Hemostasis & Coagulation Flashcards

1
Q

What are the primary steps of hemostasis?

A
  1. Vascular spasm
  2. Formation of the platelet plug
  3. Fibrin formation
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2
Q

steps of platelet plug formation

A

adhesion
activation
aggregation

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3
Q

adhesion

A

-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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4
Q

activation

A

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

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5
Q

prostacycline

A

causes vasodilation

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6
Q

thromboxane A2

A

causes vasoconstriction

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7
Q

aggregation

A

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

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8
Q

secondary hemostasis

A

-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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9
Q

clotting factors made in the liver

A

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

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10
Q

clotting factors not made in the liver

A

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

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11
Q

clotting cascade

A

formation and cross-linking of fibrin to stabilize the clot

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12
Q

intrinsic pathway initiation

A

injury to the inside of the blood vessel

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13
Q

intrinsic pathway factor cascade

A

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

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14
Q

intrinsic pathway drug

A

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

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15
Q

intrinsic pathway labs

A

aPTT & ACT

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16
Q

extrinsic pathway initiation

A

injury occurring outside the blood vessel

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17
Q

extrinsic pathway factor cascade

A

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

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18
Q

intrinsic pathway drug

A

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

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19
Q

extrinsic pathway labs

A

PT & INR

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20
Q

final common pathway initiation

A

factor 8 intrinsic or factor 7 extrinsic

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21
Q

final common pathway factor cascade

A

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)

22
Q

stages of cell based coagulation model

A

initiation
amplification
propagation

23
Q

DIC stage 1

A

Hypercoaguable state with secondary fibrinolysis

24
Q

DIC stage 2

A

Hypocoaguable state

25
Q

TEG R time

A

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

26
Q

TEG K time

A

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

27
Q

TEG alpha angle

A

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

28
Q

TEG maximum amplitude

A

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

29
Q

TEG LY30

A

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

30
Q

Fibrinolysis

A

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

31
Q

tPA & uPA

A

Concert plasminogen to plasmin

32
Q

Can increase risk of intraoperative bleeding

A

Garlic
Gingko
Ginger
Fish oil

33
Q

Von Willebrands

A

Type 1: deficiency
*Treat DDAVP or cryo

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

34
Q

Cryoprecipitate

A

factors I, VIII, XIII

35
Q

hemophilia A

A

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

36
Q

hemophilia B

A

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

37
Q

Bebulin

A

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

38
Q

K-Centra

A

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

39
Q

DIC

A

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

40
Q

DIC treatment

A

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

41
Q

HIT

A

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

42
Q

Type 1 HIT

A

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

43
Q

Type 2 HIT

A

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

44
Q

liver disease

A

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

45
Q

renal disease

A

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

46
Q

anemia most important adverse effect

A

decreased tissue oxygen delivery

47
Q

which way does the dissociation curve shift for anemia

A

right (offloads to the tissues)

48
Q

RBCs

A

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

49
Q

Platelets

A

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

50
Q

FFP

A

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

51
Q

Cryoprecipitate

A

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