Anatomy
1 questionsNerves of pharyngeal arch develop from
NEET-PG 2018 - Anatomy NEET-PG Practice Questions and MCQs
Question 171: Nerves of pharyngeal arch develop from
- A. Mesoderm
- B. Neural crest cells (Correct Answer)
- C. Neuroectoderm
- D. Ectoderm
Explanation: ***Neural crest cells*** - **Neural crest cells** are a multipotent, migratory population of cells that arise from the dorsal part of the neural tube and contribute to a wide array of tissues, including the nerves of the pharyngeal arches (clefts). [1] - They give rise to components of the peripheral nervous system, including **sensory ganglia**, autonomic ganglia, and some cranial nerves associated with the pharyngeal arches. [2] *Mesoderm* - **Mesoderm** is one of the three primary germ layers that forms during early embryonic development. - It primarily gives rise to muscle, bone, connective tissue, and the circulatory system, but not the nerves of the pharyngeal structures. *Neuroectoderm* - **Neuroectoderm** refers to the part of the ectoderm that gives rise to the nervous system, but specifically it differentiates into the neural tube and neural crest. - While neural crest cells originate from neuroectoderm, the direct derivative for the pharyngeal nerves are the **neural crest cells** themselves after migration. *Ectoderm* - The **ectoderm** is the outermost of the three germ layers and gives rise to the epidermis, hair, nails, and the nervous system. - While the nervous system originates from ectoderm, the specific cell type for pharyngeal arch nerves is the **neural crest**, which is a specialized derivative of the ectoderm.
ENT
1 questionsWhich of the following is true regarding Singer's nodule?
NEET-PG 2018 - ENT NEET-PG Practice Questions and MCQs
Question 171: Which of the following is true regarding Singer's nodule?
- A. Laser therapy is treatment of choice
- B. It occurs at junction of anterior 1/3rd and posterior 2/3rd (Correct Answer)
- C. Requires excision as its potentially malignant
- D. Most common symptom is pain
Explanation: ***Correct: It occurs at junction of anterior 1/3rd and posterior 2/3rd*** **Singer's nodules**, also known as **vocal cord nodules**, are typically found at the junction of the **anterior one-third and posterior two-thirds** of the true vocal cords. This area experiences the most vibratory stress and contact during phonation, making it prone to trauma from vocal abuse, leading to the formation of bilateral benign lesions. *Incorrect: Laser therapy is treatment of choice* **Voice therapy** is the **first-line treatment** for Singer's nodules, aiming to modify vocal behaviors and reduce vocal strain. **Surgery**, including laser therapy or microlaryngeal excision, is reserved for cases that do not respond to conservative voice therapy and when nodules significantly impair vocal function. *Incorrect: Requires excision as its potentially malignant* Singer's nodules are **benign lesions** with no malignant potential. They are not considered premalignant and do not undergo malignant transformation. Surgical excision is considered only if voice therapy fails after adequate trial and the nodules continue to cause significant dysphonia. *Incorrect: Most common symptom is pain* The most common symptom associated with Singer's nodules is **hoarseness** or **dysphonia** (altered voice quality). The voice may sound breathy, rough, or strained. **Pain is generally not a prominent symptom** of vocal cord nodules, which helps differentiate them from other laryngeal pathologies like laryngitis or vocal cord polyps with inflammation.
