NEET-PG 2019 Practice Questions

Q: Foot drop is caused due to injury to which nerve?

Common Peroneal Nerve. Common peroneal nerve - Injury to the common peroneal nerve (also known as the common fibular nerve) leads to weakness or paralysis of the muscles responsible for dorsiflexion and eversion of the foot. - This results in a condition called foot drop, where the foot cannot be lifted at the ankle, causing a characteristic high-stepping or steppage gait. Obturator Nerve - The obturator nerve primarily innervates the adductor muscles of the thigh, which are responsible for pulling the legs together. - Injury to this nerve would cause difficulty with leg adduction and sensation over the medial thigh, not foot drop. Tibial Nerve - The tibial nerve innervates the muscles of the posterior compartment of the leg, responsible for plantarflexion and inversion of the foot. - Damage to the tibial nerve would result in an inability to stand on tiptoes or reduced sensation in the sole of the foot, not foot drop. Femoral Nerve - The femoral nerve innervates the quadriceps femoris muscle, essential for knee extension, and also provides sensation to the anterior thigh and medial leg. - Injury to this nerve would primarily lead to weakness in knee extension and difficulty climbing stairs, not foot drop.

Q: Ammonia causes depletion of which of the following in TCA cycle?

Alpha-ketoglutarate. ***Alpha-ketoglutarate*** - Ammonia is detoxified in the brain by conversion to **glutamine**, a process that consumes **alpha-ketoglutarate** in the glutamate dehydrogenase reaction (alpha-ketoglutarate + NH3 + NADH glutamate + NAD+). - The depletion of **alpha-ketoglutarate** in the TCA cycle impairs cellular respiration and ATP production, contributing to the neurological dysfunction seen in hyperammonemia. *Malate* - While malate is a component of the TCA cycle, its depletion is not a direct consequence of ammonia detoxification. - Ammonia metabolism primarily impacts the availability of alpha-ketoglutarate through the synthesis of glutamate and glutamine. *Oxaloacetate* - Although **oxaloacetate** is a key intermediate in the TCA cycle, its levels are not directly depleted by ammonia metabolism. - **Oxaloacetate** can be replenished through anaplerotic reactions, even if the TCA cycle is slightly inhibited due to alpha-ketoglutarate depletion. *Fumarate* - **Fumarate** is an intermediate of the TCA cycle and is not directly consumed or depleted by the ammonia detoxification pathway. - Its levels would only indirectly be affected if the overall flux of the TCA cycle is significantly reduced due to depletion of other intermediates.

Q: Defect in Menkes disease:

ATP7A (Copper-transporting ATPase). ***ATP7A (Copper-transporting ATPase)*** - **Menkes disease** is an X-linked recessive disorder characterized by a defect in the **ATP7A gene**, which encodes a copper-transporting ATPase. - This defect leads to impaired intestinal absorption and cellular transport of copper, resulting in **copper deficiency** in various tissues despite adequate dietary intake. *Prolyl oxidase* - **Prolyl oxidase** is involved in proline metabolism, and defects are not associated with Menkes disease. - Deficiency of this enzyme is usually linked to hyperprolinemia. *Prolyl hydroxylase* - **Prolyl hydroxylase** is an enzyme critical for the hydroxylation of proline residues in collagen, a step essential for collagen stability. - While collagen synthesis requires copper (for lysyl oxidase), a direct defect in prolyl hydroxylase is not the cause of Menkes disease. *Lysyl oxidase* - **Lysyl oxidase** is a copper-dependent enzyme required for the cross-linking of collagen and elastin, contributing to connective tissue strength. - Although lysyl oxidase activity is reduced in Menkes disease due to copper deficiency, the primary defect is in the **ATP7A transporter**, not the lysyl oxidase enzyme itself.

Q: All of the following are not true with respect to erythema multiforme except?

Targetoid lesions are seen. ***Targetoid lesions are seen*** - **Erythema multiforme (EM)** is characterized by distinctive **targetoid lesions** (target lesions) with three concentric zones: a dusky center, a pale middle ring, and an erythematous outer ring. - These lesions are a hallmark of EM and differentiate it from many other dermatological conditions. *Most commonly due to leukemia* - **Erythema multiforme** is most commonly associated with **infections**, particularly **herpes simplex virus (HSV)**, rather than leukemia. - Other common triggers include **mycoplasma infections** and certain **medications**. *Steroids are the drug of choice* - For typical, mild **erythema multiforme**, **topical steroids** may be used for symptomatic relief, but they are generally **not the drug of choice** for severe or widespread disease. - **Systemic steroids** are controversial and not routinely recommended for uncomplicated EM, as they may prolong the course or lead to recurrences, though they might be considered in severe cases or to prevent progression to Stevens-Johnson syndrome. *Koebner's phenomenon is seen* - The **Koebner phenomenon** (isomorphic response), where new lesions appear at sites of trauma, is classically associated with conditions like **psoriasis**, **lichen planus**, and **vitiligo**. - It is **not typically seen** in erythema multiforme.

