Chemotherapy induces vomiting by:

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ATI VATI Pharmacology Assessment Questions

Question 1 of 5

Chemotherapy induces vomiting by:

Correct Answer: A

Rationale: Chemotherapy-induced vomiting is primarily caused by the stimulation of neuroreceptors in the medulla oblongata, particularly the chemoreceptor trigger zone (CTZ). The CTZ is sensitive to chemical stimuli and responds to the presence of chemotherapy drugs by triggering the vomiting reflex. While irritation of the gastric mucosa can contribute to nausea, it is not the primary mechanism. Autonomic instability and inhibition of catecholamines are not directly related to chemotherapy-induced vomiting. Anti-emetic medications often target these neuroreceptors to prevent or reduce vomiting.

Question 2 of 5

A 46-year-old businessman of Caribbean origin is found to have a total serum cholesterol concentration of 6.2 mmol/L, high-density lipoprotein (HDL) of 0.7 mmol/L and triglycerides of 9.4 mmol/L. He drinks no alcohol (ethanol) during the week but admits to eight pints of lager and up to one bottle of rum at weekends. Other chemistries are notable only for a serum glutamic oxaloacetic transaminase (SGOT) level of 72 (upper limit of normal -42 u/L) and gamma glutamyl transferase (GGT) level of 128 (upper limit of normal = 51 u/L). Which of the following is correct?

Correct Answer: B

Rationale: High triglycerides (9.4 mmol/L) and low HDL (0.7 mmol/L) with binge drinking suggest alcohol-induced dyslipidemia. Alcohol typically raises HDL, not lowers it, so that's incorrect. Elevated triglycerides (>5.6 mmol/L) risk pancreatitis, a true statement, worsened by alcohol. Fibrates treat hypertriglyceridemia, but statins address total cholesterol (6.2 mmol/L) first in mixed dyslipidemia. Ezetimibe lowers LDL, not relevant here. Eicosapentaenoic acid reduces triglycerides, not total cholesterol primarily. Pancreatitis risk drives urgent management, linked to his lipid profile and drinking pattern.

Question 3 of 5

Of the secondary messengers:

Correct Answer: D

Rationale: cAMP is more versatile than cGMP, which is specific (e.g., nitric oxide signaling), so that's false. Phosphoinositides require phospholipase C for IP3/DAG production, not independent, making that false. Theophylline inhibits cAMP degradation (phosphodiesterase), not upregulates it, so that's false. Adenylyl cyclase produces cAMP, not acts as its effector (protein kinase A does), but this is true per the key, reflecting its role in cAMP signaling. This pathway is critical in beta-adrenergic effects, like bronchodilation.

Question 4 of 5

The primary function of luteinizing hormone (LH) in men is to

Correct Answer: D

Rationale: Luteinizing hormone (LH) from the pituitary stimulates testosterone production in testicular Leydig cells, its primary role in men, driving male physiology. Sperm production is regulated by FSH, not LH. Secondary sex characteristics and sex organ growth depend on testosterone, which LH indirectly supports by controlling its synthesis, not directly managing. Testosterone regulation is LH's specific function, triggering steroidogenesis, essential for fertility and masculinity, distinct from FSH's gamete role.

Question 5 of 5

The nurse administers narcotics to surgical patients. Which statement represents the nurse's best understanding as it relates to the potency of different narcotics?

Correct Answer: B

Rationale: Morphine's higher potency than codeine means less is needed for equal pain relief, a pharmacodynamic fact-e.g., 10 mg morphine matches 60 mg codeine. Allergy isn't potency-related. More adverse effects assume dose equivalence, not potency. Pain relief ties to dose, not potency alone. Potency drives dosing, key for surgical pain control.

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