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: Base of sphenoid fuses with occiput at the age of -

20 years. ***20 years*** - The **spheno-occipital synchondrosis** typically fuses by the age of **20 to 25 years**, marking the cessation of growth in the cranial base. - This fusion is an important indicator of skeletal maturity and is often used in **forensic anthropology** for age estimation. *30 years* - Fusion of the **spheno-occipital synchondrosis** beyond the early twenties is considered late and is not the typical age for this event. - By 30 years, most cranial sutures and synchondroses are already fused. *40 years* - At 40 years of age, the **spheno-occipital synchondrosis** would have been completely fused for many years, making this an incorrect age for the fusion process itself. - This age is well past the usual developmental timeframe for cranial base closure. *50 years* - Fusion at 50 years would be an **anomalous finding** as this synchondrosis is known to fuse much earlier in life. - By this age, the skull is fully mature, and fusion events of this nature have long since completed.

Q: A patient presents with skin involvement and collar stud ulceration in the intestine observed on radiography. What is the most likely diagnosis?

Ulcerative colitis. ***Ulcerative colitis*** - **Collar stud ulcers** are a classic radiographic finding in **ulcerative colitis**, occurring when superficial ulcers undermine the mucosa. - While skin involvement can occur in ulcerative colitis (e.g., **erythema nodosum**, **pyoderma gangrenosum**), the characteristic intestinal ulcers are a strong indicator. *TB intestine* - Intestinal tuberculosis typically presents with **transverse ulcers** and **strictures**, often in the ileocecal region, rather than collar stud ulcers. - Skin involvement is less common and usually manifests as **lupus vulgaris** or **scrofuloderma**, which are distinct from the general "skin involvement" mentioned. *Intestinal Amebiasis* - Amebic colitis causes characteristic **flask-shaped ulcers** in the colon due to the parasite invading the submucosa, which are distinct from collar stud ulcers. - Skin involvement is rare but can occur as **cutaneous amebiasis**, presenting as chronic ulcers, which is not suggested by the general term. *Crohn's disease* - Crohn's disease is characterized by **skip lesions**, **transmural inflammation**, and **cobblestoning**, with deep, linear ulcers and fissures. - While skin manifestations like **erythema nodosum** and **pyoderma gangrenosum** can occur, classical collar stud ulcers are not typical for Crohn's disease.

Q: Which genetic condition is considered the most lethal due to monosomy?

Autosomal monosomy. ***Autosomal monosomy*** - **Autosomal monosomy** is the most lethal form of monosomy because it involves the loss of an entire autosome, leading to a severe imbalance in gene dosage. [1] - The human body cannot typically survive with the loss of a whole autosome, resulting in early embryonic or fetal demise. [1] *Chromosomal monosomy* - This is a broader term that includes both **autosomal monosomy** and **sex chromosome monosomy**. - While many forms of chromosomal monosomy are lethal, **sex chromosome monosomy (e.g., Turner syndrome)** is survivable, making the general term "chromosomal monosomy" less specific for the *most lethal* condition. [1] *Autosomal trisomy* - **Autosomal trisomy** involves an extra copy of an autosome (e.g., Trisomy 21 for Down syndrome), which, while causing significant health issues, is generally less lethal than the complete loss of an autosome. [1] - Many individuals with autosomal trisomies can survive to birth and beyond, unlike most cases of autosomal monosomy. [1] *Chromosomal trisomy* - This refers to having an extra copy of any chromosome, including **autosomes** and **sex chromosomes**. - While conditions like **Trisomy 13 (Patau syndrome)** and **Trisomy 18 (Edwards syndrome)** are highly lethal, the presence of *extra* genetic material is typically less universally lethal than the *absence* of an entire autosome. [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 168-169.

