NEET-PG 2013 - Internal Medicine Practice Questions

Q: Which of the following glands is NOT typically involved in Multiple Endocrine Neoplasia type II A (MEN II A)?

Pituitary gland. ***Pituitary gland*** - The **pituitary gland** is not a characteristic component of **MEN II A**. It is, however, associated with **Multiple Endocrine Neoplasia type I (MEN I)**, which involves the 3 Ps: **pituitary**, **parathyroid**, and **pancreas** [1]. - **MEN IIA** classically involves **medullary thyroid carcinoma**, **pheochromocytoma**, and **parathyroid hyperplasia** [1]. *Thyroid gland* - The **thyroid gland** is centrally involved in MEN IIA, specifically through the development of **medullary thyroid carcinoma (MTC)**, a hallmark feature. - MTC arises from the parafollicular C cells of the thyroid and secretes **calcitonin**. *Parathyroid gland* - The **parathyroid gland** is often involved in MEN IIA, typically presenting as **parathyroid hyperplasia** or adenoma, leading to **primary hyperparathyroidism**. - This typically results in elevated **parathyroid hormone** levels and **hypercalcemia**. *Adrenal gland* - The **adrenal gland** is a key player in MEN IIA due to the occurrence of **pheochromocytoma**, a tumor of the adrenal medulla. - Pheochromocytomas can be bilateral and secrete **catecholamines**, leading to hypertension and other symptoms.

Q: Autoimmune thyroiditis is associated with all except which of the following?

Psoriasis. ***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].

Q: What is the most appropriate initial management for paralysis resulting from organophosphorus poisoning?

Supportive care, including respiratory support. **Supportive care, including respiratory support** * **Paralysis** in organophosphorus poisoning (OPP) is often due to **nicotinic effects** at the neuromuscular junction, leading to respiratory muscle weakness and failure [2]. * **Respiratory support** through mechanical ventilation is crucial to maintain oxygenation and prevent complications while awaiting the effects of antidotal therapy [1], [2]. * *Atropine to counteract muscarinic symptoms* * **Atropine** primarily blocks **muscarinic receptors**, effectively treating symptoms like bradycardia, bronchorrhea, and miosis [2]. * It does **not reverse the nicotinic effects** responsible for muscle paralysis and respiratory failure. * *Oximes to reactivate acetylcholinesterase* * **Oximes (e.g., pralidoxime)** reactivate **acetylcholinesterase**, thereby addressing the underlying cause of acetylcholine accumulation [2]. * They are most effective if given **early** before irreversible aging of the enzyme occurs, but their effect on established paralysis can be limited without concurrent respiratory support [2]. * *No specific antidote* * This statement is incorrect; **atropine** and **oximes** are specific antidotes for organophosphorus poisoning [2]. * While these antidotes are vital, initial management prioritizing **airway and breathing support** is paramount due to the life-threatening respiratory paralysis [1].

Q: What is the most common location of gastrinoma?

Duodenum. ***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.

Q: Which of the following is NOT a feature of Peutz-Jeghers syndrome?

Autosomal recessive inheritance. ***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.

Q: Which of the following statements about Gilbert syndrome is false?

Causes cirrhosis. ***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].

Q: Anemia with reticulocytosis is seen in -

Hemolysis. ***Hemolysis*** - Reticulocytosis indicates a compensatory response to anemia, often occurring in hemolytic processes where the **bone marrow increases red blood cell production** in response to red blood cell destruction. - Conditions like **sickle cell disease** or **autoimmune hemolytic anemia** lead to hemolysis, further confirming increased reticulocyte count. *Iron deficiency anemia* - Typically presents with a **low reticulocyte count** as the bone marrow does not have sufficient iron to produce new red blood cells. - This condition is characterized by **microcytic, hypochromic** red blood cells due to inadequate iron stores. *Vitamin B12 deficiency* - Often results in a **macrocytic anemia** with a variable reticulocyte count; however, reticulocytosis is generally not seen initially. - This deficiency affects DNA synthesis, leading to ineffective erythropoiesis and the presence of **megaloblastic changes**. *Aplastic anemia* - Characterized by a **decrease in all types of blood cells** (pancytopenia) and typically has a **low reticulocyte count** due to bone marrow failure. - There is insufficient production of red blood cells, hence **reticulocytosis is not observed**.

