NEET-PG 2013 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: 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: 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: Linitis plastica is a type of ?

Manifestation of gastric cancer. ***Diffuse carcinoma of stomach*** - Linitis plastica is a specific type of **gastric cancer** characterized by **thickening of the stomach wall**, leading to a rigid, non-distensible abdomen [1]. - It often presents with **significant weight loss** and **early satiety**, distinguishing it from other stomach conditions. *Benign ulcer* - Benign ulcers do not cause the **extensive wall thickening** or **desmoplastic response** seen in linitis plastica [1]. - They typically heal with treatment and are associated with typical ulcer symptoms, unlike the progressive nature of linitis plastica. *Plastic like lining of stomach* - While linitis plastica describes a **plastic-like appearance**, it is not classified as a mere lining change but rather a sign of underlying **malignancy** [1]. - This option misrepresents it as a benign condition rather than a serious **stomach adenocarcinoma**. *GIST* - Gastrointestinal stromal tumors (GIST) are **soft tissue tumors** of mesenchymal origin, differing fundamentally from the **invasive** characteristics of linitis plastica [2]. - GISTs typically present with **mass lesions** in the GI tract, not the diffuse rigidity seen in linitis plastica [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 779-780. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 779.

Q: Centrilobular necrosis of the liver may be seen with?

CCl4. ***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.

Q: When two different chemicals act on two different receptors and their responses are opposite to each other on the same cell, this phenomenon is called?

Physiological antagonism. ***Physiological antagonism*** - This occurs when two drugs act on **different receptors** to produce **opposite physiological effects** within the same system or cell, effectively canceling each other out [1]. - A classic example is the opposing actions of **histamine** (causing bronchoconstriction) and **adrenaline** (causing bronchodilation) on the bronchi [1]. *Chemical antagonism* - This involves a direct **chemical interaction** between two drugs that results in the **inactivation of one or both** of them. - An example is the binding of **chelating agents** to heavy metals, forming an inert complex. *Reversible antagonism* - This describes antagonism where the antagonist binds to the receptor and can be **displaced by a higher concentration of the agonist**. - It does not specifically describe antagonists acting on different receptors or producing opposing physiological effects. *Competitive antagonism* - This occurs when an antagonist directly **competes with an agonist for the same binding site** on a receptor [1]. - The antagonist, while not producing a response itself, prevents the agonist from binding and activating the receptor.

Q: What is the air remaining in the lung after normal expiration?

Functional Residual Capacity (FRC). ***Functional Residual Capacity (FRC)*** - **FRC** represents the volume of air remaining in the lungs after a **normal expiration**. - It is the sum of the **expiratory reserve volume (ERV)** and the **residual volume (RV)**. *Tidal Volume (TV)* - **TV** is the volume of air inspired or expired with a **normal breath**. - It does not represent the total air remaining in the lungs after expiration. *Residual Volume (RV)* - **RV** is the volume of air remaining in the lungs after a **maximal expiration**. - It is a component of FRC but does not fully describe the air remaining after a *normal* expiration. *Vital Capacity (VC)* - **VC** is the maximum volume of air that can be exhaled after a **maximal inspiration**. - It represents the maximum amount of air that can be exchanged with a single breath, not the air remaining after normal expiration.

Q: Maximum voluntary ventilation is:

150 L/min. ***150 L/min*** - The **Maximum Voluntary Ventilation (MVV)** represents the largest volume of air that can be breathed in and out using maximal effort over a 10-15 second period. - While it varies among individuals, a typical average value for a healthy adult is approximately **150-170 L/min**. *25 L/min* - This value is significantly lower than the typical MVV; 25 L/min is closer to a normal **resting minute ventilation** (tidal volume multiplied by respiratory rate). - Resting minute ventilation reflects the volume of air exchanged at rest, not the maximum capacity. *50 L/min* - This value is still considerably lower than the average MVV and does not represent the maximum capacity of the respiratory system. - It might be seen in individuals with **severe pulmonary impairment** or at a very high resting metabolic rate. *100 L/min* - While higher than resting values, 100 L/min is generally below the average maximum voluntary ventilation for a healthy adult. - It could represent a MVV in individuals with **mild to moderate respiratory compromise** or less effort during the test.

Q: When blood pressure falls below 40 mm Hg, which mechanism of regulation is working?

CNS ischemic reflex. ***CNS ischemic reflex*** - The **CNS ischemic reflex** is activated when blood pressure falls below 60 mmHg, with maximal activation below 40 mmHg, indicating severe ischemia in the brain's vasomotor center. - This reflex elicits an intense **sympathetic vasoconstriction** and cardiac stimulation to prioritize blood flow to the brain even at the expense of other organs. *Chemoreceptor response* - The chemoreceptor reflex is primarily activated by a decrease in **arterial pO2**, an increase in **pCO2**, or a decrease in **pH**. - While it can increase blood pressure, it is not the primary or most profound regulatory mechanism specifically triggered by extremely low blood pressure (below 40 mmHg) to prevent brain ischemia. *Baroreceptor response* - **Baroreceptors** are most sensitive to changes in blood pressure within the normal to moderately hypotensive range (e.g., 60-180 mmHg). - At very low pressures (below 40-50 mmHg), baroreceptors become **less sensitive** or "saturated," and their effectiveness in raising blood pressure significantly diminishes. *None of the options* - This option is incorrect because the **CNS ischemic reflex** specifically functions as a powerful, last-ditch mechanism to maintain cerebral blood flow during severe hypotension which is a life saving reflex during conditions like hemorrhage.

Question 1

What is the most common location of gastrinoma?

Accepted Answer

Duodenum

Answer

Pancreas

Answer

Jejunum

Answer

Gall bladder

Question 2

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 3

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 4

Linitis plastica is a type of ?

Accepted Answer

Manifestation of gastric cancer

Answer

Benign ulcer

Answer

GIST

Answer

Plastic-like appearance of stomach lining

Question 5

Centrilobular necrosis of the liver may be seen with?

Accepted Answer

CCl4

Answer

Arsenic

Answer

Ethanol

Answer

Phosphorus

Question 6

When two different chemicals act on two different receptors and their responses are opposite to each other on the same cell, this phenomenon is called?

Accepted Answer

Physiological antagonism

Answer

Chemical antagonism

Answer

Reversible antagonism

Answer

Competitive antagonism

Question 7

Which of the following statements about breathing is incorrect?

Accepted Answer

Normal breathing occurs when transpulmonary pressure is 5-8 cm H2O

Answer

Inspiration is an active process

Answer

Expiration during quiet breathing is passive

Answer

Compliance is influenced by multiple factors including surfactant.

Question 8

What is the air remaining in the lung after normal expiration?

Accepted Answer

Functional Residual Capacity (FRC)

Answer

Tidal Volume (TV)

Answer

Residual Volume (RV)

Answer

Vital Capacity (VC)

Question 9

Maximum voluntary ventilation is:

Accepted Answer

150 L/min

Answer

25 L/min

Answer

50 L/min

Answer

100 L/min

Question 10

When blood pressure falls below 40 mm Hg, which mechanism of regulation is working?

Accepted Answer

CNS ischemic reflex

Answer

Chemoreceptor response

Answer

Baroreceptor response

Answer

None of the options

NEET-PG 2013

Internal Medicine

Pathology

Pharmacology

Physiology