Uworld Nclex Review 3 Exam 100% Correct Questions And Answers | Rated A+

Uworld Nclex Review 3 Exam 100% Correct Questions And Answers | Rated A+ A 65-year-old woman comes to the emergency department with progressive fatigue and lower- extremity paresthesias. Medical history is otherwise insignificant and the patient takes no medications. Laboratory studies show a mean corpuscular volume of 112 fL. Upper gastrointestinal endoscopy shows atrophic mucosa in the gastric body and fundus and a normal- appearing antrum. Destruction of which of the following gastric layers is most likely responsible for this patient's symptoms? - answerUpper glandular layer - The combination of lower- extremity paresthesias, macrocytic red blood cells (RBCs), and gastric body and fundal atrophy is highly suggestive of pernicious anemia (PA). PA is an autoimmune disorder caused by the cell-mediated destruction of parietal cells, oxyntic (pale pink) cells found predominantly in the upper glandular layer of the gastric body and fundus. Over time, progressive parietal cell destruction leads to chronic atrophic gastritis (ie, autoimmune gastritis), characterized histologically by a CD4-predominate inflammatory infiltrate, oxyntic gland atrophy, and intestinal metaplasia (ie, replacement of normal epithelia with goblet cells). Parietal cells are responsible for the secretion of hydrochloric acid and intrinsic factor, a glycoprotein that is involved in the absorption of B12 (cobalamin, an essential nutrient). After a critical number of parietal cells are destroyed and hepatic stores of cobalamin are depleted, patients develop B12 deficiency. This results in a megaloblastic anemia, characterized by macro-ovalocytes (elevated mean corpuscular volume, oval-shaped RBCs) and hypersegmented neutrophils. Patients also develop neurologic dysfunction due to demyelination of the dorsal and lateral spinal tracts, resulting in paresthesias and ataxia. A 69-year-old hospitalized woman is evaluated for new-onset weakness of the right foot. The patient has a history of chronic hip pain due to osteoarthritis and underwent left total hip arthroplasty under general anesthesia while in the right lateral decubitus position 2 days ago. Since the surgery, she has had difficulty moving her right foot. Other medical conditions include lumbar spinal stenosis, hypertension, type 2 diabetes mellitus, and a small ischemic stroke with no residual deficit. On examination of the right lower extremity, the patient is unable to dorsiflex or evert the foot or extend the toes. Sensation is decreased over the dorsum of the right foot. The rest of the neurologic examination of the right lower extremity is normal. Injury to which of the following structures is the most likely cause of this patient's current symptoms? - answerCommon fibular nerve - The common fibular (peroneal) nerve originates in the popliteal fossa as the lateral branch of the sciatic nerve. From there, it courses laterally around the head and neck of the fibula before dividing into the deep and superficial fibular nerves. Because of its proximity to the lateral neck of the fibula, the common fibular nerve is particularly susceptible to compression from a leg cast or during prolonged time in the lateral decubitus position (eg, during surgical procedures). Common fibular neuropathy characteristically presents with deficits involving both the deep fibular (eg, weakness in foot dorsiflexion and toe extension) and the superficial fibular (eg, weakness in foot eversion, sensory loss over the dorsal foot) nerves. In an ambulatory patient, gait examination typically shows foot drop due to loss of dorsiflexion, with the affected foot lifted high off the ground to compensate (ie, steppage gait). A 45-year-old man comes to the hospital with acute onset of severe chest pain and diaphoresis. The patient describes the pain as "squeezing," different from any discomfort he has ever had. He has a past medical history of hypertension, and his father underwent coronary artery bypass grafting at age 50. The patient is diagnosed with acute ST-elevation myocardial infarction and undergoes an urgent coronary intervention with stent placement into the right coronary artery. He is also started on high-intensity atorvastatin therapy, along with antiplatelet therapy and appropriate medications to control blood pressure. Four weeks later, the patient's total cholesterol level is 140 mg/dL, down from 200 mg/dL before discharge. Which of the following has most likely increased as the result of the therapy? - answerLDL receptor density - HMG-CoA reductase inhibitors (statins) inhibit the rate-limiting enzyme in hepatic cholesterol synthesis. In response to these changes, hepatocytes increase their surface expression of the LDL receptor to increase uptake of circulating LDL. Treatment generally produces a 20%-50% reduction in serum cholesterol and LDL concentration. A 36-year-old man comes to the office for follow-up regarding hepatitis C. The patient was last seen 3 years ago for a 2-week history of fatigue, nausea, and decreased appetite; at that time, he was diagnosed with hepatitis C infection due to injection drug use. The patient was offered treatment but declined. He is currently healthy and feels well. There is no family history of liver disease. The patient currently does not use illicit drugs or alcohol. Vital signs are normal. BMI is 26 kg/m2. Examination is normal. Laboratory results are as follows: Albumin 3.6 g/dL Total bilirubin 1.7 mg/dL Aspartate aminotransferase (SGOT) 54 U/L Alanine aminotransferase (SGPT) 62 U/L Hepatitis B surface antigen negative Hepatitis B surface antibody positive Anti-hepatitis C virus antibody positive Hepatitis C RNA positive HIV antibody negative Liver ultrasound is negative for cirrhosis or masses. If a liver biopsy is performed, wh - answerLymphocytic infiltration of portal tracts - Most cases of Hepatitis C (~80%) progress to chronic HCV, which is predominantly characterized by portal tract-based lymphocytic infiltration, including lymphoid follicles, and fibrosis. Chronic inflammation causes persistent hepatocyte injury and can involve the hepatocytes adjacent to the portal tracts (ie, interface activity). After several decades, chronic HCV can progress to cirrhosis characterized by abnormal hepatic architecture with extensive fibrosis and the formation of bridging fibrous septa that surround regenerative parenchymal nodules. A 38-year-old woman, gravida 1