Prostaglandins and Eicosanoids — MCQs
Which of the following is not a definite use for Prostaglandin E2 (PGE2)?
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?
Reverse cholesterol transport is mediated by which lipoprotein?
Lipid is required in the average diet because it:
What is the concentration of the reagent used for determining the Reichert-Meissl number?
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: 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 3: 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 4: 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 5: 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 6: 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 7: 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 8: Reverse cholesterol transport is mediated by which lipoprotein?
- A. HDL (Correct Answer)
- B. VLDL
- C. LDL
- D. IDL
Explanation: **Explanation:** **Reverse Cholesterol Transport (RCT)** is the physiological process by which excess cholesterol is removed from peripheral tissues (like macrophages in the arterial wall) and transported back to the liver for excretion in bile. **HDL (High-Density Lipoprotein)** is the primary mediator of this process, which is why it is clinically referred to as "Good Cholesterol." The process involves: 1. **Efflux:** Free cholesterol is moved from cells to nascent HDL via **ABCA1 transporters**. 2. **Esterification:** The enzyme **LCAT** (Lecithin-Cholesterol Acyltransferase) converts free cholesterol into cholesterol esters, trapping them in the HDL core. 3. **Hepatic Uptake:** HDL delivers these esters to the liver via **SR-BI receptors** or transfers them to other lipoproteins via **CETP**. **Why other options are incorrect:** * **VLDL (Very Low-Density Lipoprotein):** Synthesized in the liver to transport endogenous triglycerides to peripheral tissues. * **LDL (Low-Density Lipoprotein):** Known as "Bad Cholesterol," it transports cholesterol **from** the liver **to** peripheral tissues. High levels are associated with atherosclerosis. * **IDL (Intermediate-Density Lipoprotein):** A transient product formed during the conversion of VLDL to LDL; it is not involved in RCT. **High-Yield NEET-PG Pearls:** * **Apo A-I:** The major apoprotein associated with HDL and a potent activator of LCAT. * **Tangier Disease:** A genetic deficiency of ABCA1 transporters resulting in extremely low HDL levels and orange-colored tonsils. * **Anti-atherogenic property:** HDL prevents foam cell formation, reducing the risk of Coronary Artery Disease (CAD).
Question 9: Lipid is required in the average diet because it:
- A. has a high caloric value
- B. provides essential fatty acids (Correct Answer)
- C. aids in absorption of carbohydrates
- D. is necessary for storage of carbohydrates
Explanation: **Explanation:** The primary nutritional requirement for lipids in the diet is to provide **Essential Fatty Acids (EFAs)**—specifically **Linoleic acid (omega-6)** and **Alpha-linolenic acid (omega-3)**. These are termed "essential" because the human body lacks the enzymes (**desaturases** beyond carbon 9) required to synthesize them de novo. These fatty acids are vital precursors for the synthesis of eicosanoids (prostaglandins, leukotrienes) and are structural components of cell membranes. **Analysis of Options:** * **Option A (High caloric value):** While lipids are the most energy-dense macronutrient (9 kcal/g), this is a characteristic, not the primary biological *requirement*. The body can derive sufficient calories from carbohydrates and proteins if necessary. * **Option C & D (Carbohydrate metabolism):** Lipids do not aid in the absorption of carbohydrates, nor are they necessary for their storage. Carbohydrates are stored as glycogen in the liver and muscles. **High-Yield NEET-PG Pearls:** 1. **EFA Deficiency:** Clinically presents as **Phrynoderma** (follicular hyperkeratosis/toad skin), poor wound healing, and alopecia. 2. **Fat-Soluble Vitamins:** Dietary lipids are also essential for the absorption of Vitamins **A, D, E, and K**. 3. **Arachidonic Acid:** It is considered "semi-essential" because it can be synthesized from Linoleic acid. 4. **Energy Storage:** Lipids are stored in the body as **Triacylglycerols (TAGs)** in adipose tissue, which serves as the body's main energy reservoir.
Question 10: What is the concentration of the reagent used for determining the Reichert-Meissl number?
- A. 0.1 N KOH (Correct Answer)
- B. 0.5 N KOH
- C. 0.1 N NaOH
- D. 0.5 N NaOH
Explanation: **Explanation:** The **Reichert-Meissl (RM) number** is a critical analytical constant used in lipid biochemistry to determine the amount of volatile, water-soluble fatty acids (primarily butyric and caproic acid) present in a fat or oil. **Why 0.1 N KOH is correct:** The RM number is defined as the number of milliliters of **0.1 N Potassium Hydroxide (KOH)** required to neutralize the steam-volatile, water-soluble fatty acids distilled from 5 grams of fat. KOH is the standard alkali used in this titration process because it effectively neutralizes the short-chain fatty acids (like butyric acid) that are characteristic of milk fats. **Analysis of Incorrect Options:** * **0.5 N KOH (B):** This concentration is too high. 0.5 N KOH is typically used in the determination of the **Saponification Number**, where a stronger alkali is needed to hydrolyze all fatty acids in a sample. * **0.1 N and 0.5 N NaOH (C & D):** While Sodium Hydroxide (NaOH) is a strong base, the standard protocol for RM number specifically mandates KOH. In lipid chemistry, KOH is preferred for many titrations because it is more soluble in organic solvents (like ethanol) often used during the preparation of fat samples. **High-Yield Clinical Pearls for NEET-PG:** * **Significance:** The RM number is primarily used to detect the **adulteration of Ghee or Butter**. * **Normal Value:** Pure Ghee/Butter has a high RM number (typically **24–30**) due to its high content of butyric acid. * **Adulteration:** If butter is adulterated with animal fats or vegetable oils (which have very low RM numbers, usually <1), the RM value of the sample will significantly decrease. * **Related Constant:** The **Polenske Number** also uses 0.1 N KOH but measures steam-volatile, water-**insoluble** fatty acids (like caprylic and capric acid).
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free