NEET-PG 2018 Practice Questions

Q: What is the primary tensor of the vocal cords?

Cricothyroid. ***Cricothyroid*** - The **cricothyroid muscle** is the principal tensor of the vocal cords, responsible for stretching and thinning them. - It achieves this by tilting the **thyroid cartilage** forward relative to the **cricoid cartilage**, increasing the distance between the **thyroid** and **arytenoid cartilages**. *Lateral Cricoarytenoid* - This muscle primarily functions as an **adductor** of the vocal cords, bringing them together. - It rotates the **arytenoid cartilages** medially, closing the **rima glottidis**. *Thyroarytenoids* - The **thyroarytenoid muscles** are located within the vocal cords and primarily act to **shorten and relax** the vocal cords. - They also contribute to **adduction** and can internally tense the vocal folds, but their main role is *not* primary tension. *Posterior cricoarytenoids* - The **posterior cricoarytenoid muscles** are the *only* muscles responsible for **abducting** (opening) the vocal cords. - They rotate the **arytenoid cartilages** laterally, thus widening the **rima glottidis**.

Q: Ureteric bud develops from:

Mesonephros. ***Mesonephros*** - The **ureteric bud** arises as an outgrowth of the **mesonephric duct** (Wolffian duct), which is the duct of the mesonephros. - The ureteric bud emerges from the **caudal portion of the mesonephric duct** near its entry into the cloaca around the 5th week of development. - It plays a crucial role in forming the **collecting system of the kidney**, including the ureter, renal pelvis, major and minor calyces, and collecting ducts. - **Note:** While technically the ureteric bud arises from the mesonephric duct (not the mesonephric tubules), "mesonephros" is accepted as the answer referring to the mesonephric duct system. *Metanephros* - The **metanephric mesoderm** (metanephric blastema) is induced by the ureteric bud to form the **definitive kidney**. - The metanephros forms the **nephrons** (from Bowman's capsule to distal convoluted tubule). - It does not give rise to the ureteric bud; rather, it interacts with it through **reciprocal induction**. *Pronephros* - The **pronephros** is the first, transient, and **non-functional** kidney structure in human embryonic development. - It appears in the **cervical region** around week 4 and completely **regresses** by week 5. - It does not contribute to the formation of the ureteric bud or the adult kidney. *Genital sinus* - The **urogenital sinus** is derived from the ventral part of the cloaca after division by the urorectal septum. - It gives rise to the **bladder**, parts of the urethra, and contributes to external genitalia. - It is not involved in the development of the ureteric bud or the kidney's collecting system.

Q: Which enzyme deficiency causes Lesch-Nyhan syndrome?

Hypoxanthine-guanine phosphoribosyltransferase (HGPRT). ***Hypoxanthine-guanine phosphoribosyltransferase (HGPRT)*** - **Lesch-Nyhan syndrome** is an X-linked recessive disorder caused by a severe deficiency of the enzyme **HGPRT**. - This deficiency leads to a buildup of **uric acid** due to impaired purine salvage, as well as neurologic dysfunction and self-mutilation. *Xanthine oxidase deficiency* - This deficiency leads to **xanthinuria**, characterized by high levels of xanthine in the urine, which can cause **kidney stones**. - It does not cause the severe neurological and behavioral symptoms seen in Lesch-Nyhan syndrome. *Adenine phosphoribosyltransferase (APRT) deficiency* - Deficiency of **APRT** causes a rare disorder resulting in the overproduction of **2,8-dihydroxyadenine**, which can form renal stones. - While it is involved in purine metabolism, it does not lead to the specific clinical presentation of Lesch-Nyhan syndrome. *AMP deaminase deficiency* - **AMP deaminase deficiency** is a relatively common enzyme defect that can cause exercise-induced myalgia or fatigue. - It affects muscle function and energy metabolism but is not associated with the severe hyperuricemia and neurobehavioral symptoms of Lesch-Nyhan syndrome.

Q: Trilene is degraded by:

Cytochrome P450 oxidation. ***Cytochrome P450 oxidation*** - **Trichloroethylene (Trilene)** was historically used as an inhalational anesthetic and industrial solvent - In humans, it undergoes **hepatic metabolism primarily through cytochrome P450 enzymes**, particularly **CYP2E1** - The oxidation pathway produces metabolites including **chloral hydrate, trichloroethanol, and trichloroacetic acid** - This is a classic example of **Phase I detoxification** involving oxidative biotransformation - The metabolites are then conjugated (Phase II) or excreted renally *Glutathione conjugation* - While some chlorinated compounds undergo glutathione conjugation as a Phase II reaction - For trichloroethylene, **oxidation by CYP450 is the primary metabolic pathway**, not direct glutathione conjugation - GSH conjugation may occur with some metabolites but is not the main degradation route *Direct renal excretion* - Trilene is **lipophilic** and requires hepatic metabolism before elimination - Direct renal excretion without biotransformation is **minimal** - Metabolites (after oxidation) are excreted via kidneys *Acetylation* - **Acetylation** is a Phase II conjugation reaction typically for compounds with **amino or sulfonamide groups** - Trichloroethylene lacks the appropriate functional groups for acetylation - This pathway is **not involved** in Trilene metabolism

Q: According to WHO classification, severe thinness is defined as a BMI below which value?

