NEET-PG 2015 Practice Questions

Q: Which gene is responsible for the production of COX type 3?

COX I gene. ***COX I gene*** - COX-3 is an **alternatively spliced variant** of the **COX-1 gene** (specifically, a splice variant of the COX-1 mRNA that retains intron 1). - While it was initially thought to be a distinct gene, research has shown that it arises from the same genetic locus as COX-1. *COX 2 gene* - The COX-2 gene encodes for the **inducible cyclooxygenase enzyme**, which is responsible for prostaglandin synthesis during inflammation. - It is a separate gene from COX-1 and has distinct regulatory mechanisms and physiological roles. *COX 3 gene* - There is currently **no distinct gene in humans** specifically identified as "COX-3". - COX-3 refers to a protein isoform derived from the COX-1 gene, not a separate genetic locus. *None of the above* - This option is incorrect because COX-3 is indeed derived from the **COX-1 gene** through alternative splicing. - The existence of COX-3 as a distinct protein product has been demonstrated, although its precise physiological role in humans is still under investigation.

Q: Which of the following is NOT a function of glycosaminoglycans?

Transport of lipids in the bloodstream. ***Transport of lipids in the bloodstream*** - Glycosaminoglycans (GAGs) generally do not play a direct role in the **transport of lipids** in the bloodstream. Lipid transport is primarily mediated by **lipoproteins** (e.g., chylomicrons, VLDL, LDL, HDL). - While some GAGs might interact with lipoproteins in the extracellular matrix, their fundamental role is not lipid transport but rather structural and signaling functions. *Lubrication of joints* - This is a well-established function of GAGs, particularly **hyaluronic acid**, which contributes to the **viscoelastic properties of synovial fluid**, reducing friction in joints. - Hyaluronic acid helps maintain the **hydration** and **shock-absorbing capacity** of articular cartilage. *Wound healing process* - Glycosaminoglycans, especially **hyaluronic acid** and **heparin sulfate**, are crucial in **wound healing** processes, where they modulate inflammation, cell migration, and tissue remodeling. - They provide a **scaffold for cell proliferation** and differentiation in the wound bed. *Anticoagulant activity* - **Heparin**, a highly sulfated glycosaminoglycan, is a potent **anticoagulant** that works by activating **antithrombin III**, thereby inhibiting various coagulation factors like thrombin. - Other GAGs, like **heparan sulfate** found on cell surfaces, also exhibit mild anticoagulant properties.

Q: IPC 201 deals with which of the following?

Embalming a body before an autopsy. ***Embalming a body before an autopsy*** - **IPC (Indian Penal Code) 201** addresses the destruction of evidence or giving false information to screen an offender, specifically focusing on actions that impede justice in criminal investigations. - While not explicitly listing "embalming a body," judicial interpretations and legal precedents recognize that **embalming a body before an autopsy**, when an autopsy is required, would fall under **destruction of evidence** by significantly altering or obliterating crucial forensic clues. *Providing false information to the police* - This act is covered under different sections of the IPC, such as **IPC 182 (False information with intent to cause public servant to use his lawful power to the injury of another person)**, not solely IPC 201. - IPC 201 specifically pertains to actions taken to **screen an offender from legal punishment** by destroying evidence or giving false information, implying a more direct link to a committed offense. *Causing grievous hurt to another person* - This is addressed by **IPC 320 to 326 (Of Hurt)**, which deals with various types of grievous hurt and their punishments. - IPC 201 is related to acts that obstruct justice after a crime, rather than the commission of the crime itself. *Kidnapping a person* - This offense is covered under **IPC 359 to 369 (Of Kidnapping and Abduction)**, detailing different forms of kidnapping and their respective punishments. - Similar to grievous hurt, kidnapping is an original offense, whereas IPC 201 deals with actions taken post-offense to cover up criminal activity.

Q: What does ristocetin testing indicate in von Willebrand disease?

Decreased agglutination. ***Decreased agglutination*** - In von Willebrand disease, **ristocetin induces less agglutination** due to a deficiency or dysfunction of von Willebrand factor. - This results in **impaired platelet adhesion** [1], crucial for effective hemostasis. *Increased agglutination* - Would suggest an increased platelet interaction, which is **not characteristic of von Willebrand disease**. - It can occur in conditions with enhanced von Willebrand factor, unlike in this case. *No agglutination* - Suggests complete lack of platelet interaction, which is **not typical** in von Willebrand disease. - There is often some level of interaction, albeit reduced, not a total absence of agglutination. *Normal agglutination* - Indicates no abnormalities, which **contradicts the known pathology** of von Willebrand disease. - Patients typically demonstrate decreased levels of agglutination, not normal findings in this test.

