Pathophysiological process template

CASE STUDY

Mr Black, a 61 year old businessman was watching the 7pm television news when he developed sudden onset of difficulty in speaking and drooping of the right side of his mouth. He was not able to lift his right arm or stand up. His wife immediately called the ambulance. The paramedics, using the FAST protocol assessed Mr Black as having had a stroke and transported him to a hospital with an acute stroke thrombolysis centre. He was admitted to the Emergency Department at 8pm.

History obtained from wife.

Mr Black was diagnosed with hypertension 10 years ago for which he takes Metopropol daily. He smokes about one packet of cigarettes/day and drinks alcohol socially. There is no history of serious illnesses or allergies. His father died of a heart attack at the age of 60.

Vital signs

BP 150/80 mmHg

Pulse 90bpm and regular

Respirations 20 breaths/minute

Temperature 36.5???? C

SaO2 95%

Neurological examination

Pupils equal – 2mm and reactive to light

Right facial droop

Paralysis of right arm and weakness of the right leg

Normal strength in the left arm and leg

Decreased sensation on right side of the body

Right knee and ankle reflexes moderately brisk compared with those on the left

Plantar response is extensor on the right and flexor on the left

Difficulty with speech repeats yes to all questions

Laboratory tests

Full blood count all values within normal range

Blood glucose level 6.5 mmol/L

Electrolytes, urea and creatinine all values within normal range

ECG normal sinus rhythm

CT brain scan (2hours from symptom onset)

No intracranial haemorrhage or mass lesions. Suggestion of early ischaemic changes in left hemisphere.

Diagnosis

Mr Black is diagnosed with a left middle cerebral artery distribution stroke. He is assessed as being eligible for thrombolytic therapy.

Management

IV Alteplase (8.1mL bolus over minute; 72.9 mL added to 50mL sodium chloride infused over 60 minutes via a volumetric control pump).

Continue antihypertensive medication

24 hours after completion of alteplase follow-up CT brain scan if bleeding excluded commence Assasantin???? SR capsule twice a day

PART 1 Pathophysiology template

Complete a pathophysiology template for an ischaemic stroke that affects the dominant left cerebral hemisphere (400 words).

PART 2- Questions related to the case study

Question 1 (450 words) Explain the pathogenesis that leads to the structural and functional changes resulting from Mr Blacks stroke.

Question 2 (150 words) Explain how two of Mr Blacks clinical manifestations are related to the structural and functional changes caused by the stroke.

Question 3 (250 words) Relating your discussion to the pathogenesis of Mr Blacks condition, explain the mode of action of Alteplase and Assasantin.

Ischemic Stroke

Pathophysiological process template

The diseases whose symptoms are given in the case study are for ischemic stroke. Therefore Mr. Black is suffering from this disorder.

Ischemic stroke is a strike that is characterized with a sudden loss in blood circulation to the brain area. As a result nreulogic function in the body gets lost (Crystal, 1996).There are two types of strokes hemorrhagic or ischemic where Ischemic is the most common one and they are also caused by thrombosis

A stroke occurs once there is an interruption of the blood supply in the brain. This deprives the brain nutrients as well as oxygen which may result in death of the brain cells. Ischemic stroke results once an artery blockage or narrowing occurs (Crutchlow, 2002). This cause reduced blood flow that is severe to the brain. There are also some cases when some people experience a blood flow disruption to their brain. Blood clot in the arteries that supplies blood to the brain also result in Ischemic strioke.These blood clots are caused by fatty deposits in the arteries.

Pathogenesis, it is clear that ischemic stroke occurs as a result of interruption in the cerebral blood flow to the brain.Ischamic contributes to the production of metabolism energy and depolarization of cells leading to the calcium ions accumulation in the intracellular space. There is also production of radicals and acidosis (Moore, 1951). In case the blood disruption is severe death of the cell occurs. This result from activation of receptors like N methyl D.A normal adult brain has a blood flow of 50 to 60 mL/100g/minute and when it falls below 18 mL/100g/minute evoked sensory potentials disappears. This can also be viewed from another perspective where if the blood flow goes below 12 mL/100g/minute, infraction occurs (Morris, 2005). Therefore, a blood flow of 10 and 20 mL/100g/minute is reliable with ischemic penumbra

A medical history for those patients suffering from ischemic stroke seeks to find out on the risk factors atherosclerotic as well as cardiac disease. The most common stroke signs include hemiplegic, loss in hemisensory, a partial or complete hemianopia, and unexpected lessen in consciousness (Matfin, 2009). It is important to note the time when a patient was last without a stroke symptoms.

