Endocrinology Practice Questions

Q: A 45-year-old male with type 2 diabetes mellitus on metformin 1000 mg twice daily presents with HbA1c of 8.5%. His serum creatinine is 2.8 mg/dL (eGFR 28 mL/min/1.73m²) and he has a history of two episodes of heart failure in the past year. His BMI is 32 kg/m². Which of the following would be the most appropriate addition to his current therapy?

Empagliflozin. ***Empagliflozin*** - **SGLT2 inhibitors** like empagliflozin are now recommended down to **eGFR ≥20 mL/min/1.73m²** per **ADA 2024 guidelines** for **cardiorenal protection**, making this patient with eGFR 28 an appropriate candidate. - This patient has **two episodes of heart failure**, which is a **Class I indication** for SGLT2 inhibitor therapy due to proven cardiovascular benefits and **heart failure risk reduction**. *Sitagliptin* - **DPP-4 inhibitors** can be used in renal failure with **dose adjustment**, but they only offer a modest HbA1c reduction (**0.5–0.8%**). - This reduction would be **insufficient** to reach the target glycemic goal for a patient starting at an **HbA1c of 8.5%**. *Pioglitazone* - **Pioglitazone** is strictly contraindicated in patients with a history of **heart failure** because it causes **fluid retention** and peripheral edema. - Initiation of this medication could lead to an acute **exacerbation** of the patient's pre-existing cardiac condition. *Insulin glargine* - While **insulin** has no renal contraindications and provides potent glycemic control, it does not offer the **cardiorenal protective benefits** that this high-risk patient requires. - **SGLT2 inhibitors** are preferred in patients with **heart failure** and **CKD** due to their proven cardiovascular and renal outcomes, making empagliflozin the superior choice.

Q: A 50-year-old man with obesity presents with fatigue, facial rounding, and proximal muscle weakness. Initial screening shows elevated 24-hour urinary free cortisol. Serum cortisol remains elevated after low-dose dexamethasone suppression test but suppresses with high-dose dexamethasone. ACTH level is 85 pg/mL (normal 10-60). Analyze these findings to determine the anatomical source of excess cortisol production.

Pituitary adenoma producing excess ACTH. ***Pituitary adenoma producing excess ACTH*** - The elevated **ACTH level (85 pg/mL)** confirms the patient has **ACTH-dependent Cushing syndrome**, which points toward either a pituitary source or an ectopic source. - Cortisol suppression with a **high-dose dexamethasone suppression test (HDDST)** is characteristic of **Cushing disease** (pituitary adenoma), as these tumors retain partial sensitivity to negative feedback. *Adrenal adenoma with autonomous cortisol secretion* - Adrenal adenomas secrete cortisol autonomously, which would lead to a **suppressed ACTH level** (less than 5 pg/mL) due to negative feedback on the pituitary. - These tumors do not suppress with dexamethasone because they are not under the control of the **hypothalamic-pituitary-adrenal (HPA) axis**. *Exogenous glucocorticoid administration* - Factitious or therapeutic use of glucocorticoids results in **low ACTH levels** and low 24-hour urinary free cortisol (unless testing for synthetic analogs). - It leads to **bilateral adrenal atrophy** rather than the hyperfunctioning state indicated by the clinical and lab markers in this patient. *Primary adrenal hyperplasia independent of ACTH* - This condition involves autonomous cortisol production by the adrenal glands, leading to an appropriately **suppressed serum ACTH**. - Like adrenal adenomas, this pathology will not demonstrate suppression during a **high-dose dexamethasone test**. *Ectopic ACTH production from small cell lung cancer* - Ectopic sources typically present with **extremely high ACTH levels** and fail to suppress with **high-dose dexamethasone** because the tumors lack legitimate glucocorticoid receptors. - Patients with ectopic ACTH often have more severe, rapid-onset symptoms such as **profound hypokalemia** and significant hyperpigmentation.

