Anatomy
1 questionsLeft-Right movement of skull occurs at:-
NEET-PG 2019 - Anatomy NEET-PG Practice Questions and MCQs
Question 201: Left-Right movement of skull occurs at:-
- A. C6-C7
- B. C2-C3
- C. Atlanto-axial joint (Correct Answer)
- D. Atlanto-occipital joint
Explanation: ***Atlanto-axial joint*** - The **atlanto-axial joint** (between C1 and C2) is primarily responsible for **rotation of the head** (left-right movement), allowing for approximately 50-60 degrees of rotation. - This joint's structure, particularly the **pivot joint** formed by the dens of C2 and the atlas, facilitates this extensive rotational movement. *C6-C7* - The C6-C7 vertebral segment primarily contributes to **flexion, extension**, and some lateral bending of the neck. - It has limited capacity for **rotational movement** compared to the atlanto-axial joint. *C2-C3* - The C2-C3 vertebral segment contributes to general **neck mobility**, including flexion, extension, and lateral bending. - While there is some rotational component, it is significantly **less pronounced** than at the atlanto-axial joint. *Atlanto-occipital joint* - The **atlanto-occipital joint** (between C0 and C1) is primarily responsible for **flexion and extension** of the head, similar to nodding "yes." - It allows for very **limited rotation** of the head.
Anesthesiology
2 questionsWhich of the following anesthetic agent is not painful on intravenous administration?
Drug that does not cause cardiac depression:
NEET-PG 2019 - Anesthesiology NEET-PG Practice Questions and MCQs
Question 201: Which of the following anesthetic agent is not painful on intravenous administration?
- A. Propofol
- B. Etomidate
- C. Ketamine (Correct Answer)
- D. Methohexital
Explanation: ***Ketamine*** - **Ketamine** is known for causing minimal pain on intravenous administration compared to other common induction agents. - Its mechanism of action as an **NMDA receptor antagonist** does not involve irritation of venous endothelium to the same extent as some other anesthetics. *Propofol* - **Propofol** is infamous for causing significant **injection pain** due to its formulation, which contains soybean oil, glycerol, and egg lecithin, acting as a direct irritant to the intima of veins. - The pain is often described as a **burning sensation** and can be severe enough to require pre-treatment with lidocaine. *Etomidate* - **Etomidate**, like propofol, can cause significant pain on injection, although generally less severe than propofol. - The pain is thought to be related to its **propylene glycol vehicle**, which can cause venous irritation. *Methohexital* - **Methohexital**, a barbiturate, is associated with a moderate incidence of **injection site pain and thrombophlebitis**. - Its alkaline pH and direct irritation of the **venous intima** are the primary reasons for patient discomfort during administration.
Question 202: Drug that does not cause cardiac depression:
- A. Thiopentone
- B. Ketamine
- C. Propofol
- D. Etomidate (Correct Answer)
Explanation: ***Etomidate*** - Etomidate is known for its **cardiovascular stability**, making it a preferred induction agent in patients with **compromised cardiac function**. - It maintains **myocardial contractility** and does not typically cause a significant drop in blood pressure. *Thiopentone* - Thiopentone causes **dose-dependent myocardial depression** and peripheral vasodilation. - This can lead to a significant **decrease in blood pressure** and cardiac output, especially in hypovolemic patients. *Propofol* - Propofol is a potent **vasodilator** and can cause significant **myocardial depression**, leading to hypotension. - Its cardiovascular effects are often more pronounced than those of other induction agents, necessitating careful titration. *Ketamine* - Ketamine causes indirect cardiovascular stimulation (due to **sympathetic nervous system activation**), but direct myocardial depression. - While it often increases heart rate and blood pressure, this is a compensatory mechanism and its direct effect on the myocardium is depressant.
