Endocrinology Practice Questions

Q: Medical adrenalectomy is seen with:

Mitotane. **Explanation:** **Correct Answer: C. Mitotane** **Medical Adrenalectomy** refers to the pharmacological destruction or functional suppression of the adrenal cortex, mimicking a surgical removal. **Mitotane** is the drug of choice for this process. It is a derivative of the insecticide DDT and acts as a **cytotoxic antineoplastic agent** specifically targeting the adrenal cortex. It works via two primary mechanisms: 1. **Direct Adrenolytic Action:** It causes mitochondrial damage and necrosis of the cells in the *zona fasciculata* and *zona reticularis*, leading to atrophy of the gland. 2. **Biochemical Inhibition:** It inhibits enzymes involved in steroidogenesis (such as 11-beta-hydroxylase) and alters the peripheral metabolism of steroids. It is primarily used in the treatment of **inoperable Adrenocortical Carcinoma** and occasionally in refractory Cushing’s Syndrome. **Why other options are incorrect:** * **Vincristine & Vinblastine (Options A & B):** These are Vinca alkaloids that inhibit microtubule formation (M-phase specific). Their primary toxicities are neurological (Vincristine) and bone marrow suppression (Vinblastine), with no specific destructive effect on the adrenal glands. * **Methotrexate (Option D):** An antimetabolite that inhibits dihydrofolate reductase (DHFR). It is used for malignancies, ectopic pregnancy, and autoimmune conditions (RA/Psoriasis), but does not cause adrenal necrosis. **High-Yield Clinical Pearls for NEET-PG:** * **Other drugs causing "Medical Adrenalectomy" (Functional):** Ketoconazole, Metyrapone, and Aminoglutethimide (these inhibit steroid synthesis rather than destroying the tissue). * **Mitotane Side Effect:** It is highly lipophilic and can cause significant GI distress and neurological symptoms (ataxia, lethargy). * **Nelson’s Syndrome:** Be aware that rapid reduction of cortisol (via surgery or drugs) can lead to an ACTH-secreting pituitary adenoma and hyperpigmentation.

Q: Which of the following is NOT true about dyshormonogenesis?

It follows autosomal dominant inheritance.. **Explanation:** **Dyshormonogenesis** refers to a group of genetic defects in the enzymatic pathways required for thyroid hormone synthesis [1]. 1. **Why Option A is the Correct Answer (The False Statement):** Dyshormonogenesis follows an **autosomal recessive** inheritance pattern, not autosomal dominant [1]. Most cases result from loss-of-function mutations in both alleles of genes encoding enzymes like TPO, thyroglobulin, or the sodium-iodide symporter. 2. **Analysis of Other Options:** * **Option B:** The most common biochemical defect in dyshormonogenesis is a deficiency or dysfunction of the **Thyroid Peroxidase (TPO)** enzyme, which impairs the organification of iodide [1]. * **Option C:** In mild enzymatic defects, increased TSH levels can compensate for the biosynthetic block, leading to a **euthyroid goiter**. However, severe defects typically present as congenital hypothyroidism (cretinism) [1]. * **Option D:** **Pendred Syndrome** is a classic example caused by mutations in the *SLC26A4* gene (encoding pendrin). It is characterized by a triad of sensorineural hearing loss, goiter, and a positive perchlorate discharge test (indicating an organification defect/TPO dysfunction). **High-Yield Clinical Pearls for NEET-PG:** * **Perchlorate Discharge Test:** Used to diagnose iodide organification defects (positive if >10-15% of the tracer is discharged). * **Goiter:** Unlike thyroid agenesis, dyshormonogenesis typically presents with a goiter due to chronic TSH overstimulation. * **Most common cause of Congenital Hypothyroidism:** Thyroid Dysgenesis (80-85%); Dyshormonogenesis accounts for the remaining 10-15% [1].

Q: An obese patient presented with random blood sugar 400 mg%, urine sugar +++, and ketones. Which drug is most useful in management?

