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In medical school it can also be painful to learn and teach a coagulation cascade. The reason you hate the coagulation cascade is that there are a lot of Roman numerals with arrows back and forth? I’m gonna try to simplify things with a significant clinical correlation here. I know that without realizing it, many of you are tempted to dig up a waterfall and print it out on forensic documents. But that won’t help you, and I advise you to study the coagulation cascade for a few minutes and not just read it.

Coefficients of coagulation – mnemonic

During my medical studies I read this reminder in a book and it is still very useful:

The first person said that cancer leads to disease, the other said that the protein was high in fat.

  1. factor I : Fibrinogen (First)
  2. Factor II : Prothrombin (male)
  3. Factor III : Thromboplasty or tissue factor (narrative)
  4. Factor IV : Calcium (cancer)
  5. Factor V : Unstable factor (lead), proxelerine.
  6. Coefficient VI: Axeler (reminder: excluded because it does not play a role in blood coagulation)
  7. Factor VII : Stable factor (disease), proconvertin.
  8. Factor VIII : Anti-haemophilic factor A (other)
  9. Factor IX : Christmas factor (Chap), antihemophilic factor B
  10. X factor : Stewart (Said) power factor, autoprombin III
  11. Factor XI : Plasma Thromboplastin Background or PTA (protein)
  12. Factor XII : Heigemann’s coefficient (high), glass or contact factor.
  13. Factor XIII: Fibrin or fibrinase stabilizing factor (fat)

Coagulation cascade – simplified

A complex and detailed cascade can be found in the manual.

1. The goal of the coagulation cascade is to deposit fibrin, the final step:

  • factor I: fibrinogen, which is converted into fibrin.
  • Factor XIII : The fibrin stabilizing factor that crosses the fibrin.

2. The coagulation cascade is activated by 2 pathways, the external and the internal, which are cultivated in a common way. The factors involved in a common path can be memorized mnemonically: 1 X 2 X 5 = 10.

  • factor II (prothrombin) : When activated on thrombin, factors I and XIII are activated.
  • Coefficient V (unstable factor): if activated, Coefficient II is activated.
  • X-factor (Stewart power factor): activated on the internal and external rail; if activated, factor II is activated.

3. Tissue Factor Way:

Donkey bridge:Tissue factor – factor 3 and 3 + 7 = 10 (total displacement). Therefore, the factors involved in the alien route are Factor III and Factor VII.

4. Internal path (wound path) :

Memory support:Factors 12 to 8 are part of the internal path, with the exception of factor 10, which is part of the global path. Therefore, the factors involved in the inner journey : Factor XII, Factor XI, Factor IX and Factor VIII.

Facts to consider regarding the thrombosis cascade

1. All blood coagulation factors are proteins and synthesize in the liver, except:

  • Factor IV : Calcium
  • Protein-carrying factor VIII: vWF (von Willebronde factor)

2. Think of a small cycle of positive feedback on a common path:

  • The activated factor V (Va) activates factor II (IIa or thrombin).
  • Activated factor II (IIa or thrombin) activates factor V.

3. Activation of factors II, VII, IX and X requires calcium (factor IV) and phospholipid (PL) . Vitamin K-dependent coagulation factors are most susceptible to liver disease and warfarin. The external channel is assigned and therefore PT/INR is cancelled. The normal duration of the broadcast is 12 to 16 seconds. Prothrombin time (PT) and International Standardised Ratio (INR) are equal. The NRM is the parameter for monitoring a patient’s physical exertion. If the patient’s CT matches the check, then the M.O.D. is 1. Vitamin K deficiency is also responsible for the haemorrhagic disease in neonates. The release of delta grains by thrombocytes leads to the release of calcium, which is necessary for the coagulation cascade during hemostasis.

4. When the alien staircase becomes frequent, it interacts with TFPI (Tissue Factor Pathway Inhibitor) and deactivates the alien staircase by inhibiting VIIa and Xa. However, factor Xa also activates factor II (protromine) to thrombin, which in turn activates the internal signal path (factor XI and factor IX).