Q: A 62-year-old diabetic patient is enrolled in a telemedicine program with remote monitoring. His continuous glucose monitor shows nocturnal hypoglycemia at 3 AM for three consecutive nights, but morning fasting glucose is elevated at 180 mg/dL. What is the most appropriate next step?

Reduce evening insulin dose and provide bedtime snack. Reduce evening insulin dose and provide bedtime snack - This presentation describes the Somogyi phenomenon, where nocturnal hypoglycemia triggers a surge in counter-regulatory hormones (like glucagon and cortisol), leading to rebound fasting hyperglycemia. - Remote Continuous Glucose Monitoring (CGM) is essential for identifying this pattern, as the primary intervention is to reduce evening insulin or provide a snack to prevent the 3 AM drop [1]. Switch to morning insulin administration only - Removing evening insulin entirely can lead to poor glycemic control throughout the night and uncontrolled basal glucose production. - Managing Type 2 diabetes usually requires a balanced basal-bolus or long-acting regimen that cannot be achieved with morning-only dosing. Increase evening insulin dose to control morning hyperglycemia - Increasing the evening dose would worsen the nocturnal hypoglycemia, potentially leading to dangerous seizures or coma during sleep [1]. - This is a common error when clinicians rely only on fasting glucose levels without checking midnight or 3 AM glucose values [1]. Add metformin to evening regimen - While Metformin suppresses hepatic gluconeogenesis, it does not address the underlying hypoglycemic trigger caused by insulin excess in this scenario. - Adding more glucose-lowering medication without adjusting the insulin would likely exacerbate the Somogyi effect rather than stabilize the patient.

Q: A 19-year-old transgender woman on feminizing hormone therapy presents with galactorrhea and serum prolactin of 85 ng/mL (normal <25). Which component of her therapy is most likely responsible?

Cyproterone acetate. ***Cyproterone acetate*** - **Cyproterone acetate** is a potent **progestogen** and anti-androgen that can cause **hyperprolactinemia** by exerting a **dopamine-antagonistic** effect or stimulating lactotroph hyperplasia. - It is a well-documented cause of **galactorrhea** and significant prolactin elevation in transgender individuals receiving feminizing therapy. *Finasteride* - **Finasteride** is a **5-alpha reductase inhibitor** that prevents the conversion of testosterone to dihydrotestosterone (DHT) and does not significantly impact **prolactin** levels. - Its primary side effects relate to **sexual dysfunction** and erectile issues rather than stimulation of the pituitary gland or breast discharge. *Spironolactone* - **Spironolactone** acts as an **androgen receptor antagonist** and a weak inhibitor of androgen synthesis; it is not associated with elevated serum **prolactin**. - While it may cause **gynecomastia** through estrogenic-like effects, it does not typically induce **galactorrhea** or pituitary lactotroph changes. *Transdermal estradiol patches* - While **estrogen** can stimulate the growth of **lactotrophs**, transdermal delivery results in stable levels that are less likely to cause sudden, marked elevations in **prolactin** compared to high-dose oral therapy. - In the context of combined therapy, **Cyproterone acetate** is considered a more potent and specific pharmacological trigger for significant **prolactinemia** than standard doses of estradiol patches.

Q: Which hormone therapy is primarily used for feminizing gender-affirming hormone therapy in transgender women?

Estradiol with anti-androgen. ***Estradiol with anti-androgen*** - **Estradiol** (oral, transdermal, or injectable) is the primary hormone used to promote feminizing characteristics like **breast development** and female-pattern **fat redistribution**. - **Anti-androgens** (e.g., **spironolactone** or cyproterone acetate) are necessary to suppress **endogenous testosterone** levels to typical female ranges. *Testosterone cypionate* - This is an **androgen** used primarily for **masculinizing** hormone therapy in transgender men or for treating male hypogonadism. - Administration in transgender women would counteract feminization by promoting **virilization** and increasing muscle mass. *Progesterone alone* - Progesterone is occasionally added to regimens for its potential effect on **breast development** or libido, but it is not the primary feminizing agent. - Use of **progesterone alone** is insufficient to suppress testosterone or achieve significant feminization without **estradiol**. *Selective estrogen receptor modulators* - **SERMs** like tamoxifen or **raloxifene** act as estrogen agonists in some tissues and antagonists in others, which is inconsistent with goal of full feminization. - These are generally avoided in transgender women because they may inhibit **breast development**, which is a primary goal of feminizing therapy.

