Endocrinology — MCQs

A 67-year-old woman presents to the clinic for evaluation of numbness in her feet, with symptoms that started gradually and are more noticeable now. There is no weakness in her feet or difficulty walking. Her past medical history is significant for Type 2 diabetes for the past 10 years, for which she currently takes metformin and glyburide. Physical examination confirms sensory loss in the feet to touch and vibration. Which of the following is most characteristic of diabetic neuropathy?

Q1045Easy

Which is NOT a clinical feature of Addison's disease?

Q1046Easy

All of the following are clinical features of Cushing's syndrome except?

Q1047Medium

Diabetes mellitus is present in which of the following conditions, except?

Q1048Easy

Which of the following hormonal patterns is found in primary hypothyroidism?

Q1049Easy

Alcoholic ketoacidosis is best managed with?

Q1050Easy

In which of the following conditions radioactive iodine can be used in Graves' disease?

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 1041: Which of the following is true of adrenal suppression due to steroid therapy?

A. It is not associated with atrophy of the adrenal glands.
B. It is less likely to occur in patients receiving inhaled steroids. (Correct Answer)
C. It should be expected in anyone receiving more than 5 mg of prednisolone daily.
D. Following cessation, the stress response normalizes after 8 weeks.

Explanation: Adrenal suppression occurs due to the exogenous administration of glucocorticoids, which triggers negative feedback on the Hypothalamic-Pituitary-Adrenal (HPA) axis, leading to decreased production of CRH and ACTH [2]. **1. Why Option B is Correct:** Inhaled corticosteroids (ICS) are designed to act locally on the airway mucosa. While high doses can lead to systemic absorption, the risk of HPA axis suppression is significantly lower compared to systemic (oral or IV) therapy because of extensive first-pass metabolism in the liver and lower systemic bioavailability. **2. Why Other Options are Incorrect:** * **Option A:** Chronic suppression of ACTH leads to **disuse atrophy** of the adrenal cortex (specifically the zona fasciculata and reticularis). * **Option C:** Adrenal suppression is generally expected in patients taking **>20 mg/day** of Prednisolone for more than 3 weeks [1]. Doses <5 mg/day (physiologic replacement) are unlikely to cause suppression [1]. * **Option D:** Recovery of the HPA axis is a slow, tiered process. While basal cortisol levels may normalize within weeks, the **full stress response** (ability to increase cortisol during trauma or surgery) can take **up to 6–12 months** to fully recover after cessation of long-term therapy [1]. **Clinical Pearls for NEET-PG:** * **Gold Standard Test:** The **Insulin Tolerance Test (ITT)** is the gold standard to assess the integrity of the HPA axis, though the Short ACTH Stimulation test is more commonly used in clinical practice. * **Steroid Cover:** Patients with suspected HPA suppression undergoing surgery require "stress doses" of hydrocortisone to prevent an Addisonian crisis. * **Tapering Rule:** Never abruptly stop steroids if the patient has been on a suppressive dose for >3 weeks; gradual tapering is mandatory to allow the HPA axis to wake up [1].

Question 1042: Schmidt syndrome includes all of the following conditions except?

A. Adrenal insufficiency
B. Hypothyroidism
C. Type-1 Diabetes Mellitus
D. Chronic Candidiasis (Correct Answer)

Explanation: **Explanation:** Schmidt syndrome, also known as **Autoimmune Polyglandular Syndrome Type 2 (APS-2)**, is an autosomal dominant condition with variable penetrance [1]. It is characterized by the mandatory presence of **Autoimmune Adrenal Insufficiency (Addison’s disease)** along with autoimmune thyroid disease and/or Type-1 Diabetes Mellitus [1], [2]. **Why Chronic Candidiasis is the correct answer:** Chronic Mucocutaneous Candidiasis (CMC) is the hallmark of **APS Type 1** (also known as APECED syndrome), not APS Type 2 [1]. APS Type 1 typically presents in childhood with a classic triad: CMC, Hypoparathyroidism, and Adrenal Insufficiency [1]. Its absence is a key clinical differentiator for Schmidt syndrome. **Analysis of incorrect options:** * **Adrenal Insufficiency (Option A):** This is the primary component of Schmidt syndrome. It is almost always present and is usually the first manifestation [2]. * **Hypothyroidism (Option B):** Autoimmune thyroid disease (Hashimoto’s thyroiditis) is a frequent component [1], [3]. The combination of Addison’s and Hypothyroidism is specifically referred to as Schmidt syndrome [1]. * **Type-1 Diabetes Mellitus (Option C):** T1DM is frequently associated with APS-2 [2], [3]. When T1DM is present alongside Addison’s and Thyroid disease, it is sometimes called Carpenter’s syndrome (a subset of APS-2). **High-Yield Clinical Pearls for NEET-PG:** * **APS Type 1 Triad:** Candidiasis, Hypoparathyroidism, Addison’s (Mnemonic: **CHA**) [1]. * **APS Type 2 (Schmidt):** Addison’s + Thyroid disease +/– T1DM [1]. It is more common in females and typically presents in adulthood (3rd–4th decade). * **Treatment Caution:** In Schmidt syndrome, always treat the adrenal insufficiency with steroids **before** starting thyroxine to avoid precipitating an acute adrenal crisis.

