NEET-PG 2013 — Internal Medicine
157 Previous Year Questions with Answers & Explanations
Which of the following statements regarding falciparum malaria is false?
Which condition is primarily associated with tetany?
Which of the following is NOT a recommended primary management option for a patient with a snake bite?
Which of the following is used in the treatment of well-differentiated thyroid carcinoma?
What is the primary vascular abnormality associated with intestinal angiodysplasia?
Classification of aortic dissection depends on.
Migraine is due to
Response to iron therapy in iron deficiency anemia is denoted by?
Which of the following is NOT a feature of Peutz-Jeghers syndrome?
Which of the following statements about Alport's syndrome is incorrect?
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 1: Which of the following statements regarding falciparum malaria is false?
- A. Haemoglobinuria and renal failure
- B. Hypoglycemia
- C. Cerebral malaria
- D. Adequately prevented with chloroquine therapy (Correct Answer)
Explanation: ***Adequately prevented with chloroquine therapy*** - This statement is **false** because many strains of *Plasmodium falciparum* are now **resistant to chloroquine**, making it ineffective for prevention or treatment in most endemic areas [1]. - The widespread **drug resistance** of *P. falciparum* to chloroquine means it is no longer considered an adequate preventative measure. *Haemoglobinuria and renal failure* - These are **true** complications of severe *Falciparum malaria*, often termed **"blackwater fever"**, due to massive **intravascular hemolysis** and subsequent **acute kidney injury** [1]. - Renal failure can result from **hemoglobinuria**, **hypovolemia**, and **acidosis** associated with severe infection. *Hypoglycemia* - **Hypoglycemia** is a **true** and life-threatening complication of severe *Falciparum malaria*, particularly in children, pregnant women, and patients treated with **quinine** [1]. - It occurs due to increased **glucose consumption** by parasites and host cells, impaired **gluconeogenesis**, and drug-induced **insulin secretion**. *Cerebral malaria* - **Cerebral malaria** is a **true**, severe, and often fatal neurological complication of *Falciparum malaria*, characterized by **impaired consciousness** or **coma** [1]. - It is caused by **sequestration** of parasitized red blood cells in the **cerebral microvasculature**, leading to **microcirculatory obstruction** and inflammation.
Question 2: Which condition is primarily associated with tetany?
- A. None of the options
- B. Hyperparathyroidism
- C. Hypercalcemia
- D. Hypocalcemia (Correct Answer)
Explanation: ***Hypocalcemia*** - **Tetany** is a neuromuscular hyperexcitability state resulting from critically low levels of **ionized calcium** in the extracellular fluid [2]. - Reduced extracellular calcium increases neuronal membrane excitability, leading to spontaneous and repetitive nerve discharges and muscle contractions. *Hypercalcemia* - **Hypercalcemia** refers to elevated calcium levels, which *decreases* neuromuscular excitability. - Symptoms typically involve **fatigue, weakness, constipation, and kidney stones**, rather than tetany [1]. *Hyperparathyroidism* - **Primary hyperparathyroidism** is a common cause of **hypercalcemia** due to increased PTH secretion [3]. - Therefore, it leads to symptoms associated with high calcium, not low calcium and tetany. *None of the options* - This option is incorrect because **hypocalcemia** is a well-established cause of tetany.
Question 3: Which of the following is NOT a recommended primary management option for a patient with a snake bite?
- A. Wash with soap and water (Correct Answer)
- B. Reassure the patient
- C. Splinting and immobilization
- D. Keep the site of bite below heart level
Explanation: ***Wash with soap and water*** - Washing the bite with soap and water is **NOT** a recommended primary management option for a snake bite as it can spread the **venom**, potentially worsening the local effects and systemic absorption [1]. - The focus should be on **immobilization and minimizing movement** to restrict venom spread [1], [3]. *Splinting and immobilization* - **Immobilization** of the bitten limb is crucial to reduce venom dissemination through the **lymphatic system** [1], [2]. - This helps to **slow the absorption** of venom into the systemic circulation [1], [3]. *Reassure the patient* - **Anxiety and panic** can increase heart rate and metabolism, potentially accelerating venom absorption. - **Reassurance** helps to calm the patient, which can slow the spread of venom and improve cooperation with treatment [1], [2]. *Keep the site of bite below heart level* - Keeping the affected limb **below heart level** helps to reduce blood flow and, consequently, the systemic spread of venom [1]. - This simple maneuver can **delay the onset** of systemic toxic effects [1].
