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NUR 654 Midterm - 200+ Verified Q&A | Endocrine, Cancer, Pain Management, Reproductive, Neuro - 2025/2026 | Grand Canyon University

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NUR 654 Midterm - 200+ Verified Q&A | Endocrine, Cancer, Pain Management, Reproductive, Neuro - 2025/2026 | Grand Canyon University

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NUR 654 Midterm - 200+ Verified Q&A | Endocrine,
Cancer, Pain Management, Reproductive, Neuro -
2025/2026 | Grand Canyon University


1. A patient with type 2 diabetes on metformin and empagliflozin develops euglycemic diabetic
ketoacidosis (euDKA) after starting a ketogenic diet. Which mechanism best explains the euDKA
in this context?

A. Metformin-induced lactic acidosis shifting to ketoacidosis
B. Empagliflozin increases glucagon secretion and ketogenesis, while reduced carbohydrate intake depletes
glycogen stores
C. Ketogenic diet directly causes metabolic acidosis independent of SGLT2 inhibition
D. Combined therapy impairs renal ketone excretion leading to accumulation

Answer: B
Rationale: SGLT2 inhibitors like empagliflozin increase glucagon secretion and reduce insulin,
promoting ketogenesis. When carbohydrate intake is severely restricted, glycogen stores are low, leading
to euDKA despite near-normal glucose levels. Metformin does not cause euDKA, and the ketogenic diet
alone does not explain the euglycemic presentation. Renal ketone excretion is not impaired by these
drugs.


2. A patient with metastatic castration-resistant prostate cancer (mCRPC) is started on
abiraterone acetate plus prednisone. Which laboratory parameter requires the most frequent
monitoring due to the drug's mechanism?

A. Serum creatinine and BUN
B. Serum potassium and blood pressure
C. Liver transaminases and bilirubin
D. Complete blood count with differential

Answer: B
Rationale: Abiraterone inhibits CYP17A1, reducing androgen synthesis but also causing
mineralocorticoid excess (due to ACTH feedback), leading to hypertension, hypokalemia, and fluid
retention. Prednisone mitigates these effects but monitoring of potassium and blood pressure is
essential. Liver function monitoring is also important but less frequent than electrolytes and BP. Renal
and hematologic effects are not primary.


3. A patient with chronic neuropathic pain from diabetic peripheral neuropathy has inadequate
relief from gabapentin 900 mg/day. Which of the following dose adjustments or adjuncts is most
appropriate based on current guidelines?

A. Increase gabapentin to 1800 mg/day in divided doses
B. Switch to pregabalin 150 mg twice daily




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,C. Add tramadol 50 mg four times daily
D. Add amitriptyline 25 mg at bedtime

Answer: A
Rationale: First-line treatment for diabetic peripheral neuropathy includes gabapentinoids. Gabapentin
should be titrated up to 1800-3600 mg/day (in divided doses) before considering alternatives.
Pregabalin is also first-line but switching without maximizing gabapentin is not optimal. Tramadol is
second-line due to abuse potential, and amitriptyline is effective but often reserved due to
anticholinergic side effects.


4. A patient with endometriosis and severe dysmenorrhea fails to respond to NSAIDs and
combined hormonal contraceptives. Which of the following mechanisms underlies the use of
gonadotropin-releasing hormone (GnRH) antagonists in this condition?

A. Competitive blockade of estrogen receptors in endometrial tissue
B. Suppression of pituitary LH and FSH secretion by inhibiting GnRH receptors
C. Inhibition of aromatase conversion of androgens to estrogens
D. Downregulation of GnRH receptors after initial stimulation

Answer: B
Rationale: GnRH antagonists (e.g., elagolix) competitively block pituitary GnRH receptors, causing rapid
suppression of LH and FSH, thereby reducing ovarian estrogen production. This alleviates
endometriosis symptoms. In contrast, GnRH agonists initially stimulate then downregulate receptors
(option D). Options A and C describe mechanisms of selective estrogen receptor modulators and
aromatase inhibitors, respectively.


5. A patient with Parkinson's disease on levodopa/carbidopa experiences motor fluctuations and
dyskinesias. Which adjunctive therapy is most appropriate to reduce off-time by inhibiting
catechol-O-methyltransferase (COMT)?

A. Rasagiline
B. Pramipexole
C. Entacapone
D. Benztropine

Answer: C
Rationale: Entacapone is a COMT inhibitor that prolongs the half-life of levodopa, reducing off-time in
patients with motor fluctuations. Rasagiline is a MAO-B inhibitor, pramipexole is a dopamine agonist,
and benztropine is an anticholinergic. COMT inhibition specifically addresses wearing-off phenomena
by preventing peripheral metabolism of levodopa.


6. A patient with anaplastic thyroid cancer has a BRAF V600E mutation. Which targeted therapy
would be most appropriate?
A. Sorafenib
B. Dabrafenib plus trametinib
C. Lenvatinib
D. Vandetanib




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,Answer: B
Rationale: BRAF V600E mutation is common in anaplastic thyroid cancer. Dabrafenib (BRAF inhibitor)
plus trametinib (MEK inhibitor) is approved for this indication, as dual blockade of the MAPK pathway
improves outcomes. Sorafenib and lenvatinib are multikinase inhibitors used for differentiated thyroid
cancer. Vandetanib targets RET mutations in medullary thyroid cancer.


