Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 981: For FITTER, what is the shortest needle length in mm that should be used?

A. 4 (Correct Answer)
B. 5
C. 6
D. 8

Explanation: The **FITTER (Forum for Injection Technique and Therapy Expert Recommendations)** guidelines emphasize that the primary goal of insulin injection is to deliver the drug into the **subcutaneous (SC) space** while avoiding accidental **intramuscular (IM)** injection. **1. Why 4 mm is the correct answer:** The human skin (epidermis and dermis) thickness at injection sites rarely exceeds 2.5 mm, regardless of BMI, age, or ethnicity. A **4 mm needle** is the shortest available length and is considered the **gold standard** for all patients (including obese individuals). It is long enough to pass through the skin into the SC tissue but short enough to significantly reduce the risk of painful IM injections, which can cause unpredictable glucose fluctuations and hypoglycemia. **2. Why the other options are incorrect:** * **5 mm & 6 mm:** While these were previously common, they increase the risk of IM injection, especially in children, thin adults, or when injecting into the limbs. * **8 mm:** This length is now largely discouraged for routine insulin therapy. Using an 8 mm needle often requires a skin fold (pinch-up) technique to avoid the muscle, increasing the complexity of the injection and the risk of needle-stick injuries. **High-Yield Clinical Pearls for NEET-PG:** * **Site Rotation:** Essential to prevent **Lipohypertrophy**, which can delay insulin absorption. * **No Pinch Technique:** With a 4 mm needle, a 90-degree insertion without a skin fold is recommended for most adults. * **IM Injection Risk:** Insulin absorbed from muscle acts much faster than SC insulin, leading to severe, unexplained hypoglycemia. * **Single Use:** Needles should not be reused as it causes microscopic "barbing," leading to tissue trauma and lipohypertrophy.

Question 982: Which of the following is NOT a feature of primary hyperaldosteronism?

A. Pedal edema (Correct Answer)
B. Diastolic hypertension
C. Polyuria
D. Hypokalemia

Explanation: Primary hyperaldosteronism (Conn’s syndrome) is characterized by the autonomous overproduction of aldosterone, leading to sodium retention and potassium excretion [1]. **Why Pedal Edema is NOT a feature (The "Aldosterone Escape" Phenomenon):** Despite significant sodium and water retention, patients with primary hyperaldosteronism **do not** typically develop pedal edema. This is due to the **"Aldosterone Escape"** mechanism [1]. As intravascular volume expands, the body compensates by increasing the secretion of **Atrial Natriuretic Peptide (ANP)** and increasing the pressure natriuresis in the kidneys. This results in the excretion of excess sodium and water, preventing the formation of overt edema and limiting the severity of hypernatremia [1]. **Analysis of Incorrect Options:** * **Diastolic Hypertension:** Aldosterone increases sodium reabsorption in the distal tubules, leading to volume expansion and increased peripheral resistance, which characteristically raises diastolic blood pressure. * **Polyuria:** Chronic hypokalemia causes **nephrogenic diabetes insipidus** (resistance to ADH), leading to the inability to concentrate urine, resulting in polyuria and nocturia. * **Hypokalemia:** Aldosterone promotes potassium secretion in the cortical collecting duct [1]. While 20-40% of patients may be normokalemic, hypokalemia remains a classic hallmark, often exacerbated by thiazide diuretics [1]. **High-Yield Clinical Pearls for NEET-PG:** 1. **Screening Test:** Plasma Aldosterone Concentration (PAC) to Plasma Renin Activity (PRA) ratio. A **PAC:PRA ratio > 20-30** is highly suggestive. 2. **Confirmatory Test:** Saline infusion test or Oral salt loading test. 3. **Metabolic State:** Patients typically exhibit **Hypokalemic Metabolic Alkalosis** [1]. 4. **Treatment:** Surgical excision for unilateral adenoma; **Spironolactone** or Eplerenone (Aldosterone antagonists) for bilateral adrenal hyperplasia.

Question 983: Common neurological manifestations of thyrotoxicosis include all except?

