LE3 - REVIEWER Thyroid Flashcards

Question

Which of the following complications is associated with subclinical hyperthyroidism? A. Bradycardia B. Osteopenia C. Hypothyroidism D. Decreased bone turnover

Answer 1

B. Osteopenia Rationale: Subclinical hyperthyroidism can lead to decreased bone density (osteopenia), increasing the risk of fractures due to the effects of mild thyroid hormone excess on bone metabolism.

Answer 2

C. No treatment is required Rationale: In most cases of subclinical hyperthyroidism, especially if asymptomatic, no treatment is necessary. However, the condition should be monitored for progression or complications.

Answer 3

A. Ventricular hypertrophy Rationale: Subclinical hyperthyroidism can cause cardiovascular changes, including ventricular hypertrophy, due to increased heart activity related to thyroid hormone effects on the cardiovascular system.

Answer 4

D. Adrenal insufficiency Rationale: Subclinical hyperthyroidism is not associated with adrenal insufficiency. It is primarily linked to cardiac complications (arrhythmias, ventricular hypertrophy) and bone density reduction (osteopenia).

Answer 5

C. No treatment is required; monitor thyroid function periodically. Rationale: This patient has subclinical hyperthyroidism, characterized by low TSH with normal T4 and T3 levels. Since she is asymptomatic, treatment is not needed, but her thyroid function should be monitored for any changes or progression to overt hyperthyroidism.

Answer 6

D. Cardiac arrhythmias Rationale: Subclinical hyperthyroidism is associated with an increased risk of cardiac arrhythmias, particularly in older adults with pre-existing heart conditions like atrial fibrillation. Monitoring and managing cardiac health is crucial in these patients.

Answer 7

B. Increase calcium and vitamin D intake, but no specific treatment for thyroid is needed. Rationale: Subclinical hyperthyroidism can contribute to bone loss, but antithyroid treatment is not typically recommended unless there is significant progression. Calcium and vitamin D supplementation can help manage the osteopenia while thyroid function is monitored.

Answer 8

A. Start beta-blockers for symptomatic management of palpitations. Rationale: Beta-blockers can be used to manage palpitations in patients with subclinical hyperthyroidism, especially if symptoms like tachycardia or arrhythmias occur. Antithyroid drugs or more invasive treatments are not indicated unless progression to overt hyperthyroidism occurs.

Answer 9

B. Preeclampsia Rationale: Preeclampsia is a well-known precipitating factor for thyroid storm in pregnant women, especially due to its stress on cardiovascular and metabolic systems. Precipitating Factors: Preeclampsia, anemia, and sepsis are common triggers in pregnant women with thyrotoxicosis.

Answer 10

B. Propylthiouracil (PTU) Rationale: PTU is preferred in thyroid storm as it not only blocks thyroid hormone synthesis but also inhibits the peripheral conversion of T4 to the more active T3 form.

Answer 11

A. 1-2 hours Rationale: Iodine should be administered 1-2 hours after PTU to inhibit thyroid hormone release. Administering it earlier can fuel the thyroid hormone production if hormone synthesis is not already blocked

Answer 12

B. Block peripheral conversion of T4 to T3 Rationale: Corticosteroids, such as dexamethasone, are used in thyroid storm to block the peripheral conversion of T4 to T3, which helps reduce the active thyroid hormone load in the body.

Answer 13

B. Propylthiouracil (PTU) and propranolol Rationale: PTU is the first-line treatment in thyroid storm during pregnancy, as it blocks the synthesis of thyroid hormones and inhibits T4 to T3 conversion. Propranolol is used for heart rate control.

Answer 14

B. Administer lithium carbonate Rationale: In cases of iodine anaphylaxis, lithium carbonate is used as an alternative to iodine therapy because it inhibits thyroid hormone release without triggering an allergic reaction.

Answer 15

B. Reversible heart failure if thyroid hormone levels are controlled Rationale: Thyrotoxicosis-induced cardiomyopathy is reversible once thyroid hormone levels are controlled. The heart's function can recover fully after stabilization of the hyperthyroid state.

Answer 16

B. Preterm delivery and heart failure Rationale: Uncontrolled thyroid storm in pregnancy can lead to serious complications, including preterm delivery, preeclampsia, heart failure, and perinatal mortality.

Answer 17

D. Propranolol Rationale: Propranolol is the beta-blocker of choice for controlling tachycardia in thyroid storm as it not only reduces heart rate but also inhibits peripheral conversion of T4 to T3.

Answer 18

D. Lithium carbonate Rationale: Lithium carbonate is used as an alternative to iodine in patients with iodine anaphylaxis because it inhibits thyroid hormone release without triggering an allergic reaction.

