Internal Medicine
3 questionsWhat is the most common location of gastrinoma?
Which of the following statements about Gilbert syndrome is false?
Which of the following is NOT a feature of Peutz-Jeghers syndrome?
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 211: 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.
Question 212: 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 213: 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
2 questionsLinitis plastica is a type of ?
Centrilobular necrosis of the liver may be seen with?
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 211: Linitis plastica is a type of ?
- A. Benign ulcer
- B. GIST
- C. Manifestation of gastric cancer (Correct Answer)
- D. Plastic-like appearance of stomach lining
Explanation: ***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.
Question 212: 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.
Pharmacology
1 questionsWhen two different chemicals act on two different receptors and their responses are opposite to each other on the same cell, this phenomenon is called?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 211: 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?
- A. Physiological antagonism (Correct Answer)
- B. Chemical antagonism
- C. Reversible antagonism
- D. Competitive antagonism
Explanation: ***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.
Physiology
4 questionsWhich of the following statements about breathing is incorrect?
What is the air remaining in the lung after normal expiration?
Maximum voluntary ventilation is:
When blood pressure falls below 40 mm Hg, which mechanism of regulation is working?
NEET-PG 2013 - Physiology NEET-PG Practice Questions and MCQs
Question 211: Which of the following statements about breathing is incorrect?
- A. Inspiration is an active process
- B. Normal breathing occurs when transpulmonary pressure is 5-8 cm H2O (Correct Answer)
- C. Expiration during quiet breathing is passive
- D. Compliance is influenced by multiple factors including surfactant.
Explanation: ***Normal breathing occurs when transpulmonary pressure is 5-8 cm H2O*** - This statement is **incorrect** because it misrepresents transpulmonary pressure during normal breathing. - Normal **transpulmonary pressure** during quiet breathing typically ranges from approximately **3-6 cm H2O** during inspiration, with an average of about **5 cm H2O** at functional residual capacity. - The range "5-8 cm H2O" is too high for normal quiet breathing. While transpulmonary pressure can reach 8 cm H2O during deeper inspiration, stating this as the range for "normal breathing" is inaccurate. - Transpulmonary pressure is the difference between alveolar pressure and pleural pressure (P_L = P_alv - P_pl), which drives lung inflation. *Expiration during quiet breathing is passive* - During quiet breathing, **expiration is a passive process** driven by the **elastic recoil of the lungs** and chest wall. - No active muscular contraction is required for air to leave the lungs during unforced expiration. *Inspiration is an active process* - **Inspiration is an active process** requiring muscular contraction, primarily of the **diaphragm and external intercostal muscles**. - These muscles contract to increase the thoracic volume, which decreases intrapleural and alveolar pressures, drawing air into the lungs. *Compliance is influenced by multiple factors including surfactant* - **Lung compliance**, a measure of the lung's distensibility, is significantly influenced by **surfactant**. - Surfactant reduces **surface tension** in the alveoli, preventing their collapse and increasing compliance.
Question 212: What is the air remaining in the lung after normal expiration?
- A. Tidal Volume (TV)
- B. Residual Volume (RV)
- C. Functional Residual Capacity (FRC) (Correct Answer)
- D. Vital Capacity (VC)
Explanation: ***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.
Question 213: Maximum voluntary ventilation is:
- A. 25 L/min
- B. 50 L/min
- C. 100 L/min
- D. 150 L/min (Correct Answer)
Explanation: ***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.
Question 214: When blood pressure falls below 40 mm Hg, which mechanism of regulation is working?
- A. CNS ischemic reflex (Correct Answer)
- B. Chemoreceptor response
- C. Baroreceptor response
- D. None of the options
Explanation: ***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.