Board Review 1-Clotting

Front 1

Of the various types of white blood cells (leukocytes), which is most abundant?

Back 1

neutrophils (also referred to as polymorphonuclear leukocytes) are the most abundant WBCs

Front 2

Neutrophils comprise what percent of the total WBC (leukocyte) population? What stimulates the neutrophil count to increase?

Back 2

neutrophils are 55% of the leukocyte population. Any inflammatory stimulus, including bacterial infection, increases the neutrophil count.

Front 3

what is the normal platelet count?

Back 3

150,000 to 400,000 platelets per ml

Front 4

Where is erythropoietin made? What stimulate the release of erythropoietin do?

Back 4

The kidneys make 90% of the erythropoietin and the liver 10%. Erythropoietin is released in response to hypoxia. Erythropoietin stimulates bone marrow to produce and release red blood cells.

Front 5

what are the steps in primary hemostasis

Back 5

adhesion, activation, aggregation of plts, fibrin production

Front 6

plts have an avg lifespan of how many days

Back 6

8-12

Front 7

what is the normal plt count

Back 7

150,000-400,000

Front 8

when vascular endothelium is damaged and the sub endothelium of the blood vessel is exposed what anchors the plt to the collagen layer of the sub endothelium

Back 8

vWF

Front 9

what does vWf promote

Back 9

: plt adhesion

Front 10

where is vWf made and released from

Back 10

endothelial cells

Front 11

what is the most common inherited coagulation defect

Back 11

von willebrands disease

Front 12

what is DDAVP

Back 12

a non pressor analog of arginine vasopressin

Front 13

what is the dose of DDAVP

Back 13

.3 ug/kg IV infusion over 15-20 minutes

Front 14

what is a side effect in children when using DDAVP

Back 14

hyponatremia

Front 15

what is the traditional treatment of vW disease

Back 15

cryoprecipitate, or DDAVP

Front 16

what does cryoprecipitate consist of

Back 16

VIII and I

Front 17

: Pts who do not respond to DDAVP should receive what

Back 17

cryo or factor VIII

Front 18

Thrombin activates the plt by combining with the thrombin receptor on the plt to release what

Back 18

TXA2 and ADP

Front 19

what does TXA2 do

Back 19

it vasoconstricts

Front 20

what does ADP do

Back 20

attracts more plts

Front 21

what does TXA2 and ADP uncover

Back 21

fibrinogen receptors and fibrinogen attaches to its receptors and links plts together

Front 22

what does TXA2 do

Back 22

increases ADP release, opens fibrinogen receptors, vasoconstricts

Front 23

how does ASA render plts dysfunctional

Back 23

the acetyl group of ASA causes acetylation of cyclooxygenase

Front 24

How long does ASA render plts dysfunctional

Back 24

8-12 days

Front 25

what is the rate limiting step in the conversion of AA to TXA2

Back 25

cyclooxygenase

Front 26

How long do NSAIDS render plts dysfunctional

Back 26

24-48 hours

Front 27

how does ticlid work

Back 27

inhibits ADP-induced fibrinogen aggregation of plt drugs

Front 28

How does persantine work

Back 28

it increases cAMP in plts and thus prevents aggregation of plts

Front 29

cyclooxygenase converts AA to what initially

Back 29

prostaglandin G2

Front 30

what is PGG2 metabolized to

Back 30

PGH2

Front 31

what is the most common acquired blood clotting defect

Back 31

inhibition of cyclooxygenase by ASA and NSAIDS

Front 32

What is the name of factor I, where is it made and is it Vit K dependent

Back 32

fibrinogen/liver/no

Front 33

what is Factor II called, where is it made and is it Vit K dependent

Back 33

prothrombin/liver/yes

Front 34

what is Factor III called, where is it made and is it Vit K dependent

Back 34

 tissue factor or thromboplastin
 vascular wall and cells
 release by traumatized cells
 Not vit k dependent