Answer 19

C. It has a rapid onset and short half-life, allowing for easy titration. Rationale: Esmolol is ideal in acute settings like thyroid storm due to its rapid onset and short duration of action, allowing for precise control of heart rate.

Answer 20

B. Block peripheral conversion of T4 to T3 Rationale: Corticosteroids like dexamethasone are used in thyroid storm to inhibit the peripheral conversion of T4 to T3, reducing the active hormone levels in circulation.

Answer 21

C. To improve cardiovascular stability Rationale: Managing precipitating factors like preeclampsia is crucial for cardiovascular stability, as pregnancy complications add strain to an already taxed cardiovascular system during thyroid storm.

Answer 22

C. Euthyroidism Rationale: In most cases, neonates born to mothers with Graves' disease are euthyroid (normal thyroid function), though around 1% may develop clinical hyperthyroidism.

Answer 23

C. Presence of thyroid-stimulating TSH-receptor antibodies in the mother Rationale: The best predictor of perinatal thyrotoxicosis is the presence of thyroid-stimulating TSH-receptor antibodies in a mother with Graves' disease. These antibodies can cross the placenta and affect the fetus.

Answer 24

A. Goitrous hypothyroidism Rationale: Goitrous hypothyroidism can occur due to maternal administration of thioamides, which can reduce fetal thyroid hormone production, causing goiter and hypothyroidism in the fetus.

Answer 25

C. Intra-amniotic thyroxine Rationale: For a hypothyroid fetus with thyromegaly, the recommended treatment is intra-amniotic thyroxine, which helps to correct the hypothyroid state.

Answer 26

A. Transplacental passage of thyrotropin receptor-blocking antibodies Rationale: Non-goitrous hypothyroidism in fetuses can result from the transplacental passage of thyrotropin receptor-blocking antibodies, which impair thyroid function without causing goiter.

Answer 27

B. Perform intra-amniotic thyroxine injection Rationale: The presence of fetal thyromegaly indicates possible hypothyroidism due to maternal thioamide therapy. The next step is to administer intra-amniotic thyroxine to correct fetal hypothyroidism.

Answer 28

B. Placental transfer of thyroid-stimulating antibodies Rationale: Fetal thyrotoxicosis in this case is likely due to the transplacental passage of thyroid-stimulating antibodies from the mother. These antibodies stimulate the fetal thyroid gland, leading to increased hormone production.

Answer 29

B. Placental transfer of maternal thioamide Rationale: The neonate's hypothyroidism is most likely due to placental transfer of methimazole (thioamide) from the mother. Thioamides can cross the placenta and inhibit thyroid hormone synthesis in the fetus, leading to hypothyroidism.

Answer 30

B. To measure fetal thyroid hormone levels Rationale: Cord blood sampling is performed to measure fetal thyroid hormone levels and assess thyroid function in utero, particularly in cases where the fetus may be hypothyroid or thyrotoxic.

Answer 31

C. Neonatal levothyroxine therapy Rationale: The neonate with hypothyroidism and goiter likely needs levothyroxine therapy to restore normal thyroid function, especially since maternal PTU therapy has likely suppressed thyroid hormone production.

Answer 32

B. Elevated levels of hCG Rationale: Hyperemesis gravidarum is associated with high levels of hCG, which can stimulate the thyroid gland, leading to increased thyroxine (T4) production and decreased TSH levels.

Answer 33

C. No treatment Rationale: Gestational thyrotoxicosis seen in hyperemesis gravidarum is transient and typically resolves by mid-pregnancy without the need for antithyroid medications.

Answer 34

B. Gestational trophoblastic disease Rationale: Gestational trophoblastic disease (GTD) leads to markedly elevated hCG levels, which overstimulate the TSH receptor, causing increased thyroid hormone production and hyperthyroidism.

Answer 35

B. They normalize by mid-pregnancy Rationale: In hyperemesis gravidarum, thyroid hormone levels (T4) typically normalize by mid-pregnancy as hCG levels decline.

Answer 36

A. Hyperthyroidism due to high levels of hCG Rationale: In gestational trophoblastic disease, the excessive hCG levels can overstimulate the TSH receptor, leading to hyperthyroidism.

Answer 37

B. Gestational thyrotoxicosis from hyperemesis gravidarum; no treatment needed Rationale: The patient’s symptoms, elevated T4, low TSH, and high hCG levels are consistent with gestational thyrotoxicosis secondary to hyperemesis gravidarum. Thyroid function typically normalizes without treatment by mid-pregnancy.