Ischemic stroke holds about a quarter of strokes that occur when a blood clot or a thrombus is formed. The blood clot blocks the flow of the blood to a part of the brain. In another case an embolus may occur when a blood clot formation occurs somewhere in the body, this clot has a possibility of being carried to the brain and can cause ischemic stroke.

According research it is clear that most people who suffer from ischemic stroke experiences long life disability. There is also a likelihood of people who have stroke to suffer another within a span of five years. About 40 percent of people who have stroke experience severe moderate impairments while another 20 percent dies (Minagar, 2005). It is also notable that physical as well as mental impairments that results from stroke never resolves in an year of therapy and mostly persist for the lifetime of the patient.

A precise ischemic stroke diagnosis, cause and location are important when a patient visits a medical center with the symptoms discussed in this paper. This can be done through laboratory test and through the use of advanced imaging diagnostic tests. The other ways is by use of a CT scan, CTA, and cerebral angiogram, among others.

There is no distinguished d cure for a stroke, but there are medical as well, as surgical advanced ischemic stroke treatments that are advanced. These treatments are aimed at giving stroke patients with hope of finest recovery. Some of the treatments include medications aimed at dissolving blood clots and therapies to reduce brain swelling. Medications that protect the brain from damage and support measures are now available.

Stroke prevention is a strategy that is same to that of preventing a heart disease. These health recommendations include, curbing and controlling hypertension by ensuring a low blood pressure. Lowering the cholesterol concentration and saturated fat in the diet is important. It is advisable to quite tobacco use; maintain a healthy weight and feeding on a rich diet both in fruits and vegetables.

Question 1 Part 2

Ischemic stroke common pathway is lack of enough blood flow in the cerebral tissues. This is because of narrowed or blockage in the arteries that ends to the brain or within the brain. These types of strokes can be subdivided into thrombotic and embolic. Narrowing of the arteries commonly results from atherosclerosis, which is fatty plaques lining occurrence in the blood vessels (Flomin, 2008). When these plaques grows the blood vessels becomes narrow and the blood flow beyond is reduced. Atherosclerotic plaque contains some damaged areas that cause a blood clot which ends up blocking the blood vessels or a thrombotic stroke. This is what led to Mr. Black difficulty in speaking and his mouth drooling from the precise part of his mouth (Minagar, 2005). Mr. Black was not in a position to raise his right arm or support him upright. These signs show that Mr. Black left side of the body was had dead cells. There is a drastic reduction in the blood flow such that cells are undergoing a cellular death.

The laboratory tests conducted yielded  the results as follows, full  blood count-all values within normal range ,blood glucose level-6.5 mmol/L ,electrolytes urea and  creative -all values within normal range ECG-normal sinus rhythm. CT brain scans no intracranial hemorrhage or mass lesion (Moore, 1945). There is pathogenesis that leads to the structural and functional changes resulting from Mr. Black’s stroke. The tissues that boders the infant cores or the ischemic penumbra of Mr Black is not fully damaged. The functionality of these areas is rendered by reduced blood flow, but it is partially metabolically active (Moore, 1945). Cells in the left part of Mr. blacks body are endangered to damage and might go through apoptosis after several hours ,but incase blood flow  and oxygen concentration is restored after the start of the stroke there is potentiality of recovering them.

Other vision problems associated with stroke includes those with an increased light sensitivity. It is also clear that there is brain complexity while adjusting to different light levels. (Lehne, 2010). The rate of blinking may slow following a stroke and /or there may be incomplete eye closure with a partial blink, which will cause a part of the cornea to dry resulting in the eye feeling uncomfortable.

Question 2

The cerebrum forms the largest part of the brain. It comprises of a right and left hemisphere. In most cases, people’s right hemisphere takes charge of the functions of the left side of the body as well as many cognitive functions of the body. Therefore, a right stroke happens when a body blood supply to the left side of the brain is interrupted. The brain tissue dies due to lack of oxygen and nutrients from the blood. In accordance to Mr. Black’s manifestation we see that he has his left arm paralyzed and his left leg not as strong as before.  He also drools from the mouth down. All these are may be caused by a blood flow blockage which may be because of a clot from another part of the body. The clot cuts off flows through the blood extending the trap to a vessel that supplies the brain (Lee, 2011). There are also clots that form in the arteries that supply the brain with blood.