Q: Which is an immunological marker of type I diabetes?

GAD. **Explanation:** Type 1 Diabetes Mellitus (T1DM) is characterized by the autoimmune destruction of insulin-producing pancreatic beta cells [1]. This process is mediated by T-cells and is associated with the presence of specific autoantibodies that serve as diagnostic and predictive markers [2]. **Why GAD is correct:** **Glutamic Acid Decarboxylase (GAD65) antibodies** are the most sensitive and persistent immunological markers for T1DM. GAD is an enzyme involved in the synthesis of the neurotransmitter GABA, but it is also expressed in pancreatic beta cells. GAD antibodies are particularly useful in clinical practice because they remain detectable for years after diagnosis, unlike other antibodies that may disappear shortly after the onset of the disease. They are also used to diagnose **LADA** (Latent Autoimmune Diabetes in Adults). **Analysis of Incorrect Options:** * **Anti-endothelial antibody:** These are associated with systemic vasculitides (like Kawasaki disease) or certain connective tissue disorders, not diabetes. * **Anti-saccharomyces cerevisiae antibody (ASCA):** This is a classic marker for **Crohn’s Disease**, used to differentiate it from Ulcerative Colitis. **High-Yield Clinical Pearls for NEET-PG:** * **Other T1DM Markers:** Islet Cell Antibodies (ICA), Insulin Autoantibodies (IAA), and **Zinc Transporter 8 (ZnT8)** antibodies. * **ZnT8** is often cited as the most specific marker for beta-cell destruction. * **HLA Association:** T1DM is strongly linked to **HLA-DR3 and HLA-DR4** [2]. * **Screening:** The presence of two or more of these antibodies in an asymptomatic child indicates a near 100% lifetime risk of developing clinical T1DM.

Q: A man presents with weakness, tachycardia, sweating, and palpitations on fasting, which are promptly relieved with food intake. What is the most probable diagnosis?

Insulinoma. ### Explanation The clinical presentation described is a classic manifestation of **Whipple’s Triad**, which is the hallmark of an **Insulinoma**. **1. Why Insulinoma is correct:** Insulinoma is a rare neuroendocrine tumor of the pancreatic beta cells that secretes insulin autonomously, regardless of blood glucose levels. The patient exhibits symptoms of **fasting hypoglycemia**: * **Autonomic symptoms:** Tachycardia, sweating, and palpitations (due to catecholamine release). * **Neuroglycopenic symptoms:** Weakness and confusion. * **Relief with food:** The prompt resolution of symptoms after eating completes Whipple’s Triad, making Insulinoma the most probable diagnosis. **2. Why the other options are incorrect:** * **Pancreatic carcinoma:** Typically presents with painless obstructive jaundice, weight loss, and abdominal pain. It does not cause fasting hypoglycemia. * **Carcinoid syndrome:** Characterized by flushing, diarrhea, and wheezing due to serotonin release [1]. Symptoms are usually triggered by alcohol or stress, not fasting. * **Zollinger-Ellison syndrome (Gastrinoma):** Caused by excessive gastrin secretion leading to severe peptic ulcers and chronic diarrhea, not hypoglycemia. **3. High-Yield NEET-PG Pearls:** * **Whipple’s Triad:** 1. Symptoms of hypoglycemia; 2. Low plasma glucose (<55 mg/dL); 3. Relief of symptoms after glucose administration. * **Diagnosis:** The gold standard is the **72-hour supervised fast**. * **Biochemical markers:** During hypoglycemia, an insulinoma patient will show **elevated Insulin**, **elevated C-peptide**, and **elevated Pro-insulin** levels, with **absent urinary sulfonylureas** [1]. * **Localization:** Most insulinomas are small, benign, and solitary. Endoscopic ultrasound (EUS) is highly sensitive for localization. * **Association:** 10% are associated with **MEN1 syndrome** (usually multiple tumors).

