NEET-PG 2012 Practice Questions

Q: Ovarian fossa is formed by all except?

Round ligament of ovary. ***Round ligament of ovary*** - The **round ligament of ovary** (ovarian ligament) connects the ovary to the lateral wall of the uterus and does NOT form any boundary of the ovarian fossa [1]. - It lies medial to the ovary and is not involved in forming the depression of the ovarian fossa [1]. - This ligament anchors the ovary but is separate from the peritoneal boundaries defining the fossa [1]. *Obliterated umbilical artery* - The **obliterated umbilical artery** (medial umbilical ligament) forms the **anterior boundary** of the ovarian fossa [2]. - This is a key anatomical landmark running along the lateral pelvic wall anterior to the ovary [2]. *Internal iliac artery* - The **internal iliac artery** forms the **posterior boundary** of the ovarian fossa [2]. - It lies on the lateral pelvic wall, deep and posterior to the ovarian fossa [2]. - This is one of the main structures defining the fossa's posterior limit [2]. *Ureter* - The **ureter** runs along the lateral pelvic wall and forms part of the **posterior/floor boundary** of the ovarian fossa [2]. - It passes posteroinferior to the ovary, contributing to the fossa's posterior limits [2].

Q: In bladder injury, pain is referred to which of the following areas?

Lower abdominal wall. ***Correct Option: Lower abdominal wall*** - **Referred pain** from the bladder is typically felt in the **suprapubic region** of the lower abdominal wall due to shared visceral and somatic afferent innervation. - The **parietal peritoneum** overlying the bladder is innervated by somatic nerves that also supply the abdominal wall. - This convergence of visceral afferents from the bladder and somatic afferents from the abdominal wall at the spinal cord level (particularly S2-S4) results in referred pain to the suprapubic area. *Incorrect Option: Upper part of thigh* - Pain in the upper thigh is more commonly associated with conditions affecting the **hip joint**, **femoral nerve**, or **inguinal region**. - Bladder innervation does not primarily refer pain to the upper thigh. *Incorrect Option: Flank* - Flank pain is typically associated with conditions of the **kidneys** or **ureters**, such as **nephrolithiasis** or **pyelonephritis**. - The bladder's referred pain pattern does not usually extend to the flank. *Incorrect Option: Penis* - While bladder irritation can sometimes cause sensations in the penis, it is more often associated with conditions like **urethritis**, **cystitis**, or **prostatitis**. - Direct referred pain from bladder injury to the penis is less common than to the lower abdominal wall.

Q: Fluoroacetate inhibits?

Aconitase. ***Aconitase*** - **Fluoroacetate** is metabolically converted to **fluorocitrate**, which is a potent competitive inhibitor of **aconitase**. - **Aconitase** is the enzyme responsible for converting **citrate to isocitrate** in the **Krebs cycle**, and its inhibition blocks the cycle. *Citrate synthase* - This enzyme is responsible for the formation of **citrate** from **acetyl-CoA** and **oxaloacetate**. - While fluoroacetate indirectly affects the cycle, it does not directly inhibit **citrate synthase**. *Succinate dehydrogenase* - This enzyme is part of the **Krebs cycle** and the **electron transport chain**, converting **succinate to fumarate**. - **Malonate** is a competitive inhibitor of succinate dehydrogenase, not **fluoroacetate**. *Alpha-ketoglutarate dehydrogenase* - This enzyme catalyzes the conversion of **alpha-ketoglutarate to succinyl-CoA** in the **Krebs cycle**. - Specific inhibitors of this enzyme include **arsenite** and **mercury compounds**, but not fluoroacetate.

Q: Organ that can utilize glucose, fatty acids and ketone bodies is:

Skeletal muscle. ***Skeletal muscle*** - Skeletal muscle is highly adaptable and can utilize **glucose**, **fatty acids (FAs)**, and **ketone bodies** as fuel sources, especially during prolonged exercise or starvation. - Its metabolic flexibility allows it to switch between these substrates depending on their availability and the body's energy demands. *Liver* - The liver is central to metabolism but primarily **produces ketone bodies** from fatty acids rather than utilizing them as a major fuel source for its own energy needs. - While it uses glucose and FAs, its role in ketone body metabolism is largely synthetic. *Brain* - The brain preferentially uses **glucose** as its primary fuel. - During prolonged starvation, it can adapt to utilize **ketone bodies** as an alternative fuel source, but it does not significantly use fatty acids directly. *RBC* - Red blood cells (RBCs) lack mitochondria and therefore rely exclusively on **anaerobic glycolysis** for energy, metabolizing only **glucose**. - They cannot utilize fatty acids or ketone bodies.