Answer 38

B. Overstimulation of the thyroid by hCG; gestational trophoblastic disease Rationale: In this case, the significantly elevated hCG due to a molar pregnancy (a form of gestational trophoblastic disease) is overstimulating the thyroid via the TSH receptor, causing hyperthyroidism.

Answer 39

A. Levels will normalize by mid-pregnancy; monitor in the second trimester Rationale: In gestational thyrotoxicosis, thyroid hormone levels typically normalize by mid-pregnancy as hCG levels decrease, so no treatment is needed, but thyroid function should be rechecked in the second trimester to confirm normalization.

Answer 40

C. hCG overstimulation of the TSH receptor; manage the molar pregnancy Rationale: The primary cause of hyperthyroidism in gestational trophoblastic disease is hCG overstimulation of the TSH receptor, leading to increased thyroid hormone production. The key to management is treating the underlying molar pregnancy, which will help normalize the thyroid function.

Answer 41

A. Thyroid function will normalize; no treatment needed Rationale: In cases of gestational thyrotoxicosis associated with hyperemesis gravidarum, thyroid function typically normalizes by mid-pregnancy without the need for treatment.

Answer 42

C. Antithyroid peroxidase antibodies (anti-TPO) Rationale: Anti-TPO antibodies cause autoimmune destruction of the thyroid gland, commonly associated with Hashimoto’s thyroiditis, making it the leading cause of hypothyroidism in pregnancy.

Answer 43

C. High TSH and normal thyroxine (T4) Rationale: Subclinical hypothyroidism is characterized by elevated TSH with normal thyroxine levels (T4), indicating that the thyroid gland is slightly underactive but still producing adequate thyroid hormone. Hypothyroidism: High TSH, low T₄ (and sometimes low T₃). Hyperthyroidism: Low TSH, high T₄ and/or T₃.

Answer 44

B. Weight loss Rationale: Weight loss is not typically seen in hypothyroidism. In contrast, hypothyroidism is more commonly associated with weight gain, fatigue, cold intolerance, and constipation.

Answer 45

B. Subclinical hypothyroidism Rationale: Subclinical hypothyroidism is more common than overt hypothyroidism in pregnancy, affecting more women (23 per 1000 pregnancies compared to 2-10 per 1000 for overt hypothyroidism).

Answer 46

B. Infertility, miscarriage, or preterm labor Rationale: Untreated overt hypothyroidism can lead to infertility, spontaneous abortion, and preterm labor due to the significant impact of thyroid hormones on pregnancy and fetal development.

Answer 47

A. Restart levothyroxine at a higher dose and monitor TSH Rationale: The patient has overt hypothyroidism, confirmed by her high TSH and low T4. The appropriate treatment is to restart levothyroxine, ensuring adequate thyroid hormone levels to support pregnancy.

Answer 48

B. Subclinical hypothyroidism; consider levothyroxine and monitor TSH Rationale: The patient’s elevated TSH and normal T4 are consistent with subclinical hypothyroidism. Levothyroxine may be considered, especially in pregnancy, to prevent complications, and TSH should be monitored regularly.

Answer 49

A. Overt hypothyroidism; risk of miscarriage or preterm labor Rationale: The patient has overt hypothyroidism, as indicated by her high TSH and low T4 levels, along with classic hypothyroid symptoms. If untreated, she is at risk for miscarriage, preterm labor, and other pregnancy complications.

Answer 50

B. Start levothyroxine and monitor TSH during pregnancy Rationale: The patient likely has subclinical hypothyroidism (elevated TSH with normal T4). During pregnancy, treatment with levothyroxine is recommended to avoid potential complications like preterm birth and impaired fetal development.

Answer 51

A. Recheck thyroid function in 6-8 weeks, initiate levothyroxine if TSH rises Rationale: The patient’s mildly elevated TSH with normal T4 is consistent with subclinical hypothyroidism. It is important to monitor thyroid function during pregnancy, as rising TSH levels may warrant levothyroxine treatment to prevent complications.

Answer 52

A. Type 1 diabetes mellitus Rationale: Type 1 diabetes mellitus is associated with autoimmune conditions, including subclinical hypothyroidism. Autoimmune diseases often coexist, increasing the risk.

Answer 53

C. TSH >10 mU/L Rationale: In cases of subclinical hypothyroidism, treatment with thyroxine is generally initiated when TSH exceeds 10 mU/L.

Answer 54

B. Increased estrogen production Rationale: Pregnancy increases the need for thyroxine due to increased estrogen production, which raises thyroid-binding globulin levels, thus increasing the demand for thyroid hormone.

