Coagulation Cascade: A Series of Limericks - Clinical Chemistry

Coagulation Cascade: A Series of Limericks
Mark A. Vande Haar and Karyn A. Fay*
Intrinsic:
Hageman factor 1 with contact from collagen
can be sufficient to convert the zymogen.
Fitzgerald’s 2 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 IXa 3 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.
Extrinsic:
If you’re dying from a traumatic hemorrhage,
your body can make its own bandage.
Factor III is released,
and calcium completes
the VIIa 6 and TF 7 assemblage.
Common:
The common pathway’s where it all comes together
and saves you from the brink of the nether.
Factors X, V 8 , and IV 9
put their foot in the door
and then thrombin 10 starts building the anchor.
This one can be a tough customer:
factor II 11 converts I 12 to a monomer.
Factors V and VIII swoop
in positive feedback loops 13
and XIIIa 14 transmutes fibrin polymer.
Unveiling the Right Side
Clinical Chemistry 56:8 (2010) 1369

Fibrinolysis:
Lysis is launched by tissue plasminogen activator. 15
This enzyme causes serine to splinter.
Now plasmin’s 16 adrift
inciting a rift,
and D fragments can bind with twin sisters. 17
Interactions:
Factor VIII 18 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.
Regulation:
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.
1370 Clinical Chemistry 56:8 (2010)
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
and down-regulation
is at work in this thrombotic scene.
But wait, there’s still more to be regulated!
Thrombin itself will be moderated.
AT III 20 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
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.
Michigan Tech University, Houghton, MI.
*Address correspondence to this author at: Michigan Tech University, 1400
Townsend Drive, Dow 734, Houghtoh, MI 49931. Fax 906-487-3167; e-mail
kafay@mtu.edu.
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.
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.
DOI: 10.1373/clinchem.2010.150052
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 inactivates
kallikrein and plasmin.
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Clinical Chemistry 56:8 (2010) 1371