Internal Medicine
2 questionsStunning of myocardium without any acute coronary syndrome is:-
Mean transformation time for HIV to AIDS is:-
NEET-PG 2018 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 171: Stunning of myocardium without any acute coronary syndrome is:-
- A. Restrictive cardiomyopathy
- B. Subendocardial infarction
- C. Transmural infarction
- D. Takotsubo cardiomyopathy (Correct Answer)
Explanation: ***Takotsubo cardiomyopathy*** - This condition involves **transient systolic dysfunction** of the left ventricle, often triggered by severe emotional or physical stress, mimicking a heart attack but without **coronary artery obstruction**. - The apical and mid-ventricular segments of the left ventricle become akinetic or hypocinetic, causing the heart to take on a shape resembling an octopus trap (**takotsubo**). *Restrictive cardiomyopathy* - This is a condition where the walls of the ventricles become **stiff** and **lose their flexibility**, preventing the heart from filling properly. - It is typically caused by conditions like **amyloidosis** or **sarcoidosis**, leading to impaired diastolic function, not transient stunning. *Subendocardial infarction* - This refers to a **heart attack** that affects only the **inner layer** of the heart muscle (**subendocardium**) due to reduced blood flow [2]. - It is a form of **acute coronary syndrome** where there is irreversible myocardial necrosis, unlike the temporary dysfunction in stunning [1]. *Transmural infarction* - This is a **severe form of heart attack** where the entire thickness of the heart muscle wall is affected, usually due to a **complete blockage of a coronary artery** [2]. - This also represents **acute coronary syndrome** with widespread myocardial necrosis, which is fundamentally different from a reversible stunning of the myocardium [1].
Question 172: Mean transformation time for HIV to AIDS is:-
- A. 12 years
- B. 9 years
- C. 5 years
- D. 10 years (Correct Answer)
Explanation: ***10 years*** - The mean transformation time from initial **HIV infection** to the development of **AIDS** in untreated individuals is approximately 10 years [1]. - This time frame represents the average duration of the **clinical latency period**, during which the viral load increases and CD4+ T-cell count gradually declines [1]. *12 years* - While some individuals may progress to AIDS later than 10 years, 12 years is not recognized as the **mean transformation time**. - This longer period might be seen in individuals with slower disease progression or those initiating **antiretroviral therapy (ART)** at later stages. *9 years* - This duration is slightly shorter than the generally accepted mean, though some individuals may progress more rapidly. - Factors like **higher viral load** at infection, coinfections, or certain genetic predispositions can accelerate progression. *5 years* - A transformation time of 5 years is considered a **rapid progression** to AIDS. - This rapid progression is typically seen in a minority of HIV-infected individuals, often associated with factors such as high baseline viral load, genetic susceptibility, or co-infection with other pathogens.
Obstetrics and Gynecology
1 questionsWhich of the following is the most common cause of perforation of uterus in non-pregnant state?
NEET-PG 2018 - Obstetrics and Gynecology NEET-PG Practice Questions and MCQs
Question 171: Which of the following is the most common cause of perforation of uterus in non-pregnant state?
- A. Dilatation and curettage (Correct Answer)
- B. Laparoscopy
- C. IUCD
- D. Carcinoma Endometrium
Explanation: ***Dilatation and curettage*** - **Dilatation and curettage (D&C)** is the most frequent iatrogenic cause of uterine perforation in the non-pregnant state due to the blind nature of the procedure, especially in cases of uterine anatomical variations or reduced uterine wall integrity. - The risk of perforation is higher in postmenopausal women due to **atrophic, thinned uterine walls**, and in procedures performed for conditions like endometrial hyperplasia or polyps. *Laparoscopy* - While laparoscopic procedures involve inserting instruments into the abdomen, **uterine perforation during laparoscopy itself is rare**, as it usually involves instrumentation *outside* the uterus unless direct uterine manipulation or hysteroscopy is part of the procedure. - Laparoscopy more commonly results in complications like bowel or vascular injury due to trocar insertion, rather than uterine perforation. *IUCD* - **Intrauterine contraceptive device (IUCD)** insertion can cause uterine perforation, but it is less common than with D&C, with an estimated incidence of 1-2 per 1000 insertions. - Perforation during IUCD insertion is typically an immediate event, whereas D&C-related perforations can occur at any stage of the curettage. *Carcinoma Endometrium* - **Endometrial carcinoma** does not typically cause spontaneous uterine perforation, though it can weaken the uterine wall, making it more susceptible to perforation during diagnostic or therapeutic procedures like D&C. - Perforation directly attributable to the carcinoma itself without instrumental intervention is exceedingly rare.
