Description of the Patient Case The patient was a 30-year-old white woman who had delivered a child via cesarean section. She had no chronic conditions or previous surgeries and no severe diseases in her patient history. The patient was prescribed codeine for managing post-cesarean pain; the dosage was adjusted for the woman’s age and weight, and she took no more than the prescribed dose. Nevertheless, while on codeine, the patient experienced the adverse effects of dizziness and nausea. The woman also saw that her breastfed baby was lethargic and showed a lack of appetite. The patient shared her observations of these adverse effects with her physician, who recommended the discontinuation of codeine. When the medicine was discontinued, both the patient and her infant returned to their normal condition and demonstrated no above-mentioned symptoms. Factors Influencing Pharmacokinetics and Pharmacodynamics The patient’s response to codeine can be explained by several individual variations. The first factor is genetic variants that change the person’s drug metabolism, which are the most prevalent genetic mechanism modifying drug responses (Rosenthal & Burchum, 2017). Codeine refers to opioids, and its effect is exerted through opioid receptors located throughout the body (Dean, 2017). However, since this medicine is a prodrug, its effect is highly dependent on metabolism, which converts it into morphine that possesses stronger analgesic properties (Dean, 2017). This conversion requires the liver enzyme CYP2D6, which metabolizes codeine into morphine via the process called O- demethylation (Dean, 2017). Usually, only 5-10% of codeine is converted into morphine, with 80% of the administered dose being transformed into inactive metabolites (Dean, 2017). Yet, this conversion rate may be different in some patients because of the varied activity of the CYP2D6 enzyme. The activity of the CYP2D6 enzyme depends on the individual’s genotype. Patients with low enzyme activity are called “poor metabolizers” because they receive little morphine from codeine, while those with higher activity of this enzyme are “ultrarapid metabolizers” (Kwon & Flood, 2020). Given that the dose administrated to the patient in the described case was normal for her age and weight but resulted in the symptoms of intoxication, it may be concluded that the patient was an ultrarapid metabolizer. The second factor that may have influenced the patient’s response to codeine is physiologic alterations due to pregnancy. Research indicates that the activity level of the CYP2D6 enzyme usually rises in pregnancy (Dean, 2017). Since the patient in the case gave birth shortly before codeine administration, it may be assumed that the elevated enzyme activity level was still present. This would result in greater conversion of codeine into morphine than expected, causing dizziness and nausea in the mother and lethargy in the breastfed infant. Finally, the patient’s response to the drug may be explained by a lack of dose adjustment to the patient’s race. Studies show that Caucasians require a lower dose of codeine than Asians (Baber et al., 2015). The patient belonged to the Caucasian race, meaning that her appropriate dose of codeine should have been low