Endocrinology Practice Questions

Q: A 35-year-old male with a history of severe bronchial asthma for several months now complains of weight gain and the development of purple stretch marks. Physical examination showed BP 149/95 mmHg, supraclavicular fullness, thinned skin with areas of bruising, and decreased strength in proximal muscles. Laboratory investigations showed reduced serum cortisol and reduced plasma ACTH. An electrolyte workup in this patient will most likely reveal?

Iatrogenic cause. ### Explanation **1. Why "Iatrogenic cause" is correct:** The patient presents with classic features of **Cushing’s Syndrome** (weight gain, purple striae, hypertension, supraclavicular fullness, and proximal myopathy) [1]. However, the laboratory findings show **reduced serum cortisol** and **reduced plasma ACTH**. This biochemical profile (Low ACTH + Low Cortisol) indicates **Secondary Adrenal Insufficiency**. In the context of severe bronchial asthma, the patient has likely been using long-term exogenous glucocorticoids (oral or inhaled). Exogenous steroids provide systemic glucocorticoid activity (causing the Cushingoid appearance) while simultaneously suppressing the Hypothalamic-Pituitary-Adrenal (HPA) axis via negative feedback. This leads to low endogenous cortisol and ACTH levels. In iatrogenic Cushing's syndrome, cortisol levels are low unless the patient is taking a corticosteroid like prednisolone that cross-reacts in immunoassays [2]. **2. Why other options are incorrect:** * **Pituitary tumor (Cushing’s Disease):** Would show **High ACTH** and **High Cortisol** [1]. * **Tumor of the adrenal cortex:** Would show **Low ACTH** (due to feedback) but **High endogenous Cortisol** [2]. * **Lung cancer (Ectopic ACTH):** Small cell lung cancer typically causes **High ACTH** and **High Cortisol**, often presenting with severe hypokalemia rather than classic fat redistribution. **3. NEET-PG Clinical Pearls:** * **Most common cause of Cushing’s Syndrome:** Iatrogenic (exogenous steroid use). * **Most common endogenous cause:** Cushing’s Disease (Pituitary adenoma). * **Proximal Myopathy:** A key clinical differentiator; Cushing’s causes muscle wasting, whereas simple obesity does not [1]. * **The "Paradox":** Iatrogenic Cushing’s is the only state where a patient looks "Cushingoid" but has low laboratory cortisol levels (unless the specific synthetic steroid used is cross-reactive in the assay) [2].

Q: Which of the following is seen in secondary hyperparathyroidism?

Chronic hypocalcemia. ### Explanation **Secondary Hyperparathyroidism (sHPT)** is a compensatory physiological response where the parathyroid glands become overactive in an attempt to correct low serum calcium levels [1]. **1. Why Chronic Hypocalcemia is Correct:** The hallmark of sHPT is **chronic hypocalcemia** (or low-normal calcium) [2]. The most common cause is **Chronic Kidney Disease (CKD)** [1]. In CKD, the kidneys fail to excrete phosphate (leading to hyperphosphatemia) and fail to activate Vitamin D (1,25-dihydroxyvitamin D deficiency) [4]. Both low Vitamin D and high phosphate lead to low serum ionized calcium [4]. This persistent hypocalcemia acts as a potent stimulus for the parathyroid glands to secrete excessive **Parathyroid Hormone (PTH)** to restore calcium homeostasis [3]. **2. Analysis of Incorrect Options:** * **A. Chronic hypercalcemia:** This is the hallmark of **Primary Hyperparathyroidism** (usually due to an adenoma) or **Tertiary Hyperparathyroidism** (autonomous secretion after long-standing CKD) [1,4]. * **C & D. Magnesium levels:** While magnesium can influence PTH secretion (severe hypomagnesemia actually inhibits PTH release), it is not the primary driver or the characteristic finding used to define secondary hyperparathyroidism in standard clinical scenarios [2]. **3. NEET-PG High-Yield Pearls:** * **Primary HPT:** ↑ PTH, ↑ Calcium, ↓ Phosphate [1]. * **Secondary HPT:** ↑ PTH, **↓/Normal Calcium**, ↑ Phosphate (in CKD) or ↓ Phosphate (in Vitamin D deficiency/malabsorption) [2,4]. * **Tertiary HPT:** ↑↑ PTH, ↑ Calcium (seen in long-term dialysis patients where glands become autonomous) [4]. * **Key Radiology:** Look for "subperiosteal bone resorption" (especially in phalanges) and "Salt and Pepper" appearance of the skull (Osteitis Fibrosa Cystica) [4].

