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Eicosanoids

Tier 4 · #29 of 33 · lower yield · topic 3.15 — every high-yield fact from the book chapter, exam-ready.

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  1. Front
    What is the 20-carbon polyunsaturated fatty acid precursor of all eicosanoids ?
    Back
    Arachidonic acid (20:4)
  2. Front
    Which enzyme catalyzes the committed, rate-limiting upstream step of eicosanoid synthesis by releasing arachidonic acid from membrane phospholipids?
    Back
    Phospholipase A2 (PLA2)
  3. Front
    From which position of membrane glycerophospholipids does phospholipase A2 cleave arachidonic acid ?
    Back
    The sn-2 position
  4. Front
    Eicosanoids are made on ____ and never stored.
    Back
    demand
  5. Front
    After arachidonic acid is released, which two competing enzyme families determine whether the cell makes prostaglandins/thromboxanes versus leukotrienes ?
    Back
    Cyclooxygenase (COX) and lipoxygenase (LOX)
  6. Front
    How do corticosteroids broadly suppress eicosanoid production at its source?
    Back
    They induce lipocortin (annexin A1) , which inhibits PLA2
  7. Front
    From which essential dietary fatty acid does the body synthesize arachidonic acid ?
    Back
    Linoleic acid (18:2, omega-6)
  8. Front
    Why must linoleic acid come from the diet (be essential)?
    Back
    Mammalian cells cannot introduce double bonds beyond carbon 9 from the carboxyl end
  9. Front
    Prostaglandin H2 synthase is universally known by what name?
    Back
    Cyclooxygenase (COX)
  10. Front
    COX is bifunctional: name its two distinct catalytic activities.
    Back
    Cyclooxygenase activity and peroxidase activity
  11. Front
    The cyclooxygenase activity of COX inserts two O2 molecules into arachidonic acid to produce which bicyclic hydroperoxide?
    Back
    PGG2
  12. Front
    The peroxidase activity of COX reduces PGG2 to which central branch-point product?
    Back
    PGH2
  13. Front
    Which prostaglandin is the immediate central hub from which all prostaglandins and thromboxanes are derived?
    Back
    PGH2
  14. Front
    Which COX isoenzyme is the constitutive form expressed steadily in nearly all tissues for physiological housekeeping?
    Back
    COX-1
  15. Front
    Which COX isoenzyme is the inducible form upregulated by cytokines (TNF, IL-1, IL-6) in inflamed tissue?
    Back
    COX-2
  16. Front
    In the gastric mucosa , what protective functions do COX-1 -generated prostaglandins serve?
    Back
    Stimulate protective mucus secretion and bicarbonate production
  17. Front
    Which is the only COX isoenzyme present in mature platelets ?
    Back
    COX-1
  18. Front
    Why can mature platelets not synthesize new COX after release from megakaryocytes?
    Back
    They have no nucleus , so they cannot synthesize new protein
  19. Front
    Which processes (inflammation, pain, fever) does COX-2 primarily mediate?
    Back
    Inflammation, pain, and fever
  20. Front
    Which COX product, made predominantly in platelets , promotes platelet aggregation and vasoconstriction?
    Back
    Thromboxane A2 (TXA2)
  21. Front
    Which cells synthesize prostacyclin (PGI2) ?
    Back
    Vascular endothelial cells
  22. Front
    What are the two opposing actions of prostacyclin (PGI2) ?
    Back
    Inhibits platelet aggregation and causes vasodilation
  23. Front
    TXA2 vs PGI2 — which promotes clotting (aggregation + vasoconstriction)?
    Back
    TXA2 ( PGI2 does the opposite)
  24. Front
    By what mechanism does aspirin inhibit COX ?
    Back
    It irreversibly acetylates Ser530 (transfers an acetyl group )
  25. Front
    Which serine residue does aspirin acetylate on COX-1 ?
    Back
    Ser530
  26. Front
    Aspirin's inhibition of COX is ____ (reversible/irreversible).
    Back
    irreversible
  27. Front
    Why does a single dose of aspirin abolish platelet TXA2 for the platelet's entire ~10-day lifespan?
    Back
    Platelets are anucleate and cannot make new COX-1 to replace the irreversibly acetylated enzyme
  28. Front
    What is the mechanistic basis for using low-dose aspirin as an antiplatelet drug?
    Back
    It irreversibly acetylates platelet COX-1 , permanently abolishing TXA2 synthesis for the platelet lifespan
  29. Front
    By what mechanism do classical NSAIDs (ibuprofen, naproxen, indomethacin) inhibit COX ?
    Back
    Competitive, reversible inhibition (no covalent bond)
  30. Front
    Celecoxib is what type of COX inhibitor?
    Back
    A selective COX-2 inhibitor
  31. Front
    Why does selective COX-2 inhibition ( celecoxib ) increase cardiovascular thrombotic risk?
    Back
    It reduces endothelial COX-2-dependent PGI2 (anti-clotting) more than platelet COX-1-dependent TXA2 , tilting the balance toward thrombosis
  32. Front
    If ibuprofen is taken just before aspirin , how can it blunt aspirin's antiplatelet effect?
    Back
