Correct Answer: A

Rationale: Fractures caused by disease processes are termed pathological fractures. Diseases like osteoporosis weaken bones, increasing susceptibility to fractures. Conditions like cancer can invade bone tissue, causing structural fragility. Pathological fractures occur without significant trauma, distinguishing them from those caused by external injuries, which require high-impact forces to break otherwise healthy bones. Traumatic fractures stem from external forces, not from disease processes. This assertion neglects the reality of pathological fractures, which result from diseases undermining the bone's natural strength. Healthy bones typically endure significant stress before fracturing, and the absence of disease makes fractures from minimal trauma highly unlikely. This reasoning excludes pathological fractures caused by internal illnesses or conditions weakening bone structures.

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: 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.

Correct Answer: C

Rationale: Glucagon IM is inappropriate for a glucose of 85 mg/dL, which is within normal preprandial ranges of 70-100 mg/dL. It is reserved for severe hypoglycemia with symptoms like unconsciousness. Calling the MD is unnecessary when blood glucose is in the normal range and the patient is symptomatic. Nutritional intake is the next logical step in management. Holding insulin and allowing the patient to eat is appropriate for 85 mg/dL. Nutritional intake stabilizes glucose levels, maintaining euglycemia without risking hypoglycemia from insulin. Administering 10 units of Humalog risks causing hypoglycemia, as this dose is excessive for a glucose level of 85 mg/dL. Insulin use is not indicated here. Administering dextrose IVP unnecessarily increases glucose levels. It is inappropriate unless the patient is symptomatic and glucose levels drop below 70 mg/dL. Administering 7 units of Humalog risks hypoglycemia for a glucose level of 85 mg/dL, as the dose is excessive and unnecessary without elevated glucose. Administering 5 units of Humalog poses a risk for hypoglycemia and is not indicated with normal glucose levels. Nutritional intake alone suffices. Administering 15 units of Humalog is inappropriate and dangerous for a normal glucose level, as it likely induces hypoglycemia. Insulin use should be avoided here.

Correct Answer: B

Rationale: Administering 1 mg of glucagon intramuscularly stimulates glycogenolysis in the liver, increasing blood glucose levels. However, it is slower in onset compared to IV dextrose, which is critical in a non-arousable patient with a dangerously low blood glucose level of 50 mg/dL. Time efficiency is vital in this emergency. Administering 25 g of dextrose IV pushes glucose directly into the bloodstream, providing an immediate increase in blood glucose. This is the most appropriate action for a non-arousable, hypoglycemic patient. Normal blood glucose ranges between 70-100 mg/dL fasting, making this an emergency requiring prompt correction. Encouraging the patient to eat may be effective in mild hypoglycemia, but not for a critically low level like 50 mg/dL in a non-arousable patient. This delay can result in prolonged neuroglycopenic effects, worsening the patient's condition. Administering 7 units of Humalog insulin would worsen the hypoglycemia by facilitating glucose uptake into cells, which is contraindicated in this situation. Instead, glucose administration is required to correct the hypoglycemia immediately.