Biochemistry
1 questionsClinical effect of vitamin D is reduced by ?
NEET-PG 2013 - Biochemistry NEET-PG Practice Questions and MCQs
Question 661: Clinical effect of vitamin D is reduced by ?
- A. Simultaneous ingestion of lactose
- B. Simultaneous ingestion of phytates (Correct Answer)
- C. None of the options
- D. Acidic environment
Explanation: ***Simultaneous ingestion of phytates*** - **Phytates (phytic acid)** found in whole grains, nuts, seeds, and legumes can **reduce the clinical effect of vitamin D** through multiple mechanisms - Phytates **chelate calcium** and form insoluble calcium-phytate complexes, reducing calcium absorption - Since **vitamin D and calcium metabolism are closely linked**, impaired calcium absorption indirectly reduces vitamin D efficacy - Phytates can also **directly bind to vitamin D** in the gastrointestinal tract, reducing its bioavailability - Studies show that **high phytate intake increases vitamin D requirements** and can impair vitamin D status *Simultaneous ingestion of lactose* - Lactose does **not reduce** vitamin D absorption or efficacy - In fact, **dairy products are commonly fortified** with vitamin D, and the presence of lactose does not interfere with its beneficial effects - Lactose may actually **enhance calcium absorption**, which works synergistically with vitamin D *Acidic environment* - Vitamin D is a **fat-soluble vitamin** absorbed primarily in the small intestine - An acidic environment (stomach acid) is **not known to inhibit** vitamin D absorption - The absorption process occurs in the **alkaline environment of the small intestine** where fat-soluble vitamins are absorbed with dietary fats *None of the options* - This is **incorrect** as phytates do reduce the clinical effect of vitamin D through calcium chelation and direct binding mechanisms
Microbiology
2 questionsAn adolescent male developed vomiting and diarrhea 1 hour after having food from a restaurant. The most likely pathogen is?
Which of the following bacteria is known to exhibit antigenic variation?
NEET-PG 2013 - Microbiology NEET-PG Practice Questions and MCQs
Question 661: An adolescent male developed vomiting and diarrhea 1 hour after having food from a restaurant. The most likely pathogen is?
- A. Clostridium perfringens
- B. Vibrio parahaemolyticus
- C. Staphylococcus aureus (Correct Answer)
- D. Salmonella
Explanation: ***Staphylococcus aureus*** - The rapid onset of symptoms (within 1 hour) strongly suggests **pre-formed toxin ingestion**, which is characteristic of *Staphylococcus aureus* food poisoning. - While the typical incubation period is **1-6 hours** (average 2-4 hours), onset within 1 hour can occur with **high toxin loads** in contaminated food. - **Vomiting** is often the predominant symptom, occurring shortly after consuming contaminated food, which distinguishes it from other bacterial causes. *Clostridium perfringens* - Onset of symptoms caused by *Clostridium perfringens* is typically **8-16 hours** after ingestion, which is much longer than observed here. - It primarily causes **diarrhea and abdominal cramps** due to toxin production in the intestine, with minimal vomiting. *Vibrio parahaemolyticus* - Symptoms usually appear **4-96 hours** (average 12-24 hours) after consuming contaminated seafood, which is a longer incubation period than described. - It typically causes **watery diarrhea**, abdominal cramps, nausea, and occasional vomiting, but not within 1 hour. *Salmonella* - The incubation period for *Salmonella* infection is typically **6-72 hours** (average 12-36 hours), making it highly unlikely for symptoms to appear within 1 hour. - **Diarrhea, fever, and abdominal cramps** are common with *Salmonella*, but rapid-onset vomiting from pre-formed toxin is not its mechanism.
Question 662: Which of the following bacteria is known to exhibit antigenic variation?
- A. Yersinia
- B. Bordetella
- C. Brucella
- D. Borrelia (Correct Answer)
Explanation: ***Borrelia*** - *Borrelia* species, particularly *Borrelia burgdorferi* (causing **Lyme disease**), are known for extensive **antigenic variation** of their outer surface proteins (Osps), especially OspC. - This variation helps the bacteria evade the host's immune response, contributing to persistent infection. *Yersinia* - While *Yersinia* species produce various virulence factors, including proteins that interfere with immune cell function, they are not primarily known for the type of rapid and extensive **antigenic variation**seen in *Borrelia*. - Their immune evasion strategies often involve modifying host cell signaling pathways and resisting phagocytosis. *Bordetella* - *Bordetella pertussis*, causative agent of **whooping cough**, varies its expression of adhesins and toxins through **phase variation**, which is a form of phenotypic switching. - However, this is distinct from the frequent and sequential changes in surface antigens (antigenic variation) observed in *Borrelia*. *Brucella* - *Brucella* species are **intracellular pathogens** that primarily evade the immune system by surviving and replicating within host cells. - They do not typically engage in significant **antigenic variation** of their surface components as a primary immune evasion mechanism.
Pharmacology
7 questionsWhat is the mechanism of action of clofibrate in lipid metabolism?
Drug that binds bile acids in the intestine and prevents their return to liver via the enterohepatic circulation?
