Certain types of art erial pathology, brain tumour, and the use of medications may besides cause intracerebral haemorrhage (Farrell Dempsey, 2014b). Bleeding related to the condition is most commonly arterial and normally occurs in the putamen and coterminous internal capsule, cerebral lobes, basal ganglia, thalamus, cerebellum and brain stem (Farrell Dempsey, 2014b).Intracranial aneurism is dilation of the walls of a cerebral artery developing because of weakness in the arterial wall (Farrell Dempsey, 2014b). Presumed causes of aneurysms are weakness in arterial walls, congenital abnormalities, hypertensive vascular affection, head trauma, infection, or advancing age. Aneurysms can occur in both area of the brain but commonly occur at the circle of Willis arteries. Arteries affected by aneurysms are the internal carotid artery, anterior cerebral artery, anterior communicating artery, posterior communicating artery, posterior cerebral artery and middle cerebral artery (Farrell Dempsey, 2014b).Ar teriovenous malformations are caused by abnormalities in embryonic developing or are the result of trauma. It is the formation of a mass of arteries and veins without a capillary bed, whose absence, leads to dilation of arteries and veins with eventual(prenominal) rupture. This type of haemorrhage is common in younger people (Farrell Dempsey, 2014b).Subarachnoid haemorrhage may occur because of arteriovenous malformation, intracranial aneurysm, trauma or hypertension. Most common causes are leaking aneurysms in the area of the circle of Willis or a congenital arteriovenous malformation of the brain (Farrell Dempsey, 2014b).Both ischaemic and haemorrhagic stroke ease up modifiable and non-modifiable precipitating factors. Modifiable factors are those that can be changed and let in(Al-Asadi Habib, 2014 Jarvis, 2012)Non-modifiable factors are those that cannot be changed or altered, and in concert with modifiable risk factors, can indicate populations at higher risk. The factors a re(Al-Asadi Habib, 2014 Jarvis, 2012)Question 2The nursing care required for the patient within the archetypal 24 hours would initially include a neurological assessment, especially if thrombolytic therapy has been administered (Hinkle McKenna Guanci, 2007). Nurses need to use the Glasgow coma scale (GCS), check springy signs pupil reaction and limb assessment. If the GCS falls during or after treatment, patients need to endure an urgent CT scan to get up haemorrhagic stroke. These observations need to be recorded every 15 minutes for the first 2 hours after thrombolytic therapy, then every hour for the next 24 to 48 hours (Hinkle McKenna Guanci, 2007). type O therapy will only need to be administered if the patient becomes hypoxic, which occurs if the oxygen saturation (SaO2) levels fall below 95% saturation. Blood sugar levels need to be monitored, as it is common for post stroke patients to become hyperglycaemic. Patients to a fault need to be in an electric bed with the c ot sides up and the head at a 30-degree angle, which trim downs the risks of choking and falls (Catangui Slark, 2012). Suction should be available at the bedside in case of angioedma. Electrocardiograms need to be performed regularly to detect any abnormal changes in optic rhythm. The patient is already in atrial fibrillation but this may alter if thrombolytic therapy is administered, as such, this requires assessment on an hourly basis. The nurse should also take the magazine to provide information to family members regarding the patients treatment (Felicilda-Reynaldo, 2013). The patient and family need to be informed why thrombolytic therapy is needed, what the desired outcomes are and if there are any adverse effects. When this treatment is needed, it is often in an emergency and can be frightening for family members to see their loved one in pain or distress (Felicilda-Reynaldo, 2013).Question 3Thrombolysis is the division of a blood clot or thrombus by the infusion of a fibr inolytic agent ( doses that are capable of breaking atomic pile fibrin, the main persona of blood clots) into the blood (Tiziani, 2013). Thrombolytic agents act by activating plasminogen to form a proteolytic enzyme, plasmin, which attaches to fibrin, and consequently, breaks down the clot (Tiziani, 2013 Catangui Slark, 2012) this process is called clot resolution. Thrombolytic agents vary in there action, for example, Alteplase and Reteplase, are recombinant tissue plasminogen activator (r-tPA) doses that have fibrin specific actions, adhering to fibrin saltation plasminogen, Tenecteplase, a genetically engineered tissue plasminogen activator (tPA) shares similar traits (Tiziani, 2013 Catangui Slark, 2012). In contrast, Streptokinase is a non-specific plasminogen activator, which attaches itself to both fibrin bound plasminogen and unbound plasminogen (Tiziani, 2013).The use of thrombolytic agents on stroke patients is time-critical. Catangui Slark (2012), supported by Hinkl e McKenna Guanci (2007) and Farrell Dempsey (2014b), describe a sic of contraindications for the use of thrombolysis in stroke patients, these include