NEET-PG 2020 — Internal Medicine
61 Previous Year Questions with Answers & Explanations
In renal transplant recipients, which is the likely organism causing reactivation disease within 1 to 4 months after surgery?
A patient presents with clustered, white lesions on the buccal mucosa, typically near the upper molars. These lesions are pathognomonic for measles. What are these lesions called?
In multiple sclerosis, where does the defect occur?
A middle-aged male presented with a history of fatigue and tiredness. On investigation, he had a hemoglobin level of 8 g/dL and a mean corpuscular volume (MCV) of 110 fl, with the peripheral smear showing macrocytes and hypersegmented neutrophils. Which of the following is the most likely cause of these findings in this patient?
A 13-year-old child visits the OPD with complaints of not attaining menarche, and has a karyotype of 46,XX. On examination, there is clitoromegaly. Which enzyme is likely deficient?
Most common cause of death in SLE in children
A 42-year-old patient with obstructive jaundice. Alp, Ggt, haptoglobin all increased. The most likely cause is:
MC location of gastrinoma in MEN-1 syndrome?
Which of the following is commonly seen in Pituitary apoplexy?
Esophageal manometry was performed - it revealed panesophageal pressurization with distal contractile integrity as >450mm Hg pressure in the body. What will be the diagnosis?
NEET-PG 2020 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 1: In renal transplant recipients, which is the likely organism causing reactivation disease within 1 to 4 months after surgery?
- A. EBV
- B. CMV (Correct Answer)
- C. HSV
- D. VZV
Explanation: ***CMV*** - **Cytomegalovirus (CMV)** is the most common viral infection causing significant morbidity and mortality in solid organ transplant recipients, often leading to **reactivation disease** within 1 to 4 months post-transplant due to immunosuppression [1]. - CMV disease can manifest in various forms, including **fever**, **leukopenia**, **gastroenteritis**, and potentially organ-specific involvement, mimicking transplant rejection [3]. *EBV* - **Epstein-Barr Virus (EBV)** reactivation is a concern in transplant recipients but is more strongly associated with the development of **post-transplant lymphoproliferative disorder (PTLD)**, which tends to occur later than the 1-4 month window for typical CMV reactivation [1]. - While EBV can cause a mononucleosis-like syndrome, its timeline and common severe complications differ from the typical CMV reactivation pattern [2]. *HSV* - **Herpes Simplex Virus (HSV)** reactivation is typically seen much earlier in transplant recipients, often within the first few weeks (usually 1-2 weeks) post-transplant [1]. - HSV reactivation typically presents as **mucocutaneous lesions** (e.g., cold sores, genital ulcers) rather than systemic disease in the 1-4 month window [3]. *VZV* - **Varicella-Zoster Virus (VZV)** reactivation (shingles) occurs in transplant recipients, but it generally has a slightly later onset than CMV, often beyond 4 months post-transplant or less commonly within the 1-4 month window [1]. - VZV reactivation typically presents as **dermatomal rash** and pain, which is distinct from the systemic symptoms of CMV disease.
Question 2: A patient presents with clustered, white lesions on the buccal mucosa, typically near the upper molars. These lesions are pathognomonic for measles. What are these lesions called?
- A. Leukoplakia
- B. Koplik spots (Correct Answer)
- C. Kaposi spots
- D. None of the options
Explanation: ***Koplik spots*** - These are pathognomonic for **measles (rubeola)** and appear as small, **white or bluish-white lesions** on an erythematous base on the buccal mucosa. - They typically precede the characteristic rash of measles by 1-2 days, making them a crucial early diagnostic sign. *Leukoplakia* - Refers to **thickened, white patches** on the mucous membranes that cannot be scraped off and are often precancerous. - These lesions are usually associated with chronic irritation (e.g., tobacco use) and are not a feature of viral infections like measles. *Kaposi spots* - This term is **not typically used** to describe oral lesions, particularly in the context of measles. - Kaposi sarcoma involves **purple or brown skin lesions** associated with HHV-8 infection, commonly seen in immunocompromised individuals. *None of the options* - This option is incorrect because **Koplik spots** accurately describe the buccal mucosal lesions pathognomonic for measles.
