Phys And Pathophys - Clotting Stuff

Front 1

what are the four steps in formation of the platelet plug

Back 1

adhesion, activation, aggregation, and production of fibrin

Front 2

activation of the platelet is when

Back 2

the platelet exposes receptors that will attach to fibrin

Front 3

aggregation of platelets is when

Back 3

the clot calls in more platelets

Front 4

VonWillebrand's factor is

Back 4

VIII:vWF - an autosomal dominant trait that prevents the platelets from adhering to the collagen layer to begin plug formation

Front 5

function of VonWillebrand's factor is

Back 5

it is released by the subendothelium to anchor platelets to the collagen layer of the subendothelium by having one end attach to the platelet and the other to the collagen recepto9r

Front 6

VonWillebrand's factor is made by

Back 6

the endothelial cells

Front 7

symptoms of VonWillebrand's factor deficiency

Back 7

epistaxis, mucosal bleeding, and superficial bleeding

Front 8

treatments for Von Willebrand's deficiency are

Back 8

DDAVP, cryoprecipitate, and concentrated factor VIII, FFP

Front 9

DDAVP is aka

Back 9

desmopressin or D-amino-d-arginine vasopressin (this is a NON pressor analog of arginine vasopressin)

Front 10

DDAVP works by

Back 10

causing the release of endogenous stores of vWF

Front 11

DDAVP

Back 11

0.3 ug/kg IV over 15 - 20 minutes

Front 12

DDAVP effect

Back 12

releases from stores - platelet adhesion will increase in 30 minutes and last 4 - 6 hours (occasionally may repeat dose) - will not work if patient has no endogenous stores

Front 13

side effect of DDAVP

Back 13

hyponatremia in kids, rare in adults

Front 14

if pt's do not respond to DDAVP, then give

Back 14

cryoprecipitate or concentrated factor VIII (possibly also FFP)

Front 15

cryoprecipitate includes factors

Back 15

I, VIII, and XIII

Front 16

what activates the platelets?

Back 16

Thrombin, Thrombaxane A2, ADP, others

Front 17

Thrombin is Factor

Back 17

IIa

Front 18

precursor to thrombin is

Back 18

prothrombin

Front 19

when the platelet is activated it makes and releases

Back 19

thromboxane A2 and ADP which accelerate platelet activation on nearby platelets

Front 20

the drug persantine used to

Back 20

work on affecting ADP

Front 21

fibrin binding sites exposed during platelet activation are

Back 21

GPIIb3a receptors

Front 22

what drugs bind to the GPIIb3a receptors

Back 22

Reopro, integrelin, aggrestat

Front 23

treatment for bleeding associated with GPIIb3a receptor drugs is

Back 23

platelets to wash out effect of the drugs

Front 24

white clot means

Back 24

when the fibrin from one platelet binds to another platelet and forms a spider web like white mesh (before any RBC's get caught in it)

Front 25

studies show that regional anesthesia

Back 25

may reduce platelet aggregation

Front 26

stopping white clot formation would be useful in

Back 26

preventing clot formation in the heart

Front 27

aspirin works by

Back 27

rendering cyclooxygenase nonfunctional because the acetyl group of aspirin acetylizes the cyclo oxygenase for the duration of the platelet lifespan

Front 28

lifespan of the platelet is

Back 28

8 - 12 days

Front 29

rate limiting step in the conversion of arachidonic acid to prostaglandins and thromboxane A2 is

Back 29

cyclo oxygenase

Front 30

delay elective sugeries for how long after aspirin

Back 30

2 weeks

Front 31

if cannot delay surgery and patient is on aspirin

Back 31

give platelets

Front 32

the laboratory value that correlates with platelet function best is

Back 32

bleeding time

Front 33

NSAIDS work by

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temporarily inhibiting cyclooxygenase and thrombaxane A2 production

Front 34

NSAIDS effect lasts for how long

Back 34

24 - 48 hours

Front 35

ticlopidine or ticlid work by

Back 35

inhibiting ADP

Front 36

persantine (dipyridamole) works by

Back 36

increasing cylcic AMP in the platelet causing inhibited aggregation

Front 37

what is the most common acquired blood clotting defect encountered in anesthesia

Back 37

inhibition of the cyclo oxygenase production by aspirin or nsaids

Front 38

two ways to fibrin production

Back 38

intrinsic and extrinsic pathways

Front 39

extrinsic pathway is measured by what lab value

Back 39

PT

Front 40

coumadin affects what pathway

Back 40

extrinsic and final common pathway

Front 41

pneumonic for the extrinsic pathway

Back 41

you can purchase the extrinsic pathway for 37 cents

Front 42

characteristic of the extrinsic pathway

Back 42

very fast - 15 seconds

Front 43

the extrinsic pathway is initiated by

Back 43

endothelial damage causing a release of a substance called tissue factor

Front 44

the basic extrinsic pathway is

Back 44

endothelial damage - tissue factor (III) release - complexes with facto VII

Front 45

clotting pathway regulated by

Back 45

several positive and negative feedback loops

Front 46

warfarin is in a family of drugs called

Back 46

coumarins

Front 47

coumarins work by

Back 47

competing fro binding sites within the liver

Front 48

factors dependent on vitamin K for production are

Back 48

factors II, VII, IX, and X

Front 49

Vitamin K begins to work in

Back 49

3 - 6 hours of administration

Front 50

if surgery is emergent and patient is on coumadin give

Back 50

FFP (works immediately) and then vitamin K

Front 51

labs that will be elevated if patient is on coumadin

Back 51

PT and INR

Front 52

why is INR different than PT

Back 52

PT's sometimes vary between hospitals so INR (international normalized ratio) was created to standardize lab results

