A. 2+ Deep Tendon Reflexes. A 2+ deep tendon reflex is considered normal and does not indicate worsening preeclampsia. Severe preeclampsia is often associated with hyperreflexia, typically 3+ or 4+, which can signal worsening central nervous system involvement and an increased risk for seizures.

B. Platelets of 20,000. A platelet count of 20,000 is dangerously low and suggests the development of HELLP syndrome, a severe complication of preeclampsia that includes hemolysis, elevated liver enzymes, and low platelets. This condition increases the risk of spontaneous bleeding and requires immediate medical intervention.

C. Urine output of 75 ml per hour. A urine output of 75 mL per hour is adequate and does not indicate worsening kidney function. In severe preeclampsia, oliguria (urine output less than 30 mL per hour) is a more concerning sign, as it suggests impaired renal perfusion and possible acute kidney injury.

D. 1+ Proteinuria. While proteinuria is a key feature of preeclampsia, a 1+ reading is mild and not necessarily indicative of worsening disease. Severe preeclampsia is typically associated with proteinuria of 3+ or higher, along with other symptoms such as hypertension, headache, and visual disturbances.

A. Right-sided epigastric pain. Epigastric pain, especially on the right side, is a concerning sign of preeclampsia and may indicate liver involvement due to elevated liver enzymes or HELLP syndrome. This symptom should be assessed further as it suggests worsening disease progression.

B. Uterine contractions. Uterine contractions are not a defining feature of preeclampsia. They are more commonly associated with preterm labor rather than hypertension-related complications. While preeclampsia can lead to preterm birth, contractions alone do not confirm or negate the condition.

C. Bright red painless vaginal bleeding. Bright red painless vaginal bleeding is more indicative of placenta previa or another obstetric complication rather than preeclampsia. Preeclampsia primarily presents with hypertension, proteinuria, and systemic symptoms rather than vaginal bleeding.

D. Severe headache. A severe headache is a classic symptom of preeclampsia, often due to elevated blood pressure and cerebral edema. Persistent headaches that do not resolve with usual interventions should be evaluated promptly as they may indicate worsening hypertension or an impending seizure.

E. Visual disturbances. Visual disturbances such as blurred vision, photophobia, or seeing spots are common in preeclampsia and can signal cerebral edema or increased intracranial pressure. This is a significant warning sign requiring immediate assessment.

F. Dull backache. A dull backache is more commonly associated with musculoskeletal strain, labor, or a urinary tract infection rather than preeclampsia. While discomfort can be present in pregnancy, it is not a defining symptom of preeclampsia.

A. "An ectopic pregnancy does not need major treatment and can be delivered vaginally." This statement is incorrect. An ectopic pregnancy involves the fertilized ovum implanting outside the uterus, most commonly in a fallopian tube, which poses serious risks to the mother. The pregnancy cannot be carried to term, and it requires prompt medical intervention, such as medication or surgery, to prevent life-threatening complications.
B. "An ectopic pregnancy involves a fertilized ovum outside the uterus that cannot be transferred to the uterus." This is an accurate explanation of an ectopic pregnancy. The fertilized egg implants outside the uterus, most commonly in the fallopian tubes, and cannot develop into a viable pregnancy. The condition requires immediate treatment to prevent tube rupture and internal bleeding.
C. "An ectopic pregnancy involves a cancerous fertilized ovum in either fallopian tube." This is incorrect. An ectopic pregnancy is not cancerous. It refers to a pregnancy where the fertilized ovum implants in an abnormal location outside the uterus, most commonly the fallopian tubes, not involving cancerous growth.
D. "An ectopic pregnancy involves a fertilized ovum in the vagina." This statement is incorrect. An ectopic pregnancy occurs when the fertilized ovum implants outside the uterus, but it does not implant in the vagina. The condition most commonly involves the fallopian tubes but can also occur in other locations such as the cervix, ovary, or abdominal cavity.

