Internal Medicine
5 questionsAutoimmune thyroiditis is associated with all except which of the following?
What is the most common location of gastrinoma?
Which of the following is NOT a feature of Peutz-Jeghers syndrome?
Which of the following statements about Gilbert syndrome is false?
Response to iron therapy in iron deficiency anemia is denoted by?
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 111: Autoimmune thyroiditis is associated with all except which of the following?
- A. DM
- B. Myasthenia gravis
- C. SLE
- D. Psoriasis (Correct Answer)
Explanation: ***Psoriasis*** - Psoriasis is generally not associated with **autoimmune thyroiditis**, which is more commonly linked to other autoimmune disorders [1]. - Autoimmune thyroiditis does not typically result in the **skin changes** seen in psoriasis, distinguishing them clinically. *Sly* - Sly syndrome, while a genetic disorder, is not directly connected to **autoimmune thyroiditis**. - Conditions like Sly syndrome are metabolic and do not involve the autoimmune pathways typically seen in thyroiditis. *Myasthenia gravis* - Myasthenia gravis is an **autoimmune neuromuscular disorder** that can occur concurrently with thyroid diseases, particularly **thyroiditis** [1]. - Both conditions arise from **autoimmune processes**, making their association plausible [1]. *DM* - Diabetes Mellitus (DM), particularly Type 1, is often linked with other autoimmune diseases, including **autoimmune thyroiditis** [2]. - They share a common **autoimmune pathway**, making them more likely to co-occur than psoriasis [2].
Question 112: 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 113: 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 114: 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 115: 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
4 questionsCentrilobular necrosis of the liver may be seen with?
Hurthle cell carcinoma is a variant of which type of carcinoma?
Flexner-Wintersteiner rosette is seen in-
Donath-Landsteiner antibody is seen in?
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: Hurthle cell carcinoma is a variant of which type of carcinoma?
- A. Medullary carcinoma
- B. Papillary carcinoma
- C. Follicular carcinoma (Correct Answer)
- D. Anaplastic carcinoma
Explanation: **Follicular carcinoma** - **Hürthle cell carcinoma**, also known as **oxyphilic follicular carcinoma**, is a specific variant of **follicular carcinoma of the thyroid**. - It is characterized by the presence of large polygonal cells with abundant eosinophilic, granular cytoplasm known as **Hürthle cells** (or oxyphil cells) within the neoplastic growth. *Medullary carcinoma* - **Medullary carcinoma** originates from the **parafollicular C cells** of the thyroid, which produce calcitonin. - It is histologically distinct, featuring nests or cords of cells often associated with **amyloid deposits**, and is not related to Hürthle cell morphology. *Papillary carcinoma* - **Papillary carcinoma** is the most common type of thyroid cancer, characterized by distinctive **nuclear features** such as **Orphan Annie eye nuclei**, nuclear grooves, and intranuclear cytoplasmic inclusions. - Its histological origin and morphological appearance are different from Hürthle cell neoplasms, which are follicular in origin. *Anaplastic carcinoma* - **Anaplastic carcinoma** is a highly aggressive and undifferentiated thyroid malignancy with a very poor prognosis. - It is characterized by pleomorphic, giant, and spindle cells and lacks the specific differentiation seen in follicular or Hürthle cell tumors.
Question 113: Flexner-Wintersteiner rosette is seen in-
- A. Retinoblastoma (Correct Answer)
- B. Hepatoblastoma
- C. Nephroblastoma
- D. Neuroblastoma
Explanation: ***Retinoblastoma*** - Flexner-Wintersteiner rosettes are **characteristic histological features** seen in retinoblastoma, indicating retinal differentiation [1]. - These rosettes reflect the **presence of photoreceptor-like structures**, which are specific to this type of tumor [1]. *Hepatoblastoma* - Histologically, hepatoblastoma shows **primitive epithelial cells** and **mixed patterns**, not Flexner-Wintersteiner rosettes. - It is primarily associated with **liver** and does not present with retinal differentiation. *Nephroblastoma* - Nephroblastoma, or Wilms tumor, typically exhibits **triphasic histology** (epithelial, stromal, and blastemal components) without rosette formation. - It primarily affects the **kidney** and does not involve the retina. *Neuroblastoma* - Neuroblastoma is characterized by **small round blue cells** and **neuroid differentiation** but lacks Flexner-Wintersteiner rosettes. - This tumor usually arises in the **adrenal glands** or sympathetic nervous system, not in retinal tissue. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Eye, p. 1342.
Question 114: 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.
Pharmacology
1 questionsWhich of the following drugs is known to have low first pass metabolism?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 111: Which of the following drugs is known to have low first pass metabolism?
- A. Lidocaine
- B. Propranolol
- C. Theophylline (Correct Answer)
- D. Morphine
Explanation: ***Theophylline*** - **Theophylline** exhibits **low first-pass metabolism**, meaning a significant portion of the orally administered drug reaches systemic circulation unchanged. - This characteristic contributes to its relatively **high bioavailability** when given orally. *Lidocaine* - **Lidocaine** undergoes extensive **first-pass metabolism** in the liver, leading to very low oral bioavailability. - Due to this, it is typically administered **parenterally** (e.g., intravenously or topically) to achieve therapeutic concentrations. *Propranolol* - **Propranolol** is known for its significant **first-pass metabolism**, which results in a much lower bioavailability after oral administration compared to intravenous. - This extensive metabolism necessitates higher oral doses to achieve the same therapeutic effect as parenteral administration. *Morphine* - **Morphine** also undergoes substantial **first-pass metabolism** in the liver, where it is primarily glucuronidated. - This leads to a lower oral bioavailability compared to other routes of administration and contributes to a higher oral dose requirement.