Endocrinology Practice Questions

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].

Q: A middle-aged male patient who was involved in a road traffic accident and brought to the emergency department in an unconscious state. A computed tomography (CT) scan of the abdomen revealed a splenic laceration, and emergency splenectomy was performed. The patient was then transferred to the intensive care unit (ICU). Despite receiving a bolus of normal saline, his blood pressure remained low in the postoperative period. On examination, he was afebrile, had a moon-like face with central obesity, and exhibited violet striae on his abdomen. A repeat CT scan of the chest, abdomen, and pelvis showed no evidence of hemorrhage. What is the next best step in managing this patient?

Administer hydrocortisone 100 mg IV. ***Administer hydrocortisone 100 mg IV*** - The patient's presentation with **hypotension unresponsive to fluid resuscitation**, combined with a **moon-like face**, **central obesity**, and **violet striae**, strongly suggests **adrenal insufficiency** as a complication of **Cushing's syndrome**. [1] - **Adrenal crisis** requires immediate administration of **stress-dose corticosteroids** to prevent cardiovascular collapse. [1] *Return to the operating room for exploratory laparotomy* - A **repeat CT scan** confirmed no evidence of hemorrhage, ruling out **active bleeding** as the cause of refractory hypotension. - Therefore, subjecting the patient to another surgery without evidence would be unnecessary and introduce additional risks. *Administer vancomycin and piperacillin/tazobactam* - The patient is **afebrile**, and there are no signs or symptoms suggestive of a **postoperative infection**. - Initiating broad-spectrum antibiotics without an indication in an already compromised patient is not appropriate and could contribute to **antibiotic resistance**. *Perform MRI of the spine.* - There is nothing in the patient's presentation that suggests **spinal cord injury** as the cause of his current unstable condition. - While the patient was in a **road traffic accident**, the primary issues are related to **hemodynamic instability** and suspected **endocrine dysfunction**, not neurological deficit.

Q: Nelson syndrome is associated with:

Bilateral adrenalectomy. ***Bilateral adrenalectomy*** - **Nelson syndrome** develops in a subset of patients with Cushing's disease after **bilateral adrenalectomy**. [1] - It is caused by the loss of negative feedback from adrenal cortisol on the pituitary, leading to continued growth of an existing **ACTH-secreting pituitary adenoma**. *Prophylactic craniospinal irradiation* - **Craniospinal irradiation** is a radiotherapy technique used to treat disseminated cancers like medulloblastoma but is not directly associated with the etiology of Nelson syndrome. - While pituitary tumors can be treated with radiotherapy, this is typically given once a tumor has caused symptoms, not prophylactically in this context. *Subarachnoid hemorrhage* - **Subarachnoid hemorrhage** is bleeding into the space between the brain and the surrounding membrane, often caused by ruptured **aneurysms** or **trauma**. - It is a neurological emergency unrelated to the development of Nelson syndrome. *BRCA2 mutation* - **BRCA2 mutations** are strongly associated with an increased risk of developing various cancers, most notably **breast** and **ovarian cancer**. - This genetic mutation is not linked to the pathogenesis of Nelson syndrome, which is an endocrine complication following surgery.

Q: A young patient presented with hypertension and a 24-hour urinary metanephrine level of 1.4 mg, the most likely causes are -

VonHippelLindau syndrome. ***Von Hippel-Lindau syndrome*** - This syndrome is a **hereditary condition** predisposing individuals to various tumors, including **pheochromocytomas**, which cause elevated **metanephrines** and hypertension. - The combination of **hypertension** in a young patient and an elevated **24-hour urinary metanephrine level** (indicating excessive catecholamine production) strongly suggests a pheochromocytoma, which is frequently associated with Von Hippel-Lindau syndrome. *Medullary carcinoma thyroid* - This cancer is associated with **MEN 2 syndromes** and produces **calcitonin**, leading to hypocalcemia, but not typically elevated metanephrines or hypertension directly from the thyroid. - While it can be associated with **pheochromocytoma** (as part of MEN 2), it is not the direct cause of the elevated metanephrines. *Grave's disease* - **Grave's disease** is an autoimmune disorder causing **hyperthyroidism**, characterized by symptoms like goiter, exophthalmos, and weight loss. - While it can cause hypertension due to increased cardiac output, it does not lead to elevated **urinary metanephrine levels**, which are specific to catecholamine excess. *Pseudohypoparathyroidism* - This is a genetic disorder characterized by **target organ resistance to parathyroid hormone (PTH)**, leading to hypocalcemia and hyperphosphatemia [1]. - It does not cause hypertension or elevated **urinary metanephrine levels**.

Q: What is the preferred insulin regimen during pregnancy?

