NEET-PG 2012 Practice Questions

Q: Glycogen synthase is activated by?

Insulin. **Insulin** - Insulin activates **glycogen synthase** through a signaling cascade that dephosphorylates the enzyme, shifting it to its active form (glycogen synthase a). - This activation promotes **glycogen synthesis** in the liver and muscles, lowering blood glucose levels. *Glucagon* - **Glucagon** primarily acts to increase blood glucose levels by activating **glycogen phosphorylase** and inhibiting glycogen synthase. - It promotes the breakdown of glycogen (glycogenolysis) rather than its synthesis. *Epinephrine* - **Epinephrine** (adrenaline) also promotes **glycogenolysis** (glycogen breakdown) by activating glycogen phosphorylase. - Its main role is to provide rapid energy during stress, not to store glucose as glycogen. *AMP* - **AMP** (adenosine monophosphate) is a key allosteric activator of **AMP-activated protein kinase (AMPK)**, which phosphorylates and inactivates glycogen synthase. - High AMP levels signal a low energy state, prompting ATP-generating pathways like glycogenolysis, not glycogen synthesis.

Q: Which isoform of LDH is raised in Anemia ?

LDH 2. ***Correct: LDH 2*** - **LDH 2 (H3M1)** is highly abundant in **red blood cells (RBCs)**, second only to LDH 1. - In **hemolytic anemia**, there is increased destruction of red blood cells, leading to the release of intracellular LDH isoforms into the bloodstream. - Both **LDH 1 and LDH 2 are significantly elevated** in hemolytic anemia, as RBCs contain predominantly these two isoforms. - The elevation of LDH 2 is particularly notable and diagnostically useful in anemia, especially hemolytic conditions. *Incorrect: LDH 1* - **LDH 1 (H4)** is the most abundant isoform in **heart muscle** and is also present in **red blood cells**. - While LDH 1 is indeed elevated in hemolytic anemia, this option is not the best answer in this context. - LDH 1 elevation is classically associated with **myocardial infarction**. *Incorrect: LDH 4* - **LDH 4 (HM3)** is present in various tissues, including **liver, skeletal muscle, and kidneys**, but in lower concentrations. - Not the primary isoform associated with anemia. *Incorrect: LDH 5* - **LDH 5 (M4)** is predominantly found in the **liver and skeletal muscles**. - Elevation of LDH 5 typically indicates **liver damage, muscle injury, or malignancies**, not primarily anemia.

Q: Chylomicron remnants are associated with ?

Apo-E. ***Apo-E*** - **Apolipoprotein E (Apo-E)** is a crucial apolipoprotein on the surface of chylomicron remnants, acting as a **ligand for the LDL receptor-related protein 1 (LRP1)** in the liver. - This binding facilitates the **hepatic uptake and clearance** of chylomicron remnants from circulation. *Apo-A* - **Apo-AI** is the primary apolipoprotein of **HDL** and plays a key role in reverse cholesterol transport by activating **lecithin-cholesterol acyltransferase (LCAT)**. - While chylomicrons *acquire* some Apo-AI from HDL, it is not the primary apolipoprotein defining their remnants' hepatic clearance. *Apo-C* - **Apo-CII** is a vital activator of **lipoprotein lipase (LPL)**, which metabolizes triglycerides in chylomicrons and VLDL. - **Apo-CIII** inhibits LPL and hinders receptor-mediated uptake, but **Apo-E** is the key for remnant recognition and uptake, not Apo-C in general. *Apo-B100* - **Apo-B100** is the main structural apolipoprotein of **LDL** and **VLDL**, serving as the ligand for the LDL receptor, mediating their hepatic uptake. - While chylomicrons have **Apo-B48**, which is a truncated form of Apo-B100, Apo-B100 itself is not found on chylomicron remnants.

Q: What is Little's area, also known as Kiesselbach's plexus?

Anteroinferior nasal septum. ***Anteroinferior nasal septum*** - **Little's area**, or **Kiesselbach's plexus**, is a well-vascularized region located on the **anteroinferior portion of the nasal septum**. - This area is a common site for **anterior epistaxis** (nosebleeds) due to its superficial position and rich anastomotic blood supply from several arteries. *Anteroinferior lateral wall* - While the lateral nasal wall also contributes to the nasal blood supply, the specific region of **Little's area** is on the **septum**, not the lateral wall. - The **lateral wall** contains structures like the turbinates and their associated vascular networks, which are distinct from Kiesselbach's plexus. *Posteroinferior lateral wall* - The **posterior and inferior aspects** of the nasal cavity are not where Kiesselbach's plexus is predominantly located. - Bleeding from this posterior region often indicates **posterior epistaxis**, which can be more severe and difficult to control. *Posteroinferior nasal septum* - The **posterior nasal septum** is supplied by different arteries, such as branches of the **sphenopalatine artery**. - Bleeding from this part of the septum is also considered **posterior epistaxis** and is not typically associated with Kiesselbach's plexus.