Q: A mother brings her 10-year-old son to the OPD due to a family history of medullary carcinoma of the thyroid in his father and grandparents. There are no abnormal findings on physical examination. Which of the following tests would you perform?

Urine vanillylmandelic acid (VMA) level. **Explanation:** The clinical scenario describes a child with a strong family history of **Medullary Thyroid Carcinoma (MTC)**, which strongly suggests **Multiple Endocrine Neoplasia Type 2 (MEN 2)** syndrome (specifically MEN 2A or 2B). These syndromes are inherited in an autosomal dominant fashion due to mutations in the **RET proto-oncogene** [1]. **Why Option C is correct:** Patients with MEN 2 are at high risk for developing **Pheochromocytoma** (often bilateral) in addition to MTC [1]. In clinical practice, when a patient is suspected of having MEN 2, it is mandatory to **rule out Pheochromocytoma before any surgical intervention** for the thyroid. This is because an undiagnosed pheochromocytoma can lead to a fatal hypertensive crisis during anesthesia or surgery. Screening is done via 24-hour **Urine VMA**, metanephrines, or plasma free metanephrines [1]. **Why other options are incorrect:** * **Options A, B, and D:** Serum insulin, glucagon, and somatostatin are markers for pancreatic islet cell tumors [1]. These are characteristic of **MEN 1** (Wermer’s Syndrome), which involves the "3 Ps": Pituitary, Parathyroid, and Pancreas. MEN 1 is *not* associated with Medullary Thyroid Carcinoma. **High-Yield Clinical Pearls for NEET-PG:** * **MEN 2A (Sipple Syndrome):** MTC + Pheochromocytoma + Parathyroid Hyperplasia. * **MEN 2B:** MTC + Pheochromocytoma + Mucosal Neuromas + Marfanoid Habitus. * **Prophylactic Thyroidectomy:** In children with known RET mutations, thyroidectomy is often performed early (before age 5 in MEN 2A, or within the 1st year in MEN 2B) because MTC in these patients is highly aggressive [1]. * **Rule of thumb:** Always screen for and treat Pheochromocytoma *first* before addressing the thyroid.

Question 1

A 45-year-old male with type 2 diabetes mellitus on metformin 1000 mg twice daily presents with HbA1c of 8.5%. His serum creatinine is 2.8 mg/dL (eGFR 28 mL/min/1.73m²) and he has a history of two episodes of heart failure in the past year. His BMI is 32 kg/m². Which of the following would be the most appropriate addition to his current therapy?

Accepted Answer

Empagliflozin

Answer

Sitagliptin

Answer

Pioglitazone

Answer

Insulin glargine

Question 2

A 60-year-old man with type 2 diabetes on metformin and insulin presents with 3 days of nausea, vomiting, and diffuse abdominal pain. He appears ill and confused. Vital signs: BP 95/60 mmHg, HR 115/min, RR 28/min, T 37.2°C. Labs show glucose 380 mg/dL, pH 7.28, HCO3 18 mEq/L, anion gap 24, serum osmolality 310 mOsm/kg, negative urine ketones, creatinine 2.8 mg/dL (baseline 1.1), lactate 8.2 mmol/L. Apply physiological principles to determine the primary acid-base and metabolic disturbance.

