Endocrinology Practice Questions

Q: Which of the following is seen in Conn's syndrome?

Hypokalemia. ***Hypokalemia*** - In Conn's syndrome (primary hyperaldosteronism), excessive **aldosterone** secretion leads to increased renal reabsorption of sodium and excretion of **potassium** and hydrogen ions, resulting in hypokalemia. - This persistent electrolyte imbalance can manifest clinically as muscle weakness, fatigue, and cardiac arrhythmias. *Hypertension* - While hypertension is a prominent feature of Conn's syndrome due to increased sodium reabsorption and water retention, it is a **symptom** or **consequence** of the condition, not the underlying biochemical derangement that defines the syndrome itself. - The elevated aldosterone causes volume expansion and increased vascular tone, leading to systemic hypertension. *Metabolic alkalosis* - Metabolic alkalosis can occur in Conn's syndrome due to the renal excretion of **hydrogen ions** in exchange for sodium reabsorption. - However, it is a **secondary effect** of the hyperaldosteronism and is not the primary defining biochemical abnormality like hypokalemia. *Edema* - Edema is generally **not a common or prominent** feature of Conn's syndrome despite the increased sodium reabsorption. - The body's "escape phenomenon" often limits significant fluid retention and overt edema, preventing gross fluid overload.

Q: Which of the following clinical problems is NOT associated with hypothyroidism?

Weight loss is associated with hypothyroidism.. Weight loss is associated with hypothyroidism. - Hypothyroidism is characterized by a **decreased metabolic rate**, leading to common symptoms like **weight gain** and difficulty losing weight [1]. - Therefore, **weight loss** is not a typical clinical problem associated with hypothyroidism; rather, it is often seen in hyperthyroidism [1]. *Menorrhagia is associated with hypothyroidism.* - Hypothyroidism can lead to **menorrhagia** (heavy menstrual bleeding) due to impaired coagulation factor synthesis and altered estrogen metabolism. - The **slowed metabolism** can affect the breakdown of estrogen, leading to prolonged endometrial stimulation. *Early abortions are associated with hypothyroidism.* - **Untreated hypothyroidism** in pregnant individuals is associated with an increased risk of **early pregnancy loss** and recurrent miscarriages. - This is thought to be due to an inadequate uterine environment and hormonal imbalances critical for a viable pregnancy. *Galactorrhoea is associated with hypothyroidism.* - Hypothyroidism can cause **hyperprolactinemia** due to increased **thyrotropin-releasing hormone (TRH)**, which stimulates prolactin release. - Elevated prolactin levels can lead to **galactorrhoea** (milk production unrelated to childbirth or breastfeeding).

Q: Which of the following is not a marker for hyperparathyroidism?

Alteration in serum calcitonin levels. ***Alteration in serum calcitonin levels*** - While calcitonin plays a role in calcium regulation, its levels are generally **not directly altered** in primary hyperparathyroidism. - Calcitonin is secreted by **parafollicular C cells of the thyroid gland** and acts to lower plasma calcium, *Increase in serum calcium* - **Hypercalcemia** is a hallmark of primary hyperparathyroidism, as excess PTH mobilizes calcium from bones and increases renal reabsorption [2]. - Prolonged elevation can lead to symptoms like **"stones, bones, groans, and psychic overtones"** [1]. *Increase in serum parathyroid hormone (PTH) levels* - An **elevated PTH level** is the primary diagnostic criterion for primary hyperparathyroidism [1]. - This indicates an overactive parathyroid gland, which is responsible for **regulating calcium homeostasis**. *Subperiosteal bone resorption of phalanges* - This is a classic radiographic finding in advanced **primary hyperparathyroidism**, particularly in the **distal phalanges**. - It results from the continuous action of **excess PTH on osteoclasts**, leading to bone breakdown [1].

Q: The commonest cause of primary hyperparathyroidism is what?

Solitary parathyroid adenoma. ***Solitary parathyroid adenoma*** - A **solitary parathyroid adenoma** is the cause of **80-85%** of primary hyperparathyroidism cases [2]. - This benign tumor leads to excessive parathyroid hormone (PTH) secretion, causing **hypercalcemia** [3]. *Parathyroid carcinoma* - **Parathyroid carcinoma** is a very rare cause of primary hyperparathyroidism, accounting for less than **1%** of cases. - While it also causes hypercalcemia, its clinical presentation is often more severe with significantly higher PTH and calcium levels, often with a palpable neck mass. *Chronic kidney disease* - **Chronic kidney disease** is a common cause of **secondary hyperparathyroidism**, not primary hyperparathyroidism [2]. - In secondary hyperparathyroidism, low calcium and vitamin D levels (due to impaired kidney function) stimulate the parathyroid glands to produce more PTH [1], [2]. *Parathyroid hyperplasia* - **Parathyroid hyperplasia**, involving enlargement of all four parathyroid glands, accounts for about **10-15%** of primary hyperparathyroidism cases. - It is the second most common cause after solitary adenomas, but still less frequent.

Q: Which of the following is a common laboratory finding in hypothyroidism?

