Thromboxanes MCQs With Answer

Introduction: Thromboxanes MCQs With Answer is a focused study resource for B. Pharm students exploring thromboxane biology and pharmacology. This short primer emphasizes key concepts such as eicosanoids, biosynthesis from arachidonic acid via cyclooxygenase (COX), the role of TXA2 in platelet aggregation and vasoconstriction, thromboxane receptors (TP), measurement of metabolites like TXB2, and clinical pharmacology including aspirin and COX inhibitors. Questions reinforce mechanisms, assays, receptor signaling, and therapeutic implications in thrombosis, pulmonary vasoconstriction, and inflammation. Now let’s test your knowledge with 30 MCQs on this topic.

Q1. What is the primary biochemical precursor for thromboxane synthesis?

• Arachidonic acid
• Linoleic acid
• Cholesterol
• Phosphatidylcholine

Correct Answer: Arachidonic acid

Q2. Which enzyme initially converts arachidonic acid to prostaglandin H2 (PGH2), the common substrate for thromboxane synthesis?

• Cyclooxygenase (COX)
• Lipoxygenase (LOX)
• Thromboxane synthase
• Phospholipase A2

Correct Answer: Cyclooxygenase (COX)

Q3. Which enzyme directly converts PGH2 to thromboxane A2 (TXA2)?

• Thromboxane synthase
• Prostacyclin synthase
• 5-lipoxygenase
• COX-2

Correct Answer: Thromboxane synthase

Q4. Which thromboxane molecule is the biologically active platelet agonist?

• TXA2 (Thromboxane A2)
• TXB2 (Thromboxane B2)
• 11-dehydro-TXB2
• Prostacyclin (PGI2)

Correct Answer: TXA2 (Thromboxane A2)

Q5. What is the primary receptor for thromboxane on platelets and vascular smooth muscle called?

• Thromboxane-prostanoid (TP) receptor
• Prostacyclin (IP) receptor
• Leukotriene B4 receptor
• Histamine H1 receptor

Correct Answer: Thromboxane-prostanoid (TP) receptor

Q6. Which G-protein pathways are most commonly activated by the TP receptor?

• Gq and G12/13
• Gs only
• Gi only
• Gs and Gi

Correct Answer: Gq and G12/13

Q7. What are the principal physiological effects of thromboxane A2?

• Platelet aggregation and vasoconstriction
• Vasodilation and inhibition of aggregation
• Bronchodilation and mucus secretion
• Leukocyte chemotaxis and fever

Correct Answer: Platelet aggregation and vasoconstriction

Q8. How does aspirin reduce thromboxane-mediated platelet activation?

• Irreversible inhibition of platelet COX-1, preventing TXA2 formation
• Competitive antagonism at the TP receptor
• Inhibition of thromboxane synthase only
• Enhancement of prostacyclin synthesis

Correct Answer: Irreversible inhibition of platelet COX-1, preventing TXA2 formation

Q9. Why is low-dose aspirin used for cardiovascular prophylaxis?

• It selectively decreases platelet TXA2 synthesis, reducing thrombosis risk
• It increases endothelial PGI2 production to prevent vasospasm
• It blocks TP receptors on vascular smooth muscle
• It inhibits thromboxane metabolite excretion

Correct Answer: It selectively decreases platelet TXA2 synthesis, reducing thrombosis risk

Q10. Which urinary metabolite is commonly measured clinically as an index of systemic thromboxane production?

• 11-dehydro-TXB2
• TXA2
• PGH2
• Leukotriene C4

Correct Answer: 11-dehydro-TXB2

Q11. Which prostanoid primarily opposes thromboxane actions in the vasculature?

• Prostacyclin (PGI2)
• PGE2
• PGD2
• LTC4

Correct Answer: Prostacyclin (PGI2)

Q12. Which drug is a selective thromboxane receptor (TP) antagonist developed for antiplatelet effect?

• Terutroban
• Clopidogrel
• Aspirin
• Heparin

Correct Answer: Terutroban

Q13. Which synthetic analogue of TXA2 is widely used in research to activate TP receptors?

• U46619
• Iloprost
• Latanoprost
• Montelukast

Correct Answer: U46619

Q14. Overproduction of thromboxane contributes to which pulmonary condition via vasoconstriction?

• Pulmonary hypertension
• Emphysema due to alveolar destruction
• Primary pulmonary fibrosis
• Pneumothorax

Correct Answer: Pulmonary hypertension

Q15. Which COX isoform predominates in platelets and is responsible for TXA2 generation?

• COX-1
• COX-2
• COX-3
• 5-LOX

Correct Answer: COX-1

Q16. Why can selective COX-2 inhibitors increase thrombotic risk?