Accepted Answer

Hyperosmolar hyperglycemic state complicated by lactic acidosis from metformin

Answer

Alcoholic ketoacidosis with concurrent diabetic emergency

Answer

Sepsis-induced lactic acidosis with stress hyperglycemia

Answer

Mixed metabolic acidosis from uremia and starvation ketosis

Answer

Diabetic ketoacidosis with renal failure from volume depletion

Question 3

A 38-year-old woman presents with hypertension (170/105 mmHg), hypokalemia (2.9 mEq/L), and metabolic alkalosis. Plasma aldosterone is elevated at 35 ng/dL (normal 4-31) and plasma renin activity is suppressed at 0.2 ng/mL/hr (normal 0.5-3.5). CT scan shows a 2.5 cm left adrenal mass. She also reports recent diagnosis of hyperthyroidism and is being evaluated for a neck mass. Synthesize these findings to evaluate for an underlying unifying diagnosis requiring modified treatment approach.

Accepted Answer

Multiple endocrine neoplasia type 2 requiring RET proto-oncogene testing and comprehensive screening

Answer

Carney complex requiring cardiac myxoma screening before adrenal surgery

Answer

Ectopic ACTH syndrome from thyroid carcinoma causing bilateral adrenal hyperplasia

Answer

Coincidental adrenal adenoma and Graves' disease requiring separate standard treatments

Answer

Isolated aldosterone-producing adenoma requiring unilateral adrenalectomy only

Question 4

A 50-year-old man with obesity presents with fatigue, facial rounding, and proximal muscle weakness. Initial screening shows elevated 24-hour urinary free cortisol. Serum cortisol remains elevated after low-dose dexamethasone suppression test but suppresses with high-dose dexamethasone. ACTH level is 85 pg/mL (normal 10-60). Analyze these findings to determine the anatomical source of excess cortisol production.

Accepted Answer

Pituitary adenoma producing excess ACTH

Answer

Adrenal adenoma with autonomous cortisol secretion

Answer

Exogenous glucocorticoid administration

Answer

Primary adrenal hyperplasia independent of ACTH

Answer

Ectopic ACTH production from small cell lung cancer

Question 5

A 62-year-old diabetic patient is enrolled in a telemedicine program with remote monitoring. His continuous glucose monitor shows nocturnal hypoglycemia at 3 AM for three consecutive nights, but morning fasting glucose is elevated at 180 mg/dL. What is the most appropriate next step?

Accepted Answer

Reduce evening insulin dose and provide bedtime snack

Answer

Switch to morning insulin administration only

Answer

Increase evening insulin dose to control morning hyperglycemia

Answer

Add metformin to evening regimen

Question 6

A 19-year-old transgender woman on feminizing hormone therapy presents with galactorrhea and serum prolactin of 85 ng/mL (normal <25). Which component of her therapy is most likely responsible?

Accepted Answer

Cyproterone acetate

Answer

Finasteride

Answer

Spironolactone

Answer

Transdermal estradiol patches

Question 7

Which hormone therapy is primarily used for feminizing gender-affirming hormone therapy in transgender women?

Accepted Answer

Estradiol with anti-androgen

Answer

Testosterone cypionate

Answer

Progesterone alone

Answer

Selective estrogen receptor modulators

Question 8

Which is an immunological marker of type I diabetes?

Accepted Answer

GAD

Answer

Anti-endothelial antibody

Answer

Anti-saccharomyces antibody

Answer

None of the above

Question 9

A man presents with weakness, tachycardia, sweating, and palpitations on fasting, which are promptly relieved with food intake. What is the most probable diagnosis?

Accepted Answer

Insulinoma

Answer

Pancreatic carcinoma

Answer

Carcinoid syndrome

Answer

Zollinger-Ellison syndrome

Question 10

A mother brings her 10-year-old son to the OPD due to a family history of medullary carcinoma of the thyroid in his father and grandparents. There are no abnormal findings on physical examination. Which of the following tests would you perform?

Accepted Answer

Urine vanillylmandelic acid (VMA) level

Answer

Serum insulin level

Answer

Serum glucagon level

Answer

Serum somatostatin level

Endocrinology — MCQs

Endocrinology — MCQs

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