NEET-PG 2013 - Internal Medicine Practice Questions

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: Type 3 respiratory failure occurs due to ?

Post-operative atelectasis. ***Post-operative atelectasis*** - **Type 3 respiratory failure**, also known as **perioperative respiratory failure**, is characterized by hypoxemia occurring typically after surgery. - **Atelectasis**, the collapse of lung tissue, is a common cause of hypoxemia in the post-operative period due to shallow breathing, pain, and anesthesia affecting lung volumes. *Kyphoscoliosis* - This condition leads to a **restrictive lung disease** due to chest wall deformity, causing chronic respiratory failure. [1] - It more typically results in **Type 2 respiratory failure** (hypercapnic) due to impaired ventilation over time. [1] *Flail chest* - Flail chest is a severe chest wall injury causing paradoxical movement, leading to **acute respiratory failure**. - It is often associated with **Type 1 (hypoxemic)** or **Type 2 (hypercapnic)** respiratory failure due to trauma-induced lung injury and impaired mechanics. *Pulmonary fibrosis* - This is a progressive interstitial lung disease causing **restrictive ventilatory defect** and impaired gas exchange. - It leads to chronic **Type 1 respiratory failure** (hypoxemic) as the lung tissue becomes stiff and scarred.

Q: Chronic atrophy of adrenal gland will result in which hormone deficiency ?

Cortisol. ***Cortisol*** - **Chronic atrophy of the adrenal gland**, often seen in conditions like **Addison's disease** [1], primarily leads to a deficiency of **glucocorticoids**, the main one being cortisol [2]. - **Cortisol** is produced in the **zona fasciculata** of the adrenal cortex, which is highly susceptible to damage in atrophic conditions [2]. *Aldosterone* - While aldosterone is produced in the adrenal cortex (**zona glomerulosa**), its deficiency is more characteristic of primary adrenal insufficiency affecting the entire cortex, not necessarily solely from 'chronic atrophy' which can have varied pathophysiology [2]. - In some autoimmune forms of adrenal atrophy (Addison's disease), **aldosterone deficiency** can occur, but **cortisol deficiency** is a more universal and defining feature [1][3]. *Dehydroepiandrosterone (DHEA)* - **DHEA** is an adrenal androgen produced in the **zona reticularis** of the adrenal cortex [2]. Its deficiency is also common in adrenal atrophy. - However, **cortisol deficiency** generally has more immediate and life-threatening clinical consequences compared to DHEA deficiency. *Epinephrine* - Epinephrine is produced by the **adrenal medulla**, which is distinct from the adrenal cortex where atrophy typically occurs in conditions causing hormone deficiencies. - Therefore, **adrenal gland atrophy** primarily affecting the cortex would not lead to **epinephrine deficiency** as the medulla usually remains functional.

Q: Which of the following does not synthesize von Willebrand factor?

Hepatocytes. ***Hepatocytes*** - Von Willebrand factor (vWF) is primarily synthesized by **endothelial cells** and **megakaryocytes** [1], not hepatocytes. - Hepatocytes are responsible for synthesizing other proteins like **clotting factors**, but not vWF. *Megakaryoctyes* - Megakaryocytes play a crucial role in the synthesis of **platelet-derived factors**, including von Willebrand factor (vWF) [1]. - They release vWF into the bloodstream, facilitating platelet adhesion, especially in vascular injury sites. *None* - The option implies all listed cell types synthesize vWF, which is incorrect, as **only endothelial cells and megakaryocytes** produce it [1]. - Suggests a misunderstanding of the synthesis of coagulation-related factors, as hepatocytes do not produce vWF. *Endothelial cells* - Endothelial cells are the primary source of **von Willebrand factor** [1], releasing it to assist in platelet aggregation and clotting. - They are essential for the body's response to vascular injury, facilitating hemostasis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 669-670.

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: 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: 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.

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 one of the following is the most common CNS tumor associated with type I neurofibromatosis?

Optic nerve glioma. ***Optic nerve glioma*** - **Optic nerve gliomas** are the most frequently encountered central nervous system tumors in patients with **Type 1 neurofibromatosis (NF1)**, occurring in about 15% of individuals. - They are typically low-grade **astrocytomas** and can cause vision loss and proptosis depending on their size and location. *Meningioma* - While more common in **Type 2 neurofibromatosis (NF2)**, meningiomas can occur in NF1, but are not the most common CNS tumor. - Meningiomas are tumors that arise from the **meninges**, the membranes surrounding the brain and spinal cord. *Acoustic schwannoma* - **Bilateral acoustic schwannomas (vestibular schwannomas)** are the hallmark feature of **Type 2 neurofibromatosis (NF2)**, not NF1 [1]. - These tumors arise from the Schwann cells of the **vestibulocochlear nerve** and can cause hearing loss and balance issues [1]. *Low grade astrocytoma* - While optic nerve gliomas are a type of low-grade astrocytoma, this option is too general; **optic nerve glioma** is the specific and most common presentation in NF1. - Other forms of low-grade astrocytomas can occur in NF1 but are not as universally characteristic as optic nerve gliomas.

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].

Question 1

What is the most common location of gastrinoma?

Accepted Answer

Duodenum

Answer

Pancreas

Answer

Jejunum

Answer

Gall bladder

Question 2

Type 3 respiratory failure occurs due to ?

Accepted Answer

Post-operative atelectasis

Answer

Kyphoscoliosis

Answer

Flail chest

Answer

Pulmonary fibrosis

Question 3

Chronic atrophy of adrenal gland will result in which hormone deficiency ?

Accepted Answer

Cortisol

Answer

Aldosterone

Answer

Dehydroepiandrosterone (DHEA)

Answer

Epinephrine

Question 4

Which of the following does not synthesize von Willebrand factor?

Accepted Answer

Hepatocytes

Answer

Endothelial cells

Answer

Megakaryocytes

Answer

None of the options

Question 5

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

Accepted Answer

Autosomal dominant

Answer

Nerve deafness

Answer

Glomerulonephritis

Answer

X-linked

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

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

Question 8

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 9

Which one of the following is the most common CNS tumor associated with type I neurofibromatosis?

Accepted Answer

Optic nerve glioma

Answer

Meningioma

Answer

Acoustic schwannoma

Answer

Low grade astrocytoma

Question 10

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

NEET-PG 2013 — Internal Medicine