Endocrinology Practice Questions

Q: Which of the following is NOT a typical effect of hypoparathyroidism on bones?

Brown tumors. Hypoparathyroidism typically does not lead to direct **bone resorption** or the formation of **bone lesions** like brown tumors. The condition results in low serum calcium, but the skeletal effects are not characterized by any of the changes noted in the other options. *Subperiosteal Resorption of Bone* - This is commonly seen in **hyperparathyroidism**, where increased osteoclastic activity leads to bone resorption [1]. Parathyroid hormone (PTH) acts on the skeleton to increase osteoclastic bone resorption; thus, in hypoparathyroidism, there is **decreased bone turnover** with no subperiosteal resorption occurring [1]. *Brown tumours* - Brown tumors are associated with **hyperparathyroidism** due to osteitis fibrosa cystica, characterized by **osteoclastic resorption** [1]. Prolonged exposure of bone to high levels of PTH is associated with these changes, which do not occur in hypoparathyroidism [1]. *Multiple Cysts in Bone* - Multiple bone cysts often represent conditions such as **osteitis fibrosa cystica** in **hyperparathyroidism** or other osteolytic lesions [2]. Hypoparathyroidism primarily leads to a reduction in bone remodeling without promoting cyst formation.

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

Excess stimulation of the HPO axis. ***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.

Q: 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

Solitary Toxic Adenoma. 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**.

Q: In which condition is Chvostek's sign typically observed?

Hypoparathyroidism. Hypoparathyroidism - **Chvostek's sign** is a clinical manifestation of **hypocalcemia**, which is a hallmark of hypoparathyroidism [1]. - It involves a twitch of facial muscles elicited by tapping the **facial nerve** anterior to the ear. Hypercalcemia - **Hypercalcemia** is the opposite of hypocalcemia and would not cause increased neuromuscular excitability [2]. - Patients with hypercalcemia might experience symptoms like **fatigue**, **constipation**, and **bone pain** [2]. Insulinoma - An **insulinoma** is a tumor that produces excessive insulin, leading to **hypoglycemia**, not issues with calcium balance. - Symptoms are primarily related to low blood sugar, such as **confusion** and **tachycardia**. Diabetes mellitus - **Diabetes mellitus** is a metabolic disorder characterized by **high blood glucose levels** due to insulin deficiency or resistance. - It is not directly associated with calcium imbalances that would cause Chvostek's sign.

Q: Hyperpigmentation is seen with which hormone?

ACTH. ***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**.

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

Sodium levels may appear to increase. ***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.

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

Hyperkalemia. 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.

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

< 180 mg/dl. ***< 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.

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

Decrease insulin dosage. ***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].

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

Tuberculosis. ***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 1

Which of the following is NOT a typical effect of hypoparathyroidism on bones?

Accepted Answer

Brown tumors

Answer

Osteosclerosis

Answer

Multiple bone cysts

Answer

None of the above

Question 2

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

Accepted Answer

Excess stimulation of the HPO axis

Answer

Hypogonadotropic hypogonadism

Answer

Anosmia

Answer

Amenorrhea

Question 3

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

Accepted Answer

Solitary Toxic Adenoma

Answer

Benign Thyroid Nodule

Answer

Follicular Carcinoma

Answer

Toxic Multinodular Goiter

Question 4

In which condition is Chvostek's sign typically observed?

Accepted Answer

Hypoparathyroidism

Answer

Hypercalcemia

Answer

Insulinoma

Answer

Diabetes mellitus

Question 5

Hyperpigmentation is seen with which hormone?

Accepted Answer

ACTH

Answer

TSH

Answer

FSH

Answer

LH

Question 6

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

Accepted Answer

Sodium levels may appear to increase

Answer

Sodium levels decrease

Answer

Sodium levels remain unchanged

Answer

Relative sodium deficiency may occur

Question 7

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

Accepted Answer

Hyperkalemia

Answer

Diastolic Hypertension without edema

Answer

Low Plasma Renin Activity

Answer

Hyperaldosteronism which is not suppressed by volume expansion

Question 8

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

Accepted Answer

< 180 mg/dl

Answer

< 200 mg/dl

Answer

< 100 mg/dl

Answer

< 140 mg/dl

Question 9

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

Accepted Answer

Decrease insulin dosage

Answer

Increase insulin dosage

Answer

Maintain current insulin dosage

Answer

Add a different medication

Question 10

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

Accepted Answer

Tuberculosis

Answer

Autoimmune

Answer

HIV

Answer

Malignancy

Endocrinology — MCQs

Endocrinology — MCQs

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