Exam #2: Hemodynamics III Flashcards Preview

General Pathology > Exam #2: Hemodynamics III > Flashcards

Flashcards in Exam #2: Hemodynamics III Deck (30):
1

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

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

2

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

- Make a 50:50 mixture of patient plasma and normal plasma
- Factor= clotting will occur
- Inhibitor= no clotting

3

What are the does dependent effects of Heparin and Warfarin?

- Low dose heparin= PTT prolonged
- Low dose warfarin= PT prolonged

BOTH will be prolonged at HIGH doses

4

What are the special considerations regarding anticoagulation and the elderly?

- Increased age= increased sensitivity
- Increased drug interactions

Possibly increased bleeding independent of other factors

5

What are the contraindications to warfarin therapy?

1) Pregnancy
2) Risk of hemorrhage>benefit

E.g.
- uncontrolled alcohol or drug abuse
- unsupervised dementia/ psychosis

6

What are the signs of warfarin overdose?

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

7

What is Warfarin Necrosis?

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.

8

What causes Warfarin Necrosis?

- 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)

9

What is Heparin-induced Thrombocytopenia?

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

10

What are the platelet abnormalities?

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

11

What are the coagulopathies?

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

*Mom

12

What is Bernard-Soulier Disease?

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

13

What is Glanzmann's Thrombasthenia?

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

14

What is Thrombotic Thrombocytopenic Purpura (TTP)?

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

15

What is Idiopathic Thrombocytopenic Purpura (ITP)?

This is a disease caused by autoantibodies to platelets
- Splenomegaly

*****Treated with thrombopoetin

16

What is Aplastic Anemia?

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

17

What is von Willebrand's disease?

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

18

Describe the clinical presentation of vWF disease?

Most patients are asymptomatic, but other may:
- bruise easily
- nosebleed
- gingival bleeding
- heavy periods

19

Generally, what is Hemophilia?

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

What is the defect in Hemophilia A?

Factor VIII
- most common

21

What is the defect in Hemophilia B?

Factor IX

22

What is the defect in Hemophilia C?

Factor XI

23

How is Hemophilia treated?

Recombinant factor

24

What are the complications of Hemophilia?

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

25

What is DIC?

"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

What is a consumptive coagulopathy?

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

27

Outline the pathophysiology of DIC.

N/A

28

How is DIC diagnosed?

D-dimer

29

What is a D-Dimer?

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

30

How is DIC treated?

- Treat the underlying cause
- Blood products and heparin as needed