The case Study Essay Example

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The case Study 4

Lecturer’s Name

Part 1: Pathophysiological template

Date: 5th August, 2013

Date the patient was admitted: 4th August, 2013 at 8pm.

Patient presentation:

Mr Black is a male who is 61 years old. He developed a difficulty in speaking as well as the drooping of the right side of his mouth at 7 pm. Mr Black could also not lift his right arm, neither could he stand. He was admitted to the emergency department after suffering a stroke at 8 pm.

Symptoms and History:

Mr Black’s symptoms were: difficulty in speaking, drooping of the right side of the mouth, unable to lift the right arm, unable to stand, and he also had a difficulty with speech (Uchino, Pary, & Grotta, 2011).

Mr Black has been suffering from hypertension which was diagnosed 10 years ago, and for this he takes Metopropol every day. He takes alcohol socially, but smokes heavily, about a packet of cigarettes daily. Mr Black’s father died at the age of 60, due to heart attack (Kasiman, Lundholm, Sandin, et al., 2012).

He has no history of serious allergies or even illnesses.

Physical exam:

Vital signs:

BP 150/ 80 mmHg

Pulse 90 bpm and regular

Respiration 20 breaths/ minute

Temperature 36.5◦C

Neurological examination:

Pupils equal- 2mm and reactive to light;

Paralysis of right arm and right leg weakness;

Right facial droop;

Normal left leg and arm strength.

Decreased right side of the body sensation;

Plantar response in extensor on the right and flexor on the left;

Right ankle and knee reflexes are moderately brisk when compared to the left ones.

Difficulty with speech; repeats yes to every question.

Labs and diagnostic tests:

Full blood count- all values within the normal range;

Blood glucose level- 6.5 mmol/L;

Electrolytes, urea and creatinine- all values within the normal range;

ECG- normal sinus rhythm;

CT brain scan (2 hrs from the onset of symptoms);

No mass lesions or haemorrhage –indicates early ischaemic changes in the left hemisphere.


Left middle cerebral artery distribution stroke.

Past medical history:

Diagnosed with hypertension 10 years ago;

No major allergies or illnesses.

Medical care plan:

Thrombolytic therapy; (Uchino, Pary, & Grotta, 2011).

Continue the hypertension treatment.

Medication and management:

IV Alteplase (8.1 ml bolus over minute; 72.9 ml added to 50 ml sodium chloride infused over 60 minute via volumetric control pump) (Gonzalez, Hirsch, & Lev, 2010).

Antihypertensive medication — Metropol

CT brain scan 24hrs after completing alteplase; if no bleeding, commence Assasantin- SR capsule twice in a day (Macrez, Ali, Toutirais, et al., 2011).

Part 2: Pathogenesis of ischaemic stroke

In the past years, stroke has risen to be one of the major causes of morbidity and mortality in the world. Studies show that ischaemic stroke itself accounts for 80- 85% of the strokes reported in the world, each year (Williams, Carter, Hysi et al., 2013). Ischaemic stroke occurs when there is reduced blood flow in the brain, and this result to tissue damage in the brain. When the supply of blood to the brain is disrupted the cells in the brain are deprived and denied the necessary oxygen and glucose vital for their functioning (Matarin, Singleton, Hardy, & Meschia, 2010). This is because it is the blood that transports oxygen and nutrients to the entire body, and the brain receiving almost 20% of the blood. The blood circulation disruption occurs in case of a clot blocking the blood vessel in the brain (Williams, Carter, Hysi et al., 2013). 45% of ischaemic strokes occur as a result of artery thrombus, while 20 % are embolic caused.

Thrombosis, the major cause of ischaemic stroke, form in the intracranial and extracranial arteries, after the roughening of the intima. This causes plague to form along the vessels which are injured, permitting platelets to adhere and then aggregate. This in turn causes coagulation to be activated, hence causing thrombosis to form at the plague site. What follows is a decrease of the blood flowing through the intracranial and extracranial systems and the function is maintained by the collateral circulation (Allen, & Bayraktutan, 2009). When the collateral circulation also fails, there is a compromise in perfusion, which leads to a decrease in perfusion, and eventually cell death.