Biochemistry
1 questionsType-I hyperlipoproteinemia is caused by deficiency of:-
NEET-PG 2019 - Biochemistry NEET-PG Practice Questions and MCQs
Question 201: Type-I hyperlipoproteinemia is caused by deficiency of:-
- A. Lipoprotein lipase (Correct Answer)
- B. Elevated triglycerides in plasma
- C. Elevated LDL
- D. Elevated cholesterol
Explanation: ***Lipoprotein lipase*** - **Type I hyperlipoproteinemia**, also known as **familial lipoprotein lipase deficiency**, is caused by a genetic defect leading to **deficiency or defect in lipoprotein lipase (LPL)** or its cofactor **apolipoprotein C-II**. - LPL is crucial for the **hydrolysis of triglycerides** in chylomicrons and VLDL at the capillary endothelium. - This enzymatic deficiency leads to **massive accumulation of chylomicrons** and severe hypertriglyceridemia (often >1000 mg/dL). - Clinical features include **eruptive xanthomas, lipemia retinalis, hepatosplenomegaly**, and **recurrent pancreatitis**. *Elevated triglycerides in plasma* - This is indeed the **most prominent laboratory finding** in Type I hyperlipoproteinemia, with triglyceride levels often exceeding 1000-2000 mg/dL. - However, this is the **consequence/manifestation** of the LPL deficiency, not the underlying cause. - The question asks what causes Type I hyperlipoproteinemia, which is the enzyme deficiency itself. *Elevated LDL* - Type I hyperlipoproteinemia typically has **normal or even reduced LDL levels**. - **Elevated LDL** is characteristic of **Type IIa hyperlipoproteinemia (familial hypercholesterolemia)**, which involves defects in LDL receptor or ApoB-100. - Type I primarily affects **chylomicron metabolism**, not LDL. *Elevated cholesterol* - Cholesterol levels are typically **normal or only mildly elevated** in Type I hyperlipoproteinemia. - The triglyceride elevation is disproportionately massive compared to any cholesterol elevation. - Significant isolated cholesterol elevation points to Type IIa or IIb dyslipidemias.
Community Medicine
2 questionsFor the population of 10,000, how much area is required per year for a trench method sanitary landfill pit of 2m depth?
Which vaccine requires annual updates due to frequent antigenic changes?
NEET-PG 2019 - Community Medicine NEET-PG Practice Questions and MCQs
Question 201: For the population of 10,000, how much area is required per year for a trench method sanitary landfill pit of 2m depth?
- A. 3 acres
- B. 4 acres
- C. 2 acres
- D. 1 acre (Correct Answer)
Explanation: ***1 acre*** - For a **trench method sanitary landfill** with a 2m depth, the required area per year for a population of 10,000 is approximately **1 acre**. - This estimation accounts for the typical volume of solid waste generated by this population size and the compaction achieved in well-managed landfills. *3 acres* - An area of **3 acres** would be significantly larger than typically required for a population of 10,000 for a 2m deep trench landfill. - This might be needed for a much larger population, less compaction, or a shallower landfill depth. *4 acres* - **4 acres** is an excessive amount of land for the stated population and landfill depth, suggesting inefficiency or a miscalculation in waste volume or density. - Such a large area would likely imply either very low waste compaction or a much larger population than specified. *2 acres* - While closer than 3 or 4 acres, **2 acres** is still generally more than what is needed for a 10,000 population with a 2m deep trench landfill. - This could be considered if the waste generation rate is higher than average or if compaction is less efficient.
Question 202: Which vaccine requires annual updates due to frequent antigenic changes?
