Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 1711: Diabetic ketoacidosis is said to be present if:

A. Hyperglycemia, glycosuria, hyperkalemia, and hypocalcemia are present.
B. Hypoglycemia, hypokalemia, hypercalcemia, and ketonemia are present.
C. Hypoglycemia, ketonemia, ketonuria, and hypokalemia are present.
D. Hyperglycemia, heavy glycosuria, ketonemia, ketonuria, and acidosis are present. (Correct Answer)

Explanation: ***Hyperglycemia, heavy glycosuria, ketonemia, ketonuria, and acidosis are present.*** [1], [3] - **Diabetic ketoacidosis (DKA)** is characterized by **uncontrolled hyperglycemia** (blood glucose > 250 mg/dL), metabolic acidosis (pH < 7.3, bicarbonate < 18 mEq/L), and the presence of **ketones** in the blood (ketonemia) and urine (ketonuria). - The heavy glycosuria reflects the body's attempt to excrete excess glucose through the kidneys. *Hyperglycemia, glycosuria, hyperkalemia, and hypocalcemia are present.* - While **hyperglycemia** and **glycosuria** are present in DKA, **hyperkalemia** is often seen due to the acidosis shifting potassium out of cells, but it is not a defining diagnostic criterion. [2] - **Hypocalcemia** is not a primary diagnostic feature of DKA; calcium levels are generally normal or may even be slightly elevated due to hemoconcentration. *Hypoglycemia, hypokalemia, hypercalcemia, and ketonemia are present.* - **Hypoglycemia** contradicts the definition of DKA, which is characterized by **hyperglycemia**. - While **ketonemia** is a feature, **hypokalemia** and **hypercalcemia** are not defining diagnostic criteria for DKA. Hypokalemia may develop during treatment, but patients often present with normal or high potassium. [2] *Hypoglycemia, ketonemia, ketonuria, and hypokalemia are present.* - **Hypoglycemia** is a direct contradiction to the diagnostic criteria of DKA, which requires **hyperglycemia**. - Although **ketonemia** and **ketonuria** are features of DKA, **hypokalemia** is not a defining characteristic at presentation and typically develops during insulin therapy. [2]

Question 1712: Which type of hypercholesterolemia is characterized by a genetic defect in the LDL receptor, leading to markedly elevated LDL levels?

A. Type I
B. Type IIa (Correct Answer)
C. Type IIb
D. Type III

Explanation: ***Type IIa*** - This type of hypercholesterolemia, also known as **familial hypercholesterolemia (FH)**, is caused by a genetic defect in the **LDL receptor gene**. - The dysfunctional or absent LDL receptors lead to impaired clearance of **LDL particles** from the blood, resulting in markedly elevated **LDL cholesterol levels**. *Type I* - Type I hypercholesterolemia (also called familial chylomicronemia syndrome) is characterized by a deficiency in **lipoprotein lipase (LPL)** or its cofactor **apoC-II**. - This leads to a severe accumulation of **chylomicrons** and **very-low-density lipoprotein (VLDL)**, causing extremely high triglyceride levels, not primarily elevated LDL. *Type IIb* - Type IIb hypercholesterolemia, or **familial combined hyperlipidemia**, involves elevated levels of both **LDL** and **VLDL**. - It is typically associated with overproduction of VLDL and impaired clearance of VLDL and LDL, but the primary defect is not specifically in the LDL receptor. *Type III* - Type III hypercholesterolemia, or **familial dysbetalipoproteinemia**, is characterized by a defect in **apoE**, leading to impaired clearance of **chylomicron remnants** and **VLDL remnants (IDL)**. - This results in elevated levels of both cholesterol and triglycerides, primarily due to the accumulation of these specific remnant lipoproteins, not a defect in LDL receptors.

Question 1713: The drug of choice in a 50-year-old patient presenting with hyperglycemia and ketoacidosis?

