Coagulation Disorders Flashcards

1
Q

Heparin Induced Thrombocytopenia

A

Caused by abnormal antibodies that activate platelets, causing clots to form and depleting platelet counts in blood
Consumes the platelets, to be rendered useless. Impaired ability to clot

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2
Q

Antidote for heparin:

A

protamine sulfate

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3
Q

warfarin side effects:

A

cholesterol microemboli

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4
Q

Anticoagulants

A

Anticoagulant: prevent to body from completing the clotting cascade and developing a blood clot. Prevents clot formation; does not break down existing clots. NOT A THROMBOLYTIC

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5
Q

Heparin and LMWH

A
  • Heparin: enhances antithrombin III activity
    o Decreases thrombin activity
    o Decreases prothrombinase
  • LMWH
    o Also enhances AT-III activity but more specific to prothrombinase (active factor X)
    o Fever adverse effects than heparin
    o Less risk of thrombocytopenia compared to heparin
  • Used for acute thromboembolic disorder including DVT, PE, unstable angina, and evolving MI
  • Prophylaxis for clotting
  • Monitor PTT when on heparin.

Warfarin, apixaban, rivaroxiban are all anticoagulants

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6
Q

Anti-platelets (ex. aspirin)

A
  • antagonize the receptors that communicate with platelets, thereby preventing platelet aggregation, and preventing clot formation.
  • inhibit platelet aggregation
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7
Q

Receptors used in platelet aggregation

A

ADP receptors

glycoprotein IIb/IIIa receptors

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8
Q

Thrombolytics

A

breakdown existing clots. Converts plasminogen to plasmin, which then degrades fibrin in clots.

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9
Q

Anti-fibrinolytics

A

refers to drugs that prevent the breakdown of fibrin/existing clots, thereby preventing excessive bleeding. does this by displacing plasminogen from fibrin, inhibiting fibrinolysis.

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10
Q

PT - prothrombin time

A

measures the time it takes plasma to clot when exposed to tissue factor, which assess the extrinsic and common pathways of coagulation.

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11
Q

aPTT: activated partial thromboplastin time

A

measures the time it takes plasma to clot when exposed to substances that activates the contact factors, which assesses the intrinsic and common pathways of coagulation

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12
Q

INR

A

international normalized ratio): the normal range for PT varies by laboratory and reagent/instrument combination, therefore the result is always reported along with a control factor, which is the INR. INR results will be similar on a blood sample tested in any library using any thromboplastin reagent/instrument system when calibrated correctly.

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13
Q

what conditions are antiplatelet agents prescribed for?

A
  • Reduce risk of CVA/MI
  • Reducing thrombolytic events post – CVA/MI
  • Prevent DVT
  • Prevent thrombi formation unstable angina/coronary stents
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14
Q

Foods that interfere with coagulation: counter effects of anticoagulant

A

o Foods high in vitamin K will counter the effects of the anticoagulant
o Alcohol is high in vitamin K, as well as cranberry juice
o Kale, spinach, Brussel sprouts, collards, mustard greens, chard, broccoli, asparagus

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15
Q

Foods that are natural anticoagulants

A

o Turmeric/ginger/garlic/cayenne pepper

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16
Q

• Know which nursing assessments need to be performed prior to the administration of a thrombolytic and WHY

A
  • Need to give thrombolytics ASAP. Ideally in less than an hour. Can be given a max of 4.5 hours after CVA has occurred.
  • Obtain complete health history including allergies and drug history
  • Obtain baseline vital signs
  • Obtain lab values for clotting times and CBC
17
Q

• When would an anti-fibrinolytic be administered and what is important to assess for in the patient’s history prior to administration?

A

o Used to prevent and treat excessive bleeding post-op
o Usually given during or after surgery so the site will stop bleeding
o Heavy menstrual bleeding
o Displaces plasminogen from fibrin. Inhibits fibrinolysis
o Assess clotting time, CBC

18
Q

Process of Hemostasis: Three major steps

A
  1. intrinsic and extrinsic pathways both lead to formation of prothrombinase
  2. prothrombinase coverts prothrombin to thrombin
  3. thrombin coverts fibrinogen to fibrin
  4. fibrin strands trap RBCs forming a clot.
19
Q

Role of platelet in hemostasis

A

o Platelets adhere to and aggregate at site of injury in vessel
o Platelet activation leads to formation of fibrin network that trap RBCs forming clot

20
Q

Role of Cofactors in hemostasis

A

o Ca2+ and vitamin K are critical for synthesis of clotting factors

21
Q

Platelet disorders

A
  • Due to decreased production resulting in low platelet counts (thrombocytopenia) – not able to clot as easily
    o Bone marrow suppression
    o Folic acid and B12 deficiency
    o Decreased thrombopoietin (in liver failure) – platelets <100
  • Hemophilia and von Willebrand’s disease
    o Genetic conditions result in in absence of clotting factors  difficulty clotting
22
Q

Warfarin

A
  • Reduced vit K (active vitamin K) is a cofactor for the production of clotting factors including thrombin and prothrombinase
  • Warfarin inhibits two enzymes necessary for formation of reduced vitamin K.
  • Monitor INR when on Warfarin
23
Q

Thrombolytics: tPA

A

Plasmin – tissue-plasminogen activator (tPA) and urokinase-plasminogen activator convert plasminogen into active plasmin which breaks down fibrin.