Question 4: Which of the following is used in the treatment of well-differentiated thyroid carcinoma?
- A. I131 (Correct Answer)
- B. 99m Tc
- C. 32p
- D. MIBG
Explanation: ***I131*** - **Radioactive iodine (I131)** is specifically absorbed by **well-differentiated thyroid cancer cells** because these cells retain the ability to uptake iodine, unlike other types of cancer cells. - Used for **ablating residual thyroid tissue** after surgery and for treating **metastatic well-differentiated thyroid carcinoma** [1]. *99m Tc* - **Technetium-99m (99m Tc)** is primarily used for **diagnostic imaging** (e.g., thyroid scans, bone scans), not for therapeutic treatment of thyroid cancer. - It has a short half-life and emits gamma rays, making it suitable for imaging but generally not for delivering sustained radiation for therapeutic effect. *32p* - **Phosphorus-32 (32p)** is a beta-emitting radionuclide used in the treatment of certain hematological malignancies, such as **polycythemia vera**, and for palliative treatment of bone metastases. - It is not selectively taken up by thyroid cancer cells and therefore is not used in the treatment of thyroid carcinoma. *MIBG* - **Metaiodobenzylguanidine (MIBG)**, often labeled with I123 (diagnostic) or I131 (therapeutic), is used in the diagnosis and treatment of **neuroendocrine tumors** like **pheochromocytoma** and **neuroblastoma**. - Its uptake mechanism targets cells of neuroectodermal origin, which is distinct from the iodine uptake mechanism of thyroid cells.
Question 5: What is the primary vascular abnormality associated with intestinal angiodysplasia?
- A. Arteriovenous malformation (Correct Answer)
- B. Capillary hemangioma (usually superficial)
- C. Malignant tumor
- D. Cavernous hemangioma
Explanation: ***AV malformation*** - **Intestinal angiodysplasia** is characterized by abnormal **arteriovenous (AV) connections**, leading to vascular lesions in the gut [1]. - These malformations can cause **chronic gastrointestinal bleeding** due to fragility of the blood vessels [1]. *Capillary hemangioma* - This is a **benign vascular tumor** often found in the skin or subcutaneous tissue, not specifically associated with intestinal vascular changes. - **Capillary hemangiomas** typically do not cause significant gastrointestinal bleeding as seen in angiodysplasia. *Malignant tumor* - Intestinal angiodysplasia is a **benign condition** and not a malignant tumor, therefore it does not fit the characteristics of malignancy. - **Malignant tumors** usually present with different symptoms and underlying pathophysiology than angiodysplasia. *Cavernous hemangioma* - This type of hemangioma involves larger vascular channels and is typically more associated with the liver than the intestines. - **Cavernous hemangiomas** do not relate to the intestinal bleeding patterns seen in angiodysplasia.
Question 6: Classification of aortic dissection depends on.
- A. Cause of dissection
- B. Level of aorta affected (Correct Answer)
- C. Extent of symptoms
- D. Percentage of aorta affected
Explanation: The classification of aortic dissection is primarily based on the **segment of the aorta involved**, typically divided into Stanford and DeBakey classifications [1]. This classification helps determine **management strategies** and prognosis based on the affected aortic region (ascending or descending) [1]. Understanding the classification is crucial for guiding **treatment decisions** and predicting outcomes [1]. The classification is more concerned with **anatomical location** rather than the etiology, such as hypertension or collagen disorders [1].
Question 7: Migraine is due to
- A. Cortical spreading depression (Correct Answer)
- B. Dilatation of cranial blood vessels
- C. Constriction of cranial blood vessels
- D. Inflammation of the meninges
Explanation: ***Cortical spreading depression*** - The current understanding is that **cortical spreading depression (CSD)** is the initiating event in migraine with aura, characterized by a wave of neuronal and glial depolarization that spreads across the cerebral cortex, leading to a temporary shutdown of neuronal activity [1]. - CSD is thought to activate the **trigeminal nerve**, subsequently causing the release of inflammatory neuropeptides and contributing to the pain phase [1]. *Dilatation of cranial blood vessels* - While **vasodilation of intracranial and extracranial blood vessels** does occur during the headache phase of migraine, it is now considered a *consequence* of the initial neurological events rather than the primary cause [1]. - This vasodilation contributes to the throbbing sensation of migraine pain but does not explain the aura or the initiation of the attack. *Constriction of cranial blood vessels* - **Vasoconstriction** was previously thought to be the cause of the migraine aura, but this theory has largely been disproven. - While some temporary constriction may precede CSD, it is not the primary mechanism behind the migraine attack. *Inflammation of the meninges* - While **neurogenic inflammation** of the meninges, involving the release of inflammatory mediators like **calcitonin gene-related peptide (CGRP)**, does play a role in sensitizing the trigeminal system and contributing to migraine pain, it is a downstream effect. - It is not the initial trigger for a migraine attack but rather part of the pain pathway activated by events like CSD.
