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Based on the information in the case study, which type of stroke is Mrs Smith likely to have suffered? Mrs Smith has demonstrated the clinical manifestations of a trans ischaemic attack (TIA) the symptoms of a the TIA are similar to a Ischaemic stroke although patients become asymptomatic within 24 hours and in seventy five percent of patients they become asymptomatic of any neurological dysfunction or deficits within an hour of the onset of the TIA (Craft, & Gordon 2011, pp. 190-192). The TIA is caused by a thrombus or emboli compounded by carotid stenosis of the blood vessel.
However, the insufficient blood supply is restored before acute cerebral infarction can occur. If a TIA lasts for more than twenty four hours it is then identified as a thrombotic stroke. In Craft & Gordon (2011, pp. 190-191) the physiology of the ischaemic stroke is similar to the TIA but much more severe. The ischaemic stroke occurs when an artery carrying oxygenated blood and glucose becomes blocked; blood flow is greatly reduced from an occlusion, resulting in hypoxia. In turn causing cerebral oedema and cerebral infarction occurs resulting in permanent brain damage.
Cerebral dysfunction is dependent on the location of the occlusion. Mrs Smith’s symptoms suggest the cerebellum and brain stem have been affected by the TIA (Brain Foundation 2011). In the treatment for the TIA it is extremely important to identify conclusively that a haemorrhagic stroke is not occurring. Thrombolytic therapy introduces a tissue plamaminogen activator, this dissolves blood clots. In the occurrence of the haemorrhagic stroke and introduction of thrombolytic therapy exasperation of the haemorrhage results, potentially resulting in mortality (Craft & Gordon 2011, p.194; Bryant & knights 2011, p. 395).
References Bryant, B & Knights, K 2011, Pharmacology for health professionals, 3rd edn. , Elsevier, Australia. Craft, J Gordon, C 2011, ‘Alterations in neurological function across the life span’, in J Craft, C Gordon, A Tiziani (eds), Understanding pathophysiology, Elsevier Mosby, Chatswood, NSW, pp. 188-226. Brain foundation 2011, A-Z of disorders, Stroke, Brain Foundation, Sydney, viewed 30 June 2011, . 3. Would it be appropriate to consider treating this patient with tissue plasminogen activator (tPA, alteplase)?
How does this drug work? Treating Mrs Smith with tissue plasminogen activator (tPA) or alteplase would be advisable after the evidence from the magnetic resonance imagery (MRI) scan confirmed no haemorrhagic conditions existed, even though the presenting symptoms greatly suggest a transient ischaemic attack (TIA) has occurred (Brain Foundation 2011). Tissue plasminogen activator is a fibrinolytic drug which is used to treat thromboembolic disorders, such as ischaemic strokes. These agents initiate secondary fibrinolysis to occur; altering the haemostatic capability.
The primary purpose of this agent is to clear occluded blood vessels within the systemic circulation (Bryant & Knights 2011, pp. 534-536). The occlusion, caused by a haemostatic plug or thrombus is comprised of a fibrous protein called fibrin. This protein polymerises to create a tightly woven mesh, trapping platelets within the fibrin fibre meshwork, resulting in the creation of the haemostatic plug. Proceeding this process, the lumen of the blood vessel will become retracted, restricting or occluding the blood flow within the systemic circulation (Brain Foundation 2011; Craft, Gordon & Tiziani 2011, p.390).
Therapeutic action is achieved by an intravenous introduction of plasminogen activator agent to catalyse into plasmin factor XIIa enabling the destruction of the thrombi. Tissue plasminogen activator engages fibrinolysis; processing occurs by cleaving the single chain plasminogen into two chains linked by a disulfide bond, resulting in the molecular product of plasmin. Plasmin will then directly catalyse the fibrin substrate structure, using enzymatic activity to dissolve the thrombi (Therapeutics Goods Administration 2011).
This in-turn re-establishes the circulation, reducing the fibrin into fibrin-degradation products cleared by the fibrinolytic system and metabolized by the liver. References Brain foundation 2011, A-Z of disorders, Stroke, Brain Foundation, Sydney, viewed 30 June 2011, . Bryant, B & Knights, K 2011, Pharmacology for health professionals, 3rd edn. , Elsevier, Australia. Therapeutic Goods Administration 2011, Australian Public Assessment Report for Alteplase, viewed 05 August 2011.