LE3 - REVIEWER Thyroid Flashcards
Which of the following statements about thyroid physiology in pregnancy is correct?
A. Thyroid hormone is not essential for fetal brain development until after the fetal thyroid gland is functional.
B. Maternal serum thyroid-stimulating hormone (TSH) increases significantly in early pregnancy due to increased metabolic demands.
C. Human chorionic gonadotropin (hCG) can weakly stimulate TSH receptors, leading to lower TSH levels in early pregnancy.
D. Maternal thyroid hormone does not cross the placenta, so fetal thyroid development is independent of maternal thyroid function.
C. Human chorionic gonadotropin (hCG) can weakly stimulate TSH receptors, leading to lower TSH levels in early pregnancy.
Rationale: hCG structurally mimics TSH and can stimulate TSH receptors, causing a transient decrease in maternal TSH levels during early pregnancy. Maternal thyroid hormone is essential for fetal brain development, especially before the fetal thyroid becomes functional.
Which of the following changes occurs in maternal thyroid function during the first trimester of pregnancy?
A. Decreased production of thyroxine-binding globulin (TBG)
B. Increased secretion of thyrotropin-releasing hormone (TRH)
C. Decreased TSH levels due to hCG stimulation of TSH receptors
D. Decreased free thyroxine (T4) levels
C. Decreased TSH levels due to hCG stimulation of TSH receptors
Rationale: During early pregnancy, the increase in hCG causes a decrease in TSH levels due to weak stimulation of TSH receptors. Thyroxine-binding globulin (TBG) levels increase, and free T4 levels initially rise, leading to the suppression of TRH.
What percentage of fetal thyroxine (T4) is derived from maternal sources after the fetal thyroid gland begins functioning?
A. 10%
B. 20%
C. 30%
D. 50%
C. 30%
Rationale: Approximately 30% of fetal thyroxine (T4) comes from maternal sources even after the fetal thyroid begins synthesizing its own thyroid hormone. This maternal contribution is critical for normal brain development.
What is the primary reason for a decrease in maternal TSH levels in early pregnancy?
A. Increased production of thyrotropin-releasing hormone (TRH)
B. Increased thyroid hormone production by the fetus
C. Weak stimulation of TSH receptors by high levels of hCG
D. Direct suppression by progesterone
C. Weak stimulation of TSH receptors by high levels of hCG
Rationale: hCG, produced in large quantities during early pregnancy, has a structural similarity to TSH, leading to weak stimulation of the TSH receptor and resulting in lower maternal TSH levels.
A 28-year-old woman in her first trimester of pregnancy presents for a routine prenatal visit. She reports mild fatigue but denies any other symptoms. Her laboratory results show slightly elevated free T4 levels and a decreased TSH level. She is concerned about these findings and asks if they will affect her pregnancy.
Question: What is the most likely explanation for her lab results, and what advice should you provide her?
A. She has subclinical hyperthyroidism and should be started on antithyroid medications.
B. This is a normal physiological change in early pregnancy due to elevated hCG levels, and no treatment is necessary.
C. She has overt hypothyroidism, and levothyroxine should be initiated.
D. These results suggest Graves’ disease, and she should be referred to an endocrinologist for further evaluation.
B. This is a normal physiological change in early pregnancy due to elevated hCG levels, and no treatment is necessary.
Rationale: In early pregnancy, hCG can cause a mild increase in free T4 and suppression of TSH. This is a normal physiological response, and treatment is not required unless other symptoms or significant thyroid dysfunction is present.
A 32-year-old woman with a history of Graves’ disease that was treated with radioiodine therapy two years ago becomes pregnant. She is currently asymptomatic. During her first prenatal visit, her TSH is found to be low, and free T4 is slightly elevated.
Question: What is the most appropriate next step in managing her thyroid function during pregnancy?
A. Start her on a low dose of methimazole.
B. Continue to monitor her thyroid function closely without starting any treatment.
C. Initiate high-dose propylthiouracil (PTU) to control her thyroid hormone levels.
D. Administer iodine supplementation to reduce thyroid hormone production.
B. Continue to monitor her thyroid function closely without starting any treatment.
Rationale: Pregnancy often leads to a remission of Graves’ disease due to the immune modulation that occurs during this period. The mildly elevated free T4 and low TSH could be due to hCG-related TSH suppression rather than recurrent Graves’ disease, so close monitoring without immediate treatment is recommended unless overt hyperthyroidism develops.