Question 8: Response to iron therapy in iron deficiency anemia is denoted by?
- A. Increase in hemoglobin
- B. Reticulocytosis (Correct Answer)
- C. Restoration of enzymes
- D. Increase in iron binding capacity
Explanation: Reticulocytosis - Reticulocytosis is one of the earliest signs of a positive response to iron therapy in iron deficiency anemia, occurring within 5-10 days. - It signifies that the bone marrow is effectively producing new red blood cells after iron supplementation. Restoration of enzymes - While iron is a crucial component of many enzymes (e.g., catalase, cytochrome oxidase), its restoration takes time and is not the primary immediate indicator of therapeutic response. - Clinical improvement and other hematological parameters precede the full restoration of enzyme function. Increase in hemoglobin - An increase in hemoglobin is a definitive sign of successful treatment, but it occurs later than reticulocytosis, typically visible after several weeks to months of therapy. - Hemoglobin levels rise as the new, iron-sufficient red blood cells fully mature and replace the older, iron-deficient ones. Increase in iron binding capacity - In iron deficiency anemia, total iron-binding capacity (TIBC) is typically increased due to more transferrin being available to bind iron [1]. - Successful iron therapy would lead to a decrease in TIBC as transferrin sites become saturated with iron, not an increase.
Question 9: Which of the following is NOT a feature of Peutz-Jeghers syndrome?
- A. Mucocutaneous pigmentation
- B. Autosomal recessive inheritance (Correct Answer)
- C. Autosomal dominant
- D. Hamartomatous polyp
Explanation: ***High risk of malignancy*** - Peutz-Jeghers syndrome is primarily associated with **benign hamartomatous polyps**, not a **high risk of malignancy**, which distinguishes it from other syndromes. - Although patients may develop cancers [1], the syndrome itself does not inherently denote a high malignancy risk like other syndromes such as familial adenomatous polyposis. *Autosomal dominant* - This syndrome is indeed **autosomal dominant**, caused by mutations in the STK11 gene. - Families with this condition typically show **vertical transmission**, characteristic of autosomal dominant inheritance. *Hamartomatous polyp* - Individuals with Peutz-Jeghers syndrome develop **hamartomatous polyps**, which are a hallmark feature of the condition [1]. - These polyps can occur in the gastrointestinal tract and are benign lesions rather than adenomatous type seen in other syndromes [1]. *Mucocutaneous pigmentation* - Mucocutaneous pigmentation, such as **freckling around the lips and buccal mucosa**, is a key clinical feature of Peutz-Jeghers syndrome. - This pigmentation usually appears in childhood and is often a distinguishing sign of the syndrome.
Question 10: Which of the following statements about Alport's syndrome is incorrect?
- A. Nerve deafness
- B. Glomerulonephritis
- C. Autosomal dominant (Correct Answer)
- D. X-linked
Explanation: ***Autosomal dominant*** - While there are rare autosomal dominant forms, the most common and classic presentation of **Alport's syndrome is X-linked recessive**, affecting males more severely. - This statement is incorrect because it implies that autosomal dominant inheritance is the primary or typical mode, which is not true for the majority of cases. *Nerve deafness* - **Sensorineural hearing loss**, particularly for high frequencies, is a common and characteristic extra-renal manifestation of Alport's syndrome. - This symptom typically progresses with age and is a key diagnostic feature. *Glomerulonephritis* - **Progressive glomerulonephritis** is the hallmark renal feature of Alport's syndrome, leading to hematuria, proteinuria, and eventually end-stage renal disease. - It is caused by mutations in collagen type IV genes, which disrupt the integrity of the glomerular basement membrane. *X-linked* - The majority of Alport's syndrome cases (about 85%) are **X-linked recessive**, caused by mutations in the *COL4A5* gene located on the X chromosome. - This explains why males are more severely affected and typically present with earlier onset and more rapid progression of renal disease.