Endocrinology Practice Questions

Q: Which of the following is a component of the classic triad used for clinical diagnosis of pheochromocytoma?

Headache. ***Headache*** - **Headache** is a key symptom in the classic triad for pheochromocytoma, caused by the **vasoconstrictive effects** of catecholamine surges. - The other two components of the classic triad are **palpitations** and **sweating**. *Hyperkalemia* - **Hyperkalemia** is not a typical manifestation of pheochromocytoma; rather, these tumors produce **catecholamines** that can lead to hyperglycemia. - Mineralocorticoid excess (e.g., in aldosteronism) is more commonly associated with electrolyte imbalances like hyperkalemia or hypokalemia. *Hypertension* - While **hypertension** is a hallmark feature of pheochromocytoma, it is a general sign rather than one of the specific three components of the classic clinical triad used for initial diagnostic suspicion. - The classic triad focuses on the most prominent and specific symptoms that suggest a **catecholamine-secreting tumor**. *Bradycardia* - **Bradycardia** is contrary to the expected cardiovascular effects of pheochromocytoma, which typically causes **tachycardia** (palpitations) due to excessive catecholamine release. - Catecholamines, such as **epinephrine** and **norepinephrine**, increase heart rate and myocardial contractility.

Q: Which of the following is a classic feature of pheochromocytoma?

Episodic hypertension. Episodic hypertension - Episodic hypertension is a hallmark symptom of pheochromocytoma, caused by the intermittent release of large amounts of catecholamines (epinephrine and norepinephrine) from the tumor. - These episodes often manifest with a sudden onset of headache, palpitations, sweating, and anxiety, alongside a sharp rise in blood pressure. [1] Hypoglycemia - Pheochromocytoma typically causes hyperglycemia, not hypoglycemia, due to the catecholamine-induced breakdown of glycogen and inhibition of insulin release. - Catecholamines increase blood glucose levels by stimulating glycogenolysis and gluconeogenesis. [1] Hyperkalemia - Catecholamines, particularly epinephrine, can actually cause a shift of potassium into cells, potentially leading to hypokalemia in some situations, not hyperkalemia. [1] - Hyperkalemia is not a characteristic feature of pheochromocytoma and would suggest other underlying conditions. [1] Bradycardia - Patients with pheochromocytoma usually experience tachycardia and palpitations due to the direct chronotropic effects of excess catecholamines on the heart. - Bradycardia is contrary to the expected physiological response to high levels of circulating catecholamines, which stimulate beta-adrenergic receptors. [1]

Q: Which electrolyte disturbance is seen in primary hyperaldosteronism?

Hypokalemia. ***Hypokalemia*** - **Aldosterone** normally promotes sodium reabsorption and potassium excretion in the renal tubules [1]. - In primary hyperaldosteronism, excessive aldosterone production leads to increased potassium excretion, resulting in **hypokalemia** [1], [2]. *Hyperkalemia* - **Hyperkalemia** (high potassium) is the opposite of what occurs in primary hyperaldosteronism [1]. - Aldosterone's primary action is to increase potassium secretion, so excess aldosterone would not cause potassium retention. *Hyponatremia* - **Hyponatremia** (low sodium) is not typical in primary hyperaldosteronism; instead, **hypernatremia** or normal sodium levels may be observed due to increased sodium reabsorption. - The increased sodium reabsorption also leads to increased water reabsorption which can lead to **hypervolemia** but **normonatremia** [3]. *Hypercalcemia* - **Hypercalcemia** (high calcium) is not directly associated with primary hyperaldosteronism. - Calcium regulation is primarily controlled by parathyroid hormone and vitamin D, not aldosterone.

Q: A male patient with purple striae, thin skin, non-healing wound, and pedunculated abdomen, most probable cause?

Hypercortisolism. Hypercortisolism - **Purple striae** are characteristic due to the breakdown of collagen and elastic fibers from excessive **cortisol**. - **Thin skin**, **non-healing wounds**, and a **pedunculated abdomen** (central obesity) are all classic signs of chronic high cortisol levels, as seen in **Cushing's syndrome** [1]. *Insulin resistance* - While insulin resistance can lead to conditions like **acanthosis nigricans** and **obesity**, it typically does not cause purple striae or thin skin directly. - It's often associated with **type 2 diabetes**, polycystic ovary syndrome, but not the specific dermatological features presented. *Hypothyroidism* - Hypothyroidism symptoms include **dry skin**, **coarse hair**, **fatigue**, and **weight gain**, but not typically purple striae or thin skin. - It can cause **non-pitting edema** (myxedema), which is distinct from the described skin changes. *Genetic connective tissue disorder* - Genetic connective tissue disorders like **Ehlers-Danlos syndrome** can cause thin, fragile skin and poor wound healing. - However, they do not typically present with the characteristic **purple striae** or **pedunculated abdomen** that point specifically to hypercortisolism.

Q: Which condition results from hypersecretion of growth hormone in adults?

