Prostaglandins and Eicosanoids — MCQs
Which of the following is not a definite use for Prostaglandin E2 (PGE2)?
All of the following are classical mediators of inflammation, except which of the following?
What is an atypical side effect of montelukast?
Zileuton is:-
Chemotaxis is mediated by-
Which of the following is the MOST accurate statement regarding thromboxane A2?
Mechanism of action of aspirin in pain relief is:
Which organ does not utilise ketone bodies?
What is the role of cholesterol present in LDL?
Which receptors are present in the liver for the uptake of LDL?
Prostaglandins and Eicosanoids Indian Medical PG Practice Questions and MCQs
Question 1: Which of the following is not a definite use for Prostaglandin E2 (PGE2)?
- A. Induces labour
- B. Keeps patency of PDA (Correct Answer)
- C. Contraception
- D. Therapeutic abortion
Explanation: ***Keeps patency of PDA*** - **Prostaglandin E1 (PGE1)**, not PGE2, is used to maintain the patency of the **ductus arteriosus** in neonates with certain congenital heart defects. - PGE1 causes **vascular smooth muscle relaxation**, preventing closure of the ductus arteriosus. *Contraception* - **PGE2 analogs** are used in various forms of contraception, including emergency contraception and for cervical ripening before elective abortion. - They act by inducing **uterine contractions** and can interfere with implantation or facilitate expulsion of a fertilized egg. *Induces labour* - **PGE2 (dinoprostone)** is commonly used clinically to induce labor by promoting **cervical ripening** and stimulating **uterine contractions**. - It is administered as a vaginal gel or insert to prepare the cervix for delivery. *Therapeutic abortion* - **PGE2 analogs** are used to induce therapeutic abortion, particularly in the second trimester, by causing powerful **uterine contractions** that lead to the expulsion of the fetus. - They are often used in combination with other agents to enhance their efficacy.
Question 2: All of the following are classical mediators of inflammation, except which of the following?
- A. Prostaglandins
- B. Interleukin-1 (IL-1)
- C. Tumour necrosis factor-alpha (TNF-alpha)
- D. Myeloperoxidase (MPO) (Correct Answer)
Explanation: ***Myeloperoxidase*** - **Myeloperoxidase** is primarily an enzyme involved in the microbial killing process in neutrophils, not a typical mediator of inflammation. - It catalyzes the production of **hypochlorous acid** (HOCl) during the oxidative burst, more related to pathogen destruction than inflammation mediation. *Tumour necrosis factor-a (TNF-a)* - **TNF-a** is a key pro-inflammatory cytokine that plays a significant role in systemic inflammation and is involved in the acute phase response [1][3]. - It promotes the recruitment of immune cells to sites of inflammation and is involved in the activation of the inflammatory process [1][3]. *Prostaglandins* - **Prostaglandins** are lipid mediators derived from arachidonic acid that have various roles, including enhancing inflammation and pain signaling [1][2]. - They contribute to vasodilation, increased vascular permeability, and sensitization of nociceptors during inflammatory responses [1][2]. *Interleukin-1* - **Interleukin-1** (IL-1) is a crucial inflammatory cytokine that stimulates immune responses and is involved in both acute and chronic inflammation [1][3]. - It can induce fever and promote the expression of adhesion molecules on endothelial cells, facilitating leukocyte migration [1][3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 95-96. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 97-99.
Question 3: What is an atypical side effect of montelukast?
- A. Goodpasture syndrome
- B. Membranous glomerulonephritis
- C. Bronchial asthma
- D. Churg-Strauss syndrome (Correct Answer)
Explanation: ***Churg-Strauss syndrome*** - The apparent development of **Churg-Strauss syndrome** (eosinophilic granulomatosis with polyangiitis) has been reported in patients treated with montelukast, although it is believed to be related more to the unmasking of the disease rather than a direct drug effect. - This typically occurs when **corticosteroids** are tapered or withdrawn as montelukast takes over, revealing the underlying vasculitis. *Goodpasture syndrome* - **Goodpasture syndrome** is an autoimmune disease causing rapidly progressive glomerulonephritis and pulmonary hemorrhage, characterized by anti-glomerular basement membrane (GBM) antibodies. - There is no established association between montelukast use and the development of Goodpasture syndrome. *Membranous glomerulonephritis* - **Membranous glomerulonephritis** is a common cause of nephrotic syndrome, characterized by immune complex deposition on the glomerular basement membrane. - This condition is not typically linked to the use of montelukast. *Bronchial asthma* - **Bronchial asthma** is the condition montelukast is used to treat, acting as a leukotriene receptor antagonist to reduce inflammation and bronchoconstriction. - It is a primary indication for the drug, not a side effect.
