Anatomy
1 questionsWhich muscle is not part of the superficial anterior compartment of the forearm?
NEET-PG 2013 - Anatomy NEET-PG Practice Questions and MCQs
Question 261: Which muscle is not part of the superficial anterior compartment of the forearm?
- A. FDS
- B. FCR
- C. Palmaris longus
- D. Flexor pollicis longus (FPL) (Correct Answer)
Explanation: **Flexor pollicis longus (FPL)** - The **FPL** is located in the **deep anterior compartment** of the forearm, differentiating it from the superficial muscles [1]. - Its primary function is **flexion of the thumb's interphalangeal joint**, requiring a deeper anatomical position for mechanical advantage [1]. *FDS* - The **Flexor digitorum superficialis (FDS)** is a key muscle of the superficial anterior compartment, visible just beneath the skin and fascia. - It is responsible for **flexing the middle phalanges** of the medial four digits. *FCR* - The **Flexor carpi radialis (FCR)** is situated in the superficial anterior compartment, running obliquely across the forearm. - It functions in **flexion and abduction of the wrist**. *Palmaris longus* - The **Palmaris longus** is a superficial anterior compartment muscle, though it is absent in a significant portion of the population. - When present, its main action is **flexion of the wrist** and tightening of the palmar aponeurosis.
Biochemistry
1 questionsWhich of the following is activated by calmodulin?
NEET-PG 2013 - Biochemistry NEET-PG Practice Questions and MCQs
Question 261: Which of the following is activated by calmodulin?
- A. Muscle phosphorylase
- B. Calcium/calmodulin-dependent protein kinase (Correct Answer)
- C. Phospholipase C
- D. Adenylyl cyclase
Explanation: ***Calcium/calmodulin-dependent protein kinase*** - **Calmodulin** is a **calcium-binding messenger protein** that, when bound to calcium, undergoes a conformational change allowing it to activate various enzymes, including **calcium/calmodulin-dependent protein kinases** (CaMKs). - CaMKs play crucial roles in many cellular processes, including **metabolism**, **gene expression**, and **neurotransmission**, by phosphorylating target proteins. *Muscle phosphorylase* - **Muscle phosphorylase** (glycogen phosphorylase) is primarily activated by **epinephrine**, **AMP**, and **nerve stimulation** (via calcium), but not directly by calmodulin. - Its activation leads to the breakdown of **glycogen** into glucose-1-phosphate. *Phospholipase C* - **Phospholipase C (PLC)** is typically activated by **G protein-coupled receptors** and **tyrosine kinase receptors**, leading to the production of **inositol trisphosphate (IP3)** and **diacylglycerol (DAG)**. - While it plays a role in calcium signaling upstream (releasing calcium from stores), it is not directly activated by calmodulin. *Adenylyl cyclase* - **Adenylyl cyclase (AC)** is a key enzyme in generating **cyclic AMP (cAMP)**, and is commonly regulated by **G proteins** (specifically Gs and Gi subunits). - While certain isoforms (AC1, AC3, AC8) can be directly activated by calcium/calmodulin, **CaMK** remains the most classical and direct example of calmodulin activation.
Internal Medicine
2 questionsWhich of the following is NOT a feature of Peutz-Jeghers syndrome?
Which of the following statements about Alport's syndrome is incorrect?
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 261: Which of the following is NOT a feature of Peutz-Jeghers syndrome?
- A. Mucocutaneous pigmentation
- B. Autosomal recessive inheritance (Correct Answer)
- C. Autosomal dominant
- D. Hamartomatous polyp
Explanation: ***High risk of malignancy*** - Peutz-Jeghers syndrome is primarily associated with **benign hamartomatous polyps**, not a **high risk of malignancy**, which distinguishes it from other syndromes. - Although patients may develop cancers [1], the syndrome itself does not inherently denote a high malignancy risk like other syndromes such as familial adenomatous polyposis. *Autosomal dominant* - This syndrome is indeed **autosomal dominant**, caused by mutations in the STK11 gene. - Families with this condition typically show **vertical transmission**, characteristic of autosomal dominant inheritance. *Hamartomatous polyp* - Individuals with Peutz-Jeghers syndrome develop **hamartomatous polyps**, which are a hallmark feature of the condition [1]. - These polyps can occur in the gastrointestinal tract and are benign lesions rather than adenomatous type seen in other syndromes [1]. *Mucocutaneous pigmentation* - Mucocutaneous pigmentation, such as **freckling around the lips and buccal mucosa**, is a key clinical feature of Peutz-Jeghers syndrome. - This pigmentation usually appears in childhood and is often a distinguishing sign of the syndrome.
Question 262: Which of the following statements about Alport's syndrome is incorrect?