Acromegaly. ***Acromegaly*** - **Acromegaly** is the clinical syndrome that results from **hypersecretion of growth hormone (GH)** in adults, after the growth plates have fused [1], [3]. - This leads to characteristic symptoms such as the **enlargement of hands, feet, and facial features**, as well as various systemic complications [1]. *Gigantism* - **Gigantism** results from **hypersecretion of GH during childhood or adolescence**, before the epiphyseal growth plates have fused [1]. - This condition leads to **excessive linear growth** and an abnormally tall stature [1]. *Growth hormone deficiency* - **Growth hormone deficiency** is caused by the **underproduction** or lack of growth hormone secretion. - In children, it leads to **delayed growth and short stature**, while in adults, it can cause changes in body composition and metabolism. *Cushing's syndrome* - **Cushing's syndrome** is caused by prolonged exposure to **high levels of cortisol**, not growth hormone [2]. - Its symptoms include central obesity, a "moon face," "buffalo hump," and skin thinning, which are distinct from those of excess growth hormone [2].

Q: A 40F presents with double vision, headaches, and a progressively enlarging thyroid mass. She has proptosis and limited eye movement. TSH is suppressed. Likely cause of her symptoms?

Graves' orbitopathy. Graves' orbitopathy - The combination of **proptosis**, **limited eye movement (ophthalmoplegia)** causing double vision, and a suppressed TSH (indicating hyperthyroidism) is highly characteristic of **Graves' disease** with orbital involvement [1]. - An **enlarging thyroid mass** further supports Graves' disease, as it often presents with goiter and hyperthyroidism, leading to the autoimmune sequelae in the orbit [1]. *Pituitary adenoma* - While it can cause **headaches** and **double vision** due to oculomotor nerve compression, a pituitary adenoma would not typically cause a progressively **enlarging thyroid mass** or **proptosis** with suppressed TSH. - Hypersecreting pituitary adenomas (e.g., ACTH, GH) affect other endocrine axes, and non-secreting ones primarily cause mass effect. *Orbital cellulitis* - This is an **acute infection** of the orbital tissues, usually presenting with **pain, fever, rapidly progressing proptosis**, and erythema, which is not suggested by the chronic and progressive nature of this patient's symptoms. - It would not be associated with a suppressed TSH or an enlarged thyroid gland. *Thyroid carcinoma* - A thyroid carcinoma can present as an **enlarging thyroid mass** and may cause local symptoms like dysphagia or hoarseness if advanced, but it does not directly cause **proptosis**, **double vision**, or suppressed TSH. - Although some rare thyroid cancers can metastasize to the orbit, primary presentation with bilateral proptosis and ophthalmoplegia is not typical.

Q: A 50-year-old male with diabetes presents with severe burning pain in his feet. Medications have been ineffective. What is the most appropriate next step in management?

Trial of pregabalin. ***Trial of pregabalin*** - **Pregabalin**, a gamma-aminobutyric acid (GABA) analog, is a first-line treatment for **diabetic neuropathic pain** due to its efficacy in modulating neurotransmitter release [2]. - Given that previous medications have been ineffective for **severe burning pain** [1] in diabetic neuropathy, exploring other pharmacological options like pregabalin is the most appropriate next step [2]. *Prescribe opioid analgesics* - **Opioid analgesics** are generally reserved for neuropathic pain that is refractory to other treatments due to concerns about tolerance, dependence, and significant side effects [1]. - They are not considered a first-line or early second-line treatment for **diabetic neuropathy**, especially when other agents like pregabalin have not yet been trialed [2]. *Prescribe corticosteroids* - **Corticosteroids** are potent anti-inflammatory agents but are not indicated for the chronic management of **diabetic neuropathic pain**, which is primarily a nerve damage issue rather than an inflammatory one. - Long-term steroid use carries significant risks and would likely worsen diabetes control, making it an inappropriate choice. *Refer for physical therapy* - **Physical therapy** can be beneficial for managing some aspects of diabetic neuropathy, such as improving balance or muscle strength, but it is unlikely to directly alleviate severe burning neuropathic pain as a primary monotherapy. - While a valuable adjunctive treatment, it is not the most appropriate initial next step for directly addressing severe pain symptoms when pharmacological options are still available [2].

Q: In a 25-year-old male diagnosed with decreased bone density, which hormone should be assessed first?

Testosterone level. Detailed Explanation: ***Testosterone level*** - In a young male with **decreased bone density**, an underlying cause like **hypogonadism** (low testosterone) should be investigated as testosterone plays a crucial role in bone formation and maintenance [1]. - **Androgens** (like testosterone) are important for achieving peak bone mass and preventing bone loss in men [1]. In hypogonadism, the pathogenesis of bone loss is similar to post-menopausal osteoporosis, as testosterone deficiency results in an increase in bone turnover and uncoupling of bone resorption from bone formation [1]. *Insulin level* - Poorly controlled **diabetes** can negatively affect bone health, but assessing insulin levels directly is not typically the first step in investigating decreased bone density. - **Insulin resistance** or Type 1 diabetes can indirectly impact bone through inflammation or metabolic imbalances, but it's not the primary hormonal deficiency directly linked to reduced bone density in a young male. *Estrogen level* - While estrogen is crucial for bone health in both sexes, in a young male, **estrogen levels** are usually assessed secondary to testosterone, as testosterone is aromatized to estrogen and is the primary sex hormone [1]. - Significant **estrogen deficiency** in males is rare and usually indicates severe hypogonadism where testosterone would be low too. *Parathyroid hormone level* - **Parathyroid hormone (PTH)** regulates calcium and phosphate levels and is assessed to rule out hyperparathyroidism or hypoparathyroidism, which can affect bone density. - However, in a young male, **PTH** would typically be considered after initial evaluation of sex hormones and other more common causes of osteoporosis.

