Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 1421: A 40 year old lady with temporal field defects and galactorrhoea is most likely to have-

A. Lactational failure
B. Pituitary macroadenoma (Correct Answer)
C. Pregnancy
D. Craniopharyngioma

Explanation: ***Pituitary macroadenoma*** - **Temporal field defects** (bitemporal hemianopsia) are a classic symptom of a pituitary macroadenoma due to compression of the **optic chiasm** by the expanding tumor [1]. - **Galactorrhoea** is often caused by hyperprolactinemia, which is frequently associated with **prolactinomas**, a type of pituitary adenoma [1]. *Lactational failure* - Lactational failure would present with the **absence** of milk production or poor milk supply, not galactorrhoea (milk production outside of breastfeeding). - This condition does not cause **temporal field defects**, which are indicative of a mass effect on vision. *Pregnancy* - While pregnancy can cause galactorrhoea due to hormonal changes, it does not typically lead to **temporal field defects**. - **Visual field defects** in pregnancy would suggest a more serious underlying neurological issue, not a normal physiological response to pregnancy. *Craniopharyngioma* - Craniopharyngiomas are typically **suprasellar tumors** that can cause visual field defects due to optic chiasm compression, similar to pituitary adenomas. - However, craniopharyngiomas are not typically associated with **galactorrhoea**; they are more often linked to hypothalamic-pituitary dysfunction leading to hormone deficiencies, not hyperprolactinemia [1].

Question 1422: Pseudohyponatremia is found in all of the following EXCEPT:

A. Extreme hyperproteinemia
B. Severe hyperglycemia
C. Aldosterone excess (Correct Answer)
D. Severe hyperlipemia

Explanation: ***Aldosterone excess*** - **Aldosterone excess** typically leads to increased **sodium reabsorption** [2] and potassium excretion [1], which can result in **hypernatremia** or normal sodium levels, but not pseudohyponatremia. - It does not interfere with the measurement of plasma sodium concentration. *Extreme hyperproteinemia* - **Extreme hyperproteinemia** leads to an increase in the non-aqueous component of plasma, causing a falsely low sodium reading when measured by **flame photometry** (indirect ion-selective electrodes). - This is because the sodium concentration in the **aqueous phase** remains normal, but the total plasma volume is disproportionately high due to protein. *Severe hyperglycemia* - **Severe hyperglycemia** causes an **osmotic shift** of water from the intracellular to the extracellular compartment, diluting extracellular sodium. This can cause **translocational hyponatremia**, which is a form of pseudohyponatremia. - For every 100 mg/dL increase in glucose above normal, serum sodium typically decreases by 1.6-2.4 mEq/L. *Severe hyperlipemia* - **Severe hyperlipemia** (hypertriglyceridemia) falsely lowers the measured sodium concentration due to the large volume occupied by lipids in the plasma sample. - Similar to hyperproteinemia, this is an artifact of measurement methods that assume a constant proportion of plasma is water, causing a low reading even though sodium concentration in plasma water is normal.

Question 1423: Starvation and diabetes mellitus can lead to ketoacidosis. Which of the following features is in favor of ketoacidosis due to diabetes mellitus?

A. Increase in glucagon/insulin ratio, increased cAMP and increased blood glucose (Correct Answer)
B. Decreased insulin, increased free fatty acid with normal blood glucose
C. Elevated insulin and free fatty acid with hyperglycemia
D. Decreased insulin, increased free fatty acid which is not equivalent to blood glucose