Question 1043: Which of the following is NOT a feature of primary thyrotoxicosis?

A. Tremors
B. Warm extremities
C. Diarrhea
D. Intolerance to cold (Correct Answer)

Explanation: Explanation: Thyrotoxicosis is a clinical state resulting from inappropriate high levels of circulating thyroid hormones ($T_3$ and $T_4$). Thyroid hormones act as a "metabolic accelerator," increasing the basal metabolic rate (BMR) and upregulating beta-adrenergic receptors [1]. Why "Intolerance to Cold" is the correct answer: Primary thyrotoxicosis leads to increased thermogenesis (heat production). Consequently, patients develop heat intolerance and prefer cold environments [1]. Cold intolerance is a hallmark feature of hypothyroidism, where the BMR is low and the body cannot generate sufficient heat. Analysis of incorrect options: * Tremors: Excess thyroid hormone increases sensitivity to catecholamines and affects the neurological system. This typically manifests as a fine, high-frequency kinetic tremor, best seen in outstretched hands [1]. * Warm extremities: Increased metabolism and the need to dissipate excess heat lead to peripheral vasodilation. This results in skin that is characteristically warm, moist, and velvety [1]. * Diarrhea: Thyroid hormones stimulate gut motility [1]. While frank diarrhea occurs in severe cases, most patients report an increased frequency of bowel movements or malabsorption. Clinical Pearls for NEET-PG: * Apathetic Hyperthyroidism: Seen in the elderly; typical hypermetabolic features (like tremors/tachycardia) may be absent, presenting instead with depression or atrial fibrillation [2]. * Cardiovascular Sign: Look for "bounding pulses" and a wide pulse pressure due to increased stroke volume and decreased peripheral resistance [1]. * Eye Signs: Lid lag and lid retraction are due to sympathetic overactivity (seen in all thyrotoxicosis), whereas Exophthalmos is specific to Graves' Disease (due to TSH-receptor antibodies) [1].

Question 1044: A 67-year-old woman presents to the clinic for evaluation of numbness in her feet, with symptoms that started gradually and are more noticeable now. There is no weakness in her feet or difficulty walking. Her past medical history is significant for Type 2 diabetes for the past 10 years, for which she currently takes metformin and glyburide. Physical examination confirms sensory loss in the feet to touch and vibration. Which of the following is most characteristic of diabetic neuropathy?

A. It is usually bilateral. (Correct Answer)
B. Pain is not a feature.
C. It most commonly affects the brain.
D. It spares the autonomic system.

Explanation: **Explanation:** The patient presents with classic symptoms of **Distal Symmetric Polyneuropathy (DSPN)**, the most common form of diabetic neuropathy [1]. **1. Why Option A is correct:** Diabetic neuropathy is a length-dependent process caused by metabolic and microvascular damage to the nerves [1]. It typically presents in a **"stocking-and-glove" distribution**, meaning it is **bilateral, symmetrical**, and starts in the longest nerves (the feet) [1]. The symmetry is a hallmark feature that helps distinguish it from other conditions like mononeuritis multiplex. **2. Why the other options are incorrect:** * **Option B:** Pain is a very common feature. Up to 50% of patients experience "positive" symptoms such as burning, tingling, or lancinating pain, which is often worse at night. * **Option C:** Diabetic neuropathy primarily affects the **Peripheral Nervous System (PNS)** and the Autonomic Nervous System [1]. It does not typically affect the brain (Central Nervous System). * **Option D:** Diabetes frequently involves the **Autonomic Nervous System**, leading to complications such as resting tachycardia, orthostatic hypotension, gastroparesis, and erectile dysfunction [3]. **Clinical Pearls for NEET-PG:** * **First sign:** Loss of vibratory sensation (tested with a 128-Hz tuning fork) and loss of ankle jerks [1], [2]. * **Screening:** Annual screening using the **10-g Semmes-Weinstein monofilament** is essential to identify feet at risk for ulceration [2]. * **Management:** Strict glycemic control is the only way to prevent progression. For symptomatic pain, first-line agents include **Pregabalin, Duloxetine, or Gabapentin**. * **Metformin Link:** Long-term metformin use (as seen in this patient) can cause **Vitamin B12 deficiency**, which can mimic or exacerbate diabetic neuropathy. Always check B12 levels in these patients.

