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Hematology Flashcards

0
Q

Thrombin function

A

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

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1
Q

Initial 3 responses to vascular injury

A

Vasoconstriction
Platelet adhesion
Thrombin generation

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2
Q

Actions of Antithrombin III

A

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

Heparin binds Antithrombin III

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3
Q

Protein C and S function

A

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

Protein S- vitamin K dependent, protein C cofactor

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4
Q

Factors that cause fibrinolysis (no clot)

A

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

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5
Q

Clotting factor with shortest half life

A

Factor VII (7)

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6
Q

Only clotting factor NOT synthesized in liver

A

Factor VIII (8)

Synthesized in endothelium

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7
Q

Vitamin K dependent factors

A

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

Protein C, S

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8
Q

Thromboxane (TXA2)

A

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

“Box in platelets”

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9
Q

Coagulation factor with highest amount of vWF VIII

A

Cryoprecipitate

Tx in Von Willebrand dz, hemophilia A VIII def

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10
Q

Coagulation factor with highest amount of all factors

A

FFP

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11
Q

Causes release of VIII and vWF from endothelium

A

DDAVP

Conjugated estrogens

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12
Q

PT measures

A

Factors II, V, VII, X, fibrinogen

Best test for liver synthetic function

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13
Q

Factors not measured with PTT

A

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

For anticoagulation: PTT 60-90

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14
Q

Want ACT (activated clotting time)

A

Routine anticoag 150-200

Cardiopulmonary bypass 400

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15
Q

What is most common congenital bleeding disorder?

A

VonWillebrand dz

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16
Q

Vonwillebrand dz

A

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

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17
Q

What is factor VIII deficiency?

A

Hemophilia A

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

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18
Q

What is Christmas Dz?

A

Hemophilia B
IX (9) def

Need 50% preop
Long PTT, normal PT

Tx:factor IX or FFP

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19
Q

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

A

Glanzmann’s thrombocytopenia

20
Q

Platelet disorders

A

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)

21
Q

Plavix works by…

A

ADP rec antagonist- blocks so plts can’t bind

Tx: platlets

22
Q

HIT - Heparin Induced Thrombocytopenia

A

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

23
Q

DIC disseminated intravascular coagulation

A

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

Long PT and PTT

Tx: underlying cause

24
Q

ASA

A

Inhibits cyclooxygenase in platelets
Stop 7d before sx

Keep platelets > 50,000 before sx, > 20,000 after sx

25
Q

Conditions causing hypercoagulability

A 
Factor V Leiden
Hyper homocysteinemia
Protein C or S deficiency
Anti-thrombin III deficiency
Lupus
Polycythemia Vera
26
Q

Most common congenital hypercoagulability disorder

A

Factor V Leiden

27
Q

Factor V Leiden

A

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

28
Q

Hyperhomocysteinemia

A

Homocysteine auto-oxidizes and reacts with reactive oxygen intermediates, damaging endothelial cells and increasing the risk of thrombus formation

Tx: folic acid & B12

29
Q

Anti thrombin III Def causes?

A

Thrombus formation
Heparin does not work for treatment

Tx: AT III concentrate or FFP

30
Q

Most common cause of acquired hypercoagulability

A

Tobacco

31
Q

Warfarin induced skin necrosis

A

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

Tx: heparin

32
Q

Key element in the development of arterial thrombosis

A

Endothelial injury

33
Q

Most common location that PE come from

A

ileofemoral region

34
Q

Tx of refractory bleeding in AV malformations

A

Thalidomide- stops angiogenesis

35
Q

Way heparin works

A

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

36
Q

Argatroban

A

Direct thrombin inhibitor (stop clot)

Metabolized in liver
Good for pts with HIT

37
Q

Bivalirudin

A

Reversible direct thrombin inhibitor ( no clot)

38
Q

Procoagulants: amicar (aminocaproic acid)

A

Stops fibrinolysis by stopping plasmin

Use: DIC, thrombolytic overdoses

39
Q

Thrombolytics

A

Streptokinase
Urokinase
tPA

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

40
Q

Treatment of DIC

A

Treat underlying cause

Decreased ATIII, plasminogen

41
Q

Platelet function

A

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

42
Q

Vascular endothelium maintains no clotting by these factors…

A

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

43
Q

The liver synthesizes all coagulation factors except….

A

Factor VIII (8)

44
Q

Thrombin works by….

A

Activating platelets

Activating the coagulation cascade - factors 5,7,8

45
Q

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

A

Activation of plasmin

Plasminogen activated by tPA/urokinase/strepokinase—-> activates plasmin

Plasmin—> digests fibrin! factors 5, 8, 12, 2(prothrombin)

46
Q

Aspirin and NSAIDs work by….

A

Block COX—> mediates synthesis of thromboxanes and prostaglandins

Asa - not reversible
NSAIDs - reversible

47
Q

Thromboxane A2 works by…

A

Vasoconstriction
Platelet aggregation
Platelet activation

48
Q

Plavix works by…

A

Blocking platelet receptors

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