Insulin. **Explanation:** The patient presents with significant hyperglycemia (RBS 400 mg/dL), glycosuria, and **ketonuria**. This clinical triad is highly suggestive of **Diabetic Ketoacidosis (DKA)** [3] or severe insulin deficiency. **Why Insulin is the Correct Choice:** Insulin is the definitive treatment for any patient presenting with ketosis. In the presence of ketones, there is an absolute or relative deficiency of insulin leading to lipolysis and ketone body formation. Insulin is required to: 1. Inhibit further ketogenesis by suppressing lipolysis. 2. Facilitate glucose uptake into cells. 3. Correct the metabolic acidosis [5]. Oral hypoglycemic agents (OHAs) are ineffective and contraindicated in the management of acute ketosis or DKA. **Why Other Options are Incorrect:** * **Glibenclamide (Sulfonylurea):** It works by stimulating insulin release from pancreatic beta cells [4]. In an acute state of ketosis, the pancreas cannot produce enough insulin to overcome the crisis, and the onset of action is too slow. * **Troglitazone (Thiazolidinedione):** These are insulin sensitizers that take weeks to reach maximum effect. Furthermore, Troglitazone was withdrawn globally due to severe hepatotoxicity. * **Metformin (Biguanide):** It is the first-line drug for stable Type 2 Diabetes but is **contraindicated** in states of severe dehydration or metabolic acidosis (like DKA) due to the risk of worsening lactic acidosis. **High-Yield Clinical Pearls for NEET-PG:** * **DKA Diagnosis:** Look for the "D-K-A" triad: Diabetes (Glucose >250 mg/dL), Ketones (positive in urine/serum), and Acidosis (pH <7.3 or Bicarbonate <18 mEq/L) [1]. * **Management Priority:** The first step in DKA management is aggressive fluid resuscitation (Normal Saline), followed by intravenous regular insulin [2]. * **Insulin Choice:** Regular (Short-acting) insulin is the preparation of choice for managing acute hyperglycemic emergencies [2].

Q: Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is diagnosed by all EXCEPT:

Normal blood urea nitrogen. **Explanation:** The diagnosis of **SIADH** is based on the **Bartter-Schwartz criteria**. It is a condition of "euvolemic hyponatremia" where excessive ADH leads to water retention and secondary solute loss [1]. **Why Option C is the correct answer (The Exception):** In SIADH, the expansion of total body water leads to a **dilutional effect** and increased renal clearance of urea. Therefore, a characteristic finding in SIADH is a **Low Blood Urea Nitrogen (BUN <10 mg/dL)** and low serum uric acid. A "Normal" BUN (typically 10–20 mg/dL) actually points away from SIADH and suggests other causes of hyponatremia or underlying renal impairment. **Analysis of Incorrect Options:** * **A & B (Hyponatremia & Decreased Serum Osmolality):** These are the hallmarks of SIADH [2]. Excessive water reabsorption dilutes the extracellular fluid, leading to hypotonic hyponatremia (Serum Na <135 mEq/L and Osmolality <280 mOsm/kg). * **D (Normal Thyroid Function):** To diagnose SIADH, one must **exclude** other causes of euvolemic hyponatremia. Both hypothyroidism and adrenal insufficiency (glucocorticoid deficiency) can mimic SIADH; thus, normal thyroid and adrenal functions are mandatory diagnostic requirements [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Urine Findings:** Urine osmolality is inappropriately high (>100 mOsm/kg, often > serum) and urine sodium is high (>40 mEq/L) due to the absence of hypovolemia. * **Volume Status:** Patients are clinically **euvolemic** (no edema, no JVP elevation) [2]. * **Treatment:** Fluid restriction is the first-line treatment. For severe cases, Vaptans (ADH antagonists) or hypertonic saline may be used. * **Caution:** Rapid correction of hyponatremia can lead to **Osmotic Demyelination Syndrome (Central Pontine Myelinolysis).**

Q: What is the cause of infertility in hypothyroidism?

