Exam #2: Hemodynamics III Flashcards

1
Q

What is the difference between a PT, PTT, & INR?

A

PT= Prothrombin time, extrinsic pathway, warfarin

INR= International Normalized Ratio–a way to compensate for differences in tissue factor; normally you’ll order a PT/INR

PTT= Partial thromboplastin time, intrinsic pathway, heparin

*****Note that a good PT/INR when you want a patient to be anticoagulated is 2-3

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2
Q

How do you figure out if a person has a factor deficiency or an inhibitor?

A
  • Make a 50:50 mixture of patient plasma and normal plasma
  • Factor= clotting will occur
  • Inhibitor= no clotting
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3
Q

What are the does dependent effects of Heparin and Warfarin?

A
  • Low dose heparin= PTT prolonged
  • Low dose warfarin= PT prolonged

BOTH will be prolonged at HIGH doses

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4
Q

What are the special considerations regarding anticoagulation and the elderly?

A
  • Increased age= increased sensitivity
  • Increased drug interactions

Possibly increased bleeding independent of other factors

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5
Q

What are the contraindications to warfarin therapy?

A

1) Pregnancy
2) Risk of hemorrhage>benefit

E.g.

  • uncontrolled alcohol or drug abuse
  • unsupervised dementia/ psychosis
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6
Q

What are the signs of warfarin overdose?

A

Any unusual bleeding

  • Melena or hematochezia
  • Hematuria
  • Excessive menstrual bleeding
  • Bruising
  • Excessive nosebleeds or bleeding gums
  • Persistent bleeding from superficial injuries
  • Bleeding from a tumor, ulcer, or other lesion
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7
Q

What is Warfarin Necrosis?

A

This is a condition seen 3-5 days s/p warfarin therapy initiation; patients develop skin lesions that progress from localized pain and erythema to a necrotic eschar.

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8
Q

What causes Warfarin Necrosis?

A
  • Warfarin Necrosis is most commonly seen in patients with low levels of Protein C
  • Protein C normally has anticoagulant & fibrinolytic activity
  • Synthesis of Protein C is Vitamin K dependent
  • Warfarin causes depletion of already low Protein C, leading to an acutely hypercoabuable state prior to anticoagulation
  • Thrombosis occurs in dermal vessels

*****Because of this, patients should be started on Heparin & then given warfarin i.e. Lovenox (low molecular weight heparin)

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9
Q

What is Heparin-induced Thrombocytopenia?

A

This is a potential complication of heparin therapy that leads to a prothromic state, even in the face of thrombocytopenia & heparin.

  • More common with unfractionated heparin than low molecular weight heparin
  • Immune system forms antibodies against heparin and Platelet Factor 4 (the receptor for heparin on platelets)/ Heparin complexes, which has three effects:
    1) Platelet activation
    2) Platelet aggregation
    3) Platelet consumption

Thus, a thrombocytopenia (low platelets) develops from platelet consumption & a prothrombic state is developed . Can lead to extensive venous thrombosis, venous limb gangrene, and secondary skin ulcer

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10
Q

What are the platelet abnormalities?

A

1) Bernard-Soulier Disease
2) Glanzmann’s Thromboasthenia
3) Thrombotic Thryomctopenic Purpura (TTP)
4) Idiopathic Thrombocytopenic Purpura
5) Aplastic Anemia–Pancytopenia

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11
Q

What are the coagulopathies?

A

Von Willebrand’s Disease
- Deficiency in vWF in the ECM such that platelet binding by GpIb is prevented

*Mom

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12
Q

What is Bernard-Soulier Disease?

A

This is an autosomal recessive disorder caused by a defect in platelet adhesion, specifically, glycoprotein Ib.
- This is the glycoprotein on platelets that binds to vWF in the ECM

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13
Q

What is Glanzmann’s Thrombasthenia?

A

This is a defect in platelet aggregation caused specifically by a defect in glycoprotein IIb & IIIa.
- I.e. this disease prevents fibrinogen cross-bridging & platelet aggregation

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14
Q

What is Thrombotic Thrombocytopenic Purpura (TTP)?

A

This is a disease caused by antibodies directed against the von Willebrand factor cleaving protease, ADAMTS-13

  • Can’t split vWF & platelets
  • At risk for bleeding as well as thrombi
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15
Q

What is Idiopathic Thrombocytopenic Purpura (ITP)?

A

This is a disease caused by autoantibodies to platelets
- Splenomegaly

*****Treated with thrombopoetin

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16
Q

What is Aplastic Anemia?

A

Bone marrow leads to pancytopenia; you’re not making any of your blood cells

17
Q

What is von Willebrand’s disease?

A

This is a deficiency of vWF & is the most common bleeding disorder

18
Q

Describe the clinical presentation of vWF disease?

A

Most patients are asymptomatic, but other may:

  • bruise easily
  • nosebleed
  • gingival bleeding
  • heavy periods
19
Q

Generally, what is Hemophilia?

A

Coagulopathy caused by specific coagulation cascade factor deficiencies

All have the same clinical presentation
- Severe bleeding from minor trauma, especially in types A & B

20
Q

What is the defect in Hemophilia A?

A

Factor VIII

- most common

21
Q

What is the defect in Hemophilia B?

A

Factor IX

22
Q

What is the defect in Hemophilia C?

A

Factor XI

23
Q

How is Hemophilia treated?

A

Recombinant factor

24
Q

What are the complications of Hemophilia?

A

1) Deep internal bleeding
2) Joint damage
3) Transfusion transmitted infection
4) Adverse reaction to factor
5) Intracranial hemorrhage

25
Q

What is DIC?

A

“Disseminated Intravasulcar Coagulation”

Systemic activation of the coagulation system that leads to widespread fibrin thrombi in the microcirculation
- Of note, this widespread thrombosis causes platelet & coagulation protein CONSUMPTION–>bleeding catastrophe

*****This is referred to as a “consumptive coagulopathy”m

26
Q

What is a consumptive coagulopathy?

A

Depletion of platelets & coagulation factors that causes the patient to be at an increased risk of bleeding

27
Q

Outline the pathophysiology of DIC.

A

N/A

28
Q

How is DIC diagnosed?

A

D-dimer

29
Q

What is a D-Dimer?

A

D-dimer is an assay that measures plasmin-cleaved insoluble cross-linked fibrin

30
Q

How is DIC treated?

A
  • Treat the underlying cause

- Blood products and heparin as needed