Internal Medicine
4 questionsWhat is the most common location of gastrinoma?
Which of the following is NOT a feature of Peutz-Jeghers syndrome?
Response to iron therapy in iron deficiency anemia is denoted by?
Thalassemia gives protection against ?
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 111: What is the most common location of gastrinoma?
- A. Pancreas
- B. Duodenum (Correct Answer)
- C. Jejunum
- D. Gall bladder
Explanation: ***Duodenum*** - The **duodenum** is the most common site for gastrinomas, accounting for over **half of all cases**, particularly in sporadic gastrinoma and Zollinger-Ellison syndrome. - These tumors are often **small** and **multiple** in the duodenum, making them challenging to locate. *Pancreas* - Pancreatic gastrinomas are also common, representing approximately **25-40% of cases**, but are less frequent than duodenal gastrinomas. - Pancreatic gastrinomas tend to be **larger** and more amenable to surgical resection when compared to duodenal gastrinomas. *Jejunum* - Gastrinomas found in the jejunum are **rare**, accounting for only a small percentage of cases. - The small intestine distal to the duodenum is an **uncommon site** for primary gastrinoma formation. *Gall bladder* - The **gallbladder** is not a typical location for gastrinoma development. - Gastrinomas are neuroendocrine tumors that arise from **gastrin-producing cells**, which are not found in the gallbladder.
Question 112: 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 113: 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 114: Thalassemia gives protection against ?
- A. Protection against filaria
- B. Protection against kala-azar
- C. Protection against leptospirosis
- D. Protection against malaria (Correct Answer)
Explanation: Protection against malaria - Individuals with thalassemia, particularly thalassemia trait, have some degree of protection against severe forms of malaria, specifically Plasmodium falciparum [1]. - The altered red blood cell structure and reduced hemoglobin content in thalassemia make the red blood cells less hospitable for the parasites, hindering their replication and survival [1]. Protection against filaria - Filaria is caused by parasitic worms (nematodes) transmitted by mosquitoes, leading to lymphatic filariasis (elephantiasis) or onchocerciasis (river blindness). - Thalassemia's primary impact is on red blood cell health and oxygen transport, offering no known protective effect against nematode infections or their associated pathology. Protection against kala-azar - Kala-azar (visceral leishmaniasis) is caused by Leishmania parasites transmitted by sandflies, primarily affecting the reticuloendothelial system (spleen, liver, bone marrow). - There is no established scientific evidence indicating that thalassemia provides protection against Leishmania infections or their clinical manifestations. Protection against leptospirosis - Leptospirosis is a bacterial infection caused by Leptospira bacteria, typically acquired through contact with contaminated water or animal urine. - Thalassemia is a genetic blood disorder; its physiological effects are unrelated to the mechanisms of infection or immunity against bacterial pathogens like Leptospira.
Microbiology
1 questionsPersons with heterozygous sickle cell trait are protected from infection by:
NEET-PG 2013 - Microbiology NEET-PG Practice Questions and MCQs
Question 111: Persons with heterozygous sickle cell trait are protected from infection by:
- A. Pneumococcus
- B. P. falciparum (Correct Answer)
- C. P. vivax
- D. Salmonella
Explanation: ***P. falciparum*** - Individuals with heterozygous sickle cell trait have a **protective effect** against severe malaria caused by *P. falciparum* due to altered red blood cell morphology [1][2]. - The sickle hemoglobin (HbAS) provides a **selective advantage**, reducing the severity of malaria infections and the parasitic load [2][3]. *P. vivax* - Sickle cell trait does not confer significant protection against *P. vivax*, which primarily infects non-sickled red blood cells [2]. - The infection still occurs in individuals with the trait because it specifically affects the reticulocyte count, which is less impacted by sickling. *Salmonella* - While sickle cell disease is linked with increased susceptibility to **Salmonella infections**, the sickle cell trait itself does not provide protection against it [2]. - The trait does not influence immunity or susceptibility to bacterial pathogens like *Salmonella*. *Pneumococcus* - Individuals with sickle cell trait still have a normal risk of **invasive pneumococcal disease**, similar to those without the trait [2]. - Protection against *Pneumococcus* primarily relates to vaccination status and not to hemoglobinopathies. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 398-400. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 50-51.
