Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 1571: Which of the following is NOT typically associated with Kallmann's syndrome?

A. Hypogonadotropic hypogonadism
B. Anosmia
C. Amenorrhea
D. Excess stimulation of the HPO axis (Correct Answer)

Explanation: ***Excess stimulation of the HPO axis*** - Kallmann's syndrome is characterized by **hypogonadotropic hypogonadism**, meaning there is a deficiency in the secretion of **gonadotropin-releasing hormone (GnRH)** [1] from the hypothalamus. - This deficiency leads to *reduced* stimulation of the **hypothalamic-pituitary-ovarian (HPO)** axis, not excess stimulation. *Amenorrhea* - **Amenorrhea** (absence of menstruation) is a common presentation in females with Kallmann's syndrome due to the **hypogonadotropic hypogonadism**. - The lack of GnRH results in insufficient **follicle-stimulating hormone (FSH)** and **luteinizing hormone (LH)**, preventing ovarian function and regular menstrual cycles. *Hypogonadotropic hypogonadism* - This is a **defining feature** of Kallmann's syndrome, where the **hypothalamus fails to produce enough GnRH**, leading to low levels of FSH and LH from the pituitary. - The low gonadotropin levels subsequently cause the gonads (testes or ovaries) to produce insufficient sex hormones, resulting in **delayed or absent puberty** [1]. *Anosmia* - **Anosmia** (the inability to smell) is a classic and diagnostic feature of Kallmann's syndrome, distinguishing it from other forms of hypogonadotropic hypogonadism. - It occurs because the **GnRH-producing neurons** originate in the olfactory placode and fail to migrate correctly into the hypothalamus during embryonic development, disrupting both smell and GnRH secretion.

Question 1572: Thyroid nodule in a 65 year old male who is clinically euthyroid is most likely to be

A. Follicular adenoma (Correct Answer)
B. Multinodular goiter
C. Thyroid cyst
D. Follicular carcinoma

Explanation: ***Follicular adenoma*** - Typically presents as a **solitary, well-defined nodule** in euthyroid patients, making it a common finding in this demographic. - It is often **benign** and can be differentiated from malignancies through imaging and cytological evaluation. *Multinodular goiter* - Usually involves multiple nodules rather than a **single nodule**, and patients often present with thyroid dysfunction [1]. - More common in women, and does not fit the profile of a solitary nodule in a euthyroid male. *Follicular Carcinoma* - While it can present as a nodule, it typically involves **elevated risk factors** such as family history and certain genetic mutations. - Euthyroid status alone is insufficient for a diagnosis of malignancy without further alarming features. *Thyroid Cyst* - Cysts are usually **fluid-filled** and may not present as solid nodules, which are common in cases described. - They tend to be **asymptomatic** and are generally **benign**, lacking the solid characteristics of a follicular adenoma.

Question 1573: A 65 year old female presents with a swelling in the neck diagnosed as a solitary thyroid nodule. The patient is investigated and a scan shows increased uptake of iodine. Serum T3 and T4 are elevated . Most probabe diagnosis is

A. Benign Thyroid Nodule
B. Solitary Toxic Adenoma (Correct Answer)
C. Follicular Carcinoma
D. Toxic Multinodular Goiter

Explanation: A **solitary toxic adenoma** is a single thyroid nodule that autonomously produces thyroid hormones, leading to **hyperthyroidism**. The increased iodine uptake on scan reflects its hyperfunctional state, and elevated **T3/T4** confirms hyperthyroidism. [2] - The combination of a **solitary nodule**, **increased iodine uptake**, and **elevated thyroid hormone levels** is pathognomonic for a solitary toxic adenoma. [2] *Benign Thyroid Nodule* - A **benign thyroid nodule** without hyperfunction would typically show **normal or decreased iodine uptake** and **normal T3/T4** levels. [2] - While benign, such a nodule alone does not explain the **elevated T3/T4** or **increased iodine uptake**. *Follicular Carcinoma* - **Follicular carcinoma** is a type of thyroid cancer that typically presents as a **cold nodule** (decreased iodine uptake) and is usually **non-functional**, meaning it does not cause hyperthyroidism with elevated T3/T4. [2] - The presence of **increased iodine uptake** and **hyperthyroidism** makes follicular carcinoma highly unlikely. *Toxic Multinodular Goiter* - A **toxic multinodular goiter** involves **multiple nodules**, not a solitary one, that are autonomously functional and cause hyperthyroidism. [1] - While it causes **hyperthyroidism** and **increased iodine uptake**, the key differentiating factor here is the presentation as a **solitary nodule**.

Question 1574: In a patient with hypoglycemia, what is the appropriate dose adjustment of insulin?