Explanation: ***Increase in glucagon/insulin ratio, increased cAMP and increased blood glucose*** - In **diabetic ketoacidosis (DKA)**, there is a severe relative or absolute lack of **insulin**, leading to an unopposed action of **glucagon** [1]. This results in a significantly **elevated blood glucose** due to increased **gluconeogenesis** and glycogenolysis [3]. - The increased **glucagon-to-insulin ratio** activates **adenylate cyclase**, leading to an increase in **cAMP**, which promotes fatty acid oxidation and ketone body formation. *Decreased insulin, increased free fatty acid with normal blood glucose* - This description is characteristic of **starvation ketoacidosis**, where insulin levels are low and free fatty acids are elevated, but **blood glucose** is typically normal or slightly reduced due to preserved glucose regulation in the absence of exogenous glucose [4]. - In **diabetic ketoacidosis**, a hallmark is **hyperglycemia** (elevated blood glucose), which differentiates it from starvation [2]. *Decreased insulin, increased free fatty acid which is not equivalent to blood glucose* - While both decreased insulin and increased free fatty acids are common to both starvation and diabetic ketoacidosis, the phrase "not equivalent to blood glucose" is vague and doesn't explicitly state the expected **hyperglycemia** seen in DKA. - The key distinguishing feature for **diabetic ketoacidosis** is the high blood glucose, which is not clearly indicated here. *Elevated insulin and free fatty acid with hyperglycemia* - **Elevated insulin** with hyperglycemia in the context of ketoacidosis is contradictory for DKA. DKA is primarily caused by **insulin deficiency**. - While **hyperglycemia** and **elevated free fatty acids** are present in DKA, the absence of insufficient insulin or an unfavorable glucagon/insulin ratio makes this option incorrect for distinguishing DKA.

Question 1424: True about osteoporosis

A. Normal serum phosphate levels
B. Normal serum alkaline phosphatase level
C. Normal serum calcium levels
D. All of the options (Correct Answer)

Explanation: ***All of the options*** - In **primary osteoporosis**, serum levels of calcium, phosphate, and alkaline phosphatase are typically **normal**, distinguishing it from other metabolic bone diseases [1]. - The diagnosis of osteoporosis is based on **bone mineral density (BMD)** measurements, not on abnormalities in these serum markers [3]. *Normal serum phosphate levels* - While correct that serum phosphate is usually normal in osteoporosis, this option alone does not encompass the full biochemical picture [1]. - Osteoporosis is primarily a disorder of **bone quantity**, not systemic mineral metabolism, so levels of **calcium and phosphate remain homeostatically regulated** [1]. *Normal serum alkaline phosphatase level* - Similarly, a normal alkaline phosphatase level reflects the absence of significantly increased **osteoblast activity** or **bone turnover** that would be seen in conditions like osteomalacia or Paget's disease [2]. - This observation is a key biochemical finding, but it is not the only normal lab value. *Normal serum calcium levels* - Normal serum calcium is characteristic of osteoporosis, as **parathyroid hormone** and **vitamin D** regulation of calcium remains intact [4]. - Hypercalcemia or hypocalcemia would suggest alternative diagnoses or complications, such as **primary hyperparathyroidism** or **vitamin D deficiency** [4].

Question 1425: A 35 year old female presents to the OPD with headaches and high blood pressure. On investigations, increased aldosterone levels with low renin levels are seen and a diagnosis of Conn's syndrome is made. Excess secretion of aldosterone can cause all except

A. Hypertension
B. Hypokalemia
C. Increase in plasma Na+ > 7 meq/L
D. Slight increase in ECF volume (Correct Answer)

Explanation: Slight increase in ECF volume - While aldosterone increases sodium reabsorption, the resulting ECF expansion is usually more than 'slight' and contributes significantly to hypertension [1]. - A significant increase in ECF volume is a hallmark of aldosterone excess due to its role in sodium and water retention [3]. *Hypertension* - Aldosterone causes sodium and water retention, leading to an increase in extracellular fluid volume and subsequently blood pressure [3]. - This is a primary clinical manifestation of Conn's syndrome. *Hypokalemia* - Aldosterone promotes the secretion of potassium into the renal tubules, leading to increased urinary excretion of potassium [2]. - Excessive aldosterone levels therefore result in hypokalemia, which is a classic feature of primary hyperaldosteronism [2]. *Increase in plasma Na+ > 7 meq/L* - While aldosterone increases sodium reabsorption, the increase in plasma sodium concentration is typically mild and rarely exceeds a few mEq/L [1]. - The elevated ECF volume triggers mechanisms that prevent severe hypernatremia, making a rise of more than 7 mEq/L unlikely [1].