Pathology
1 questionsWhich of the following is the most important infiltrate in rheumatoid arthritis?
NEET-PG 2018 - Pathology NEET-PG Practice Questions and MCQs
Question 171: Which of the following is the most important infiltrate in rheumatoid arthritis?
- A. Dendritic cells
- B. CD4+ Helper cells
- C. Macrophages (Correct Answer)
- D. Neutrophils
Explanation: ***Macrophages*** - **Macrophages** are crucial in rheumatoid arthritis synovium due to their role in producing **pro-inflammatory cytokines** like TNF-̑, IL-1, and IL-6, which drive joint destruction [1], [2]. - They also contribute to the **pannus formation** and degrade cartilage and bone through the release of proteases [1]. *Dendritic cells* - While present in the synovium, **dendritic cells primarily function as antigen-presenting cells**, initiating T-cell responses. - Their direct contribution to tissue damage and chronic inflammation is less prominent than that of macrophages. *CD4+ Helper cells* - **CD4+ T helper cells** orchestrate the immune response by activating B cells and macrophages, but they are not the primary effector cells causing direct tissue damage [3]. - They secrete cytokines that promote inflammation but do not directly participate in tissue degradation. *Neutrophils* - **Neutrophils are abundant in the synovial fluid** during acute flares, contributing to inflammation and breakdown of cartilage through the release of enzymes. - However, their role in the chronic, sustained synovial inflammation and tissue destruction characteristic of RA is less significant compared to macrophages. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 677-678. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 105-106. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1212.
Pharmacology
2 questionsColonoscopy performed on a 25 year old woman with eating disorder showed dark brown to black pigmentary deposit in the lining of the large intestine. Histopathology of biopsy revealed pigment laden macrophages within the lamina propria. On probing, the woman revealed use of laxatives for 9 months to lose weight. What could be the probable laxative agent that could have caused these findings?
Which drug increases bone formation in osteoporosis?
NEET-PG 2018 - Pharmacology NEET-PG Practice Questions and MCQs
Question 171: Colonoscopy performed on a 25 year old woman with eating disorder showed dark brown to black pigmentary deposit in the lining of the large intestine. Histopathology of biopsy revealed pigment laden macrophages within the lamina propria. On probing, the woman revealed use of laxatives for 9 months to lose weight. What could be the probable laxative agent that could have caused these findings?
- A. Castor oil
- B. Bisacodyl
- C. Senna (Correct Answer)
- D. Sorbitol
Explanation: ***Senna*** - Chronic use of **anthraquinone laxatives** like senna [1] leads to **melanosis coli**, characterized by dark brown pigment in the colon. - Histopathology reveals **pigment-laden macrophages** in the lamina propria, confirming melanosis coli. *Castor oil* - **Castor oil** is a stimulant laxative that acts on the small intestine but does not typically cause **melanosis coli**. - Its primary action is to increase fluid secretion and bowel motility, rather than pigment deposition. *Bisacodyl* - **Bisacodyl** is a stimulant laxative that works locally in the colon to increase fluid and electrolyte secretion and stimulate peristalsis. - It works on different pharmacological mechanisms and typically does not cause the characteristic **pigment-laden macrophages** that define melanosis coli. *Sorbitol* - **Sorbitol** is an osmotic laxative that works by drawing water into the colon, softening stools and promoting bowel movements. - It does not induce the characteristic **darkening of the colonic mucosa** or the specific histological changes observed in melanosis coli.
Question 172: Which drug increases bone formation in osteoporosis?