Question 4: Zileuton is:-
- A. Phospholipase inhibitor
- B. Leukotriene receptor antagonist
- C. 5-Lipoxygenase inhibitor (Correct Answer)
- D. Cyclooxygenase inhibitor
Explanation: ***5-Lipoxygenase inhibitor*** - **Zileuton** specifically inhibits **5-lipoxygenase**, an enzyme crucial for the synthesis of **leukotrienes**. - By blocking this enzyme, zileuton reduces the production of **pro-inflammatory leukotrienes**, which are involved in the pathophysiology of **asthma**. *Phospholipase inhibitor* - **Phospholipase A2 inhibitors** like **corticosteroids** act upstream by preventing the release of **arachidonic acid**, a precursor to both prostaglandins and leukotrienes. - Zileuton's action is more specific to the **leukotriene pathway**, occurring after arachidonic acid is already formed. *Cyclooxygenase inhibitor* - **Cyclooxygenase (COX) inhibitors** (like NSAIDs) block the synthesis of **prostaglandins** and **thromboxanes** from arachidonic acid. - Zileuton does not affect the COX pathway but rather targets the **lipoxygenase pathway**. *Leukotriene receptor antagonist* - **Leukotriene receptor antagonists** (e.g., Montelukast, Zafirlukast) block the binding of leukotrienes to their receptors, preventing their downstream effects. - While both target the **leukotriene pathway**, zileuton works by **inhibiting their production**, not their receptor binding.
Question 5: Chemotaxis is mediated by-
- A. Histamine
- B. Leukotriene C4 and C3a
- C. Bradykinin
- D. Leukotriene B4 and C5a (Correct Answer)
Explanation: ***Leukotriene B4 and C5a*** - Both **Leukotriene B4** [2] and **C5a** [1] are potent **chemoattractants** that guide the migration of neutrophils and other immune cells to sites of inflammation. - They are crucial in amplifying the **immune response**, particularly during acute inflammatory reactions. *Histamine* - Primarily involved in **vasodilation** and increased **vascular permeability**, rather than mediating chemotaxis. - Does not specifically attract immune cells to sites of injury or infection like leukotrienes do. *Bradykinin* - Mainly functions in **pain sensation** and promoting **vascular permeability**, not as a direct chemotactic agent. - It influences inflammation but does not effectively recruit immune cells to tissues. *Leukotriene C4 and C3a* - **Leukotriene C4** is involved in bronchoconstriction, while **C3a** [1] has roles in the complement system but is less potent than C5a in chemotaxis. - These mediators have different primary roles in inflammation, lacking the specificity of B4 and C5a for leukocyte attraction. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 99-100. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 95-96.
Question 6: Which of the following is the MOST accurate statement regarding thromboxane A2?
- A. Formed by platelets
- B. Formed from PGG2/PGH2
- C. Prothrombogenic (Correct Answer)
- D. Vasoconstrictor
Explanation: ***ABCD*** - Thromboxane A2 is primarily **formed by platelets** [1] and is derived from **PGG2/PGH2**, having a significant role in **hemostasis**. - It is known to be **prothrombogenic** [1] and acts as a **vasoconstrictor** [2], enhancing platelet aggregation and promoting localized increases in **vascular resistance**. *ACB* - This option indicates only a partial representation of thromboxane A2's functions and formation. - It misses the comprehensive list of effects and does not mention it as a **vasoconstrictor** or its role in hemostasis. *ABC* - Like , it lacks recognition of all relevant characteristics of thromboxane A2. - Thus, it omits the **vasodilator** function, even though thromboxane A2 acts mainly as a **vasoconstrictor**. *ABCDE* - Including **E as vasodilator** contradicts the well-known actions of thromboxane A2, which does not promote vasodilation [2]. - Thus, this ssentially misrepresents thromboxane A2 as it primarily promotes **vasoconstriction** and is **prothrombogenic**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 130. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 95-96.
