Internal Medicine
3 questionsWhich 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 121: 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 122: 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 123: 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.
Microbiology
1 questionsPersons with heterozygous sickle cell trait are protected from infection by:
NEET-PG 2013 - Microbiology NEET-PG Practice Questions and MCQs
Question 121: 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
5 questionsCentrilobular necrosis of the liver may be seen with?
Peliosis hepatis is caused by all except?
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 121: 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 122: 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 123: 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 124: 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 125: 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.
Pharmacology
1 questionsWhich of the following statements about clonidine is incorrect?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 121: Which of the following statements about clonidine is incorrect?
- A. Alpha 2 receptor agonist
- B. Sudden withdrawal causes rebound hypertension
- C. Controls loose motions due to diabetic neuropathy
- D. First line for AMI (Correct Answer)
Explanation: ***First line for AMI*** - Clonidine is **not first-line** for **Acute Myocardial Infarction (AMI)** as it can cause **bradycardia** and **hypotension**, potentially worsening cardiac output. - First-line AMI treatments include **thrombolytics**, **antiplatelet agents** (aspirin), **beta-blockers**, and **ACE inhibitors** for optimal cardiac protection. *Alpha 2 receptor agonist* - Clonidine is indeed an **alpha-2 adrenergic receptor agonist** that acts centrally in the **medulla oblongata**. - It reduces **sympathetic outflow** from the CNS, leading to decreased **heart rate**, **blood pressure**, and **peripheral vascular resistance**. *Sudden withdrawal causes rebound hypertension* - Abrupt clonidine discontinuation causes dangerous **rebound hypertension** due to sudden loss of **sympathetic inhibition**. - **Gradual tapering** over 1-2 weeks is essential to prevent this potentially life-threatening complication. *Controls loose motions due to diabetic neuropathy* - Clonidine effectively treats **diabetic diarrhea** by stimulating **alpha-2 receptors** in the enteric nervous system. - It **slows intestinal transit** and **enhances fluid absorption**, making it useful for **autonomic neuropathy-related** gastrointestinal symptoms.