Front 35

what is Factor IV called, where is it made and is it Vit K dependent

Back 35

calcium/diet/no

Front 36

what is Factor V, where is it made and is it Vit K dependent

Back 36

proaccelerin/liver and other tissues/no

Front 37

what is Factor VII called, where is it made and is it Vit K dependent

Back 37

proconvertin/liver/yes

Front 38

what is Factor VIII: C called, where is it made and is it Vit K dependent

Back 38

antihemophilic factor/liver/no

Front 39

what is Factor VIII:vWF called, where is it made and is it Vit K dependent

Back 39

Von Willebrand factor/vascular endothelial cells/no

Front 40

what is Factor IX called, where is it made and is it Vit K dependent

Back 40

christmas factor/liver and other tissues/yes

Front 41

what is Factor X called, where is it made and is it Vit K dependent

Back 41

stuart-prower factor/liver/yes

Front 42

what is Factor XI called, where is it made and is it Vit K dependent

Back 42

plasma thromboplastin antecedent/liver/no

Front 43

what is Factor XII called, where is it made and is it Vit K dependent

Back 43

hageman factor/liver/no

Front 44

what is Factor XIII called, where is it made and is it Vit K dependent

Back 44

fibrin stabilizing factor/liver and other tissues/no

Front 45

where is prekallikrein factor made and is it vit K dependent

Back 45

liver/no

Front 46

where is high molecular weight kininogen factor made and is it Vit K dependent

Back 46

liver/no

Front 47

what are the Vit K dependent factors

Back 47

2,7,9,10

Front 48

what factor causes the cross-linking of fibrin strands

Back 48

coag factor XIII

Front 49

after plts aggregate what happens

Back 49

fibrin is weaved into plts and cross linked

Front 50

Heparin affects what pathway

Back 50

intrinsic

Front 51

what pathway does coumadin affect

Back 51

extrinsic

Front 52

what factors comprise the intrinsic path

Back 52

12, 11, 9, 8

Front 53

what factors comprise the extrinsic path

Back 53

3 and 7

Front 54

what factors comprise the common path

Back 54

10, 5, 2, 1, 13

Front 55

Hemophilia A (factor VIII:C deficiency) is a genetic disorder, describe it

Back 55

it is a sex linked genetic disorder that is carried by the female member of a kindred and effects males almost exclusively

Front 56

how do you treat hemophilia A

Back 56

FFP and cryo, VIII in low concentration

Front 57

How is hemophilia B (christmas disease) treated

Back 57

heat treated, concentrated preparations of factor IX are available

Front 58

what is the best (although not great) measure of plt function

Back 58

a standardized skin bleeding time

Front 59

what is the most common reason for coagulopathy in pts receiving massive blood transfusions is the lack of what

Back 59

functioning plts

Front 60

Plts in stored blood are nonfunctional after how many days

Back 60

1 to 2 days

Front 61

what is the only clinical indication for transfusion of PRBC

Back 61

to increase the oxygen carrying capacity of the blood

Front 62

all pro-coagulants except what are in FFP

Back 62

plts

Front 63

cryoprecipitate contains what

Back 63

factor VIII, factor I and factor XIII

Front 64

what does activated antithrombin III bind to

Back 64

thrombin (IIa) and factor Xa greatly and factors IX, XI, and XII to a lesser degree

Front 65

what disease processes are associated with antithrombin III deficiency

Back 65

nephrotic syndrome and cirrhosis of liver

Front 66

what is adequate heparinization indicated by

Back 66

ACT greater than 400

Front 67

what should you do if the ACT is not greater than 400 (if indicated of course)

Back 67

give FFP

Front 68

how does protamine work

Back 68

combines electrostatically with heparin (positive substance combines with negative substance) to form an inactive salt

Front 69

how does coumadin work

Back 69

binds to Vit K receptors in the liver and competitively inhibit Vit K

Front 70

what is a normal bleeding time

Back 70

3-10 minutes

Front 71

what is a normal PT

Back 71

12-14 seconds

Front 72

what is a normal PTT

Back 72

25-35 seconds

Front 73

what is a normal thrombin time

Back 73

12 - 20 seconds

Front 74

what is a normal ACT

Back 74

80-150 seconds

Front 75

how does plasminogen work

Back 75

it works itself into a clot and tPA and urokinase type drugs convert it to plasmin and thus breaks down fibrin into FSP

Front 76

where is tPa made

Back 76

in the endothelial cells

Front 77

what stimulates tPa release

Back 77

venous stasis and thrombin

Front 78

where is tPa found

Back 78

limits stores in blood and has little affinity for fibrin, thus activates any circulating plasminogen

Front 79

what produces streptokinase

Back 79

beta-hemolytic streptococci and also has little affinity for fibrin

Front 80

how does aprotinin work

Back 80

it inhibits plasmin, thus fibrin breakdown is slowed

Front 81

how does amicar work

Back 81

by inhibiting binding of plasmin to fibrin

Front 82

why should you never give aprotinin twice

Back 82

anaphylaxis potential

Front 83

what are some conditions that contribute to DIC

Back 83

: sepsis, hemolysis, transfusion reaction, ischemia, trauma, hypotension/hypo-perfusion, OB emergencies, aneurysms, hamangiomas, allograft rejections, glomerulonephritis

Front 84

how does DIC present

Back 84

bleeding, oozing from tubes, wounds and IV sites

Front 85

what are some lab abnormalities with DIC

Back 85

decreased plts, decreased fibrinogen, decreased prothrombin, decreased level of V, VIII, and XIII, and increased FSP

Front 86

what is the most common cause of isolated high PT

Back 86

liver disease

Front 87

what is transfused blood deficient in

Back 87

plts and V & VIII

Front 88

what is diffuse bleeding usually caused by

Back 88

thrombocytopenia