Question 3

The common pathway of ischemic stroke is lack of sufficient blood flow to perfuse cerebral tissue, because of blocked arteries that leads to the brain or those within the brain. Ischemic strokes can be broadly subdivided into thrombotic and embolic strokes (Lehne, 2010). This explains the action of the mode of action of Alteplase and Assasantin.

Assasantin is used in the prevention of ischemic further strokes. It contains aspirins and dipyridame which works differently to prevent blood platelets from blocking the blood vessels which causes stroke. This form of medication is taken by those people who had suffered from stroke to prevent a further occurrence of the disorder. Diet observation is important as it determines on the functionality of the drug. It acts well when taken with a meal. The medicine should be swallowed with help of water and should not be chewed. Some of its side effects include vomiting, gastritis, skin problems among others.

Alteplase helps in treating ischemic stroke where 0.9mg/kg is infused in an hour’s time. Clogged catheters are cleared through the injection of 2mg/2ml solution in the clogged catheters. Alteplase helps in breaking down clots and it is drug injected able directly to a vein (Tortora, 2010). To increase on its action in the body inject able drug is far greater than that which occurs naturally. The point here is to help in dissolving of the blood clots that forms in the veins affecting the cerebral blood flow which results into a stroke. It is an enzyme that is found naturally in the body and causes blood clots to dissolve. One of its side effects is that it interferes with the body ability to stop bleeding or the blood platelets.

References

Bordow, R. A., Ries, A. L., & Morris, T. A. (2005). Manual of clinical problems in pulmonary medicine. Philadelphia: Lippincott Williams & Williams.

Crystal, R. G. (1996). Alpha 1-antitrypsin deficiency: Biology, pathogenesis, clinical manifestations, therapy. New York: Marcel Dekker.

Crystal, R. G. (1996). Alpha 1-antitrypsin deficiency: Biology, pathogenesis, clinical manifestations, therapy. New York: Marcel Dekker.

Crutchlow, E. M. (2002). Pathophysiology. Therefore, NJ: Slack.

Essential texts Jenkins, G. W., Kemnitz, C. P., & Anatomy and physiology from science to life (2nd ed.). Hoboken, NJ: John Wiley & Sons.

Huether, S. E., & McCance, K. L. (2008). Understanding pathophysiology. St. Louis, Mo: Mosby/Elsevier.

International Symposium on Retinal Degenerations, Anderson, R. E., LaVail, M. M., Holyfield, J. G., & Mandal, M. N. A. (2010). Retinal degenerative diseases: Laboratory and therapeutic investigations. New York: Springer.

Lehne, R. A., (2010). Pharmacology for nursing care (7th ed.). St. Louis, Mo: Saunders/Elsevier.

Lee, R. C., Cravalho, E. G., & Burke, J. F. (2011). Electrical trauma: The pathophysiology, manifestations and clinical management. Cambridge: Cambridge University Press.

Mufson, M. A., Heck, C. A., & Nesler, S. M. (2002). Pathophysiology: PreTest self-assessment and review. New York: McGraw-Hill, Medical Pub. Division.

Minagar, A., & Alexander, J. S. (2005). Inflammatory disorders of the nervous system: Pathogenesis, immunology, and clinical management. Totowa, N.J: Humana Press.

Moore, R. A. (1951). A textbook of pathology: Pathologic anatomy in relation to the causes, pathogenesis, and clinical manifestations of disease. Philadelphia: Saunders.

Moore, R. A. (1945). A textbook of pathology: Pathologic anatomy in relation to the causes, pathogenesis, and clinical manifestations of disease. Philadelphia: Saunders.

Porth, C. M., & Matfin, G. (Eds.). (2009). Pathophysiology: Concepts of altered health states (8th ed.). Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins.

Swanson, T. A., Kim, S. I., & Flomin, O. E. (2008). Pathophysiology: II. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins.

Sigel, A., Sigel, H., Sigel, R. K. O., & Ebooks Corporation. (2006). Neurodegenerative diseases and metal ions. Chichester, West Sussex, England: Wiley.

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