A. Increase insulin dosage
B. Decrease insulin dosage (Correct Answer)
C. Maintain current insulin dosage
D. Add a different medication

Explanation: ***Decrease insulin dosage*** - Hypoglycemia indicates that the current insulin dose is too high, causing blood glucose levels to drop excessively [1]. - Reducing the insulin dosage helps prevent future episodes of low blood sugar by allowing blood glucose to remain within a healthier range [1]. *Increase insulin dosage* - Increasing insulin would further lower blood glucose, exacerbating the **hypoglycemia** and potentially leading to a more severe and dangerous state. - This action is appropriate for **hyperglycemia**, not hypoglycemia. *Maintain current insulin dosage* - Maintaining the current dose would not address the problem, as it has already proven to be too much for the patient, causing the **hypoglycemic episodes** [1]. - This approach would leave the patient at continued risk for recurrent hypoglycemia. *Add a different medication* - While other medications might be used in diabetes management, adding a new one without adjusting the existing insulin dose could further complicate blood glucose control. - The immediate and most direct action for **hypoglycemia** caused by insulin is to adjust the insulin itself [1].

Question 1575: What is the recommended postprandial capillary glucose level (in mg/dl) for adequate diabetes control?

A. < 180 mg/dl (Correct Answer)
B. < 200 mg/dl
C. < 100 mg/dl
D. < 140 mg/dl

Explanation: ***< 180 mg/dl*** - This is the **recommended target** for postprandial (1-2 hours after a meal) capillary glucose levels in most non-pregnant adults with diabetes to achieve **adequate glycemic control** [1], [2]. - Maintaining levels below 180 mg/dl helps to minimize the risk of **long-term microvascular and macrovascular complications**. *< 100 mg/dl* - While this is an ideal fasting glucose level, it is generally **too low for postprandial glucose**, and attempting to maintain such levels might increase the risk of **hypoglycemia** in many patients with diabetes [1]. - This target is more appropriate for **fasting or pre-meal glucose** goals. *< 140 mg/dl* - This is a **more stringent target** that may be appropriate for some individuals with diabetes, particularly those who are carefully managed and at low risk of hypoglycemia. - However, for the general population with diabetes, **< 180 mg/dl is the more commonly accepted and achievable goal** for postprandial readings [2]. *< 200 mg/dl* - A postprandial glucose level of < 200 mg/dl is considered **good control** in some contexts, but it's often a **less strict target** than < 180 mg/dl for optimal long-term management. - While better than uncontrolled high levels, consistently approaching 200 mg/dl may still contribute to **increased risk of complications** over time compared to tighter control.

Question 1576: Most common cause of Addison's Disease in India is:

A. Autoimmune
B. HIV
C. Tuberculosis (Correct Answer)
D. Malignancy

Explanation: ***Tuberculosis*** - In India, **tuberculosis** is the most common cause of **Addison's disease** due to the high prevalence of TB infections. - Adrenal involvement in TB can lead to gradual destruction of the adrenal cortex, resulting in **adrenal insufficiency**. *Autoimmune* - **Autoimmune adrenalitis** is the leading cause of Addison's disease in developed Western countries. - It involves the destruction of adrenal cortical cells by the body's own immune system, often associated with other autoimmune conditions. *Malignancy* - **Malignancy**, particularly metastatic cancer to the adrenals, can cause adrenal insufficiency but is a less common primary cause of Addison's disease overall. - While possible, it is not the most prevalent cause in India compared to infectious etiologies. *HIV* - **HIV infection** can lead to adrenal dysfunction, but it's typically through opportunistic infections like CMV, cryptococcosis, or direct HIV effects, rather than being the direct cause of widespread adrenal destruction. - It increases the risk of adrenal insufficiency but is not the most common etiology in India for Addison's disease.

Question 1577: Female with blood sugar of 600 mg% and sodium of 110 mEq. Insulin was given, what will happen to serum sodium levels ?

A. Sodium levels may appear to increase (Correct Answer)
B. Sodium levels decrease
C. Sodium levels remain unchanged
D. Relative sodium deficiency may occur

Explanation: ***Sodium levels may appear to increase*** - The patient's initial presentation with severe hyperglycemia (600 mg%) and hyponatremia (110 mEq/L) suggests **hyperglycemia-induced pseudohyponatremia**. - **Insulin administration** will lower blood glucose, causing water to shift back into the cells from the extracellular space, thereby correcting the dilutional effect and leading to an **apparent increase in serum sodium levels**. *Sodium levels decrease* - This is incorrect because the hyponatremia in this scenario is largely **dilutional** due to hyperglycemia. - As glucose levels decrease with insulin, the osmotic drive for water movement out of cells diminishes, leading to **normalization**, not further decrease, of sodium concentration. *Sodium levels remain unchanged* - This is incorrect because the underlying cause of the initial low sodium is dilution from high glucose. - Once **hyperglycemia is treated**, the osmotic gradient changes, and water shifts, directly impacting and changing the serum sodium concentration. *Relative sodium deficiency may occur* - This option is incorrect because the initial hyponatremia is not primarily due to an absolute lack of sodium in the body but rather a **dilutional effect** caused by the osmotic pull of glucose. - As hyperglycemia resolves, the extracellular fluid becomes less diluted, and the measured sodium concentration will **rise**, not indicate a deficiency.