Q: Which type of artery is most commonly involved in PAN?

Muscular. ***Muscular*** - **Polyarteritis nodosa (PAN)** predominantly affects **medium to small-sized muscular arteries**, leading to inflammation, necrosis, and microaneurysms [1]. - This involvement often causes **organ ischemia** and symptoms related to the affected organs, such as the kidneys, gastrointestinal tract, and skin [1]. *Elastic* - **Elastic arteries**, such as the aorta and its major branches, are typically spared in PAN due to their larger size and distinct histological structure. - Diseases like **Takayasu arteritis** or **Giant cell arteritis** are more commonly associated with vasculitis affecting large elastic arteries. *Arterioles* - While arterioles can be affected in various forms of vasculitis, they are not the primary target in classic PAN. - Involvement of arterioles is more characteristic of **microscopic polyangiitis** or **Churg-Strauss syndrome** [2]. *Capillaries* - **Capillaries** are the smallest blood vessels, and their involvement is rare in PAN. - Conditions like **Henoch-Schönlein purpura** or some drug-induced vasculitides more typically affect capillaries, often resulting in palpable purpura [2].

Q: Where does the oxidation of drugs mainly take place?

Smooth ER. **Smooth ER** - The **smooth endoplasmic reticulum (SER)** is rich in enzymes, particularly the **cytochrome P450 system**, which is primarily responsible for phase I **oxidation reactions** of many drugs and xenobiotics [1]. - These oxidative reactions typically **increase the polarity** of drugs, making them easier to excrete [1]. *Nucleus* - The nucleus primarily contains the cell's **genetic material** (DNA) and is involved in **gene expression** and replication. - It does not contain the necessary enzymatic machinery for the major oxidative metabolism of drugs. *Rough ER* - The **rough endoplasmic reticulum (RER)** is characterized by the presence of **ribosomes** and is mainly involved in the **synthesis, folding, modification, and transport of proteins** destined for secretion or insertion into membranes [2]. - While it plays a role in protein synthesis, it is not the primary site for drug oxidation. *Cytoplasm* - The cytoplasm contains various organelles and is the site of many metabolic pathways, including **glycolysis** and some **phase II drug metabolism** (e.g., glucuronidation, sulfation) [1]. - However, the bulk of phase I **oxidative drug metabolism** does not occur in the general cytoplasm but rather within the smooth ER due to the concentration of relevant enzymes there [1].

Q: What is an atypical side effect of montelukast?

Churg-Strauss syndrome. ***Churg-Strauss syndrome*** - The apparent development of **Churg-Strauss syndrome** (eosinophilic granulomatosis with polyangiitis) has been reported in patients treated with montelukast, although it is believed to be related more to the unmasking of the disease rather than a direct drug effect. - This typically occurs when **corticosteroids** are tapered or withdrawn as montelukast takes over, revealing the underlying vasculitis. *Goodpasture syndrome* - **Goodpasture syndrome** is an autoimmune disease causing rapidly progressive glomerulonephritis and pulmonary hemorrhage, characterized by anti-glomerular basement membrane (GBM) antibodies. - There is no established association between montelukast use and the development of Goodpasture syndrome. *Membranous glomerulonephritis* - **Membranous glomerulonephritis** is a common cause of nephrotic syndrome, characterized by immune complex deposition on the glomerular basement membrane. - This condition is not typically linked to the use of montelukast. *Bronchial asthma* - **Bronchial asthma** is the condition montelukast is used to treat, acting as a leukotriene receptor antagonist to reduce inflammation and bronchoconstriction. - It is a primary indication for the drug, not a side effect.

Q: What is the nature of the relationship between insulin and glucose concentration in the human body?

