NEET-PG 2018 Practice Questions

Q: What type of joint is formed by the costal cartilages of the 8th and 9th ribs?

Interchondral joint. ***Interchondral joint*** - The **8th, 9th, and 10th costal cartilages** articulate with the cartilage immediately above them, forming **interchondral joints**. - These are typically **synovial plane joints** that allow for some gliding movement during respiration. *Costochondral joint* - This joint type is formed between the **rib bone** and its respective **costal cartilage**. - These are **primary cartilaginous joints (synchondroses)** and are generally immobile. *Synovial joint* - While interchondral joints are a type of synovial joint, this option is too general and does not specify the unique anatomical arrangement. - Synovial joints are characterized by a **joint capsule**, **synovial fluid**, and **articular cartilage**, allowing for free movement. *Costovertebral joint* - This joint is formed between the **head of a rib** and the **bodies of two adjacent vertebrae** and their intervertebral disc. - It is a **synovial plane joint** crucial for respiratory mechanics, but not related to the articulation of costal cartilages with each other.

Q: Modified Mallampati grading is used in assessment of -

Difficulty of intubation. ***Difficulty of intubation*** - The **Modified Mallampati score** assesses the visibility of pharyngeal structures, which directly correlates with the ease or difficulty of performing **direct laryngoscopy** and **endotracheal intubation**. - A higher Mallampati class (e.g., III or IV) indicates less visibility of the soft palate, uvula, and pillars, suggesting a more difficult airway and increased likelihood of a challenging intubation. *Obstruction of the airway* - While a high Mallampati score might indirectly indicate potential for **airway obstruction** during anesthesia due to anatomical features, its primary purpose is not to diagnose or quantify existing airway obstruction. - Airway obstruction is more directly assessed by monitoring breathing sounds, respiratory effort, and oxygen saturation. *Aspiration-related death* - The **Mallampati score** helps predict the difficulty of securing the airway but does not directly assess the risk of **aspiration**. - Aspiration risk is evaluated based on factors like gastric contents, gag reflex, and patient positioning. *Endotracheal intubation procedure* - The **Modified Mallampati score** helps in **planning the intubation procedure** by identifying potential difficulties but is not a measure of the intubation procedure itself. - It is a **pre-procedure assessment tool** to gauge airway anatomy, not a description or evaluation of the steps involved in endotracheal intubation.

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: 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 gene is primarily associated with Cowden syndrome?

PTEN. ***PTEN*** - Cowden syndrome is an **autosomal dominant** inherited disorder caused by germline mutations in the **PTEN (phosphatase and tensin homolog) tumor suppressor gene**. - The PTEN gene plays a crucial role in cell growth, proliferation, and apoptosis, and its dysfunction leads to uncontrolled cell growth and the development of multiple **hamartomas** and increased cancer risk. *TP53* - Mutations in the **TP53 gene** are primarily associated with Li-Fraumeni syndrome, a different inherited cancer predisposition syndrome characterized by a high risk of various cancers including sarcomas, breast cancer, and adrenocortical carcinoma. - While both inherited cancer syndromes involve tumor suppressor gene mutations, the specific gene affected and the clinical presentation differ significantly. *RB1* - The **RB1 gene** is a tumor suppressor gene primarily associated with **retinoblastoma**, a rare childhood eye cancer, and an increased risk of other cancers like osteosarcoma. - It plays a critical role in cell cycle regulation, and its mutation leads to uncontrolled cell division in the retina and other tissues. *KRAS* - The **KRAS gene** is an oncogene, not a tumor suppressor gene, and its mutations are frequently found in various sporadic cancers, particularly **colorectal cancer**, pancreatic cancer, and lung cancer. - KRAS mutations lead to constitutive activation of signaling pathways that promote cell growth and survival, but they are not the primary genetic cause of inherited Cowden syndrome.

Q: Which drug decreases the bone resorption in osteoporosis?

Risedronate. ***Risedronate*** - **Risedronate** is a **bisphosphonate**, a class of drugs that inhibits osteoclast activity, thereby decreasing **bone resorption**. - By reducing the rate at which bone is broken down, it helps to preserve **bone mineral density** in patients with osteoporosis. *Teriparatide* - **Teriparatide** is a **parathyroid hormone analog** that primarily works by stimulating **osteoblast activity** to promote new bone formation. - While it treats osteoporosis, its primary mechanism is **anabolic** (bone building), not directly decreasing bone resorption as its main effect. *Cortisone* - **Cortisone** is a **glucocorticoid** that can actually *worsen* osteoporosis by increasing **bone resorption** and decreasing **bone formation** with long-term use. - It is used to treat inflammatory conditions, not to decrease bone resorption for osteoporosis. *Cimetidine* - **Cimetidine** is an **H2-receptor antagonist** used to reduce stomach acid production, commonly for conditions like GERD or ulcers. - It has no known effect on **bone metabolism** or **osteoporosis**.