Question 7: Mechanism of action of aspirin in pain relief is:
- A. Enhances opioid action
- B. Activates serotonin receptors
- C. Inhibits COX enzymes (Correct Answer)
- D. Blocks NMDA receptors
Explanation: **Inhibits COX enzymes** - **Aspirin** exerts its analgesic effects primarily by **irreversibly inhibiting** cyclooxygenase (COX) enzymes, particularly COX-1 and COX-2. - This inhibition reduces the synthesis of **prostaglandins**, which are important mediators of pain and inflammation. *Enhances opioid action* - Opioids primarily act on **opioid receptors** in the central nervous system to reduce pain perception. - Aspirin does not directly enhance opioid action; while they can be used together for additive pain relief, their mechanisms are distinct. *Activates serotonin receptors* - Activation of **serotonin receptors** (5-HT receptors) can play a role in pain modulation, but aspirin's primary mechanism is not through these receptors. - Some antidepressants and triptans exert their effects via serotonin receptors. *Blocks NMDA receptors* - **NMDA receptors** are involved in neuronal excitability and the processing of pain signals, particularly in chronic pain. - Drugs that block NMDA receptors, such as ketamine, have analgesic properties but this is not the mechanism of action for aspirin.
Question 8: Which organ does not utilise ketone bodies?
- A. Liver (Correct Answer)
- B. Brain
- C. Skeletal muscles
- D. Cardiac muscles
Explanation: **Explanation** The correct answer is **A. Liver**. **1. Why the Liver cannot utilize Ketone Bodies:** The liver is the primary site for **ketogenesis** (the synthesis of ketone bodies), but it cannot utilize them for energy. This is because the liver lacks the essential enzyme **Thiophorase** (also known as Succinyl-CoA:3-ketoacid CoA transferase). In extrahepatic tissues, Thiophorase converts Acetoacetate into Acetoacetyl-CoA by transferring a CoA group from Succinyl-CoA. Without this enzyme, the liver cannot activate ketone bodies to enter the TCA cycle, preventing a "futile cycle" where the liver would consume the fuel it is supposed to export to the rest of the body. **2. Why the other options are incorrect:** * **B. Brain:** During prolonged fasting or starvation, the brain adapts to use ketone bodies (specifically 3-hydroxybutyrate and acetoacetate) as its primary energy source, reducing its dependence on glucose. * **C & D. Skeletal and Cardiac Muscles:** These tissues possess high levels of Thiophorase. In the early stages of fasting, muscles are the primary consumers of ketone bodies to spare glucose for the brain. **High-Yield NEET-PG Pearls:** * **Rate-limiting enzyme of Ketogenesis:** HMG-CoA Synthase (Mitochondrial). * **Ketone bodies include:** Acetone (non-metabolizable, excreted in breath), Acetoacetate, and β-Hydroxybutyrate. * **Site of Ketogenesis:** Mitochondria of hepatocytes. * **Key Enzyme for Utilization:** Thiophorase (absent in Liver). * **Clinical Sign:** "Fruity odor" of breath in Diabetic Ketoacidosis (DKA) is due to the excretion of Acetone.
Question 9: What is the role of cholesterol present in LDL?
- A. Represents primarily cholesterol that is being removed from peripheral cells.
- B. Binds to a receptor and diffuses across the cell membrane.
- C. On accumulation in the cell inhibits replenishment of LDL receptors. (Correct Answer)
- D. When enters a cell, suppresses activity of acyl-CoA; cholesterol acytransferase ACAT.