- A. Measles
- B. Rubella
- C. Influenza (Correct Answer)
- D. BCG
Explanation: ***Influenza*** - The influenza virus undergoes frequent **antigenic drift** and **antigenic shift**, which are changes in its surface proteins (hemagglutinin and neuraminidase). - These constant changes necessitate annual updates to the influenza vaccine to match the circulating strains predicted for the upcoming flu season. *Measles* - The measles virus is **antigenically stable**, meaning it does not frequently change its surface proteins. - Due to its stability, a highly effective and long-lasting vaccine can be produced, and annual updates are not required. *Rubella* - The rubella virus is also **antigenically stable**, similar to measles. - A single vaccine, usually given as part of the MMR (Measles, Mumps, Rubella) vaccine, provides long-term immunity without the need for annual revision. *BCG* - The Bacillus Calmette-Guérin (BCG) vaccine targets *Mycobacterium tuberculosis* and is not subject to frequent antigenic changes. - It is a live-attenuated vaccine that provides long-lasting immunity, and annual boosters or updates are not necessary.
Internal Medicine
1 questionsA patient with rheumatoid arthritis on Methotrexate, steroids and NSAIDs for past 4 months has had no retardation of disease progression. What is the next rational step in management?
NEET-PG 2019 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 201: A patient with rheumatoid arthritis on Methotrexate, steroids and NSAIDs for past 4 months has had no retardation of disease progression. What is the next rational step in management?
- A. Continue Methotrexate and steroids at higher dose
- B. Stop oral Methotrexate and start parenteral Methotrexate
- C. Add Sulfasalazine (Correct Answer)
- D. Start treatment with anti-TNF alpha drugs
Explanation: Focus on **Add Sulfasalazine**: - Since the patient has not responded to **Methotrexate** alone, adding a second conventional synthetic **disease-modifying antirheumatic drug (DMARD)** like **Sulfasalazine** is a common and appropriate step in a **treat-to-target strategy** for rheumatoid arthritis [1]. - This approach aims to achieve **disease remission** or **low disease activity** by combining therapies to enhance efficacy. *Continue Methotrexate and steroids at higher dose* - Increasing the dose of **Methotrexate** might be considered if the current dose is sub-optimal, but after 4 months with no improvement, simply continuing current medications at higher doses without adding another agent is less likely to significantly alter **disease progression** [1]. - Prolonged higher-dose **steroids** carry significant risks and are generally used for symptom control, not primary disease modification. *Stop oral Methotrexate and start parenteral Methotrexate* - Switching to **parenteral Methotrexate** is considered if **oral Methotrexate** absorption is an issue or if the patient experiences gastrointestinal side effects [1]. - While parenteral administration can improve bioavailability, it doesn't represent a change in therapeutic strategy for **uncontrolled disease activity**. *Start treatment with anti-TNF alpha drugs* - **Biologic DMARDs** like **anti-TNF alpha drugs** are typically reserved for patients who have failed **two or more conventional synthetic DMARDs**, including **Methotrexate**, or in cases of severe, rapidly progressing disease [2]. - While effective, they are more expensive and have different side effect profiles, making them a later-line treatment in the management algorithm [2].
Pathology
1 questionsGlanzmann thrombasthenia is due to defect in:-
NEET-PG 2019 - Pathology NEET-PG Practice Questions and MCQs
Question 201: Glanzmann thrombasthenia is due to defect in:-
- A. Gp VI
- B. Thromboxane A2
- C. Gp Ia/IIa
- D. Gp IIb/IIIa (Correct Answer)
Explanation: ***Gp IIb/IIIa*** - Glanzmann thrombasthenia is a **rare, inherited bleeding disorder** characterized by a defect or deficiency in the **glycoprotein IIb/IIIa (Gp IIb/IIIa) complex** on the platelet surface [1]. - This complex is crucial for platelet aggregation as it acts as the receptor for **fibrinogen**, which links activated platelets together [1]. *Gp VI* - **Glycoprotein VI (Gp VI)** is a collagen receptor on platelets, important for initial **platelet adhesion and activation** at sites of vascular injury. - Defects in Gp VI are associated with milder bleeding disorders, not Glanzmann thrombasthenia. *Thromboxane A2* - **Thromboxane A2 (TXA2)** is a potent **vasoconstrictor** and **platelet aggregator** synthesized by platelets. - Disorders in TXA2 synthesis or response, such as aspirin-induced platelet dysfunction, cause bleeding but are biochemically distinct from Glanzmann thrombasthenia. *Gp Ia/IIa* - The **glycoprotein Ia/IIa (Gp Ia/IIa) complex** (also known as integrin ̡2̢1) is another **collagen receptor** on platelets, mediating platelet adhesion to collagen. - Defects in Gp Ia/IIa lead to a different type of mild bleeding disorder, affecting initial adhesion rather than aggregation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 668-669.