Answer 55

B. Preterm birth and low birth weight Rationale: Untreated subclinical hypothyroidism in pregnancy is associated with a higher risk of preterm birth, low birth weight (LBW), and other adverse outcomes like placental abruption and stillbirths.

Answer 56

B. Subclinical hypothyroidism; monitor TSH levels and consider levothyroxine Rationale: This patient has subclinical hypothyroidism (elevated TSH, normal T4), and treatment should be considered, especially since she is pregnant, with TSH being close to the 10 mU/L threshold.

Answer 57

B. Increase the dose by 25-50 ug/day every 4-6 weeks Rationale: During pregnancy, thyroxine requirements increase due to elevated estrogen levels, so the dose of levothyroxine should be adjusted by 25-50 ug/day every 4-6 weeks to maintain normal thyroid hormone levels.

Answer 58

B. Continue the current levothyroxine dose and recheck TSH in 4-6 weeks Rationale: The patient’s current TSH and free T4 levels are within normal range, indicating that her current levothyroxine dose is adequate. TSH should be monitored every 4-6 weeks during pregnancy.

Answer 59

B. Iodine supplementation is recommended at 220 ug/day Rationale: Iodine supplementation is essential during pregnancy, with a recommended daily intake of 220 ug/day to support thyroid function and prevent iodine deficiency-related complications.

Answer 60

B. Her untreated subclinical hypothyroidism contributed to preterm birth and low birth weight Rationale: Untreated subclinical hypothyroidism during pregnancy is associated with preterm birth, low birth weight, and increased risk of NICU admissions. Thyroid function plays a significant role in fetal development and pregnancy outcomes.

Answer 61

A. Thyroid agenesis or dyshormonogenesis Rationale: Thyroid agenesis (absence of the thyroid gland) or dyshormonogenesis (abnormal thyroid hormone synthesis) accounts for 75% of cases of congenital hypothyroidism.

Answer 62

B. Levothyroxine replacement therapy Rationale: Aggressive levothyroxine replacement therapy is critical in treating congenital hypothyroidism to prevent cognitive impairments and improve long-term developmental outcomes.

Answer 63

B. Preterm infants Rationale: Preterm infants are at risk for transient hypothyroxinemia, a temporary decrease in thyroxine (T4) levels that often resolves without requiring long-term treatment.

Answer 64

B. Administer levothyroxine and monitor TSH and free T4 levels Rationale: The infant has congenital hypothyroidism due to thyroid agenesis, and the recommended treatment is levothyroxine replacement therapy to normalize thyroid hormone levels and promote normal cognitive development.

Answer 65

C. Monitor thyroid function and expect resolution without treatment Rationale: Transient hypothyroxinemia in preterm infants typically resolves on its own. These infants should be monitored rather than treated unless thyroid function worsens or symptoms develop.

Answer 66

C. Placental transfer of maternal thyroid-blocking antibodies Rationale: Transient hypothyroidism in newborns can be caused by the placental transfer of maternal thyroid-blocking antibodies, which may temporarily inhibit thyroid function but typically resolves over time.

Answer 67

C. 8% Rationale: Congenital hypothyroidism is associated with major anomalies in about 8% of cases, and these infants may have additional congenital defects, requiring a multidisciplinary approach to care.

Answer 68

C. Destructive lymphocytic thyroiditis Rationale: Postpartum thyroiditis is primarily caused by destructive lymphocytic thyroiditis, often triggered by an increase in thyroid autoantibodies.

Answer 69

C. Weight loss Rationale: Weight loss is typically associated with hyperthyroidism but is not a common symptom of postpartum thyroiditis. Symptoms include depression, palpitations, and memory impairment.

Answer 70

C. Beta-blockers Rationale: Beta-blockers are commonly used to manage the hyperthyroid symptoms of postpartum thyroiditis, such as palpitations and anxiety.

Answer 71

B. Postpartum thyroiditis; treat with beta-blockers for symptoms Rationale: This patient has postpartum thyroiditis, which can cause hyperthyroid symptoms in the early phase. Beta-blockers are the first-line treatment to manage symptoms like palpitations.

Answer 72

B. Start levothyroxine for hypothyroidism Rationale: The patient has transitioned to the hypothyroid phase of postpartum thyroiditis. Levothyroxine is indicated to treat hypothyroidism, particularly given her symptoms of fatigue and cognitive changes.

Answer 73

A. Destructive lymphocytic thyroiditis Rationale: Postpartum thyroiditis is typically caused by destructive lymphocytic thyroiditis, which is associated with autoimmune conditions such as Type 1 diabetes.