• They reduce endothelial PGI2 synthesis while sparing platelet TXA2, shifting the balance toward thrombosis
• They directly activate TP receptors on platelets
• They increase thromboxane synthase expression in liver
• They enhance leukotriene synthesis causing vasospasm

Correct Answer: They reduce endothelial PGI2 synthesis while sparing platelet TXA2, shifting the balance toward thrombosis

Q17. Which laboratory assay directly assesses platelet aggregation influenced by thromboxane?

• Platelet aggregometry
• Serum creatinine
• ELISA for C-reactive protein
• Coagulation factor VIII assay

Correct Answer: Platelet aggregometry

Q18. What is the approximate biological half-life of TXA2 in the circulation?

• About 30 seconds
• About 10 minutes
• About 24 hours
• About 2 hours

Correct Answer: About 30 seconds

Q19. Which molecule is the stable, inactive hydrolysis product of TXA2 often measured in serum assays?

• TXB2
• TXA3
• PGI2
• PGE1

Correct Answer: TXB2

Q20. Which class of drugs directly inhibits thromboxane synthase activity?

• Thromboxane synthase inhibitors (e.g., dazoxiben)
• Selective serotonin reuptake inhibitors
• Beta blockers
• ACE inhibitors

Correct Answer: Thromboxane synthase inhibitors (e.g., dazoxiben)

Q21. Which blood component is the chief source of thromboxane A2 in hemostasis?

• Platelets
• Endothelial cells
• Neutrophils
• Red blood cells

Correct Answer: Platelets

Q22. Activation of TP receptors on platelets typically results in which intracellular change?

• Increase in intracellular calcium concentration
• Decrease in cAMP with no calcium change
• Activation of adenylate cyclase to raise cAMP
• Opening of K+ channels to hyperpolarize the cell

Correct Answer: Increase in intracellular calcium concentration

Q23. Thromboxane contributes to bronchoconstriction; this makes it relevant in which respiratory condition?

• Asthma
• Pneumonia caused by bacteria
• Pulmonary embolism due to clots
• Interstitial lung disease due to fibrosis

Correct Answer: Asthma

Q24. Besides aggregation, TXA2 promotes which morphological change in platelets during activation?

• Shape change (filopodia/lamellipodia formation)
• Formation of erythrocyte rouleaux
• Membrane blebbing in endothelial cells only
• Complete platelet lysis

Correct Answer: Shape change (filopodia/lamellipodia formation)

Q25. Which medication would directly reduce platelet TXA2 production when taken chronically at low dose?

• Aspirin (low-dose)
• Ibuprofen (intermittent low dose)
• Nifedipine
• Warfarin

Correct Answer: Aspirin (low-dose)

Q26. Measurement of serum TXB2 after clotting is used to assess what platelet capacity?

• Platelet capacity to generate TXA2
• Platelet count only
• Red blood cell aggregation
• Endothelial nitric oxide production

Correct Answer: Platelet capacity to generate TXA2

Q27. A genetic loss-of-function mutation in the TP receptor would most likely cause which clinical sign?

• Bleeding tendency due to impaired platelet aggregation
• Hypercoagulability with recurrent thrombosis
• Elevated blood pressure due to vasoconstriction
• Excessive bronchoconstriction and asthma exacerbations

Correct Answer: Bleeding tendency due to impaired platelet aggregation

Q28. Which prostanoid is therapeutically used as an antiplatelet vasodilator and functionally opposes thromboxane?

• Iloprost (stable prostacyclin analogue)
• Misoprostol (PGE1 analogue)
• Latanoprost (PGF2α analogue)
• Bimatoprost

Correct Answer: Iloprost (stable prostacyclin analogue)

Q29. Thromboxane A synthase acts on which intermediate substrate in the prostanoid pathway?

• PGH2
• AA (arachidonic acid) directly
• PGE2
• Leukotriene A4

Correct Answer: PGH2

Q30. Excessive thromboxane activity is most directly associated with which pathological process?

• Atherothrombosis and platelet-mediated thrombus formation
• Impaired wound healing due to reduced fibroblast activity
• Decreased inflammation and immune suppression
• Reduced vascular smooth muscle tone causing hypotension

Correct Answer: Atherothrombosis and platelet-mediated thrombus formation

G S Sachin

I am a Registered Pharmacist under the Pharmacy Act, 1948, and the founder of PharmacyFreak.com. I hold a Bachelor of Pharmacy degree from Rungta College of Pharmaceutical Science and Research. With a strong academic foundation and practical knowledge, I am committed to providing accurate, easy-to-understand content to support pharmacy students and professionals. My aim is to make complex pharmaceutical concepts accessible and useful for real-world application.

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