What should the nurse anticipate teaching a patient with a new report of heartburn?

Choice A 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.

Choice B rationale

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.

Choice C rationale

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.

Choice D rationale

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.

Choice 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.

Choice B rationale

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.

Choice C rationale

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.

Choice D rationale

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.