Answer 74

B. Ultrasound Rationale: Ultrasound is the preferred diagnostic tool for evaluating thyroid nodules during pregnancy because it is safe and provides detailed imaging. Radioiodine scanning is contraindicated due to the potential risks to the fetus.

Answer 75

A. Before mid-pregnancy Rationale: Fine needle aspiration (FNA) is best performed before mid-pregnancy to evaluate suspicious thyroid nodules and determine if they are benign or malignant.

Answer 76

B. 24-26 weeks gestation Rationale: Thyroidectomy for a confirmed malignant thyroid nodule should be performed during the 24-26 weeks gestation period, as this is considered the safest window for surgery during pregnancy.

Answer 77

C. 4 cm Rationale: Cystic thyroid lesions greater than 4 cm should be evaluated further to assess the risk of malignancy, although cystic lesions are less likely to be malignant compared to solid ones.

Answer 78

B. Two-fold increase in 1,25-dihydroxyvitamin D to increase calcium absorption Rationale: During pregnancy, 1,25-dihydroxyvitamin D levels increase two-fold to enhance gastrointestinal calcium absorption to meet the growing fetal demands for calcium.

Answer 79

C. Increased intestinal absorption of calcium due to elevated 1,25-dihydroxyvitamin D Rationale: During pregnancy, 1,25-dihydroxyvitamin D levels increase to improve intestinal absorption of calcium, which helps compensate for increased calcium loss through the kidneys.

Answer 80

B. 300 mg/day; increase dietary calcium and ensure adequate vitamin D intake Rationale: The fetus requires 300 mg/day of calcium in late pregnancy. The mother can meet this demand by increasing dietary calcium intake and ensuring she gets enough vitamin D for optimal calcium absorption.

Answer 81

C. Acts as a hypocalcemic hormone by opposing PTH Rationale: Calcitonin is a hypocalcemic hormone that opposes the action of PTH by inhibiting bone resorption and lowering blood calcium levels, especially during pregnancy.

Answer 82

B. Increased levels of 1,25-dihydroxyvitamin D increase maternal calcium absorption Rationale: During pregnancy, 1,25-dihydroxyvitamin D levels increase, enhancing calcium absorption from the gastrointestinal tract to ensure that the fetus receives sufficient calcium for proper development.

Answer 83

B. Primary hyperparathyroidism or cancer Rationale: Hypercalcemia in 90% of cases is due to primary hyperparathyroidism or malignancy. These conditions increase the levels of circulating calcium by increasing PTH or tumor-secreted factors that mimic PTH.

Answer 84

D. Weight gain Rationale: Common symptoms of hypercalcemia include renal calculi, stupor, pancreatitis, nausea, and vomiting. Weight gain is not typically associated with hyperparathyroidism.

Answer 85

B. Neonatal tetany Rationale: Hyperparathyroidism can lead to neonatal tetany due to severe hypocalcemia in the newborn, as well as complications such as stillbirth and preterm delivery.

Answer 86

B. Serum calcium is greater than 1.0 mg/dL above normal values Rationale: Surgical excision is indicated when serum calcium levels are greater than 1.0 mg/dL over normal values or if the patient has symptomatic adenomas.

Answer 87

A. Diuresis with normal saline or furosemide Rationale: In cases of hypercalcemic crisis, emergency treatment includes diuresis with normal saline or furosemide to lower calcium levels and prevent complications such as stupor or renal failure.

Answer 88

B. Hypercalcemia due to hyperparathyroidism; initiate diuresis with normal saline or furosemide Rationale: The patient’s elevated calcium and PTH levels along with renal calculi indicate hypercalcemia due to hyperparathyroidism. Diuresis with normal saline or furosemide is the appropriate treatment to lower calcium levels.

Answer 89

C. Diuresis with normal saline or furosemide Rationale: The patient is in a hypercalcemic crisis, requiring urgent diuresis with normal saline or furosemide to reduce her calcium levels and stabilize her condition.

Answer 90

B. Oral phosphate supplementation and surgery after delivery Rationale: In asymptomatic patients with mild hypercalcemia, oral phosphate supplementation can be used to manage calcium levels, and surgery can be postponed until after delivery unless the patient becomes symptomatic.

Answer 91

A. Preterm delivery and neonatal tetany Rationale: Hyperparathyroidism during pregnancy increases the risk of preterm delivery, stillbirth, and neonatal tetany due to severe hypocalcemia in the neonate.

Answer 92

C. Between 24-26 weeks gestation Rationale: If surgery is necessary for hyperparathyroidism, the safest time for surgical excision during pregnancy is between 24-26 weeks gestation, minimizing risk to both the mother and fetus.