Insulin NPH + Lispro. ***Insulin NPH + Lispro*** - **NPH insulin** is a preferred basal insulin during pregnancy due to its long-standing safety record and intermediate duration of action [1]. - **Insulin Lispro** is a rapid-acting insulin analog that is safe and effective for postprandial glucose control in pregnant women [1]. *Insulin Regular + NPH* - While NPH is safe, **regular insulin** has a slower onset and longer duration compared to rapid-acting analogs, making it less ideal for precise postprandial control [2]. - Achieving tight glycemic control with regular insulin can be challenging due to its peak action occurring later, potentially leading to **postprandial hyperglycemia** or **unpredictable hypoglycemia** [2]. *Insulin Degludec* - **Insulin Degludec** is a newer ultra-long-acting insulin analog, and while effective, there is currently limited data on its long-term safety during pregnancy. - Due to insufficient robust safety data, it is generally **not the preferred first-line basal insulin** for pregnant women. *Insulin Lispro + Insulin regular* - This combination lacks a dedicated **basal insulin** component, which is crucial for maintaining fasting and between-meal glucose levels [2]. - Relying solely on rapid-acting and short-acting insulins without basal coverage would likely result in **poor glycemic control** throughout the day and night [1].

Q: Which clinical features are specifically associated with congenital adrenal hyperplasia due to 21-hydroxylase deficiency?

Female pseudohermaphroditism. ***All of the above*** - 21-hydroxylase deficiency leads to a lack of cortisol and aldosterone, causing adrenal crisis. Thus, **hyponatremia**, **hyperkalemia**, and **ambiguous genitalia** in females are clinical features associated with this condition [1]. - It also results in **female pseudohermaphroditism** due to excess androgen exposure in utero, showcasing the spectrum of symptoms seen [1]. *Hyponatremia and hyperkalemia* - While these are common electrolyte abnormalities seen in adrenal crisis due to **aldosterone deficiency**, they don't capture the entire clinical picture of 21-hydroxylase deficiency [1]. - Focusing solely on these abnormalities neglects significant features like **ambiguous genitalia** and **pseudohermaphroditism**. *Ambiguous genitalia in females* - This is indeed a critical feature of 21-hydroxylase deficiency but does not represent the full array of clinical manifestations involved [1]. - The deficiency also affects electrolyte balance which is a crucial aspect, thereby making it insufficient as a standalone answer. *Female pseudohermaphroditism* - While **female pseudohermaphroditism** due to androgen excess is a key characteristic, it is just one of multiple clinical features of this condition [1]. - This option overlooks **hyponatremia**, **hyperkalemia**, and **ambiguous genitalia**, which are all critical for a comprehensive understanding of the disorder [1].

Q: All of the following may be associated with primary aldosteronism, except:

Von-Hippel-Lindau syndrome. ***Von-Hippel-Lindau syndrome*** - **Von Hippel-Lindau (VHL) syndrome** is a genetic disorder commonly associated with tumors such as **pheochromocytomas**, **renal cell carcinoma**, hemangioblastomas, and pancreatic neuroendocrine tumors, but not primary aldosteronism. - While VHL can involve adrenal glands (pheochromocytomas being a common manifestation), it does not directly cause **aldosterone overproduction** leading to primary aldosteronism. *Adrenal adenoma* - A **solitary adrenal adenoma** is the most common cause of primary aldosteronism, often referred to as **Conn's syndrome** [1]. - These benign tumors autonomously secrete **aldosterone**, leading to hypertension and hypokalemia [1]. *Adrenal hyperplasia* - **Bilateral adrenal hyperplasia** is the second most common cause of primary aldosteronism, where both adrenal glands produce excessive aldosterone. - This condition is often managed medically rather than surgically, in contrast to unilateral adenomas [1]. *Adrenal carcinoma* - Although rare, a **functional adrenal carcinoma** can cause primary aldosteronism by overproducing aldosterone [1]. - These malignant tumors are typically larger and more aggressive than adenomas [1].

Q: Which of the following is the most prominent clinical manifestation of primary hyperaldosteronism (Conn's syndrome)?

Hypertension. ** Hypertension** - **Hypertension** is the most prominent and consistent clinical manifestation of primary hyperaldosteronism, present in nearly all patients. - The excessive aldosterone leads to increased **sodium reabsorption** and water retention, directly causing elevated blood pressure [2], [3]. *Hypokalemia* - While **hypokalemia** is common in primary hyperaldosteronism due to increased renal potassium excretion, it is not universally present and can be absent in a significant portion of patients (up to 30-50%). - Therefore, hypertension is a more reliable and prominent symptom for initial suspicion [3]. *Hyperkalemia* - **Hyperkalemia** is inconsistent with primary hyperaldosteronism; the hallmark of the condition is **potassium wasting** and **hypokalemia**, not elevated potassium levels [2]. - Aldosterone's primary role includes promoting potassium excretion, so hyperkalemia would indicate a different underlying pathology, such as adrenal insufficiency [2]. *Expansion of Extracellular and Plasma volume* - While increased aldosterone does lead to **expansion of extracellular and plasma volume** due to sodium and water retention, this is a physiological consequence that contributes to hypertension rather than being the most prominent *clinical manifestation* itself [1]. - Hypertension is the direct observable and measurable clinical symptom that drives investigation [3].

Q: What is the most common cause of hypercalcemia in outpatient settings?