Q: A couple has two children and is currently unable to conceive. The father is diagnosed with hypogonadotropic hypogonadism. Which of the following statements is false regarding his condition?

Normal testosterone levels. **Explanation:** Hypogonadotropic hypogonadism (Secondary Hypogonadism) is characterized by a failure of the pituitary gland or hypothalamus to produce the gonadotropins required to stimulate the testes [1]. **Why Option B is the Correct Answer (The False Statement):** In hypogonadotropic hypogonadism, the primary defect lies in the low secretion of **LH and FSH**. Since LH is responsible for stimulating Leydig cells to produce testosterone, a deficiency in LH directly leads to **low testosterone levels** [2]. Therefore, stating that testosterone levels are "normal" is clinically incorrect. **Analysis of Other Options:** * **Option A (Low LH and FSH):** This is the hallmark of secondary hypogonadism. The "hypo-hypo" state implies that both the stimulatory hormones (gonadotropins) and the end-product (testosterone) are low [1]. * **Option C (Oligospermia):** FSH is essential for stimulating Sertoli cells and maintaining spermatogenesis. Low FSH leads to impaired sperm production, resulting in oligospermia or azoospermia, explaining the couple's secondary infertility [3]. * **Option D (High prolactin levels):** Hyperprolactinemia is a common cause of secondary hypogonadism. High prolactin inhibits the pulsatile release of GnRH from the hypothalamus, leading to decreased LH/FSH and subsequent hypogonadism [2]. **NEET-PG High-Yield Pearls:** * **Primary vs. Secondary:** In Primary Hypogonadism (e.g., Klinefelter syndrome), LH/FSH are **high** (Hypergonadotropic). In Secondary, they are **low/normal** (Hypotropic) [2]. * **Kallmann Syndrome:** A key differential for congenital hypogonadotropic hypogonadism, characterized by **anosmia** (loss of smell) due to failure of GnRH neuron migration. * **Initial Investigation:** The first step in evaluating a male with low testosterone and low LH/FSH is often checking **Serum Prolactin** and performing an **MRI of the sella** to rule out a pituitary adenoma [2].

Q: A patient presents with increased serum calcium and decreased serum phosphate. What is the most likely diagnosis?

Primary hyperparathyroidism. ### Explanation The biochemical hallmark of **Primary Hyperparathyroidism (PHPT)** is the combination of **hypercalcemia** and **hypophosphatemia** [1, 2]. **Pathophysiology:** In PHPT, there is autonomous secretion of Parathyroid Hormone (PTH), usually due to a solitary parathyroid adenoma [2]. PTH increases serum calcium through three mechanisms: 1. **Bone:** Increases osteoclastic bone resorption [1]. 2. **Kidney:** Increases distal tubular reabsorption of calcium and **decreases proximal tubular reabsorption of phosphate** (phosphaturic effect) [1]. 3. **Intestine:** Indirectly increases calcium absorption by stimulating the synthesis of 1,25-(OH)₂ Vitamin D (Calcitriol) [1]. The inhibition of phosphate reabsorption in the kidneys leads to increased urinary phosphate excretion, resulting in low serum phosphate levels [1]. **Analysis of Incorrect Options:** * **Secondary Hyperparathyroidism:** This is a compensatory rise in PTH due to **hypocalcemia** (commonly from Vitamin D deficiency or Chronic Kidney Disease) [2]. Serum calcium is typically low or low-normal. * **Malignancy:** While malignancy is a common cause of hypercalcemia (often via PTHrP), serum phosphate is usually **normal or elevated** unless there is a specific co-existing tubular defect. * **Osteoporosis:** This is a disease of bone density; routine serum calcium, phosphate, and PTH levels are typically **normal**. **NEET-PG High-Yield Pearls:** * **Most common cause of PHPT:** Solitary Parathyroid Adenoma (85%). * **Classic Clinical Pentad:** "Stones (renal calculi), bones (osteitis fibrosa cystica), abdominal groans (peptic ulcers/pancreatitis), psychic moans (depression), and fatigue overtones." * **Biochemical Marker:** High PTH, High Ca²⁺, Low PO₄³⁻, and increased urinary cAMP. * **X-ray finding:** Subperiosteal bone resorption (most common in the radial aspect of middle phalanges) and "Salt and pepper" appearance of the skull.

Q: A patient with IDDM injects a mixture of NPH insulin and crystalline zinc (Regular) insulin before breakfast (at 7 AM) and before dinner (at 8 PM) each day. She reports the following average self-monitored RBS for the past week.

