NEET-PG 2013

1544 Questions — Page 10 of 155

Internal Medicine

4 questions

Q91

Cryoprecipitate is useful in which of the following conditions?

Q92

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

Q93

Which of the following statements about Gilbert syndrome is false?

Q94

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

NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs

Question 91: Cryoprecipitate is useful in which of the following conditions?

A. Hemophilia A
B. Thrombosthenia
C. Warfarin reversal
D. Afibrinogenemia (Correct Answer)

Explanation: ***Afibrinogenemia*** - Cryoprecipitate is rich in **fibrinogen**, factor VIII, factor XIII, von Willebrand factor, and fibronectin. It is the only blood product with a substantial concentration of fibrinogen. - **Afibrinogenemia** (or hypofibrinogenemia) is a condition characterized by low or absent levels of fibrinogen, a critical clotting factor that cryoprecipitate replaces effectively. *Hemophilia A* - Hemophilia A is a deficiency of **Factor VIII**. While cryoprecipitate contains factor VIII, **recombinant Factor VIII concentrates** are the preferred treatment due to better safety (reduced risk of viral transmission) and more precise dosing [1]. - Cryoprecipitate was historically used for Hemophilia A before the availability of safer, more specific factor concentrates [2]. *Thrombosthenia* - Thrombasthenia is a platelet function disorder characterized by defective **glycoprotein IIb/IIIa receptors** on platelets, leading to impaired platelet aggregation. - Cryoprecipitate does not contain platelets or factors that directly correct platelet function, making **platelet transfusions** the treatment of choice for severe bleeding in thrombasthenia. *Warfarin reversal* - Warfarin reversal is primarily achieved using **Vitamin K**, which restores levels of functional clotting factors II, VII, IX, and X. - For rapid reversal in emergencies, **prothrombin complex concentrate (PCC)** is preferred because it contains high concentrations of these vitamin K-dependent factors, addressing the primary deficiency caused by warfarin [1].

Question 92: 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 93: 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 94: 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.

Pathology

3 questions

Q91

Flexner-Wintersteiner rosette is seen in-

Q92

Centrilobular necrosis of the liver may be seen with?

Q93

What are Councilman bodies and in which condition are they typically observed?

NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs

Question 91: 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 92: 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 93: 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

2 questions

Q91

Which of the following drugs is known to have low first pass metabolism?

Q92

What is the mechanism of metabolism for alcohol, aspirin, and phenytoin at high doses?

NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs

Question 91: 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.

Question 92: What is the mechanism of metabolism for alcohol, aspirin, and phenytoin at high doses?

A. First pass kinetics
B. First order kinetics
C. Zero order kinetics (Correct Answer)
D. Second order kinetics

Explanation: ***Zero order kinetics*** - This mechanism occurs when the **metabolic enzymes become saturated at high drug concentrations**, leading to a constant amount (not a constant percentage) of drug being eliminated per unit time. - Alcohol, aspirin, and phenytoin are examples of drugs that exhibit **saturable metabolism**, transitioning from first-order to zero-order kinetics at higher doses. *First pass kinetics* - This describes the **metabolism of a drug by the liver or gut wall enzymes before it reaches systemic circulation** after oral administration. - While relevant to the oral bioavailability of these drugs, it does not describe the specific mechanism of elimination at high doses. *First order kinetics* - In this mechanism, a **constant fraction or percentage of the drug is eliminated per unit of time**, meaning the rate of elimination is directly proportional to the drug concentration. - Most drugs follow first-order kinetics at therapeutic doses because metabolizing enzymes are not saturated. *Second order kinetics* - This is a **less common pharmacokinetic model** where the rate of elimination is proportional to the square of the drug concentration or involves two reactants. - It does not typically describe the common elimination patterns of most drugs, including alcohol, aspirin, and phenytoin.

Surgery

1 questions

Q91

Which condition typically presents with irregular, hard palpable masses in the breast?