Question 1578: Which of the following is NOT a criterion for the diagnosis of Primary Hyperaldosteronism?

A. Diastolic Hypertension without edema
B. Low Plasma Renin Activity
C. Hyperkalemia (Correct Answer)
D. Hyperaldosteronism which is not suppressed by volume expansion

Explanation: Primary hyperaldosteronism is typically characterized by **hypokalemia** due to excessive aldosterone-mediated potassium excretion in the urine, not hyperkalemia [1]. Hyperkalemia would suggest other conditions, such as **adrenal insufficiency** or kidney disease, rather than primary hyperaldosteronism [2]. *Diastolic Hypertension without edema* - **Diastolic hypertension** is a common presentation of primary hyperaldosteronism due to increased **sodium and water retention**, leading to expanded extracellular volume. - The absence of significant edema is also common, as the body often develops an **"escape phenomenon"** where natriuresis occurs despite high aldosterone, preventing overt fluid overload [3]. *Low Plasma Renin Activity* - In primary hyperaldosteronism, the high aldosterone levels **suppress renin secretion** through negative feedback mechanisms. - Therefore, a **low plasma renin activity** (PRA) or plasma renin concentration (PRC) is a key diagnostic feature [4]. *Hyperaldosteronism which is not suppressed by volume expansion* - Normally, volume expansion would suppress aldosterone secretion. However, in primary hyperaldosteronism, aldosterone production is **autonomous** and remains elevated even after volume expansion. - This lack of suppression is a critical diagnostic criterion, often assessed through various **confirmatory tests** like saline infusion or oral sodium loading.

Question 1579: Hyperpigmentation is seen with which hormone?

A. TSH
B. ACTH (Correct Answer)
C. FSH
D. LH

Explanation: ***ACTH*** - In conditions like **Addison's disease**, the adrenal glands' inability to produce cortisol leads to increased **ACTH** (adrenocorticotropic hormone) secretion due to a lack of negative feedback [3], [4]. - ACTH is derived from proopiomelanocortin (POMC), which also gives rise to alpha-melanocyte-stimulating hormone (α-MSH). Elevated ACTH levels can thus stimulate melanocytes, causing **hyperpigmentation** in skin folds, buccal mucosa, and pressure points [4]. *FSH* - **FSH** (follicle-stimulating hormone) primarily regulates the development of **follicles in the ovaries** and sperm production in the testes [1]. - There is no known direct association between excessive FSH levels and **hyperpigmentation**. *TSH* - **TSH** (thyroid-stimulating hormone) stimulates the **thyroid gland** to produce thyroid hormones (T3 and T4) [1]. - While thyroid disorders can affect skin texture and moisture, there is no direct link between elevated TSH and **hyperpigmentation**. *LH* - **LH** (luteinizing hormone) plays a key role in **ovulation** in females and testosterone production in males [2]. - High LH levels are not associated with **hyperpigmentation**.

Question 1580: What is the best indicator for assessing short-term control of blood glucose levels over a period of 2-3 weeks?

A. Serum fructosamine (Correct Answer)
B. Blood sugar
C. Urine sugar
D. HbA1c

Explanation: ***Serum fructosamine*** - **Fructosamine** reflects the glycation of serum proteins, primarily albumin, which has a shorter half-life (around 17-20 days) compared to hemoglobin. - This allows it to assess average blood glucose control over the preceding **2-3 weeks**, making it suitable for short-term monitoring. *HbA1c* - **HbA1c** (glycated hemoglobin) reflects average blood glucose levels over the lifespan of red blood cells, typically **2-3 months** [1]. - While an excellent long-term indicator, its longer time frame makes it less suitable for assessing short-term changes over just 2-3 weeks [1]. *Blood sugar* - A single **blood sugar** measurement (fasting or random) provides an instantaneous snapshot of glucose levels at that specific moment [2]. - It does not reflect average glucose control over a period of 2-3 weeks and is highly influenced by recent food intake and activity [2]. *Urine sugar* - **Urine sugar** levels indicate that the kidney's reabsorption capacity for glucose has been exceeded, resulting in glucose spilling into the urine [3]. - This is a qualitative or semi-quantitative measure that primarily reflects very high blood glucose levels and is not a reliable indicator of averaged glucose control over any specific time frame [3].

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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