Answer 93

B. Parathyroid or thyroid surgery Rationale: The most common cause of hypoparathyroidism is accidental damage or removal of the parathyroid glands during parathyroid or thyroid surgery, leading to insufficient PTH production.

Answer 94

B. Skeletal demineralization Rationale: Fetal skeletal demineralization can occur in cases of maternal hypoparathyroidism due to impaired calcium regulation and hypocalcemia.

Answer 95

C. 1,25-dihydroxyvitamin D3 Rationale: 1,25-dihydroxyvitamin D3 is the active form of vitamin D used to enhance calcium absorption in patients with hypoparathyroidism.

Answer 96

A. To prevent hyperphosphatemia, which can worsen hypocalcemia Rationale: A low-phosphate diet is recommended to prevent hyperphosphatemia

Answer 97

C. Large doses of vitamin D Rationale: Patients with hypoparathyroidism require large doses of vitamin D to maintain calcium levels due to the lack of PTH.

Answer 98

B. Hypoparathyroidism due to thyroid surgery; treat with 1,25-dihydroxyvitamin D3 and calcium Rationale: The patient has hypoparathyroidism caused by thyroid surgery, leading to hypocalcemia. The treatment includes 1,25-dihydroxyvitamin D3 and calcium supplementation to correct calcium levels.

Answer 99

C. To prevent hyperphosphatemia, which can worsen hypocalcemia Rationale: A low-phosphate diet helps prevent hyperphosphatemia, which can worsen hypocalcemia in patients with hypoparathyroidism, as phosphate competes with calcium.

Answer 100

B. Skeletal demineralization Rationale: Skeletal demineralization can occur in the fetus if the mother's hypoparathyroidism is not well controlled, leading to insufficient calcium for fetal bone development.

Answer 101

B. It enhances gastrointestinal calcium absorption Rationale: 1,25-dihydroxyvitamin D3 plays a critical role in enhancing gastrointestinal calcium absorption, which is essential for managing hypocalcemia in patients with hypoparathyroidism.

Answer 102

A. Increase her calcium and vitamin D supplementation Rationale: In hypoparathyroidism, maintaining adequate calcium and vitamin D levels is essential, especially during pregnancy. Increasing supplementation helps manage slight hypocalcemia and prevent complications.

Answer 103

B. Fractures Rationale: Pregnancy-induced osteoporosis often results in bone fractures, especially in weight-bearing bones, due to reduced bone density.

Answer 104

A. Prolonged bed rest Rationale: Prolonged bed rest reduces mechanical stress on bones, leading to decreased bone density and increasing the risk of pregnancy-induced osteoporosis. Causes Heparin use: Long-term use of heparin, particularly during pregnancy, can contribute to osteoporosis. Prolonged bed rest: Immobility can result in decreased bone density, leading to osteoporosis. Corticosteroid therapy: Long-term corticosteroid use is a well-known risk factor for osteoporosis.

Answer 105

B. Heparin Rationale: Long-term heparin use during pregnancy is associated with a higher risk of osteoporosis and bone fractures due to its effects on bone density.

Answer 106

B. Sickle cell anemia Rationale: Idiopathic osteonecrosis of the femoral head is often associated with sickle cell anemia, which can lead to poor blood supply to the bone and contribute to necrosis.

Answer 107

A. Calcium and vitamin D supplementation Rationale: The primary treatment for pregnancy-induced osteoporosis includes calcium and vitamin D supplementation to support bone health and prevent further bone loss.

Answer 108

A. Pregnancy-induced osteoporosis; treat with calcium and vitamin D supplementation Rationale: The patient’s fracture and back pain, along with her prolonged bed rest, suggest pregnancy-induced osteoporosis. Calcium and vitamin D supplementation is the appropriate treatment to support bone health.

Answer 109

B. Sickle cell anemia; treat with calcium and vitamin D Rationale: The patient’s sickle cell anemia is contributing to the development of idiopathic osteonecrosis of the femoral head. Treatment should include calcium and vitamin D to prevent further bone loss.

Answer 110

B. Heparin use; start calcium and vitamin D supplementation Rationale: Heparin use is a risk factor for pregnancy-induced osteoporosis. The recommended treatment is calcium and vitamin D supplementation to mitigate bone loss.

Answer 111

A. Corticosteroid therapy; treat with calcium and vitamin D supplementation Rationale: Corticosteroid therapy is a known risk factor for osteoporosis, especially in pregnant women. Treatment should include calcium and vitamin D to support bone health and prevent further fractures.

