Free Anesthesia In-Training Exam Sample Questions

See why TrueLearn is a trusted resource for thousands of medical students and residents. We understand that it’s all about the content. That’s why we have high-yield anesthesia practice questions written and screened by physician authors, which are regularly updated to ensure our SmartBanks stay up-to-date with exam blueprint changes. Below is a free anesthesia exam sample question to showcase what we mean.

Try This ABA ITE Sample Question from the 2025 New Edition

A 59-year-old man with a history of end-stage renal disease on intermittent hemodialysis presents to the ED after a fall. He is found to have a fracture of the femoral neck and is brought to the OR for emergent repair. He last received dialysis 2 days before the injury. Which of the following metabolic derangements is MOST likely to be seen on initial chemistry analysis?

A. Hypocalcemia
B. Hypomagnesemia
C. Hypophosphatemia

The Answer and Explanation

Did you get it right? The correct answer is A.

Hypocalcemia is the electrolyte abnormality most likely to be seen perioperatively on initial chemistry analysis for this patient and is common in end-stage renal disease (ESRD) due to two primary etiologies. It can be caused by increased serum phosphorus due to the increased complexing of phosphorus with calcium, resulting in a decreased serum availability of free calcium ions. Hypocalcemia is also caused by decreased renal production of 1,25-dihydroxy vitamin D, resulting in decreased enteral absorption of calcium from dietary sources. Although ESRD has implications for every organ system in the body, one of the most relevant to anesthesiologists is its effect on the metabolic system. ESRD typically causes a wide range of clinically significant metabolic derangements. Patients tend to exist in an acidemic state, which is transiently corrected with dialysis.

The hypervolemia associated with ESRD is due to a failure to excrete sodium effectively; however, the resultant increase in total body water maintains an essentially normal sodium level. Weight gain from this increased water is typically offset by a decrease in lean body mass, resulting in minimal change in total body weight in patients with ESRD. In ESRD, potassium is not effectively excreted at the level of the distal collecting tubule. Although gastrointestinal excretion is enhanced in patients with ESRD, it is not usually enough to mitigate the loss of renal excretion of potassium. In addition, metabolic acidosis and protein catabolism result in increased serum potassium, and both are common in the ESRD state. Osmolality may increase if dialysis is not received regularly. However, due to the inability to eliminate free water in urine, serum osmolality is relatively diluted, and the effect of increased serum solute is attenuated. Serum blood urea nitrogen and creatinine levels are markedly elevated in ESRD due to a loss of renal elimination.

The increase in phosphorus seen in ESRD involves more than just decreased phosphorus excretion, although this factor plays a role. As chronic kidney disease (CKD) progresses, the kidneys lose their ability to secrete calcitriol, the hormone responsible for stimulating bone growth. The calcitriol loss is balanced by an increase in parathyroid hormone, which increases bony turnover and mobilizes phosphorus from the bones. As the kidneys lose their ability to excrete phosphorus, serum phosphorus levels will increase, leading to the hyperphosphatemia seen in ESRD.

Albumin is decreased in ESRD due to decreased synthesis and increased catabolism of albumin. The pathophysiology of these changes is likely due to the systemic inflammatory state accompanying ESRD. A state of acidemia tends to occur in the later stages of CKD and in ESRD. As the kidneys lose their ability to excrete organic anions, the anion gap will expand to an average of ∼ 20 mmol/L with an appropriate decrease in serum bicarbonate levels. It is especially crucial to be mindful of this change after surgery. The inflammatory changes and tissue injury may result in increased production of organic anions, which may exceed the body’s ability to compensate. This result can precipitate further acidemia or hyperkalemia and its associated harmful cardiac effects.

Incorrect Answer Explanations

Answer B: Magnesium tends to increase in ESRD due to decreased excretion instead of being low, as in hypomagnesemia. However, magnesium levels may be normal or even low in some patients due to poor intake and absorption of nutritional magnesium. Answer C: When coupled with decreased phosphorus excretion in ESRD, serum phosphorus levels tend to rise in patients with ESRD rather than being low, as in hypophosphatemia. The loss of calcitriol excretion and the subsequent unopposed parathyroid hormone action tend to mobilize phosphorus from the bones.

