Internal Medicine
4 questionsAutoimmune thyroiditis is associated with all except which of the following?
Which of the following statements about Gilbert syndrome is false?
Which of the following is NOT a feature of Peutz-Jeghers syndrome?
What is the most common location of gastrinoma?
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 101: 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 102: 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 103: 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 104: 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.
Pathology
3 questionsFlexner-Wintersteiner rosette is seen in-
Centrilobular necrosis of the liver may be seen with?
What are Councilman bodies and in which condition are they typically observed?
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 101: 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 102: 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 103: What are Councilman bodies and in which condition are they typically observed?
- A. Wilson's disease
- B. Ballooning degeneration of hepatocytes
- C. Acute viral hepatitis (Correct Answer)
- D. Alcoholic liver disease
Explanation: **Option G*****Acute viral hepatitis*** - Councilman bodies are **characteristic histological findings** in acute viral hepatitis, associated with apoptotic hepatocytes [1]. - They represent **necrosis** of liver cells, which is commonly seen during the acute phase of viral infections affecting the liver [1]. *Alcoholic cirrhosis* - While liver damage is present, Councilman bodies are not typical; they are more associated with acute conditions rather than the chronic nature of cirrhosis. - **Fibrosis** and **bridging necrosis** are evident in alcoholic cirrhosis, distinct from the **acute necrotic changes** seen in viral hepatitis. *Ballooning of cells - Damaged cells show diffuse swelling known as ballooning degeneration.* - Ballooning degeneration indicates **cellular swelling**, often noted in conditions like steatosis or alcoholic liver disease, but does not lead to the formation of Councilman bodies. - These changes are different from the **pyknotic or karyolytic changes** associated with Councilman bodies in acute infections. *Hepatic cell necrosis - The necrosis is usually focal or centirzonal.* - This refers to various types of necrosis in the liver but does not specifically indicate the presence of Councilman bodies, which are linked with apoptotic cells. - While necrosis is common in hepatic pathology, Councilman bodies are particularly associated with **viral hepatitis**. *Wilson's disease* - Although it causes liver damage, it typically results in **copper accumulation** and associated features, not specifically Councilman bodies in its pathology. - The findings in Wilson's disease include **hepatocellular degeneration** without the distinct apoptotic features seen in **acute viral hepatitis**. Option F*Autoimmune hepatitis* - This condition may cause liver cell damage and necrosis but does not typically show Councilman bodies in its histological profile. - It primarily shows **interface hepatitis** and **lymphocytic infiltration**, contrasting with the **apoptotic bodies** seen in acute viral scenarios. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 386-387.
Pharmacology
3 questionsWhich antiglaucomatous drug is known to cause spasm of accommodation?
Besides its properties of decreasing intraocular pressure, timolol is preferred in the treatment of glaucoma because it
Which drug has the highest plasma protein binding?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 101: Which antiglaucomatous drug is known to cause spasm of accommodation?
- A. Timolol
- B. Pilocarpine (Correct Answer)
- C. Dorzolamide
- D. Latanoprost
Explanation: ***Pilocarpine*** - **Pilocarpine** is a **direct-acting muscarinic agonist** that contracts the **ciliary muscle**. - Contraction of the ciliary muscle leads to **accommodation spasm** and a forward movement of the **iris-lens diaphragm**, which also helps to open the **trabecular meshwork**, facilitating aqueous outflow. *Timolol* - **Timolol** is a **beta-blocker** that reduces aqueous humor production by blocking beta-adrenergic receptors on the ciliary epithelium. - It does not directly affect the **ciliary muscle** or cause accommodation spasm. *Dorazolamide* - **Dorzolamide** is a **carbonic anhydrase inhibitor** that reduces aqueous humor production. - Its mechanism of action does not involve the ciliary body's mechanical action and therefore does not cause **accommodation spasm**. *Latanoprost* - **Latanoprost** is a **prostaglandin analog** that increases uveoscleral outflow of aqueous humor. - It does not directly affect the ciliary muscle's contraction or cause **accommodation spasm**.
Question 102: Besides its properties of decreasing intraocular pressure, timolol is preferred in the treatment of glaucoma because it
- A. Is a selective beta-adrenoceptor blocker
- B. Increases outflow of aqueous humor
- C. Produces no miosis (Correct Answer)
- D. Possesses membrane stabilizing activity
Explanation: ***Produces no miosis*** - Timolol, a **non-selective beta-blocker**, decreases intraocular pressure without affecting pupillary size. - This is a **key advantage** in glaucoma treatment as miosis (pupil constriction) can worsen vision, especially in patients with cataracts. - Unlike **miotics** (e.g., pilocarpine), timolol does not cause pupillary constriction, making it better tolerated. *Possesses membrane stabilizing activity* - While some beta-blockers possess **membrane-stabilizing activity** (local anesthetic effect), this property is not a primary reason for timolol's preference in glaucoma. - This action is more relevant in antiarrhythmic uses of beta-blockers due to its effect on cardiac action potentials. *Increases outflow of aqueous humor* - Timolol primarily reduces intraocular pressure by **decreasing the production of aqueous humor**, not by increasing its outflow. - Drugs like **pilocarpine** (a cholinergic agonist) or **prostaglandin analogs** increase outflow. *Is a selective beta-adrenoceptor blocker* - Timolol is a **non-selective beta-blocker**, meaning it blocks both beta-1 and beta-2 adrenergic receptors. - Its non-selectivity is associated with systemic side effects (e.g., bronchospasm, bradycardia), and selective beta-blockers like **betaxolol** exist but are not the primary reason for timolol's preference in glaucoma.
Question 103: Which drug has the highest plasma protein binding?
- A. Warfarin (Correct Answer)
- B. Verapamil
- C. Aspirin
- D. GTN
Explanation: ***Warfarin*** - **Warfarin** exhibits very **high plasma protein binding**, typically greater than 99%, primarily to albumin. - This high binding capacity means that only a small fraction of the drug is free and pharmacologically active. - Due to high protein binding, warfarin is susceptible to drug interactions when displaced from albumin. *Verapamil* - **Verapamil** has a relatively high plasma protein binding, around 90%, but it is not as high as warfarin. - Its binding is predominantly to **albumin** and alpha-1-acid glycoprotein. *Aspirin* - **Aspirin** (acetylsalicylic acid) has moderate plasma protein binding, usually between 50-90%, depending on the dosage. - It binds to **albumin** and can displace other protein-bound drugs. *GTN* - **Glyceryl trinitrate (GTN)** has moderate plasma protein binding, approximately 60%. - Its rapid onset and short duration of action are primarily due to its extensive first-pass metabolism and quick redistribution, rather than protein binding characteristics.