Hemostasis 1

britt611's version from 2017-01-27 04:27

Section 1

Question Answer
What are 5 factors involved in hemostasis?platelets, vessels, coagulation factors, fibrinolytic factors, inhibitors
Define primary hemostasisformation of initial platelet plug (3 As) at site of vessel injury
define secondary hemostasisformation of the fibrin clot from coagulation factors
define fibrinolysiscontrolled break down of the clot
hemostasis vs coagulation coagulation is a part of hemostasis
What are the 3 As of primary hemostasisAdhesion, activation, aggregation
Blood vessels are normally....non thrombogenic
when do blood vessels become procoagulantwith the right stimuli or injury, for ex. can produce tissue factor to start coagulation cascase, vWF
What are plateletscytoplasmic fragments of megakaryocytes, produced in the B<
define thrombopoiesisprocess of plt formation
how long do plts circulate for5-9 days
what are plts called in non-mammalian vertebratesthrombycytes

Section 2

Question Answer
What does the cascade in secondary hemostasis lead tofibrin formation
What are the 2 phases of secondary hemostasisintrinsic and extrinsic
What is the key factor in the extrinsic pathwayTissue factor activation
What does the intrinsic pathway contribute to?thrombin ?
What is the main pathway for initiation extrinsic phase
What is the function of the common pathway?prothrombin activation for produciton of thrombin
What is the pathways of fibrinolysisplasminogen --> plasmin --> makes fibrin --> fibrin degradation production
What is the main activator of plasminTPA- tissue plasminogen activation
what is the main enzyme in fibrinolysisplasmin
what inhibits plasminalpha 1 antiplasmin
what inhibits plasminogen to plasminplasminogen activator - inhibitor type 1 (PAI-1)
What are fDPsare breakdown products of both fibrinogen and fibrn
what are D-dimersbreakdown production ONLY of cross-linked fibrine
What is good to evaluated hemostasisD-dimers
what are 3 natural (endogenous) anticoagulantsanti-thrombin III, protein C, TFPI (tissue factor pathway inhibitor)
What is the function of anti-thrombin IIIbindes and inactivates thrombin
how is anti-thrombin III enhanced heparin
what activates protein Cthrombin
What is the function of protein Cinactivates factors V and VIII leading to anitcoagulation
What is protein C facilitated by?protein S

Section 3

Question Answer
what are 3 factors that are involved in disorders of primary hemostasisblood vessels, platelets, platelet associated factors (vWF)
What are clinical signs of a primary hemostasis disorderpetechia, ecchymoses and/or bleeding of mm and skin, epistaxis, bleeding/oozing at IV cath site
What are 2 types of blood vessel disorders (primary hemostasis)acquired and hereditary
what is the most common acquired blood vessel disordervasculitis - usually infection related
what is an example of an hereditary blood vessel disorder of primary hemostasisehler danlos syndrome - collagen disorder
What is a common distorder of primary hemostasisdecreased plt number and/or function
what are clinical signs of platelet disorders of primary hemostasispetechia, ecchymoses on the mm and skin, spontaneous bleeding when plt count is <20,000
What are 4 mechanisms of thrombocytopenia1. decreased plts production, 2. increased plt destruction, 3. increase plt consumption, 4. increased platelet sequestration

Section 4

Question Answer
What are causes of decreased platelet production drugs, (chloramphenicol, grrsefulvin, chemotherapy), increased/abnormal estrogen exposure, infectious agents (feLV, EIA, BVD, parvo), toxins (aflatoxin, bracken fern), chemicals, radiation, myelophthisis
what are some examples of infectious agents that can cause decrease platelet production FeLV, EIA, BVD, Parvo
what are some examples of toxins that can cause decrease plt production aflatoxin, bracken fern
What is the main cause of increased plt destruction leading to thrombocytopeniaIMT- immune mediated thrombocytopenia (<10,000)
define IMTplts destryed in the periphery faster than being produced
describe the typical signalment for IMT OES, cocer spaniel, poodle, Female
what are the clinical signs for IMTepistaxis, hematuria, petechiae
how is IMT diagnosedbone marrow, IgG detection
how do you treat IMTcorticosteroid, other immune suppresions
what is IMT sometimes associated withIMHA, SLE
Besides IMT what is 2 other ways to cause increased plt destruction?drug induced (heparin -releated horse or trimethoprim sulfa in dogs), secondary immune mediated destruction destruction (distemper, EIA, rickettsial infection)
what are some examples of how thrombocytopenia does drug induced can cause heparin -releated in horses, trimethoprim-sulfa in dogs
What is a cause of increased plt consumption leading to thrombycytopenia DIC (disseminated intravascular coagulation)
define consumptive coagulopathyplts coagulation factors consumed in hypercoagulation, follwed by hypocaogaulation
horses vs dog/cats DIChorses- may see early evidence of thrombosis, dog/cat- see signs of hypocoagulation only (bleeding/oozing and petechiae)
What causes DICDIC is a syndrome secondary to underlying cause (sepsis, trauma, neoplasia, snake bite, severe inflammation
what is the triad of DICthrombocytopenia, coagulation factor depletion, increased fibinolysis
How is DIC diagnosedif all 3 parts of the triad are present- only suspected if 2 are present
what is the only real reasonfor increased platelete sequestration?splenomegaly
what are causes of splenomegal?neoplasia, infection, torsion
what are 2 types of thrombyocytosisprimary (essential thrombycythenmia), secondary
what is primary thromboyctosis RARE myeloproliferative disorder that causes uncontrolled bone marrow plt production
what are 3 types of secondary thrombocytosisreactive, rebound, iron deficiency-associated
what is the most common cause of thrombocytosisreactive- any inflammatory disorder can cause it
what does rebound thrombycytosis follow?recovers from thrombocytopenia
how does iron deficiency cause thrombocytosispossible hormonal cross-talk (EPO stimulating megakaryocytes)
What is the important clinical aspect of thrombycytosisthere are NO clinical signs!

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