Q: Cystic medial necrosis is seen in?

Marfan syndrome. ***Marfans syndrome*** - Cystic medial necrosis is a prominent feature of Marfan syndrome, leading to **aortic dilation** and increased risk of dissection [1] [2]. - It is associated with **connective tissue abnormalities**, specifically affecting elastic fibers in the aorta [2]. *Kawasaki disease* - Primarily affects children, leading to **vasculitis** of medium-sized arteries, especially the coronary arteries. - Does not characteristically cause **cystic medial necrosis** in the aorta. *Friedrichs ataxia Pattern* - An autosomal recessive disorder characterized by degeneration of spinal cord and peripheral nerves, not related to cystic medial necrosis. - Presents with **ataxia**, **scoliosis**, and **diabetes**, lacking cardiovascular changes associated with cystic medial necrosis. *Downs syndrome* - A genetic condition resulting from **trisomy 21**, associated with various congenital anomalies but not specifically with cystic medial necrosis. - Includes features like **heart defects** but does not involve the aortic changes seen in Marfan syndrome. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 511-512. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 153-154.

Q: Which of the following conditions can lead to pulmonary infarction?

Blockage of 2nd and 3rd generation end arteries. ***Blockage of 2nd and 3rd generation end arteries*** - These are **true end arteries** beyond the reach of **bronchial collateral circulation**, making pulmonary infarction more likely when blocked. - The **dual blood supply** (pulmonary and bronchial arteries) is compromised at this level, leading to tissue necrosis and infarction. *Saddle embolus at bifurcation* - A **saddle embolus** typically causes **sudden death** or **acute cor pulmonale** rather than pulmonary infarction. - The **main pulmonary artery bifurcation** is proximal enough that **bronchial collateral circulation** can still maintain tissue viability. *Arterioles being blocked* - **Arterioles** are small vessels that can be compensated by the **dual blood supply** from both pulmonary and bronchial circulations. - The **bronchial artery collaterals** can provide adequate perfusion to prevent infarction at this level. *None of the above* - This option is incorrect as **blockage of 2nd and 3rd generation end arteries** does cause pulmonary infarction. - The lung's **dual circulation** protects against infarction except when **true end arteries** are involved.

Q: What change is seen in the vessels during the initial stage of Raynaud's phenomenon?

No pathological changes (functional vasospasm only). ***No pathological changes (functional vasospasm only)*** - Raynaud's phenomenon, particularly **primary Raynaud's** (Raynaud's disease), is characterized by **functional vasospasm** of arterioles, especially in fingers and toes, in response to cold or stress [1]. - In its initial stages, there are no structural changes or pathological alterations within the vessel walls; the vasoconstriction is entirely **functional** [1]. *Thrombosis* - **Thrombosis** involves the formation of a blood clot within a vessel, obstructing blood flow. - While severe Raynaud's can, in rare cases, lead to digital ischemia and microthrombosis, it is **not the primary or initial change** seen in typical Raynaud's phenomenon. *Fibrinoid necrosis* - **Fibrinoid necrosis** is a type of vascular damage associated with severe autoimmune diseases or malignant hypertension, where fibrin and plasma proteins deposit in the vessel wall. - This is a **structural, irreversible change** and is not characteristic of the initial, functional vasospasm seen in Raynaud's phenomenon. *Hyaline sclerosis* - **Hyaline sclerosis** is a change in small arteries and arterioles, often seen in benign essential hypertension or as part of the aging process, where the vessel wall thickens and becomes hyaline (glassy) due to plasma protein leakage and fibrosis. - This represents a **chronic structural change** and is not the acute, intermittent, functional vasoconstriction defining the initial stage of Raynaud's. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 520-522.

Q: Gastric secretions are essential for absorption of -

Cobalamin. ***Cobalamin*** - **Intrinsic factor**, secreted by gastric parietal cells, is crucial for the absorption of **vitamin B12 (cobalamin)** in the terminal ileum [1]. - Without sufficient intrinsic factor, **pernicious anemia** can develop due to impaired B12 absorption [2]. *Fat* - Fat digestion primarily occurs in the **small intestine** with the help of **bile salts** and **pancreatic lipases**. - While gastric lipase begins some fat digestion, it's not essential for overall fat absorption. *Thiamine* - **Thiamine (vitamin B1)** is absorbed in the jejunum and ileum, primarily via **active transport** and passive diffusion. - Gastric secretions do not play a direct, essential role in its absorption. *Folic acid* - **Folic acid** is absorbed in the **duodenum and jejunum** as monoglutamates after being deconjugated from polyglutamate forms. - This process is not directly dependent on gastric secretions [2].

Q: Central stellate scar is typically associated with which of the following conditions?

