Internal Medicine
5 questionsWhat is the most common location of gastrinoma?
Which of the following statements about Gilbert syndrome is false?
Which of the following is NOT a feature of Peutz-Jeghers syndrome?
Thalassemia gives protection against ?
Response to iron therapy in iron deficiency anemia is denoted by?
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 131: 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 132: Which of the following statements about Gilbert syndrome is false?
- A. Normal liver histology
- B. Autosomal dominant
- C. Elevated bilirubin levels are present
- D. Causes cirrhosis (Correct Answer)
Explanation: ***Causes cirrhosis*** - **Gilbert syndrome** is a benign condition characterized by intermittent unconjugated hyperbilirubinemia and does **not lead to cirrhosis** [1]. - Cirrhosis is a severe form of **liver scarring** resulting from chronic damage, which is not a feature of Gilbert syndrome. *Normal liver histology* - The liver structure and function in individuals with Gilbert syndrome are typically **normal**, distinguishing it from other liver disorders [2]. - Histological examination of liver biopsies usually reveals no abnormalities, reflecting the **benign nature** of the condition. *Autosomal dominant* - Gilbert syndrome is inherited in an **autosomal recessive** pattern, not autosomal dominant [2]. - It results from a reduction in the activity of the **UGT1A1 enzyme**, which is responsible for bilirubin conjugation [1], [2]. *Elevated bilirubin levels are present* - Individuals with Gilbert syndrome experience **intermittent unconjugated hyperbilirubinemia**, meaning their indirect bilirubin levels are elevated [3]. - This elevation is usually mild and can be exacerbated by stress, fasting, or illness, but it is typically **harmless** [1], [2].
Question 133: 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 134: 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.
Question 135: 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.
Pathology
5 questionsLinitis plastica is a type of ?
What are Councilman bodies and in which condition are they typically observed?
Donath-Landsteiner antibody is seen in?
Which of the following statements about sickle cell anemia is false?
Which of the following statements is false regarding hereditary spherocytosis?
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 131: 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.
Question 132: What are Councilman bodies and in which condition are they typically observed?
- A. Wilson's disease
- B. Ballooning degeneration of hepatocytes
- C. Acute viral hepatitis (Correct Answer)
- D. Alcoholic liver disease
Explanation: **Option G*****Acute viral hepatitis*** - Councilman bodies are **characteristic histological findings** in acute viral hepatitis, associated with apoptotic hepatocytes [1]. - They represent **necrosis** of liver cells, which is commonly seen during the acute phase of viral infections affecting the liver [1]. *Alcoholic cirrhosis* - While liver damage is present, Councilman bodies are not typical; they are more associated with acute conditions rather than the chronic nature of cirrhosis. - **Fibrosis** and **bridging necrosis** are evident in alcoholic cirrhosis, distinct from the **acute necrotic changes** seen in viral hepatitis. *Ballooning of cells - Damaged cells show diffuse swelling known as ballooning degeneration.* - Ballooning degeneration indicates **cellular swelling**, often noted in conditions like steatosis or alcoholic liver disease, but does not lead to the formation of Councilman bodies. - These changes are different from the **pyknotic or karyolytic changes** associated with Councilman bodies in acute infections. *Hepatic cell necrosis - The necrosis is usually focal or centirzonal.* - This refers to various types of necrosis in the liver but does not specifically indicate the presence of Councilman bodies, which are linked with apoptotic cells. - While necrosis is common in hepatic pathology, Councilman bodies are particularly associated with **viral hepatitis**. *Wilson's disease* - Although it causes liver damage, it typically results in **copper accumulation** and associated features, not specifically Councilman bodies in its pathology. - The findings in Wilson's disease include **hepatocellular degeneration** without the distinct apoptotic features seen in **acute viral hepatitis**. Option F*Autoimmune hepatitis* - This condition may cause liver cell damage and necrosis but does not typically show Councilman bodies in its histological profile. - It primarily shows **interface hepatitis** and **lymphocytic infiltration**, contrasting with the **apoptotic bodies** seen in acute viral scenarios. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 386-387.
Question 133: Donath-Landsteiner antibody is seen in?