A. Hyperreflexia
B. Muscle wasting
C. Chorea (Correct Answer)
D. Proximal myopathy without fasciculations

Explanation: Thyrotoxicosis (excess thyroid hormone) significantly impacts the neuromuscular system by increasing metabolic rate and enhancing beta-adrenergic sensitivity. [2] **Why Chorea is the Correct Answer (The Exception):** While thyrotoxicosis can cause various movement disorders, **Chorea is a rare manifestation**, not a "common" one. It is typically seen in specific cases like Graves' disease (possibly due to autoimmune mechanisms or hypersensitivity of dopamine receptors in the basal ganglia) but is not a routine clinical finding compared to the other options. **Analysis of Other Options:** * **A. Hyperreflexia:** This is a hallmark sign. Excess thyroid hormone shortens the contraction and relaxation phases of deep tendon reflexes, leading to "brisk" reflexes. * **B. Muscle Wasting:** Chronic thyrotoxicosis leads to a catabolic state where protein breakdown exceeds synthesis, resulting in visible muscle wasting, particularly in the shoulder and pelvic girdles. [1] * **D. Proximal Myopathy without Fasciculations:** Thyrotoxic myopathy characteristically affects proximal muscles (difficulty climbing stairs or combing hair). [1] Crucially, unlike lower motor neuron diseases (e.g., ALS), it occurs **without fasciculations**, making this a classic clinical description. **High-Yield Clinical Pearls for NEET-PG:** * **Thyroid Storm:** Look for extreme hyperthermia, tachycardia, and altered mental status (delirium/coma). * **Hypokalemic Periodic Paralysis:** A rare but high-yield neurological complication of thyrotoxicosis, more common in Asian males, characterized by sudden muscle weakness after high-carb meals or exercise. * **Tremors:** The tremor in thyrotoxicosis is typically high-frequency, low-amplitude, and fine (best seen by placing a sheet of paper on outstretched hands). [2]

Question 984: Which of the following statements is true about hypercalcemia?

A. Treatment of the primary cause
B. Malignancy does not produce hypercalcemia
C. IV fluids with furosemide are given
D. Amidronate is not effective (Correct Answer)

Explanation: ### **Explanation** **Correct Answer: D. Amidronate is not effective** The management of hypercalcemia focuses on increasing renal excretion and inhibiting bone resorption. **Bisphosphonates** are the mainstay of treatment for hypercalcemia of malignancy [2]. However, **Amidronate** is not a standard clinical bisphosphonate used for this purpose. The potent, nitrogen-containing bisphosphonates used in clinical practice are **Pamidronate** and **Zoledronic acid**. These drugs inhibit osteoclast activity, effectively lowering serum calcium levels over 2–4 days. #### **Analysis of Incorrect Options:** * **A. Treatment of the primary cause:** While treating the underlying etiology (e.g., surgery for primary hyperparathyroidism) is the definitive long-term management, it is **not** the immediate priority in acute, symptomatic hypercalcemia [1]. The immediate goal is stabilization via hydration and calciuresis. * **B. Malignancy does not produce hypercalcemia:** This is false. Malignancy is the **most common cause of hypercalcemia in hospitalized patients**, occurring via PTHrP production (Squamous cell CA), local osteolysis (Multiple Myeloma), or Vitamin D production (Lymphoma) [3]. * **C. IV fluids with furosemide are given:** While aggressive hydration with Normal Saline (0.9% NaCl) is the first-line treatment, the routine use of **Furosemide is no longer recommended** unless the patient is in fluid overload or heart failure. It does not significantly increase calcium excretion beyond hydration alone and can worsen dehydration. #### **NEET-PG High-Yield Pearls:** * **Most common cause overall:** Primary Hyperparathyroidism (usually asymptomatic outpatients) [3]. * **First-line treatment:** Aggressive IV hydration (Normal Saline) [1]. * **Drug of choice for malignancy-associated hypercalcemia:** Zoledronic acid (more potent than Pamidronate). * **ECG finding:** Shortened QT interval. * **Refractory cases:** Denosumab (RANKL inhibitor) or Calcitonin (for rapid, short-term reduction).

Question 985: Which of the following is associated with secondary hyperparathyroidism?