Question 3: In multiple sclerosis, where does the defect occur?
- A. Oligodendrocytes
- B. Myelin sheath (Correct Answer)
- C. Node of Ranvier
- D. Neuroglial cells
Explanation: ***Myelin sheath*** - Multiple sclerosis (MS) is an autoimmune disorder characterized by the destruction of the **myelin sheath** in the central nervous system [3]. - The demyelination of nerve fibers impairs the **conduction of electrical signals**, leading to a wide range of neurological symptoms [3]. *Oligodendrocytes* - **Oligodendrocytes** are the cells responsible for **producing and maintaining the myelin sheath** in the central nervous system [1]. - While oligodendrocytes are directly involved in myelination, the primary defect in MS is the **destruction of the myelin itself**, not primarily a defect in the oligodendrocytes' ability to produce it initially [3]. *Node of Ranvier* - The **nodes of Ranvier** are gaps in the myelin sheath that allow for **saltatory conduction** of nerve impulses [1]. - While damage to the myelin sheath around the nodes can affect their function, the primary defect in MS is the **loss of the insulating myelin material**, not a structural defect in the nodes themselves [2]. *Neuroglial cells* - **Neuroglial cells** (or glial cells) encompass various cell types, including oligodendrocytes, astrocytes, microglia, and ependymal cells, which support neurons [4]. - While glial cells (specifically oligodendrocytes) are involved in myelin production, and other glial cells like microglia can contribute to the inflammatory response in MS, the **direct defect leading to neurological impairment is the destruction of the myelin sheath**, not a general defect in all neuroglial cells [4].
Question 4: A middle-aged male presented with a history of fatigue and tiredness. On investigation, he had a hemoglobin level of 8 g/dL and a mean corpuscular volume (MCV) of 110 fl, with the peripheral smear showing macrocytes and hypersegmented neutrophils. Which of the following is the most likely cause of these findings in this patient?
- A. Chronic alcohol use (Correct Answer)
- B. Ancylostoma duodenale infection
- C. Chronic kidney disease
- D. Colorectal cancer
Explanation: ***Chronic alcoholism*** - **Macrocytic anemia** with a **hemoglobin level of 8 g/dL** is commonly seen in chronic alcoholism due to impaired erythropoiesis and folate deficiency. [1] - The **peripheral smear** showing **hypersegmented neutrophils** is indicative of megaloblastic anemia, often linked to **alcoholism**. [1] *Chronic renal failure* - Typically causes **normocytic anemia** due to inadequate erythropoietin production, not macrocytic anemia. [2] - While uremic effects can impact erythropoiesis, they usually do not produce **hypersegmented neutrophils** found in megaloblastic anemia. *Colon cancer* - More commonly causes **microcytic anemia** due to **iron deficiency** from chronic blood loss rather than macrocytic anemia. [2] - **Macrocytic anemia** with hypersegmented neutrophils would not be expected in most cases of colon cancer. *Ancylostoma duodenale infestation* - This hookworm infection typically leads to **microcytic anemia** due to **iron deficiency**, not macrocytic. [2] - The presence of **macrocytes** and **hypersegmented neutrophils** does not correlate with this type of anemia.
Question 5: A 13-year-old child visits the OPD with complaints of not attaining menarche, and has a karyotype of 46,XX. On examination, there is clitoromegaly. Which enzyme is likely deficient?