Q: A 62-year-old woman with type 2 diabetes presents with persistent hyperglycemia despite the maximum use of oral hypoglycemic agents. What is the next best step in management?

Start insulin therapy. ***Start insulin therapy*** - When **maximum doses** of oral hypoglycemic agents (OHAs) fail to achieve glycemic targets in type 2 diabetes, **insulin therapy** is generally the next recommended step. - This ensures effective glucose control and prevents long-term complications associated with **persistent hyperglycemia** [1]. *Increase oral hypoglycemics* - The patient is already on the **maximum use of oral hypoglycemic agents**, meaning further increases are unlikely to be effective and could increase side effects. - Continued escalation of OHAs beyond their maximum effective dose is not a standard or safe practice for glycemic control. *Add GLP-1 receptor agonist* - While **GLP-1 receptor agonists** can be beneficial, they are often considered *before* reaching maximal OHA therapy or in conjunction with insulin, not necessarily as the *next best step* when maximal OHAs have already failed. - In cases of **persistent hyperglycemia** despite maximal OHA use, insulin is typically the most potent and effective option for immediate and sustained glycemic control [1]. *Diet and lifestyle modification* - Diet and lifestyle modifications are **fundamental** for all diabetic patients and should always be emphasized, but in this scenario, they have likely already been implemented. - For **persistent hyperglycemia** despite maximal pharmacotherapy, lifestyle changes alone are insufficient to achieve adequate glycemic targets.

Question 1

Which of the following is a component of the classic triad used for clinical diagnosis of pheochromocytoma?

Accepted Answer

Headache

Answer

Hyperkalemia

Answer

Hypertension

Answer

Bradycardia

Question 2

Which of the following is a classic feature of pheochromocytoma?

Accepted Answer

Episodic hypertension

Answer

Hypoglycemia

Answer

Hyperkalemia

Answer

Bradycardia

Question 3

Which electrolyte disturbance is seen in primary hyperaldosteronism?

Accepted Answer

Hypokalemia

Answer

Hyperkalemia

Answer

Hyponatremia

Answer

Hypercalcemia

Question 4

A male patient with purple striae, thin skin, non-healing wound, and pedunculated abdomen, most probable cause?

Accepted Answer

Hypercortisolism

Answer

Insulin resistance

Answer

Hypothyroidism

Answer

Genetic connective tissue disorder

Question 5

Which condition results from hypersecretion of growth hormone in adults?

Accepted Answer

Acromegaly

Answer

Gigantism

Answer

Growth hormone deficiency

Answer

Cushing's syndrome

Question 6

A 40F presents with double vision, headaches, and a progressively enlarging thyroid mass. She has proptosis and limited eye movement. TSH is suppressed. Likely cause of her symptoms?

Accepted Answer

Graves' orbitopathy

Answer

Pituitary adenoma

Answer

Orbital cellulitis

Answer

Thyroid carcinoma

Question 7

A 50-year-old male with diabetes presents with severe burning pain in his feet. Medications have been ineffective. What is the most appropriate next step in management?

Accepted Answer

Trial of pregabalin

Answer

Prescribe opioid analgesics

Answer

Prescribe corticosteroids

Answer

Refer for physical therapy

Question 8

What is the role of leptin in energy homeostasis, and what are the current evidence-based therapeutic approaches for managing leptin resistance in obesity?

Accepted Answer

Leptin decreases appetite, use lifestyle modifications and evidence-based pharmacotherapy

Answer

Leptin decreases appetite, use bariatric surgery for severe obesity

Answer

Leptin increases appetite, use GLP-1 receptor agonists

Answer

Leptin increases appetite, use lifestyle modifications and caloric restriction

Question 9

In a 25-year-old male diagnosed with decreased bone density, which hormone should be assessed first?

Accepted Answer

Testosterone level

Answer

Insulin level

Answer

Estrogen level

Answer

Parathyroid hormone level

Question 10

A 62-year-old woman with type 2 diabetes presents with persistent hyperglycemia despite the maximum use of oral hypoglycemic agents. What is the next best step in management?

Accepted Answer

Start insulin therapy

Answer

Increase oral hypoglycemics

Answer

Add GLP-1 receptor agonist

Answer

Diet and lifestyle modification

Endocrinology — MCQs

Endocrinology — MCQs

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