Question 1045: Which is NOT a clinical feature of Addison's disease?

A. Hypoglycemia
B. Hyponatremia
C. Hypopigmentation (Correct Answer)
D. Hyperkalemia

Explanation: **Explanation** Addison’s disease (Primary Adrenocortical Insufficiency) is characterized by the destruction of the adrenal cortex, leading to a deficiency of cortisol, aldosterone, and adrenal androgens [1]. **Why Hypopigmentation is the Correct Answer:** In primary adrenal insufficiency, low cortisol levels trigger a compensatory increase in **ACTH** (Adrenotropic Hormone) secretion from the pituitary. ACTH is derived from a precursor molecule called **POMC** (Proopiomelanocortin). POMC also produces **MSH** (Melanocyte-Stimulating Hormone). High levels of ACTH/MSH stimulate melanocytes, leading to **hyperpigmentation** (especially in skin creases, scars, and buccal mucosa), not hypopigmentation. **Analysis of Incorrect Options:** * **Hypoglycemia:** Cortisol is a counter-regulatory hormone that promotes gluconeogenesis. Its absence leads to impaired glucose production and increased insulin sensitivity. * **Hyponatremia:** Aldosterone deficiency leads to renal wasting of sodium [2]. Additionally, cortisol deficiency increases ADH secretion (dilutional hyponatremia). * **Hyperkalemia:** Aldosterone normally promotes potassium excretion in the distal tubule. Its absence results in potassium retention and metabolic acidosis [2]. **NEET-PG High-Yield Pearls:** * **Most common cause:** Autoimmune adrenalitis (Western world); Tuberculosis (Developing countries/India) [1], [2]. * **Cosyntropin Stimulation Test:** The gold standard for diagnosis (failure of cortisol to rise >18 µg/dL) [2]. * **Secondary Adrenal Insufficiency:** Caused by pituitary failure. Key difference: **No hyperpigmentation** (low ACTH) and **no hyperkalemia** (mineralocorticoid production is preserved via the RAAS system). * **Classic Triad:** Hyponatremia, Hyperkalemia, and Azotemia.

Question 1046: All of the following are clinical features of Cushing's syndrome except?

A. Insulin resistance
B. Menorrhagia (Correct Answer)
C. Violaceous striae
D. Centripetal obesity

Explanation: **Explanation:** Cushing’s syndrome results from chronic exposure to excessive glucocorticoids. The correct answer is **Menorrhagia** because hypercortisolism typically leads to **amenorrhea or oligomenorrhea**, rather than heavy menstrual bleeding. [1] **Why Menorrhagia is the correct answer (The Exception):** Excess cortisol exerts a negative feedback effect on the hypothalamus, suppressing the secretion of Gonadotropin-Releasing Hormone (GnRH). This leads to decreased levels of LH and FSH, resulting in hypogonadotropic hypogonadism. Clinically, this manifests as menstrual irregularities, most commonly **oligomenorrhea** (infrequent periods) or secondary **amenorrhea** (absence of periods), often accompanied by hirsutism due to co-secretion of adrenal androgens. [1] **Analysis of Incorrect Options:** * **Insulin resistance:** Cortisol is a potent "diabetogenic" hormone. It increases gluconeogenesis in the liver and inhibits glucose uptake in peripheral tissues, leading to secondary diabetes mellitus or impaired glucose tolerance. * **Violaceous striae:** These are wide (>1 cm), reddish-purple stretch marks typically found on the abdomen, thighs, and breasts. They occur because cortisol inhibits fibroblasts and causes collagen breakdown, making the skin thin and fragile. [1] * **Centripetal obesity:** This is the hallmark of Cushing’s. Cortisol causes redistribution of fat from the extremities to the trunk, resulting in "lemon on a matchstick" appearance, "buffalo hump" (supraclavicular/dorsocervical fat pads), and "moon facies." [1] **High-Yield NEET-PG Pearls:** * **Screening Test of Choice:** 24-hour urinary free cortisol or Low-Dose Dexamethasone Suppression Test (LDDST). [2] * **Most Common Cause:** Iatrogenic (exogenous steroids). [1] * **Most Common Endogenous Cause:** Cushing’s Disease (Pituitary adenoma). [1] * **Proximal Myopathy:** Cortisol causes muscle wasting, leading to difficulty climbing stairs or rising from a chair. [1]

Question 1047: Diabetes mellitus is present in which of the following conditions, except?