    Ibuprofen occupies the COX-1 active site and physically blocks aspirin from reaching Ser530
  33. Front
    Which lipoxygenase isoform is the principal one in eicosanoid biology, expressed in leukocytes, mast cells, and eosinophils ?
    Back
    5-lipoxygenase (5-LOX)
  34. Front
    5-LOX inserts oxygen at carbon 5 of arachidonic acid to form which initial intermediate?
    Back
    5-HPETE (5-hydroperoxyeicosatetraenoic acid)
  35. Front
    Which unstable epoxide is the committed precursor for all leukotrienes ?
    Back
    Leukotriene A4 (LTA4)
  36. Front
    Which leukotriene , formed by hydrolysis of LTA4 , is a potent neutrophil chemotactic agent ?
    Back
    LTB4
  37. Front
    LTA4 conjugated with glutathione produces which leukotriene (then processed to LTD4 and LTE4 )?
    Back
    LTC4
  38. Front
    What collective name is given to LTC4, LTD4, and LTE4 ?
    Back
    Cysteinyl leukotrienes
  39. Front
    By what older name were the cysteinyl leukotrienes formerly known?
    Back
    Slow-reacting substances of anaphylaxis (SRS-A)
  40. Front
    Cysteinyl leukotrienes are central mediators of which disease via bronchospasm , vascular permeability, and mucus secretion?
    Back
    Asthma
  41. Front
    Montelukast (Singulair) treats asthma by blocking the receptor for which leukotriene ?
    Back
    LTD4
  42. Front
    Do aspirin and NSAIDs inhibit the 5-LOX (leukotriene) pathway?
    Back
    No — they act only on the COX pathway
  43. Front
    In aspirin-exacerbated respiratory disease , why does blocking COX trigger bronchospasm?
    Back
    Arachidonic acid is shunted into the LOX pathway , increasing leukotriene production
  44. Front
    Which omega-3 fatty acid from fish oil competes with arachidonic acid at both COX and LOX ?
    Back
    EPA (eicosapentaenoic acid)
  45. Front
    EPA generates which series of prostaglandins, thromboxanes, and leukotrienes ?
    Back
    Series-3 prostaglandins/thromboxanes and series-5 leukotrienes ( much weaker pro-inflammatory effects )
  46. Front
    EPA and DHA are precursors to which specialized pro-resolving mediators that actively terminate inflammation?
    Back
    Resolvins and protectins
  47. Front
    Does increasing dietary omega-3 abolish COX/LOX activity?
    Back
    No — it modulates the substrate pool to produce a less aggressive eicosanoid signature
  48. Front
    What does the Greek root "eikosi" (in eicosanoid ) mean?
    Back
    Twenty
  49. Front
    Aspirin irreversibly acetylates Ser530 on which COX isoenzyme(s)?
    Back
    Both COX-1 and COX-2
  50. Front
    By what two reaction types does the liver convert linoleic acid into arachidonic acid ?
    Back
    Desaturation and elongation (adding double bonds and extending the chain by two-carbon units)
  51. Front
    In how many carbons does each elongation step extend the chain during arachidonic acid synthesis from linoleic acid ?
    Back
    Two carbons per step
  52. Front
    Which named synthase converts PGH2 to thromboxane A2 in platelets ?
    Back
    Thromboxane synthase
  53. Front
    Give the full structural shorthand of arachidonic acid (chain length, double bonds, geometry, positions).
    Back
    20:4, all-cis Δ5,8,11,14
  54. Front
    At which four carbons are the cis double bonds of arachidonic acid located?
    Back
    Carbons 5, 8, 11, and 14
  55. Front
    What is the physiological purpose of balancing platelet TXA2 against endothelial PGI2 ?
    Back
    It keeps blood fluid in healthy vessels yet allows clot formation only where it is needed
  56. Front
    Besides EPA , which other omega-3 fatty acid is a precursor of resolvins and protectins ?
    Back
    DHA (docosahexaenoic acid)
  57. Front
    A diet chronically low in omega-3 fatty acids elevates which three pro-inflammatory cytokines as a biochemical backdrop?
    Back
    TNF, IL-1, and IL-6
  58. Front
    How do eicosanoids act and how long do they last after synthesis?
    Back
    As ultra-local (autocrine/paracrine) hormones , made on demand and destroyed within seconds to minutes — never stored
  59. Front
    Functional split: which branch yields the mediators of pain, fever, and clotting?
    Back
    The COX branch ( prostaglandins and thromboxanes ); 5-LOX yields the leukotrienes of allergic inflammation and bronchoconstriction
  60. Front
    Which branch produces the mediators of allergic inflammation and bronchoconstriction?
    Back
    The 5-LOX branch ( leukotrienes )
  61. Front
    LTB4 vs the cysteinyl leukotrienes (LTC4/D4/E4) — which one is the neutrophil chemoattractant?
    Back
    LTB4 (the cysteinyl leukotrienes cause bronchoconstriction instead)
  62. Front
    Reversibility contrast: aspirin vs classical NSAIDs (ibuprofen/naproxen) vs celecoxib as COX inhibitors?
    Back
    Aspirin = irreversible covalent (acetylates Ser530); classical NSAIDs = reversible competitive ; celecoxib = selective COX-2

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