Hemostasis & Coagulation Flashcards by Kelly K

What are the primary steps of hemostasis?

Vascular spasm
Formation of the platelet plug
Fibrin formation

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steps of platelet plug formation

adhesion
activation
aggregation

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adhesion

-dependent on factor VIII:v (vWF)
-GpIb receptor on platelet attaches to vWF on endothelium
-vWF is released from endothelial cells

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activation

-thrombin combines with thrombin receptor on platelet
-platelet changes shape and releases mediators (ADP, Thromboxane A2, serotonin)

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prostacycline

causes vasodilation

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thromboxane A2

causes vasoconstriction

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aggregation

-ADP & thromboxane A2 uncovers GpIIb/IIIa receptors
-fibrin links platelets together
-clot is water-soluble

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secondary hemostasis

-fibrin is key player
-involves the extrinsic, intrinsic, and final common pathways along with all 12 clotting factors
-makes clot water insoluble

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clotting factors made in the liver

1, 2, 5, 7, 8, 9, 10, 11, 12, 13

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clotting factors not made in the liver

3-vascular wall of extravascular cell membranes
4- diet
8v (vWF)- vascular endothelial cells

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clotting cascade

formation and cross-linking of fibrin to stabilize the clot

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intrinsic pathway initiation

injury to the inside of the blood vessel

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intrinsic pathway factor cascade

12-11-9-8
twelvE > EleveN > NinE > EighT

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intrinsic pathway drug

Heparin
Intrinsic = I = IV (route of administration of Heparin)

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intrinsic pathway labs

aPTT & ACT

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extrinsic pathway initiation

injury occurring outside the blood vessel

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extrinsic pathway factor cascade

3-7
*warfarin is cheap aka 37 cents
*3+7=10 (10 starts final common pathway)

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intrinsic pathway drug

Coumadin
Extrinsic = E = esophagus (route of administration of Coumadin)

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extrinsic pathway labs

PT & INR

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final common pathway initiation

factor 8 intrinsic or factor 7 extrinsic

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final common pathway factor cascade

10-5-2-1 (&13-fibrin stabilizing factor)
*1x2x5=10
*keep halfing to get to 1 (10x0.5=5, 5x0.5=2.5, 2x.05=1)

stages of cell based coagulation model

initiation
amplification
propagation

DIC stage 1

Hypercoaguable state with secondary fibrinolysis

DIC stage 2

Hypocoaguable state

TEG R time

-Time to start clot -5-10 minutes -problem with coagulation factors -treat: FFP

TEG K time

-Time until clot reaches a fixed strength -1-3 minutes -problem with fibrinogen -treat with cryo

TEG alpha angle

-speed of fibrin accumulation -53-72 degrees -problem with fibrinogen -treat with cryo

TEG maximum amplitude

-highest vertical amplitude -50-70 mm -problem with platelets -treat with platelets and/or DDAVP

TEG LY30

-percentage of amplitude reduction 30 minutes after MA -0-8% -problem with fibrinolysis -treat with TXA or Amicar

Fibrinolysis

-main player is plasmin -plasminogen is inactive form (in all clots) -plasmin breaks down fibrin into fibrin split products -D-dimer

tPA & uPA

Concert plasminogen to plasmin

Can increase risk of intraoperative bleeding

Garlic Gingko Ginger Fish oil

Von Willebrands

Type 1: deficiency *Treat DDAVP or cryo Type 2: dysfunction Type 3: absent *Treat cryo or Factor 8 concentrate

Cryoprecipitate

factors I, VIII, XIII

hemophilia A

factor VIII deficiency treat: FFP, cryo, Factor VIII concentrate

hemophilia B

factor IX deficiency treat: heat-treated factor IX, K-Centra, Bebulin,

Bebulin

Factors II, IX, and X *vitamin K dependent factors

K-Centra

inactivated factors II, XII, IX, and X *vitamin K dependent factors diet FFP: also has protein C & S and AT3

DIC

-fibrinogen receptor left open -decreased platelets and factors I,II, V, VIII, XIII

DIC treatment

-platelets -FFP or factor concentrate -Vitamin K -antifibrinolytic

HIT

thrombocytopenia resistance to heparin thrombosis positive assay -treat: DC heparin, administer direct thrombin inhibitors (bivalirudin)

Type 1 HIT

-direct heparin action of platelet aggregation -onset 1-4 days -seen with high dose therapy

Type 2 HIT

-indirect action by heparin platelet factor 4 IgG -onset 5-14 days -severe thrombocytopenia -any heparin dose -serious clinical sequelae -treat: plasmapheresis

liver disease

problems with platelet plug -treat: FFP, cryo, Vitamin K

renal disease

platelet dysfunction, defective vWF -treat: dialysis, cryo, DDAVP

anemia most important adverse effect

decreased tissue oxygen delivery

which way does the dissociation curve shift for anemia

right (offloads to the tissues)

RBCs

-1 unit increases Hct 3-4% -increase O2 carrying capacity

Platelets

-active bleeding or platelet level for procedure -1 unit increased count by 20-50,000

FFP

-all factors & antithrombin -1 dose = 1 vial AT3 -for bleeding, deficient coag factors, coumadin reversal, vWF disease, AT3 deficiency

Cryoprecipitate

-factors 1, VIII, XIII -1 unit increases fibrinogen by 50 mg/dl -for bleeding and fibrin deficiency, hemophilia A, vWB disease