High TSH. ### High TSH - In **primary hypothyroidism**, the thyroid gland fails to produce adequate thyroid hormones (**T3** and **T4**). [1] - This leads to a compensatory increase in **TSH** release from the pituitary gland, attempting to stimulate the thyroid. [1] *Low T3* - While **low T3** can be present in hypothyroidism, **low free T4** is generally a more sensitive and specific marker for the diagnosis of primary hypothyroidism. [1] - T3 levels can sometimes remain normal or only slightly reduced even in overt hypothyroidism, especially in the early stages. *High cholesterol* - **Elevated cholesterol**, particularly **LDL (low-density lipoprotein)**, is a common metabolic consequence of hypothyroidism due to decreased catabolism of lipids. [2] - However, it is a metabolic complication rather than a direct hormonal lab finding defining hypothyroidism. *High Triglycerides* - **High triglycerides** can also be observed in hypothyroidism due to impaired lipid metabolism and reduced lipoprotein lipase activity. - Similar to elevated cholesterol, it is a metabolic consequence, not a primary diagnostic marker for the thyroid hormone imbalance itself.

Q: Middle-aged female with a mass in the sella turcica, what is the hormone level that is increased?

Prolactin. ***Prolactin*** - A mass in the **sella turcica** suggests a **pituitary adenoma**, and the most common type is a **prolactinoma** [1]. - **Prolactinomas** cause an elevation in **prolactin levels**, leading to symptoms like galactorrhea, amenorrhea, and infertility in women [1]. *Thyroxine* - An increase in **thyroxine** usually indicates **hyperthyroidism**, which results from thyroid gland dysfunction or a TSH-secreting pituitary adenoma, not typically a mass directly causing elevated thyroxine. - While TSH-secreting adenomas are rare causes of thyrotoxicosis, a non-functional or prolactin-secreting pituitary mass would not directly increase peripheral thyroxine levels [2]. *ADH* - **Antidiuretic hormone (ADH)**, also known as vasopressin, is primarily involved in water balance. - While ADH can be affected by pituitary lesions, an increase would typically lead to **syndrome of inappropriate ADH secretion (SIADH)**, causing hyponatremia, which is not the primary presentation for most sella turcica masses. *Estrogen* - **Estrogen** levels are regulated by the ovaries under the influence of FSH and LH from the pituitary. - While pituitary masses can affect gonadotropin secretion (FSH/LH), leading to changes in estrogen, the mass itself does not directly secrete estrogen.

Q: Which of the following conditions is least likely to cause hypercalcemia?

SLE. ***SLE*** - **Systemic lupus erythematosus (SLE)** is an autoimmune disease rarely associated with hypercalcemia. While various electrolyte imbalances can occur in SLE, hypercalcemia is not a typical manifestation, and other calcium-related issues like hypocalcemia (due to renal involvement or vitamin D deficiency) might be more common [3], [4]. - The inflammatory and immune mechanisms in SLE do not generally promote the increased production of activated **vitamin D** or significant bone resorption seen in other causes of hypercalcemia. *TB* - **Tuberculosis (TB)**, particularly disseminated forms, can cause hypercalcemia due to **granuloma formation** [1]. - These **granulomas** contain **macrophages** that have aberrant 1-alpha-hydroxylase activity, leading to increased production of **1,25-dihydroxyvitamin D**, which enhances calcium absorption from the gut and bone resorption [1]. *Berylliosis* - **Berylliosis** is a chronic inflammatory disease caused by exposure to beryllium, characterized by **granuloma formation** in various organs, most commonly the lungs. - Similar to sarcoidosis and TB, the **granulomas** in berylliosis can produce **1,25-dihydroxyvitamin D**, leading to increased calcium absorption and subsequent **hypercalcemia** [1]. *Sarcoidosis* - **Sarcoidosis** is known to cause **hypercalcemia** in a significant percentage of patients (around 10-20%) [1], [2]. - The mechanism involves **macrophages** within the **granulomas** producing **1,25-dihydroxyvitamin D**, which leads to increased intestinal calcium absorption and bone resorption [1].

Q: The best marker for hyperthyroidism is

TSH. ***TSH*** - **TSH (Thyroid-Stimulating Hormone)** is the most sensitive and specific initial test for evaluating thyroid function. - In **hyperthyroidism**, the thyroid gland produces excess thyroid hormones (T3 and T4), which suppresses TSH release from the pituitary gland, leading to **very low or undetectable TSH levels**. *T3* - While **elevated T3 levels** are diagnostic of hyperthyroidism, TSH is a more sensitive initial screen. - Some patients, particularly those with **T3 toxicosis**, may have elevated T3 but normal T4. *T4* - **Elevated T4 levels** are a key indicator of hyperthyroidism, but TSH often reflects changes in thyroid hormone status earlier and is more sensitive for screening. - **Free T4** is preferred over total T4 as it is not affected by protein binding changes. *Thyroglobulin* - **Thyroglobulin** is a protein produced by the thyroid gland and is primarily used as a **tumor marker** in patients with differentiated thyroid cancer after thyroidectomy. - It is **not a primary diagnostic marker for hyperthyroidism**, although it can be elevated in conditions causing thyroid destruction or inflammation.

