A 28-year-old client at 32 weeks gestation reports dull lower back pain, pelvic pressure, and an increase in vaginal discharge. The nurse suspects preterm labor. Which finding would confirm true preterm labor?

Metformin is a biguanide that improves insulin sensitivity in peripheral tissues and inhibits hepatic gluconeogenesis. In PCOS, hyperinsulinemia stimulates the theca cells to produce excess androgens, leading to hirsutism and anovulation. Reducing insulin levels helps restore the normal hormonal balance required for follicle maturation.

A. Block ovulation: Metformin is actually used to induce or restore regular ovulation in PCOS patients by correcting the underlying metabolic dysfunction. It is not a contraceptive and does not suppress the pituitary-gonadal axis. Improved insulin levels allow the body to resume a normal ovulatory menstrual cycle.

B. Decrease insulin resistance: By enhancing the action of insulin at the cellular level, metformin lowers circulating insulin concentrations. This reduction decreases the stimulus for ovarian androgen production, which is the primary driver of PCOS symptoms. It addresses the metabolic root cause of the syndrome, improving systemic health.

C. Reduce estrogen levels: PCOS is often characterized by "unopposed estrogen" due to a lack of progesterone from anovulation. Metformin's primary role is not the direct reduction of estrogen, but rather the management of insulin signaling. Restoring ovulation through metformin use will eventually lead to healthier progesterone-estrogen ratios.

D. Stimulate LH surge: Metformin does not directly act on the anterior pituitary to trigger a luteinizing hormone surge. Instead, it creates an internal environment where the dominant follicle can develop naturally. The LH surge eventually occurs as a secondary result of restored follicular health and proper estrogen feedback.

Phenylketonuria (PKU) is an autosomal recessive disorder caused by a deficiency of the hepatic enzyme phenylalanine hydroxylase. This leads to the toxic accumulation of the amino acid phenylalanine, which causes irreversible neurological damage and intellectual disability. Screening occurs via a neonatal heel stick shortly after birth.

A. Fluid restriction: There is no physiological basis for limiting fluid intake in infants with PKU. Adequate hydration is necessary for metabolic stability and renal function. Treatment focuses on the chemical composition of the intake rather than the total volume of fluid consumed.

B. Iron supplementation: While maintaining general nutrition is important, iron does not affect the metabolic pathway of phenylalanine. PKU management is specifically concerned with amino acid metabolism rather than hematological parameters. Iron status is managed independently of a PKU diagnosis.

C. High-protein diet: Standard high-protein foods like meat, dairy, and eggs are extremely high in phenylalanine and are strictly forbidden. Consumption of these foods would lead to a rapid rise in neurotoxic levels of the amino acid. A high-protein diet is contraindicated for these patients.

D. Phenylalanine-restricted diet: The mainstay of therapy is a life-long diet that limits phenylalanine while providing enough tyrosine and other essential nutrients. This involves special medical formulas and low-protein foods to maintain blood levels within the therapeutic range. This prevents cognitive impairment.