- A. 17-alpha hydroxylase
- B. 21-alpha hydroxylase (Correct Answer)
- C. 11-alpha hydroxylase
- D. 3-beta hydroxysteroid dehydrogenase
Explanation: ***21-alpha hydroxylase*** - A deficiency in **21-alpha hydroxylase** leads to **Congenital Adrenal Hyperplasia (CAH)**, shunting precursors towards **androgen production**. - In a 46,XX individual, this results in **virilization** such as **clitoromegaly** and **primary amenorrhea** due to excess androgens suppressing gonadotropin release and ovarian function. *17-alpha hydroxylase* - Deficiency in **17-alpha hydroxylase** in a 46,XX individual would lead to impaired sex steroid synthesis but **excess mineralocorticoids**, causing **hypertension** and **hypokalemia**. - While it causes **primary amenorrhea** due to lack of estrogen, it typically presents with **female external genitalia** that are underdeveloped, not virilized with clitoromegaly. *11-alpha hydroxylase* - There is no known functional enzyme called **11-alpha hydroxylase** in the steroid synthesis pathway. The relevant enzyme is **11-beta hydroxylase**, which, when deficient, leads to **CAH** with virilization and hypertension. - Assuming it refers to 11-beta hydroxylase, deficiency would cause **virilization** in 46,XX females but also lead to **hypertension** due to accumulation of 11-deoxycorticosterone, which is not mentioned in the presentation. *3-beta hydroxysteroid dehydrogenase* - Deficiency of **3-beta hydroxysteroid dehydrogenase** impairs the synthesis of **all classes of adrenal steroids** (glucocorticoids, mineralocorticoids, and sex steroids). - In 46,XX individuals, it leads to **females with ambiguous genitalia** (due to accumulation of DHEA) and **salt wasting**, but typically does not cause overt clitoromegaly and amenorrhea in the manner seen with 21-hydroxylase deficiency.
Question 6: Most common cause of death in SLE in children
- A. Libman sacks endocarditis
- B. Lupus cerebritis
- C. Lupus nephritis
- D. Anemia and infections (Correct Answer)
Explanation: ***Anemia and infections*** - **Infections** are a leading cause of death in pediatric SLE patients, often due to immunosuppression from the disease itself or its treatment. Although pediatric Systemic Lupus Erythematosus (SLE) is not a primary immune deficiency, the susceptibility to encapsulated bacteria and recurrent infections seen in primary B- and T-lymphocyte deficiencies mirrors the infection risks managed in these patients [1]. - **Anemia** can contribute to overall morbidity and mortality, although it is less directly a cause of death than severe infections or organ failure. *Lupus nephritis* - While **lupus nephritis** is a common and severe manifestation of SLE in children and a major cause of morbidity, particularly long-term kidney failure, it is not the most frequent immediate cause of death. - Advancements in treatment for nephritis have improved prognosis, shifting the leading cause of mortality to other factors. *Lupus cerebritis* - **Lupus cerebritis** (neuropsychiatric SLE) can be life-threatening, causing seizures, stroke, or psychosis, but it is less common as the primary cause of death compared to infections. - Its presence usually indicates severe disease requiring intensive treatment, but not the most common direct cause of death. *Libman sacks endocarditis* - **Libman-Sacks endocarditis** involves sterile vegetations on heart valves and is a known complication of SLE, but it rarely causes acute mortality in children. - It is more often associated with chronic complications like valvular dysfunction or a source of emboli rather than being the most common cause of death.
Question 7: A 42-year-old patient with obstructive jaundice. Alp, Ggt, haptoglobin all increased. The most likely cause is:
- A. Alcohol
- B. Lead
- C. Biliary obstruction (Correct Answer)
- D. None of the options
Explanation: ***Alcohol*** - Chronic **alcohol consumption** leads to hepatic injury, causing cholestasis and increased levels of **Alkaline Phosphatase (ALP)** and **Gamma-glutamyl transferase (GGT)** [1, 2]. - Increased **haptoglobin** indicates hemolysis or hepatic dysfunction, commonly seen in alcohol-related liver disease [1]. *Lead* - Lead poisoning typically causes **anemia** and affects **erythropoiesis**, but does not generally increase ALP and GGT levels significantly. - The classic presentation involves **neurological** deficits and **peripheral neuropathy**, rather than obstructive jaundice. *Chronic rf* - Chronic renal failure primarily affects **uremia** and renal function tests, with minimal impact on liver function tests like ALP and GGT. - It is not directly associated with **increased haptoglobin**, which is usually elevated in liver disease. *None of the above* - This option implies that none of the listed causes could lead to the observed lab changes, which is incorrect as **alcohol** is a known cause [1, 2]. - Enhancing liver damage from substances other than alcohol is not applicable based on the information given.