Drug of choice for familial hypercholesterolemia?
Which of the following statements about hypolipidemic drugs is false?
Which of the following drugs inhibits the activation of plasminogen?
Mechanism of action of tranexamic acid is
Why do NSAIDs cause gastric ulcers?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 661: What is the mechanism of action of clofibrate in lipid metabolism?
- A. Inhibits lipolysis in adipose tissue.
- B. Inhibits HMG CoA reductase.
- C. Binds bile acids and bile salts in the small intestine.
- D. Increases lipoprotein lipase activity through PPAR alpha, leading to enhanced lipolysis of triglycerides. (Correct Answer)
Explanation: ***Increases lipoprotein lipase activity through PPAR alpha, leading to enhanced lipolysis of triglycerides.*** - Clofibrate, a **fibrat**e, acts as an agonist for **peroxisome proliferator-activated receptor alpha (PPAR-α)**. - Activation of PPAR-α leads to increased synthesis of **lipoprotein lipase (LPL)**, which enhances the breakdown of **triglycerides** in VLDL particles. *Inhibits lipolysis in adipose tissue.* - This mechanism is characteristic of **niacin (nicotinic acid)**, which reduces the release of free fatty acids from adipose tissue. - Clofibrate's primary action is not focused on inhibiting lipolysis in adipose tissue. *Inhibits HMG CoA reductase.* - This is the mechanism of action for **statins** (e.g., simvastatin, atorvastatin), which are used to reduce cholesterol synthesis. - Clofibrate does not directly inhibit HMG CoA reductase. *Binds bile acids and bile salts in the small intestine.* - This mechanism is characteristic of **bile acid sequestrants** (e.g., cholestyramine, colestipol). - These drugs prevent the reabsorption of bile acids, leading to increased cholesterol conversion to bile acids in the liver.
Question 662: Drug that binds bile acids in the intestine and prevents their return to liver via the enterohepatic circulation?
- A. Niacin
- B. Fenofibrate
- C. Cholestyramine (Correct Answer)
- D. Gugulipid
Explanation: ***Cholestyramine*** - **Cholestyramine** is a **bile acid-binding resin** that sequesters bile acids in the intestine, preventing their reabsorption. - This interruption of the **enterohepatic circulation** leads to increased synthesis of new bile acids from cholesterol in the liver, thus lowering plasma LDL cholesterol. *Niacin* - **Niacin (nicotinic acid)** reduces the hepatic synthesis and secretion of **VLDL**, which in turn lowers LDL and triglyceride levels. - It works primarily through mechanisms related to fat metabolism in the liver and adipose tissue, not direct bile acid binding in the intestine. *Fenofibrate* - **Fenofibrate** is a **PPAR-α agonist** that primarily reduces triglyceride levels by increasing fatty acid oxidation and lipoprotein lipase activity, and secondarily increases HDL. - Its main action is on lipid metabolism in the liver and peripheral tissues, not by binding bile acids in the gut. *Gugulipid* - **Gugulipid** is a phytosterol derived from the guggul tree, sometimes used in traditional medicine for cholesterol management. - Its purported mechanism involves increasing **bile acid excretion** and inhibiting cholesterol biosynthesis, but it does not directly bind bile acids in the same manner as resins like cholestyramine.
Question 663: Drug of choice for familial hypercholesterolemia?
- A. Nicotinic acid
- B. Lovastatin (Correct Answer)
- C. Cholestyramine
- D. Gemfibrozil
Explanation: ***Lovastatin*** - **Statins** (HMG-CoA reductase inhibitors) are the **first-line therapy** for familial hypercholesterolemia as they effectively lower **LDL cholesterol** levels by inhibiting cholesterol synthesis [1]. - While other agents can be used adjunctively, statins like lovastatin are the cornerstone for managing this genetic condition [2]. *Nicotinic acid* - **Nicotinic acid** (niacin) primarily lowers **triglycerides** and increases **HDL cholesterol**, but it is less potent than statins for reducing LDL-C, especially in familial hypercholesterolemia [1]. - Its use is often limited by significant **side effects** like flushing. *Cholestyramine* - **Cholestyramine** is a **bile acid sequestrant** that binds to bile acids in the intestine, preventing their reabsorption and mildly lowering LDL cholesterol. - It is less effective than statins and often causes **gastrointestinal side effects** such as constipation and bloating. *Gemfibrozil* - **Gemfibrozil** is a **fibrate**, primarily used to lower **triglyceride levels** and increase HDL cholesterol. - It has minimal impact on LDL cholesterol compared to statins and is not the primary treatment for familial hypercholesterolemia [2].
Question 664: Which of the following statements about hypolipidemic drugs is false?