Answer 112

B. Calcium and vitamin D supplementation Rationale: In cases of osteonecrosis related to sickle cell anemia, treatment with calcium and vitamin D is essential to support bone health and reduce the risk of further complications.

Answer 113

A. Corticotropin-releasing hormone (CRH) Rationale: The placenta secretes CRH during pregnancy, which leads to an increase in serum corticotropin levels.

Answer 114

B. Pheochromocytoma Rationale: Pheochromocytoma, a chromaffin tumor that secretes catecholamines (e.g., adrenaline), is particularly dangerous during pregnancy due to its association with hypertensive crises.

Answer 115

D. Hypotension Rationale: Hypotension is not a common symptom of pheochromocytoma. Instead, hypertensive crises, seizures, and anxiety attacks are frequent due to excess catecholamine secretion.

Answer 116

C. 24-hour urine catecholamine metabolite quantification Rationale: During pregnancy, 24-hour urine catecholamine metabolite quantification is the preferred test to diagnose pheochromocytoma, as imaging methods like CT and MRI are avoided.

Answer 117

B. 16-20 weeks gestation Rationale: Laparoscopic adrenalectomy is recommended between 16-20 weeks gestation in cases of pheochromocytoma to manage the tumor and avoid complications later in pregnancy.

Answer 118

C. 24-hour urine catecholamine metabolite quantification Rationale: 24-hour urine catecholamine metabolite quantification is the safest and most accurate diagnostic test for pheochromocytoma during pregnancy. Imaging such as CT and MRI is avoided due to risks to the fetus.

Answer 119

A. Laparoscopic adrenalectomy Rationale: Laparoscopic adrenalectomy between 16-20 weeks gestation is the recommended treatment for pheochromocytoma to remove the tumor and prevent hypertensive crises, which pose significant risks to both the mother and fetus.

Answer 120

A. Alpha-adrenergic blockers Rationale: Alpha-adrenergic blockers are the first-line treatment for controlling hypertension in patients with pheochromocytoma. These medications help to counteract the effects of excess catecholamines.

Answer 121

A. Beta-blockers Rationale: After initiating alpha-adrenergic blockers, beta-blockers can be added to further control heart rate and reduce the risk of hypertensive episodes in patients with pheochromocytoma.

Answer 122

C. Iatrogenic corticosteroid use Rationale: Iatrogenic corticosteroid use (due to long-term treatment with corticosteroids) is the most common cause of Cushing syndrome in pregnancy.

Answer 123

B. Truncal obesity Rationale: Truncal obesity is a hallmark feature of Cushing syndrome, along with moon facies, buffalo hump, and cutaneous striae.

Answer 124

B. 24-hour urine free cortisol measurement Rationale: The 24-hour urine free cortisol measurement is the standard diagnostic test to confirm Cushing syndrome, as it reflects excess cortisol production. Diagnosis is confirmed by: Elevated 24-hour urine free cortisol levels. Elevated plasma cortisol that does not respond to dexamethasone suppression.

Answer 125

C. Preterm delivery Rationale: Untreated Cushing syndrome during pregnancy increases the risk of preterm delivery and high perinatal morbidity and mortality.

Answer 126

C. Adrenalectomy Rationale: The definitive treatment for Cushing syndrome caused by an adrenal adenoma is adrenalectomy, which removes the tumor causing excess cortisol production.

Answer 127

B. Cushing syndrome due to iatrogenic corticosteroid use Rationale: The patient’s signs (moon facies, truncal obesity, striae) and elevated cortisol levels are consistent with Cushing syndrome, most likely caused by iatrogenic corticosteroid use for her chronic autoimmune condition.

Answer 128

B. Preterm delivery Rationale: Untreated Cushing syndrome during pregnancy is associated with an increased risk of preterm delivery and high perinatal morbidity and mortality.

Answer 129

A. Laparoscopic adrenalectomy Rationale: The definitive treatment for Cushing syndrome caused by an adrenal adenoma is laparoscopic adrenalectomy, which removes the source of excess cortisol production Management includes surgical resection of adrenal or pituitary adenomas

Answer 130

A. Ketoconazole Rationale: Ketoconazole blocks steroidogenesis but can affect the male fetus by interfering with testicular function, so it must be used with caution in pregnant women.

Answer 131

B. Hypertension, gestational diabetes, and heart failure Rationale: Untreated Cushing syndrome can lead to serious maternal complications such as hypertension, gestational diabetes, and heart failure, increasing the risk of maternal death.

Answer 132

B. Hyperprolactinemia Rationale: Prolactinoma causes hyperprolactinemia, leading to symptoms such as amenorrhea and galactorrhea.

