INI-CET 2013

Q: Which of the following induces apoptosis in a cell?

Glucocorticoids. ***Glucocorticoids*** - **Glucocorticoids** are known to induce apoptosis in various cell types, particularly lymphocytes, making them useful in **lymphoid malignancies**. - They activate a complex signaling pathway that leads to the activation of pro-apoptotic proteins and the suppression of anti-apoptotic proteins, ultimately resulting in **programmed cell death**. *Isoprenoids* - **Isoprenoids** are a large class of organic compounds derived from isoprene, involved in various metabolic processes like cholesterol synthesis and protein prenylation, but do not directly induce apoptosis. - While some isoprenoid precursors or inhibitors of isoprenoid synthesis can affect cell proliferation or survival, isoprenoids themselves are not primary apoptosis inducers. *Myristic acid* - **Myristic acid** is a saturated fatty acid primarily involved in protein myristoylation, a post-translational modification essential for various cellular functions. - It is not known to be a direct inducer of apoptosis but can influence signaling pathways that may indirectly impact cell survival or death. *Oleic acid* - **Oleic acid** is a monounsaturated fatty acid that is a major component of cell membranes and is involved in energy storage and signaling. - It is generally considered cytoprotective and can even inhibit apoptosis in some contexts, rather than inducing it. [Practice more INI-CET 2013 questions on OnCourse]

Q: What is true about ribozymes?

Peptidyl transferase activity. **Explanation:** **Ribozymes** are non-protein enzyme molecules composed of RNA that possess catalytic activity. This discovery challenged the traditional dogma that all enzymes are proteins. 1. **Why Option A is Correct:** The most clinically significant ribozyme in human biology is the **23S rRNA** (in prokaryotes) or **28S rRNA** (in eukaryotes) of the large ribosomal subunit. This RNA molecule acts as a **Peptidyl transferase**, catalyzing the formation of peptide bonds during protein synthesis (translation). This confirms that the ribosome is essentially a ribozyme. 2. **Analysis of Incorrect Options:** * **Option B (Cut DNA):** Enzymes that cut DNA at specific sites are **Restriction Endonucleases**, which are protein-based enzymes, not ribozymes. * **Option C (DNA Synthesis):** DNA synthesis is mediated by **DNA Polymerases**, which are complex protein enzymes. While RNA primers are needed, the catalytic synthesis is not ribozyme-mediated. * **Option D (GTPase activity):** GTPase activity in translation is associated with protein factors like **EF-Tu or EF-G**, not the catalytic RNA itself. **High-Yield Facts for NEET-PG:** * **Examples of Ribozymes:** Peptidyl transferase, RNase P (cleaves tRNA precursors), and SnRNAs (involved in splicing/spliceosomes). * **Mechanism:** Like protein enzymes, ribozymes lower activation energy through specific tertiary folding and metal ion stabilization. * **Nobel Prize:** Thomas Cech and Sidney Altman won the Nobel Prize in 1989 for the discovery of catalytic properties of RNA. * **Clinical Relevance:** Ribozymes are being researched as "molecular scissors" for gene therapy to target and destroy viral RNA (e.g., HIV) or oncogenic mRNA. [Practice more INI-CET 2013 questions on OnCourse]

Q: A dead body is having cadaveric lividity of bluish green color. The most likely cause of death is by poisoning due to:

Hydrogen sulfide. ***Hydrogen sulfide*** - **Hydrogen sulfide poisoning** classically causes a **bluish-green cadaveric lividity** due to the formation of sulfhemoglobin. - This distinct discoloration is a key indicator often noted during post-mortem examination in cases of hydrogen sulfide exposure. *Hydrocyanic acid* - **Hydrocyanic acid poisoning** typically leads to a **cherry-red lividity** due to the inhibition of cytochrome oxidase, preventing tissue oxygen utilization, which is different from the bluish-green color described. - The bright red color results from the persistence of oxygenated hemoglobin in the venous blood. *Oleander* - **Oleander poisoning** affects the heart, causing **cardiac arrhythmias** and bradycardia, but does not typically produce a characteristic or distinct cadaveric discoloration like the bluish-green hue. - Lividity would generally be a more typical reddish-purple, consistent with simple hypostasis. *Sodium nitrite* - **Sodium nitrite poisoning** causes **methemoglobinemia**, leading to a characteristic **chocolate-brown or grayish-blue lividity** due to the oxidation of hemoglobin, which differs from the specific bluish-green described. - This change is due to the formation of methemoglobin, which cannot carry oxygen effectively. [Practice more INI-CET 2013 questions on OnCourse]

Q: Which of the following is true about degenerative myopia?