Pathology
4 questionsCentrilobular necrosis of the liver may be seen with?
Peliosis hepatis is caused by all except?
Gastric carcinoma is associated with all of the following EXCEPT:
Linitis plastica is a type of ?
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 111: Centrilobular necrosis of the liver may be seen with?
- A. Arsenic
- B. Ethanol
- C. CCl4 (Correct Answer)
- D. Phosphorus
Explanation: ***CCl4*** - **Carbon tetrachloride (CCl4)** is the **classic and prototypical** hepatotoxin that causes **centrilobular (zone 3) necrosis**. - The **centrilobular zone (zone 3)** is particularly vulnerable due to its high concentration of **cytochrome P450 enzymes**, which metabolize CCl4 into **toxic free radicals (trichloromethyl radicals)**. - This is the **most characteristic** cause of centrilobular necrosis in toxicology and is the preferred answer for exam purposes. *Ethanol* - **Ethanol** can also cause **centrilobular necrosis** in **alcoholic hepatitis**, as zone 3 is most susceptible to hypoxic injury and oxidative stress. - However, alcoholic liver disease presents with a **spectrum of changes** including steatosis (earliest), hepatitis with ballooning degeneration and Mallory-Denk bodies, and eventual cirrhosis. - While centrilobular necrosis occurs in alcoholic hepatitis, **CCl4 remains the prototype** for pure centrilobular necrosis in exam contexts. *Phosphorus* - **Elemental phosphorus** toxicity causes **periportal (zone 1) necrosis**, which is the opposite pattern from centrilobular necrosis. - It also causes widespread fatty change and hemorrhagic necrosis within the liver. *Arsenic* - **Arsenic poisoning** causes **diffuse/generalized hepatocellular necrosis** and cholestasis, rather than the specific centrilobular pattern. - Chronic exposure is associated with non-cirrhotic portal fibrosis and portal hypertension.
Question 112: Peliosis hepatis is caused by all except?
- A. OC pills
- B. Danazol
- C. Anabolic steroids
- D. Analgesics (Correct Answer)
Explanation: ***Analgesics*** - While various drugs can cause liver injury, **analgesics** are not typically associated with the development of **peliosis hepatis**. [1] - **Peliosis hepatis** involves blood-filled cysts in the liver and is linked to specific agents, not common pain relievers. *Anabolic steroids* - **Anabolic steroids** are a well-known cause of **peliosis hepatis**, especially with prolonged high-dose use. - They can induce sinusoidal dilation and hemorrhage, leading to **blood-filled cysts** in the liver. *OC pills* - **Oral contraceptive pills** (OCPs) containing estrogen have been implicated in the development of **peliosis hepatis**, though it is rare. - The estrogen component is thought to affect the **vascular endothelium** and sinusoidal integrity of the liver. *Danazol* - **Danazol**, an attenuated androgen, is strongly associated with **peliosis hepatis** and other liver complications. - It can cause severe damage to the **hepatic sinusoids**, leading to the characteristic blood-filled cavities. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 847-848.
