Physio 2 - Hemo 2

drraythe's version from 2015-06-09 01:26

The Erythron (continued)

Question Answer
what is polycythemia? increase in RBC numbers
what is primary polycythemia? what kind of disorder can this be called? RARE. lack of feedback control = uncontrolled RBC production. (myeloproliferative disorder). Hct can be up to 60-70%. this means high viscosity of blood and reduced blood flow.
what animal has naturally high PCV values?sighthounds!
what is secondary polycythemia? physiological response to O2 deficiency (high altitude, cardiac failures, lung diseases). Hct increases by a few %, plasma unchanged.
what is transient polycythemia? spleenic contraction due to excitement/exercise. **horses, cats, sighthounds. Elevated PCV, normal PP
what is relative polycythemia?*not a true polycythemia. caused by dehydration/fluid loss so all blood components relatively more concentrated (hemoconcentration). shows as increased PCV and PP
what determines a blood group?antigens on surface of RBC.
two types of blood type antigens arethose with natural antibodies, those without natural antibodies
explain blood type with natural antibodies. examples?within weeks of being born, animal develops antibodies against non-present antigens = natural antibodies present in plasma against other blood types (antigens aquired via food). ex) O-A-B in people, A-B in cats
explain blood type with no natural antibodies. examples?unless animal is exposed to antigen (typically though blood transfusion) no antibodies develop. **only SOME blood types are highly antigenic ex: dogs DEA 1.1,1.2, etc. horses A,C,Q, etc. cattle B, J, A, F, etc.
if mismatched transfusion with natural antibodies?recipients antibodies react with donors RBCs (MAJOR reaction), leads to intravascular agglutination, block capillaries, shock. also phagocytosis/rupture of attacked RBCs -> precip. of excess Hb, renal blockage -> acute renal failure
if mismatched transfusion with no natural antibodies?after transfusion THEN antibodies develop (perhaps delayed mild reaction occurs after first transfusion)...however second transfusion of same antigenic RBCs -> full blown immune response as in animal with initial natural antibodies.
do what to avoid transfusion mismatches?blood typing/cross matching of recipients plasma with donors RBCs
highly antigenic dog blood groups are?DEA 1.1, 1.2, and 7
what is major cross matching?expose donors RBCs to recipients plasma and observe for agglutination
what is minor cross matching?expose recipients RBCs to donors plasma and observe for agglutination
akitas have what unique attribute of their blood cells?microcytic