Front 53

how does vitamin K work to reduce effect of coumadin

Back 53

it does not reduce affects of coumadin, just tips the scales in favor of vitamin K dependent factor production (II, VII, IX, X)

Front 54

vitamin K dependent factors are

Back 54

II, VII, IX, X

Front 55

the intrinsic pathway is measured by

Back 55

PTT and ACT (activated coagulation time)

Front 56

the pneumonic for the intrinsic pathway is

Back 56

if you can't get the intrinsic pathway for $12, then you can get it for $11.98

Front 57

speed of the intrinsic pathway is

Back 57

1 - 6 minutes

Front 58

the intrinsic pathway is initiated by

Back 58

the blood itself (flow stress) or exposure of the blood to collagen in a traumatized blood vessel wall

Front 59

the intrinsic pathway is

Back 59

blood trauma activates factor XII (HMW kininogen and prekalikrein) then XI is activated plus Ca++ activates IX, which triggers VIIIa (thrombin) then the common pathway factor X

Front 60

the final common pathway begins with

Back 60

activation of factor X

Front 61

factor Xa produces

Back 61

prothrombin

Front 62

the final common pathway is

Back 62

prothrombin with Ca++ and activator produces thrombin which allows for conversion of fibrinogen to fibrin fibers which bind to the GPIIb3a receptors. Thrombin also helps with the cross linking of fibrin fibers

Front 63

hemophilia A is

Back 63

an x-linked recessive genetic disorder producing absence or reduction of factor VIIIc

Front 64

clinical manifestations of hemophilia A is

Back 64

joint ans skeletal muscle hemorrhage, bruising, and hemorrhage after trauma (deep tissue bleeding) but limited bleeding after minor cuts

Front 65

lab results for hemophilia A

Back 65

normal PT and platelet count, abnormal PTT

Front 66

treatment for hemophilia A is

Back 66

factor VIII concentrate, FFP, and cryoprecipitate - mild cases may also be treated with DDAVP which releases both VIIIc and VIIIvW

Front 67

anesthetic implications for hemophilia A is

Back 67

no deep IM injections, no regionals, watch for bleeding in airway, most bleeding can be controlled with anesthesia, coexisting diseases of HIV and hepatits possible

Front 68

factor VIII's half life

Back 68

8 hours - so may need to be repeated

Front 69

what else to remember with factor VIII

Back 69

pooled product so should be heat treated for HIV

Front 70

PTT measures what pathway

Back 70

intrinsic

Front 71

how many factor VIII units/ml in FFP

Back 71

1 unit per ml

Front 72

how many factor VIII units/ml in cryoprecipitate

Back 72

10 units per ml

Front 73

how many factor VIII units/ml in factor VIII concentrate

Back 73

40 units per ml

Front 74

Hemophilia B is aka

Back 74

Christmas disease

Front 75

hemophilia B is

Back 75

an X-linked coag disorder that causes deficient factor IX, indistinguishable from hemophilia A except for factor assay

Front 76

treatment for hemophilia B is

Back 76

pooled factor IX, and FFP (but no cryoprecipitate)

Front 77

factor IV is

Back 77

calcium

Front 78

calcium is involved in

Back 78

both intrinsic and extrinsic pathways as accelerants of several reactions in the clotting cascade so the ionized calcium levels will affect the bleeding time (higher or lower levels will make it faster or slower?)

Front 79

antithrombin III is made

Back 79

in the liver

Front 80

antithrombin III binds

Back 80

II, Xa, IX, XI, XII

Front 81

antithrombin III binds strongest

Back 81

II (thrombin) and Xa

Front 82

antithrombin III works by

Back 82

binding the clotting factors and removing them from circulation therefore it is an anticlotting factor

Front 83

heparin works by

Back 83

increasing antithrombin III's binding to thrombin by more than 1000x. antithrombin III is a required cofactor for heparin

Front 84

most common reason a patient is unresponsive to heparin is

Back 84

an antithrombin III deficiency

Front 85

treat antithrombin III deficiency with

Back 85

FFP since it contains all the clotting factors

Front 86

homeostasis in the blood is maintained by

Back 86

a balance between clotting and anticlotting factors

Front 87

acquired antithrombin III deficiency is seen in

Back 87

liver cirrhosis and nephrotic syndrome - also long term birth control use

Front 88

heparin lab values will show

Back 88

an elevated PTT and ACT

Front 89

if you give a big dose of heparin for your heart patient but can't get the
ACT over 400 like the heart surgeons like then

