Hemostasis ABSITE Killer Review

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Hemostasis

Intrinsic path (PTT): exposed collagen + XII -> XI, IX -> X which activates thrombin to produce fibrin
Extrinsic path (PT): tissue factor + VII -> activated X -> fibrin
X is common to both pathways
XIII crosslinks fibrin to form ‘plug’. PT is best single test to evaluate synthetic function of the liver.

Banked blood is low in 2,3-DPG which increases Hgb affinity for O2 (left shift)
Cryo contains fibrinogen and vWF-VIII; used in vWD, hemophilia A, and DIC if fibrinogen low
Vit K inhibits II, VII, IX, X, protein C and protein S
Protein C degrades active V and VIII. Protein S helps protein C
V and VIII are labile factors, low levels stored in blood
Factor VIII only factor not made in liver (made by reticuloendothelial system)

Von Willebrand’s Disease: long PTT, long bleeding time, +ristocetin test. Type I and III have low amounts of vWF, respond to ddAVP; type II is qualitatively poor vWF
Autosomal dominant (only one beside Rosenthal’s XI deficiency). Only inherited coagulopathy with long bleeding time.
Rx with VIII, vWF or cryoprecipitate

ddAVP causes release of vWF, useful also in pts on ASA or w/uremic plt

Glanzman’s thrombasthenia: plts have IIb/IIIa receptor deficiency. Decr plt aggregation

Bernard Soulier: Ib deficiency, decr adherence to exposed collagen

VII deficiency causes long PT, normal PTT

Hemophilia A = VIII deficiency, sex-linked recessive, replace to 100% levels pre-op
Have long PTT, normal PT. Newborn has VIII from mom, may not bleed at circumcision

Hemophilia B = IX deficiency = Christmas disease, also sex-linked. achieve 50% levels pre-op

Hemophiliac joint = do not aspirate; ice, ROM therapy, give factor VIII

Lupus anticoagulant: antiphospholipid antibodies, not necessarily with Luppus and generally pro-coagulant;
Dx: long Russel viper venom time, long PTT which does not correct by adding normal plasma

Factor XII = Hagemann factor; activated by cardiopulmonary bypass -> need for heparin

Factor V Leyden = resistance to activated protein C = common cause of DVT

Plasmin degrades fibrinogen, is inhibited by alpha-2-plasmin inhibitor

Heparin binds/activates ATIII and inactivates factors 9-12; prolongs PTT; counteract with protamine

epsilon-ACA (epsilon amino caproic acid) inhibits fibrinolysis, is the Rx for overdose of thrombolytics; thrombin is best test to monitor thrombolysis

DIC: low platelets, prolonged PT/PTT, low fibrinogen, high fibrin split products

HIT: ‘white clot syndrom’, thrombocytopenia due to anti-platelet antibody causing plt aggregation. Use dextran to anticoagulate. Generally see after 5 days of heparin, less frequent with LMWH

Prostacyclin = PGI2: from endothelium, decr plt aggregation, vasodilatation, bronchial relaxation

Thromboxane: from platelets, opposite effects of above

Best preop test fro pt on NSAIDS/ASA is bleeding time