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pathoma
secondary hemostasis and disorders
| Question | Answer |
|---|---|
| what does the coagulation cascade produce that will turn fibrinogen in the primary platelet plug into fibrin? | thrombin |
| what produces coagulation factors? | the liver |
| what are 3 things that will activate the circulating inactive coagulation factors? | 1. exposure to an activating substance (tissue thromboplastin activates factor 7, subendothelial collagen activates factor 12) 2. phospholipid surface of the platelets 3. Ca (from platelet dense grandules) |
| what are clinical features of seconday hemostatsis abnl? | deep tissue bleeding into muscles and joints (hemarthrosis) and rebleeding after surgical procedures (circumscision and wisdom teeth removal) |
| what does prothrombin time (PT) measure? | the extrinsic pathway- factor 7 (less numbers in the extrinsic pathwya is measured by the lab w less letters). and it measures teh common pathway- factors 2, 5, 10 and fibrinogen |
| what does partial thromboplastin (PTT) time measure? | the intrinsic pathway (factors 12, 11, 9, 8) and common pathway factors- 2, 5, 10 and fibrinogen. |
| hemophila A is a deficiency in what? | factor 8 deficiency. |
| what is the etiology of hemophila A? | its mostly genetic- x linked recessive (MC in males) but can be sporadic- de novo without mutation |
| PTT, PT, platelet count and bleeding time lab measures for hemophila A? | def in factor 8 is part of intrinsic pathway, so the PTT will be prolonged but PT will be normal. you have normal platelet count and bleeding time, with decreased factor 8 levels. |
| treatment for hemophila A? | recombinant factor 8 |
| what is christmas disease? | hemophila B, factor 9 deficiency. similar to hemophila A but the def is 9. |
| what is the major testing to determine the difference btw coagulation factor inhibitor disease (ab against coag factor- MC 8) and hemophila A? | when you mix the pts blood with normal plasma, the PTT in hemophila pts will increase bc you are gaining some factor 8. however in coagulation factor inhibitor, the ab will attack the factor 8 in normal plasma- so PTT will NOT correct |
| what is the MC inherited coagulation disorder/ | vWF deficiency |
| a low vWF will impair what part of hemostasis | the platelet adhesion |
| bleeding time, PTT, PT levels for a pt with vWF disease? | you have prolonged bleeding time, normal PT but prolonged PTT (bc vWF stabilizes factor 8) but dont have clinical sxs of decreased factor 8 |
| what is the major test for vWF disease? | ristocetin test- its a test that will induce platelet aggregation by causing vWF to bind to gp1b on platelets. a lack of vwf will show a lack of aggregation= abnl test |
| what is the treatment for vWF disease?*** | ADH (desmopressin) will induces weibel-palade bodies on endothelial cells to release vwf. |
| what activates vitamin K in the liver? | epoxide reductase |
| what factors does vitamin K gamma carboxylase? | 2, 7, 9, 10, protein C and S too. |
| why do newborns often have vit K deficiency, how do we normally correct this? | newborns dont have the normal colonic bacteria yet, which is what produces vit K. at birth we give all newborns vitK injection. |
| how does malabsorption lead to vit K deficiency? | malabsorption leads to a deficiency in fat soluble vitamins- D,E,A,K** |
| how does liver failure cause abnl secondary hemostasis? | liver produces coagulation factors, failure = a lack of those factors. also liver will activate vit K by epoxide reductase. |
| how does a large volume transfusion cause hemostasis disroders? | it will dilute the coagulation factors |
| how can heparin induced thrombocytopenia cause thrombosis? | the platelets that were destroyed can activate remaining platelets = thrombosis |
| what is DIC? | you have widespread microthrombi that cause ischemia and infarction- and d/t platelets being used up you have increased bleeding at IV sites and mucosal surfaces |
| DIC is almost always secondary to another disease process, how do OB complications induce DIC? | amniotic fluid has tissue thromboplastin which will activate the extrinsic pathway = coagulation |
| how does sepsis induce DIC? | endotoxins from bacterial wall and cytokines induce endothelial cells to make tissue factor |
| how does adenocarcinoma induce DIC? | mucin from adenoca activates coagulation |
| what activates DIC in acute promyelocytic leukemia? | primary granules |
| what are the lab findings in DIC? the platelet count, PT/PTT, fibrinogen levels? | platelet count will be decreased, PT/PTT increased, decreased fibrinogen. |
| what is the BEST screening test for DIC? what is it | D dimer test, it is derived from the splitting of cross-linked fibrin (NOT fibrinogen) |
| what si the treatment for DIC? | transfusing blood products and cryopreciptate (has coagulation factors) |
| what does tpa do? | converts plasminogen to plasmin |
| what does plasmin do? | cleaves fibrin and serum fibrinogen, destroys coagulation factors, and blocks platelet aggregation |
| what does alpha2- antiplasmin do? | inactivates plasmin |
| how does a radical prostatectomy cause excess fibrinolysis? | bc it will release urokinase which activtes plasmin |
| how does cirrhosis of the liver cause disorder of fibrinolysis? | it causes a reduction in alpha2- antiplasmin |
| what are the PT, PTT, bleeding time, platelet count and D dimer results in excess fibrinolysis? | increased PT/PTT (plasmin destroys coagulation factors), increased bleeding time w normal platelet count. no increased D dimer (serum fibrinogen is lysed, but d dimers not formed bc no thrombi are present- its pathological activation) |
| what is the treatment for excess fibrinolysis? | aminocaproic acid to block activation of plasminogen |
Created by:
afrank1