coagulation Flashcards

1
Q

hemostasis (arrest of bleeding) is achieved in what three ways

A
  1. vascular contraction (vasospasm)
  2. platelet adhesion, activation, and aggregation
  3. fibrin formation and reinforcement of the platelet plug
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2
Q

What is a factor that is produced from endothelial cells and inhibits platelet adhesion

A

PGI2

  • Prostacyclin (also called prostaglandin I2)
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3
Q

What factor in platelets binds to fibronogen in blood stream

A

GPIIb/IIIa

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4
Q

What are the three functions of thrombin

A
  1. positive feedback on intrinsic pathway
  2. activate platelets
  3. catalyze conversion of fibrinogen to fibrin
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5
Q

What factors are part of the intrinsic pathway

A

8, 9, 11, 12

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6
Q

What factors are part of the extrinsic pathway

A
  • tissue factor
  • VII
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7
Q

Damage to the blood vessel endothelium causes release of

A

von Willebrand factor (vWF)

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8
Q

Binding of platelets to collagen (through glycoprotein 1a (GP 1a)) and vWF (through GP 1b) activates the bound platelets to release

A

ADP, thromboxane A2 (TXA2), and serotonin (5-HT)

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9
Q

What are three natural inhibitors of coagulation in the body

A
  • Antithrombin III
  • Tissue factor pathway inhibitor (TFPI) – blocks the activity of TF/VIIa
  • Protein C – with its cofactor, protein S, destroys factors Va and VIIIa
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10
Q

PTT evaluates which pathway

A

intrinsic

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11
Q

PT and INR evaluate which pathway

A

extrinsic pathway

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12
Q

PTT monitors action of which drug

A

Heparin

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13
Q

INR (PT) monitors action of which drug

A

warfarin

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14
Q

list the High-molecular weight heparins

A

Heparin sodium (Liquaemin®)

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15
Q

List the Low molecular weight heparins

A
  • Enoxaparin (Lovenox®)
  • Fondaparinux (Arixtra®): synthetic pentasaccharide
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16
Q

List the Direct thrombin inhibitors

A
  • Lepirudin (Refludan®)
  • Argatroban (Novastan®)
  • Dabigatran (Pradaxa®)
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17
Q

List the Direct inhibitors of factor Xa

A
  • Rivaroxaban (Xarelto®)
  • Apixaban (Eliquis®)
  • Edoxaban
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18
Q

What is Heparin

A

a heterogenous mix of sulfated mucopolysaccharies; action from a unique pentasaccharide

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19
Q

MOA of Heparin

A
  • accelerates Antithrombin III activity
    • mainly affects Xa and thrombin
  • is recycled and stays active after releasing from inactivated clotting factor
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20
Q

When is heparin used

A
  • anticoagulant -> operations and IV catheters
  • prophylaxis against thrombosis (DVT and PE)
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21
Q

route of administration of heparin

A

IV only, onset of action is immediate

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22
Q

adverse effects of heparin

A
  • hemorrhage
  • heparin induced thrombocytopenia (HIT)
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23
Q

treatment of hemorrhage from heparin

A

Protamine sulfate

24
Q

contraindications/precautions to taking heparin

A
  • renal or hepatic dysfunction
25
Q

The low molecular weight heparins, Enoxaparin (Lovenox®) and Fondaparinux (Arixtra®) are similar to HMW heparins except:

A
  • main inhibitory action is on Factor Xa
  • can be injected subcutaneously
  • lower incidence of HIT
26
Q

Does protamine sulfate have an effect on Enoxaparin (Lovenox®) and Fondaparinux (Arixtra®)

A
  • Enoxaparin (Lovenox®): does not completely reverse
  • Fondaparinux (Arixtra®): no effect
27
Q