Increasing both the 7 AM and 8 PM doses of regular insulin. ***Increasing both the 7 AM and 8 PM doses of regular insulin*** - **Regular insulin** peaks 2-4 hours after injection, directly controlling **postprandial glucose** after breakfast and dinner meals. - The elevated **post-breakfast** and **post-dinner** readings indicate inadequate regular insulin coverage for meal-related glucose spikes. *Increasing the 7 AM dose of NPH insulin* - **NPH insulin** has a longer duration (12-18 hours) and primarily controls **fasting glucose** and pre-meal readings, not postprandial spikes. - The **normal fasting** and **pre-dinner** glucose levels suggest adequate NPH coverage, making this adjustment inappropriate. *Increasing both 7 AM and 8 PM doses of NPH insulin* - **NPH insulin** from the morning dose peaks around **pre-dinner time**, while evening NPH controls **overnight** and **fasting glucose**. - Since **fasting** and **pre-dinner** readings are normal, increasing NPH would risk **hypoglycemia** during these periods. *Increasing the 7 AM dose of regular insulin* - This would only address the **post-breakfast hyperglycemia** but would not correct the elevated **post-dinner** glucose readings. - A **split-mixed regimen** requires adjustment of both regular insulin doses when postprandial control is inadequate at both meals.

Q: A patient presents with polyuria and elevated prolactin levels. There is a family history of the father dying due to renal stones. The patient has a Ca2+ of 12 g% and PTH levels of 260 IU/L. What is the most likely diagnosis?

MEN 1. **Explanation:** The clinical presentation points towards **Multiple Endocrine Neoplasia Type 1 (MEN 1)**, also known as Wermer’s Syndrome. This autosomal dominant condition is characterized by the "3 Ps": **P**arathyroid, **P**ancreas, and **P**ituitary tumors. [1] 1. **Parathyroid (95% of cases):** The patient has hypercalcemia (12 mg/dL) and significantly elevated PTH (260 IU/L), indicating primary hyperparathyroidism. [3] The family history of renal stones in the father suggests a genetic predisposition to hypercalcemia [1] and occasionally, primary hyperparathyroidism presents with severe life-threatening hypercalcemia often due to dehydration. [3] 2. **Pituitary (30-40%):** Elevated prolactin levels indicate a prolactinoma, the most common pituitary tumor in MEN 1. 3. **Pancreas:** While not explicitly mentioned, polyuria in this context could be due to hypercalcemia (nephrogenic diabetes insipidus) [2] or potentially a co-existing gastrinoma/insulinoma. **Why other options are incorrect:** * **MEN 2:** Characterized by Medullary Thyroid Carcinoma and Pheochromocytoma. While MEN 2A includes hyperparathyroidism, it does **not** involve pituitary tumors (prolactinoma). * **PGA 1 (APS-1):** Characterized by the triad of Chronic Mucocutaneous Candidiasis, Autoimmune Hypoparathyroidism (low calcium), and Addison’s disease. This patient has *high* calcium. * **Autoimmune Polyendocrinopathy:** Usually involves glandular destruction (hypofunction) rather than the hormone-secreting tumors seen here. **Clinical Pearls for NEET-PG:** * **MEN 1 Gene:** Located on Chromosome **11q13** (encodes Menin protein). * **First manifestation:** Hyperparathyroidism is usually the earliest and most common sign of MEN 1. * **Screening:** In suspected MEN 1, the most sensitive initial screen is ionized calcium and PTH. [1] * **Pituitary:** Prolactinoma is the most common, followed by GH-secreting tumors.

Q: A 14-year-old boy presents with a 3-month history of increasing weakness, easy fatigability, and weight loss. He also reports recent onset of nausea, vomiting, and abdominal pain. His blood pressure is markedly decreased, and he has increased pigmentation of his skin creases. What is the most likely diagnosis?