A 25-year-old pregnant woman at 10 weeks of gestation presents with fatigue, weight gain, and cold intolerance. Her thyroid function tests reveal an elevated TSH level and low free T4.
Question: What is the potential risk to her fetus if her hypothyroidism is not properly treated during pregnancy?
A. Increased risk of fetal hyperthyroidism
B. Increased risk of fetal hypothyroidism and impaired brain development
C. Increased maternal risk of postpartum thyroiditis
D. Increased fetal risk of congenital heart disease
B. Increased risk of fetal hypothyroidism and impaired brain development
Rationale: Untreated maternal hypothyroidism can lead to inadequate thyroid hormone transfer to the fetus, which is critical for normal brain development, especially before the fetal thyroid begins functioning around 12 weeks of gestation.
Which of the following best describes the pathophysiology of Graves’ disease?
A. Thyroid-stimulating blocking antibodies prevent the thyroid from producing hormones.
B. Thyroid-stimulating autoantibodies attach to thyrotropin receptors, causing hyperthyroidism.
C. Thyroid peroxidase antibodies destroy thyroid tissue, leading to hypothyroidism.
D. Fetal lymphocytes attack the maternal thyroid, causing thyroid dysfunction.
B. Thyroid-stimulating autoantibodies attach to thyrotropin receptors, causing hyperthyroidism.
Rationale: In Graves’ disease, thyroid-stimulating autoantibodies bind to the TSH receptor and activate it, causing overproduction of thyroid hormones and thyroid gland enlargement.
Thyroid peroxidase antibodies (TPO-Ab) are associated with which of the following pregnancy complications?
A. Preeclampsia
B. Gestational diabetes
C. Placental abruption and increased risk of abortion
D. Macrosomia
C. Placental abruption and increased risk of abortion
Rationale: TPO antibodies are present in 10-20% of pregnant women and are associated with autoimmune thyroiditis, which can lead to thyroid failure, increased risk of abortion, and placental abruption.
Which mechanism explains why autoimmune thyroid disease is more common in females than males?
A. Women have higher estrogen levels, which stimulate thyroid antibodies.
B. Fetal lymphocytes persist in the maternal circulation, leading to immune dysregulation.
C. Male fetuses transfer autoimmune antibodies to the mother during pregnancy.
D. Females have a stronger immune system that is more prone to attack the thyroid.
B. Fetal lymphocytes persist in the maternal circulation, leading to immune dysregulation.
Rationale: Fetal-to-maternal cell trafficking allows fetal lymphocytes to persist in maternal circulation for up to 20 years, contributing to the development of autoimmune thyroid diseases in women.
Which autoimmune thyroid disease is potentially caused by the maternal microchimerism of male fetal cells expressing the SRY sex-determining gene?
A. Graves’ disease
B. Hashimoto’s thyroiditis
C. Subacute thyroiditis
D. Papillary thyroid carcinoma
B. Hashimoto’s thyroiditis
Rationale: Maternal microchimerism, where male fetal cells expressing the SRY gene remain in maternal circulation, has been linked to the development of Hashimoto’s thyroiditis, an autoimmune thyroid condition.
Case Scenario:
A 30-year-old pregnant woman in her first trimester presents with fatigue, weight loss, and palpitations. Her thyroid function tests show low TSH and elevated free T4. She also tests positive for thyroid-stimulating autoantibodies.
Question: What is the most likely diagnosis and the underlying mechanism of her condition?
A. Hashimoto’s thyroiditis; thyroid destruction by thyroid peroxidase antibodies.
B. Graves’ disease; activation of thyrotropin receptors by thyroid-stimulating autoantibodies.
C. Subacute thyroiditis; inflammation of the thyroid gland causing hormone release.
D. Euthyroid; physiological changes in pregnancy leading to temporary thyroid hormone imbalance.
B. Graves’ disease; activation of thyrotropin receptors by thyroid-stimulating autoantibodies.
Rationale: The patient presents with classic hyperthyroid symptoms (weight loss, palpitations, fatigue), and her lab results show low TSH and high T4. The presence of thyroid-stimulating autoantibodies indicates Graves’ disease, where these antibodies activate the TSH receptor, causing hyperthyroidism.