Ischaemic stroke which is embolic occurs when a clot is lodged on the cerebral vessel after travelling a long distance (Williams, Carter, Hysi et al., 2013). Emboli can be a form of fat, blood or even air travelling from other parts of the body to the brain. Arteritis, infection, age, hereditary genes or even abuse of drugs like alcohol and tobacco can also cause ischaemic stroke (Kasiman, Lundholm, Sandin, et al., 2012). When the blood is prevented from going to the brain it affects that side of the brain. If the dominant hemisphere is affected, it affects language and mobility. This is because it is the dominant hemisphere that controls language function. Most right- handed people have the left hemisphere as the dominant (Williams, Perry, & Watkins, 2010). When ischaemic stroke occurs there are changes that take place in the victim’s body. There are exaggerated reflexes, sudden confusion which can cause trouble in speech, seeing can become trouble, or it can only be only by one eye (Macrez, Ali, Toutirais, et al., 2011). There occurs trouble in walking, moving and coordination; there can also be loss of balance. There also occurs sudden weakness and numbness of the leg, arm, or even the face, mostly on one side of the body. These changes occur as a result of dead or damaged cells and tissues in the brain which is responsible for the normal functioning of the body (Gonzalez, Hirsch, & Lev, 2010).

Mr Black has a problem with speech whereby he answers all question with yes. This is a clear indication of ischaemic stroke in the left hemisphere. This is because; the left dominant hemisphere is responsible for the functioning of language and speech (Rymer & Silverman, 2009). Mr Black’s another clinical manifestation is a decrease in body sensation on the right side. This is a common clinical feature with a dominant left hemisphere cerebral lesion, which leads to ischaemic stroke (Williams, Perry, & Watkins, 2010). After there is a clot in the blood vessels which disrupts blood circulation to the brain, the brain is deprived off the necessary nutrients and oxygen necessary for normal functioning. These functions like pH, temperature as well as nutrition (Deb, Sharma, & Hassan, 2010). When the oxygen and nutrients do not reach the left hemisphere of the brain, the cells and tissues die, hence there is no coordination between the receptors, the central nervous system and the effectors. Therefore, the central nervous system on the left hemisphere lacks sensitivity and cannot give commands to the part of the body that it governs.

Mr Black’s condition has led to the administering of various medications to curb his condition as well as control his hypertension condition. Among the drugs administered there are Alteplase and Assasantin®, and each of these medicine have their different purposes in the case of Mr Black as explained here forth. Assasantin is being administered in order to prevent transient ischaemic attacks, as well as a way of preventing a second occurrence of ischaemic stroke (Rymer & Silverman, 2009). Ateplase on the other hand is used in order to lyse the already formed thrombin. It binds to the fibrins in the thrombus and it converts the plasminogen that is trapped into plasmin and goes ahead to initiate local fibrinolysis. This in turn helps in breaking down of any present thrombotic occlusions. Cathflo Activase (Alteplase) is specified for functional restoration to the (CVADs) central venous access devices as gauged by the withdrawal of blood ability (Rymer & Silverman, 2009).

The administering of Assasantin® and Alteplase is to ensure that the ischaemic stroke suffered by Mr Black is managed and a recurrent of the ischaemic stroke is reduced or even terminated (Uchino, Pary, & Grotta, 2011). This is because; these drugs lyse the blood clots already in the blood vessels which could be causing the ischaemic stroke, in this way reducing fatality (Deb, Sharma, & Hassan, 2010). They also lyse other clots in the blood vessels which, if left in place, can trigger ischaemic stroke, hence reducing the chances of the stroke recurring.


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, 5:226.Circ Cardiovasc GenetKasiman, K., Lundholm, C., Sandin, S., et al. (2012). Familial effects on ischemic stroke: the role of sibling kinship, sex, and age of onset.

, 10:471.Lancet NeurolMacrez, R., Ali, C., Toutirais, O. et al. (2011). Stroke and the immune system: from pathophysiology to new therapeutic strategies.

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Gonzalez, R., Hirsch, J. & Lev, M. (2010). Acute Ischemic stroke: imaging and intervention. New York: Springer.

Rymer & Silverman, I. (2009). Ischemic stroke: An atlas of investigation and treatment. Oxford: Clinical publishing.

Uchino, K., Pary, J. & Grotta, J. (2011). Acute stroke care. Cambridge: Cambridge university press.