Small Ani. Med- Coagulation 2

wilsbach's version from 2015-12-06 17:24

membranes--> termination (And summary)

Question Answer
what is happening in the termination step?When the factors tell us to STOP making thrombin.
the signal to tell everything to stop making thrombin is prolly related to what where?mostly related to receptors on the surface of the cells (Membrane LPs, Thrombomodulin, Protein C receptors, HSPG, ADPase) and plasma factors (ATIII, TFPI) which limit the reaction just to where it needs to be.
******WHaT HAPPENED IN INITIATION?VII/TF --> IXa, local IIa (via local Xa) [Factor 7 and Tissue Factor interact which results in 9a, local 2a (via local 10a) ]
*****WHAT HAPPENED IN AMPLIFICATION?Plt activation by IIa (Thrombin) which causes VIIIa & Va at surface (8a and 5a)
*****what happened IN PROPAGATION?IXa/VIIIa --> Xa/Va --> lots of IIa [9a and 8a which is tenase makes lots of Xa, Xa then interacts with 5a to make LOTS of 2a(thrombin) ]
**what happens in termination step?Stray factors removed from system
what is Thromboelastography / Thromboelastometry? ONLY TEST which tells us if a pt is HYPERcoagulable. Gives us a better assessment of the WHOLE process of coagulation.
**only test that tells you if the pt is hypercoagulable?Thromboelastography / Thromboelastometry (pt tests and such you can only interpret if slow=hypo, cant determine if hyper from fast response)


Question Answer
what are some examples of Surface bleeding, and where do you think the problem is in coag if you get these signs?SURFACE BLEEDING--> petechia/ecchymosis, epistaxis, hemoptysis, hematemesis, melena, hematochezia, hematuria, etc---> THINK PLATELET NUMBER OR FXN PROBLEM
what are some examples of Cavitary bleeding, and where do you think the problem is in coag if you get these signs?CAVITARY--> Hemoabdomen, hemothorax, hematoma, this is likely due to a COAG FACTOR DEFECT OR DEFICIENCY
if you have petechia and your platelet number is normal, is it not a prob with platelets?STILL A PROB WITH PLATELETS, just prolly fxn not number (thrombocytopathia
what is thrombocytopathia?means prob with platelet FXN not NUMBER
what kinda problem is von Willebrand's dz? who is the poster child?THROMBOCYTOPATHIA, DOBERMANS
(said in class) test for thrombocytopathia? (platelet fxn test)BMBT (buccal mucosal bleeding time) -- don't bother doing if you know there is low platelet numbers.
a complete/thorough panel to check all coag stuff--> what three things would you be looking at and what tests would you need to do?need to look at platelet number, platelet function, and the coag factors. So you'd need to do a CBC, BMBT, AND a PT/PTT
what is normal and what is abnormal about coag in a dog with von Willebrand's dz?Normal platelet count and normal coag times. This is a THROMBOCYTOPATHIA tho, so there is an ABNORMAL BMBT, and abnormal clinical bleeding if they suffer an injury. If not injured, often show no signs of bleeding (rarely have spontaneous bleeding tho)
if you are worried about this dobie with a fam history of vWD, what can you do testing wise?there are specific vWF tests
how do you tx vWD?TRANSFUSION-- just replacing the factors. (vWF in plasma transfusion) (if you gotta cut them, give them plasma BEFORE you do it) (he mentioned in class there is a drug named desmopressin too which can inc levels if theyre just partial cases)
vWD vs hemophilia: which gets spontaneous bleeding?hemophilia, bc hemophilia is a factor prob (vWD is a platelet dz)
DIFF BETWEEN HEMOPHILIA TYPE A VERSUS TYPE B??TYPE A: factor VIII deficiency (remember 8 in propagation step where it combines with 9a to make tenase) TYPE B: factor IX deficiency (the other part of the tenase in propagation)
which is X-linked- hemophilia or vWD? if X-linked, WHO tends to get it?HEMOPHILIA-- MALES
factor XII (12) deficiency-- WHO tends to get this? How important clinically? What happens? what test you do?common in DSH (cats). Not actually important clinically bc does not cause clinical signs of bleeding, but DOES cause inc aPTT (and is common enough where you will get a ton of cats with longer aPTTs- he usually ignores it)
which rodenticides do we usually see causing problems?Anti-coagulant rodenticide ( 1st or 2nd generation) like Brodifacoum, Diphacinone, Bromadiolone (1st gen is warfarin) and 2ndd generations have super long half lifes compared for first generation
omg doc! my cat ate a rat that ate anti-coag rodenticide! How bad should I freak out right now??Probably have to eat it directly, Not from eating poisoned rodents (so dogs tend to eat straight up rodenticide more than cats)
explain the pathogenesis of anti-coag redenticidethe drug antagonizes vitamin K enzyme (Inhibits Vit. K epoxide reductase), which dec stores of K in the liver (decreased hepatic stores of functional Vit. K), which means we have the inability to recycle our coag factors (inability to activate new coagulation factors or to recycle old ones). (normally as coag factors get activated and unactivated we can re-process them) so basically end up with a deficiency in all our vit-k dependent factors (decreased circulating levels of these factors)
how fast for rodenticide related problems to show up? Clinical signs?Not an immediate effect, Based upon half lives: Hemostasis abn w/in 1 day. C.S. ~2-4 days after exposure
which factor is the first to be affected by rodenticide, and why?one with shortest half life- factor 7. ...which is also the most important one for starting coag lol.
***dear god what are the vit-K dependant factors?2,7,9,10!
how do you dx rodenticide poisoning? which coag tests are affected? what are some SPECIFIC tests?sometimes Presumptive, based on Hx, C.S., labwork... ↑ PT, PTT, ACT, PIVKA. SPECIFICALLY: Serum screening (antemortem), Liver tissue levels (post-mortem)
what is the tx for rodenticide poisoning?PLASMA!!! Plasma will replace the missing factors. Can give red cells if needed to control the anemia. And can give vit K1 NOT JUST ANY VIT K, K1!!! If it's been within hours you can induce emesis.
what is DIC? What parts of the coag system are affected? What are the tests which are abnormal?Severe, global, dysregulation of hemostasis....ALL parts of the system are affected, so They are hypo AND hypercoagulable. MANY DIFF ABNORMALITIES ON TESTS, including Platelets(bmbt), coag tests (osPT, aPTT) AND have ~FDPs and D-DIMERS present))
if you see making clots AND bleeding....DIC