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A 35-year-old woman with a history of Hashimoto’s thyroiditis presents to the clinic at 20 weeks of pregnancy. Her thyroid peroxidase antibody (TPO-Ab) test is positive. She is concerned about how this may affect her pregnancy.
Question: What is the most appropriate counseling for this patient regarding the risks associated with TPO antibodies in pregnancy?
A. TPO antibodies will likely cause hyperthyroidism, increasing the risk of preeclampsia.
B. TPO antibodies may lead to thyroid failure, increasing the risk of abortion and placental abruption.
C. TPO antibodies are benign and have no effect on the pregnancy outcome.
D. TPO antibodies will cause congenital hypothyroidism in the fetus.
B. TPO antibodies may lead to thyroid failure, increasing the risk of abortion and placental abruption.
Rationale: TPO antibodies are associated with autoimmune thyroiditis and thyroid failure. This increases the risk of pregnancy complications such as abortion and placental abruption, and the patient should be monitored closely for thyroid function throughout the pregnancy.
A 32-year-old woman with a history of three pregnancies, including one male child, presents with fatigue and weight gain 18 months postpartum. She reports a strong family history of autoimmune diseases. Laboratory testing reveals elevated TSH and positive TPO antibodies.
Question: What is the most likely diagnosis, and what mechanism might explain the development of her condition?
A. Graves’ disease; thyroid-stimulating antibodies cross-reacting with fetal antigens.
B. Subacute thyroiditis; inflammation from fetal microchimerism.
C. Hashimoto’s thyroiditis; fetal lymphocytes from her male child contributing to autoimmune thyroiditis.
D. Postpartum thyroiditis; normal fluctuation of thyroid hormones after pregnancy.
C. Hashimoto’s thyroiditis; fetal lymphocytes from her male child contributing to autoimmune thyroiditis.
Rationale: The patient’s elevated TSH and positive TPO antibodies suggest Hashimoto’s thyroiditis, an autoimmune thyroid disease. The mechanism may involve maternal microchimerism, where fetal lymphocytes from her male child persist in her circulation and contribute to the autoimmune process.
What is the most common symptom of hyperthyroidism in pregnancy?
A. Weight gain despite increased appetite
B. Bradycardia
C. Tachycardia with elevated sleeping pulse rate
D. Hypotension
C. Tachycardia with elevated sleeping pulse rate
Rationale: Tachycardia, especially during rest (elevated sleeping pulse rate), is a hallmark sign of hyperthyroidism in pregnancy due to the overproduction of thyroid hormones.
Which thioamide drug is preferred for treating hyperthyroidism during the first trimester of pregnancy?
A. Methimazole
B. Propylthiouracil (PTU)
C. Levothyroxine
D. Radioactive iodine
B. Propylthiouracil (PTU)
Rationale: PTU is the preferred treatment for hyperthyroidism in the first trimester due to a lower risk of teratogenic effects compared to methimazole, which is associated with birth defects when used early in pregnancy.
Which of the following is a known adverse effect of propylthiouracil (PTU) that warrants discontinuation of the drug?
A. Transient leukopenia
B. Agranulocytosis
C. Mild rash
D. Weight gain
B. Agranulocytosis
Rationale: Agranulocytosis, a severe decrease in white blood cell count, is a rare but serious side effect of PTU. The drug should be discontinued immediately if the patient develops symptoms such as fever or sore throat, which may indicate this condition.
Why is methimazole avoided during the first trimester of pregnancy?
A. It causes hepatotoxicity in the mother.
B. It is associated with fetal congenital defects such as esophageal atresia and aplasia cutis.
C. It is ineffective at controlling hyperthyroidism.
D. It causes maternal hypothyroidism.
B. It is associated with fetal congenital defects such as esophageal atresia and aplasia cutis.
Rationale: Methimazole is associated with specific congenital malformations, including esophageal atresia and aplasia cutis, when used in the first trimester. Therefore, it is avoided during early pregnancy and preferred in the second trimester.