Q: Which of the following statements about Alport's syndrome is incorrect?

Autosomal dominant. ***Autosomal dominant*** - While there are rare autosomal dominant forms, the most common and classic presentation of **Alport's syndrome is X-linked recessive**, affecting males more severely. - This statement is incorrect because it implies that autosomal dominant inheritance is the primary or typical mode, which is not true for the majority of cases. *Nerve deafness* - **Sensorineural hearing loss**, particularly for high frequencies, is a common and characteristic extra-renal manifestation of Alport's syndrome. - This symptom typically progresses with age and is a key diagnostic feature. *Glomerulonephritis* - **Progressive glomerulonephritis** is the hallmark renal feature of Alport's syndrome, leading to hematuria, proteinuria, and eventually end-stage renal disease. - It is caused by mutations in collagen type IV genes, which disrupt the integrity of the glomerular basement membrane. *X-linked* - The majority of Alport's syndrome cases (about 85%) are **X-linked recessive**, caused by mutations in the *COL4A5* gene located on the X chromosome. - This explains why males are more severely affected and typically present with earlier onset and more rapid progression of renal disease.

Q: Thalassemia gives protection against ?

Protection against malaria. 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.

Q: Response to iron therapy in iron deficiency anemia is denoted by?

Reticulocytosis. 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 1

Which of the following glands is NOT typically involved in Multiple Endocrine Neoplasia type II A (MEN II A)?

Accepted Answer

Pituitary gland

Answer

Thyroid gland

Answer

Parathyroid gland

Answer

Adrenal gland

Question 2

Autoimmune thyroiditis is associated with all except which of the following?

Accepted Answer

Psoriasis

Answer

DM

Answer

Myasthenia gravis

Answer

SLE

Question 3

What is the most appropriate initial management for paralysis resulting from organophosphorus poisoning?

Accepted Answer

Supportive care, including respiratory support

Answer

Atropine to counteract muscarinic symptoms

Answer

Oximes to reactivate acetylcholinesterase

Answer

No specific antidote

Question 4

What is the most common location of gastrinoma?

Accepted Answer

Duodenum

Answer

Pancreas

Answer

Jejunum

Answer

Gall bladder

Question 5

Which of the following is NOT a feature of Peutz-Jeghers syndrome?

Accepted Answer

Autosomal recessive inheritance

Answer

Mucocutaneous pigmentation

Answer

Autosomal dominant

Answer

Hamartomatous polyp

Question 6

Which of the following statements about Gilbert syndrome is false?

Accepted Answer

Causes cirrhosis

Answer

Normal liver histology

Answer

Autosomal dominant

Answer

Elevated bilirubin levels are present

Question 7

Anemia with reticulocytosis is seen in -

Accepted Answer

Hemolysis

Answer

Iron deficiency anemia

Answer

Vitamin B12 deficiency

Answer

Aplastic anemia

Question 8

Which of the following statements about Alport's syndrome is incorrect?

Accepted Answer

Autosomal dominant

Answer

Nerve deafness

Answer

Glomerulonephritis

Answer

X-linked

Question 9

Thalassemia gives protection against ?

Accepted Answer

Protection against malaria

Answer

Protection against filaria

Answer

Protection against kala-azar

Answer

Protection against leptospirosis

Question 10

Response to iron therapy in iron deficiency anemia is denoted by?

Accepted Answer

Reticulocytosis

Answer

Increase in hemoglobin

Answer

Restoration of enzymes

Answer

Increase in iron binding capacity

NEET-PG 2013 — Internal Medicine