Bottom Line

Myriad metabolic derangements occurring in the setting of end-stage renal disease may be clinically significant to anesthesiologists. Potassium is typically elevated, whereas calcium tends to be decreased. Patients tend to exist in an acidemic state, which is transiently corrected with dialysis.

Another Free Anesthesia ITE Sample Question

Which of the following MOST accurately describes the mechanism of neuraxial opioid administration?

A. Primarily leads to systemic absorption and subsequent central effects that inhibit nociception
B. Produces locally mediated inhibitory effects on the spinal cord only
C. Reduces ascending nociceptive signaling via binding in the substantia gelatinosa

The Answer and Explanation

Did you get it right? The correct answer is C.

Neuraxial opioid administration results in multiple effects, including the inhibition of nociceptive nerve impulses via ligand-mediated binding within the substantia gelatinosa of the spinal cord, resulting in reduced neurotransmitter release. Direct effects on the medulla and periaqueductal gray areas that project neurons into the spinal cord cause inhibition of ascending pain transmission from the dorsal horn as well.

Systemic opioid administration produces a complex interplay between several brain areas that results in analgesia. Primarily, however, neuraxial opioids have a direct effect on the spinal cord, although there is evidence that systemic absorption also occurs and can produce effects in areas of the brain. During neuraxial opioid administration, the binding of neuraxial opioids at presynaptic and postsynaptic neurons within the substantia gelatinosa of the spinal cord lead to suppression of substance P and glutamate secretion. The transmission of nociceptive information arising from the dorsal horn toward the brain (ie, ascending pathway) is inhibited via this process. Correspondingly, descending nociceptive signaling from the midbrain and periaqueductal gray area inhibit the flow of ascending nociceptive firing from dorsal horn neurons through inhibitory projections into the spinal cord. Several brain areas are involved in pain modulation outside the spinal cord. These areas include the cingulate cortex, insula, orbitofrontal cortex, and the brainstem. Positron emission scan results provide evidence that the descending nociceptive signaling ending in the dorsal horn from areas such as the periaqueductal gray and rostral ventromedial medulla are disrupted by the administration of opioids and play a role in nociceptive inhibition as well. Clearly, there is an incredibly complex interplay between human neurophysiology and opioid receptor–binding substances. Neuraxial opioids may produce more pronounced effects in the spinal cord, but systemic effects may also be responsible for some of the analgesic qualities of neuraxial infusion of the drugs.

Incorrect Answer Explanations

Answer A: Although some theorists have suggested the infusion of opioids does lead to systemic absorption, the primary nociceptive inhibition after neuraxial infusion results from local uptake by the spinal cord. In the case of less lipid-soluble opioids, the brainstem and brain will see the effects of these medications via movement through the central spinal fluid to the brain. The extended effects and late respiratory depression caused by morphine demonstrate this behavior of lipid-insoluble opioids. Answer B: Some systemic absorption does occur after neuraxial infusion, and the movement of opioids up the spinal column and to the brainstem and brain via the cerebral spinal fluid also occurs, resulting in analgesic effects as well.

Bottom Line

Neuraxial opioids have a complex mechanism of action, primarily mediated by the inhibition of ascending nociceptive nerve impulses from the spinal cord via ligand-mediated binding within the substantia gelatinosa. The reduction of substance P and glutamate release at presynaptic and postsynaptic neurons within the spinal cord is primarily responsible for reduced pain transmission with neuraxial opioids. Effects in the brain and brainstem also occur through systemic absorption and passage through the cerebrospinal fluid, resulting in projections into the spinal cord that inhibit pain transmission from the dorsal horn as well. For more information, see:

• American Board of Anesthesiology Keyword. “Neuraxial opioids: Mechanism (A)”
• Gropper M, et al. Miller’s Anesthesia. Ch. 45: Spinal, Epidural, and Caudal Anesthesia. Section: Opioids. 9th ed.
• George MJ. The site of action of epidurally administered opioids and its relevance to postoperative pain management. Anaesthesia, 2006;61:659-664.