Hageman factor1 with contact from collagen
can be sufficient to convert the zymogen.
Fitzgerald’s2 not needed,
but often has speeded
the addition of “a” to XI.
When your body’s subjected to contusing,
factor XI can help stop the bruising.
With calcium’s aid,
factor IXa3 is made,
and from here on it gets more confusing.
You may think all this stuff is insipid,
but with calcium, VIIIa, and some phospholipids,4
tenase is formed
as per the norm,
and at prothrombinase,5 intrinsic has ended.
If you’re dying from a traumatic hemorrhage,
your body can make its own bandage.
Factor III is released,
and calcium completes
The common pathway’s where it all comes together
and saves you from the brink of the nether.
put their foot in the door
and then thrombin10 starts building the anchor.
This one can be a tough customer:
Factors V and VIII swoop
in positive feedback loops13
and XIIIa14 transmutes fibrin polymer.
Lysis is launched by tissue plasminogen activator.15
This enzyme causes serine to splinter.
Now plasmin’s16 adrift
inciting a rift,
and D fragments can bind with twin sisters.17
Factor VIII18 and von Willebrand’s factor stick,
and with platelets they help “make blood thick.”
This starts the plug
and it makes me quite smug
to know I won’t die from this prick.
Protein C, with V and VIII, interacts.
A serine protease, these factors it cracks.
And with great behest
promotes coag. arrest
by scaling feedback loops to contract.
Thrombin will activate more protein C
slowing hemostasis against I, V, VIII, and XIII.19
Much more deflation
is at work in this thrombotic scene.
But wait, there’s still more to be regulated!
Thrombin itself will be moderated.
AT III20 will append
to XI, IX, and X
and protease function has just been obliterated.
I hope that you find this to fit,
because for it I have used up my wit.
You’ve made me love heme.
About blood I will dream,
and next semester we’ll write up a skit!
Unveiling the Right Side highlights the creative side of our readers and members of the clinical chemistry community. From photography to poetry, this section is dedicated to encouraging chemists to think with their left and right sides. Share your passion and submit to www.clinchem.org! For more information, please see the Information for Authors at http://www.clinchem.org/info_ar/info_authors.shtml. The opinions expressed in “Unveiling the Right Side” are those of individual authors and unless clearly labeled do not represent the opinions or policies of the Journal.
Author Contributions: All authors confirmed they have contributed to the intellectual content of this paper and have met the following 3 requirements: (a) significant contributions to the conception and design, acquisition of data, or analysis and interpretation of data; (b) drafting or revising the article for intellectual content; and (c) final approval of the published article.
Authors’ Disclosures of Potential Conflicts of Interest: Upon manuscript submission, all authors completed the Disclosures of Potential Conflict of Interest form. Potential conflicts of interest:
Employment or Leadership: K.A. Fay, Michigan Tech University, Aspirus Keweenaw Hospital.
Consultant or Advisory Role: None declared.
Stock Ownership: None declared.
Honoraria: K.A. Fay, University of Wisconsin La Crosse.
Research Funding: None declared.
Expert Testimony: None declared.
Role of Sponsor: The funding organizations played no role in the design of study, choice of enrolled patients, review and interpretation of data, or preparation or approval of manuscript.
↵1. Hageman factor is also known as factor XII, which is a contact factor.
↵2. Fitzgerald factor is also known as high molecular weight kininogen. This forms a complex with kallikrein (formed by prekallikrein) to help factor XI convert to Xla.
↵3. Factor IX, Christmas factor, is a vitamin K-dependent factor.
↵4. Platelet factor 3 (PF3) is part of the tenase complex.
↵5. The prothrombinase complex activates prothrombin (factor II) to thrombin (factor IIa) and includes factors Xa and Va, calcium ions, and phospholipids.
↵6. Proconvertin is known as factor VII, another vitamin K-dependent factor.
↵7. TF stands for tissue factor, factor III.
↵8. Proaccelerin (factor V) is predominantly activated by thrombin (factor IIa).
↵9. Calcium (factor IV), along with factor Va and platelet-activating factor 3, has a role in activating factor II and IIa.
↵10. Prothrombin (factor II), after activation, activates I, V, VIII, and XIII, VIIIa works in the intrinsic pathway and Va enter a positive feedback loop with Xa as stated in this limerick.
↵11. Factor II (prothrombin), when activated, becomes thrombin, which activates factor I.
↵12. Factor I is fibrinogen.
↵13. VIlla:C (antihemophilic factor) enhances coagulation as part of the tenase complex, which activates factor X and causes more activation of factor VIII downstream (positive feedback loop). Factor V (labile factor) forms part of the prothrombinase complex, which activates prothrombin (factor II), which activates more factor V (also positive feedback loop).
↵14. Factor XIIIa is fibrin-stabilizing factor. It covalently cross-links fibrin polymers to form a stable fibrin polymer network—a stable fibrin clot.
↵15. TPA is a serine protease that activates plasminogen to plasmin.
↵16. Plasmin breaks down fibrin to X fragments, then further to Y and D fragments. The Y fragment is broken down to an E and a D fragment.
↵17. This refers to the formation of D-dimers.
↵18. Factor VIII is composed of 2 separate molecular entities, a carrier protein called von Willebrand factor (vWF) and a procoagulant called factor VIII:C.
↵19. Thrombin also activates factors I, V, VIII, and XIII, which generally upregulates hemostatis.
↵20. Antithrombin III is a general serine protease inhibitor. It also activates kallikrein and plasmin.
- © 2010 The American Association for Clinical Chemistry