Question 1426: A 40-year-old female presents with multiple lytic bone lesions, fracture clavicle and periosteal resorption of 2nd and 3rd metatarsals. What is the most likely diagnosis?

A. Osteomalacia
B. Hyperparathyroidism (Correct Answer)
C. Renal osteodystrophy
D. Hyperthyroidism

Explanation: ***Hyperparathyroidism*** - **Multiple lytic bone lesions**, **fracture clavicle**, and **periosteal resorption** (especially in the phalanges and metatarsals) are classic radiological findings of **osteitis fibrosa cystica**, which is characteristic of severe hyperparathyroidism. - The combination of these bone changes strongly indicates excessive **parathyroid hormone** leading to increased **osteoclastic activity** and bone demineralization. *Osteomalacia* - Characterized by **softening of the bones** due to defective mineralization, typically manifesting as generalized bone pain, muscle weakness, and sometimes **pseudofractures**. - Does not typically present with **lytic lesions** or **periosteal resorption** as the primary radiographic features. *Renal osteodystrophy* - A spectrum of bone disorders in patients with **chronic kidney disease**, often involving features of both **osteomalacia** and **hyperparathyroidism**, including **osteitis fibrosa cystica**. - While it can present with similar bone changes, the scenario does not explicitly mention **renal failure** as an underlying condition, making primary hyperparathyroidism a more direct diagnosis for these specific findings. *Hyperthyroidism* - Can lead to increased **bone turnover** and a generalized reduction in **bone mineral density**, increasing the risk of **osteoporosis** and fractures. - However, it does not typically cause localized **lytic bone lesions** or specific **periosteal resorption**.

Question 1427: Cerebral salt wasting occurs due to which of the following?

A. SIADH
B. Hyper secretion of ANP (Correct Answer)
C. Low cortisol secretion
D. Low aldosterone secretion

Explanation: Cerebral salt wasting (CSW) is characterized by hyponatremia and volume depletion due to excessive renal sodium excretion. While the exact mechanism is complex, elevated levels of atrial natriuretic peptide (ANP) are thought to play a significant role in promoting natriuresis [1]. ANP and related molecules increase intracellular cGMP, which inhibits sodium transport via ENaC and inhibits sodium reabsorption in the renal tubules [1], [2]. Syndrome of inappropriate antidiuretic hormone (SIADH) also causes hyponatremia, but it leads to euvolemia or mild hypervolemia, not volume depletion [3]. Low cortisol secretion, as seen in adrenal insufficiency, can lead to hyponatremia due to both decreased free water clearance and increased ADH secretion, but it is not the primary mechanism of CSW. Low aldosterone secretion, also seen in adrenal insufficiency, can cause hyponatremia and hyperkalemia due to impaired renal sodium reabsorption and potassium excretion [3].

Question 1428: Primary Hyperparathyroidism is associated with -

A. Increased serum PTH and Hypercalcemia (Correct Answer)
B. Decreased serum PTH and Hyporcalcemia
C. Decreased serum PTH and Hypercalcemia
D. Increased serum PTH and Hyporcalcemia

Explanation: ***Increased serum PTH and Hypercalcemia*** - **Primary hyperparathyroidism** results from an autonomous overproduction of **parathyroid hormone (PTH)**, usually by an adenoma or hyperplasia [1]. - This excess PTH leads to increased calcium reabsorption from bones and kidneys, causing **hypercalcemia** [2][4]. *Decreased serum PTH and Hyporcalcemia* - This combination is characteristic of **hypoparathyroidism**, where insufficient PTH production leads to low calcium levels [3]. - Primary hyperparathyroidism, by definition, involves *increased* PTH [4]. *Decreased serum PTH and Hypercalcemia* - This might be seen in cases of **non-PTH-mediated hypercalcemia**, such as malignancy, where high calcium levels suppress normal PTH secretion [4]. - However, in primary hyperparathyroidism, PTH would be **elevated** [1]. *Increased serum PTH and Hyporcalcemia* - This scenario typically points to **secondary hyperparathyroidism**, where the parathyroid glands are overactive in response to chronic low calcium levels (e.g., due to **chronic kidney disease** or **Vitamin D deficiency**) [1][3]. - In primary hyperparathyroidism, the elevated PTH directly *causes* hypercalcemia [4].