Explanation: ### Explanation The primary role of LDL (Low-Density Lipoprotein) is to transport cholesterol from the liver to peripheral tissues. This process is tightly regulated by the **Goldstein and Brown pathway** of receptor-mediated endocytosis. **1. Why Option C is Correct:** When LDL binds to the LDL receptor (ApoB-100/E receptor), it is internalized. Once inside the cell, the cholesterol is released. An increase in free intracellular cholesterol triggers a feedback mechanism to prevent "cholesterol overload." It **downregulates the synthesis of new LDL receptors** by inhibiting the transcription of the LDL receptor gene (via SREBP suppression). This reduces further uptake of LDL from the blood. **2. Why the Other Options are Incorrect:** * **Option A:** This describes **HDL (High-Density Lipoprotein)**, which is involved in "Reverse Cholesterol Transport," moving cholesterol from peripheral cells back to the liver. * **Option B:** LDL does not "diffuse" across the membrane. It enters the cell via **clathrin-coated pits** through a specific process called **receptor-mediated endocytosis**. * **Option D:** Intracellular cholesterol actually **activates** ACAT (Acyl-CoA: cholesterol acyltransferase). ACAT promotes the esterification of free cholesterol into cholesterol esters for storage, thereby reducing the toxic levels of free cholesterol within the cell. **High-Yield Clinical Pearls for NEET-PG:** * **Rate-Limiting Step:** Intracellular cholesterol inhibits **HMG-CoA Reductase**, the rate-limiting enzyme of de novo cholesterol synthesis. * **Familial Hypercholesterolemia (Type IIa):** Caused by a genetic defect or absence of LDL receptors, leading to drastically elevated plasma LDL and premature atherosclerosis. * **Apolipoprotein:** The primary apoprotein associated with LDL is **ApoB-100**. * **Statins:** These drugs inhibit HMG-CoA Reductase, leading to a compensatory *increase* in LDL receptor expression, which clears more LDL from the circulation.
Question 10: Which receptors are present in the liver for the uptake of LDL?
- A. Apolipoprotein E
- B. Apolipoprotein A and Apolipoprotein E
- C. Apolipoprotein E and Apolipoprotein B100 (Correct Answer)
- D. Apolipoprotein B100
Explanation: **Explanation:** The **LDL receptor (LDLR)**, also known as the **Apo B100/E receptor**, is a cell surface glycoprotein primarily expressed in the liver. It plays a critical role in cholesterol homeostasis by mediating the endocytosis of cholesterol-rich lipoproteins. **Why Option C is Correct:** The LDL receptor has a high affinity for two specific ligands: 1. **Apolipoprotein B100:** Found on **VLDL, IDL, and LDL**. This is the primary ligand for the uptake of LDL particles. 2. **Apolipoprotein E:** Found on **Chylomicron remnants, VLDL, and IDL**. Apo E has a much higher affinity for the LDLR than Apo B100, allowing the liver to efficiently clear remnant particles. Because the receptor recognizes both proteins, it is physiologically defined by its dual specificity for Apo E and Apo B100. **Analysis of Incorrect Options:** * **Option A:** Apo E is a ligand for the LDLR and the LRP (LDL Receptor-Related Protein), but this option is incomplete as it ignores the primary ligand for LDL itself (B100). * **Option B:** Apo A (specifically A-I) is associated with **HDL** and interacts with ABCA1/SR-B1 receptors, not the LDL receptor. * **Option D:** While B100 is the sole apolipoprotein on LDL, the receptor itself is genetically and structurally designed to bind both B100 and E. **High-Yield Clinical Pearls for NEET-PG:** * **Familial Hypercholesterolemia (Type IIa):** Caused by a genetic defect or deficiency in the **LDL receptor**, leading to secondary elevations in plasma LDL and premature atherosclerosis. * **PCSK9 Inhibitors:** PCSK9 is an enzyme that degrades LDL receptors. Inhibitors (e.g., Alirocumab) increase the recycling of these receptors to the cell surface, lowering LDL levels. * **Wolman Disease:** A lysosomal storage disease where a deficiency in acid lipase prevents the release of free cholesterol from LDL after it has been internalized by the receptor.
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