- A. PNH
- B. Waldenstrom's macroglobulinemia
- C. Malaria
- D. Paroxysmal cold hemoglobinuria (Correct Answer)
Explanation: ***Paroxysmal cold hemoglobinuria*** - **Donath-Landsteiner antibody** is a **biphasic IgG autoantibody** that binds to red blood cells in the cold and causes **hemolysis** upon warming, characteristic of paroxysmal cold hemoglobinuria. - This antibody has **anti-P specificity**, meaning it targets the P antigen on red blood cells, leading to complement activation and cell lysis. *PNH* - **Paroxysmal nocturnal hemoglobinuria** (PNH) is characterized by a deficiency in **GPI-anchored proteins** on red blood cells, notably **CD55** and **CD59**, making them susceptible to complement-mediated lysis. - It is not associated with the Donath-Landsteiner antibody; rather, it is identified by **flow cytometry** showing absence of CD55/CD59. *Waldenstrom's macroglobulinemia* - This is a **B-cell lymphoma** characterized by the overproduction of **monoclonal IgM antibodies**, leading to hyperviscosity syndrome and other symptoms. - It does not involve Donath-Landsteiner antibodies or cold-induced hemolysis in the same manner as paroxysmal cold hemoglobinuria. *Malaria* - **Malaria** is caused by **Plasmodium parasites** that infect and destroy red blood cells, leading to hemolytic anemia and fever. - While it causes **hemolysis**, it is not mediated by the Donath-Landsteiner antibody; the destruction is primarily due to parasitic replication and immune responses against infected cells.
Question 134: Which of the following statements about sickle cell anemia is false?
- A. Sickle cells are present in sickle cell anemia.
- B. Target cells are commonly seen in sickle cell anemia.
- C. Ringed sideroblasts are associated with sickle cell anemia. (Correct Answer)
- D. Howell Jolly bodies can be found in sickle cell anemia.
Explanation: ***Ringed sideroblast*** - **Ringed sideroblasts** are not typically associated with sickle cell anemia; they are indicative of disorders like **sideroblastic anemia**. - In sickle cell anemia, the primary findings include **hemolysis** and ineffective erythropoiesis, not ringed sideroblasts [3]. *Howell jolly bodies* - These bodies are remnants of nuclear material and can be found in individuals with **spleen dysfunction**, which can occur in sickle cell anemia [1]. - They are actually a common finding due to **hyposplenism** or **asplenia** in patients with sickle cell disease [2]. *Sickle cells* - The presence of **sickle-shaped red blood cells** is a hallmark of sickle cell anemia, caused by the mutation in the **beta-globin chain** [3]. - These sickle cells are responsible for the characteristic complications of the disease, such as **vaso-occlusive crises** [1][3]. *Target cells* - Target cells, or **codocytes**, are often seen in disorders like **thalassemia** and liver disease, and can also be present in sickle cell anemia. - They are formed due to an increase in the **surface area to volume ratio** of red blood cells, often secondary to **membrane abnormalities** seen in sickle cell changes [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 644-646. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 570-571. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599.
Question 135: Which of the following statements is false regarding hereditary spherocytosis?
- A. Defect in ankyrin
- B. Reticulocytosis
- C. Decreased MCHC (Correct Answer)
- D. Normal to increased MCV
Explanation: ***Decreased MCHC*** - Hereditary spherocytosis typically presents with an **increased MCHC** due to the spherocytes being more concentrated. - MCHC is a measure of the hemoglobin concentration in red blood cells, and in spherocytosis, this value is often elevated rather than decreased. *Defect in ankyrin* - This is a true statement; hereditary spherocytosis is associated with a defect in **ankyrin**, a protein that helps maintain the cell's membrane structure [2]. - Mutations in ankyrin lead to instability of the red blood cell membrane, resulting in spherocyte formation [2]. *Decreased MCV* - In hereditary spherocytosis, MCV is often **normal or slightly increased**, as it reflects the volume of red blood cells, which can be misinterpreted due to the presence of spherocytes. - Spherocytes are smaller cells, which can mistakenly suggest a falsely decreased MCV if not properly interpreted [1]. *Reticulocytosis* - This condition typically presents with **reticulocytosis** as a response to hemolysis, indicating the bone marrow is producing more red blood cells to compensate [1]. - The presence of reticulocytosis is a common finding in hereditary spherocytosis due to increased destruction of spherocytes. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-598. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 640-641.