Question 8: MC location of gastrinoma in MEN-1 syndrome?
- A. Jejunum
- B. Ileum
- C. Duodenum
- D. Pancreas (Correct Answer)
Explanation: ***Pancreas*** - In **Multiple Endocrine Neoplasia type 1 (MEN-1) syndrome**, gastrinomas are most commonly found in the **pancreas**. - While sporadic gastrinomas are frequently duodenal, the **genetic predisposition of MEN-1** shifts the primary location to the pancreas. *Duodenum* - **Sporadic gastrinomas** without MEN-1 syndrome are most frequently located in the **duodenum**, particularly the first and second parts. - However, in the context of **MEN-1**, the pancreas becomes the predominant site for gastrinoma development. *Jejunum* - The jejunum is an **uncommon location** for gastrinomas in both sporadic cases and those associated with MEN-1. - Gastrinomas found in the jejunum are typically **rare** and often associated with more aggressive disease or disseminated metastasis. *Ileum* - The ileum is an **extremely rare site** for gastrinomas. - Gastrinomas developing in the ileum are usually **ectopic** and are not typically the primary location in either sporadic cases or MEN-1 syndrome.
Question 9: Which of the following is commonly seen in Pituitary apoplexy?
- A. Headache (Correct Answer)
- B. Hypertension
- C. Hypotension
- D. Vomiting
Explanation: ***Headache*** - **Severe headache** is the most common symptom of pituitary apoplexy, resulting from the sudden expansion of a pituitary mass due to hemorrhage or infarction [1]. - The rapid increase in pressure within the sella turcica, especially on the **dura mater**, causes intense pain. *Hypertension* - While stress can elevate blood pressure, **hypertension** is not a characteristic or direct symptom of acute pituitary apoplexy itself. - Instead, the condition often leads to **adrenal insufficiency**, which is associated with hypotension [1]. *Hypotension* - **Hypotension** is a common and serious manifestation of pituitary apoplexy, often due to acute **adrenal insufficiency** caused by the destruction of ACTH-producing cells [1]. - Reduced ACTH leads to decreased cortisol production, impairing vascular tone and fluid balance. *Vomiting* - **Vomiting** is a common symptom in pituitary apoplexy, often accompanying the severe headache. - It results from the increased **intracranial pressure** and irritation of pathways in the brainstem.
Question 10: Esophageal manometry was performed - it revealed panesophageal pressurization with distal contractile integrity as >450mm Hg pressure in the body. What will be the diagnosis?
- A. Type 2 achalasia
- B. Type 3 achalasia (Correct Answer)
- C. Jackhammer esophagus
- D. Type 1 achalasia (classic achalasia)
Explanation: The diagnosis is Type 3 achalasia. This condition is characterized by panesophageal pressurization, indicating diffuse, simultaneous contractions throughout the esophagus. The high distal contractile integrity (>450 mmHg pressure) further supports Type 3 achalasia, which involves significant spastic contractions. In contrast, while high-resolution manometry allows for the accurate classification of these motility abnormalities [1], other types present differently. Type 1 achalasia (classic achalasia) is marked by failed esophageal peristalsis and absent or minimal esophageal pressurization [1]. The primary characteristic is incomplete or absent lower esophageal sphincter (LES) relaxation, not hypercontractility [1]. Type 2 achalasia is identified by esophageal panesophageal pressurization (simultaneous contractions), but with normal to high contractile pressures, not the extremely high values seen here. Jackhammer esophagus involves hypercontractility (distal contractile integral >8000 mmHg·cm·s) and is characterized by rapid, repetitive, and fragmented contractions, rather than the diffuse panesophageal pressurization and spasticity typical of Type 3 achalasia [2].