A. Hemochromatosis
B. Ataxia telangiectasia (Correct Answer)
C. Friedreich's ataxia
D. Motor neuron disease

Explanation: The correct answer is **B. Ataxia telangiectasia**. While this condition is associated with severe **insulin resistance**, patients typically maintain normal or near-normal glucose levels due to compensatory hyperinsulinemia; overt clinical diabetes mellitus is not a standard feature of the syndrome. **Analysis of Options:** * **Hemochromatosis (Option A):** Known as "Bronze Diabetes," iron deposition in the pancreas causes direct damage to beta cells (insulin deficiency) and liver damage (insulin resistance), making diabetes a classic complication. * **Friedreich's Ataxia (Option C):** Approximately 10–20% of patients develop diabetes mellitus. The mechanism involves mitochondrial dysfunction leading to both impaired insulin secretion and peripheral insulin resistance. * **Motor Neuron Disease (Option D):** Several studies have linked MND (specifically ALS) with abnormal glucose metabolism and a higher prevalence of diabetes, likely due to metabolic stress and shared genetic pathways. **Clinical Pearls for NEET-PG:** 1. **Secondary Diabetes:** Always look for "Bronze Diabetes" (Hemochromatosis) and "Endocrine Diabetes" (Cushing’s, Acromegaly, Pheochromocytoma, Glucagonoma) [1]. 2. **Ataxia Telangiectasia Triad:** Cerebellar ataxia, oculocutaneous telangiectasia, and immunodeficiency (IgA deficiency). It is an autosomal recessive disorder involving the *ATM* gene. 3. **High-Yield Association:** While Ataxia telangiectasia shows insulin resistance [2], **Friedreich's Ataxia** is the neurodegenerative disorder most classically associated with clinical **Diabetes Mellitus** in exam questions.

Question 1048: Which of the following hormonal patterns is found in primary hypothyroidism?

A. T3 decrease, T4 decrease, TSH increase (Correct Answer)
B. T3 decrease, T4 increase, TSH decrease
C. T3 normal, T4 normal, TSH increase
D. T3 decrease, T4 decrease, TSH normal

Explanation: ### Explanation **1. Why the Correct Answer is Right (Option A)** Primary hypothyroidism occurs due to the failure of the thyroid gland itself (e.g., Hashimoto’s thyroiditis). When the thyroid gland cannot produce sufficient hormones, levels of **T4 (Thyroxine)** and **T3 (Triiodothyronine)** fall. This drop triggers the **negative feedback mechanism** on the anterior pituitary [1], leading to a compensatory and marked **increase in Thyroid Stimulating Hormone (TSH)** [1]. TSH is the most sensitive indicator for primary thyroid disease. **2. Why the Other Options are Incorrect** * **Option B:** This pattern (Low T3, High T4, Low TSH) is physiologically inconsistent. High T4 would typically suppress TSH, and T3 would usually be elevated in hyperthyroid states. * **Option C:** This pattern (Normal T3/T4, High TSH) represents **Subclinical Hypothyroidism**. While it is a precursor to primary hypothyroidism, the question asks for the pattern of established primary hypothyroidism where hormone levels have already fallen. * **Option D:** This pattern (Low T3/T4, Normal TSH) suggests **Secondary (Central) Hypothyroidism**, where the pituitary fails to respond to low thyroid levels by increasing TSH production [2]. **3. Clinical Pearls for NEET-PG** * **Gold Standard Screening:** Serum **TSH** is the single best initial test for screening thyroid dysfunction. * **T3 vs. T4:** In early primary hypothyroidism, T4 levels drop before T3. T3 may remain in the normal range for a long time due to increased peripheral conversion; however, in overt disease, both are low. * **Wolff-Chaikoff Effect:** Transient hypothyroidism caused by the ingestion of a large amount of iodine. * **Myxedema Coma:** The most severe expression of primary hypothyroidism, characterized by altered mental status and hypothermia.

Question 1049: Alcoholic ketoacidosis is best managed with?