Which of the following treatments for hyperthyroidism is contraindicated in pregnancy?
A. Propylthiouracil (PTU)
B. Methimazole
C. Subtotal thyroidectomy
D. Radioactive iodine ablation
D. Radioactive iodine ablation
Rationale: Radioactive iodine ablation is contraindicated during pregnancy because it can destroy the fetal thyroid gland and result in fetal hypothyroidism or abortion.
Case Scenario:
A 26-year-old woman, who is 10 weeks pregnant, presents with palpitations, weight loss despite adequate food intake, and tremors. Her physical exam reveals tachycardia, a mildly enlarged thyroid gland, and mild exophthalmos. Laboratory results show elevated free T4 and suppressed TSH levels.
Question: What is the most appropriate initial treatment for this patient?
A. Methimazole 10-40 mg/day
B. Radioactive iodine therapy
C. Propylthiouracil (PTU) 50-150 mg 3 times daily
D. Subtotal thyroidectomy
C. Propylthiouracil (PTU) 50-150 mg 3 times daily
Rationale: PTU is the preferred treatment for hyperthyroidism in the first trimester of pregnancy due to its lower risk of causing fetal malformations. Methimazole should be avoided during this period due to its association with congenital defects.
1=0-13
2=14-27
3=28-37
A 32-year-old pregnant woman in her second trimester is being treated for hyperthyroidism with propylthiouracil (PTU). During her follow-up visit, she reports a sore throat and fever. Her lab work shows a low white blood cell count.
Question: What is the next best step in management?
A. Continue PTU and monitor her symptoms.
B. Discontinue PTU and initiate methimazole.
C. Refer the patient for radioactive iodine therapy.
D. Increase the PTU dose and repeat blood work in 2 weeks.
B. Discontinue PTU and initiate methimazole.
Rationale: The patient’s symptoms and low white blood cell count suggest agranulocytosis, a known side effect of PTU. The drug should be discontinued, and methimazole, which is safer in the second trimester, should be started.
A 30-year-old woman who is 25 weeks pregnant is diagnosed with uncontrolled hyperthyroidism. Despite medical therapy with PTU, her symptoms persist. After discussing treatment options, the decision is made to proceed with surgery.
Question: What is the most appropriate timing for performing a subtotal thyroidectomy in this patient?
A. First trimester
B. Second trimester
C. Third trimester
D. Immediately postpartum
B. Second trimester
Rationale: If surgery is required for hyperthyroidism during pregnancy, the second trimester is the safest time to perform a thyroidectomy because it minimizes the risks to both the mother and fetus. Surgery is generally avoided during the first and third trimesters due to the higher risks of miscarriage and preterm labor.
A 28-year-old pregnant woman in her third trimester presents with a history of hyperthyroidism managed with methimazole. At a routine prenatal visit, her physician expresses concern that the baby may have been exposed to the drug.
Question: What complication should be considered in the newborn due to methimazole exposure?
A. Fetal hypothyroidism
B. Congenital aplasia cutis
C. Hyperthyroidism
D. Fetal thyroid gland destruction
B. Congenital aplasia cutis
Rationale: Methimazole use during the first trimester is associated with congenital malformations, including aplasia cutis, a condition characterized by the absence of a portion of the skin. This is why methimazole is avoided in the first trimester, although it is considered safe in later stages of pregnancy.
What is the characteristic laboratory finding in subclinical hyperthyroidism?
A. Elevated TSH with normal T4 and T3 levels
B. Low TSH with normal T4 and T3 levels
C. Elevated TSH with elevated T4 levels
D. Low TSH with elevated T4 levels
B. Low TSH with normal T4 and T3 levels
Rationale: Subclinical hyperthyroidism is defined by a low TSH level with normal thyroid hormone (T4 and T3) levels. This differentiates it from overt hyperthyroidism, where T4 and/or T3 levels would be elevated.
Which of the following complications is associated with subclinical hyperthyroidism?
A. Bradycardia
B. Osteopenia
C. Hypothyroidism
D. Decreased bone turnover
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.
What is the most appropriate management for a patient diagnosed with subclinical hyperthyroidism and no significant symptoms?