- A. Nerve deafness
- B. Glomerulonephritis
- C. Autosomal dominant (Correct Answer)
- D. X-linked
Explanation: ***Autosomal dominant*** - While there are rare autosomal dominant forms, the most common and classic presentation of **Alport's syndrome is X-linked recessive**, affecting males more severely. - This statement is incorrect because it implies that autosomal dominant inheritance is the primary or typical mode, which is not true for the majority of cases. *Nerve deafness* - **Sensorineural hearing loss**, particularly for high frequencies, is a common and characteristic extra-renal manifestation of Alport's syndrome. - This symptom typically progresses with age and is a key diagnostic feature. *Glomerulonephritis* - **Progressive glomerulonephritis** is the hallmark renal feature of Alport's syndrome, leading to hematuria, proteinuria, and eventually end-stage renal disease. - It is caused by mutations in collagen type IV genes, which disrupt the integrity of the glomerular basement membrane. *X-linked* - The majority of Alport's syndrome cases (about 85%) are **X-linked recessive**, caused by mutations in the *COL4A5* gene located on the X chromosome. - This explains why males are more severely affected and typically present with earlier onset and more rapid progression of renal disease.
Pathology
5 questionsMALT lymphoma is positive for which of the following markers?
Intracorpuscular hemolytic anemia is seen in ?
Centrilobular necrosis of the liver may be seen with?
Which of the following statements about Polycythemia vera is false?
Which of the following statements is true regarding light microscopy findings in minimal change disease?
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 261: MALT lymphoma is positive for which of the following markers?
- A. CD20 (Correct Answer)
- B. CD19
- C. CD43
- D. CD5
Explanation: ***CD20*** - MALT lymphoma is a type of **B-cell non-Hodgkin lymphoma**, and CD20 is a **pan B-cell marker consistently expressed** in MALT lymphomas. - CD20 positivity is **crucial for diagnosis** and is the **primary therapeutic target** for anti-CD20 monoclonal antibody therapy (Rituximab). - In diagnostic practice, **CD20 is the most important B-cell marker** for identifying MALT lymphoma and guiding treatment decisions. *CD19* - CD19 is also a **pan B-cell marker** and is **typically positive in MALT lymphoma** along with CD20. - However, in the context of this question, **CD20 is the preferred answer** because it is the **standard diagnostic marker emphasized in clinical practice** and the **primary therapeutic target**. - Both markers are positive, but CD20 has greater **clinical and therapeutic significance** in MALT lymphoma management. *CD43* - CD43 is primarily a **T-cell and myeloid marker**, but can show **aberrant expression in 40-50% of MALT lymphomas**. - While it may be positive in some cases, it is **not a defining B-cell lineage marker** and is not used as a primary diagnostic criterion for MALT lymphoma. - Its variable expression makes it **less reliable** than consistent B-cell markers like CD20. *CD5* - CD5 is typically associated with **T-cells** and certain B-cell lymphomas, particularly **chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL)** and **mantle cell lymphoma**. - **MALT lymphoma is characteristically CD5-negative**, which is an important feature for **differentiating it from CD5+ B-cell lymphomas**.
Question 262: Intracorpuscular hemolytic anemia is seen in ?
- A. Thalassemia (Correct Answer)
- B. Infection
- C. Thrombotic thrombocytopenic purpura (TTP)
- D. Autoimmune hemolytic anemia
Explanation: ***Thalassemia*** - Thalassemia is characterized by **intracorpuscular hemolysis** due to defective hemoglobin synthesis, leading to premature destruction of red blood cells [1][2]. - It manifests as **microcytic anemia** with associated **extramedullary erythropoiesis** in severe cases [1]. *Autoimmune hemolytic anemia* - This condition leads to **extravascular hemolysis**, primarily affecting red blood cells in the spleen, not within the plasma [2]. - It is often associated with **positive direct Coombs test**, indicating reactants on the RBC surface. *TIP* - TIP (Thrombotic Microangiopathy) primarily involves **microangiopathic hemolytic anemia** and is not classified as intracorpuscular [2]. - The hemolysis in TIP occurs due to **microthrombi**, causing damage to red blood cells as they pass through narrowed vessels. *Infection* - Infections can lead to **hemolysis**, but this is typically **extravascular** due to splenic clearance or due to other mechanisms like **malaria** [2]. - The hemolytic mechanism is not intracorpuscular, as seen in conditions like thalassemia. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 601-602. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 596-597.
Question 263: Centrilobular necrosis of the liver may be seen with?