Focal nodular hyperplasia (FNH). ***Focal nodular hyperplasia (FNH)*** - FNH is a benign liver lesion characterized by a central fibrous scar with radiating septa, giving it the characteristic appearance of a **central stellate scar** on imaging. - This scar contains **malformed blood vessels** and bile ductules, which are key diagnostic features. - On dynamic imaging, FNH typically shows **spoke-wheel arterial enhancement** pattern and the central scar shows **delayed enhancement** on MRI. *Hepatic adenoma* - Hepatic adenomas are typically composed of sheets of **hepatocytes** with absent portal triads and are usually **homogeneous** on imaging without a central scar. - They are associated with **oral contraceptive use** and have a risk of hemorrhage and malignant transformation. *Chronic liver disease* - Chronic liver disease, such as **cirrhosis**, is characterized by widespread **fibrosis** and **nodule formation** throughout the liver, but it does not typically present with a solitary lesion with a central stellate scar. - The scarring in cirrhosis is diffuse and leads to architectural distortion, rather than a focal central scar. *Hepatocellular carcinoma* - Hepatocellular carcinoma (HCC) typically presents as a **vascular mass** that may or may not be solitary, usually arising in the context of chronic liver disease or cirrhosis. - Although the **fibrolamellar variant of HCC** (seen in younger patients without cirrhosis) can show a central scar, this is less common and the scar typically shows **hypointensity on T2-weighted imaging**, unlike FNH where the scar is **hyperintense on T2**. - Typical HCC does not show a distinct central stellate scar as a characteristic feature.

Q: IVC filter is used in the following situations except -

As primary treatment for acute DVT. ***As primary treatment for acute DVT*** - The **primary treatment** for **acute deep vein thrombosis (DVT)** is **anticoagulation therapy** (heparin, warfarin, or DOACs) to prevent clot propagation and embolization. - An **IVC filter** is **NOT primary therapy**—it is reserved for specific situations and does not treat the underlying thrombosis. - **Indications for IVC filter include:** - Absolute **contraindication to anticoagulation** (active bleeding, recent hemorrhagic stroke) - **Recurrent PE despite adequate anticoagulation** - Complications from anticoagulation therapy - Therefore, using IVC filter as primary treatment for acute DVT is **incorrect and not indicated**. *Negligible size of emboli* - While IVC filters trap **large emboli**, the concept of "negligible size emboli" is not a standard clinical consideration for filter placement. - IVC filters are indicated based on **risk of PE** and **contraindications to anticoagulation**, not based on emboli size assessment. *To reduce symptoms* - **IVC filters** do not reduce symptoms of DVT such as pain, swelling, or discomfort. - They function as a **mechanical barrier** to prevent emboli from reaching pulmonary circulation. - Symptom management requires anticoagulation, compression therapy, and leg elevation. *To prevent progress of native blood vessel disease* - IVC filters do not influence progression of underlying **vascular disease** such as atherosclerosis or chronic venous insufficiency. - Their sole function is **mechanical prevention of PE**, not disease modification.

Question 1

Glycogen synthase is activated by?

Accepted Answer

Insulin

Answer

Glucagon

Answer

AMP

Answer

Epinephrine

Question 2

Which isoform of LDH is raised in Anemia ?

Accepted Answer

LDH 2

Answer

LDH 5

Answer

LDH 4

Answer

LDH 1

Question 3

Chylomicron remnants are associated with ?

Accepted Answer

Apo-E

Answer

Apo-C

Answer

Apo-A

Answer

Apo-B100

Question 4

What is Little's area, also known as Kiesselbach's plexus?

Accepted Answer

Anteroinferior nasal septum

Answer

Anteroinferior lateral wall

Answer

Posteroinferior lateral wall

Answer

Posteroinferior nasal septum

Question 5

Cystic medial necrosis is seen in?

Accepted Answer

Marfan syndrome

Answer

Friedreich's ataxia

Answer

Down syndrome

Answer

Kawasaki disease

Question 6

Which of the following conditions can lead to pulmonary infarction?

Accepted Answer

Blockage of 2nd and 3rd generation end arteries

Answer

Saddle embolus at bifurcation

Answer

Arterioles being blocked

Answer

None of the above.

Question 7

What change is seen in the vessels during the initial stage of Raynaud's phenomenon?

Accepted Answer

No pathological changes (functional vasospasm only)

Answer

Thrombosis

Answer

Fibrinoid necrosis

Answer

Hyaline sclerosis

Question 8

Gastric secretions are essential for absorption of -

Accepted Answer

Cobalamin

Answer

Fat

Answer

Thiamine

Answer

Folic acid

Question 9

Central stellate scar is typically associated with which of the following conditions?

Accepted Answer

Focal nodular hyperplasia (FNH)

Answer

Hepatic adenoma

Answer

Chronic liver disease

Answer

Hepatocellular carcinoma

Question 10

IVC filter is used in the following situations except -

Accepted Answer

As primary treatment for acute DVT

Answer

To reduce symptoms

Answer

Negligible size of emboli

Answer

To prevent progress of native blood vessel disease

NEET-PG 2012

Biochemistry

ENT

Pathology

Physiology

Radiology

Surgery