< 16. ***Correct: < 16 kg/m²*** - The WHO classifies **BMI < 16 kg/m²** as **severe thinness (Grade 3 thinness)** - This represents critically low body weight with significant health risks - Values like 12, 13, 14, or 15 all fall into this severe thinness category *18* - BMI **18.5-24.9 kg/m²** is classified as **normal/healthy weight** by WHO - BMI **17.0-18.49 kg/m²** is classified as **mild thinness (Grade 1)** - 18 is not the threshold for severe thinness *14* - 14 kg/m² is **an example of a value** that falls within severe thinness - However, the question asks for the **threshold/cutoff value**, which is **16 kg/m²** - Any BMI below 16 (including 14, 13, 12) indicates severe thinness *13* - Like option 14, this is **a value within** the severe thinness range - The **defining threshold** is **< 16 kg/m²**, not 13 - The question asks for the classification cutoff, not an example value within the range

Q: Where will be the placement location for Auditory Brainstem Implant?

Recess of 4th ventricle. ***Recess of 4th ventricle*** - An **Auditory Brainstem Implant (ABI)** is placed on the **cochlear nucleus** in the brainstem, which is anatomically located near the **lateral recess of the fourth ventricle**. - The implant stimulates these nuclei directly, bypassing the damaged auditory nerve in patients who cannot benefit from cochlear implants. *Scala tympani* - The **scala tympani** is the location for electrode placement in a **cochlear implant**, not an auditory brainstem implant. - Cochlear implants stimulate the intact auditory nerve within the cochlea. *IAC* - The **internal auditory canal (IAC)** houses the auditory and facial nerves, but it is not the target site for an ABI. - The ABI is designed for patients whose auditory nerve (which passes through the IAC) is non-functional. *Back of ear* - The "back of the ear" is the general area where the **external processor of a cochlear implant** or a **bone-anchored hearing aid** is typically worn, not the surgical placement site for an ABI. - The ABI's internal component is surgically placed within the cranium.

Q: Which of the following is a cause of hypokalemic metabolic alkalosis with hypertension?

Liddle syndrome. ***Liddle syndrome*** - It is an **autosomal dominant** disorder characterized by a mutation in the **ENaC channel**, leading to increased sodium reabsorption and potassium excretion, thus causing **hypokalemia**, **metabolic alkalosis**, and **hypertension**. [1] - This condition mimics **primary hyperaldosteronism** but has **low plasma renin activity** and **low aldosterone levels**. [1] *Bartter syndrome* - This is a genetic disorder affecting the **Na-K-2Cl cotransporter** in the **thick ascending limb** of the loop of Henle, leading to **salt wasting** and compensatory **renin-angiotensin-aldosterone system activation**. - It presents with **hypokalemia**, **metabolic alkalosis**, but typically with **normal or low blood pressure**, not hypertension. *Gitelman syndrome* - This is an autosomal recessive disorder affecting the **thiazide-sensitive Na-Cl cotransporter** in the **distal convoluted tubule**. - It causes **hypokalemic metabolic alkalosis**, hypomagnesemia, and hypocalciuria, but patients are typically **normotensive** or **hypotensive**, distinguishing it from Liddle syndrome. *Renal tubular acidosis* - This is a group of disorders characterized by the **kidneys' inability to excrete acid** or **reabsorb bicarbonate**, leading to **metabolic acidosis**. [2] - While it can cause electrolyte abnormalities, hypokalemia is a feature of certain types (e.g., RTA type 1 and 2), but the defining feature is **metabolic acidosis**, not metabolic alkalosis, and it is not typically associated with hypertension from the primary tubular defect. [2]

Q: Which condition is associated with congenital adrenal hyperplasia?

Female pseudohermaphroditism. ***Female pseudohermaphroditism*** - In **21-hydroxylase deficiency**, the most common form of CAH, virilization of a female fetus occurs due to excessive **androgen production** [2], [3]. - This leads to ambiguous genitalia in genetically female (XX) infants, presenting as **female pseudohermaphroditism** [2]. *Male pseudohermaphroditism* - This condition occurs when a **genetically male individual (XY)** has external genitalia that are undervirilized or ambiguous. - It is typically caused by inadequate **androgen synthesis** or action, such as in **androgen insensitivity syndrome**, which is not the primary presentation of CAH [2]. *True pseudohermaphroditism* - This term refers to individuals who possess both **ovarian and testicular tissue**, either in separate gonads or as ovotestes [1], [2]. - It is distinct from CAH, where gonadal tissue is uniform (either ovaries or testes), but the external genitalia are ambiguous due to hormonal imbalances [2]. *Sequential pseudohermaphroditism* - This term is not a recognized medical classification for conditions like CAH. - It does not describe a specific developmental anomaly of the reproductive system related to adrenal function.