When is the direct thrombin inhibitor, Lepirudin (Refludan®) used

A
  • given as alternative in patients with h/o HIT
  • use in patients with poor liver function
    • do not use in patients with poor renal function
28
Q

route of administration of Lepirudin and Argatroban

A

IV

29
Q

when is the direct thrombin inhibitor Argatroban used

A
  • given as an alternative in patients with h/o HIT
  • use in patients with poor renal function
    • do not use in poor liver function
30
Q

route of administration of the the direct thrombin inhibitor Dabigatran

A

oral

31
Q

all new oral anticoagulants have the black box warning

A
  • avoid abrupt discontinuation without adequate alternative anticoagulation
  • Dabigatran has predictable anticoagulant effects
32
Q

route of administration of direct inhibitors of factor Xa

A

oral

33
Q

when are direct inhibitors of factor Xa used

A
  • DVT, PE, and prophylaxis
  • Rivaroxaban -> any patients
  • Apixaban (Eliquis®) and Edoxaban: patients with non-valvular AFIB
34
Q

MOA of warfarin

A
  • inhibits vitamin K epoxide reductase
  • interferes with synthesis of II, VII, IX, X, protein C and S
35
Q

peak effect of warfarin

A

after 48 hours

  • takes time to go off of warfarin too
36
Q

when is warfarin used

A
  • prevents development of emboli
    • no effect on already formed thrombi
  • uses:
    • DVT
    • thromboembolism
  • given chronically
37
Q

route of administration of warfarin

A

oral

38
Q

how is action of warfarin reversed

A
  1. vitamin K with discontinuation of warfarin -> takes time
  2. fresh frozen plasma -> immediate
39
Q

why does warfarin have to be coadministered with heparin for the first 5 days

A
  • warfarin quickly reduced levels of Protein C (short half life)
    • increases chance for warfarin-induced thrombosis -> cutaneous necrosis and infarction
40
Q

when is warfarin contraindicated

A

pregnancy (category X)

41
Q

Warfarin has LOTS of drug interactions. list some

A
  • drugs that affect
    • vit K
    • clotting factors : estrogen/pregnancy
    • platelet aggregation/function - aspirin
    • inhibit microsomal liver enzymes
    • induce liver microsomal enzymes
42
Q

list thrombolytic agents

A
  • Alteplase or Tissue plasminogen activator or t-PA
  • Reteplase (Retevase® )
  • Tenecteplase (TNKase®)
43
Q

MOA of thrombolytic agents

A
  • convert plasminogen to plasmin which cleaves fibrin and fibrinogen
44
Q

when are thrombolytic agents given

A
  • lysis of clots -> re-establish tissue perfusion
  • severe PE, DVT, and arterial thrombosis
45
Q

What makes Tenecteplase different from other thrombolytic agents

A
  • longer plasma half life
  • single IV injection
  • more fibrin specific
46
Q

MOA Urokinase

A
  • directly activates plasminogen
  • not clot-fibrin specific -> generalized systemic fibrinolysis
47
Q

list the Antifibrinolytics

A
  • Aminocaproic acid
  • Tranexamic acid
48
Q

MOA of Aminocaproic acid (Amicar®), Tranexamic acid (Cyklokapron®)

A
  • inhibits plasminogen activation -> decreases plasmin formation
49
Q

when are antifibrinolytics used

A

Reversal of fibrinolytic therapy

  • used for bleeding
50
Q

MOA of Aspirin

A
  • irreversible inhibition of COX enzyme -> decrease TXA2
    • lasts the life of the platelet 7-10 days
51
Q

when is ASA used

A

secondary prevention of cardiovascular events in most patients with established cardiovascular disease

52
Q

MOA of Clopidogrel (Plavix®), Ticlopidine (Ticlid®)

A
  • irreversibly block the ADP receptor on platelets
    • inhibits platelet aggregation
53
Q

when are Clopidogrel (Plavix®), Ticlopidine (Ticlid®) used

A

used in patients who are allergic to ASA

54
Q

DOC to prevent thrombosis in patients undergoing placement of coronary stents

A

Clopidogrel (Plavix®), Ticlopidine (Ticlid®)

  • Clopidigrel is frequently preferred over ticlodipine – because of better side effect profile and dosing
55
Q

List the inhibitors of GPIIB/IIIa receptor

A
  • Abciximab (ReoPro®)
  • Eptifibatide (Integrilin®)
  • Tirofiban (Aggrastat®)
56
Q

route of administration of GPIIB/IIIa receptor inhibitors

A

IV