Question Answer
what is hemostasis?sequence of responses that stop bleeding
5 steps of hemostasis?(1) vascular spasm (2) platelet plug formation (3) blood clot formation (coagulation) (4) healing (5) clot removal (fibrinolysis)
what is primary hemostasis?platelet plug formation
what is secondary hemostasis?blood clot formation (coagulation)
another name for platelet?thrombocyte
what has a nucleate platelet?birds and reptiles
origin of platelets? pluripotent stem cell -> myeloid stem cell -> CFU-Meg (colony forming unit-meg) -> megakaryoblast -> megakaryocyte -> framentation to platelets
what controls production of platelets?hepatic thrombopoietin
contents of a platelet?**contractile proteins (actin, myosin, thrombosthenin), ADP+ATP, prostaglandins+serotonin+clotting factors+ endothelial growth factors+etc, calcium
functions of a platelet (4)release chemicals that promote vasospasem, formation of platelet plugs, release of factors that promote coagulation, healing processes
two main purposes of vasospasm?reduce blood flow/loss, facilitate subsequent steps of hemostasis
what causes vasospasm immediately?release of ENDOTHELIN from damaged cells ("im IN trouble!" )
what causes vasospasm AFTER immediate reaction (later?)release of THROMBOXANE A2 (a prostaglandin derivative) and serotonin from platelets (SERa, who is SPAStic carried a BOX of PLATEs)
what causes/releases vWF (von Willebrand Factor)?damage to endothelial cells causes them to release vWF.
after released, what does vWF bond to?damaged cell membranes and collagen fibers
after vWF is bonded what happens?vWF undergoes a conformation change and expresses receptor sites for platelets. Then platelets bind.
what does binding of platelets to vWF activate platelets to do? (aka what does an activated platelet do?) (1-6) (just list, explanations later) 1) send out pseudopodia 2) release serotonin/thromboxane A2. 3) release ADP and thromboxane A2 4) release ADP and fibronectin 5) release platelet factors (V and VII) and calcium. 6) expose receptor sites for fibrinogen and prothrombin
what does releasing serotonin and and thromboxane A2 do?promote vasospasm
what does releasing ADP and thromboxane A2 do?attract more platelets
what does releasing ADP and fibronectin do?promote adhesion (glue like substance)
what does releasing platelet factors and calcium do?part of clotting process
how long does it take for loose plug to be formed to seal off injury site?1-2 minutes
what type of bleeding can be a result of platelet plug formation not occuring?petechial bleeding
three stages of clot formation (secondary hemostasis) are?1) EXTRINSIC and/or INTRINSIC pathway lead to formation of prothrombin-activator complex. 2) COMMON pathway begins (activation of prothrombin to thrombin). 3) conversion of soluble fibrinogen to insoluable fibrin (via thrombin)
what is the extrinsic system of clot formation based on? what is the initial factor released?tissue based. injured tissue expresses tissue factor THROMBOPLASTIN (EXtroverts get PLASTerd)
what does thromoboplastin do? how long does it take to do it?in extrinsic system of clot formation, activates enzymatic cascade (factors VII, X, V, Ca++) which lead to prothrombin activator complex. 15-30 sec
what is the intrinsic system of clot formation based on? caused by what type of reaction? what is the initial factor released?plasma-based. change in surface charge of endothelial membranes cause binding/activation of plasma factor XII (so, caused by INFLAMMATORY reactions e.g. endotoxins, or activated platelets. bleeding not necessary!
what does Factor XII do? how long does it take to do it?activated enzymatic cascade (kallekrein, factors XI, IX, VII, X, V, Ca++) which lead to prothrombin activator complex. takes 1-6 min
how would you describe the relationship between extrinsic and intrinsic systems of clot formation?extrinsic system is faster and more powerful, the intrinsic system serves as an amplifier, although they are both activated simultaneously in most cases.
what does the prothrombin activator complex (common pathway) do?converts proenzyme prothrombin to the active enzyme thrombin
what is prothrombin? what is its synthesis dependent on? where does it attach itself?it's a hepatic alpha globulin, with vit. K dependent synthesis. it attaches itself to activated platelets
what are the effects of thrombin? (2)1) positive feedback effect on extrinsic/intrinsic system and platelet aggregation 2) FIBRIN formation (thrombin hydrolyses FIBRINOGEN to FIBRIN
what happens when thrombin hydrolyses soluable fibrinogen into fibrin?the insoluble fibrin monomers polymerize into long fibers and crosslink to form a meshwork in and around the platelet plug. this makes a STABLE clot.
how long does it take bleeding to stop after the injury?3-6 min.
what happens within the next 30 minutes after clot formation?CLOT RETRACTION: platelets contract more and pull fibrin threads together, which tightens the clot and pulls injured blood vessel edges together.
what is the fluid that remains after hemostasis?serum (plasma minus clotting factors)
how does healing take place after a stable, retracted clot has formed? (factor/ cells involved? )platelets secrete ENDOTHELIAL GROWTH FACTOR, which attracts fibroblasts to the clot site. the fibroblasts use the fibrin meshwork as scaffolding to begin to repair.
what is the removal of a clot called?fibrinolysis
how does fibrionlysis occur? (time frame, chemicals involved, etc) (3 steps)(1) 1-2 days after clot formation, the injured tissue+endothelium slowly releases a "tissue plasminogen activator" (t-PA). (2) t-PA activates hepatic plasma factor plasminogen to plasmin = proteolytic enzyme. (3) plasmin hydrolyses fibrin fibers + clotting factors = FDPs (fibrin degradation products) and then FDPs are removed by macrophages
what does tissue plasminogen activator do?released from injured tissue and endothelium to turn plasminogen to plasmin (a proteolytic enzyme)
what does plasmin do?it hydrolyses fibrin fibers and clotting factors into fibrin degredation products, which are eaten by macrophages
body's defense against unwanted hemostasis?smooth endothelial cells to prevent platelet adhesion and activation. intact endothelial cells + WBCs secrete PROSTACYCLIN and nitrous oxide to inhibit platelet adhesion (blood smoothly bikes (cycles) along while high on nitrous)
what does prostacyclin and nitrous oxide do?prevent platelet adhesion
how does the body prevent excessive clot formation? (3 ways)(1) fibrin binds thrombin which limits fibrin formation and pos. feedback. (2) ANTI-THROMBIN III (alpha globulin) deactivates thrombin and other clotting factors. (3) heparin from mast cells/basophils combines with antithrombin III and augments its effects
how does fibrin prevent excessive clot production?it binds thrombin
what does anti-thrombin III do?deactivates thrombin/ other clotting factors
what can augment anti-thrombin's effects?heparin from mast cells and basophils
in vitro anticoagulation agents?Ca++ binding agents (citrate, oxalate, EDTA), heparin
in vivo anticoagulation agents?heparin, vit. K antagonists, prostaglandin synthesis inhibitors (NSAIDs)
what is a lab hemostasis test you can perform? expected results?(mucosal) record time until bleeding stops after a small standard incision into skin or mucosa (expected time 1-5 minutes)
what is OSPT? what does it measure? expected time?one stage prothrombin time. measures extrinsic and common pathway. expected time <10sec. measures clot formation in citrated plasma after addition of tissue factor, platelet factors, and calcium. (O as in outer as in Extrinsic)
what is APTT? what does it measure? expected time?(activated partial thromboplastin time) measures intrinsic and common pathway. expected time 60-120 sec. measures clot formation after clean venipuncture in citrated plasma and addition of contact activator (diatomaceous earth), platelets factors and calcium
what is a bleeding disorder called?coagulopathy
what are the 4 bleeding disorders? (4, list)thrombocytopenia, von Willebrands disease (form I,II,III), vit. K deficiency, hemophilias
what is thrombocytopenia?decreased production (bone marrow, drugs, FeLV) or increased destruction (immune mediated) or consumption of thrombocytes
what is von Willebrands Disease?(mild/ severe/ fatal) *most common bleeding disorder, due to genetic lack or insufficiency of vWF. Platelets fail to adhere to injury sites which results in spontaneous bleeding (petechial or ecchymotic) **highest prevalence in dobermans
how can rodentacide cause coagulopathies?coumarin is a vit K antagonist. therefore it impairs liver synthesis of several clotting factors including prothrombin.
what is the rarest coagulopathy?hemophilia (genetic deficiency in a clotting factor)
what is thrombosis?clotting in a unbroken vessel.
what might cause a thrombosis?stasis (impaired flow), artherosclerosis, trauma, parasites, tumors.
what happens if a thrombus dislodges?embolism, which can block a blood vessel and cause ischemia
example of common embolism in vet med? what species? due to what?aortic thromboembolism in cats, AKA saddle thrombus. Due to myocardial diseases...clot forms in L atrium and moves into aorta (often lodges at caudal trifurcation and blocks blood into illiac aa.)

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