Increase in prolactin. **Explanation:** The correct answer is **B. Increase in prolactin**. **Pathophysiology:** In primary hypothyroidism, low levels of circulating thyroid hormones (T3 and T4) trigger a feedback mechanism that increases the secretion of **Thyrotropin-Releasing Hormone (TRH)** from the hypothalamus. TRH acts as a potent stimulator for both the thyrotrophs (releasing TSH) and the lactotrophs in the anterior pituitary. Consequently, elevated TRH leads to **hyperprolactinemia**. High prolactin levels interfere with the pulsatile secretion of **Gonadotropin-Releasing Hormone (GnRH)** from the hypothalamus. This disruption inhibits the release of LH and FSH, leading to anovulation, luteal phase defects, and ultimately, infertility. **Analysis of Options:** * **Option A (Decrease in prolactin):** This is incorrect. Low prolactin is not associated with hypothyroidism; rather, the loss of negative feedback in hypothyroidism specifically drives prolactin levels upward. * **Option C & D:** These are incorrect based on the established hormonal axis described above. **High-Yield Clinical Pearls for NEET-PG:** * **First-line Investigation:** In a patient presenting with galactorrhea and infertility, always check **TSH** levels first to rule out primary hypothyroidism before considering a prolactinoma. * **Treatment:** Infertility caused by hypothyroidism is often reversible. Treating the underlying condition with **Levothyroxine** typically normalizes TRH and prolactin levels, restoring regular ovulatory cycles. * **Associated Symptoms:** Patients may also present with menstrual irregularities like **menorrhagia** (most common) or oligomenorrhea.

Question 1

A patient presents with headache and flushing, and has a family history of medullary thyroid carcinoma. What investigation is most appropriate for this patient?

Accepted Answer

Fractionated plasma metanephrines

Answer

Chest X-ray

Answer

Measurement of 5-hydroxyindoleacetic acid (5-HIAA)

Answer

Intravenous pyelography

Question 2

Medical adrenalectomy is seen with:

Accepted Answer

Mitotane

Answer

Vincristine

Answer

Vinblastine

Answer

Methotrexate

Question 3

Which of the following causative factors is not involved in the pathogenesis of diabetic gangrene?

Accepted Answer

Myelopathy

Answer

Infection

Answer

Atherosclerosis

Answer

Osteoarthropathy

Question 4

Which of the following is NOT true about dyshormonogenesis?

Accepted Answer

It follows autosomal dominant inheritance.

Answer

The most common abnormality is with thyroid peroxidase activity.

Answer

Young patients may present with euthyroid goiter.

Answer

Pendred syndrome is a classic example of dyshormonogenesis due to TPO deficiency.

Question 5

An obese patient presented with random blood sugar 400 mg%, urine sugar +++, and ketones. Which drug is most useful in management?

Accepted Answer

Insulin

Answer

Glibenclamide

Answer

Troglitazone

Answer

Metformin

Question 6

A patient, after bilateral adrenalectomy, develops gradual loss of vision, hyperpigmentation of the skin, and headache. What is the likely cause of these symptoms?

Accepted Answer

Nelson's syndrome

Answer

Addison's disease

Answer

Cushing's disease

Answer

Harrison's syndrome

Question 7

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is diagnosed by all EXCEPT:

Accepted Answer

Normal blood urea nitrogen

Answer

Hyponatremia

Answer

Decreased serum osmolality (< 280 mosm/kg)

Answer

Normal thyroid function

Question 8

What is the cause of infertility in hypothyroidism?

Accepted Answer

Increase in prolactin

Answer

Decrease in prolactin

Answer

Both

Answer

None

Question 9

A 29-year-old person, known diabetic on oral hypoglycemic agents for 3 years, has lost weight and never had diabetic ketoacidosis. His grandfather is diabetic, but his father is not. Which of the following is the likely diagnosis?

Accepted Answer

Diabetes Mellitus type II

Answer

Maturity Onset Diabetes of the Young (MODY)

Answer

Diabetes Mellitus type I

Answer

Pancreatic diabetes

Question 10

A 40-year-old non-diabetic woman presents to the emergency department with hypoglycemia. The paramedics suspect an insulin overdose, while you suspect an insulinoma. Which laboratory result would confirm your suspicion of insulinoma?

Accepted Answer

Insulin level is inappropriately high for the degree of hypoglycemia and is accompanied by a detectable C-peptide level

Answer

Insulin level is significantly elevated compared to C-peptide level

Answer

Insulin level is significantly lower than C-peptide level

Answer

Insulin antibody level is equal to the insulin level

Endocrinology — MCQs

Endocrinology — MCQs

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