Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
CPII Exam 3
Lecture 8: Blood Coagulation and Hemostasis
| Question | Answer |
|---|---|
| hemostasis | ability to stop bleeding by maintaining the integrity of the blood vessels; process by which blood is prevented from leaking out of damaged blood vessels |
| 3 mechanisms of hemostasis | vascular spasm, platelet plug formation, blood clotting (coagulation) |
| vascular spasms (mechanical phase) | when blood vessel is injured, vessels CONSTRICT triggered by: injury to smooth muscle, chemicals released from endothelial cells, platelets, reflexes involving local pain receptors |
| thrombocytes | function is HEMOSTASIS via formation of a PLATELET PLUG (CLOTTING!!) |
| platelet plug formation (mechanical phase) | outer lining of blood vessel is injured |
| platelet adhesion (platelet plug formation step 1) | exposed sub-layer contains proteins that attract PLATELETS to adhere to it; required VON WILLEBRAND FACTOR |
| platelet plug formation step 2 | vessel wall produces tissue factors that activate to lead to formation of THROMBIN |
| platelet aggregation (platelet plug formation step 3) | THROMBIN causes platelets to change shape and intertwine with each other |
| platelet plug formation step 4 | platelets squeeze together to form a PRIMARY HEMOSTATIC PLUG |
| platelet plug formation step 5 | thrombin also converts FIBRINOGEN (a soluble plasma protein) to FIBRIN |
| platelet plug formation step 6 | FIBRIN attaches to platelet surface and helps CEMENT platelets in place |
| platelet release reaction | platelets release CLOTTING FACTORS to activate NEIGHBORING PLATELETS; also release SEROTONIN and THROMBOXANE that cause VASOCONTRICTION to decrease blood flow) |
| coagulation cascade | a series of chemical rxns which lead to FIBRIN FORMATION |
| coagulation cascade RESULT | formation of a gel-like mass through the activation of coagulation factors |
| coagulation cascade END | ends with a break down of the clot, called FIBRINOLYSIS |
| coagulation cascade -> chemical phase | both clotting factors and chemicals released from the platelets and damaged tissue are needed for coagulation to take place; consists of 2 pathways and 13 clotting factors separated into INTRINSIC and EXTRINSIC |
| what happens when an intrinsic/extrinsic factor is activated? | both pathways continue to the COMMON PATHWAY |
| what starts the COMMON pathway? | starts with the activation of FACTOR X (factor 10) which leads to the production of THROMBIN and FIBRIN |
| extrinsic pathway | quicker, with fewer steps; damaged tissue releases tissue factor (THROMBOPLASTIN) that leads to the production of factor X |
| intrinsic pathway | all factors necessary for blood clotting are present in the blood; relies on production of a PHOSPHOLIPID from external surface of platelets, leads to production of factor X |
| clot dissolution | clots are NOT permanent; at the same time the clot if being formed, the ENDOTHELIUM produced substances that will eventually dissolve the clot (PLASMIN) |
| fibrinolysis | process by which the clot is removed |
| thrombosis | formation of a clot in an INTACT vessel |
| thrombus | noun, clot formed in thrombosis -> saddle thrombus or FATE |
| embolus | movement through the blood of clot, air bubble, fat from a broken bone, or debris -> FATE (feline aortic thromboembolism, pulmonary embolism (embolus lodged in lungs) |
| vitamin K | not directly involved in CLOT FORMATION, but needed for synthesis of the following clotting factors: II (2), VII (7), IX (9), X (10) |
| clotting disorders | animals that are unable to form clots could have interference at any point of coagulation, leading to bleeding disorders; can be due to CONGENITAL or ACQUIRED defects in: coagulation proteins, platelets, vasculature |
