Anatomy
1 questionsWhat type of joint is formed by the costal cartilages of the 8th and 9th ribs?
NEET-PG 2018 - Anatomy NEET-PG Practice Questions and MCQs
Question 61: What type of joint is formed by the costal cartilages of the 8th and 9th ribs?
- A. Synovial joint
- B. Costochondral joint
- C. Costovertebral joint
- D. Interchondral joint (Correct Answer)
Explanation: ***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.
Anesthesiology
1 questionsModified Mallampati grading is used in assessment of -
NEET-PG 2018 - Anesthesiology NEET-PG Practice Questions and MCQs
Question 61: Modified Mallampati grading is used in assessment of -
- A. Difficulty of intubation (Correct Answer)
- B. Obstruction of the airway
- C. Aspiration-related death
- D. Endotracheal intubation procedure
Explanation: ***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.
Biochemistry
2 questionsWhich enzyme deficiency causes Lesch-Nyhan syndrome?
Trilene is degraded by:
NEET-PG 2018 - Biochemistry NEET-PG Practice Questions and MCQs
Question 61: Which enzyme deficiency causes Lesch-Nyhan syndrome?
- A. Hypoxanthine-guanine phosphoribosyltransferase (HGPRT) (Correct Answer)
- B. Xanthine oxidase
- C. Adenine phosphoribosyltransferase (APRT)
- D. AMP deaminase
Explanation: ***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.
Question 62: Trilene is degraded by:
- A. Glutathione conjugation
- B. Cytochrome P450 oxidation (Correct Answer)
- C. Direct renal excretion
- D. Acetylation
Explanation: ***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
Internal Medicine
1 questionsWhich of the following is a cause of hypokalemic metabolic alkalosis with hypertension?
NEET-PG 2018 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 61: Which of the following is a cause of hypokalemic metabolic alkalosis with hypertension?
- A. Liddle syndrome (Correct Answer)
- B. Bartter syndrome
- C. Gitelman syndrome
- D. Renal tubular acidosis
Explanation: ***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]
Pathology
1 questionsWhich gene is primarily associated with Cowden syndrome?
NEET-PG 2018 - Pathology NEET-PG Practice Questions and MCQs
Question 61: Which gene is primarily associated with Cowden syndrome?
- A. PTEN (Correct Answer)
- B. RB1
- C. KRAS
- D. TP53
Explanation: ***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.
Pharmacology
1 questionsWhich drug decreases the bone resorption in osteoporosis?
NEET-PG 2018 - Pharmacology NEET-PG Practice Questions and MCQs
Question 61: Which drug decreases the bone resorption in osteoporosis?
- A. Teriparatide
- B. Risedronate (Correct Answer)
- C. Cortisone
- D. Cimetidine
Explanation: ***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**.
Physiology
1 questionsIn hypovolemic shock there is -
NEET-PG 2018 - Physiology NEET-PG Practice Questions and MCQs
Question 61: In hypovolemic shock there is -
- A. Efferent arteriolar constriction
- B. Increased blood flow to kidney
- C. Decreased cardiac output (Correct Answer)
- D. Afferent arteriolar constriction
Explanation: ***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.
Surgery
2 questionsWhere will be the placement location for Auditory Brainstem Implant?
What is the cutoff for surgery in an abdominal aortic aneurysm in asymptomatic patients?
NEET-PG 2018 - Surgery NEET-PG Practice Questions and MCQs
Question 61: Where will be the placement location for Auditory Brainstem Implant?
- A. Scala tympani
- B. Recess of 4th ventricle (Correct Answer)
- C. IAC
- D. Back of ear
Explanation: ***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.
Question 62: What is the cutoff for surgery in an abdominal aortic aneurysm in asymptomatic patients?
- A. 5.5cm (Correct Answer)
- B. 6.5cm
- C. 7.5cm
- D. 8.5cm
Explanation: ***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.