A. Diuresis. Increased urine output is a positive sign in a postpartum woman with preeclampsia, indicating that fluid shifts are occurring and the kidneys are functioning well. Magnesium sulfate does not cause fluid retention, and diuresis is not a major concern at this time.

B. Hypotension. While magnesium sulfate can cause vasodilation, leading to a mild decrease in blood pressure, severe hypotension is not the primary concern. The main hemodynamic concern postpartum is ensuring adequate uterine tone and preventing hemorrhage.

C. Increased risk for seizures. Magnesium sulfate is given to prevent eclampsia-related seizures, and its continued administration postpartum helps reduce seizure risk. The risk of seizures decreases after delivery, but stopping the infusion too early could increase the risk, making this a secondary rather than primary concern.

D. Excessive uterine bleeding. Magnesium sulfate relaxes smooth muscle, including the uterus, which can lead to uterine atony and increased postpartum hemorrhage risk. This is a critical concern in the immediate postpartum period, as uterine atony can result in life-threatening blood loss requiring urgent intervention.

A. Quantity of vaginal bleeding. While both placenta previa and abruptio placentae can cause vaginal bleeding, the amount alone does not differentiate between the two conditions. Placenta previa typically causes painless, bright red bleeding, whereas abruptio placentae often presents with concealed or variable bleeding, making quantity an unreliable distinguishing factor.

B. Presence of abdominal pain. Abdominal pain is a key differentiating factor. Placenta previa is characterized by painless vaginal bleeding, while abruptio placentae causes sudden, severe abdominal pain due to placental detachment and uterine muscle irritation. This makes the presence or absence of pain an important assessment finding.

C. Leopold's maneuver results. While Leopold’s maneuvers help determine fetal position and presentation, they do not provide definitive information about the location of the placenta or differentiate between placenta previa and abruptio placentae. Ultrasound is a more reliable diagnostic tool for this purpose.

D. Maternal blood pressure. Although abruptio placentae can lead to hypovolemic shock and blood pressure changes due to hemorrhage, maternal blood pressure alone is not a primary diagnostic criterion for differentiating between the two conditions. Other clinical findings such as pain and ultrasound results are more useful for diagnosis.

A. Oligohydramnios. Oligohydramnios, or low amniotic fluid levels, is not a primary complication of pregestational diabetes. It is more commonly associated with conditions such as fetal growth restriction, post-term pregnancy, and rupture of membranes rather than maternal hyperglycemia.

B. Congenital fetal anomalies. Poor glycemic control during preconception and early pregnancy increases the risk of congenital anomalies, particularly affecting the heart, spine, and central nervous system. Hyperglycemia during organogenesis (first 8 weeks of gestation) can lead to defects such as neural tube defects and cardiac malformations.

C. Intrauterine fetal seizures. Fetal seizures in utero are extremely rare and are not a common complication of maternal diabetes. While neonatal hypoglycemia after birth can lead to seizures, maternal hyperglycemia does not directly cause seizures in the fetus.

D. Polyhydramnios. While polyhydramnios (excess amniotic fluid) can occur in pregnancies complicated by diabetes due to fetal polyuria, it is more associated with later pregnancy. The question specifically asks about preconception and early pregnancy risks, making congenital anomalies the best answer.

A. Treat opportunistic infections. Antiretroviral drugs do not directly treat opportunistic infections. They help suppress the HIV virus, which in turn strengthens the immune system, reducing the risk of opportunistic infections, but specific infections require separate antimicrobial treatment.

B. Supplement radiation and chemotherapy. Antiretroviral therapy (ART) is not used as a supplement to radiation or chemotherapy. While HIV-positive patients can develop certain cancers like Kaposi’s sarcoma, ART is aimed at controlling HIV rather than being a direct cancer treatment.