- A. Arsenic
- B. Ethanol
- C. CCl4 (Correct Answer)
- D. Phosphorus
Explanation: ***CCl4*** - **Carbon tetrachloride (CCl4)** is the **classic and prototypical** hepatotoxin that causes **centrilobular (zone 3) necrosis**. - The **centrilobular zone (zone 3)** is particularly vulnerable due to its high concentration of **cytochrome P450 enzymes**, which metabolize CCl4 into **toxic free radicals (trichloromethyl radicals)**. - This is the **most characteristic** cause of centrilobular necrosis in toxicology and is the preferred answer for exam purposes. *Ethanol* - **Ethanol** can also cause **centrilobular necrosis** in **alcoholic hepatitis**, as zone 3 is most susceptible to hypoxic injury and oxidative stress. - However, alcoholic liver disease presents with a **spectrum of changes** including steatosis (earliest), hepatitis with ballooning degeneration and Mallory-Denk bodies, and eventual cirrhosis. - While centrilobular necrosis occurs in alcoholic hepatitis, **CCl4 remains the prototype** for pure centrilobular necrosis in exam contexts. *Phosphorus* - **Elemental phosphorus** toxicity causes **periportal (zone 1) necrosis**, which is the opposite pattern from centrilobular necrosis. - It also causes widespread fatty change and hemorrhagic necrosis within the liver. *Arsenic* - **Arsenic poisoning** causes **diffuse/generalized hepatocellular necrosis** and cholestasis, rather than the specific centrilobular pattern. - Chronic exposure is associated with non-cirrhotic portal fibrosis and portal hypertension.
Question 264: Which of the following statements about Polycythemia vera is false?
- A. Increased LAP score (Correct Answer)
- B. Increased vitamin B12 levels
- C. Leukocytosis is present
- D. Increased platelet count
Explanation: ***Decrease LAP score*** - In polycythemia vera, the **LAP (leukocyte alkaline phosphatase) score** is typically increased, indicating more mature leukocytes. - A **decrease in LAP score** is not consistent with the disease, making this statement incorrect. *Increased platelets* - Polycythemia vera often results in **thrombocytosis**, characterized by increased platelet counts [1]. - This is a common feature of the disorder, reflecting overproduction of blood cells in the bone marrow. *Leucocytosis* - Patients with polycythemia vera frequently exhibit **leucocytosis**, or increased white blood cell counts, due to hypercellularity of the bone marrow [1]. - This is an important aspect of the disease, often seen alongside increases in red blood cells and platelets. *Increased vit B12* - An elevation in **vitamin B12** levels can occur in polycythemia vera, often due to increased binding proteins. - This is a well-recognized phenomenon associated with the increased cell turnover in this condition. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 626-627.
Question 265: Which of the following statements is true regarding light microscopy findings in minimal change disease?
- A. Foot process effacement is observed under electron microscopy, not light microscopy.
- B. Anti-GBM antibodies are associated with Goodpasture syndrome, not minimal change disease.
- C. No significant changes are seen under light microscopy. (Correct Answer)
- D. IgA deposits are characteristic of IgA nephropathy, not minimal change disease.
Explanation: ***No change seen*** - In minimal change disease, **light microscopy** typically shows no significant changes, which is a key characteristic of the condition [1]. - The disease primarily affects the **podocytes** leading to **nephrotic syndrome**, while light microscopy does not reveal any abnormalities [1]. *Loss of foot process seen* - Loss of foot processes is actually observed under **electron microscopy**, not light microscopy. - Light microscopy remains normal, differentiating minimal change disease from other glomerular diseases. *IgA deposits seen* - IgA deposits are associated with **IgA nephropathy**, which is a different condition characterized by mesangial deposition. - Minimal change disease does not have **immunofluorescence** findings, and thus shows no such deposits on light microscopy [1]. *Anti GBM Abs seen* - Anti-GBM antibodies are characteristic of **Goodpasture syndrome**, which presents with significant changes in glomerular structure. - In minimal change disease, there are no **anti-GBM antibodies** or major changes visible under light microscopy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928.
Physiology
1 questionsDuring starvation, which hormone level increases?
NEET-PG 2013 - Physiology NEET-PG Practice Questions and MCQs
Question 261: During starvation, which hormone level increases?
- A. Leptin
- B. MSH
- C. Insulin
- D. Ghrelin (Correct Answer)
Explanation: ***Ghrelin*** - **Ghrelin** is often referred to as the "hunger hormone" because its levels typically rise during fasting or periods of starvation. - It stimulates **appetite** and signals the brain to increase food intake, playing a crucial role in energy balance. *Leptin* - **Leptin** is a hormone produced by **adipose tissue** that signals satiety and helps regulate long-term energy balance. - During starvation, **leptin levels typically decrease** as fat stores are depleted, which further increases appetite and reduces energy expenditure. *MSH* - **Melanocyte-stimulating hormone (MSH)** is involved in skin pigmentation and appetite regulation, but its levels do not primarily increase in response to starvation. - While MSH can influence appetite, it is often seen to decrease appetite when present in higher concentrations, which is counterintuitive during starvation. *Insulin* - **Insulin** is a hormone produced by the **pancreas** that helps regulate blood glucose levels by promoting glucose uptake into cells. - During starvation, blood glucose levels decrease, leading to a **reduction in insulin secretion** to preserve glucose for vital organs like the brain.