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Health, Medicine, Nursing
Case Study
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Pathophysiology and Pharmacology (Case Study Sample)

Dear writer This is a case study about Mrs Margaret Green. This case study require to be written in two part (part A and B) due date in different date. Therefore, this order ganna be about the part A. next order ganna be about part B. I prefer to up load all case study description and patient notes and information as file to give you clear information about the requirement. I suggest you to read the requirement for part B to get clear picture about the case study and to avoid making any clash about the requirement. If you have any questions, please do not hesitate to contact me Regard Nouf source..
Case Study
With the signs and symptoms presented by Mrs. Green, it can be concluded that she has liver failure. The liver failure can be attributed to cirrhosis or hepatitis. Cirrhosis is also known as the scarring of the liver (Alexander, Fawcett & Runciman 2006). It is an irreversible liver condition that is primarily caused by alcohol or viruses (Allen 2002). On the other hand, hepatitis is the enlargement of the liver, again caused by alcohol or viruses. Cirrhosis is however, the more severe of the two.
Signs and Symptoms
Certain signs and symptoms displayed by the patient, and which are attributed to liver failure, are discussed in the following:
a) Fatigue and Malaise Associated with Alcohol Abuse
Scarring of the liver, which eventually leads to the destruction of liver cells, can be attributed to prolonged low-grade inflammation (Alexander, Fawcett & Runciman 2006). As stated earlier, alcohol or viruses can cause liver inflammation. As a part of the inflammatory process, individuals may experience the common symptoms of body malaise and fatigue.
The fact that the patient has been experiencing these symptoms for a long period of time suggests that a disease process has been occurring in her body for quite some time. These symptoms can be associated to the patient`s drinking habit. The patient`s alcohol consumption may have caused the damage to the liver thus, aggravating the patient`s experiences of fatigue and malaise.
b) Bilateral Edema and Abdominal Tenderness
The patient has presented with bilateral edema and also abdominal tenderness. The abdominal tenderness was hypothesized to have been caused by her constipation or the accumulation of ascites. It is postulated that as the cirrhosis process continues, "the remaining liver cells proliferate to form nodules; this results in the liver becoming irregular and distorted in shape. The resistance to the flow of blood increases, which in turn leads to portal hypertension" (Alexander, Fawcett & Runciman 2006, p. 138). On the other hand, portal hypertension activates necessary vasodilatory mechanisms in order to compensate for the change in the liver`s physiology. These vasodilatory mechanisms results to the dilation of the peripheral and splanchnic arterioles, which in turn causes a drop in arterial pressure (Kashani et al. 2008). The drop in arterial pressure activates the renin-angiotensin-aldosterone system (RAAS), the sympathetic nervous system (SNS) and the release of antidiuretic hormone in order to effect homeostasis. However, as these systems are activated in the body, there becomes an increase in sodium and water retention in the kidneys. As a result, edema develops. Furthermore, "splanchnic vasodilation increases splanchnic lymph production exceeding the lymph transportation system capacity and leads to lymph leakage into the peritoneal cavity" (Kashani et al. 2008, p. 72). As a result, ascites formation occurs. Both edematous and ascites formation tendencies have been observed in the patient indicative of cirrhosis.
c) Multiple Bruises to Legs
The final sign observed from the patient was that of multiple bruises. The bruises can be attributed to low platelets and clotting factor deficiencies of the patient (Bowden & Greenberg 2009). Kang and Audu (2006) stated that liver disease affects all the five phases of coagulation. These are: "the vascular phase, the platelet phase, the fibrin formation phase, the fibrin polymerization phase, and the fibrinolysis phase" (Kang & Audu 2006, p.17). If taken in a more general context, these five phases can be attributed to vasodilation, decreased platelet and clotting factor deficiencies. Vasodilation has the effect of decreasing vessel wall and platelet interaction (Kang & Audu 2006). Thus, platelets travel to injured sites more slowly, prolonging bleeding time. The decreased number of platelets ma...
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