NEET-PG 2012 Practice Questions

Q: Blastocyst makes contact with endometrium on ?

5 - 7 days. ***5-7 days*** - The **blastocyst makes initial contact** (apposition) with the **endometrium** around **day 5-6 after fertilization**. - **Implantation**, which includes adhesion and invasion, typically begins around day 6 and is complete by day 10. - This timeframe allows the blastocyst to travel from the fallopian tube to the uterus and for the uterine lining to be optimally prepared. *< 3 days* - Within the first few days after fertilization, the zygote is still undergoing **cleavage** and development into a **morula**, then a young blastocyst, while traveling down the fallopian tube. - It has not yet reached the uterus or developed sufficiently to interact with the endometrium. *8-11 days* - By 8-11 days, the process of implantation is usually **well underway or completed**, with the blastocyst already invading the endometrial wall. - Initial contact and attachment occur prior to this period. *15-16 days* - This timeframe is well beyond the typical window for initial blastocyst contact and implantation. - By 15-16 days post-fertilization, the embryo would be undergoing **gastrulation** and early organogenesis, assuming successful implantation.

Q: Which is the primary segment of the liver drained by the right hepatic vein?

VII. ***VII*** - The **right hepatic vein** drains the **posterior segment** of the right lobe, which includes segments **VI and VII**. Segment VII is particularly well-drained by this vein. [3] - Understanding hepatic venous drainage is crucial for **surgical planning** and interpreting imaging studies of the liver. [4] *I* - Segment I, the **caudate lobe**, is unique in its venous drainage, often by small veins directly into the **inferior vena cava (IVC)** or occasionally into the left and middle hepatic veins. [1] - It has a separate blood supply and drainage which differentiates it from other segments. [4] *II* - Segment II is part of the **left lateral segment** and is primarily drained by the **left hepatic vein**. - The left hepatic vein typically drains segments II and III. [2] *IV* - Segment IV, or the **quadrate lobe**, is primarily drained by the **middle hepatic vein**. - The middle hepatic vein also drains segment VIII and the anterior aspect of segment V.

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: Major source of energy for brain in fasting/starvation?

Ketone bodies. ***Ketone bodies*** - During **prolonged fasting or starvation**, the body depletes its **glycogen stores** and begins to break down fatty acids. The liver converts these fatty acids into **ketone bodies**, such as **acetoacetate and beta-hydroxybutyrate**. - These **ketone bodies** can cross the **blood-brain barrier** and be used by the brain as an alternative energy source when glucose becomes scarce, preventing protein breakdown for gluconeogenesis. *Glucose* - While **glucose** is the primary and preferred energy source for the brain under normal physiological conditions, its availability significantly decreases during **prolonged fasting or starvation**. - The brain requires a continuous supply of glucose, but in states of severe caloric restriction, the body must conserve glucose for other critical functions and adapt by using alternative fuels. *Glycogen* - **Glycogen** is a stored form of glucose found predominantly in the **liver and muscles**. - The brain itself has minimal **glycogen stores**, which are rapidly depleted during fasting, and thus cannot be a major long-term energy source. *Fatty acids* - **Fatty acids** are a major energy source for many tissues in the body, especially during fasting, but they **cannot directly cross the blood-brain barrier** in significant amounts to fuel the brain. - Instead, **fatty acids** are metabolized into **ketone bodies** in the liver, which then serve as the brain's alternative fuel.

Q: Enzyme deficient in Type I Hyperlipidemia?

Lipoprotein lipase. ***Lipoprotein lipase*** - **Type I hyperlipidemia**, also known as **familial hyperchylomicronemia**, is characterized by a deficiency in **lipoprotein lipase (LPL)**. - LPL is crucial for hydrolyzing triglycerides in **chylomicrons** and **VLDLs** into fatty acids and glycerol, allowing their uptake by tissues. *HMG CoA reductase* - This enzyme is involved in the **rate-limiting step of cholesterol synthesis** in the liver. - While it plays a role in lipid metabolism, its deficiency is not characteristic of **Type I hyperlipidemia**. *Peroxidase* - **Peroxidase** is an enzyme involved in various oxidative reactions, including the breakdown of **hydrogen peroxide**. - It is not directly involved in the metabolism of **chylomicrons** or **triglycerides**, and its deficiency is unrelated to hyperlipidemia. *Cholesterol acyl transferase* - This enzyme, often referring to **lecithin-cholesterol acyltransferase (LCAT)** or **acyl-CoA:cholesterol acyltransferase (ACAT)**, is involved in **cholesterol esterification**. - While important for cholesterol transport and storage, its deficiency is not the primary cause of **Type I hyperlipidemia**, which is marked by severe **chylomicronemia**.

Q: Which of the following complications is commonly associated with mitral valve prolapse?