- A. Gemfibrozil causes myopathy
- B. Gemfibrozil can increase myopathy caused by statins
- C. Lovastatin can cause hepatic dysfunction
- D. Cholesterol reducing drugs are contraindicated in child less than 8 years (Correct Answer)
Explanation: ***Cholesterol reducing drugs are contraindicated in child less than 8 years*** - While cholesterol-lowering drugs are generally avoided in young children, there are specific **genetic dyslipidemias** where treatment may be initiated earlier under specialist supervision [1]. - The statement is **false** because some genetic conditions may necessitate earlier treatment, making a blanket contraindication for all children under 8 inaccurate [1]. *Gemfibrozil causes myopathy* - **Gemfibrozil** (a fibric acid derivative) can indeed cause **myopathy**, especially when used alone or in combination with other lipid-lowering agents [2]. - This adverse effect is thought to be due to its mechanism of action affecting fatty acid metabolism and muscle integrity. *Gemfibrozil can increase myopathy caused by statins* - The co-administration of **gemfibrozil** with **statins** significantly increases the risk of **myopathy** and **rhabdomyolysis** [2]. - This is primarily due to gemfibrozil inhibiting the **glucuronidation** of statins, which increases statin plasma concentrations [2]. *Lovastatin can cause hepatic dysfunction* - **Statins**, including **lovastatin**, can cause **elevations in liver transaminases** and, in rare cases, lead to **drug-induced liver injury** [1]. - Regular monitoring of liver function tests is recommended when initiating statin therapy and during follow-up [2].
Question 665: Which of the following drugs inhibits the activation of plasminogen?
- A. Streptokinase
- B. Aminocaproic acid (Correct Answer)
- C. Reteplase
- D. Clopidogrel
Explanation: ***Correct Option: Aminocaproic acid*** - **Aminocaproic acid** is an antifibrinolytic drug that acts by competitively inhibiting the activation of **plasminogen** to plasmin. - By preventing the formation of plasmin, it stabilizes blood clots and is used to treat excessive bleeding. *Incorrect Option: Streptokinase* - **Streptokinase** is a **thrombolytic agent** that forms a complex with plasminogen, converting uncomplexed plasminogen into plasmin. - This action promotes the degradation of fibrin clots, making it a **fibrinolytic drug**, not an inhibitor of plasminogen activation. *Incorrect Option: Reteplase* - **Reteplase** is a **recombinant tissue plasminogen activator (tPA)** that directly converts plasminogen to plasmin. - This drug actively promotes **fibrinolysis** and clot breakdown, making it a thrombolytic agent. *Incorrect Option: Clopidogrel* - **Clopidogrel** is an **antiplatelet drug** that inhibits platelet aggregation by irreversibly blocking the P2Y12 adenosine diphosphate (ADP) receptor on platelets. - Its mechanism of action is focused on **platelet function**, not on the plasminogen-plasmin system.
Question 666: Mechanism of action of tranexamic acid is
- A. Decrease vascular permeability
- B. Smooth muscle contraction
- C. Activates Plasmin formation
- D. Prevents fibrinolysis (Correct Answer)
Explanation: ***Correct: Prevents fibrinolysis*** - Tranexamic acid is an **antifibrinolytic agent** that works by inhibiting the activation of plasminogen to plasmin. - By preventing the formation of plasmin, it stabilizes **fibrin clots** and reduces bleeding. *Incorrect: Decrease vascular permeability* - This is primarily the mechanism of action of drugs like antihistamines or corticosteroids, which work on **inflammation** and **allergic reactions**. - Tranexamic acid does not directly target vascular permeability; its primary role is in **hemostasis**. *Incorrect: Smooth muscle contraction* - This describes the action of drugs like **vasoconstrictors** (e.g., epinephrine) or agents that promote uterine contractions (e.g., oxytocin). - Tranexamic acid has no direct effect on **smooth muscle contraction**. *Incorrect: Activates Plasmin formation* - This is the opposite of tranexamic acid's action; drugs that activate plasmin, such as **tissue plasminogen activators (tPAs)**, are used to break down clots. - Tranexamic acid specifically **inhibits plasminogen activation**, thereby preventing plasmin formation.
Question 667: Why do NSAIDs cause gastric ulcers?
- A. They increase gastric acid secretion
- B. They delay gastric emptying
- C. They inhibit the production of protective mucus
- D. They inhibit COX-1 and COX-2 enzymes (Correct Answer)
Explanation: ***They inhibit COX-1 and COX-2 enzymes*** - NSAIDs primarily exert their anti-inflammatory effects by inhibiting **cyclooxygenase (COX) enzymes**, specifically COX-1 and COX-2. - While COX-2 inhibition is responsible for anti-inflammatory action, **COX-1 inhibition** reduces the production of protective prostaglandins in the gastric mucosa, leading to a loss of mucosal integrity and an increased risk of ulceration. *They inhibit the production of protective mucus* - While NSAIDs do compromise the gastric mucosal barrier, their primary mechanism is not a direct inhibition of mucus production itself. - Instead, the reduced prostaglandin synthesis indirectly affects the quantity and quality of mucus and bicarbonate, which are crucial for mucosal defense. *They increase gastric acid secretion* - NSAIDs do not directly increase gastric acid secretion; in fact, some studies suggest a mild inhibitory effect. - The main problem is the diminished mucosal protection against the normal levels of gastric acid. *They delay gastric emptying* - Delaying gastric emptying is not a primary mechanism by which NSAIDs cause ulcers. - While some medications can affect gastric motility, this is not the key pathway for NSAID-induced gastropathy.