Q: The triad of diabetes, gallstones, and steatorrhea is associated with which of the following?

Somatostatinomas. ***Somatostatinomas*** - This **triad** is characteristic of a somatostatinoma, as somatostatin inhibits insulin release, gallbladder contraction, and pancreatic enzyme secretion. - The inhibition of **insulin release** leads to diabetes [1], blocked **cholecystokinin (CCK)** release causes gallstones, and reduced **pancreatic enzyme** secretion results in steatorrhea. *Gastrinomas* - Gastrinomas typically cause **Zollinger-Ellison syndrome**, characterized by severe peptic ulcers and diarrhea due to excessive acid production. - They are not directly associated with the specific triad of diabetes, gallstones, and steatorrhea. *VIPomas* - VIPomas are known for causing **Verner-Morrison syndrome** or pancreatic cholera, leading to severe watery diarrhea, hypokalemia, and achlorhydria. - Diabetes and gallstones are not prominent features of VIPomas. *Glucagonomas* - Glucagonomas primarily manifest with **diabetes** (due to elevated glucagon), a characteristic skin rash called **necrolytic migratory erythema**, and weight loss [1]. - While diabetes is present, gallstones and steatorrhea are not typical associations.

Q: In a patient presenting with diabetic ketoacidosis (DKA), what is the most appropriate immediate treatment?

Administration of insulin. ***Administration of insulin*** - **Insulin therapy** is critical in DKA to reverse the underlying metabolic abnormalities by stopping ketogenesis and facilitating glucose uptake into cells [1]. - It is typically administered intravenously at a continuous rate, after initial **fluid resuscitation**, to gradually lower blood glucose and resolve acidosis [1]. *Administration of an oral hypoglycemic agent* - **Oral hypoglycemic agents** are ineffective in DKA because these patients typically have an absolute or relative **insulin deficiency** and **profound insulin resistance** due to stress hormones [3]. - Moreover, they are not suitable for acutely ill patients who may have impaired gastrointestinal absorption. *Administration of bicarbonate* - **Bicarbonate administration** is generally not recommended in DKA unless the **pH is extremely low** (e.g., < 6.9 or 7.0) due to potential risks like paradoxical central nervous system acidosis and fluid overload. - The acidosis usually resolves with **insulin therapy** and **fluid resuscitation** as ketone body production ceases and they are metabolized [1]. *Close observation only* - **Diabetic ketoacidosis** is a medical emergency requiring urgent and aggressive intervention, not just observation [2]. - Delaying treatment can lead to severe complications, including **cerebral edema**, **coma**, and **death** [2].

Question 1

Which of the following is seen in Conn's syndrome?

Accepted Answer

Hypokalemia

Answer

Metabolic alkalosis

Answer

Hypertension

Answer

Edema

Question 2

Which of the following clinical problems is NOT associated with hypothyroidism?

Accepted Answer

Weight loss is associated with hypothyroidism.

Answer

Early abortions are associated with hypothyroidism.

Answer

Galactorrhoea is associated with hypothyroidism.

Answer

Menorrhagia is associated with hypothyroidism.

Question 3

Which of the following is not a marker for hyperparathyroidism?

Accepted Answer

Alteration in serum calcitonin levels

Answer

Increase in serum parathyroid hormone (PTH) levels

Answer

Subperiosteal bone resorption of phalanges

Answer

Increase in serum calcium

Question 4

The commonest cause of primary hyperparathyroidism is what?

Accepted Answer

Solitary parathyroid adenoma

Answer

Parathyroid carcinoma

Answer

Chronic kidney disease

Answer

Parathyroid hyperplasia

Question 5

Which of the following is a common laboratory finding in hypothyroidism?

Accepted Answer

High TSH

Answer

Low T3

Answer

High cholesterol

Answer

High Triglycerides

Question 6

Middle-aged female with a mass in the sella turcica, what is the hormone level that is increased?

Accepted Answer

Prolactin

Answer

Thyroxine

Answer

ADH

Answer

Estrogen

Question 7

Which of the following conditions is least likely to cause hypercalcemia?

Accepted Answer

SLE

Answer

Berylliosis

Answer

TB

Answer

Sarcoidosis

Question 8

The best marker for hyperthyroidism is

Accepted Answer

TSH

Answer

T3

Answer

T4

Answer

Thyroglobulin

Question 9

The triad of diabetes, gallstones, and steatorrhea is associated with which of the following?

Accepted Answer

Somatostatinomas

Answer

VIPomas

Answer

Gastrinomas

Answer

Glucagonomas

Question 10

In a patient presenting with diabetic ketoacidosis (DKA), what is the most appropriate immediate treatment?

Accepted Answer

Administration of insulin

Answer

Administration of an oral hypoglycemic agent

Answer

Administration of bicarbonate

Answer

Close observation only

Endocrinology — MCQs

Endocrinology — MCQs

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