- A. Teriparatide (Correct Answer)
- B. Calcitonin
- C. Risedronate
- D. Denosumab
Explanation: ***Correct Option: Teriparatide*** - **Teriparatide** is a recombinant form of **parathyroid hormone (PTH)** that, when administered intermittently, stimulates **osteoblast activity** to increase bone formation. - It is an **anabolic agent** specifically designed to build new bone, making it unique among osteoporosis treatments that primarily inhibit bone resorption. - Administered as a **daily subcutaneous injection** for up to 2 years. *Incorrect Option: Calcitonin* - **Calcitonin** is a hormone that inhibits **osteoclast activity**, thereby reducing bone resorption, but does not directly stimulate bone formation. - It may be used for pain relief in acute vertebral fractures but has a minor role in increasing bone density. *Incorrect Option: Risedronate* - **Risedronate** is a **bisphosphonate** that works by inhibiting **osteoclast-mediated bone resorption**, preventing bone breakdown. - It does not directly promote new bone formation; its primary action is to reduce bone turnover. *Incorrect Option: Denosumab* - **Denosumab** is a **monoclonal antibody** that targets and binds to **RANKL**, thereby inhibiting **osteoclast formation, function, and survival**, leading to decreased bone resorption. - Like bisphosphonates, its main mechanism is anti-resorptive, not anabolic.
Physiology
1 questionsGlucose is absorbed in the intestine by?
NEET-PG 2018 - Physiology NEET-PG Practice Questions and MCQs
Question 171: Glucose is absorbed in the intestine by?
- A. Facilitated diffusion
- B. Simple diffusion
- C. Secondary active transport (Correct Answer)
- D. Primary active transport
Explanation: ***Secondary active transport*** - Glucose absorption in the intestine primarily occurs via the **SGLT1 (sodium-glucose cotransporter 1)** protein. - SGLT1 uses the **electrochemical gradient of sodium** (established by Na+/K+-ATPase) to co-transport glucose against its concentration gradient, classifying it as secondary active transport. *Facilitated diffusion* - While **facilitated diffusion** by GLUT2 transporters is involved in glucose exit from the intestinal cells into the bloodstream, it's not the primary mechanism for uptake from the lumen. - This process does not require direct energy expenditure, but relies on a **concentration gradient**. *Simple diffusion* - **Simple diffusion** involves the movement of substances directly across the membrane, down their concentration gradient, without the help of transport proteins. - Glucose is a **hydrophilic molecule** and too large to pass through the lipid bilayer by simple diffusion. *Primary active transport* - **Primary active transport** directly uses ATP hydrolysis to move substances against their concentration gradient (e.g., Na+/K+-ATPase). - While essential for maintaining the sodium gradient, it is not the direct mechanism for glucose uptake from the intestinal lumen.
Psychiatry
1 questionsWhich of the following is true about ataxia telangiectasia?
NEET-PG 2018 - Psychiatry NEET-PG Practice Questions and MCQs
Question 171: Which of the following is true about ataxia telangiectasia?
- A. There is absence of amphicytes in different organs
- B. It is an autosomal recessive disease (Correct Answer)
- C. It is associated with normal immune function
- D. Serum levels of IgA are increased
- E. Serum alpha-fetoprotein levels are decreased
Explanation: ***It is an autosomal recessive disease*** - Ataxia telangiectasia is caused by mutations in the **ATM gene**, which is inherited in an **autosomal recessive** pattern. - This genetic defect leads to a deficiency in a protein crucial for DNA repair, causing systemic effects. *There is absence of amphicytes in different organs* - This statement is incorrect; **ataxia telangiectasia** is not characterized by an absence of amphicytes. - The term "amphicytes" is not typically associated with the defining pathological features of ataxia telangiectasia. *It is associated with normal immune function* - Ataxia telangiectasia is associated with **immunodeficiency**, particularly affecting T- and B-cell function. - Patients often experience recurrent infections due to impaired adaptive immunity, which is not a characteristic of normal immune function. *Serum levels of IgA are increased* - Patients with ataxia telangiectasia typically have **decreased serum levels of IgA**, and often IgG and IgE, leading to immunodeficiency. - Increased IgA levels are characteristic of other conditions and not ataxia telangiectasia. *Serum alpha-fetoprotein levels are decreased* - In ataxia telangiectasia, serum **alpha-fetoprotein (AFP) levels are characteristically elevated**, not decreased. - Elevated AFP is a useful diagnostic marker for this condition.