| clotting disorders CLINICAL SIGNS | purpura, petechia, ecchymoses, melena, epistaxis, hematuria |
| purpura | purple-colored patches that occur on skin or MM |
| petechia | small, pinpoint-sized red or purple discolorations of the skin or MM; <3MM |
| ecchymoses | larger patches of red or purple discolorations of the skin or MM, > 1MM |
| melena | dark, black feces due to acute blood loss in the upper GI tract (digested blood) |
| epistaxis | bleeding from one or both nostrils (unilateral or bilateral) |
| hematuria | blood in urine |
| methods to evaluate hemostasis | thrombocyte count, bleeding time test, coagulation analyzer, coagulation tests |
| thrombocyte count/platelet count | commonly performed to confirm THROMBOCYTOPENIA CAUSES: artifact, sequestration, decreased production, use, destruction (ITP) |
| bleeding time test | buccal mucosal bleeding time screening test, SENSITIVE TO PLATELET FUNCTION AND CONCENTRATION; measures clotting time (prolonged in pt's w/ platelet dysfunction or von Willebrand's disease) |
| bleeding time test NORMAL | 2-4 min |
| coagulation analyzer | used for coagulation tests (tests that can measure coagulation factors); CITRATED PLASMA (9 parts blood to 1 part citrate) or whole blood |
| coagulation tests -> prothrombin time (PT) | measures EXTRINSIC and COMMON pathway factors; also used as an indirect measure of vitamin K |
| coagulation tests -> activated partial thromboplastic time (PTT or aPTT) | measures INTRINSIC and COMMON pathway factors |
| coagulation tests -> activated clotting time | measures INTRINSIC and COMMON pathways; normal is <90 sec in SMALL ANIMALS, <180 sec in LARGE ANIMALS |
| acquired clotting disorders | liver disease (check coagulation prior to biopsy), vitamin K deficiency (Warfarin -> rodenticides, moldy sweet clover), aspirin, thrombocytopenia, disseminated intravascular coagulation (DIC) |
| hereditary clotting disorders -> hemophilia | deficiency of coagulation factor; hemophilia A -> factor VIII (8), hemophilia B -> factor IX (9), CATS -> factor XII (12) deficiency |
| hereditary clotting disorders -> von Willebrand's disease | 'platelet problem' as vWF is necessary for platelets, most common in DOBERMANS |
| hereditary clotting disorders -> vWF CLINICAL SIGNS | epistaxis or melena, NOT petechiae |
| hereditary clotting disorders -> vWF LAB FINDINGS | normal platelet concentration, prolonged BMBT, decreased serum vWF |
| acquired clotting disorders -> vitamin K deficiency CAUSES | ingestion of vitamin K antagonist (rodenticide, moldy sweet clover in cattle), decreased absorption of vitamin K, decreased synthesis |
| vitamin K is obtained from: | DIET and required BILE ACIDS for absorption in the intestines, needed for synthesis of factor II, X (2,10, both COMMON), factor IX (9, INTRINSIC), factor VII (7, EXTRINSIC) |
| acquired clotting disorders -> vitamin K antagonism | anticoagulant rodenticides, leads to rapid depletion of factors II, VII, IX, X; NOTE that NOT all rodenticides are ANTICOAGULANTS, make sure clients bring packaging with them |
| acquired clotting disorders -> vitamin K TREATMENT | emesis, activated charcoal, sorbitol |
| coumarin toxicity | dicoumarol and warfarin |
| half-life of factor VII (9) is: | SHORT |
| disseminated intravascular coagulation (DIC) | death is coming! consumptive coagulopathy secondary to a variety of other disease (hyperthemia or heat stroke); increased intravascular coagulation combined and worsened with the formation of MICROCLOTS (thrombosis) |
| DIC leads to: | multi-organ failure; most often seen in DOGS |
| DIC typical signs | petechiae, ecchymoses, melena, hematuria |
| DIC treatment | heparin and blood transfusions |
| DIC prognosis | GRAVE! better to treat underlying disease before this occurs; will see SCHISTOCYTES on blood smear |
Created by:
mkroon26
Popular Veterinary sets