A. Parathyroid adenoma
B. Marked hypercalcemia
C. Chronic renal failure (Correct Answer)
D. Parathyroidectomy relieves the symptoms

Explanation: **Explanation:** **1. Why Chronic Renal Failure (CRF) is correct:** Secondary hyperparathyroidism is a compensatory hypersecretion of Parathyroid Hormone (PTH) in response to prolonged **hypocalcemia** [1]. In Chronic Renal Failure, two main mechanisms trigger this [2]: * **Hyperphosphatemia:** Failing kidneys cannot excrete phosphate. High phosphate levels directly stimulate PTH and bind ionized calcium [3]. * **Vitamin D Deficiency:** The kidneys fail to convert 25-OH Vitamin D into its active form, **1,25-(OH)₂ Vitamin D (Calcitriol)**. This leads to decreased intestinal calcium absorption [1], [5]. The parathyroid glands undergo diffuse hyperplasia to secrete more PTH in an attempt to normalize serum calcium levels [2]. **2. Why the other options are incorrect:** * **A. Parathyroid Adenoma:** This is the most common cause of **Primary** hyperparathyroidism, where the gland autonomously overproduces PTH regardless of calcium levels [1], [4]. * **B. Marked Hypercalcemia:** Secondary hyperparathyroidism is characterized by **low or low-normal calcium** [3]. If calcium becomes high in a patient with long-standing secondary hyperparathyroidism, it suggests progression to **Tertiary hyperparathyroidism** (autonomous secretion) [2]. * **D. Parathyroidectomy:** This is the definitive treatment for Primary or Tertiary hyperparathyroidism [4]. In Secondary hyperparathyroidism, the management focuses on treating the underlying cause (e.g., phosphate binders, Vitamin D analogues, or cinacalcet). **3. High-Yield Clinical Pearls for NEET-PG:** * **Primary Hyperparathyroidism:** High PTH, High Calcium, Low Phosphate [1]. * **Secondary Hyperparathyroidism:** High PTH, **Low/Normal Calcium**, High Phosphate (in CRF) [3]. * **Tertiary Hyperparathyroidism:** Very High PTH, **High Calcium** (seen after long-term CRF or post-renal transplant) [2]. * **Radiological Hallmark:** Subperiosteal bone resorption (most common in the phalanges).

Question 986: Ocular Graves disease is associated with which of the following thyroid states?

A. Hyperthyroidism
B. Hypothyroidism
C. Euthyroid state
D. All of the above (Correct Answer)

Explanation: Graves' Ophthalmopathy (Thyroid-Associated Ophthalmopathy) is an autoimmune inflammatory disorder where antibodies (primarily TSH-receptor antibodies or TRAb) react against antigens in the retro-orbital tissues [1]. This leads to inflammation of extraocular muscles and increased orbital fat [3]. While Graves' ophthalmopathy is most commonly associated with **Hyperthyroidism** (approx. 80-90% of cases), it is an independent autoimmune process. Therefore, the clinical manifestation of eye disease does not always mirror the metabolic state of the thyroid gland: * **Hyperthyroidism:** Most patients have overt thyrotoxicosis at the time of eye symptom onset [3]. * **Euthyroid State:** Known as "Euthyroid Graves' Disease," some patients have significant ocular involvement without any biochemical evidence of thyroid dysfunction [1]. * **Hypothyroidism:** It can occur in patients with primary hypothyroidism (Hashimoto’s thyroiditis) who possess TSH-receptor stimulating antibodies. Options A, B, and C are incorrect only because they are incomplete. Selecting only "Hyperthyroidism" ignores the significant subset of patients who present with ocular symptoms while being euthyroid or hypothyroid. * **Most common cause** of both bilateral and unilateral proptosis in adults is Graves' Disease [3]. * **Smoking** is the strongest modifiable risk factor for the progression of ophthalmopathy. * **Radioactive Iodine (RAI) therapy** can potentially worsen the ophthalmopathy; steroids are often co-administered to prevent this. * **Order of muscle involvement (Mnemonic: I'M SLow):** Inferior rectus > Medial rectus > Superior rectus > Lateral rectus. * **Treatment:** Selenium (mild cases), IV Glucocorticoids (moderate-to-severe), and Orbital decompression (sight-threatening/dysthyroid optic neuropathy) [2].

Question 987: Which of the following drugs does NOT induce diabetes mellitus?