Myopic degeneration can lead to retinal detachment. **Explanation:** Degenerative (Pathological) myopia is characterized by progressive axial elongation of the eyeball, typically exceeding **26.5 mm** in length or a refractive error of **>-6 Diopters**. **Why Option B is Correct:** The hallmark of degenerative myopia is the stretching of the posterior segment. As the eyeball elongates, the retina and choroid undergo thinning and atrophy. This stretching leads to peripheral retinal degenerations, most notably **Lattice degeneration**. These weakened areas are prone to developing retinal holes or tears, which allow fluid to enter the subretinal space, leading to **Rhegmatogenous Retinal Detachment (RRD)**. **Analysis of Incorrect Options:** * **Option A:** Degenerative myopia is actually **more common in females** than in males. * **Option C:** It is defined by a refractive error **greater than -6 Diopters** (e.g., -8D, -10D). High myopia is the prerequisite for degenerative changes. * **Option D:** Instead of swelling, the optic disc typically shows **Myopic Crescent** (temporal or annular) and may appear tilted. The stretching often leads to posterior staphyloma, not edema. **High-Yield Clinical Pearls for NEET-PG:** * **Posterior Staphyloma:** The pathognomonic sign of degenerative myopia (bulging of the weakened sclera). * **Fuchs’ Spots:** Pigmented circular lesions at the macula caused by subretinal neovascularization and hemorrhage. * **Lacquer Cracks:** Linear breaks in the Bruch’s membrane. * **Vitreous:** Early liquefaction (syneresis) and Posterior Vitreous Detachment (PVD) are common. [Practice more INI-CET 2013 questions on OnCourse]

12 Previous Year Questions with Answers & Explanations

Questions

Subjects

All (12)Biochemistry (2)Forensic Medicine (1)Obstetrics and Gynecology (2)Ophthalmology (1)Orthopaedics (1)Pediatrics (2)Pharmacology (2)Surgery (1)

Biochemistry

2 questions

Which of the following induces apoptosis in a cell?

Q2Easy

What is true about ribozymes?

INI-CET 2013 - Biochemistry INI-CET Practice Questions and MCQs

Question 1: Which of the following induces apoptosis in a cell?

A. Glucocorticoids (Correct Answer)
B. Isoprenoids
C. Myristic acid
D. Oleic acid

Explanation: ***Glucocorticoids*** - **Glucocorticoids** are known to induce apoptosis in various cell types, particularly lymphocytes, making them useful in **lymphoid malignancies**. - They activate a complex signaling pathway that leads to the activation of pro-apoptotic proteins and the suppression of anti-apoptotic proteins, ultimately resulting in **programmed cell death**. *Isoprenoids* - **Isoprenoids** are a large class of organic compounds derived from isoprene, involved in various metabolic processes like cholesterol synthesis and protein prenylation, but do not directly induce apoptosis. - While some isoprenoid precursors or inhibitors of isoprenoid synthesis can affect cell proliferation or survival, isoprenoids themselves are not primary apoptosis inducers. *Myristic acid* - **Myristic acid** is a saturated fatty acid primarily involved in protein myristoylation, a post-translational modification essential for various cellular functions. - It is not known to be a direct inducer of apoptosis but can influence signaling pathways that may indirectly impact cell survival or death. *Oleic acid* - **Oleic acid** is a monounsaturated fatty acid that is a major component of cell membranes and is involved in energy storage and signaling. - It is generally considered cytoprotective and can even inhibit apoptosis in some contexts, rather than inducing it.

Question 2: What is true about ribozymes?

A. Peptidyl transferase activity (Correct Answer)
B. Cut DNA at a specific site
C. Participate in DNA synthesis
D. GTPase activity

Explanation: **Explanation:** **Ribozymes** are non-protein enzyme molecules composed of RNA that possess catalytic activity. This discovery challenged the traditional dogma that all enzymes are proteins. 1. **Why Option A is Correct:** The most clinically significant ribozyme in human biology is the **23S rRNA** (in prokaryotes) or **28S rRNA** (in eukaryotes) of the large ribosomal subunit. This RNA molecule acts as a **Peptidyl transferase**, catalyzing the formation of peptide bonds during protein synthesis (translation). This confirms that the ribosome is essentially a ribozyme. 2. **Analysis of Incorrect Options:** * **Option B (Cut DNA):** Enzymes that cut DNA at specific sites are **Restriction Endonucleases**, which are protein-based enzymes, not ribozymes. * **Option C (DNA Synthesis):** DNA synthesis is mediated by **DNA Polymerases**, which are complex protein enzymes. While RNA primers are needed, the catalytic synthesis is not ribozyme-mediated. * **Option D (GTPase activity):** GTPase activity in translation is associated with protein factors like **EF-Tu or EF-G**, not the catalytic RNA itself. **High-Yield Facts for NEET-PG:** * **Examples of Ribozymes:** Peptidyl transferase, RNase P (cleaves tRNA precursors), and SnRNAs (involved in splicing/spliceosomes). * **Mechanism:** Like protein enzymes, ribozymes lower activation energy through specific tertiary folding and metal ion stabilization. * **Nobel Prize:** Thomas Cech and Sidney Altman won the Nobel Prize in 1989 for the discovery of catalytic properties of RNA. * **Clinical Relevance:** Ribozymes are being researched as "molecular scissors" for gene therapy to target and destroy viral RNA (e.g., HIV) or oncogenic mRNA.