A. Thiamine with 10% dextrose infusion
B. Isotonic saline infusion (Correct Answer)
C. Sodium bicarbonate infusion
D. Fomepizole infusion

Explanation: **Explanation:** **Alcoholic Ketoacidosis (AKA)** typically occurs in chronic alcoholics following a binge, followed by a period of starvation and vomiting. The pathophysiology involves a combination of volume depletion, starvation (low glycogen stores), and an increased NADH/NAD+ ratio from alcohol metabolism, which shifts the metabolic balance toward the production of **beta-hydroxybutyrate**. 1. **Why Isotonic Saline is Correct:** The primary goal in AKA management is the restoration of extracellular fluid volume. **Isotonic (0.9%) Saline** is the initial fluid of choice because it corrects volume depletion, improves renal perfusion, and—crucially—increases the delivery of glucose to tissues while decreasing the stimulus for ketogenesis (by suppressing counter-regulatory hormones like glucagon and epinephrine) [1]. 2. **Why Other Options are Incorrect:** * **Thiamine with 10% Dextrose:** While dextrose is eventually needed to stimulate insulin and stop ketogenesis, and thiamine must be given to prevent Wernicke’s encephalopathy, **volume resuscitation with saline** is the immediate priority. Dextrose without saline can worsen electrolyte imbalances and does not address the underlying hypovolemia [2]. * **Sodium Bicarbonate:** Rarely indicated. AKA usually resolves rapidly with fluid and glucose; bicarbonate is reserved only for life-threatening acidemia (pH < 7.0) due to risks of paradoxical CNS acidosis. * **Fomepizole:** This is the antidote for methanol or ethylene glycol poisoning, not AKA. **High-Yield Pearls for NEET-PG:** * **The "Nitroprusside Paradox":** In AKA, the Nitroprusside test (Acetest) may be weakly positive or negative because it detects acetoacetate, whereas the predominant ketone in AKA is **beta-hydroxybutyrate**. * **Insulin:** Unlike Diabetic Ketoacidosis (DKA), **insulin is NOT required** in AKA unless the patient has comorbid diabetes, as exogenous glucose will naturally stimulate endogenous insulin release. * **The Sequence:** Always give **Thiamine before Dextrose** in alcoholics to prevent precipitating Wernicke’s Encephalopathy [2].

Question 1050: In which of the following conditions radioactive iodine can be used in Graves' disease?

A. Recurrence
B. Age less than 40 years (Correct Answer)
C. Elderly
D. Pregnant

Explanation: Radioactive Iodine (RAI), specifically **I-131**, is a definitive treatment for Graves' disease that works by emitting beta particles to cause local tissue destruction of the thyroid gland. [1] ### **Explanation of Options** * **Correct Answer (B) Age less than 40 years:** While historically there was hesitation to use RAI in younger patients due to theoretical concerns regarding carcinogenesis or genetic damage, modern clinical guidelines (including ATA) now consider RAI a safe and effective first-line or second-line therapy for adults of any age, including those under 40. [1] In the context of this specific question, it highlights the shift in clinical practice where age is no longer a contraindication. * **Option (A) Recurrence:** While RAI is used for recurrence after antithyroid drugs (ATDs), it is generally avoided if there is a recurrence after *surgery* due to altered anatomy and potential risks to the parathyroid glands. * **Option (C) Elderly:** While RAI is used in the elderly, it is often not the *preferred* first step if they have severe cardiovascular comorbidities. In such cases, ATDs are used first to achieve euthyroidism to prevent a thyroid storm triggered by RAI-induced thyroiditis. * **Option (D) Pregnant:** This is an **absolute contraindication**. [1] RAI crosses the placenta and can destroy the fetal thyroid gland, leading to permanent fetal hypothyroidism and cretinism. ### **NEET-PG High-Yield Pearls** * **Absolute Contraindications for RAI:** Pregnancy, breastfeeding, and suspected/confirmed thyroid cancer. * **Relative Contraindication:** Moderate-to-severe **Graves' Ophthalmopathy** (RAI can worsen orbitopathy; steroids are required if RAI is used). [1] * **Pre-treatment:** Patients with severe hyperthyroidism should be pre-treated with Methimazole to deplete thyroid hormone stores before RAI to prevent thyrotoxic crisis. * **Follow-up:** The most common long-term complication of RAI is **permanent hypothyroidism**, requiring lifelong Levothyroxine.

Practice by Chapter

Diabetes Mellitus

Practice Questions

Thyroid Disorders

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Adrenal Gland Disorders

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Pituitary Disorders

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Calcium and Bone Metabolism

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Reproductive Endocrinology

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Lipid Disorders

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Endocrine Hypertension

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Multiple Endocrine Neoplasia

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Obesity and Metabolic Syndrome

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Neuroendocrine Tumors

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Endocrine Emergencies

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