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Hyperplasia occurs in pregnancy, but atrophy does not. Atrophy is a reduction in cell size, which is opposite of what occurs in uterine enlargement. Muscle fibers increase in both number and size during pregnancy, making this option incorrect.

Uterine blood flow actually increases greatly in pregnancy. A decrease would compromise placental perfusion and fetal development. Normal blood flow rises from about 50 mL/min in nonpregnant state to 500–700 mL/min at term, therefore a decrease cannot explain uterine growth.

Development of new uterine cells from scratch does not occur. Instead, existing myometrial cells undergo hyperplasia and hypertrophy. Uterine cells are not newly created; the process is a modification of pre-existing smooth muscle fibers.

Increased cardiac output occurs in pregnancy due to increased blood volume and stroke volume, peaking at 30–50% above baseline. This increase improves tissue perfusion and does not cause dizziness when supine. Instead, reduced output from vena cava compression explains the symptom.

Physiological anemia in pregnancy results from plasma volume expansion exceeding red cell mass increase, leading to lower hematocrit values (normal pregnancy hemoglobin 11–12 g/dL, hematocrit 32–34%). It causes fatigue and pallor, not positional dizziness specific to lying supine.

Hyperventilation occurs due to progesterone-mediated respiratory drive increase, leading to mild respiratory alkalosis (PaCO₂ 28–32 mmHg, normal pregnancy pH 7.40–7.45). This causes dyspnea but not dizziness limited to supine position.

Decreased vascularity would make the cervix less perfused and firmer, not softer. Goodell’s sign specifically results from increased blood flow, not reduction.

Increased collagen content makes tissue more rigid and firm. In pregnancy, cervical collagen is remodeled and partially degraded, contributing to softening, not increased firmness.

Uterine contractions do not cause early cervical softening. Contractions influence cervical effacement and dilation during labor, but Goodell’s sign occurs in early pregnancy before labor begins.

Decreased clotting factors would reduce coagulation and increase the risk of bleeding, not thrombosis. Pregnancy is characterized by increased clotting factor activity, not reduction.

Increased fibrinogen levels contribute to the hypercoagulable state of pregnancy. Elevated fibrinogen enhances clot formation and is a major factor in increasing the risk of venous thromboembolism, which is one of the leading causes of maternal morbidity and mortality.

Reduced platelet count (gestational thrombocytopenia) can occur, but it is usually mild and not enough to outweigh the hypercoagulable changes. A lower platelet count actually tends toward bleeding risk, not thromboembolism.

Constipation in pregnancy is caused by decreased bowel motility and prolonged transit time due to progesterone’s effect on smooth muscle. However, it is not due to lower esophageal sphincter relaxation but rather intestinal smooth muscle relaxation.

Nausea is primarily related to increased human chorionic gonadotropin and estrogen levels, especially in the first trimester. It is not due to esophageal sphincter changes.

Gingivitis results from increased vascularity, edema, and hormonal effects on gingival tissue, often leading to bleeding gums. It is unrelated to sphincter relaxation or acid reflux.

Tidal volume does not decrease in pregnancy; it increases by 30–40% due to progesterone. A decrease would impair oxygen delivery, which is incompatible with normal pregnancy physiology.

Oxygen consumption increases by 20–30% to support maternal metabolism and fetal growth. A reduction would compromise oxygen delivery to both mother and fetus.

Functional residual capacity decreases by about 20% because the diaphragm is elevated up to 4 cm by the gravid uterus. An increase is not possible due to reduced thoracic space.

Oxytocin stimulates uterine smooth muscle contractions during labor and milk ejection from the breast. It does not influence ligament relaxation or pelvic joint mobility.

Prolactin is primarily involved in mammary gland development and initiation of lactation. It has no role in pelvic ligament relaxation or connective tissue changes in pregnancy.

Cortisol regulates metabolism and has a role in fetal lung maturation, but it does not act on pelvic ligaments or joints. Its effects are primarily catabolic and immunomodulatory, not structural relaxation.

Human placental lactogen regulates maternal glucose metabolism and increases insulin resistance to ensure fetal glucose supply. It does not act directly on neurotransmitters or cause mood swings.

Insulin regulates blood glucose by facilitating cellular glucose uptake. While hypoglycemia or hyperglycemia can cause irritability, insulin itself is not the hormonal cause of mood swings in pregnancy.

Thyroxine (T4) regulates metabolism and oxygen consumption. Abnormal thyroid hormone levels can cause anxiety or depression, but normal pregnancy mood swings are not primarily due to thyroxine.

Pregnancy-induced hypertension is a hypertensive disorder occurring after 20 weeks of gestation, defined as blood pressure ≥140/90 mmHg on two occasions. It has no relation to abdominal muscle separation and involves vascular pathophysiology, not musculoskeletal changes.

Neurological disorders affecting balance involve dysfunction of the cerebellum, vestibular system, or proprioception. Diastasis recti is purely a musculoskeletal and connective tissue condition and does not affect neural pathways or balance.

A permanent abdominal muscle tear implies actual rupture of muscle fibers. Diastasis recti does not involve tearing but rather stretching and thinning of the linea alba with separation of muscle bellies. It may improve postpartum with exercises or persist without complications of a true tear.

A 10–20% increase is too low and would not meet pregnancy demands. Such a small increase could not sustain placental blood flow or provide reserve for intrapartum hemorrhage. Scientific data consistently report expansion closer to 40–50%.

A 60–80% increase would be excessive and pathologic. This degree of hypervolemia would lead to severe hemodilution, pulmonary edema, and possible high-output cardiac failure. Physiologically, maternal cardiovascular adaptation plateaus at about 50%.

A 90–100% increase is not physiologically possible. Doubling blood volume would cause circulatory overload and profound cardiopulmonary compromise. Such levels are not compatible with normal adaptation in pregnancy.