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According to Wikipedia.

5. Antithrombin III inhibits factor IIa (thrombin) and factor X. The mechanism of antithrombin III also refers to heparin. The intracerebral canal is affected and as a result the APTT (activated partial thromboplastin time) level is increased. The typical TCA value is 26-34 seconds.

6. Protein C, S and thrombomodulin inactivate factor V and VIII by activated protein C. It also depends on vitamin K and warfarin (vitamin K inhibitor), the data could initially have a paradoxical effect of promoting coagulation as a result of the inhibition of proteins C and S. To prevent this complication, it is therefore administered with heparin in the first few days. A lack of protein C leads to thrombophilia. Thrombo-modulin is produced by all endothelial cells except those of the cerebral microcirculation. Thrombin-thrombo-modulin-anticoagulant complex.

7. Tissue plasminogen activator (tPA), such as streptokinase , converts plasminogen to plasmin. Since plasmin breaks down fibrin, tPA is used as a thrombolytic or fibrinolytic substance.

8. Factor XII is the only protein in the coagulation cascade that does not cause bleeding, but rather leads to a prothrombotic state.

9. Haemophilia is due to deficiency of factor VIII or IX. Even if the opposite is normal, bleeding is caused:

  • lack of fibrinogenesis
  • Inappropriate fibrinolysis – activation of TAFI (activated fibrinolytic thrombin inhibitor) requires a very high level of thrombin, which increases fibrin discharge by inhibiting fibrinolysis.

10. V Leiden factor is more likely to cause thrombophilia than a haemorrhagic disease. This can be explained by the fact that Factor V leiden is a mutant Factor V, which has a normal Factor V activity, but is resistant to inactivation by activated protein C. It is the most common hereditary cause of hypercoagulation, in which the normal arginine at position 506 is replaced by glutamine, making it resistant to degradation by protein C.

11.  Haemophilia A, B (Haem-A, B) and von Willebrand Disease (VWD) are the most common hereditary bleeding diseases, while congenital abnormalities of FI, FII, FV, FX, FXI, FXII or FXIII are rare. Factor XIII is usually present at birth with umbilical cord, cefalohaematoma and intracranial bleeding.

12. The Thrombin Time (TT) is used to test the conversion of fibrinogen to fibrin and depends on an adequate level of fibrinogen.

13. Fibrin degradation products (PDF) are used to assess fibrinolytic activity and increased intravascular coagulation (ICA).

14. Bleeding time (BT) is an analysis to test platelet function. Normal bleeding time is 2 to 9 minutes. It is extended in case of quantitative or qualitative platelet failure.

15. Factor XIIa (Hagman’s factor) also initiates the cynological system by converting pre-kallicin to kallicin, which in turn converts the cynogen into a genus (bradykinin). Activated Factor XII may cause activation of the film system, blood coagulation system, fibrinolytic system and complement system.

16. Fresh frozen plasma (FFPS) contains all factors of the soluble coagulation system and is indicated in patients with bleeding and multifactorial abnormalities.

17. Cryoprecipitate is a concentrated fraction of PCP rich in factor I (fibrinogen), factor VIII, factor XIII and VWF, and is therefore detected in hypofibrinogenesis, VWD and haemophilia A. It contains only 40-50% of the coagulation factors present in PCP, but it is concentrated and has a smaller volume.

18. After an injury, after a transient endothelium-mediated vaso-inhibition, tissue factor is released from the damaged cells, activating factor VII (- external route) and exposure to subendothelial collagen, causing the activation of factor XII (- internal route).

19. Tenaz Complex: Activating X factor complex (ten) –

  • Inner tube tenaz complex: IXa + VIIIa + calcium
  • Extrinique tenas complex: tissue factor + VII + calcium

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He researches and teaches simple ways to simplify complex medical subjects. He also enjoys writing poems, listening to and playing music and travelling.



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