Forensic Medicine

1 questions

A dead body is having cadaveric lividity of bluish green color. The most likely cause of death is by poisoning due to:

Obstetrics and Gynecology

1 questions

Q1Medium

Which of the following is seen in pregnancy with heart disease, which is not seen in normal pregnancy?

Ophthalmology

1 questions

Q1Medium

Which of the following is true about degenerative myopia?

Orthopaedics

1 questions

Q1Medium

In a 2-year-old child, gallows traction is applied. The child is suffering from a fracture of which bone?

Pediatrics

1 questions

Q1Medium

A 2-day-old premature neonate develops generalized tonic-clonic seizures. What is the investigation done to diagnose the underlying pathology?

Pharmacology

2 questions

Which of the following statements about methyl alcohol poisoning is incorrect?

A patient on amphotericin B develops hypokalemia with a potassium level of 2.3 mEq/L. What is the appropriate K+ supplementation required for this patient?

INI-CET 2013 - Pharmacology INI-CET Practice Questions and MCQs

Question 1: Which of the following statements about methyl alcohol poisoning is incorrect?

A. Effects are due to formic acid
B. Metabolic acidosis
C. Blindness
D. Fomepizole competitively inhibits aldehyde dehydrogenase (Correct Answer)

Explanation: ***Fomepizole competitively inhibits aldehyde dehydrogenase*** - **Fomepizole** acts as a competitive inhibitor of **alcohol dehydrogenase**, not aldehyde dehydrogenase. - By inhibiting alcohol dehydrogenase, fomepizole prevents the metabolism of methanol into toxic metabolites like formic acid. *Effects are due to formic acid* - This statement is correct. The primary toxicity of methanol poisoning is due to its metabolism into **formic acid** by alcohol and aldehyde dehydrogenases. - Formic acid is responsible for the **metabolic acidosis** and **ocular toxicity** observed. *Metabolic acidosis* - This statement is correct. Methanol poisoning leads to severe **anion gap metabolic acidosis** due to the accumulation of formic acid. - The acidosis contributes significantly to the overall toxicity and clinical manifestations. *Blindness* - This statement is correct. **Blindness** is a classic and feared complication of methanol poisoning. - **Formic acid** specifically targets the **optic nerve** and retina, leading to **optic neuropathy** and permanent vision loss.

Question 2: A patient on amphotericin B develops hypokalemia with a potassium level of 2.3 mEq/L. What is the appropriate K+ supplementation required for this patient?

A. 40 mEq over 24 hours
B. 80 mEq over 24 hours (Correct Answer)
C. 60 mEq over 24 hours
D. 100-120 mEq over 24 hours

Explanation: ***80 mEq over 24 hours***- For a potassium level of 2.3 mEq/L (moderate to severe hypokalemia), **80 mEq over 24 hours** represents appropriate aggressive replacement while maintaining safety.- This dose accounts for both the **existing deficit** and **ongoing renal potassium wasting** caused by amphotericin B, which impairs renal tubular function.- Standard guidelines recommend **60-80 mEq daily** for moderate to severe hypokalemia, divided into multiple doses with continuous cardiac monitoring.- Higher doses risk **rebound hyperkalemia** and cardiac complications [1]; replacement should be titrated based on serial potassium measurements.*40 mEq over 24 hours*- This dosage is insufficient for correcting a potassium level of 2.3 mEq/L, particularly with **ongoing drug-induced renal losses**.- It may be appropriate for mild hypokalemia (3.0-3.5 mEq/L) or maintenance therapy, but not for this clinical scenario.*60 mEq over 24 hours*- While this represents a reasonable starting dose for moderate hypokalemia, it may be **insufficient** given the severity (K+ 2.3 mEq/L) and ongoing losses from amphotericin B.- This dose might require escalation after reassessment of potassium levels.*100-120 mEq over 24 hours*- This dose **exceeds standard safe replacement protocols** and risks causing rebound hyperkalemia and cardiac arrhythmias [1].- Maximum safe infusion rates are typically **10-20 mEq/hour** (up to 40 mEq/hour only in critical situations with intensive monitoring).- Such aggressive replacement is not recommended in standard clinical practice for this scenario.

Surgery

1 questions

When a seat belt is worn, if an accident occurs, sudden deceleration can result in: