Hematology

Question 0

Thrombin function

Answer 0

Converts fibrinogen to fibrin and split products
Activates factors V and VIII
Activates platlets

Question 1

Initial 3 responses to vascular injury

Answer 1

Vasoconstriction
Platelet adhesion
Thrombin generation

Question 2

Actions of Antithrombin III

Answer 2

Anticoagulant ( no clot)
Inhibits thrombin
Inhibits factors IX, X, XI

Heparin binds Antithrombin III

Question 3

Protein C and S function

Answer 3

Protein C- vitamin K dependent, degrades factors V & VIII, degrades fibrinogen
(No clot)

Protein S- vitamin K dependent, protein C cofactor

Question 4

Factors that cause fibrinolysis (no clot)

Answer 4

TPA- tissue plasminogen activator: released from endothelium -> converts plasminogen (follow fibrinogen levels)

Plasmin: degrades factors V & VIII, fibrinogen, fibrin
-> lose platelet plug

Alpha 2 antiplasmin: inhibits plasmin, released from endothelium

Question 5

Clotting factor with shortest half life

Answer 5

Factor VII (7)

Question 6

Only clotting factor NOT synthesized in liver

Answer 6

Factor VIII (8)

Synthesized in endothelium

Question 7

Vitamin K dependent factors

Answer 7

II, VII, IX, X (2,7,9,10)

Protein C, S

Question 8

Thromboxane (TXA2)

Answer 8

From platelets
Increases platelet aggregation and promotes vasoconstriction
Triggers Ca release-> expose GpIIb/IIIa->plt to plt binding

“Box in platelets”

Question 9

Coagulation factor with highest amount of vWF VIII

Answer 9

Cryoprecipitate

Tx in Von Willebrand dz, hemophilia A VIII def

Question 10

Coagulation factor with highest amount of all factors

Answer 10

FFP

Question 11

Causes release of VIII and vWF from endothelium

Answer 11

DDAVP

Conjugated estrogens

Question 12

PT measures

Answer 12

Factors II, V, VII, X, fibrinogen

Best test for liver synthetic function

Question 13

Factors not measured with PTT

Answer 13

VII and XIII (does not pick up factor VII deficiency)

For anticoagulation: PTT 60-90

Question 14

Want ACT (activated clotting time)

Answer 14

Routine anticoag 150-200

Cardiopulmonary bypass 400

Question 15

What is most common congenital bleeding disorder?

Answer 15

VonWillebrand dz

Question 16

Vonwillebrand dz

Answer 16

Type I & II - auto dominate - type I =most common
Reduced quantity
Type III - auto recessive - most severe bleeding
Defect in vWF

Links GpIb receptor on plts to collagen
Long bleeding time

Question 17

What is factor VIII deficiency?

Answer 17

Hemophilia A

Sex-linked rec
Need 100% preop
Long PTT, normal PT

Question 18

What is Christmas Dz?

Answer 18

Hemophilia B
IX (9) def

Need 50% preop
Long PTT, normal PT

Tx:factor IX or FFP

Question 19

GpIIb/IIIa receptor deficiency on platlets ( can’t bind to each other)

Answer 19

Glanzmann’s thrombocytopenia

Question 20

Platelet disorders

Answer 20

Acquired: H2 blockers, heparin
Glanzmann’s : receptor def- can’t bind to each other
Bernard soulier: GpII rec def- can’t bind to collagen
Uremia: inhibits receptors, vWF (tx: HD, DDAVP,cryo,plts, cong estrogens)

Question 21

Plavix works by…

Answer 21

ADP rec antagonist- blocks so plts can’t bind

Tx: platlets

Question 22

HIT - Heparin Induced Thrombocytopenia

Answer 22

Due to anti platlet antibodies - IgG PF4 antibody = platelet destruction

Forms: white clot
LMWH- May have decreased risk

Tx: stop heparin
Argatroban, hirudin, ancrod or dextran for anticoag

Question 23

DIC disseminated intravascular coagulation

Answer 23

Low plts, fibrinogen
High fibrin split prod, D-Dimer

Long PT and PTT

Tx: underlying cause

Question 24

ASA

Answer 24

Inhibits cyclooxygenase in platelets Stop 7d before sx Keep platelets > 50,000 before sx, > 20,000 after sx

Question 25

Conditions causing hypercoagulability

Answer 25

``` Factor V Leiden Hyper homocysteinemia Protein C or S deficiency Anti-thrombin III deficiency Lupus Polycythemia Vera ```

Question 26

Most common congenital hypercoagulability disorder

Answer 26

Factor V Leiden

Question 27

Factor V Leiden

Answer 27

Factor V Leiden is a variant (mutated form) of human factor V that causes an increase in blood clotting (hypercoagulability). In this disorder, the Leiden form of factor V cannot be inactivated by protein C, and so clotting is increased Tx: heparin, warfarin

Question 28

Hyperhomocysteinemia

Answer 28

Homocysteine auto-oxidizes and reacts with reactive oxygen intermediates, damaging endothelial cells and increasing the risk of thrombus formation Tx: folic acid & B12

Question 29

Anti thrombin III Def causes?

Answer 29

Thrombus formation Heparin does not work for treatment Tx: AT III concentrate or FFP

Question 30

Most common cause of acquired hypercoagulability

Answer 30

Tobacco

Question 31

Warfarin induced skin necrosis

Answer 31

Due to short half life of protein C, S- increased likelihood of clotting Tx: heparin

Question 32

Key element in the development of arterial thrombosis

Answer 32

Endothelial injury

Question 33

Most common location that PE come from

Answer 33

ileofemoral region

Question 34

Tx of refractory bleeding in AV malformations

Answer 34

Thalidomide- stops angiogenesis

Question 35

Way heparin works

Answer 35

Activates AT III (no clot) Reverse: protamine (1-1.5 protamine/100U heparin) Protamine cross reacts with NPH insulin Protamine reaction: hypotension, bradycardia, decreased heart function

Question 36

Argatroban

Answer 36

Direct thrombin inhibitor (stop clot) Metabolized in liver Good for pts with HIT

Question 37

Bivalirudin

Answer 37

Reversible direct thrombin inhibitor ( no clot)

Question 38

Procoagulants: amicar (aminocaproic acid)

Answer 38

Stops fibrinolysis by stopping plasmin Use: DIC, thrombolytic overdoses

Question 39

Thrombolytics

Answer 39

Streptokinase Urokinase tPA To work- need guidewire past obstruction Follow fibrinogen levels (fibrinogen <100- inc risk of bleeding)

Question 40

Treatment of DIC

Answer 40

Treat underlying cause | Decreased ATIII, plasminogen

Question 41

Platelet function

Answer 41

Adhesion Activation Granule release- ADP, thromboxane A2, PDGF, serotonin

Question 42

Vascular endothelium maintains no clotting by these factors...

Answer 42

Prostacyclin, NO, tPA, thromboxane A2, serotonin, PDGF

Question 43

The liver synthesizes all coagulation factors except....

Answer 43

Factor VIII (8)

Question 44

Thrombin works by....

Answer 44

Activating platelets | Activating the coagulation cascade - factors 5,7,8

Question 45

In order to avoid widespread Thrombosis fibrinolysis must occur.....how does this work?

Answer 45

Activation of plasmin Plasminogen activated by tPA/urokinase/strepokinase----> activates plasmin Plasmin---> digests fibrin! factors 5, 8, 12, 2(prothrombin)

Question 46

Aspirin and NSAIDs work by....

Answer 46

Block COX---> mediates synthesis of thromboxanes and prostaglandins Asa - not reversible NSAIDs - reversible

Question 47

Thromboxane A2 works by...

Answer 47

Vasoconstriction Platelet aggregation Platelet activation

Question 48

Plavix works by...

Answer 48

Blocking platelet receptors