Q: Obliterative endarteritis in vasa vasorum is seen in -

Tertiary Syphilis. ***Tertiary Syphilis*** - **Obliterative endarteritis** of the **vasa vasorum** is a hallmark pathological finding in tertiary syphilis, particularly affecting the **aorta**. - This inflammation and occlusion of the small blood vessels supplying the aorta lead to **ischemic injury** of the aortic wall, causing **aneurysms** and **aortic regurgitation**. *Essential Hypertension* - While hypertension can lead to vascular changes like **arteriolosclerosis** and **hyperplastic arteriolosclerosis**, it does not typically involve obliterative endarteritis of the vasa vasorum. - The vascular damage in essential hypertension is more generalized to smaller arteries and arterioles, not specifically the vasa vasorum. *Systemic Lupus Erythematosus* - SLE is an **autoimmune disease** that can cause **vasculitis**, but the specific pattern of obliterative endarteritis of the vasa vasorum is not characteristic. - Vascular involvement in SLE is diverse, ranging from small vessel vasculitis to accelerated atherosclerosis, but distinct from syphilitic changes. *Pulmonary Tuberculosis* - Tuberculosis is primarily an **infectious granulomatous disease** affecting the lungs and other organs; it does not typically cause obliterative endarteritis of the vasa vasorum. - Although it can cause vascular complications like **aneurysms** (e.g., Rasmussen's aneurysm) due to erosion, the underlying mechanism is not the same as syphilitic changes.

Q: Which of the following agents requires the MOST caution when combined with spironolactone due to increased risk of hyperkalemia:

ACE inhibitors. ***ACE inhibitors*** - Spironolactone is a **potassium-sparing diuretic** that increases potassium levels by blocking aldosterone's effects in the collecting duct [1]. - **ACE inhibitors** also decrease aldosterone production [2], leading to reduced potassium excretion and a significant risk of **severe hyperkalemia** when combined with spironolactone [1, 2].*Beta-blockers* - While beta-blockers can cause a slight increase in plasma potassium by inhibiting cellular potassium uptake, this effect is generally modest and does not pose a major hyperkalemia risk when co-administered with spironolactone. - Their primary interaction concerns blood pressure and heart rate, not direct potassium handling.*Amlodipine* - Amlodipine is a **calcium channel blocker** that primarily causes vasodilation and does not significantly alter potassium balance. - Therefore, it does not substantially increase the risk of hyperkalemia when used concurrently with spironolactone.*Chlorothiazide* - Chlorothiazide is a **thiazide diuretic** that promotes potassium excretion, leading to a risk of hypokalemia. - When combined with spironolactone, a potassium-sparing diuretic, these agents can **partially offset each other's effects** on potassium balance, potentially reducing the risk of hyperkalemia compared to ACE inhibitors.

Q: What is the drug of choice for drug-induced peptic ulcer?

Proton pump inhibitors. ***Proton pump inhibitors*** - **PPIs** are the most effective agents for treating and preventing **NSAID-induced peptic ulcers** by profoundly suppressing gastric acid secretion. - They provide **rapid symptom relief** and promote ulcer healing by creating an environment conducive to mucosal repair. *Prostaglandin analogues* - **Misoprostol**, a prostaglandin E1 analogue, can prevent NSAID-induced ulcers, but its use is limited by **gastrointestinal side effects** such as diarrhea and abdominal cramping. - While they protect the gastric mucosa, their efficacy in healing established ulcers is generally **inferior to PPIs**. *H2-receptor antagonists* - **H2-blockers** are effective in reducing gastric acid, but they are **less potent** than PPIs and typically do not heal **gastric ulcers** as effectively, especially those induced by NSAIDs. - They are more commonly used for preventing **duodenal ulcers** and managing symptoms of GERD. *Antacids* - Antacids provide **immediate, temporary relief** of ulcer symptoms by neutralizing existing stomach acid. - They do not address the underlying pathology or promote **ulcer healing** and are therefore not considered the drug of choice for treatment.

Q: Which of the following is an action of muscarinic cholinergic receptors?