Primary hyperparathyroidism. **Primary hyperparathyroidism** - Accounts for the majority of hypercalcemia cases in **outpatient settings** (up to 90%). [1] - It is characterized by the **excessive secretion of parathyroid hormone (PTH)** from one or more parathyroid glands, leading to increased serum calcium levels. [1], [2] *Malignancy* - While it is the most common cause of hypercalcemia in **inpatient settings**, it is less frequent than primary hyperparathyroidism in outpatients. [1] - Often associated with **parathyroid hormone-related peptide (PTHrP)** secretion or bone metastases. [1] *Vitamin D toxicity* - This is a rare cause of hypercalcemia, usually resulting from **excessive supplementation** or medication error. [1] - It leads to increased intestinal calcium absorption and bone resorption, but is not as common as primary hyperparathyroidism. *Thiazide diuretics* - These medications can cause **mild hypercalcemia** by increasing renal calcium reabsorption. [1] - However, the hypercalcemia is typically mild and rarely as significant as that seen in primary hyperparathyroidism or malignancy.

Q: A 45-year-old woman presents with increased testosterone levels and temporal hair recession. What is the most likely diagnosis?

Polycystic Ovary Syndrome (PCOS). Polycystic Ovary Syndrome (PCOS) - PCOS is characterized by hormonal imbalances, leading to elevated androgen (testosterone) levels, which can cause symptoms like hirsutism (excess body hair), acne, and temporal hair recession in women [1]. - The elevated testosterone levels directly explain the temporal hair recession, which is a common manifestation of androgen excess in PCOS [1]. Osteoporosis - Osteoporosis is a condition of decreased bone density and increased fracture risk. - It is primarily related to estrogen deficiency and typically does not involve increased testosterone levels or temporal hair recession. Rheumatoid arthritis - Rheumatoid arthritis is an autoimmune inflammatory disease primarily affecting the joints. - It does not cause increased testosterone levels or temporal hair recession. Granulosa theca cell tumour - While granulosa cell tumors can produce hormones, they are more commonly associated with estrogen production and present with symptoms like abnormal uterine bleeding. - Although theca cell tumors can produce androgens, they are rare and typically present with more severe and rapid onset of virilization compared to the chronic presentation implied by the question [1].

Question 1

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

Question 2

A middle-aged male patient who was involved in a road traffic accident and brought to the emergency department in an unconscious state. A computed tomography (CT) scan of the abdomen revealed a splenic laceration, and emergency splenectomy was performed. The patient was then transferred to the intensive care unit (ICU). Despite receiving a bolus of normal saline, his blood pressure remained low in the postoperative period. On examination, he was afebrile, had a moon-like face with central obesity, and exhibited violet striae on his abdomen. A repeat CT scan of the chest, abdomen, and pelvis showed no evidence of hemorrhage. What is the next best step in managing this patient?

Accepted Answer

Administer hydrocortisone 100 mg IV

Answer

Return to the operating room for exploratory laparotomy

Answer

Administer vancomycin and piperacillin/tazobactam

Answer

Perform MRI of the spine.

Question 3

Nelson syndrome is associated with:

Accepted Answer

Bilateral adrenalectomy

Answer

Subarachnoid hemorrhage

Answer

Prophylactic craniospinal irradiation

Answer

BRCA2 mutation

Question 4

A young patient presented with hypertension and a 24-hour urinary metanephrine level of 1.4 mg, the most likely causes are -

Accepted Answer

VonHippelLindau syndrome

Answer

Grave's disease

Answer

Pseudohypoparathyroidism

Answer

Medullary carcinoma thyroid

Question 5

What is the preferred insulin regimen during pregnancy?

Accepted Answer

Insulin NPH + Lispro

Answer

Insulin Regular + NPH

Answer

Insulin Degludec

Answer

Insulin Lispro + Insulin regular

Question 6

Which clinical features are specifically associated with congenital adrenal hyperplasia due to 21-hydroxylase deficiency?

Accepted Answer

Female pseudohermaphroditism

Answer

All of the above features are present in 21-hydroxylase deficiency.

Answer

Hypertension due to adrenal crisis

Answer

Hypokalemia and hypernatremia

Question 7

All of the following may be associated with primary aldosteronism, except:

Accepted Answer

Von-Hippel-Lindau syndrome

Answer

Adrenal adenoma

Answer

Adrenal hyperplasia

Answer

Adrenal carcinoma

Question 8

Which of the following is the most prominent clinical manifestation of primary hyperaldosteronism (Conn's syndrome)?

Accepted Answer

Hypertension

Answer

Hyperkalemia

Answer

Hypokalemia

Answer

Expansion of Extracellular and Plasma volume

Question 9

What is the most common cause of hypercalcemia in outpatient settings?

Accepted Answer

Primary hyperparathyroidism

Answer

Malignancy

Answer

Vitamin D toxicity

Answer

Thiazide diuretics

Question 10

A 45-year-old woman presents with increased testosterone levels and temporal hair recession. What is the most likely diagnosis?

Accepted Answer

Polycystic Ovary Syndrome (PCOS)

Answer

Osteoporosis

Answer

Rheumatoid arthritis

Answer

Granulosa theca cell tumour

Endocrinology — MCQs

Endocrinology — MCQs

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