Case study Questions: Nursing (Coursework Sample)

CASE STUDY QUESTIONS-NURSING
QUESTION 1
Prioritization of care is an essential nursing process in the care and management of patients. In the five cases provided, I would prioritize my care plan according to the severity of the patient’s condition and the presence of other co-morbidities. The respiratory and the cardiovascular systems are the most important in the body, because the functionality of the other systems depends on adequate blood and oxygen supply (Zammit & Liddicoat, 2010,p. 338). In prioritizing care, I would consider patients whose disease processes affect the two systems. In this case, I would begin by formulation nursing care plans for Philip, John and Melinda. Philip has an infective exacerbation of a log standing chronic obstructive pulmonary disease (COPD). This could worsen the oxygen supply to the rest of the body and the resulting physiological stress would further make the symptoms worse (Subotic, et al., 2007,p.1293). John, on the other hand, has a cardiovascular disease, precisely, a coronary artery disease. Coronary artery diseases are known to predispose to myocardial infarction and ultimately heart failure if not managed properly at the outset (Kessler, Erdmann, & Schunkert, 2013,p. 368). Melinda, as well, has a cardiovascular disease, precisely, a ruptured aortic aneurism resulting into a subarachnoid hemorrhage. Aortic aneurism is a risk factor for stroke syndromes; therefore, early interventions may avert a potential cerebrovascular accident (CVA) (Sule, Aronow, & Sateesh, 2008, p. 141). In terms of treatment, I would prioritize my care in lieu of medications that require close monitoring of their levels to prevent toxicity or adverse events. Philip is on oxygen therapy and so needs close monitoring of the saturation levels. Oxygen toxicity results in the production of reactive oxygen species that would damage multiple cellular organs leading to disrupted physiological function (Auten & Davis, 2009, p.126). John is on heparin infusion and so will require close monitoring to prevent heparin toxicity. Heparin results in Heparin-Induced Thrombocytopenia (HIT) (O'Donnell, 2012,p. 25). Melinda, on the other hand, is on anti-hypertensive, Nimopidine. In lieu of an intracranial hemorrhage, she needs close monitoring of her neurological functions.
QUESTION 2
When reviewing Peter, I notice that his nausea is becoming worse. Peter had undergone an abdominal surgery to remove gall stones after an endoscopic retrograde cholangiopancreatography had been done. He initially presented with a history of epigastric pain for two days; however, hours later post-surgery, he complains of nausea and mild right shoulder tip pain. I review the medication chart and notice that no antiemetic had been prescribed. Anesthesia is known to cause nausea and vomiting. Nitrous oxide when used with other anesthetic agents in laparoscopic surgeries causes nausea and vomiting post operatively (Peyton & Wu CY, 2014, p. 1138). Firstly, I would consult with the intensive care team and the surgical team about the worsening vomiting of peter. It could be he is not on antiemetic because of a possible drug reaction, or by clinical judgment, it would be wise not to administer anti-emetic. Excessive vomiting results into loss of important electrolytes, in particular potassium, chloride and hydrogen ions. The resulting hydrogen ion loss results in metabolic alkalosis precipitating an increased ventilation manifested by the patient breathing in a faster rate (Khanna & Kurtzman, 2006,p. 19). Excessive vomiting causes an increased loss of water from the body. Sodium plays an essential role in the maintenance of total body water volume; therefore, in vomiting the excess sodium loss results in fluid depletion (Khanna & Kurtzman, 2006,p. 19). In my care, I would consider a fluid replacement therapy. The fluid of choice is one that has a large amount of potassium ions in order to prevent hypokalemia. In addition, I would ensure the patient is put on a nasogastric tube feed in order to replenish lost nutrients. After consultation with the intensive care team, Peter may as well be put on an anti-emetic to prevent further electrolyte losses.