Q: Which chamber of the heart is enlarged first in a patient with mitral stenosis?

Left atrium. ***Left atrium*** - **Mitral stenosis** obstructs blood flow from the left atrium to the left ventricle, leading to a build-up of pressure in the left atrium [1]. - This chronic pressure overload causes the **left atrium to dilate and hypertrophy** in an attempt to pump blood through the narrowed valve [1]. *Left ventricle* - In **mitral stenosis**, the left ventricle typically receives a reduced volume of blood, leading to a **smaller, underfilled left ventricle**, rather than enlargement. - Its workload is decreased due to reduced preload, so it does not hypertrophy or dilate primarily. *Right ventricle* - **Right ventricular enlargement** can eventually occur in severe and chronic mitral stenosis due to **pulmonary hypertension** caused by back pressure from the left atrium, but it is not the *first* chamber to be affected [1], [2]. - Increased pressure in the pulmonary circulation increases the workload on the right ventricle, leading to hypertrophy and dilation over time [1], [2]. *Right atrium* - **Right atrial enlargement** is a consequence of chronic and severe pulmonary hypertension affecting the right ventricle, which then causes back pressure into the right atrium [1]. - This is a very late manifestation of mitral stenosis, occurring after significant involvement of the left atrium and pulmonary vasculature.

Q: PGF2 alpha maximum dose in PPH management that can be given over 24 hours is:

2 mg. ***2 mg*** - The maximum recommended dose of **PGF2 alpha** (carboprost tromethamine) in a 24-hour period for PPH management is **2 mg**. - This is typically administered as 250 mcg (0.25 mg) intramuscularly every 15-90 minutes, with a total dose not exceeding 2 mg. *20 mg* - This dose is significantly higher than the recommended maximum for **PGF2 alpha** in PPH and would likely lead to severe adverse effects. - Exceeding the 2 mg limit can increase the risk of gastrointestinal, cardiovascular, and pulmonary complications. *200 mg* - This is an extremely high and dangerous dose of **PGF2 alpha**, far beyond any therapeutic range for PPH management. - Such a dose would almost certainly result in life-threatening complications. *250 mg* - While individual doses of **PGF2 alpha** are 250 mcg (0.25 mg), a total dose of 250 mg over 24 hours is vastly excessive. - This value likely confuses the single dose amount with a significantly larger incorrect total.

Q: Agent used for eliciting diagnostic differentiation of Myasthenia Gravis from Cholinergic crisis is:-

Edrophonium. ***Edrophonium*** - **Edrophonium** is a **short-acting acetylcholinesterase inhibitor** (duration 5-10 minutes) used in the **Tensilon test** to differentiate myasthenic crisis from cholinergic crisis - In **myasthenic crisis**, edrophonium temporarily improves muscle strength due to increased acetylcholine at the neuromuscular junction - In **cholinergic crisis**, it worsens weakness or shows no improvement - The rapid onset and short duration allow clear observation of transient response, making it ideal for diagnostic differentiation *Neostigmine* - **Neostigmine** is a longer-acting acetylcholinesterase inhibitor (duration 2-4 hours) used for chronic management of myasthenia gravis - Its prolonged effect makes it unsuitable for rapid diagnostic differentiation in acute crisis situations - The extended duration would make it difficult to observe transient changes and could worsen a cholinergic crisis for a prolonged period *Ecothiophate* - **Ecothiophate** is an irreversible acetylcholinesterase inhibitor used primarily in ophthalmology for glaucoma - Its irreversible action and prolonged effect (days to weeks) make it completely inappropriate for crisis differentiation - Would severely exacerbate cholinergic symptoms with sustained effect that cannot be reversed *Ambenonium* - **Ambenonium** is another long-acting acetylcholinesterase inhibitor (duration 3-8 hours) used for chronic treatment of myasthenia gravis - Similar to neostigmine, its extended duration makes it unsuitable for acute diagnostic challenge - The rapid onset and offset required for the Tensilon test cannot be achieved with this agent

Q: Cisatracurium is better than atracurium because:-

Less histamine release. ***Less histamine release*** - **Cisatracurium** causes significantly less **histamine release** compared to atracurium, reducing the risk of **hypotension** and **bronchospasm**. [1] - This makes cisatracurium a safer choice for patients with **cardiovascular instability** or **asthma**. *No active metabolites* - While cisatracurium produces **laudanosine** as a metabolite, this is also true for **atracurium**. - The difference lies in the **concentration** of laudanosine and its potential for central nervous system toxicity, which is generally lower with cisatracurium. *Shorter half-life* - **Cisatracurium** generally has a **slightly longer half-life** than atracurium, but both are characterized by a relatively rapid onset and offset of action. - Their elimination primarily occurs via **Hoffman elimination** and **ester hydrolysis**, independent of renal or hepatic function. *Better neuromuscular blockade* - Both **cisatracurium** and **atracurium** are effective **neuromuscular blockers** when administered at appropriate doses. - The "better" aspect for cisatracurium relates more to its **improved safety profile** (less histamine release) rather than a significantly superior blockade efficacy. [1]