C. Decrease viral loads in the blood. Antiretroviral drugs work by suppressing HIV replication, thereby decreasing viral load in the bloodstream. This helps maintain immune function, reduces the risk of perinatal transmission, and improves overall health outcomes. Consistent use of ART can even lower viral loads to undetectable levels, significantly reducing transmission risk.

D. Cure acute HIV/AIDS infections. There is no cure for HIV/AIDS. Antiretroviral therapy helps manage the disease by reducing viral replication and preventing progression to AIDS, but it does not eradicate the virus from the body. Lifelong adherence to ART is necessary for disease control.

A. Preterm labor. Methotrexate is not used for preterm labor. Medications such as tocolytics (e.g., nifedipine, magnesium sulfate, or terbutaline) are typically used to delay labor and improve neonatal outcomes, but methotrexate does not serve this purpose.

B. Abruptio placentae. Methotrexate is not indicated for abruptio placentae, which is the premature separation of the placenta from the uterine wall. Management of abruptio placentae focuses on stabilizing the mother, monitoring fetal well-being, and delivering the baby if necessary.

C. Pre-eclampsia. Methotrexate does not treat pre-eclampsia. The management of pre-eclampsia includes antihypertensive medications, magnesium sulfate for seizure prevention, and delivery of the baby when indicated.

D. Unruptured ectopic pregnancy. Methotrexate is the first-line treatment for an unruptured ectopic pregnancy. It works by inhibiting rapidly dividing trophoblastic cells, stopping the growth of the ectopic pregnancy while preserving the fallopian tube. It is only used in stable patients with small, unruptured ectopic pregnancies and no signs of internal bleeding.

A. Maintaining euglycemia in labor reduces the need for insulin postpartum. While insulin requirements typically decrease after delivery due to the loss of placental hormones that cause insulin resistance, the primary reason for tight glucose control during labor is to prevent neonatal complications rather than reducing postpartum insulin needs.

B. A blood glucose level above 110 puts the client at risk for infection in labor. Poorly controlled diabetes can increase infection risk over time, but transient hyperglycemia in labor is not a direct cause of infection. The focus of glucose management during labor is to prevent neonatal hypoglycemia rather than maternal infection.

C. More insulin will be available for fetal use via placental transfer. Insulin does not cross the placenta, so maternal insulin therapy does not provide insulin to the fetus. However, maternal hyperglycemia leads to increased fetal insulin production, which can cause neonatal hypoglycemia after birth.

D. An elevated blood glucose in labor increases the risk of neonatal hypoglycemia. Maternal hyperglycemia causes the fetus to produce excessive insulin in utero. After birth, when the maternal glucose supply is suddenly cut off, the infant’s high insulin levels can cause a rapid drop in blood glucose, leading to neonatal hypoglycemia, which can be dangerous if not managed properly.

A. Consuming more calories covers the insulin secreted by the fetus. The fetus does not secrete insulin to regulate maternal glucose levels. Instead, the maternal pancreas produces insulin in response to blood sugar levels, but in diabetes, maternal insulin resistance leads to excess glucose being transferred to the fetus.

B. Fetal weight gain increases as a result of the common response of maternal overeating. While some women with diabetes may have increased caloric intake, this is not the primary reason for fetal macrosomia (large birth weight). The major factor is maternal hyperglycemia leading to excess fetal insulin production and fat deposition.

C. Extra circulating glucose causes the fetus to acquire fatty deposits. In diabetic pregnancies, excess maternal glucose crosses the placenta, leading to fetal hyperinsulinemia. The increased insulin promotes fat storage and excessive fetal growth, leading to macrosomia, which increases the risk of birth complications such as shoulder dystocia.

D. Taking exogenous insulin stimulates fetal growth. Insulin does not cross the placenta, so maternal insulin therapy does not directly affect fetal growth. Instead, fetal macrosomia results from prolonged exposure to maternal hyperglycemia, which causes the fetus to produce excessive insulin and store extra fat.