A. Regular Insulin (Correct Answer)
B. Oral hypoglycemic agents
C. Lente Insulin
D. Intermediate Insulin

Explanation: ***Regular Insulin*** - **Regular insulin** is the drug of choice for treating **diabetic ketoacidosis (DKA)** because it is a **short-acting insulin** that can be administered intravenously [1]. - Given its **rapid onset** and **predictable action**, regular insulin allows for precise titration to correct hyperglycemia and resolve ketoacidosis quickly and effectively [2]. *Oral hypoglycemic agents* - **Oral hypoglycemic agents** are typically used for **type 2 diabetes mellitus** patients who are not in DKA and can produce some insulin, or for those who need to manage their blood sugar over a longer period. - They are **ineffective** in DKA due to the absolute or relative **insulin deficiency** and the severity of insulin resistance associated with the acute stress response. *Lente Insulin* - **Lente insulin** is an **intermediate-acting insulin** with a delayed onset and longer duration of action compared to regular insulin. - It is **not suitable** for the rapid correction of severe hyperglycemia and ketoacidosis in an emergency setting like DKA. *Intermediate Insulin* - **Intermediate-acting insulins** (like NPH) have a **slower onset** and a **longer duration** of action than regular insulin. - They are **not appropriate** for the acute management of DKA, which requires immediate and rigorous blood glucose control using rapid-acting or short-acting insulin.

Question 1714: What should be the minimum value of HbA1c to safely carry out a surgical procedure in an emergency setting?

A. <7
B. <8
C. <10 (Correct Answer)
D. <8

Explanation: ***<10*** - In an **emergency setting**, the priority is to proceed rapidly with surgery; current guidelines suggest that an **HbA1c <10%** is acceptable to proceed without significant delay for optimization. - While lower HbA1c is ideal, delaying an emergency procedure to achieve an HbA1c below 10% is generally **not recommended**, as the benefits of urgent surgery outweigh the risks associated with this level of glycemic control [1]. *<7* - An HbA1c of **<7% is the general target** for optimal glycemic control in most diabetic patients, especially in an elective setting. - Achieving this level in an emergency would likely require **delaying surgery**, which is not feasible or safe when immediate intervention is needed. *<8* - An HbA1c of **<8%** represents good control for many individuals, particularly older adults or those with comorbidities. - While better than 10%, it is not the absolute minimum required to proceed with an **emergency surgery**, as timely intervention is paramount. *<8* - An HbA1c of **<8%** represents good control for many individuals, particularly older adults or those with comorbidities. - While better than 10%, it is not the absolute minimum required to proceed with an **emergency surgery**, as timely intervention is paramount.

Question 1715: HAIR-AN syndrome consists of which of the following?

A. Acanthosis nigricans
B. Insulin resistance
C. Hyperandrogenism
D. All of the options (Correct Answer)

Explanation: ***All of the options*** - HAIR-AN syndrome is an acronym representing the combination of **HyperAndrogenism**, **Insulin Resistance**, and **Acanthosis Nigricans**. - This syndrome is often associated with **severe hyperinsulinemia** and is considered a severe form of polycystic ovarian syndrome (PCOS) [1]. *Acanthosis nigricans* - While **acanthosis nigricans** is a key component of HAIR-AN syndrome, it does not, by itself, define the entire syndrome. - This condition is characterized by **darkening and thickening of the skin**, particularly in body folds, and is a marker of insulin resistance. *Insulin resistance* - **Insulin resistance** is central to HAIR-AN syndrome, driving many of its metabolic and dermatological manifestations. - However, the definition of HAIR-AN syndrome requires the presence of hyperandrogenism and acanthosis nigricans in addition to insulin resistance to be complete. *Hyperandrogenism* - **Hyperandrogenism**, characterized by elevated androgen levels leading to symptoms like hirsutism and acne, is a critical feature of HAIR-AN syndrome [1]. - Similar to the other components, hyperandrogenism alone does not constitute the full syndrome, which necessitates the presence of insulin resistance and acanthosis nigricans.

Question 1716: During the evaluation of secondary amenorrhea in a 24-year-old woman, hyperprolactinemia is diagnosed. Which of the following conditions could cause increased circulating prolactin concentrations and amenorrhea in this patient?