Q: In hypovolemic shock there is -

Decreased cardiac output. ***Decreased cardiac output*** - **Hypovolemic shock** is fundamentally defined by **decreased circulating blood volume**, which leads to **decreased venous return** to the heart. - According to the **Frank-Starling mechanism**, decreased venous return leads to **decreased preload**, which results in **decreased stroke volume** and consequently **decreased cardiac output**. - This is the **primary hemodynamic characteristic** of hypovolemic shock and is present in ALL cases. - Decreased cardiac output triggers all the compensatory mechanisms seen in hypovolemic shock, including sympathetic activation and RAAS activation. *Afferent arteriolar constriction* - While afferent arteriolar constriction does occur in hypovolemic shock due to **sympathetic activation**, it is a **compensatory response** rather than the primary feature. - The predominant effect at the kidney level is actually a combination of both afferent and efferent arteriolar changes. - This occurs secondary to the decreased cardiac output. *Efferent arteriolar constriction* - **Efferent arteriolar constriction** is mediated primarily by **angiotensin II** and is actually MORE prominent than afferent constriction. - This helps **maintain glomerular filtration rate (GFR)** despite reduced renal blood flow by increasing glomerular hydrostatic pressure. - However, this is also a compensatory response, not the primary feature of hypovolemic shock. *Increased blood flow to kidney* - This is incorrect as hypovolemic shock causes **decreased renal blood flow**. - Blood is redistributed away from the kidneys to vital organs like the heart and brain through compensatory vasoconstriction.

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: What is the cutoff for surgery in an abdominal aortic aneurysm in asymptomatic patients?

5.5cm. ***5.5cm*** - For **asymptomatic patients**, an abdominal aortic aneurysm (AAA) measuring **5.5 cm or larger** is generally considered the threshold for surgical repair. - This cutoff is based on studies showing that the risk of rupture significantly increases beyond this size, outweighing the risks of elective repair. *6.5cm* - While a 6.5 cm AAA would certainly warrant repair, the **standard cutoff for elective repair is 5.5 cm** to prevent rupture. - Delaying repair until this size would expose the patient to an unnecessarily higher risk of complications. *7.5cm* - An aneurysm of 7.5 cm carries a **very high risk of rupture**, making emergency repair almost inevitable if it is not addressed proactively. - This size is well beyond the recommended threshold for elective intervention. *8.5cm* - An 8.5 cm AAA has an **extremely high and imminent risk of rupture**, which would be a life-threatening event. - Surgical intervention would be considered urgent in this scenario, as it is far past the ideal window for elective repair.

Question 1

What type of joint is formed by the costal cartilages of the 8th and 9th ribs?

Accepted Answer

Interchondral joint

Answer

Synovial joint

Answer

Costochondral joint

Answer

Costovertebral joint

Question 2

Modified Mallampati grading is used in assessment of -

Accepted Answer

Difficulty of intubation

Answer

Obstruction of the airway

Answer

Aspiration-related death

Answer

Endotracheal intubation procedure

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

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 6

Which gene is primarily associated with Cowden syndrome?

Accepted Answer

PTEN

Answer

RB1

Answer

KRAS

Answer

TP53

Question 7

Which drug decreases the bone resorption in osteoporosis?

Accepted Answer

Risedronate

Answer

Teriparatide

Answer

Cortisone

Answer

Cimetidine

Question 8

In hypovolemic shock there is -

Accepted Answer

Decreased cardiac output

Answer

Efferent arteriolar constriction

Answer

Increased blood flow to kidney

Answer

Afferent arteriolar constriction

Question 9

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 10

What is the cutoff for surgery in an abdominal aortic aneurysm in asymptomatic patients?

Accepted Answer

5.5cm

Answer

6.5cm

Answer

7.5cm

Answer

8.5cm

NEET-PG 2018

Anatomy

Anesthesiology

Biochemistry

Internal Medicine

Pathology

Pharmacology

Physiology

Surgery