Answer 133

B. Bromocriptine Rationale: Bromocriptine, a dopamine agonist, is commonly used to treat microadenomas in prolactinoma patients, including during pregnancy, as it inhibits prolactin production.

Answer 134

C. 10 mm Rationale: A pituitary tumor is classified as a macroadenoma when it is larger than 10 mm in size.

Answer 135

B. Transnasal or transseptal endoscopic resection Rationale: The preferred surgical treatment for macroadenomas is transnasal or transseptal endoscopic resection, which is minimally invasive.

Answer 136

B. Visual disturbances Rationale: An enlarging microadenoma during pregnancy can cause visual disturbances due to compression of the optic chiasm.

Answer 137

A. Pituitary microadenoma; treat with bromocriptine Rationale: The patient has a microadenoma (8 mm) with hyperprolactinemia. The first-line treatment is bromocriptine, which is a dopamine agonist that inhibits prolactin production.

Answer 138

B. Start bromocriptine to reduce tumor size and control symptoms Rationale: Bromocriptine is the preferred treatment for a microadenoma during pregnancy, as it helps shrink the tumor and controls hyperprolactinemia to relieve symptoms.

Answer 139

B. Transnasal endoscopic resection Rationale: The patient has a macroadenoma (>10 mm) with symptoms of visual disturbances due to compression of the optic chiasm. The appropriate treatment is transnasal endoscopic resection to remove the tumor.

Answer 140

B. Start bromocriptine to reduce prolactin levels and control symptoms Rationale: Bromocriptine is a dopamine agonist and is commonly used to manage prolactinomas during pregnancy, especially for microadenomas (≤10 mm). It helps reduce prolactin levels and alleviates symptoms such as galactorrhea and headaches. Surgery is typically reserved for larger tumors (macroadenomas) or cases with significant visual disturbances or rapid tumor growth.

Answer 141

C. Transnasal or transseptal endoscopic resection Rationale: The patient has a macroadenoma (>10 mm), which is compressing nearby structures and causing visual field defects. The recommended definitive treatment is transnasal or transseptal endoscopic resection, which is a minimally invasive surgical approach to remove the tumor and relieve compression. Bromocriptine can be used for smaller tumors or to control symptoms, but surgery is necessary for larger, symptomatic tumors.

Answer 142

A. Severe obstetrical blood loss Rationale: Sheehan Syndrome occurs due to pituitary ischemia and necrosis following severe obstetrical blood loss during or after childbirth.

Answer 143

B. Hypotension and failure to lactate Rationale: Sheehan Syndrome presents with persistent hypotension and failure to lactate postpartum due to a lack of pituitary hormone production.

Answer 144

B. Hormone replacement therapy Rationale: The main treatment for Sheehan Syndrome is hormone replacement therapy, as the pituitary gland fails to produce essential hormones following ischemia.

Answer 145

B. Diabetes insipidus Rationale: Diabetes insipidus can develop in patients with Sheehan Syndrome because of damage to the pituitary gland, leading to a deficiency in antidiuretic hormone (ADH).

Answer 146

A. Transsphenoidal surgery Rationale: Transsphenoidal surgery is the surgical intervention of choice when there is optic chiasm compression due to lymphocytic hypophysitis that does not respond to corticosteroid therapy.

Answer 147

B. Sheehan Syndrome; treat with hormone replacement therapy Rationale: The patient’s symptoms, especially persistent hypotension, fatigue, and failure to lactate, along with her history of severe postpartum hemorrhage, point to Sheehan Syndrome. Hormone replacement therapy is the recommended treatment to manage hormone deficiencies.

Answer 148

A. Diabetes insipidus Rationale: Diabetes insipidus should be considered in this patient, as she exhibits symptoms of excessive thirst and frequent urination. This condition can occur due to pituitary damage in Sheehan Syndrome, leading to insufficient antidiuretic hormone (ADH) production.

Answer 149

A. Pituitary infarction due to severe postpartum hemorrhage Rationale: Sheehan Syndrome is caused by pituitary infarction due to severe postpartum hemorrhage. The patient’s symptoms, including hypotension, hypoglycemia, and failure to lactate, are characteristic of this condition.v

Answer 150

B. Perform transsphenoidal surgery Rationale: In cases of lymphocytic hypophysitis with optic chiasm compression that is unresponsive to corticosteroids, transsphenoidal surgery is the recommended treatment to relieve pressure on the optic chiasm.

Answer 151

B. Hormone replacement therapy Rationale: The mainstay of treatment for Sheehan Syndrome is hormone replacement therapy, which is necessary to replace the deficient hormones produced by the pituitary gland following ischemia and necrosis.