Q: The primary defect which leads to sickle cell anemia is:

Replacement of glutamate by valine in β-chain of HbA. ***Replacement of glutamate by valine in β-chain of HbA*** - The primary defect in sickle cell anemia is a **point mutation** that leads to the replacement of **glutamic acid** with **valine** in the **sixth position** of the β-globin chain [1]. - This mutation causes the hemoglobin (HbS) to polymerize under low oxygen conditions, resulting in the characteristic **sickle-shaped red blood cells** [1]. *A nonsence mutation in the I3-chain of HbA* - A nonsense mutation leads to a **premature stop codon**, which is not the mechanism behind sickle cell anemia. - This mutation does not involve the β-globin chain, which is critical in this specific disorder. *Substitution of valine by glutamate in the a-chain of HbA* - This statement is incorrect as sickle cell anemia specifically involves the **β-chain**, not the **α-chain**. - Substituting valine with glutamate does not cause sickling but rather the opposite of the actual defect observed in this condition. *An abnormality in porphyrin part of hemoglobin* - Sickle cell anemia does not arise from **porphyrin metabolism issues**, which are related to conditions like **porphyrias**. - The primary defect is a change in the amino acid sequence, not in the porphyrin structure of hemoglobin. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599.

Q: Nutmeg liver is associated with which condition?

Right sided heart failure. ***Right sided heart failure*** - **Nutmeg liver** is a classic finding associated with **congestion** in the liver due to **right-sided heart failure**, leading to the characteristic mottled appearance [1][2]. - **Impaired venous return** from the systemic circulation causes hepatic congestion, resulting in **enlargement and fibrosis** of the liver over time [2]. *Left sided heart failure* - Left-sided heart failure primarily affects the **lungs**, leading to pulmonary congestion rather than hepatic changes. - While it can cause secondary effects on the liver over time, it does not directly cause **nutmeg liver**. *Increased pulmonary pressure* - Increased pulmonary pressure is generally associated with conditions like **pulmonary hypertension**, affecting primarily the **lungs** rather than the liver directly. - It does not lead to the **congestive changes** observed in nutmeg liver [1], which is related to right heart function. *Decreased pulmonary pressure* - Decreased pulmonary pressure would typically improve pulmonary blood flow, therefore having no association with liver congestion. - It does not contribute to the **venous stasis** seen in right heart failure, which is pivotal for nutmeg liver. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 126. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 870-872.

Q: Motilin secretion is decreased in which of the following states?

Ingested meal. ***Ingested meal*** - Motilin secretion is **decreased after a meal** due to the presence of food in the small intestine, which stimulates other gastrointestinal hormones and neuronal reflexes that inhibit motilin release. - The primary role of motilin is to stimulate **gastric and intestinal motility** during fasting, clearing residual food and preventing bacterial overgrowth, making its activity counterproductive during digestion. *Thirsty* - **Thirst** is primarily regulated by antidiuretic hormone (ADH) and the renin-angiotensin-aldosterone system, and it does not directly impact motilin secretion. - Motilin's main function is related to gut motility, largely independent of the body's hydration status. *Starving* - Motilin levels tend to be **higher during fasting or starvation**, as it plays a crucial role in initiating the **migrating motor complex (MMC)**, which sweeps undigested material through the gastrointestinal tract. - This activity prevents bacterial overgrowth and prepares the gut for the next meal; thus, its secretion is increased, not decreased. *Interdigestive state* - The **interdigestive state** refers to the period between meals, which is synonymous with a fasting or starving state. - During this period, motilin secretion is **increased** to stimulate the **migrating motor complex (MMC)**, which is essential for gut cleansing.

Q: Which mechanism is primarily responsible for the transport of glucose in renal tubular cells?

Sodium-glucose cotransport. ***Sodium-glucose cotransport*** - Glucose reabsorption in the renal tubules, particularly in the **proximal tubule**, occurs primarily via **secondary active transport** involving **sodium-glucose cotransporters (SGLTs)**. - SGLT proteins use the **sodium concentration gradient** (maintained by the Na+/K+-ATPase on the basolateral membrane) to move glucose against its concentration gradient from the tubular lumen into the cell. *Glucose diffusion* - While passive diffusion may play a minor role, it is insufficient to reabsorb the large amounts of **filtered glucose** - Diffusion would lead to significant **glucose loss in urine**, even at normal blood glucose levels. *Sodium antiport* - Antiport systems move two different ions or molecules in **opposite directions** across a membrane. - While present in renal cells, sodium antiport mechanisms are not the primary means of **glucose reabsorption**; rather, glucose transport is mostly symport. *Facilitated diffusion* - Facilitated diffusion involves carrier proteins (like **GLUT transporters**) that move molecules down their **concentration gradient**. - While GLUT transporters are present on the **basolateral membrane** of tubular cells to move glucose into the interstitium, they are not the primary mechanism for glucose uptake from the tubular lumen, which occurs against a concentration gradient.