Question 1429: A 17 years old girl who was evaluated for short height was found to have an enlarged pituitary gland. Her T4 was low and TSH was increased. Which of the following is the most likely diagnosis?

A. Thyroid target receptor insensitivity
B. TSH-secreting pituitary tumour
C. Primary hypothyroidism (Correct Answer)
D. Pituitary adenoma

Explanation: ***Primary hypothyroidism*** - **Primary hypothyroidism** leads to decreased production of thyroid hormones (low T4), which in turn causes the pituitary to produce more TSH (increased TSH) in an attempt to stimulate the thyroid [1], [3]. - The elevated TSH can lead to **pituitary hypertrophy** (enlarged pituitary gland) due to chronic stimulation, as observed in this patient. *Thyroid target receptor insensitivity* - This condition involves resistance to thyroid hormones at the tissue level, leading to elevated T4 or normal T4 and elevated TSH. However, in this case, T4 is low, which contradicts this diagnosis. - While TSH can be elevated, the primary issue is cellular resistance, not a lack of thyroid hormone synthesis. *TSH-secreting pituitary tumour* - A TSH-secreting pituitary tumor would result in **elevated TSH** and **elevated T4** (secondary hyperthyroidism), as the tumor is autonomously producing TSH. - This patient presents with **low T4**, which rules out a TSH-secreting tumor causing hyperthyroidism [2]. *Pituitary adenoma* - While a pituitary adenoma is present, the low T4 and high TSH indicate that the adenoma is a **secondary effect** of chronic TSH stimulation (due to primary hypothyroidism) leading to pituitary enlargement, rather than a primary secreting adenoma causing the thyroid dysfunction. - Non-functional pituitary adenomas can cause mass effects, but this specific hormonal profile points to the pituitary enlargement being a compensatory response.

Question 1430: A patient of 47XXY karyotype with features of hypogonadism; likely diagnosis is :

A. Turners syndrome
B. Down syndrome
C. Klinefelter's syndrome (Correct Answer)
D. Edwards syndrome

Explanation: ***Klinefelter's syndrome*** - **Klinefelter's syndrome** is characterized by a **47,XXY karyotype**, which is a genetic condition affecting males [1]. - Individuals with this syndrome often present with **hypogonadism**, leading to features such as small testes, infertility, and reduced secondary sexual characteristics [2]. *Turners syndrome* - **Turner's syndrome** is a genetic condition affecting females, characterized by a **45,X karyotype**, meaning they are missing all or part of one X chromosome [2]. - While it also involves hypogonadism, it does not present with an **XXY karyotype** or affect males [3]. *Down syndrome* - **Down syndrome**, or trisomy 21, is caused by an extra copy of chromosome 21, resulting in a **47,XX,+21 or 47,XY,+21 karyotype**. - It is characterized by intellectual disability, distinctive facial features, and developmental delays, not typically hypogonadism associated with an XXY karyotype. *Edwards syndrome* - **Edwards syndrome**, or trisomy 18, is caused by an extra copy of chromosome 18, resulting in a **47,XX,+18 or 47,XY,+18 karyotype**. - This syndrome is associated with severe developmental abnormalities, intellectual disability, and a very short lifespan, with different clinical features from the given description.

Practice by Chapter

Diabetes Mellitus

Practice Questions

Thyroid Disorders

Practice Questions

Adrenal Gland Disorders

Practice Questions

Pituitary Disorders

Practice Questions

Calcium and Bone Metabolism

Practice Questions

Reproductive Endocrinology

Practice Questions

Lipid Disorders

Practice Questions

Endocrine Hypertension

Practice Questions

Multiple Endocrine Neoplasia

Practice Questions

Obesity and Metabolic Syndrome

Practice Questions

Neuroendocrine Tumors

Practice Questions

Endocrine Emergencies

Practice Questions

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