Back 89

pt has an antithrombin III deficiency so give FFP

Front 90

smoking causes

Back 90

polycythemia and vasoconstriction

Front 91

normal value for bleeding time

Back 91

3-10 minutes

Front 92

normal platelet count

Back 92

150 - 300 cells/ml

Front 93

normal prothrombin time

Back 93

12 - 14 sec

Front 94

normal INR

Back 94

0.8 - 1.2

Front 95

normal activated partial thromboplastin time

Back 95

25 - 35 secs

Front 96

normal thrombin time (TT) is

Back 96

12 - 20 secs

Front 97

normal ACT is

Back 97

80 - 150 sec

Front 98

an INR greater than 1.15 may

Back 98

contraindicate a regional anesthetic because of increased risk of clot in the spinal cord

Front 99

plasminogen is synthesized by

Back 99

the liver

Front 100

plasminogen is

Back 100

proteins that are incorporated into the clot during formation and does nothing until activated by tPA

Front 101

tPA is aka

Back 101

tissue plasminogen activator

Front 102

tPA is produced by

Back 102

endothelial cells when stimulated by thrombin and venous stasis

Front 103

tPA works by

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binding to fibrin, converting plasminogen to active plasmin within the clot and plasmin breaks fibrin into FDP or FSP

Front 104

FDP is

Back 104

fibrin degradation products

Front 105

FSP is

Back 105

fibrin split products

Front 106

DIC labs will show

Back 106

increased levels of FDP and FSP

Front 107

some fibrinolytics are

Back 107

tPA, urokinase, streptokinase,

Front 108

urokinase is

Back 108

found in limited amounts in the blood and works like tPA

Front 109

streptokinase is made

Back 109

by beta hemolytic stretococci so can trigger development of antibodies so may not work if a repeat dose and you won't see a rise in FSP's after giving

Front 110

amicar and aprotinin work by

Back 110

slowing down bleeding by inhibiting the work of plasmin

Front 111

antifibrinolytics are

Back 111

aprotinin and amicar - which cause a slowing of the fibrinolytic system

Front 112

aprotinin works by

Back 112

inhibiting plasmin

Front 113

amicar works by

Back 113

preventing the attachment of plasmin to fibrin

Front 114

examples of complex disorders of coagulation are

Back 114

DIC, liver disease, uremia, and multiple transfusions

Front 115

define DIC

Back 115

widespread systemic activation of coagulation which results in intravascular formation of clots and thrombotic occulsion of vessel. At the same time, the consumption of platelets and coag factors may induce severe bleeding.

Front 116

#1 cause of DIC

Back 116

sepsis

Front 117

common causes of DIC seen in the or are

Back 117

ischemia, hypotension, hypoperfusion (shock)

Front 118

symptoms of DIC seen in surgery include

Back 118

oozing from tubes, wounds, vascular access sites

Front 119

other causes of DIC include

Back 119

hemolysis, brain trauma, OB emergencies

Front 120

in DIC platelet values will

Back 120

decrease

Front 121

in DIC fibrinogen levels will

Back 121

stay the same or decrease in severe cases

Front 122

in DIC, PT/PTT values will

Back 122

increase

Front 123

in DIC, factors V, VIII, XIII will

Back 123

decrease

Front 124

in DIC fibrin degradation products will

Back 124

increase

Front 125

DIC is a

Back 125

consumptive coagulopathy which means the platelets and clotting factors will be used up causing serum levels to drop and both intrinsic and extrinsic pathways will be slowed

Front 126

treatment for DIC is

Back 126

to fix the underlying problem and replace platelets and lost clotting factors

Front 127

in DIC do not give

Back 127

antifibrinolytics - will make it worse because part of the problem is an insufficient fibrinolytic system. (only give if ok with hematology b/c there is a rare version that it would help)

Front 128

DIC is an imbalance between breakdown and clotting and favors

Back 128

clotting

Front 129

In some cases, a drug to give during DIC is

Back 129

heparin

Front 130

hypercoagulable states are

Back 130

antithrombin III deficiency, protein C deficiency, and protein S deficiency

Front 131

hypercoagulable states are seen in what patient populations

Back 131

OB, oral contraceptives

Front 132

low molecular weight heparin lab values are

Back 132

not shown in any labs - so labs may be normal but clotting times not

Front 133

protein C is

Back 133

a vitamin K dependent anticoagulant synthesized by the liver. A deficiency inhibits the activation of clotting factors V and VIII and may be inherited or acquired.

Front 134

people with protein C deficiency will present with

Back 134

a history of DVT's and PE's and will usually be on oral anticoagulants - regional anesthesia may be beneficial

Front 135

protein S is

Back 135

a vitamin K dependent anticoagulant that acts as a cofactor in the protein C production

Front 136

protein S deficiency is associated with

Back 136

an increased risk for venous thromboembolism