Sigmoidal. ***Sigmoidal*** - The relationship between insulin and glucose concentration is best described as **sigmoidal**, characterized by a slow initial rise in insulin secretion at low glucose levels, followed by a steep increase at physiological glucose concentrations, and then a plateau at very high glucose levels. - This shape reflects the **beta cell's sensitivity to glucose**, where a minimal threshold of glucose is required to trigger insulin release, and then a maximal release capacity is reached. *Linear* - A **linear relationship** would imply that for every unit increase in glucose, there is a constant, proportional increase in insulin secretion, which is not physiologically accurate. - While insulin secretion does increase with glucose, the rate of increase varies significantly across different glucose concentrations. *Hyperbola* - A **hyperbolic relationship** typically suggests a rapid initial response that then gradually plateaus, often seen in enzyme kinetics. - While there is a plateau in insulin secretion at high glucose levels, the initial phase is not as rapid or proportionally inverse as a hyperbolic function would suggest. *Bell Shaped* - A **bell-shaped curve** describes a relationship where there is an optimal point, and deviations in either direction lead to a decrease in the response (e.g., enzyme activity vs. pH). - This is not characteristic of insulin secretion, as insulin levels generally continue to rise or plateau at higher glucose concentrations and do not decrease beyond an optimal point.

Q: Rebound increase in gastric acid secretion after stopping proton pump inhibitor therapy is due to?

Hypergastrinemia. ***Hypergastrinemia*** - Proton pump inhibitors (PPIs) create a state of **hypochlorhydria** (reduced stomach acid), which in turn stimulates the **G cells** in the stomach to produce more **gastrin**. - This elevated gastrin level leads to a compensatory increase in the number and activity of **parietal cells**, causing a rebound hypersecretion of acid when PPI therapy is discontinued. *Parietal cell hyperplasia* - While parietal cell hyperplasia can occur, it is a consequence of chronic **hypergastrinemia**, not the primary driver of rebound acid secretion. - The direct effect of increased gastrin stimulating existing parietal cells is more immediate and significant for the rebound phenomenon. *Increased histamine release* - Elevated histamine release from **enterochromaffin-like (ECL) cells** is a downstream effect of hypergastrinemia, as gastrin stimulates ECL cells. - While increased histamine contributes to acid secretion, the root cause for its increase in this context is the **hypergastrinemia** induced by PPIs. *Hypersensitivity of Ach receptors* - **Acetylcholine (Ach) receptors** on parietal cells are involved in direct neural stimulation of acid secretion. - There is no evidence that stopping PPIs causes an increased sensitivity of these receptors, or that this is the primary mechanism of rebound acid secretion.

Question 1

Which gene is responsible for the production of COX type 3?

Accepted Answer

COX I gene

Answer

COX 3 gene

Answer

COX 2 gene

Answer

None of the above

Question 2

Which of the following is NOT a function of glycosaminoglycans?

Accepted Answer

Transport of lipids in the bloodstream

Answer

Lubrication of joints

Answer

Wound healing process

Answer

Anticoagulant activity

Question 3

IPC 201 deals with which of the following?

Accepted Answer

Embalming a body before an autopsy

Answer

Providing false information to the police

Answer

Causing grievous hurt to another person

Answer

Kidnapping a person

Question 4

What does ristocetin testing indicate in von Willebrand disease?

Accepted Answer

Decreased agglutination

Answer

Normal agglutination

Answer

Increased agglutination

Answer

No agglutination

Question 5

Which type of artery is most commonly involved in PAN?

Accepted Answer

Muscular

Answer

Capillaries

Answer

Elastic

Answer

Arterioles

Question 6

Which of the following is a chromosomal instability syndrome?

Accepted Answer

Bloom syndrome

Answer

Fanconi anemia

Answer

Ataxia-telangiectasia

Answer

None of the options

Question 7

Where does the oxidation of drugs mainly take place?

Accepted Answer

Smooth ER

Answer

Rough ER

Answer

Cytoplasm

Answer

Nucleus

Question 8

What is an atypical side effect of montelukast?

Accepted Answer

Churg-Strauss syndrome

Answer

Goodpasture syndrome

Answer

Membranous glomerulonephritis

Answer

Bronchial asthma

Question 9

What is the nature of the relationship between insulin and glucose concentration in the human body?

Accepted Answer

Sigmoidal

Answer

Linear

Answer

Hyperbola

Answer

Bell Shaped

Question 10

Rebound increase in gastric acid secretion after stopping proton pump inhibitor therapy is due to?

Accepted Answer

Hypergastrinemia

Answer

Parietal cell hyperplasia

Answer

Increased histamine release

Answer

Hypersensitivity of Ach receptors

NEET-PG 2015

Biochemistry

Forensic Medicine

Pathology

Pharmacology

Physiology