age, blood pressure greater that 185mmHg/110mmHg, GCS score less than 8, time from barrage of symptoms less than 4 hours, or previous stroke or myocardial infarction. This is not an staring(a) list, but is relevant to the case study patient. From these indicators it can be shown that the patient falls into a menage that contraindicates the use of thrombolysis in the treatment of her condition, i.e. her blood pressure is 200mm/Hg/110mm/Hg, and that it has been at least 6 hours since onset of conditions.Question 4Aspirin is both a non-steroidal anti-inflammatory (nonsteroidal anti-inflammatory) and anti-platelet drug (Tiziani, 2013, p. 4 511). In its NSAID function, the drug acts to inhibit prostaglandin production, which is a mediator of inflammatory response and thermoregulation (McKenna Lim, 2012). The anti-platelet propertie s of the drug inhibit the production of thromboxane A2, which is a vasoconstrictor that normally increases platelet aggregation (McKenna Lim, 2012). Contraindications for this drug are for people with allergies to Salicylates, haemorrhage, and gastrointestinal bleeding (Tiziani, 2013 McKenna Lim, 2012). boldness is by oral pathway. In the context of this case study, because the patient is not eligible for thrombolysis, aspirin would be beneficial in lowering the risk of progress stroke by reducing the chance of further thrombosis forming through its anti-platelet properties. The risks in this context are exacerbation of her hypertension and possible bleeding however, in this circumstance the prescription of aspirin is appropriate.Carvedilol is a lipophilic vasodilating non-cardioselective -blocker (Leonetti Egan, 2012). This drug is used to treat hypertension by block up norepinephrine binding to 1-adrenergic receptors in addition to both 1-adrenergic and 2-adrenergic receptor s (Leonetti Egan, 2012). Contraindications for this drug include bradycardia, heart block, diabetes, and bronchospasms (McKenna Lim, 2012). Administration is by oral pathway. In the context of the case study, the administration of carvedilol is desirable because of her hypertension. It is further suggested that carvedilol contributes to a reduction in cardiac arrhythmias such as atrial fibrillation (Watson Lip, 2006). The risk associated with this drug include hepatic failure, oedema, and deterioration if the patient is in heart failure (McKenna Lim, 2012 Tiziani, 2013)Atorvostatin is a hydroxymethylglutaryl co-enzyme A (HMG-CoA) reductase inhibitor used to treat hypercholesterolaemia or hyperlipidaemia (McKenna Lim, 2012). The drug acts to inhibit production of cholesterol by blocking HMG-CoA reductase from completing the synthesis of cholesterol (Tiziani, 2013). Administration is by oral pathway. In the context of this case study, Atorvostatin is not indicated for administrat ion without further investigation into potential be causes, such as, heart disease or hypercholesterolaemia.Question 5In the context of this case study, atrial fibrillation could indicate heart disease, but further investigation would be necessary to determine this. Factors such as age, hypertension, ischaemic stroke, family history of myocardial infarction, and erratic pulse are evident and are all indicators towards heart disease (Bordignon, Corti Bilato, 2012). McKenna Lim (2012, p. 676) also associate coronary artery disease, myocardial inflammation, valvular disease, cardiomegaly, and rheumatic heart disease with atrial fibrillation.Pharmacologically, the drugs considered for intervention include heparin, warfarin, and carvedilol (Watson Lip, 2006). Both Heparin and Warfarin are anticoagulant drugs. Heparin is a fast acting, intra-venous or subcutaneously administered anticoagulant used in the acute setting, with changeover to orally administered warfarin, whose anticoagul ant effect is evident after 36-72 hour, for longer-term use (Tiziani, 2013 McKenna Lim, 2012). In context of the case study, aspirin use would be discontinued if heparin and warfarin were administered, as these drugs are recorded as having an adverse reaction (Tiziani, 2013 McKenna Lim, 2012). These drug types have contraindications for active and potential bleeding, so issues such as haemorrhoid bleeding may exclude these drugs from administration (Tiziani, 2013).As previously stated, Carvedilol is a nonselective -blocker (Leonetti Egan, 2012). This drug is administered orally and are safe in faction with heparin or warfarin (Tiziani, 2013). Contraindications for this drug include bradycardia, heart block, diabetes, and bronchospasms (McKenna Lim, 2012). This drug had both antihypertensive properties and has been shown to reduce cardiac arrhythmias such as atrial fibrillation (Watson Lip, 2006). The risk associated with this drug include hepatic failure, oedema, and deteriora tion if the patient is in heart failure (McKenna Lim, 2012 Tiziani, 2013).ConclusionThis paper has discuss and identified the pathophysiology of stroke, discussed the nursing care of the stroke patient, and identified and discussed pharmacological interventions available to treat the patient.Page 1 of 6 20/09/2016 25340 PM