Pharmacology
1 questionsHypertension and pulmonary edema associated with scorpion sting is managed by :-
NEET-PG 2019 - Pharmacology NEET-PG Practice Questions and MCQs
Question 201: Hypertension and pulmonary edema associated with scorpion sting is managed by :-
- A. Prazosin (Correct Answer)
- B. Phentolamine
- C. Spironolactone
- D. Carvedilol
Explanation: ***Prazosin*** - **Prazosin** is an **alpha-1 adrenergic receptor blocker** that causes vasodilation, reducing both preload and afterload, which is crucial in managing scorpion sting-induced **hypertension** and **pulmonary edema** [1]. - It effectively counteracts the massive catecholamine release triggered by scorpion venom, which leads to widespread vasoconstriction and increased cardiac workload [1]. *Phentolamine* - **Phentolamine** is a non-selective alpha-adrenergic blocker, but it has a shorter duration of action and is typically used for managing **hypertensive crises** during pheochromocytoma surgery. - While it can lower blood pressure, its rapid onset and short half-life make it less suitable for sustained management of scorpion sting complications compared to prazosin. *Spironolactone* - **Spironolactone** is an **aldosterone antagonist** and a potassium-sparing diuretic, primarily used in conditions like heart failure, cirrhosis, and primary hyperaldosteronism. - It is not an acute treatment for hypertension or pulmonary edema caused by scorpion venom, as its mechanism of action is too slow and indirect to counteract the immediate effects of catecholamine surge. *Carvedilol* - **Carvedilol** is a non-selective beta-blocker with alpha-1 blocking activity, commonly used in chronic heart failure and hypertension [2]. - While it has some alpha-blocking properties, its dominant **beta-blocking effects** can exacerbate pulmonary edema in an acute setting and may worsen cardiac output if bradycardia or myocardial depression occurs [2].
Radiology
1 questionsGas absent from intestine (gasless abdomen) on x-ray is seen in which condition?
NEET-PG 2019 - Radiology NEET-PG Practice Questions and MCQs
Question 201: Gas absent from intestine (gasless abdomen) on x-ray is seen in which condition?
- A. Ulcerative colitis
- B. Intussusception
- C. Acute pancreatitis (Correct Answer)
- D. Necrotizing enterocolitis
Explanation: ***Acute pancreatitis*** - In **severe acute pancreatitis**, a **gasless or relatively gasless abdomen** may be seen due to profound **ileus** with fluid accumulation displacing intestinal gas. - The marked inflammatory process can lead to complete loss of intestinal motility and fluid sequestration (third-spacing), resulting in minimal visible bowel gas on X-ray. - **Note**: Classic signs include **sentinel loop sign** (dilated jejunal loop) or **colon cut-off sign**, but in severe cases with massive ascites or fluid collections, a gasless pattern may occur. *Ulcerative colitis* - Typically presents with **dilated loops of large bowel** with visible gas and **toxic megacolon** in severe cases. - Inflammatory changes cause bowel wall thickening, but gas is usually **present and often increased**. *Intussusception* - May show a **target sign** or **meniscus sign** on imaging, with bowel loops dilated proximal to the obstruction. - Gas is typically **present** within the bowel or proximal to the invagination, not absent from the entire abdomen. *Necrotizing enterocolitis* - Characterized by **pneumatosis intestinalis** (gas in the bowel wall) and **portal venous gas**, features directly contradicting a gasless abdomen. - Shows dilated loops with gas and evidence of bowel wall necrosis - **gas is prominently present**.