NEET-PG 2015 Practice Questions

Q: What is the ionized calcium (IC) content of Ringer's lactate in mmol/L, and why is it clinically significant?

4 mmol/L. ***4 mmol/L*** - Ringer's lactate contains **calcium chloride**, contributing to its ionized calcium content of **4 mmol/L**. - This calcium is a critical component for **blood clotting** and **cardiac function**, making it clinically significant, particularly in large volume resuscitation. *130 mmol/L* - This value is close to the **sodium content** of Ringer's lactate, not its ionized calcium. - Sodium is the primary determinant of **fluid balance** and **osmolarity**, distinct from calcium's roles. *109 mmol/L* - This value approximates the **chloride content** of Ringer's lactate, which is important for acid-base balance but not its ionized calcium. - Chloride's primary role is in maintaining **electrical neutrality** and fluid distribution. *0 mmol/L* - Ringer's lactate is a **balanced electrolyte solution** and definitely contains calcium. - A value of 0 would indicate the absence of calcium, which would contradict its formulation and clinical utility, especially in scenarios requiring **electrolyte repletion**.

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 Section 191 of the Indian Penal Code (IPC) pertain to?

Giving false evidence. ***Giving false evidence*** - Section 191 of the Indian Penal Code **specifically defines the offence of giving false evidence** - It addresses situations where a person, under oath or express provision of law to state the truth, makes a statement that is false and which he/she either **knows or believes to be false**, or does not believe to be true - This section is fundamental to **maintaining the integrity of legal proceedings** and protecting against perjury *Medical negligence* - Medical negligence is typically covered under **other sections of the IPC**, such as Section 304A (causing death by negligence) or Section 338 (causing grievous hurt by act endangering life or personal safety of others) - It may also be addressed under **civil law provisions** or the Consumer Protection Act - It involves a breach of duty by a medical professional that causes harm to a patient *Hostile witness* - The concept of a hostile witness is related to **evidentiary rules in criminal procedure**, particularly under the Indian Evidence Act, 1872 - **Not defined or addressed by any specific section in the IPC** - A hostile witness is one who does not support the party that called them to testify, often contradicting their own prior statements *Assault punishment* - The punishment for assault is covered under **Sections 351 to 358 of the IPC** - These sections define what constitutes assault and criminal force, along with penalties for different degrees of such offenses - Section 191 has no connection to assault-related provisions

Q: What is the mechanism of action of ticagrelor?

Reversible inhibition of ADP action. ***Reversible inhibition of ADP action*** - **Ticagrelor** is a **P2Y12 receptor antagonist** that works by preventing ADP from binding to its receptor on platelets [2]. - This binding is **reversible**, meaning ticagrelor can dissociate from the receptor, allowing for some recovery of platelet function over time [2]. *Irreversible inhibition of ADP action* - **Clopidogrel** and **prasugrel** are examples of **irreversible P2Y12 inhibitors**, forming a permanent bond with the receptor [2]. - Irreversible inhibition leads to a longer duration of platelet inhibition, as new platelets must be generated for function to return [2]. *Reversible inhibition of GPIIb/IIIa* - **GPIIb/IIIa inhibitors** like **eptifibatide** and **tirofiban** block the final common pathway of platelet aggregation by preventing fibrinogen binding [1]. - While their action is reversible, they target a *different* mechanism than ticagrelor. *Irreversible inhibition of GPIIb/IIIa* - **Abciximab** is a GPIIb/IIIa inhibitor that binds **irreversibly** (or with very slow dissociation) to the receptor [1]. - Unlike reversible GPIIb/IIIa inhibitors, abciximab is a monoclonal antibody with a prolonged antiplatelet effect [1]. - This is still an incorrect answer as ticagrelor targets the P2Y12 receptor, not GPIIb/IIIa.

Q: All of the following are known adverse effects of thalidomide, except:

Diarrhoea. ***Diarrhoea*** - **Diarrhoea** is generally *not* considered a common or significant adverse effect of thalidomide. Constipation is more frequently reported. - While individual reactions vary, thalidomide's primary adverse effect profile does not typically include diarrhoea. *Teratogenicity* - **Teratogenicity** is the most notorious adverse effect of thalidomide, causing severe birth defects like **phocomelia** (shortened or absent limbs) in infants exposed during pregnancy. - Due to this, stringent **risk evaluation and mitigation strategies (REMS)** are in place for thalidomide use. *DVT* - Thalidomide is known to increase the risk of **venous thromboembolism (VTE)**, including **deep vein thrombosis (DVT)** and pulmonary embolism, especially in patients with multiple myeloma. - Prophylactic anticoagulation is often recommended for patients receiving thalidomide, particularly in combination with corticosteroids. *Neuropathy* - **Peripheral neuropathy** is a common and dose-limiting adverse effect of thalidomide, often presenting as numbness, tingling, and pain in the hands and feet. - It can be progressive and potentially irreversible, requiring careful monitoring and dose adjustments.

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: Which of the following statements about oral iron preparations is correct?