Q: What is mechanism of action of colchicine in acute gout?

Inhibition of leukocyte migration and microtubule function. ***Inhibition of leukocyte migration and microtubule function*** - Colchicine works by disrupting **microtubule polymerization**, which interferes with the **motility and activity of neutrophils and other inflammatory cells** [1]. - Its anti-inflammatory effect in acute gout is primarily due to the inhibition of **leukocyte migration and phagocytosis of urate crystals**, thereby reducing the inflammatory response [1]. - The mechanism involves binding to **tubulin**, preventing microtubule assembly, which affects multiple cellular processes including chemotaxis and cell division [1]. *Inhibition of purine metabolism* - This mechanism is associated with drugs like **allopurinol**, which inhibit **xanthine oxidase** to reduce uric acid production [2]. - Colchicine does not directly inhibit **purine metabolism** or uric acid synthesis; its effect is on the inflammatory response, not uric acid formation [1]. *Inhibition of uric acid conversion* - This mechanism refers to **uricosuric agents** like probenecid that increase renal excretion of uric acid. - Colchicine's action is primarily anti-inflammatory, not related to uric acid metabolism or excretion [1]. *Migration of leukocytes* - While this is partially correct, as colchicine does inhibit **leukocyte migration**, this option is incomplete. - The complete mechanism must include its action as a **microtubule inhibitor**, which is the underlying basis for all its cellular effects including inhibition of migration, phagocytosis, and inflammatory mediator release [1].

Q: Which of the following is the preferred graft material for femoropopliteal bypass?

Reversed saphenous. ***Reversed saphenous*** - The **autologous reversed saphenous vein** is considered the **gold standard** for femoropopliteal bypass due to its superior patency rates and resistance to infection. - The vein's valves are bypassed by reversing its orientation, ensuring unidirectional blood flow. *Dacron* - **Dacron (polyethylene terephthalate)** grafts are synthetic and commonly used for large-diameter arterial bypasses, such as in the aorta, but have **inferior patency in infrainguinal bypasses** compared to autologous vein. - **Higher rates of thrombosis and infection** are observed with Dacron in smaller leg vessels due to compliance mismatch and increased anastomotic intimal hyperplasia. *PTFE* - **Polytetrafluoroethylene (PTFE)** grafts are synthetic and are an option when autologous vein is unavailable, particularly for above-knee femoropopliteal bypasses. - However, PTFE generally has **lower long-term patency rates** and a higher risk of complications like **graft thrombosis and infection** compared to autologous vein grafts. *None of the options* - This option is incorrect because the **reversed saphenous vein** is indeed a preferred and highly effective graft material for femoropopliteal bypass. - The clinical evidence strongly supports its use over synthetic alternatives when available.

Question 1

What is the primary tensor of the vocal cords?

Accepted Answer

Cricothyroid

Answer

Lateral Cricoarytenoid

Answer

Thyroarytenoids

Answer

Posterior cricoarytenoids

Question 2

Ureteric bud develops from:

Accepted Answer

Mesonephros

Answer

Metanephros

Answer

Pronephros

Answer

Genital sinus

Question 3

Which enzyme deficiency causes Lesch-Nyhan syndrome?

Accepted Answer

Hypoxanthine-guanine phosphoribosyltransferase (HGPRT)

Answer

Xanthine oxidase

Answer

Adenine phosphoribosyltransferase (APRT)

Answer

AMP deaminase

Question 4

Trilene is degraded by:

Accepted Answer

Cytochrome P450 oxidation

Answer

Glutathione conjugation

Answer

Direct renal excretion

Answer

Acetylation

Question 5

According to WHO classification, severe thinness is defined as a BMI below which value?

Accepted Answer

< 16

Answer

18

Answer

14

Answer

13

Question 6

Where will be the placement location for Auditory Brainstem Implant?

Accepted Answer

Recess of 4th ventricle

Answer

Scala tympani

Answer

IAC

Answer

Back of ear

Question 7

Which of the following is a cause of hypokalemic metabolic alkalosis with hypertension?

Accepted Answer

Liddle syndrome

Answer

Bartter syndrome

Answer

Gitelman syndrome

Answer

Renal tubular acidosis

Question 8

Which condition is associated with congenital adrenal hyperplasia?

Accepted Answer

Female pseudohermaphroditism

Answer

Male pseudohermaphroditism

Answer

True pseudohermaphroditism

Answer

Sequential pseudohermaphroditism

Question 9

What is mechanism of action of colchicine in acute gout?

Accepted Answer

Inhibition of leukocyte migration and microtubule function

Answer

Inhibition of purine metabolism

Answer

Inhibition of uric acid conversion

Answer

Migration of leukocytes

Question 10

Which of the following is the preferred graft material for femoropopliteal bypass?

Accepted Answer

Reversed saphenous

Answer

PTFE

Answer

Dacron

Answer

None of the options

NEET-PG 2018

Anatomy

Biochemistry

Community Medicine

ENT

Internal Medicine

Pediatrics

Pharmacology

Surgery