Question 113: Gastric carcinoma is associated with all of the following EXCEPT:
- A. Over expression of C-met
- B. Inactivation of p53
- C. Over expression of C-erb
- D. Activation of RAS (Correct Answer)
Explanation: ***Activation of RAS*** - **RAS mutations** are relatively uncommon in gastric carcinoma compared to other gastrointestinal malignancies. While KRAS mutations can occur in approximately 10-15% of gastric cancers (particularly intestinal type), they are **far less frequent** than in **pancreatic adenocarcinoma** (~90%) or **colorectal carcinoma** (~40%). - In the context of gastric carcinoma, RAS pathway alterations are **not considered a major oncogenic driver** compared to the other molecular changes listed, making this the **LEAST characteristically associated** alteration. *Inactivation of p53* - **Inactivation of the p53 tumor suppressor gene** is one of the most frequent molecular events in gastric carcinoma, occurring in approximately **50-60% of cases**. - Loss of p53 function leads to genomic instability, uncontrolled cell proliferation, and resistance to apoptosis, contributing significantly to **tumorigenesis** and **poor prognosis**. *Over expression of C-met* - **Overexpression of C-MET**, a receptor tyrosine kinase for hepatocyte growth factor (HGF), is commonly observed in gastric carcinoma (30-40% of cases) and is strongly linked to **tumor growth**, **invasion**, and **metastasis**. - C-MET amplification and overexpression promote cell proliferation, survival, migration, and angiogenesis, making it an important **therapeutic target** in advanced gastric cancer. *Over expression of C-erb* - **Overexpression of C-erbB-2 (HER2/neu)** is found in approximately **10-20% of gastric adenocarcinomas**, particularly the intestinal type. - HER2 amplification or overexpression is a significant **prognostic and predictive biomarker**, and is specifically targeted by **trastuzumab** (Herceptin) therapy in HER2-positive advanced gastric cancer, improving survival outcomes.
Question 114: Linitis plastica is a type of ?
- A. Benign ulcer
- B. GIST
- C. Manifestation of gastric cancer (Correct Answer)
- D. Plastic-like appearance of stomach lining
Explanation: ***Diffuse carcinoma of stomach*** - Linitis plastica is a specific type of **gastric cancer** characterized by **thickening of the stomach wall**, leading to a rigid, non-distensible abdomen [1]. - It often presents with **significant weight loss** and **early satiety**, distinguishing it from other stomach conditions. *Benign ulcer* - Benign ulcers do not cause the **extensive wall thickening** or **desmoplastic response** seen in linitis plastica [1]. - They typically heal with treatment and are associated with typical ulcer symptoms, unlike the progressive nature of linitis plastica. *Plastic like lining of stomach* - While linitis plastica describes a **plastic-like appearance**, it is not classified as a mere lining change but rather a sign of underlying **malignancy** [1]. - This option misrepresents it as a benign condition rather than a serious **stomach adenocarcinoma**. *GIST* - Gastrointestinal stromal tumors (GIST) are **soft tissue tumors** of mesenchymal origin, differing fundamentally from the **invasive** characteristics of linitis plastica [2]. - GISTs typically present with **mass lesions** in the GI tract, not the diffuse rigidity seen in linitis plastica [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 779-780. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 779.
Pharmacology
1 questionsMicrovesicular fatty liver is caused by ?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 111: Microvesicular fatty liver is caused by ?
- A. Valproate (Correct Answer)
- B. Chronic diabetes mellitus (DM)
- C. Prolonged starvation
- D. Chronic inflammatory bowel disease (IBD)
Explanation: ***Valproate*** - **Valproate** is a known cause of **microvesicular steatosis**, particularly in children, due to its interference with mitochondrial fatty acid oxidation. - This can lead to severe liver injury, including **acute liver failure**, as it impairs the liver's ability to metabolize fats. *Chronic diabetes mellitus (DM)* - Chronic DM is commonly associated with **macrovesicular steatosis** (NAFLD), not microvesicular, due to insulin resistance and increased hepatic lipid synthesis. - Unlike microvesicular steatosis, macrovesicular type usually does not immediately impair mitochondrial function. *Prolonged starvation* - Prolonged starvation can lead to **fatty liver**, usually **macrovesicular steatosis**, as the body mobilizes fatty acids from adipose tissue. - While it stresses the liver, it rarely causes the specific **microvesicular** pattern of fat accumulation. *Chronic inflammatory bowel disease (IBD)* - IBD can cause various liver complications, but **microvesicular fatty liver** is not a characteristic feature. - Liver issues in IBD are more often related to **sclerosing cholangitis** or secondary to nutritional deficiencies and medications.