Different preparations have different bioavailability. ***Different preparations have different bioavailability*** - The **bioavailability** of oral iron preparations varies depending on the specific salt used, its formulation, and the presence of absorption enhancers or inhibitors. - This difference in absorption impacts the required dose and efficacy in treating **iron deficiency anemia**. *Most commonly used preparation is ferrous gluconate* - **Ferrous sulfate** is the most commonly prescribed and cost-effective oral iron preparation due to its high iron content and good bioavailability. - While ferrous gluconate is used, its iron content is lower than ferrous sulfate, making it less frequently the primary choice. *Ferrous fumarate is most efficient* - While **ferrous fumarate** has a high elemental iron content, its efficiency doesn't necessarily surpass that of ferrous sulfate or other preparations when considering factors like bioavailability and side effect profile. - **Ferrous sulfate** is often considered efficient due to its balance of elemental iron content, bioavailability, and cost-effectiveness. *Ferric preparations are more effective* - **Ferrous (Fe2+)** iron is generally better absorbed than **ferric (Fe3+)** iron, as ferric iron needs to be reduced to its ferrous form before absorption. - Unless specifically formulated for enhanced absorption (e.g., ferric maltol), ferric preparations are typically *less* effective for initial iron repletion.

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.

Q: Regarding Caisson's disease which statement among the following is CORRECT?

Pain in the joints is due to nitrogen bubbles. ***Pain in the joints is due to nitrogen bubbles*** - Caisson's disease, or **decompression sickness**, is characterized by the formation of nitrogen gas bubbles in tissues and blood due to rapid depressurization. - These gas bubbles can accumulate in joints, causing **severe pain** often referred to as "the bends." *Lung damage is caused by air embolism* - While air embolism can occur due to **pulmonary barotrauma** during ascent (rapid depressurization), the primary lung damage associated with decompression sickness is not typically directly caused by an air embolism reaching the lungs from within the body. - Air embolism from pulmonary barotrauma is a distinct complication, where air from ruptured alveoli enters the arterial circulation, potentially leading to cerebral or cardiac ischemia. *Tremors are seen due to nitrogen narcosis* - **Nitrogen narcosis** is a condition that occurs at high ambient pressures when breathing compressed air, causing a reversible alteration in consciousness similar to alcohol intoxication, but it does not primarily cause tremors. - Tremors are more characteristic of other neurological conditions or high-pressure nervous syndrome, not nitrogen narcosis itself. *High pressure Nervous syndrome can be prevented by using mixtures of Oxygen & Helium* - **High-pressure nervous syndrome (HPNS)** is indeed associated with deep dives using helium-oxygen mixtures. Its symptoms include tremors. - HPNS is actually **prevented or mitigated** by adding small amounts of narcotic gases like nitrogen to the helium-oxygen mixture (e.g., trimix) to counteract the excitatory effects of helium, rather than solely using oxygen and helium.

Question 1

What is the ionized calcium (IC) content of Ringer's lactate in mmol/L, and why is it clinically significant?

Accepted Answer

4 mmol/L

Answer

0 mmol/L

Answer

130 mmol/L

Answer

109 mmol/L

Question 2

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 3

What does Section 191 of the Indian Penal Code (IPC) pertain to?

Accepted Answer

Giving false evidence

Answer

Medical negligence

Answer

Assault punishment

Answer

Hostile witness

Question 4

What is the mechanism of action of ticagrelor?

Accepted Answer

Reversible inhibition of ADP action

Answer

Irreversible inhibition of ADP action

Answer

Reversible inhibition of GPIIb/IIIa

Answer

Irreversible inhibition of GPIIb/IIIa

Question 5

All of the following are known adverse effects of thalidomide, except:

Accepted Answer

Diarrhoea

Answer

DVT

Answer

Neuropathy

Answer

Teratogenicity

Question 6

Where does the oxidation of drugs mainly take place?

Accepted Answer

Smooth ER

Answer

Rough ER

Answer

Cytoplasm

Answer

Nucleus

Question 7

Which of the following statements best describes the underlying mechanism of heparin-induced thrombocytopenia?

Accepted Answer

Antibodies are formed against heparin-platelet factor 4 complexes.

Answer

Low molecular weight heparin can also cause heparin-induced thrombocytopenia.

Answer

Vitamin K is not an antidote for heparin-induced thrombocytopenia.

Answer

Heparin-induced thrombocytopenia can occur after several days of heparin therapy.

Question 8

Which of the following statements about oral iron preparations is correct?

Accepted Answer

Different preparations have different bioavailability

Answer

Most commonly used preparation is ferrous gluconate

Answer

Ferrous fumarate is most efficient

Answer

Ferric preparations are more effective

Question 9

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

Question 10

Regarding Caisson's disease which statement among the following is CORRECT?

Accepted Answer

Pain in the joints is due to nitrogen bubbles

Answer

Lung damage is caused by air embolism

Answer

Tremors are seen due to nitrogen narcosis

Answer

High pressure Nervous syndrome can be prevented by using mixtures of Oxygen & Helium

NEET-PG 2015

Anesthesiology

Forensic Medicine

Pharmacology

Physiology