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?
Classification of aortic dissection depends on.
What is the primary vascular abnormality associated with intestinal angiodysplasia?
Migraine is due to
Chronic atrophy of adrenal gland will result in which hormone deficiency ?
Cerebellar damage causes all of the following except?
Which of the following does not synthesize von Willebrand factor?
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: 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 6: 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 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: Chronic atrophy of adrenal gland will result in which hormone deficiency ?
- A. Aldosterone
- B. Dehydroepiandrosterone (DHEA)
- C. Epinephrine
- D. Cortisol (Correct Answer)
Explanation: ***Cortisol*** - **Chronic atrophy of the adrenal gland**, often seen in conditions like **Addison's disease** [1], primarily leads to a deficiency of **glucocorticoids**, the main one being cortisol [2]. - **Cortisol** is produced in the **zona fasciculata** of the adrenal cortex, which is highly susceptible to damage in atrophic conditions [2]. *Aldosterone* - While aldosterone is produced in the adrenal cortex (**zona glomerulosa**), its deficiency is more characteristic of primary adrenal insufficiency affecting the entire cortex, not necessarily solely from 'chronic atrophy' which can have varied pathophysiology [2]. - In some autoimmune forms of adrenal atrophy (Addison's disease), **aldosterone deficiency** can occur, but **cortisol deficiency** is a more universal and defining feature [1][3]. *Dehydroepiandrosterone (DHEA)* - **DHEA** is an adrenal androgen produced in the **zona reticularis** of the adrenal cortex [2]. Its deficiency is also common in adrenal atrophy. - However, **cortisol deficiency** generally has more immediate and life-threatening clinical consequences compared to DHEA deficiency. *Epinephrine* - Epinephrine is produced by the **adrenal medulla**, which is distinct from the adrenal cortex where atrophy typically occurs in conditions causing hormone deficiencies. - Therefore, **adrenal gland atrophy** primarily affecting the cortex would not lead to **epinephrine deficiency** as the medulla usually remains functional.
Question 9: Cerebellar damage causes all of the following except?
- A. Ataxia
- B. Past-pointing
- C. Dysmetria
- D. Hypertonia (Correct Answer)
Explanation: ***Hypertonia*** - Cerebellar lesions typically lead to **hypotonia**, a decrease in muscle tone, rather than hypertonia [1]. - Hypertonia, or increased muscle tone, is more commonly associated with lesions of the **upper motor neurons** or **basal ganglia** [2]. *Dysmetria* - **Dysmetria** is a common sign of cerebellar damage, characterized by an inability to accurately control the **range, direction, and force** of muscle movements [1]. - This leads to overshooting or undershooting a target during voluntary movements. *Ataxia* - **Ataxia**, particularly truncal or appendicular ataxia, is a cardinal symptom of cerebellar dysfunction [3]. - It refers to a lack of **voluntary coordination** of muscle movements, leading to an unsteady gait and impaired balance [3]. *Past-pointing* - **Past-pointing** is a form of dysmetria where a patient consistently points or reaches **beyond their target** [1]. - It is a specific sign that indicates a deficit in the cerebellum's ability to modulate and refine motor commands.
Question 10: Which of the following does not synthesize von Willebrand factor?
- A. Endothelial cells
- B. Hepatocytes (Correct Answer)
- C. Megakaryocytes
- D. None of the options
Explanation: ***Hepatocytes*** - Von Willebrand factor (vWF) is primarily synthesized by **endothelial cells** and **megakaryocytes** [1], not hepatocytes. - Hepatocytes are responsible for synthesizing other proteins like **clotting factors**, but not vWF. *Megakaryoctyes* - Megakaryocytes play a crucial role in the synthesis of **platelet-derived factors**, including von Willebrand factor (vWF) [1]. - They release vWF into the bloodstream, facilitating platelet adhesion, especially in vascular injury sites. *None* - The option implies all listed cell types synthesize vWF, which is incorrect, as **only endothelial cells and megakaryocytes** produce it [1]. - Suggests a misunderstanding of the synthesis of coagulation-related factors, as hepatocytes do not produce vWF. *Endothelial cells* - Endothelial cells are the primary source of **von Willebrand factor** [1], releasing it to assist in platelet aggregation and clotting. - They are essential for the body's response to vascular injury, facilitating hemostasis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 669-670.