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Multiparity with uncomplicated prior pregnancies is actually associated with a decreased risk of hyperemesis. Women who have successfully navigated previous gestations without severe vomiting have demonstrated a physiological tolerance to pregnancy hormones. Nulliparity is traditionally considered a higher risk factor than asymptomatic multiparity, as the maternal body's reaction to the initial surge of hCG is less predictable.

A singleton pregnancy at 28 weeks gestation is well beyond the typical pathogenetic window for hyperemesis gravidarum. Symptoms of hyperemesis almost universally initiate in the first trimester, typically between 4 and 9 weeks, and peak around week 12. If severe vomiting begins in the third trimester, the nurse should investigate other etiologies such as preeclampsia or acute fatty liver of pregnancy.

A history of gestational diabetes mellitus involves a primary pathology of insulin resistance and pancreatic insufficiency, which is distinct from the emetic pathways. While both conditions involve metabolic stress, there is no direct evidence that glucose intolerance stimulates the medullary centers or increases hCG production. Therefore, gestational diabetes does not increase the risk of intractable vomiting in the way that placental mass or genetic history does.

Advanced gestational age is not a risk factor because hyperemesis is a disease of the first trimester. By the second and third trimesters, human chorionic gonadotropin levels naturally decline and stabilize, leading to the resolution of symptoms in approximately 90% of cases. If severe vomiting persists beyond 20 weeks, clinicians must investigate secondary causes such as preeclampsia or late-onset gastrointestinal disorders.

Reduced placental mass would result in lower concentrations of human chorionic gonadotropin and estrogen, thereby decreasing the stimulus for vomiting. Conditions associated with small placentas, such as placental insufficiency or certain chromosomal abnormalities, are less likely to present with hyperemesis gravidarum. The condition is fundamentally driven by a high trophoblastic burden and excessive hormone production.

Decreased estrogen levels would likely result in a reduction of nausea symptoms rather than an increase. Estrogen is known to enhance the olfactory response, making pregnant women hyper-reactive to environmental odors and food scents. High levels of estradiol are consistently associated with the pathogenesis of severe vomiting, while low levels are generally protective against the hyperemetic state.

An ectopic pregnancy occurs when a fertilized egg implants outside the uterine cavity, most commonly in the fallopian tube. While this condition involves the production of human chorionic gonadotropin, the levels are typically lower than expected for the calculated gestational age. Low or slowly rising hormone levels are inconsistent with the pathophysiological drive behind hyperemesis, which requires high hormonal concentrations to stimulate the vomiting reflex.

Placenta previa is an obstetric complication where the placenta implants in the lower segment of the uterus, potentially covering the internal os. This is a condition associated with painless bleeding in the second or third trimester rather than hormonal surges in the first trimester. It does not involve an increase in trophoblastic mass or elevated hCG levels and is therefore unrelated to the development of hyperemesis gravidarum.

Gestational diabetes mellitus is a metabolic disorder characterized by insulin resistance and impaired glucose tolerance emerging during pregnancy. While it shares some metabolic complexities with hyperemesis, its pathogenesis is related to placental lactogen and maternal pancreatic function rather than hCG-mediated emesis. There is no clinical link between the development of gestational diabetes and the hormone-induced pathways that trigger severe first-trimester vomiting.