Correct Answer: B

Rationale: While alcohol is a known irritant to the gastric lining, it is not the primary cause of peptic ulcer disease. Excessive alcohol consumption contributes to mucosal damage but lacks the direct causative action of Helicobacter pylori, which colonizes the stomach lining and interferes with protective mechanisms, leading to ulcer formation. Alcohol merely exacerbates existing risk factors rather than initiating disease. Helicobacter pylori is the most common cause of peptic ulcer disease globally. Its mechanism involves producing urease, neutralizing stomach acid and enabling bacterial survival. It induces inflammation and mucosal damage, compromising the stomach's protective lining. Persistent infection leads to ulcer formation. This bacterial colonization is implicated in up to 90% of duodenal ulcers, making it the key pathogenic factor in PUD. Smoking is a risk factor for peptic ulcer disease but functions more as an aggravating agent than the primary cause.
Tobacco use increases gastric acid secretion and decreases bicarbonate production, weakening mucosal defenses. It also reduces the efficacy of Helicobacter pylori eradication therapy, prolonging ulcer disease. However, it does not directly induce the condition independently, highlighting its secondary role in PUD pathology. Stress is associated with peptic ulcer disease but is not a primary causative factor. Psychological stress can lead to hypersecretion of gastric acid, aggravating mucosal vulnerability in susceptible individuals. However, its role is predominantly indirect, amplifying existing risk factors like Helicobacter pylori infection. Stress-induced ulcers are typically seen in critical illnesses or severe physiological stress conditions, differing from PUD pathogenesis.

Correct Answer: A

Rationale: Contact isolation prevents the transmission of Clostridium difficile spores, a significant source of nosocomial infections. Private rooms reduce cross-contamination risks. Antidiarrheal use is contraindicated in Clostridium difficile infection as it may worsen colitis by retaining toxins. Prompt stool elimination is vital. Antibiotics are used to treat Clostridium difficile but educating the patient about antibiotic cessation is inappropriate as their use is essential for infection control. Stool softeners are unnecessary since diarrhea is already present, and further softening may exacerbate fluid and electrolyte loss.

Correct Answer: A

Rationale: Lispro (Humalog) is a rapid-acting insulin analog designed for mealtime glucose control. It begins action within 15 minutes, peaks in 1 hour, and lasts 2 to 4 hours. Its quick onset matches postprandial glucose spikes, enhancing glycemic control during meals and preventing hyperglycemia from carbohydrate intake. Glargine (Lantus) is a long-acting basal insulin with no peak and prolonged action. It does not target mealtime spikes but provides steady glucose control over 24 hours. Its slow onset and constant release profile are unsuitable for immediate postprandial glucose management. Detemir (Levemir) is a long-acting basal insulin, similar to glargine, with extended action for baseline glucose control. It lacks the rapid onset needed for mealtime management, making it inappropriate for postprandial hyperglycemia control, as observed in Lispro efficacy. NPH (Humulin N) is an intermediate-acting insulin with delayed onset and peak activity. It supports baseline glucose regulation but fails to address mealtime glucose control promptly. Its time profile does not align with the immediate needs of postprandial hyperglycemia management.

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: C

Rationale: Administering 1 mg of glucagon intramuscularly is unnecessary for a patient who is awake, alert, and able to swallow. Glucagon is reserved for patients who are unconscious and unable to swallow effectively to prevent choking. Administering 25 g of dextrose IVP is unnecessary in this case because the patient is alert and able to swallow. Oral intake of carbohydrates is the preferred and safer intervention for mild hypoglycemia like 69 mg/dL. Holding the insulin and encouraging the patient to eat provides glucose through dietary means, which is appropriate in a patient who is awake, alert, and hungry. A level of 69 mg/dL, though below normal, can be managed with oral glucose intake safely. Calling the MD is not the immediate priority in managing mild hypoglycemia. Intervening directly to correct the glucose level with oral intake is more appropriate and effective in this situation.