QUESTION 3
While reviewing John, I notice that the last coagulation profile reads an APTT of more than 150 seconds. In the initial treatment regime, the APTT was to be maintained between 50 and 75 seconds. A quick background past medical history of John reveals that he has a history of angina and a chronic coronary artery disease. He is on intravenous heparin infusion and aspirin at a dosage of 100mg per day. Activated Partial Thromboplastin Time (APTT), in contrast to the Prothrombin Time(PT) is an indicator of the integrity of the intrinsic and the common pathways of the coagulation cascade (Kogan, Kardakov, & Khanin, 2001, p. 300). In a normal coagulation process, calcium is essential for the formation of the fibrin clot which covers the defect on the blood vessel to prevent further blood loss. APTT is the time taken after addition of calcium ions to the time the fibrin clot is formed (Kogan, Kardakov, & Khanin, 2001, p. 300). Longer APTT means that the blood takes longer than normal to clot. In John’s case, this is attributed to the heparin intravenous infusion that he was receiving. The possible explanation is heparin over dosage. The blood is in an un-coagulable state. This condition is life threatening in case there is an undetected internal hemorrhage. The blood loss cannot easily be controlled and the patient can get into shock. In lieu of the ward protocol on intravenous heparin infusion, I would review John’s medication and adjust it by stopping the infusion for sixty minutes. Then, I would restart it at a dosage 1.0ml/hr less than previous rate for the next six hours. Stopping the infusion would provide time for the body to clear the heparin to lower blood levels. Depending on the type and molecular constitution, the biologic half-life of heparin ranges from 23 minutes to 2.48 hours (McAvoy, 1979, p. 377). Therefore, stopping it for one hour will give the body enough time to clear heparin to lower levels before the dosage can be adjusted again.
QUESTION 4
Melinda complains of a feeling of fainting when she gets out to mobilize or when she gets to the bathroom. On assessing her blood pressure, the reading is 80/40. Melinda is definitely in hypotension and soon she may be in shock. Hypotension is a clinical condition in which the blood pressure is less than 90/60 (Ashton, 2013, p. 35). In very severe cases, very low blood pressure can be life threatening. It portends that organs in the body such as the heart, brain and the kidneys do not get enough blood supply (Gordon, 2009, p. 937). Some organs such a s the kidneys when exposed to such an acute shortage of blood supply begins to shut down. Eventually, this would lead to kidney failure (Couch, 2008, p. 9). In a hypotensive state, the heart pumps faster in order to supply the little blood to the vital organs. The resultant increase in the rate of metabolism results in excessive sweating, thereby reducing the blood volume further (Ashton, 2013, p. 37). This worsens the situation.
On reviewing her history, Melinda had been admitted at the neurosurgery unit with complains of an acute onset of severe headache. She had undergone a neurosurgical procedure that involved coiling of a cerebral artery aneurism using an interventional radiological suite five days ago. The operation was successful. A CT scan done showed a subarachnoid hemorrhage from the artery that was coiled during the surgery. She also had been put on nimopidine, an anti-hypertensive, dosing at 60mg oral tablets. In my assessment, it could be blood loss in a defect at the initial interventional procedure that involved coiling of the artery. The possible cause is no-compliant to the antihypertensive medications. Rangel-Castillo, Shankar and Robertson (2008), observe that intracranial hemorrhage has two causes-primary and secondary. In this case, the important secondary causes are trauma, rupture of an aneurism, coagulation defect or a vascular malformation (p.528). Hypertension by far becomes the most prominent and prevalent cause of intracranial hemorrhages accounting for 60-70% of cases (Rangel-Castillo, Shankar, & Robertson, 2008, p. 530). Chronic hypertension results into fibrinoid necrosis, fragmentation and degeneration of the small arterioles that supply the bran parenchyma. Eventually, the walls of the arterioles weaken and they undergo a spontaneous rupture (Ramandeep & Weinberger, 2007, p. 705). Non compliance with antihypertensive medication increases the risk of developing an intracranial bleed and a controlled blood pressure reduces the risk of developing an intracranial hemorrhage (Freeman & Aguilar, 2012, p. 223).
My response to Melinda’s clinical situation is to inform the doctors on call about Melinda’s worsening signs. Melinda would require first...