7. A patient receiving morphine via patient-controlled analgesia (PCA) for acute postoperative
pain has a respiratory rate of 8 breaths/min. Which reversal agent is most appropriate and what is
its mechanism?

A. Naloxone, a competitive antagonist at mu-opioid receptors
B. Naltrexone, a long-acting antagonist at mu-opioid receptors
C. Flumazenil, a competitive antagonist at GABA-A receptors
D. Naloxone, a partial agonist at mu-opioid receptors

Answer: A
Rationale: Naloxone is a competitive mu-opioid receptor antagonist that reverses opioid-induced
respiratory depression. It is short-acting and can be titrated. Naltrexone is longer-acting and not used
for acute reversal. Flumazenil reverses benzodiazepine effects. Naloxone is not a partial agonist; it is an
antagonist.


8. A patient with polycystic ovary syndrome (PCOS) and insulin resistance is prescribed
metformin. Which of the following best describes the primary mechanism by which metformin
improves ovulatory function?

A. Direct stimulation of the pituitary to release LH and FSH
B. Reduction of hepatic gluconeogenesis and improvement of peripheral insulin sensitivity, lowering insulin
levels and reducing ovarian androgen production
C. Inhibition of ovarian aromatase activity
D. Blockade of androgen receptors in the hypothalamus

Answer: B
Rationale: In PCOS, insulin resistance leads to hyperinsulinemia, which stimulates ovarian androgen
production. Metformin improves insulin sensitivity and reduces hepatic glucose output, lowering insulin
levels. This decreases ovarian androgen secretion, improving follicular development and ovulation. It
does not directly stimulate gonadotropins or block androgen receptors.


9. A patient with multiple sclerosis experiences breakthrough disease activity despite interferon
beta therapy. Which of the following oral medications is a sphingosine-1-phosphate receptor
modulator that prevents lymphocyte egress from lymph nodes?

A. Dimethyl fumarate
B. Fingolimod
C. Teriflunomide
D. Natalizumab

Answer: B
Rationale: Fingolimod is a sphingosine-1-phosphate receptor modulator that traps lymphocytes in lymph
nodes, reducing CNS infiltration. Dimethyl fumarate has antioxidant effects, teriflunomide inhibits
pyrimidine synthesis, and natalizumab is a monoclonal antibody against alpha-4 integrin. Fingolimod is

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, oral and used for relapsing-remitting MS.


10. A patient receiving cisplatin-based chemotherapy develops acute kidney injury with
hypomagnesemia. Which mechanism best explains the hypomagnesemia?
A. Cisplatin-induced tubulointerstitial nephritis causing magnesium wasting
B. Cisplatin directly chelates magnesium in serum
C. Cisplatin increases renal excretion of magnesium by inhibiting the thick ascending limb of loop of Henle
D. Cisplatin causes syndrome of inappropriate antidiuretic hormone (SIADH) leading to dilutional
hypomagnesemia

Answer: A
Rationale: Cisplatin accumulates in renal proximal tubule cells, causing oxidative stress and apoptosis,
leading to tubulointerstitial nephritis. This results in renal magnesium wasting and hypomagnesemia.
Cisplatin does not chelate magnesium, nor does it directly inhibit the loop of Henle like loop diuretics.
SIADH is associated with hyponatremia, not hypomagnesemia.


11. In a patient with primary hyperaldosteronism, which of the following laboratory findings
would be most discordant with the expected pathophysiology?
A. Low plasma renin activity and metabolic alkalosis
B. Hypokalemia and hypertension
C. Elevated serum aldosterone and suppressed renin
D. Hyperkalemia and metabolic acidosis

Answer: D
Rationale: Primary hyperaldosteronism features excessive aldosterone, causing sodium retention,
potassium excretion, and metabolic alkalosis. Hyperkalemia and metabolic acidosis are characteristic of
hypoaldosteronism or adrenal insufficiency, not hyperaldosteronism.


12. A patient with metastatic castration-resistant prostate cancer has progression on abiraterone
and enzalutamide. Which of the following mechanisms best explains resistance to these agents?
A. Increased expression of glucocorticoid receptor bypassing androgen receptor signaling
B. Enhanced androgen receptor splice variant AR-V7 lacking ligand-binding domain
C. Upregulation of CYP17A1 leading to increased adrenal androgen synthesis
D. Mutation in the androgen receptor ligand-binding domain reducing drug affinity

Answer: B
Rationale: AR-V7 is a constitutively active splice variant that lacks the ligand-binding domain, rendering
abiraterone (which reduces androgen synthesis) and enzalutamide (which blocks the ligand-binding
domain) ineffective. Glucocorticoid receptor bypass is a resistance mechanism for enzalutamide but not
abiraterone. CYP17A1 upregulation is overcome by abiraterone. Ligand-binding domain mutations can
confer resistance to enzalutamide but not to abiraterone.


13. A patient with chronic low back pain has been on high-dose oxycodone for 6 months without
improvement in function. The provider decides to taper the opioid. Which of the following tapering
strategies is most appropriate to minimize withdrawal and monitor for adverse outcomes?




Page 4

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