A. Start antithyroid medications
B. Radioactive iodine ablation
C. No treatment is required
D. Thyroidectomy
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.
Which of the following cardiovascular conditions can occur due to subclinical hyperthyroidism?
A. Ventricular hypertrophy
B. Myocardial infarction
C. Pericarditis
D. Atrial stenosis
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.
Which of the following is NOT a known potential consequence of subclinical hyperthyroidism?
A. Cardiac arrhythmias
B. Osteopenia
C. Ventricular hypertrophy
D. Adrenal insufficiency
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).
Case Scenario:
A 65-year-old woman with no significant medical history is found to have a serum TSH level of 0.2 mU/L (reference range: 0.4-4.0 mU/L) during routine blood work. Her free T4 and T3 levels are within normal limits. She reports feeling well with no symptoms of hyperthyroidism.
Question: What is the most appropriate next step in managing this patient?
A. Start her on methimazole.
B. Perform a radioactive iodine uptake scan.
C. No treatment is required; monitor thyroid function periodically.
D. Refer for thyroidectomy.
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.
A 70-year-old man with a history of atrial fibrillation presents for a follow-up visit. Recent laboratory tests show a low TSH level of 0.1 mU/L, with normal T4 and T3 levels. He is concerned about the potential risks of his thyroid condition.
Question: What complication is most likely associated with his subclinical hyperthyroidism and should be closely monitored?
A. Bradycardia
B. Osteoporosis
C. Progression to hypothyroidism
D. Cardiac arrhythmias
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.
A 60-year-old woman with subclinical hyperthyroidism presents with a bone density scan showing signs of osteopenia. She is concerned about her thyroid condition contributing to bone loss.
Question: What is the best advice regarding the management of her subclinical hyperthyroidism in light of her osteopenia?
A. Start treatment with antithyroid medication to prevent further bone loss.
B. Increase calcium and vitamin D intake, but no specific treatment for thyroid is needed.
C. Schedule thyroid surgery to prevent complications.
D. Start her on radioactive iodine therapy.
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.
A 55-year-old woman presents with palpitations and a recent diagnosis of subclinical hyperthyroidism. Her TSH is 0.3 mU/L, and her T4 and T3 levels are normal. She is asymptomatic aside from occasional palpitations.
Question: What is the most appropriate management plan for this patient at this stage?
A. Start beta-blockers for symptomatic management of palpitations.
B. Prescribe methimazole to normalize TSH levels.
C. Refer her for radioactive iodine ablation therapy.
D. Perform a subtotal thyroidectomy.
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.
Which of the following is a common precipitating factor for thyroid storm in pregnant women?
A. Gestational diabetes
B. Preeclampsia
C. Hyperemesis gravidarum
D. Iron deficiency
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.
Which of the following is the most appropriate first-line treatment to block thyroid hormone synthesis during a thyroid storm?
A. Methimazole
B. Propylthiouracil (PTU)
C. Radioactive iodine
D. Lugol solution
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.
In the management of thyroid storm, iodine should be administered after what duration following PTU therapy?
A. 1-2 hours
B. 12-24 hours
C. 24-48 hours
D. Immediately after PTU
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
What is the primary goal of corticosteroid therapy in thyroid storm?
A. Block the release of thyroid hormone from the thyroid gland
B. Block peripheral conversion of T4 to T3
C. Promote renal clearance of excess thyroid hormone
D. Stimulate the synthesis of thyroid hormone
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.
A 30-year-old woman who is 33 weeks pregnant presents with severe agitation, tachycardia, sweating, and fever. She has a known history of untreated Graves’ disease. Her pulse is 140 bpm, and her blood pressure is 140/90 mmHg. Laboratory tests show undetectable TSH and elevated free T4. The diagnosis of thyroid storm is made.
Question: What is the first-line therapy for this patient?
A. Methimazole and propranolol
B. Propylthiouracil (PTU) and propranolol
C. Iodine therapy and esmolol
D. Radioactive iodine
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.
A 35-year-old woman presents at 36 weeks gestation with a history of Graves’ disease. She has developed heart failure and is diagnosed with thyroid storm. In addition to PTU and beta-blocker therapy, iodine therapy is considered. However, the patient has a known history of anaphylaxis to iodine-containing compounds.
