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Progesterone causes smooth muscle relaxation, decreased lower esophageal sphincter tone, and reduced gastrointestinal motility, which can contribute to bloating and constipation, not the primary mechanism for nausea and vomiting.

Estrogen is elevated in pregnancy and may have some role in enhancing sensitivity to odors, but its primary functions include uterine growth, increased blood flow, and breast tissue development. It does not directly stimulate the vomiting center.

Relaxin is secreted by the corpus luteum and placenta and functions mainly to relax pelvic ligaments and soften the cervix in preparation for delivery. It does not act on the gastrointestinal tract or central emetic pathways.

The Visual Analog Scale (VAS) is useful for quantifying subjective symptom intensity, such as pain, but it is not specific to pregnancy-related nausea and vomiting. It does not capture frequency or duration of emesis, making it less clinically useful in this setting.

The McGill Pain Questionnaire is designed to evaluate qualitative and quantitative aspects of pain perception. It does not assess gastrointestinal symptoms or vomiting patterns and is inappropriate for pregnancy-associated nausea.

The Bristol Stool Chart is a tool used to classify stool form into 7 types to evaluate bowel habits and diagnose constipation or diarrhea. It has no role in assessing nausea or vomiting during pregnancy.

Hot compresses are not recommended because they can increase vasodilation, worsen engorgement, and potentially elevate discomfort. They may also increase the risk of hyperthermia if applied excessively during pregnancy.

Avoiding physical activity is not a suitable intervention. Exercise is safe and beneficial in normal pregnancy, improving cardiovascular health and reducing complications. Limiting movement does not address the underlying cause of breast tenderness.

Limiting fluid intake is harmful, as adequate hydration is essential in pregnancy to maintain plasma volume, which normally expands by 40–50%. Reducing fluids does not relieve breast tenderness and increases risks of dehydration and hypotension.

Decreased renal blood flow is not present in early pregnancy. Instead, renal plasma flow increases by 50–80% due to systemic vasodilation mediated by progesterone and relaxin. Increased perfusion, not decreased, characterizes renal physiology in early gestation.

Reduced glomerular filtration rate is not correct because GFR increases by 40–50% above baseline in pregnancy, reaching values around 150–180 mL/min/1.73 m². This rise leads to increased clearance of urea, creatinine, and electrolytes. Normal non-pregnant creatinine is 0.6–1.1 mg/dL, but in pregnancy levels drop to 0.4–0.8 mg/dL due to elevated GFR.

An increase in antidiuretic hormone does not occur in early pregnancy. Instead, there is a mild resetting of the osmotic threshold for thirst and ADH secretion, but baseline ADH concentrations remain unchanged. Plasma osmolality decreases by about 10 mmol/kg, yet this does not directly cause urinary frequency.