Decreased heart rate. ***Decreased heart rate*** - Activation of **muscarinic cholinergic receptors (M2 receptors)** in the heart leads to a decrease in heart rate and conduction velocity. - This effect is mediated by the **vagus nerve (parasympathetic nervous system)**, which releases acetylcholine to act on these receptors. - This is the **most characteristic and clinically significant cardiovascular effect** of muscarinic receptor activation, making it the expected answer. *Skeletal muscle contraction* - **Skeletal muscle contraction** is mediated by **nicotinic acetylcholine receptors (nAChRs)** at the **neuromuscular junction**, NOT muscarinic receptors. - Nicotinic receptors are **ligand-gated ion channels** that cause direct depolarization and muscle contraction when activated. - This is the only option that is **NOT a muscarinic receptor action**. *Acid secretion in stomach* - **Gastric acid secretion** IS mediated by **M3 muscarinic receptors** on parietal cells. - Acetylcholine from the vagus nerve directly stimulates parietal cells and also stimulates histamine release from enterochromaffin-like cells. - While this is a valid muscarinic action, in the context of distinguishing muscarinic effects, **cardiac effects** (decreased heart rate) are more emphasized as the classic teaching point. *Salivation and lacrimation* - **Salivation and lacrimation** ARE mediated by **M3 muscarinic receptors** in exocrine glands. - These are classic parasympathetic/muscarinic effects taught in physiology. - However, when distinguishing key muscarinic actions, **M2 receptor-mediated cardiac effects** are typically highlighted as the primary cardiovascular manifestation, while M3 effects on glands are secondary teaching points.

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: 'Flare' in Triple response is mediated by :

Axon reflex. ***Axon reflex*** - The "flare" component of the triple response is caused by an **axon reflex**, where sensory nerve endings release **vasoactive neuropeptides** such as substance P and calcitonin gene-related peptide (CGRP). - These neuropeptides cause **vasodilation** in the surrounding area, leading to the characteristic red, irregularly shaped halo around the wheal. *Arteriolar dilation* - While arteriolar dilation is a component of the triple response and contributes to the **redness (flush)** and **flare**, it is not the direct mediator of the flare itself. - The initial arteriolar dilation is primarily due to **histamine** acting directly on the vessels, whereas the flare is a broader, neurally mediated spread of vasodilation. *Histamine release* - **Histamine** release from mast cells is the primary mediator of the initial **redness (flush)** and the formation of the **wheal** (swelling due to capillary permeability). - While histamine plays a role in the overall response, it does not directly mediate the "flare" component, which involves neuronal signaling via the axon reflex. *Local hormones* - While various **local mediators** (which could be broadly considered "local hormones" in a sense) are involved in inflammatory responses, the specific term "local hormones" is too general and does not precisely describe the mechanism of the flare. - The axon reflex, involving specific **neuropeptides**, is the precise mechanism for the flare, not a general category of local hormones.

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

Base of sphenoid fuses with occiput at the age of -

Accepted Answer

20 years

Answer

30 years

Answer

40 years

Answer

50 years

Question 3

A patient presents with skin involvement and collar stud ulceration in the intestine observed on radiography. What is the most likely diagnosis?

Accepted Answer

Ulcerative colitis

Answer

TB intestine

Answer

Intestinal Amebiasis

Answer

Crohn's disease

Question 4

Which genetic condition is considered the most lethal due to monosomy?

Accepted Answer

Autosomal monosomy

Answer

Chromosomal monosomy

Answer

Autosomal trisomy

Answer

Chromosomal trisomy

Question 5

Obliterative endarteritis in vasa vasorum is seen in -

Accepted Answer

Tertiary Syphilis

Answer

Essential Hypertension

Answer

Systemic Lupus Erythematosus

Answer

Pulmonary Tuberculosis

Question 6

Which of the following agents requires the MOST caution when combined with spironolactone due to increased risk of hyperkalemia:

Accepted Answer

ACE inhibitors

Answer

Beta-blockers

Answer

Amlodipine

Answer

Chlorothiazide

Question 7

What is the drug of choice for drug-induced peptic ulcer?

Accepted Answer

Proton pump inhibitors

Answer

Prostaglandin analogues

Answer

H2-receptor antagonists

Answer

Antacids

Question 8

Which of the following is an action of muscarinic cholinergic receptors?

Accepted Answer

Decreased heart rate

Answer

Skeletal muscle contraction

Answer

Acid secretion in stomach

Answer

Salivation and lacrimation

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

'Flare' in Triple response is mediated by :

Accepted Answer

Axon reflex

Answer

Arteriolar dilation

Answer

Histamine release

Answer

Local hormones

NEET-PG 2015

Biochemistry

Forensic Medicine

Internal Medicine

Pathology

Pharmacology

Physiology