Question: What is the best alternative therapy for this patient to control thyroid hormone release?
A. Administer Lugol’s solution
B. Administer lithium carbonate
C. Perform an emergency thyroidectomy
D. Administer dexamethasone to block hormone release
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.
A 33-year-old pregnant woman is admitted to the ICU for management of thyroid storm. Despite appropriate medical therapy with PTU, iodine, corticosteroids, and beta-blockers, she continues to have tachycardia and signs of decompensated heart failure. Echocardiography reveals dilated cardiomyopathy.
Question: What is the prognosis for her heart failure once her thyroid storm is adequately treated?
A. Permanent heart failure requiring lifelong management
B. Reversible heart failure if thyroid hormone levels are controlled
C. Requires immediate heart transplant
D. Heart failure will worsen regardless of thyroid treatment
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.
A 40-year-old woman presents at 30 weeks of gestation with severe symptoms of thyroid storm. After stabilization, she asks about the risks to her pregnancy.
Question: What are the potential complications for her pregnancy if thyroid storm remains uncontrolled?
A. Gestational diabetes
B. Preterm delivery and heart failure
C. Polyhydramnios
D. Post-term delivery and macrosomia
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.
Which beta-blocker is commonly used to control heart rate in patients with thyroid storm?
A. Atenolol
B. Metoprolol
C. Esmolol
D. Propranolol
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.
Which drug should be used in thyroid storm patients with a history of iodine anaphylaxis?
A. Methimazole
B. Sodium iodide
C. Lugol solution
D. Lithium carbonate
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.
A 29-year-old pregnant woman at 32 weeks gestation presents with thyroid storm and is treated with PTU and beta-blockers. After 1 hour, the team initiates iodine therapy. The patient improves, but her heart rate remains elevated at 130 bpm despite beta-blocker therapy. The team decides to switch to esmolol for better heart rate control.
Question: Why is esmolol preferred in this situation?
A. It has a longer duration of action.
B. It can be administered orally.
C. It has a rapid onset and short half-life, allowing for easy titration.
D. It increases the effectiveness of iodine therapy.
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.
A 32-year-old woman presents with tachycardia, fever, and altered mental status. She is 36 weeks pregnant and is diagnosed with thyroid storm. After stabilizing her with PTU, iodine, and beta-blockers, the team considers corticosteroid therapy.
Question: What is the rationale for using corticosteroids in thyroid storm management?
A. Reduce fever
B. Block peripheral conversion of T4 to T3
C. Promote excretion of thyroid hormones
D. Stabilize blood pressure
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.
A 33-year-old pregnant woman with a history of hyperthyroidism presents to the emergency department in thyroid storm. After appropriate therapy with PTU, iodine, and beta-blockers, her condition stabilizes. The medical team manages her underlying precipitating condition, preeclampsia.
Question: Why is it important to control precipitating factors such as preeclampsia in thyroid storm?
A. To reduce the risk of anemia
B. To prevent worsening of thyroid hormone production
C. To improve cardiovascular stability
D. To enhance the effect of iodine therapy
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.
What is the most common outcome for neonates born to mothers with Graves’ disease?
A. Hypothyroidism
B. Hyperthyroidism
C. Euthyroidism
D. Goiter with hyperthyroidism
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.
What is the best predictor of perinatal thyrotoxicosis in a fetus born to a mother with Graves’ disease?
A. Maternal TSH levels
B. Fetal thyromegaly on ultrasound
C. Presence of thyroid-stimulating TSH-receptor antibodies in the mother
D. Maternal free T4 levels
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.
Which fetal condition can result from maternal thioamide therapy during pregnancy?
A. Goitrous hypothyroidism
B. Fetal thyrotoxicosis
C. Non-goitrous hyperthyroidism
D. Fetal euthyroidism
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.
Which treatment is recommended for a fetus diagnosed with hypothyroidism and thyromegaly due to maternal Graves’ disease?
A. Maternal thioamides
B. Radioiodine 131I therapy
C. Intra-amniotic thyroxine
D. Fetal thyroidectomy
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.
What is the most likely cause of non-goitrous hypothyroidism in a fetus born to a mother with thyroid disease?
