Pathophysiology of Stroke

Strokes are caused by a block in the blood supply to the brain which causes a decrease in oxygen and delivery of other important supplies which facilitate proper functioning. Fifteen million cases are reported worldwide annually, although not all of these cases are mortalities, the large prevalence of strokes ranks it as the fourth leading cause of death in the United States. (Figueroa) Because of the time sensitivity associated with the lack of resources to the brain, strokes are considered a medical emergency and early recognition of symptoms can help decrease the amount of damage caused . Although strokes do not always cause death, strokes most often leave the individual with some physical and cognitive impairment.

A (assessment): Ms. O’Reilly’s vital signs are temperature of 37.5 C, pulse of 112, blood pressure of 102/52, and respirations of 24. Her respirations are still deep but have a regular rhythm. She has a CBS of 8.1 and regular insulin running as per orders. The lab work shows uncompensated metabolic acidosis with no hypoxia. Ms. O’Reilly’s neurological status has improved with a GSC of 13. Her dehydration is being treated with NS containing 40mEQ KCL/L running at 200ml/hr and potassium levels maintained at 4.

Alice Palmer has a mild brain tissue damage associated with the ischemic stroke as evidenced by a Glasgow Coma Scale score of 15. On the other hand, she has a normal heart rate of 89 beats per minute (HR 89) and a blood pressure of 155/90 mmHg. A blood pressure of 155/90 mmHg is an indication of stage 1 hypertension. Mrs. Alice Palmer is hypertensive because she refused to take medication while she was at home (Grace Meissner, 2011; Fortrat & Gharib, 2016). Further, Mrs. Alice Palmer has a left-sided hemiparesis which indicates damage to the right side of the brain. Left-sided hemiparesis is a weak muscle tone of the left side of the body which leads to faded movement and carrying out self-care activities such as dressing, bathing, and grabbing objects (Fischer et al., 2016). Moreover, damage to the right side of the brain is associated with poor memory since the limbic system is located in that region (Usher & Marriott, 2011). Also, Mrs. Alice had a bilateral visual field deficit because of the mild brain tissue damage associated with the ischemic

Patient was in the ER room when first seen. PT was with her family members and family states that she speaks little English and that she has had abdominal pain for the past day along with bloody stools. Family states that she is on calcium supplements and no other medications. Last oral intake is 24 hours ago. Family states no known past medical history. Pt is in the hospital bed in the fetal position and towards the right side. Patient's airway is clear and breathing is normal. Skin is warm and dry. Patent is AAOx4. Assessment of head, neck, and chest show no signs of deformities. Abdominal area not assessed due to severe pain. Back is without deformity. The upper extremity shows no sign of deformities or trauma. The lower extremity shows

The patient is an 85-year-old female who is brought to the ED by her family because of increasing confusion and supposedly she had a degree of altered mental status of two hours previous to presentation. In the ED she is completely worked up. CT shows advanced atrophy with microvascular changes and several lacunar infarcts nothing acute. Specific gravity in the urine reveals her to be markedly dehydrated. She culture completely, started on IV antibiotics, IV fluids and B12. On the day after admission she still presents as persistently confused. She is evaluated by PT. The patient who was formerly ambulating with a walker and allegedly driving a car is unable to be ambulated. Before the history indicates that she has a slow downward

- Coagulation inhibitors and Fibrinolysis : to Localize thrombus on injury and Prevent new thrombus formation.

Enoxaparin is a low molecular weight heparin used to prevent thrombosis, particularly post surgery. Enoxaparin binds to antithrombin III which is responsible for inhibiting coagulation by acting on factor Xa. Enoxaparin accelerates the activity of antithrombin III therefore preventing clot formation (McKenna & Lim, 2014 p766). When a blood vessel is damaged, platelets in circulating blood stick to the site of injury and release chemicals that attract more platelets causing aggregation. There are both intrinsic and extrinsic pathways causing thrombi to form to maintain a closed cardiovascular system (Hollar, 2017). Immobility increases risk of thrombus formation as the blood becomes stagnant with gravity and decreased

Mr X, a 60 year- old Caucasian male, admitted to the stroke unit with a diagnosis Left MCA infract. He presented to the emergency department right sided hemiparesis, neglect of affected limbs, dysphasia and right side facial droop. He was on cardiac monitor for close observation for 48 hours. Stroke critical care pathway and commenced and care provided as per protocol.. Stroke is a serious and deadly condition including cerebral circulation within the brain and can extremely affect a person ability to maintain a safe environment, communication and mobility as well as other activities of living. The purpose of this essay is to give an overview of the Pathophysiology of ischaemic stroke, the required nursing care and the rationale behind it, followed by medical management and treatment provided to the patient.

Venous thrombosis is a multifactorial disease. In the majority of thrombosis patients a risk factor is not detectable. Virchow's triad refers to three primary influences for thrombus formation, endothelial injury, stasis, turbulence or abnormal blood flow, and blood hypercoagulability (Kyrle, 2009). A shift in balance between procoagulant and anticoagulant of the endothelium is responsible for thrombotic state (Kyrle, 2009). Endothelial injury is the physical loss of endothelium leading to exposure of subendothelial extra-cellular matrix, adhesion of platelets, release of tissue factor, depletion of PGI2 and plasminogen activators (Kumar, 2010). Abnormal blood flow refers to turbulence that causes endothelial injury, which is a major influence

She is 74 years old, has a height of five foot six inches, and I was unable to acquire her weight. She was experiencing pain with her hammer toes at five on the pain scale. Her appetite was well. L.F. does not experience difficulty with urination or defecation, but sometimes needs assistance with going to the bathroom. She was having shortness of breath while laying down, however does not require oxygen interventions. I did have to repeat myself while performing her head to toe assessment. L.F. does not have any hearing devices. She wears corrective glasses. Her vital signs were as follows, blood pressure was 120/90 on her left arm while sitting, radial pulse rate was 84, pulse ox was 92, respirations were 20, and her temporal temperature was 97.6 ˚ F. L.F.’s radial pulses were equal in both arms. She was able to grasp my fingers equally and strongly with both hands. Her capillary refill lasted one to two seconds. Her breath sounds were normal and clear without productive or nonproductive coughing. L.F.’s apical pulse was 75 with a normal rate and rhythm, and her aortic, pulmonic, erb’s point, tricuspid, and mitral pulses had a normal rate and rhythm. Her abdomen had a round shape and bowel sounds were present and active with a low pitch in all four quadrants. L.F.’s abdomen was soft and she denied pain. She explained that she had normal passage of bowel movements without complications. She

Depending on the area of the brain that is affected by a stroke, patients may find they can no

The treatment for this patient is to replace the fluid which should stop the release of angiotensin and aldersterone. This should be accomplished with normal saline. If there is hypokalemia you would need to supplement with potassium. A proton pump inhibitor would also need to be used like prilosec to prevent further losses in hydrogen ions. If she was on any diuretics they need to be discontinued and if renal failure is

This organ system has a number of functions namely, to keep a constant body temperature as well as to ensure coagulation occurs specifically at the site of injury, as well as to ensure no added blood loss occurs to cause life-threatening effects. This process of blood coagulation is explained in three interconnected phases. In the first phase, the enzyme thrombokinase is activated due to the damage of tissue and the breaking down of platelets. Prothrombin is converted into thrombin by the disintegration of the thrombocytes, electrically charged calcium ions and other coagulation factors, as well as the blood activator and tissue activator which become involved in the coagulation process. The second phase includes production of the thrombin that transforms fibrinogen in the blood plasma into fibrin. The thrombus (or blood clotting) is formed by a fibrilliform mesh that encloses the blood cells. Lastly, the third phase, which takes place as retraction occurs of the fibres of the fibrin mesh. Solidification of the fibrous mesh takes place which closes the defect in the vascular wall. Coagulation is then followed by fibrinolysis (re-dissolution of the clot).

Thrombin is a naturally occurring protein that is present in the blood of humans and animals. The main function of thrombin is as an intermediate step during hemostasis, which slows bleeding by forming blood clots. Thrombin acts as an enzyme during an injury, converting fibrinogen to fibrin, which then causes blood clots to form. Due to its properties, thrombin’s application to the medical field includes topical surgery in the case of minor injuries as well as various other medical procedures such as neurosurgical operations. Apart from applications in the medical field, thrombin also plays significant roles by directly interacting with endothelial cells throughout the body.

As age increases, we can expect some loss of heart, lung, joint, and sexual functioning. Some loss of brain cells and mental efficiency is a normal part of