A. Beta blockers (Correct Answer)
B. Protease inhibitors
C. Antipsychotics
D. Thiazide diuretics

Explanation: **Explanation:** The correct answer is **Beta-blockers**. While beta-blockers (especially non-selective ones like Propranolol) are known to cause **dysglycemia** and can mask the symptoms of hypoglycemia, they are generally considered to have a "neutral" or slightly negative effect on glucose metabolism compared to the other options. Crucially, in the context of NEET-PG questions, they are often the "least likely" to *induce* de novo Diabetes Mellitus compared to potent diabetogenic drugs like Thiazides or Protease Inhibitors. *Note: While some studies link older beta-blockers to increased insulin resistance, newer vasodilatory beta-blockers (e.g., Carvedilol, Nebivolol) are metabolic-neutral.* **Why the other options are wrong:** * **Protease Inhibitors (e.g., Ritonavir, Indinavir):** These are notorious for causing **metabolic syndrome**, including lipodystrophy, dyslipidemia, and significant insulin resistance leading to New-Onset Diabetes After Transplantation (NODAT) or HIV-associated diabetes [1]. * **Antipsychotics (Atypical/Second Generation):** Drugs like **Clozapine and Olanzapine** cause profound weight gain and metabolic derangements, directly increasing the risk of Type 2 Diabetes. * **Thiazide Diuretics:** These induce hyperglycemia by causing **hypokalemia**, which inhibits the release of insulin from pancreatic beta cells. **High-Yield Clinical Pearls for NEET-PG:** 1. **Drug-Induced Diabetes Mnemonic (S-P-A-T):** **S**teroids (most common), **P**rotease inhibitors, **A**typical antipsychotics, **T**hiazides. 2. **Steroids:** Increase gluconeogenesis and cause peripheral insulin resistance. 3. **Phenytoin:** Can also cause hyperglycemia by inhibiting insulin release. 4. **Cyclosporine/Tacrolimus:** Common causes of post-transplant diabetes mellitus.

Question 988: All are symptoms of hyperglycemia in a diabetic patient except?

A. Polyuria
B. Weight gain (Correct Answer)
C. Fatigue
D. Recurrent skin infections

Explanation: **Explanation:** In a patient with hyperglycemia, the underlying pathophysiology is either a lack of insulin (Type 1 DM) or insulin resistance (Type 2 DM). This leads to a state of "starvation in the midst of plenty," where glucose is high in the blood but cannot enter the cells [1]. **Why Weight Gain is the Correct Answer:** Hyperglycemia typically leads to **weight loss**, not weight gain [2]. This occurs due to two main reasons: 1. **Osmotic Diuresis:** When blood glucose exceeds the renal threshold (~180 mg/dL), glucose is excreted in the urine (glycosuria), carrying water and calories with it [2]. 2. **Catabolism:** Since cells cannot utilize glucose for energy, the body shifts to breaking down stored fats and muscle proteins (proteolysis and lipolysis) to provide alternative fuel sources [2], [3]. **Analysis of Other Options:** * **Polyuria (Option A):** High blood glucose acts as an osmotic diuretic. As glucose is filtered into the renal tubules, it pulls water with it, leading to increased urine output and subsequent compensatory thirst (polydipsia) [2]. * **Fatigue (Option C):** Despite high circulating glucose, the cells are energy-deprived because glucose cannot be transported intracellularly, leading to profound lethargy [2]. * **Recurrent Skin Infections (Option D):** Hyperglycemia impairs neutrophil function (chemotaxis and phagocytosis) and provides a glucose-rich environment that promotes the growth of pathogens like *Staphylococcus aureus* and *Candida* [2]. **NEET-PG High-Yield Pearls:** * **Polyphagia:** Increased hunger despite eating, caused by the depletion of intracellular energy stores. * **Renal Threshold for Glucose:** 180 mg/dL. * **Blurred Vision:** Hyperglycemia causes osmotic swelling of the lens, altering its refractive index (reversible with glucose control). * **Weight gain** is usually a side effect of **insulin therapy** or certain oral hypoglycemics (Sulfonylureas, TZDs), but not a symptom of hyperglycemia itself.

Question 989: Which of the following is a feature of metabolic syndrome?