A. Stress
B. Hypothyroidism (Correct Answer)
C. Eating disorders
D. Adrenal disorders

Explanation: ***Hypothyroidism*** - **Primary hypothyroidism** leads to increased **TRH** (thyrotropin-releasing hormone) from the hypothalamus. TRH stimulates both **TSH** (thyroid-stimulating hormone) and **prolactin** release from the pituitary, causing hyperprolactinemia [1]. - Elevated prolactin then inhibits **GnRH** (gonadotropin-releasing hormone) secretion, leading to reduced LH and FSH, which results in **anovulation** and **amenorrhea**. *Stress* - While acute stress can transiently increase **prolactin levels**, severe and chronic stress typically leads to **hypogonadism** via effects on GnRH, but not usually hyperprolactinemia sufficient to cause prolonged amenorrhea. - Stress-induced amenorrhea is more often related to **functional hypothalamic amenorrhea**, characterized by low or normal prolactin, and is primarily a disorder of GnRH pulse generation. *Eating disorders* - Conditions like **anorexia nervosa** or **bulimia nervosa** can cause amenorrhea due to **low body weight** and nutritional deficiencies, leading to **hypothalamic dysfunction** and low estrogen levels [3]. - These disorders typically result in **hypogonadotropic hypogonadism** (low LH, FSH, and estrogen) rather than **hyperprolactinemia**. *Adrenal disorders* - Adrenal disorders like **Cushing's syndrome** or **adrenal insufficiency** can cause menstrual irregularities and amenorrhea, but they are not typically associated with **hyperprolactinemia** [2]. - **Congenital adrenal hyperplasia (CAH)** can cause androgen excess and menstrual irregularities, but prolactin levels are usually normal.

Question 1717: In a patient with primary hypothyroidism, what is the expected hormonal profile?

A. High T3, high T4, high TSH
B. Low T3, low T4, high TSH (Correct Answer)
C. Low T3, low T4, low TSH
D. Normal T3, normal T4, high TSH

Explanation: ***Low T3, low T4, high TSH*** - In **primary hypothyroidism**, the thyroid gland itself is dysfunctional, leading to reduced production of **thyroid hormones (T3 and T4)** [1]. - The pituitary gland, sensing low thyroid hormone levels, increases **TSH (thyroid-stimulating hormone)** secretion in an attempt to stimulate the failing thyroid [1]. *Low T3, low T4, low TSH* - This profile typically indicates **secondary (central) hypothyroidism**, where the pituitary gland is not producing enough TSH to stimulate a healthy thyroid [2]. - In primary hypothyroidism, the TSH would be high, not low, due to the lack of negative feedback from low T3 and T4 [4]. *High T3, high T4, high TSH* - This hormonal profile is highly suggestive of **thyroid hormone resistance** or a **TSH-secreting pituitary adenoma**, not primary hypothyroidism [3]. - In primary hypothyroidism, T3 and T4 levels are reduced, not elevated. *Normal T3, normal T4, high TSH* - This profile is characteristic of **subclinical hypothyroidism**, where TSH levels are elevated but the thyroid gland is still able to produce enough T3 and T4 to maintain normal peripheral levels. - In overt primary hypothyroidism, T3 and T4 would be low, not normal.

Question 1718: All are true about primary hyperparathyroidism except which of the following?