Q: Mechanism by which Ach decreases heart rate is by:

Delayed diastolic depolarization. ***Delayed diastolic depolarization*** - Acetylcholine (ACh) binding to muscarinic receptors on nodal cells increases **potassium permeability**, leading to a more negative maximal diastolic potential. - This slows the rate of **spontaneous depolarization** (pacemaker potential), thereby delaying the point at which the threshold for an action potential is reached and reducing heart rate. *Prolongation of action potential duration* - ACh typically **shortens** the action potential duration in atrial and nodal cells by increasing potassium efflux, which hyperpolarizes the cell and hastens repolarization. - A prolonged action potential duration would generally lead to a **slower heart rate** by increasing the refractory period, but this is achieved through different ionic mechanisms and is not the primary mechanism of ACh. *Reduction in calcium influx* - While ACh does reduce the inward **calcium current (ICa)** in nodal cells, contributing to a slower heart rate and weaker contractility, this effect primarily influences the upstroke and peak of the action potential. - The more **fundamentally important mechanism** for heart rate reduction is the impact on the pacemaker potential's slope, which is governed by altered ion conductances, predominantly potassium. *Inhibition of sympathetic activity* - ACh acts directly on **muscarinic receptors** on cardiac cells to decrease heart rate, which is a parasympathetic effect. - It does not directly inhibit sympathetic nerve activity but rather **counteracts sympathetic effects** by directly modulating cardiac cell physiology.

Q: Ptyalin is secreted by?

Salivary gland. ***Salivary gland*** - **Ptyalin**, also known as **salivary amylase**, is an enzyme produced by the salivary glands. - Its primary role is to initiate the **digestion of carbohydrates** (starches) in the mouth. *Gastric gland* - Gastric glands primarily secrete **hydrochloric acid** and **pepsinogen**, involved in protein digestion. - They do not produce ptyalin or enzymes for carbohydrate digestion. *Duodenal gland* - Duodenal glands (Brunner's glands) secrete alkaline mucus to protect the duodenum from acidic chyme. - They are not involved in the production of carbohydrate-digesting enzymes like ptyalin. *Pancreatic gland* - The pancreas produces **pancreatic amylase**, which continues starch digestion in the small intestine. - While it secretes an amylase, it is distinct from salivary amylase (ptyalin) and released into the duodenum, not the mouth.

Question 1

Ovarian fossa is formed by all except?

Accepted Answer

Round ligament of ovary

Answer

Internal iliac artery

Answer

Ureter

Answer

Obliterated umbilical artery

Question 2

In bladder injury, pain is referred to which of the following areas?

Accepted Answer

Lower abdominal wall

Answer

Flank

Answer

Upper part of thigh

Answer

Penis

Question 3

Fluoroacetate inhibits?

Accepted Answer

Aconitase

Answer

Citrate synthase

Answer

Succinate dehydrogenase

Answer

Alpha-ketoglutarate dehydrogenase

Question 4

Organ that can utilize glucose, fatty acids and ketone bodies is:

Accepted Answer

Skeletal muscle

Answer

Liver

Answer

Brain

Answer

RBC

Question 5

The primary defect which leads to sickle cell anemia is:

Accepted Answer

Replacement of glutamate by valine in β-chain of HbA

Answer

An abnormality in porphyrin part of hemoglobin

Answer

A nonsense mutation in the β-chain of HbA

Answer

Substitution of valine by glutamate in the α-chain of HbA

Question 6

Nutmeg liver is associated with which condition?

Accepted Answer

Right sided heart failure

Answer

Increased pulmonary pressure

Answer

Decreased pulmonary pressure

Answer

Left sided heart failure

Question 7

Motilin secretion is decreased in which of the following states?

Accepted Answer

Ingested meal

Answer

Thirsty

Answer

Starving

Answer

Interdigestive state

Question 8

Which mechanism is primarily responsible for the transport of glucose in renal tubular cells?

Accepted Answer

Sodium-glucose cotransport

Answer

Facilitated diffusion

Answer

Glucose diffusion

Answer

Sodium antiport

Question 9

Mechanism by which Ach decreases heart rate is by:

Accepted Answer

Delayed diastolic depolarization

Answer

Prolongation of action potential duration

Answer

Reduction in calcium influx

Answer

Inhibition of sympathetic activity

Question 10

Ptyalin is secreted by?

Accepted Answer

Salivary gland

Answer

Gastric gland

Answer

Duodenal gland

Answer

Pancreatic gland

NEET-PG 2012

Anatomy

Biochemistry

Pathology

Physiology