A. Hypoinsulinemia
B. High HDL cholesterol
C. Hyperinsulinemia (Correct Answer)
D. Type 1 diabetes mellitus

Explanation: **Explanation:** Metabolic Syndrome (also known as Syndrome X or Insulin Resistance Syndrome) is a cluster of metabolic abnormalities that significantly increase the risk of cardiovascular disease and Type 2 Diabetes Mellitus (T2DM). **Why Hyperinsulinemia is Correct:** The core pathophysiology of metabolic syndrome is **insulin resistance**. In this state, peripheral tissues (muscle, liver, and adipose tissue) do not respond adequately to normal levels of insulin [3]. To compensate and maintain normoglycemia, the pancreas secretes excessive amounts of insulin, leading to **hyperinsulinemia**. This chronic elevation of insulin contributes to other features of the syndrome, such as sodium retention (hypertension) and dyslipidemia. Adipokines like adiponectin and resistin play significant roles in the development of this resistance [4]. **Analysis of Incorrect Options:** * **A. Hypoinsulinemia:** This is a state of insulin deficiency, typically seen in late-stage Type 2 Diabetes or Type 1 Diabetes, and is the opposite of what occurs in metabolic syndrome [2]. * **B. High HDL cholesterol:** Metabolic syndrome is characterized by **low HDL cholesterol** (<40 mg/dL in men, <50 mg/dL in women) and high triglycerides. High HDL is actually a cardioprotective factor. * **C. Type 1 diabetes mellitus:** This is an autoimmune destruction of beta cells leading to absolute insulin deficiency [1]. Metabolic syndrome is specifically associated with obesity and **Type 2 Diabetes Mellitus** [3]. **High-Yield Clinical Pearls (NEET-PG):** * **NCEP ATP III Criteria:** Diagnosis requires at least 3 of the following: 1. **Waist circumference:** >102 cm (M) or >88 cm (F). 2. **Triglycerides:** ≥150 mg/dL. 3. **HDL:** <40 mg/dL (M) or <50 mg/dL (F). 4. **Blood Pressure:** ≥130/85 mmHg. 5. **Fasting Glucose:** ≥100 mg/dL. * **Acanthosis Nigricans** is a classic clinical sign of the underlying insulin resistance. * **Pro-thrombotic and Pro-inflammatory** states (elevated CRP) are also characteristic of this syndrome.

Question 990: MODY 1 is caused by mutations in which of the following genes?

A. HNF-4 alpha (Correct Answer)
B. HNF-1 alpha
C. HNF-1 beta
D. Glucokinase

Explanation: Maturity-Onset Diabetes of the Young (MODY) is a group of monogenic disorders characterized by non-insulin-dependent diabetes occurring typically before age 25, inherited in an autosomal dominant pattern [1]. **Correct Option: A (HNF-4 alpha)** MODY 1 is caused by a mutation in the **Hepatocyte Nuclear Factor-4 alpha (HNF-4α)** gene. This transcription factor is essential for the expression of genes involved in glucose transport and metabolism in pancreatic beta cells. Mutations lead to progressive beta-cell dysfunction and impaired insulin secretion. **Incorrect Options:** * **B. HNF-1 alpha:** This mutation causes **MODY 3**, which is the most common form of MODY worldwide. It is characterized by a low renal threshold for glucose (glycosuria). * **C. HNF-1 beta:** This mutation causes **MODY 5**, which is uniquely associated with renal cysts and genitourinary abnormalities (Renal Cysts and Diabetes Syndrome). * **D. Glucokinase (GCK):** This mutation causes **MODY 2**. It results in a "resetting" of the glucose sensor, leading to mild, stable fasting hyperglycemia that often does not require pharmacological treatment [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common MODY:** MODY 3 (HNF-1α). * **Most Common in Pregnancy:** MODY 2 (GCK). * **Treatment Sensitivity:** Patients with MODY 1 and MODY 3 are exquisitely sensitive to **Sulfonylureas**, which are the first-line treatment, often allowing patients to discontinue insulin. * **Key Diagnostic Clue:** Absence of beta-cell antibodies (GAD, IA-2) and low/normal insulin levels in a young, non-obese patient with a strong family history of diabetes.

Practice by Chapter

Diabetes Mellitus

Practice Questions

Thyroid Disorders

Practice Questions

Adrenal Gland Disorders

Practice Questions

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

Practice Questions

Multiple Endocrine Neoplasia

Practice Questions

Obesity and Metabolic Syndrome

Practice Questions

Neuroendocrine Tumors

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Endocrine Emergencies

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