A. Nephrolithiasis
B. Loss of lamina dura
C. Decreased calcium (Correct Answer)
D. Increased alkaline phosphatase

Explanation: ***Decreased calcium*** - Primary hyperparathyroidism is characterized by **excessive parathyroid hormone (PTH)** secretion, which leads to **hypercalcemia (increased calcium levels)**, not decreased calcium [1]. - PTH's main actions are to raise serum calcium by increasing **bone resorption**, **renal calcium reabsorption**, and **calcitriol synthesis** [2]. *Nephrolithiasis* - **Hypercalcemia** from primary hyperparathyroidism leads to increased calcium excretion in the urine, increasing the risk of **calcium oxalate stones** (nephrolithiasis) [3]. *Increased alkaline phosphatase* - PTH stimulates osteoclastic activity, leading to **increased bone turnover** and release of enzymes like **alkaline phosphatase**, particularly in cases with significant bone involvement. - Alkaline phosphatase levels may also be elevated due to **osteitis fibrosa cystica**, a severe form of bone disease associated with primary hyperparathyroidism. *Loss of lamina dura* - Chronic hyperparathyroidism can cause characteristic changes in bone, including the **resorption of the lamina dura** around the teeth, which is visible on dental radiographs. - This is a direct consequence of PTH-mediated **osteoclastic activity** in areas of high bone turnover.

Question 1719: In Swyer's syndrome, which of the following statements is true?

A. Testis is absent
B. Increased FSH and LH (Correct Answer)
C. Normal stature
D. Functional ovaries are absent

Explanation: In Swyer's syndrome, which of the following statements is true? ***Increased FSH and LH*** - In **Swyer's syndrome** (46, XY pure gonadal dysgenesis), the **gonads are streak gonads** which are non-functional and thus do not produce sex hormones [2]. - This lack of negative feedback on the hypothalamus and pituitary gland leads to **elevated levels of FSH and LH** [3], [4]. *Testis is absent* - While functional testes are absent, individuals with Swyer's syndrome typically have **streak gonads**, which are dysgenetic and non-functional remnants of gonadal tissue, not fully absent gonads [2]. - The absence of functional testicular tissue is a key feature but stating "testis is absent" is less precise than describing the dysfunctional nature of the streak gonads. *Functional ovaries are absent* - Swyer's syndrome is characterized by a **46, XY karyotype**, meaning the individual is genetically male but has female external genitalia due to a defect in testicular development [2]. - Therefore, the development of functional ovaries would be genetically impossible, and instead, streak gonads are present. *Normal stature* - Individuals with Swyer's syndrome typically have a **normal female phenotype** and are of **normal stature**. - This differentiates it from other forms of gonadal dysgenesis, such as Turner syndrome (45, XO), which is associated with short stature [1].

Question 1720: Asymptomatic hypercalcemia in a 30-year-old young male is due to:

A. Hypernephroma
B. Occult primary malignancy
C. Primary hyperparathyroidism (Correct Answer)
D. Familial hypocalciuric hypercalcemia

Explanation: ***Primary hyperparathyroidism*** - This is the most common cause of **asymptomatic hypercalcemia**, particularly in younger individuals [2] and when unrelated to malignancy [1]. - It involves excessive secretion of **parathyroid hormone (PTH)**, leading to increased calcium reabsorption from bones, kidneys, and gut [3]. *Occult primary malignancy* - While malignancy can cause hypercalcemia, it typically presents with **symptomatic hypercalcemia** and other signs of systemic illness [1]. - In a 30-year-old, a widespread occult malignancy causing asymptomatic hypercalcemia is less probable than primary hyperparathyroidism [2]. *Familial hypocalciuric hypercalcemia* - This is a rare genetic disorder characterized by **elevated serum calcium** and **low urinary calcium excretion** due to a defective calcium-sensing receptor [1]. - It is typically benign and does not require treatment for hypercalcemia, but it's important to differentiate from primary hyperparathyroidism [1]. *Hypernephroma* - **Renal cell carcinoma (hypernephroma)** can cause hypercalcemia, often via parathyroid hormone-related peptide (PTHrP) secretion [1]. - However, similar to other malignancies, it's more likely to be symptomatic and is less common than primary hyperparathyroidism as an etiology for asymptomatic hypercalcemia in a young adult [2].

Practice by Chapter

Diabetes Mellitus

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Thyroid Disorders

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Adrenal Gland Disorders

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Pituitary Disorders

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Calcium and Bone Metabolism

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Reproductive Endocrinology

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Lipid Disorders

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Endocrine Hypertension

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Multiple Endocrine Neoplasia

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Obesity and Metabolic Syndrome

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Neuroendocrine Tumors

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Endocrine Emergencies

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