Q: Risk factors for Alzheimer's include:-

Down's syndrome. ***Down's syndrome*** - Individuals with **Down's syndrome** have an extra copy of chromosome 21, which includes the **amyloid precursor protein (APP) gene**. - Overexpression of APP leads to increased production of **beta-amyloid plaques**, a hallmark pathology of Alzheimer's disease. *Parkinson's disease* - Parkinson's disease is a **neurodegenerative disorder** characterized by motor symptoms due to loss of dopaminergic neurons. - While it can be associated with **dementia (Parkinson's disease dementia)**, it is a distinct condition with different primary pathological mechanisms (alpha-synucleinopathy). *Vascular dementia* - **Vascular dementia** is caused by brain damage from conditions that impair blood flow to the brain, such as strokes or small vessel disease. - It is a **different type of dementia** with distinct etiology and neuropathology compared to Alzheimer's disease. *Huntington's disease* - **Huntington's disease** is a genetic neurodegenerative disorder characterized by involuntary movements (**chorea**), cognitive decline, and psychiatric problems. - It is caused by a mutation in the **Huntingtin gene** and has a specific pathological course unrelated to Alzheimer's.

Q: Cushing ulcers are:-

Stress ulcers in head injury. ***Stress ulcers in head injury*** - **Cushing ulcers** are acute **gastric or duodenal ulcers** that develop after a severe **head injury** or other central nervous system trauma. - The pathophysiology involves **vagal overstimulation** due to increased intracranial pressure, leading to hypersecretion of **gastric acid** and reduced mucosal blood flow. *Stress ulcers in hiatus hernia* - A **hiatus hernia** is a condition where part of the stomach protrudes through the diaphragm into the chest cavity, which can predispose to reflux and esophagitis. - While patients with hiatus hernia might develop ulcers, these are not specifically termed Cushing ulcers, and the primary cause is mechanical or reflux-related, not neurological. *Stress ulcers in burns* - **Stress ulcers** that occur in burn patients are known as **Curling ulcers**, not Cushing ulcers. - These are typically caused by **hypovolemia, vasoconstriction**, and **ischemia** of the gastrointestinal mucosa due to significant fluid loss and systemic inflammatory response. *Stress ulcers in depression* - **Depression** is a mood disorder that can influence gastrointestinal function through the **gut-brain axis**, potentially affecting motility and visceral hypersensitivity. - However, depression is not directly associated with the formation of acute stress ulcers like Cushing ulcers, which are primarily linked to severe CNS injury.

Question 1

Foot drop is caused due to injury to which nerve?

Accepted Answer

Common Peroneal Nerve

Answer

Obturator Nerve

Answer

Tibial Nerve

Answer

Femoral Nerve

Question 2

Ammonia causes depletion of which of the following in TCA cycle?

Accepted Answer

Alpha-ketoglutarate

Answer

Malate

Answer

Oxaloacetate

Answer

Fumarate

Question 3

Defect in Menkes disease:

Accepted Answer

ATP7A (Copper-transporting ATPase)

Answer

Prolyl oxidase

Answer

Prolyl hydroxylase

Answer

Lysyl oxidase

Question 4

All of the following are not true with respect to erythema multiforme except?

Accepted Answer

Targetoid lesions are seen

Answer

Most commonly due to leukemia

Answer

Steroids are the drug of choice

Answer

Koebner's phenomenon is seen

Question 5

Which chamber of the heart is enlarged first in a patient with mitral stenosis?

Accepted Answer

Left atrium

Answer

Left ventricle

Answer

Right ventricle

Answer

Right atrium

Question 6

PGF2 alpha maximum dose in PPH management that can be given over 24 hours is:

Accepted Answer

2 mg

Answer

20 mg

Answer

200 mg

Answer

250 mg

Question 7

Agent used for eliciting diagnostic differentiation of Myasthenia Gravis from Cholinergic crisis is:-

Accepted Answer

Edrophonium

Answer

Neostigmine

Answer

Ecothiophate

Answer

Ambenonium

Question 8

Cisatracurium is better than atracurium because:-

Accepted Answer

Less histamine release

Answer

No active metabolites

Answer

Shorter half-life

Answer

Better neuromuscular blockade

Question 9

Risk factors for Alzheimer's include:-

Accepted Answer

Down's syndrome

Answer

Parkinson's disease

Answer

Vascular dementia

Answer

Huntington's disease

Question 10

Cushing ulcers are:-

Accepted Answer

Stress ulcers in head injury

Answer

Stress ulcers in hiatus hernia

Answer

Stress ulcers in burns

Answer

Stress ulcers in depression

NEET-PG 2019

Anatomy

Biochemistry

Dermatology

Internal Medicine

Obstetrics and Gynecology

Pharmacology

Psychiatry

Surgery