Addison disease. **Explanation:** The clinical presentation of weakness, weight loss, hypotension, and gastrointestinal symptoms (nausea/vomiting), combined with **hyperpigmentation**, is classic for **Addison disease** (Primary Adrenocortical Insufficiency). 1. **Why Addison Disease is correct:** In primary adrenal insufficiency, the adrenal cortex fails to produce cortisol and aldosterone. The lack of cortisol triggers a compensatory increase in **ACTH** (Adrenocorticotropic Hormone) from the pituitary. ACTH is derived from Pro-opiomelanocortin (POMC), which also produces **Melanocyte-Stimulating Hormone (MSH)**. High levels of these precursors lead to the characteristic hyperpigmentation of skin creases, scars, and buccal mucosa. The lack of aldosterone leads to salt wasting, dehydration, and marked hypotension. 2. **Why other options are incorrect:** * **Cushing syndrome:** Characterized by cortisol *excess*, leading to hypertension, weight *gain* (central obesity), and striae, rather than hypotension and weight loss. * **Secondary hyperaldosteronism:** Usually presents with hypertension and edema (due to RAAS activation), not hypotension or hyperpigmentation. * **Osteitis fibrosa cystica:** A bone manifestation of hyperparathyroidism; it presents with bone pain and fractures, not adrenal symptoms. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause:** Autoimmune adrenalitis (Western world) vs. Tuberculosis (Developing countries/India). * **Electrolyte Triad:** Hyponatremia, Hyperkalemia, and Metabolic Acidosis. * **Diagnosis:** Best initial test is the **ACTH Stimulation Test** (Cosyntropin test). A failure of cortisol to rise confirms the diagnosis. * **Management:** Lifelong replacement of glucocorticoids (Hydrocortisone) and mineralocorticoids (Fludrocortisone). In "Adrenal Crisis," the priority is IV fluids and IV Hydrocortisone.

Question 1

A 35-year-old male with a history of severe bronchial asthma for several months now complains of weight gain and the development of purple stretch marks. Physical examination showed BP 149/95 mmHg, supraclavicular fullness, thinned skin with areas of bruising, and decreased strength in proximal muscles. Laboratory investigations showed reduced serum cortisol and reduced plasma ACTH. An electrolyte workup in this patient will most likely reveal?

Accepted Answer

Iatrogenic cause

Answer

Pituitary tumor

Answer

Tumor of the adrenal cortex

Answer

Lung cancer

Question 2

Which of the following is seen in secondary hyperparathyroidism?

Accepted Answer

Chronic hypocalcemia

Answer

Chronic hypercalcemia

Answer

Chronic hypomagnesemia

Answer

Chronic hypermagnesemia

Question 3

A couple has two children and is currently unable to conceive. The father is diagnosed with hypogonadotropic hypogonadism. Which of the following statements is false regarding his condition?

Accepted Answer

Normal testosterone levels

Answer

Low luteinizing hormone (LH) and follicle-stimulating hormone (FSH)

Answer

Oligospermia

Answer

High prolactin levels

Question 4

A patient presents with increased serum calcium and decreased serum phosphate. What is the most likely diagnosis?

Accepted Answer

Primary hyperparathyroidism

Answer

Secondary hyperparathyroidism due to Vitamin D deficiency

Answer

Malignancy

Answer

Osteoporosis

Question 5

What is true about thyroid storm?

Accepted Answer

It can be precipitated by surgery.

Answer

It is precipitated by infection in a hypothyroid patient.

Answer

Treatment is delayed until thyroid function test results are known.

Answer

Steroids should be withheld.

Question 6

A patient with IDDM injects a mixture of NPH insulin and crystalline zinc (Regular) insulin before breakfast (at 7 AM) and before dinner (at 8 PM) each day. She reports the following average self-monitored RBS for the past week.

Accepted Answer

Increasing both the 7 AM and 8 PM doses of regular insulin

Answer

Increasing the 7 AM dose of NPH insulin

Answer

Increasing both 7 AM and 8 PM doses of NPH insulin

Answer

Increasing the 7 AM dose of regular insulin

Question 7

A patient presents with polyuria and elevated prolactin levels. There is a family history of the father dying due to renal stones. The patient has a Ca2+ of 12 g% and PTH levels of 260 IU/L. What is the most likely diagnosis?

Accepted Answer

MEN 1

Answer

PGA 1

Answer

MEN 2

Answer

Autoimmune polyendocrinopathy

Question 8

Which one of the following is NOT an appropriate treatment for hyperthyroidism due to subacute lymphocytic thyroiditis?

Accepted Answer

Beta blockers

Answer

Propylthiouracil

Answer

Radioactive iodine ablation

Answer

Subtotal thyroidectomy

Question 9

A 14-year-old boy presents with a 3-month history of increasing weakness, easy fatigability, and weight loss. He also reports recent onset of nausea, vomiting, and abdominal pain. His blood pressure is markedly decreased, and he has increased pigmentation of his skin creases. What is the most likely diagnosis?

Accepted Answer

Addison disease

Answer

Cushing syndrome

Answer

Secondary hyperaldosteronism

Answer

Osteitis fibrosa cystica

Question 10

What is the most characteristic symptom in a patient diagnosed with Pheochromocytoma?

Accepted Answer

Paroxysmal hypertension

Answer

Sweating attacks

Answer

Weight loss

Answer

Orthostatic hypotension

Endocrinology — MCQs

Endocrinology — MCQs

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