NEET-PG 2015 Practice Questions

Q: Which of the following statements is true regarding the functions of cAMP and cGMP?

They are both second messengers.. ***They are both second messengers.*** - **cAMP (cyclic adenosine monophosphate)** and **cGMP (cyclic guanosine monophosphate)** are crucial intracellular signaling molecules. - They relay signals from **first messengers** (like hormones or neurotransmitters) received at the cell surface to intracellular targets, thus acting as second messengers. *They act on membrane receptors.* - **cAMP** and **cGMP** are *produced* in response to activation of **membrane receptors** by first messengers, but they themselves do not act directly on these receptors. - Their action is primarily *intracellular*, binding to and activating various enzymes and proteins like **protein kinases**. *All of the above statements are true* - This statement is incorrect because the claim that they act on membrane receptors is false. - Only one of the statements provided is accurate regarding the functions of cAMP and cGMP. *They act by post-translational modification.* - While cAMP and cGMP can lead to **post-translational modification** (e.g., phosphorylation by protein kinases A and G), they are not themselves the direct modifiers. - They act as **allosteric regulators** of enzymes, which then catalyze the modifications.

Q: Which of the following is not a feature of postmortem staining?

Occurs immediately after death. ***Occurs immediately after death*** - **Livor mortis** (postmortem staining/lividity) does NOT occur immediately after death - it typically begins **20-30 minutes** after death and becomes fully developed within **6-12 hours** - This is the correct answer as it represents a feature that is NOT characteristic of postmortem staining - The delay occurs because it takes time for blood to settle in capillaries due to gravity after circulation stops *Common in dependent part* - This IS a hallmark feature of postmortem staining - Gravity causes blood to pool in the **lowest parts of the body** (dependent areas) - Areas of pressure (where body contacts surface) appear pale due to **capillary compression** *Appears uniformly throughout the body* - This is also NOT a feature of postmortem staining (could be considered another correct answer) - Postmortem staining is **localized to dependent areas**, not uniform throughout - The distribution pattern helps determine body position after death in forensic investigations *Margins are sharp* - Postmortem lividity typically has **ill-defined, diffuse margins** rather than sharp borders - The transition between affected and unaffected areas is gradual - However, this is less definitively wrong compared to the timing and uniformity statements

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: IgA nephropathy is not associated with which of the following?

Decreased complement level. ***Decreased complement level*** - IgA nephropathy is typically associated with **normal serum complement levels** (C3 and C4), which is an important distinguishing feature. - Unlike post-streptococcal glomerulonephritis or lupus nephritis where complement levels are **low/decreased**, IgA nephropathy does not cause systemic complement consumption. - While complement activation does occur locally in the glomerulus (via lectin and alternative pathways), it does not lead to a decrease in serum complement levels. *Focal mesangial proliferation* - This is a **common histological finding** in IgA nephropathy, reflecting the proliferative response to IgA deposition in the mesangium. - The mesangial cells proliferate in an attempt to clear the immune deposits. *Gross hematuria concurrent with upper respiratory infection* - This is a **classic clinical presentation** of IgA nephropathy, often referred to as **synpharyngitic hematuria**. - The episode of gross hematuria typically occurs **within 1-2 days** of the onset of an upper respiratory tract infection, distinguishing it from post-streptococcal glomerulonephritis where hematuria appears 1-3 weeks later. *Immunofluorescence deposits contain IgA and IgG* - The defining feature of IgA nephropathy on immunofluorescence is the **predominant deposition of IgA**, often accompanied by C3. - While IgA is the primary immunoglobulin, **IgG and IgM can also be present** in variable amounts, but IgA must be the dominant or co-dominant immunoglobulin for the diagnosis.

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 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.

Q: What is one of the specific functions of the primary motor cortex located on the anterior edge of the pre-central gyrus?

Control of voluntary movement. ***Control of voluntary movement*** - The **primary motor cortex (M1)**, located in the **precentral gyrus**, is critically involved in generating neural impulses that control the execution of **voluntary movements**. - It plays a key role in **planning and executing complex, skilled movements**, especially of the distal musculature. *Increase extensor muscle tone* - While motor pathways influence muscle tone, the primary motor cortex's most specific role is not simply increasing extensor tone; rather, it coordinates a wide range of movements involving both flexors and extensors. - **Spasticity** or increased muscle tone (often extensor) is more commonly associated with damage to the **corticospinal tracts (upper motor neuron lesions)**, which *prevents* the fine-tuning inhibitory control from the cortex. *Perception of pain* - **Pain perception** is primarily processed in the **somatosensory cortex** (postcentral gyrus), limbic system, and insula, not the primary motor cortex. - The primary motor cortex is responsible for **motor output**, not sensory interpretation. *Inhibition of stretch reflex* - While descending motor pathways can modulate spinal reflexes, the direct and primary function of the primary motor cortex is not the specific inhibition of the stretch reflex. - The **gamma motor system** and other spinal interneurons are more directly involved in modulating the sensitivity of the stretch reflex.

Question 1

Which of the following statements is true regarding the functions of cAMP and cGMP?

Accepted Answer

They are both second messengers.

Answer

All of the above statements are true

Answer

They act on membrane receptors.

Answer

They act by post-translational modification.

Question 2

Which of the following is not a feature of postmortem staining?

Accepted Answer

Occurs immediately after death

Answer

Common in dependent part

Answer

Appears uniformly throughout the body

Answer

Margins are sharp

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

IgA nephropathy is not associated with which of the following?

Accepted Answer

Decreased complement level

Answer

Focal mesangial proliferation

Answer

Gross hematuria concurrent with upper respiratory infection

Answer

Immunofluorescence deposits contain IgA and IgG

Question 5

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 6

Obliterative endarteritis in vasa vasorum is seen in -

Accepted Answer

Tertiary Syphilis

Answer

Essential Hypertension

Answer

Systemic Lupus Erythematosus

Answer

Pulmonary Tuberculosis

Question 7

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 8

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 9

'Flare' in Triple response is mediated by :

Accepted Answer

Axon reflex

Answer

Arteriolar dilation

Answer

Histamine release

Answer

Local hormones

Question 10

What is one of the specific functions of the primary motor cortex located on the anterior edge of the pre-central gyrus?

Accepted Answer

Control of voluntary movement

Answer

Increase extensor muscle tone

Answer

Perception of pain

Answer

Inhibition of stretch reflex

NEET-PG 2015

Biochemistry

Forensic Medicine

Internal Medicine

Pathology

Pharmacology

Physiology