NP125 Med Surg Exam | Nurselytic

Correct Answer: A

Rationale: Using a Foley catheter can help prevent skin breakdown caused by prolonged contact with urine in incontinent patients, especially if they are confused or non-ambulatory and unable to use other urinary devices. Maintaining intact skin is crucial to avoiding infections and pressure injuries, making a Foley catheter a suitable intervention in specific cases when prescribed. Foley catheters are not inherently inappropriate but must be prescribed judiciously due to risks like urinary tract infections. While alternative methods may be preferable, this intervention is justified for incontinent, immobile patients with compromised mental status to protect skin integrity. It aligns with clinical guidelines and patient-specific needs.

Correct Answer: B

Rationale: Referred back pain is not a hallmark of large bowel obstruction. It typically occurs in conditions with retroperitoneal organ involvement, such as renal or pancreatic pathology. Large bowel obstruction presents primarily with abdominal distention and pain localized to the affected bowel segment due to obstruction-induced pressure and stretching. Abdominal distention is a classic sign of large bowel obstruction. Accumulated gas and stool proximal to the obstruction result in bloating and visible distention. This presentation reflects impaired bowel motility, pressure build-up, and reduced passage of contents, commonly seen in large bowel pathology. Projectile vomiting is more indicative of upper GI obstruction, such as pyloric stenosis, due to immediate pressure effects. Large bowel obstructions manifest with late vomiting as distal obstruction delays content passage. Vomiting in this case is less forceful and often accompanied by fecal material. Metabolic alkalosis is more associated with vomiting-related losses of gastric acid, as seen in upper GI pathology. Large bowel obstruction typically leads to metabolic acidosis from ischemia or bacterial overgrowth, not alkalosis, as the obstruction hampers normal bowel function and circulation.

Correct Answer: A

Rationale: Strict monitoring of intake and output in CHF patients with furosemide therapy prevents fluid overload and underhydration. Foley catheter placement accurately quantifies urine output, crucial in critically ill patients with diuretic-induced fluid shifts. This ensures precise fluid balance adjustments, improving patient outcomes. Omitting Foley catheter placement in CHF patients risks inaccurate fluid balance monitoring. Furosemide causes frequent, unpredictable urination, complicating intake-output tracking without direct measurement. This approach undermines effective management of diuretic therapy and fluid overload prevention in critical settings.

Correct Answer: A

Rationale: Insulin glargine (Lantus) is a long-acting insulin used for basal glycemic control in diabetic patients. It has a slow onset and a steady release over approximately 24 hours, mimicking natural insulin secretion to stabilize blood glucose levels and prevent fluctuations. Rapid-acting insulins, such as insulin lispro or aspart, have fast onsets and short durations to manage postprandial glucose spikes. Insulin glargine does not have these properties, as it is used for long-term basal control rather than immediate blood sugar regulation. Intermediate-acting insulins like NPH have a shorter duration and peak effect compared to long-acting insulins. Insulin glargine provides a consistent effect over 24 hours, distinguishing it from intermediate-acting options. Short-acting insulins are designed for pre-meal blood sugar control with a quick onset and limited duration. Insulin glargine does not fit this description due to its long-acting properties.

Correct Answer: A

Rationale: Metformin primarily increases peripheral insulin sensitivity, particularly in muscle and adipose tissues, facilitating glucose uptake and utilization. It inhibits hepatic glucose production through AMPK activation, reducing gluconeogenesis. Metformin also improves lipid profiles and insulin resistance without promoting insulin secretion, which minimizes the risk of hypoglycemia. Its actions target metabolic pathways, enhancing cellular glucose management for type 2 diabetes control. Metformin does not stimulate pancreatic insulin release. It acts independently of insulin production mechanisms, focusing on improving peripheral sensitivity and reducing hepatic glucose output. Drugs like sulfonylureas target beta cells for insulin release, unlike metformin, which avoids direct engagement with the pancreas, minimizing hypoglycemia risks associated with excessive insulin secretion. Stimulating glucose uptake in skeletal muscles is a partial outcome of improved insulin sensitivity induced by metformin. However, metformin's mechanism extends beyond this, involving significant hepatic effects. It does not directly stimulate glucose uptake as a sole action; rather, it enhances overall metabolic efficiency and glucose management through multiple pathways. Metformin decreases hepatic glucose production rather than increasing it. It inhibits gluconeogenesis by activating AMPK, suppressing the production of glucose from non-carbohydrate sources. This inhibition aids in reducing fasting glucose levels, which are often elevated in type 2 diabetes. The opposite action described contradicts its therapeutic role in managing hyperglycemia effectively.