A. Transplacental passage of thyrotropin receptor-blocking antibodies
B. Maternal thioamide overdose
C. Fetal thyroid agenesis
D. Excess maternal TSH secretion
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.
A 34-year-old pregnant woman at 30 weeks gestation is being monitored for Graves’ disease. Recent blood tests reveal elevated maternal thyroid-stimulating TSH-receptor antibodies. Ultrasound shows fetal thyromegaly, and the mother is on thioamide therapy.
Question: What is the best next step to manage the fetus’s thyroid condition?
A. Continue maternal thioamide therapy
B. Perform intra-amniotic thyroxine injection
C. Initiate fetal blood sampling
D. Deliver the baby early
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.
A 28-year-old woman with a history of Graves’ disease was treated with radioiodine (131I) before pregnancy. At 32 weeks gestation, she undergoes ultrasound that shows normal fetal growth, but the fetus is found to have tachycardia. There is concern for fetal thyrotoxicosis.
Question: What is the likely cause of fetal thyrotoxicosis in this case?
A. Placental transfer of maternal thyrotropin receptor-blocking antibodies
B. Placental transfer of thyroid-stimulating antibodies
C. Overproduction of thyroid hormones by the fetal thyroid gland
D. Fetal exposure to maternal thioamides
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.
A neonate is delivered at term to a mother with a 3-year history of Graves’ disease. The mother was treated with methimazole during pregnancy and was euthyroid at delivery. The infant, however, is diagnosed with hypothyroidism shortly after birth.
Question: What is the most likely cause of neonatal hypothyroidism in this case?
A. Fetal thyroid agenesis
B. Placental transfer of maternal thioamide
C. Neonatal thyroid-stimulating antibodies
D. Excessive iodine exposure during pregnancy
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.
A 32-year-old pregnant woman with Graves’ disease is treated with PTU during her pregnancy. An ultrasound performed at 28 weeks shows fetal thyromegaly. The medical team is concerned about the fetal thyroid status and plans cord blood sampling.
Question: What is the purpose of performing cord blood sampling in this scenario?
A. To assess fetal adrenal function
B. To measure fetal thyroid hormone levels
C. To confirm maternal Graves’ disease
D. To evaluate fetal lung maturity
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.
A 29-year-old woman with a history of Graves’ disease gives birth to a neonate with a goiter and signs of hypothyroidism. She had been treated with PTU throughout her pregnancy.
Question: What is the most appropriate treatment for this neonate?
A. Maternal PTU should be increased
B. Thyroid-stimulating hormone injections
C. Neonatal levothyroxine therapy
D. Neonatal corticosteroid therapy
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.
Which of the following is the primary cause of hyperthyroxinemia in hyperemesis gravidarum?
A. Increased secretion of TSH
B. Elevated levels of hCG
C. Decreased iodine intake
D. Increased production of thyroid antibodies
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.
What is the recommended treatment for gestational thyrotoxicosis in patients with hyperemesis gravidarum?
A. Propylthiouracil (PTU)
B. Methimazole
C. No treatment
D. Radioactive iodine
C. No treatment
Rationale: Gestational thyrotoxicosis seen in hyperemesis gravidarum is transient and typically resolves by mid-pregnancy without the need for antithyroid medications.
Which of the following conditions is most commonly associated with high levels of hCG stimulating the TSH receptor?
A. Thyroiditis
B. Gestational trophoblastic disease
C. Postpartum thyroiditis
D. Hashimoto’s thyroiditis
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.
How do thyroid hormone levels typically change in hyperemesis gravidarum by mid-pregnancy?
A. They remain elevated throughout the pregnancy.
B. They normalize by mid-pregnancy.
C. They decrease further by mid-pregnancy.
D. They fluctuate throughout pregnancy.
B. They normalize by mid-pregnancy
Rationale: In hyperemesis gravidarum, thyroid hormone levels (T4) typically normalize by mid-pregnancy as hCG levels decline.
Which of the following is the main thyroid-related concern in gestational trophoblastic disease?
A. Hyperthyroidism due to high levels of hCG
B. Hypothyroidism due to decreased TSH secretion
C. Euthyroid state with no thyroid involvement
D. Goitrous hypothyroidism due to iodine deficiency
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.