Infective endocarditis. Mitral valve prolapse (MVP) involves myxomatous degeneration of the mitral valve leaflets, which can create a rough surface predisposing to bacterial adhesion and subsequent infective endocarditis [1]. While the overall risk is low, patients with MVP and accompanying mitral regurgitation or thickened leaflets are at higher risk [1]. Patients with valvular heart disease are generally susceptible to bacterial endocarditis, often associated with procedures or dental hygiene [2]. Stroke - Although MVP can sometimes be associated with embolic events (e.g., from thrombi forming on the prolapsing valve), stroke is not considered a commonly associated complication. - The risk of stroke is generally higher in MVP patients with concomitant atrial fibrillation or other cardiovascular risk factors. Mitral stenosis - Mitral valve prolapse is characterized by the displacement of mitral valve leaflets into the left atrium during systole, which can lead to mitral regurgitation [3], not stenosis. - Mitral stenosis involves narrowing of the mitral valve orifice, usually due to rheumatic fever, which is a different pathophysiology [4]. Ventricular arrhythmia - While palpitations (often benign supraventricular ectopy) are common in MVP, clinically significant ventricular arrhythmias are less common. - Severe ventricular arrhythmias are more typically seen with significant underlying myocardial disease or severe mitral regurgitation causing left ventricular dysfunction.

Q: All of the following provide protection against malaria except which of the following?

PNH. ***PNH*** - Paroxysmal Nocturnal Hemoglobinuria (PNH) does not provide any **protection against malaria**; it is an acquired bone marrow disorder. - While it leads to increased hemolysis and thrombosis, it does not affect **malaria susceptibility** directly. *Duffy blood group* - The Duffy blood group has specific antigens that are a **receptor for Plasmodium vivax**, making individuals with a Duffy-negative phenotype resistant to this type of malaria. - Therefore, Duffy blood group status can indeed serve as a protective factor against certain malaria strains. *Hereditary spherocytosis* - This condition results in **spherical red blood cells** [1], causing hemolytic anemia, but it does not confer protection against malaria. - People with hereditary spherocytosis do not have a lower prevalence of malaria and may still be susceptible to infection. *Sickle cell anemia* - Individuals with sickle cell anemia often exhibit **increased resistance to malaria**, especially against Plasmodium falciparum [2]. - The sickling of red blood cells under low oxygen conditions creates an unfavorable environment for the malarial parasites to thrive [2, 3].

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.

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: Prostaglandins (PGs) in semen are secreted by?

Seminal vesicle. ***Seminal vesicle*** - The **seminal vesicles** are the primary source of **prostaglandins (PGs)** in semen, contributing significantly to the seminal fluid volume. - These PGs play a crucial role in promoting **sperm motility** and facilitating fertilization. *Prostate* - The **prostate gland** primarily secretes **citrate**, **acid phosphatase**, and **prostate-specific antigen (PSA)**, which contribute to sperm activation and semen liquefaction. - It does not significantly contribute to the prostaglandin content of semen. *Sperms* - **Spermatozoa** themselves primarily contribute genetic material and are not a significant source of prostaglandin synthesis in semen. - Their main function is fertilization, not the production of accessory gland secretions. *Testes* - The **testes** are responsible for **spermatogenesis** (sperm production) and the synthesis of **androgens** like testosterone. - They do not secrete prostaglandins into the seminal fluid.

Question 1

Blastocyst makes contact with endometrium on ?

Accepted Answer

5 - 7 days

Answer

< 3 days

Answer

8 - 11 days

Answer

15-16 days

Question 2

Which is the primary segment of the liver drained by the right hepatic vein?

Accepted Answer

VII

Answer

I

Answer

II

Answer

IV

Question 3

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

Accepted Answer

Skeletal muscle

Answer

Liver

Answer

Brain

Answer

RBC

Question 4

Major source of energy for brain in fasting/starvation?

Accepted Answer

Ketone bodies

Answer

Glucose

Answer

Glycogen

Answer

Fatty acids

Question 5

Enzyme deficient in Type I Hyperlipidemia?

Accepted Answer

Lipoprotein lipase

Answer

HMG CoA reductase

Answer

Peroxidase

Answer

Cholesterol acyl transferase

Question 6

Which of the following complications is commonly associated with mitral valve prolapse?

Accepted Answer

Infective endocarditis

Answer

Ventricular arrhythmia

Answer

Stroke

Answer

Mitral stenosis

Question 7

All of the following provide protection against malaria except which of the following?

Accepted Answer

PNH

Answer

Sickle cell anemia

Answer

Hereditary spherocytosis

Answer

Duffy blood group

Question 8

Ptyalin is secreted by?

Accepted Answer

Salivary gland

Answer

Gastric gland

Answer

Duodenal gland

Answer

Pancreatic gland

Question 9

Motilin secretion is decreased in which of the following states?

Accepted Answer

Ingested meal

Answer

Thirsty

Answer

Starving

Answer

Interdigestive state

Question 10

Prostaglandins (PGs) in semen are secreted by?

Accepted Answer

Seminal vesicle

Answer

Prostate

Answer

Sperms

Answer

Testes

NEET-PG 2012

Anatomy

Biochemistry

Internal Medicine

Pathology

Physiology