The increase in uterine size during pregnancy is primarily due to:

Cardiovascular changes in pregnancyare adaptive responses that maintain maternal and fetal perfusion. Blood volumerises by 30–50% and cardiac outputincreases by 30–50% due to higher stroke volume and heart rate. Systemic vascular resistancedecreases from progesterone-mediated vasodilation. Physiological anemiaresults from disproportionate plasma expansion. The maternal state becomes hypercoagulableto prevent postpartum hemorrhage, with increased clotting factors VII, VIII, IX, X, and fibrinogen.

Rationale for correct answers

1.Blood volume increases 30–50% to sustain uteroplacental circulation and provide a reserve for delivery blood loss. This is a normal physiologic change.

3.Physiological anemia occurs because plasma volume rises more than red cell mass. Hematocrit falls to 32–42% and hemoglobin to 11–12 g/dL, producing dilutional anemia.

5.Pregnancy is a hypercoagulable state due to increased coagulation factors and fibrinogen, which lowers fibrinolytic activity. This adaptation reduces postpartum hemorrhage risk but raises thromboembolism risk.

Rationale for incorrect answers

2.Cardiac output does not decrease. Instead, it rises by 30–50% from increased heart rate and stroke volume, peaking in mid-pregnancy. A decrease would compromise placental perfusion.

4.Systemic vascular resistance does not increase. Progesterone and prostaglandins cause vasodilation, lowering resistance to accommodate higher blood volume without severe hypertension. An increase would predispose to preeclampsia.

Take home points

• Blood volume and cardiac output increase significantly in pregnancy.

• Physiologic anemia develops due to disproportionate plasma expansion.

• Pregnancy induces a hypercoagulable state to prevent hemorrhage but raises clotting risk.

• Systemic vascular resistance decreases, distinguishing normal adaptation from hypertensive disorders.

Renal changes in pregnancyoccur due to hormonal and mechanical effects. Glomerular filtration rate (GFR)increases by 40–50% from early pregnancy, lowering serum creatinine (0.4–0.7 mg/dL) and blood urea nitrogen (BUN) (7–12 mg/dL vs non-pregnant 10–20 mg/dL). Urinary frequencyresults from increased GFR and bladder compression by the uterus. Progesteronecauses smooth muscle relaxation, leading to dilation of the renal pelvesand ureters, increasing stasis and risk for urinary tract infections. Mild glycosuriamay appear due to lower renal glucose threshold but does not always indicate gestational diabetes.

Rationale for correct answers

1.GFR increases 40–50% beginning early in pregnancy due to renal vasodilation and higher plasma volume. This is a physiologic adaptation.

2.Urinary frequency is common because of increased GFR and mechanical compression of the bladder by the enlarging uterus.

3.Dilation of renal pelves and ureters, known as hydronephrosis of pregnancy, occurs from progesterone-induced smooth muscle relaxation and uterine pressure. This increases UTI risk.

Rationale for incorrect answers

4.Serum creatinine and BUN do not increase. Instead, both decrease due to higher GFR. Normal serum creatinine in pregnancy is 0.4–0.7 mg/dL compared to 0.6–1.1 mg/dL in non-pregnant women. BUN decreases to 7–12 mg/dL.

5.Glycosuria does not always indicate gestational diabetes. It is often physiologic due to decreased renal threshold for glucose excretion. Only persistent or high-level glycosuria warrants further evaluation with glucose tolerance testing.

Take home points

• GFR increases 40–50% in pregnancy, lowering creatinine and BUN levels.

• Urinary frequency is due to both increased filtration and uterine compression.

• Ureteral and pelvic dilation increase the risk for urinary tract infections.

• Mild glycosuria is physiologic, but persistent glycosuria needs evaluation for gestational diabetes.