A 26-year-old woman at 10 weeks of gestation presents with persistent nausea, vomiting, and weight loss. Blood tests show high free thyroxine (T4) and suppressed TSH levels. Her hCG levels are significantly elevated.
Question: What is the most likely diagnosis, and what is the appropriate management for her thyroid condition?
A. Graves’ disease; treat with methimazole.
B. Gestational thyrotoxicosis from hyperemesis gravidarum; no treatment needed.
C. Subclinical hyperthyroidism; start propylthiouracil.
D. Postpartum thyroiditis; monitor and initiate beta-blockers.
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.
A 30-year-old woman with hyperemesis gravidarum at 12 weeks gestation is found to have high free T4 and undetectable TSH. Ultrasound shows a molar pregnancy, and her hCG levels are significantly elevated.
Question: What is the underlying mechanism for her thyroid dysfunction, and what condition is likely contributing to it?
A. Overstimulation of the thyroid by TSH; Hashimoto’s thyroiditis.
B. Overstimulation of the thyroid by hCG; gestational trophoblastic disease.
C. Direct stimulation of thyroid antibodies; postpartum thyroiditis.
D. Iodine deficiency; hypothyroidism.
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.
A 29-year-old pregnant woman presents at 8 weeks gestation with severe vomiting, dehydration, and weight loss. Lab results show elevated free T4 and low TSH. Her physician diagnoses gestational thyrotoxicosis secondary to hyperemesis gravidarum.
Question: What is the expected course of her thyroid hormone levels, and when should they be monitored again?
A. Levels will normalize by mid-pregnancy; monitor in the second trimester.
B. Levels will remain elevated throughout pregnancy; start methimazole.
C. Levels will fluctuate throughout pregnancy; frequent monitoring needed.
D. Levels will drop below normal by mid-pregnancy; start levothyroxine.
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.
A 28-year-old woman is diagnosed with gestational trophoblastic disease at 10 weeks gestation, and blood tests show very high hCG levels along with symptoms of hyperthyroidism. Her doctor is concerned about the risk of hyperthyroidism worsening.
Question: What is the primary cause of her thyroid dysfunction, and what is the management approach?
A. Thyroid antibody overproduction; start corticosteroids.
B. TSH overproduction; monitor and start beta-blockers.
C. hCG overstimulation of the TSH receptor; manage the molar pregnancy.
D. Iodine deficiency; supplement with iodine and monitor.
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.
A 27-year-old woman with hyperemesis gravidarum at 9 weeks gestation presents with symptoms of thyrotoxicosis. Blood tests show elevated free T4 and low TSH, and her hCG levels are markedly high.
Question: What is the expected outcome for her thyroid function by mid-pregnancy, and what treatment is needed at this time?
A. Thyroid function will normalize; no treatment needed.
B. Thyroid function will worsen; start PTU.
C. Thyroid function will remain abnormal; treat with methimazole.
D. Thyroid function will fluctuate; initiate radioactive iodine.
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.
What is the most common cause of hypothyroidism in pregnancy?
A. Graves’ disease
B. Iodine deficiency
C. Antithyroid peroxidase antibodies (anti-TPO)
D. Thyroid cancer
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.
Which of the following is the hallmark laboratory finding in subclinical hypothyroidism?
A. High TSH and low thyroxine (T4)
B. Normal TSH and high thyroxine (T4)
C. High TSH and normal thyroxine (T4)
D. Low TSH and low thyroxine (T4)
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.
Which of the following symptoms is NOT typically associated with overt hypothyroidism during pregnancy?
A. Fatigue
B. Weight loss
C. Cold intolerance
D. Constipation
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.
Which form of hypothyroidism is more common in pregnancy?
A. Overt hypothyroidism
B. Subclinical hypothyroidism
C. Hashimoto’s thyroiditis
D. Postpartum thyroiditis
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).
What is the likely impact of untreated overt hypothyroidism on pregnancy outcomes?
A. No impact, the condition resolves postpartum
B. Infertility, miscarriage, or preterm labor
C. Fetal hyperthyroidism
D. Fetal macrocephaly
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.