Internal Medicine
1 questionsWhich of the following is NOT a feature of Peutz-Jeghers syndrome?
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 291: 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.
Microbiology
1 questionsPersons with heterozygous sickle cell trait are protected from infection by:
NEET-PG 2013 - Microbiology NEET-PG Practice Questions and MCQs
Question 291: 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
8 questionsIn which condition are Michaelis Gutmann bodies typically seen?
In which condition are Pseudo-Pelger-Huët cells typically seen?
Which of the following statements is false regarding hereditary spherocytosis?
Intracorpuscular hemolytic anemia is seen in ?
Which of the following statements about sickle cell anemia is false?
Linitis plastica is a type of ?
Gastric carcinoma is associated with all of the following EXCEPT:
In glomerulus subendothelial deposits are seen in?
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 291: In which condition are Michaelis Gutmann bodies typically seen?
- A. Xanthogranulomatous
- B. Pyelonephritis
- C. Malakoplakia (Correct Answer)
- D. Nail patella syndrome
Explanation: ***Malakoplakia*** - **Michaelis-Gutmann bodies** are pathognomonic histological features of malakoplakia, representing calcified concretions containing **iron and calcium** within macrophages. - These are formed around **partially digested bacteria** within defective macrophages, appearing as basophilic inclusions with a "target-like" or "owl's eye" appearance. - Malakoplakia is a chronic granulomatous inflammatory condition most commonly affecting the **urinary tract** (bladder, kidney), but can occur in other organs. *Xanthogranulomatous* - This condition is characterized by an infiltrate of **lipid-laden macrophages** (xanthoma cells, foam cells) and occasional giant cells, but **not** Michaelis-Gutmann bodies. - It most commonly affects the kidney (**xanthogranulomatous pyelonephritis**) and is a destructive inflammatory process with a mass-like appearance. *Pyelonephritis* - Refers to **inflammation of the kidney and renal pelvis**, usually due to bacterial infection (commonly E. coli). - Histologically, it is characterized by acute or chronic inflammatory cells, neutrophil infiltration, and potential abscess formation, **without** Michaelis-Gutmann bodies. *Nail patella syndrome* - This is a **genetic disorder** (autosomal dominant) affecting primarily the **nails, bones** (absent/hypoplastic patella, elbow dysplasia), and sometimes the kidneys (glomerular disease). - It is associated with developmental abnormalities and has **no association** with Michaelis-Gutmann bodies or malakoplakia.
Question 292: In which condition are Pseudo-Pelger-Huët cells typically seen?
- A. Hairy cell leukemia
- B. Multiple myeloma
- C. Hodgkin's lymphoma
- D. Myelodysplastic syndrome (Correct Answer)
Explanation: ***Mylodysplastic syndrome*** - Pseudo-Pelger-Huet cells are characteristic and often observed in myelodysplastic syndromes, indicating an ineffective hematopoiesis [1]. - These cells appear as **hyposegmented neutrophils** and are associated with dysplastic changes in the bone marrow [1]. *Hairy cell leukemia* - Typically presents with **hairy cells** in peripheral blood and often involves splenomegaly; pseudo-Pelger-Huet cells are not usual in this condition. - Associated with **PANCYTOPENIA** and reticulin fibrosis, differing from myelodysplastic syndrome. *Hodgkin's lymphoma* - Characterized by the presence of **Reed-Sternberg cells** and typically involves lymphadenopathy. - Peripheral blood findings generally do not include pseudo-Pelger-Huet cells; the focus is on lymphatic tissue. *Multiple myeloma* - Commonly presents with **plasma cells** and related symptoms like bone pain and renal failure, not associated with pseudo-Pelger-Huet cells. - It primarily causes an increase in monoclonal proteins rather than dysplastic changes seen in myelodysplastic syndrome. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 613-614.
Question 293: 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.
Question 294: Intracorpuscular hemolytic anemia is seen in ?
- A. Thalassemia (Correct Answer)
- B. Infection
- C. Thrombotic thrombocytopenic purpura (TTP)
- D. Autoimmune hemolytic anemia
Explanation: ***Thalassemia*** - Thalassemia is characterized by **intracorpuscular hemolysis** due to defective hemoglobin synthesis, leading to premature destruction of red blood cells [1][2]. - It manifests as **microcytic anemia** with associated **extramedullary erythropoiesis** in severe cases [1]. *Autoimmune hemolytic anemia* - This condition leads to **extravascular hemolysis**, primarily affecting red blood cells in the spleen, not within the plasma [2]. - It is often associated with **positive direct Coombs test**, indicating reactants on the RBC surface. *TIP* - TIP (Thrombotic Microangiopathy) primarily involves **microangiopathic hemolytic anemia** and is not classified as intracorpuscular [2]. - The hemolysis in TIP occurs due to **microthrombi**, causing damage to red blood cells as they pass through narrowed vessels. *Infection* - Infections can lead to **hemolysis**, but this is typically **extravascular** due to splenic clearance or due to other mechanisms like **malaria** [2]. - The hemolytic mechanism is not intracorpuscular, as seen in conditions like thalassemia. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 601-602. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 596-597.
Question 295: 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 296: 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 297: 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 298: In glomerulus subendothelial deposits are seen in?
- A. Goodpasture syndrome (linear IgG deposits in the basement membrane)
- B. MPGN type I (subendothelial deposits) (Correct Answer)
- C. MPGN type II (intramembranous deposits)
- D. IgA nephropathy (mesangial IgA deposits)
Explanation: ***MPGN type I*** - **Subendothelial deposits** are a hallmark of MPGN type I, often associated with **immune complex deposition** [1]. - This condition can present with **hematuria**, **proteinuria**, and can be triggered by infections or autoimmune diseases [1]. *Good pasture syndrome* - Primarily involves **anti-GBM antibodies** leading to **glomerulonephritis** and pulmonary hemorrhage, not subendothelial deposits. - Typically, it presents with **crescent formation** in the glomeruli rather than deposits. *MPGN type II* - Characterized by **dense deposit disease**, it features **intramembranous** rather than subendothelial deposits [1]. - It is often associated with **C3 nephritic factor** and does not show classic subendothelial pathology. *IgA nephropathy* - Characterized by **IgA deposits** primarily in the **mesangium**, not subendothelially. - It presents with **hematuria** and recurrent episodes of **macrohematuria**, especially after infections. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 925-927.