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Health Assessment > Blood Disorders (Exam 2) > Flashcards

Blood Disorders (Exam 2) Flashcards

1
Q

What is the most common hereditary bleeding disorder?

**

A

vWF Disorder

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2
Q

What are the most common symptoms associated with vWF Disorder?

A
  • Easy bruising
  • Recurrent epistaxis
  • menorrhagia
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3
Q

What is the most common vonWilebrand Disease?

A

Type 1: Parial quantitative deficiency of vWF

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4
Q

What is the least common vonWillebrand?

A
  • Type 3
  • Most likely to die
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5
Q

What lab values in a vWF patient will be abnormal? Normal?

A
  • BT (bleeding time) is prolonged
  • PT/aPTT is normal
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6
Q

Treatment of vWF

A
  • Correct the deficiency of vWF
  • Desmopressin (DDVAP)
  • transfusion the missing specific factor
    * Cryoprecipitate
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7
Q

What is DDAVP?

A
  • synthetic analogue of vasopressin
  • stimulates release of vWF by endothelial cells
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8
Q

What is the dose of DDAVP?

**

A
  • 0.3 ug/kg in 50ml normal saline
  • given over 15 - 20 minutes
  • Max effect in 30 minutes
  • lasts 6-8 hours
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9
Q

Side effects of DDAVP?

A
  • Headache
  • hypotension
  • hyponatremia
  • water intoxication
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10
Q

How do you treat water intoxication and hyponatremia associated with DDAVP?

A
  • Restrict IV and Oral intake for 4-6 hours after the use of the drug.
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11
Q

Name the most serious side effect associcated with hyponatremia and water intoxication?

A

Seizures

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12
Q

At what sodium level will you see confusion and restlessness? What will their EKG show?

**

A
  • 120 mEq/L
  • Widening of QRS
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13
Q

At what sodium level will you see somulance and nausea? What will their EKG show?

**

A
  • 115 mEq/L
  • Elevated ST segment
  • Widening of QRS
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14
Q

At what sodium level will you see Seizures and death? What will their EKG show?

**

A
  • 110 mEq/L
  • Vtach or V-fib
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15
Q

If DDAVP doesn’t work for vWF, what should you use next? What risk is associated?

A
  • Cryoprecipitate
  • Infection risk d/t multiple donors and no viral attenuation
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16
Q

How much does 1unit of Cryoprecipitate raise fibrinogen levels?

A
  • 50 mg/dL
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17
Q

What is F VIII concentrate?

A
  • contains Factor VIII and vWF
  • given preoperatively and during surgery.
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18
Q

How is Factor VIII concentrate obtained?

A
  • Prepared from a pool of plasma from multiple donors
  • it UNDERGOES viral attenuation
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19
Q

Who needs to evaluate a patient with vWF before surgery?

A

A Hematologist

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20
Q

When should DDAVP be given before surgery? And what needs to be rechecked before starting surgery?

A
  • 60 minutes
  • Factor VIII levels should be rechecked and showing improvement before surgery.
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21
Q

What is not recommended for vWF and other coagulapathy patient’s during anesthesia?

A
  • Neuoaxial blocks – hematoma & bleeding
  • Arterial punctures
  • laryngeal trauma– hematoma and post op obstructions
22
Q

Number one anesthesia option for patients with vWF?

A

General Anesthesia

23
Q

What medications do we give that can increased bleeding?

A
  • Heparin
  • Warfarin
  • Fibrinolytics
  • Antiplatelets
24
Q

How does Heparin work?

A
  • inhibits thrombin.
  • Thrombin converts fibrinogen to fibrin
  • Anticoagulation effect by activating antithrombin 3
25
Q

What reverses Heparin?

A
  • Protamine
  • Very quick to reverse
26
Q

What is LMWH? And why do we give it?

A
  • Lovenox
  • effective VTE prophylaxis
  • predictable pharmacokinetic response
  • fewer effect on platelet function
  • Reduces risk of HITT
27
Q

How does Coumadin work?

A
  • interferes with hepatic synthesis of Vitamin K
  • depends on coagulation factors 2, 7, 9,10
28
Q

What medication reverses Coumadin?

A
  • Vitamin K: 6 - 8 hours—- GIVE SLOWLY
29
Q

What can you give to reverse coumadin quicker than Vitamin K?

A
  • Prothrombin complex concentrates
  • Factor 3a
  • FFP
30
Q

How do Fibrinolytics work

A
  • converts plasminogen to plasmin
  • Which cleaves fibrin
  • causing clots to dissolve
31
Q

What are some examples of fibrinolytics?

A
  • Tissue plasminogen activator (tPA)
  • Streptokinase (SK)
  • Urokinase (UK)
32
Q

How do Anti-fibrinolytics work?

A
  • Inhibits the conversion of plasminogen to plasmin
33
Q

Name 3 Antifibrinolytic agents

A
  • tranexamic acid
  • E-amiocaproic acid
  • aprotinin
34
Q

What do you do if your patient is on an antiplatelet?

A
  • d/c drugs on time
  • PLT transfusion
35
Q

What is Disseminated Intravascular Coagulopathy?

A
  • Systemic activation of the coagulation system
  • simutaneously leads to thrombus formation
  • exhausts platelet and coagulation factors
36
Q

What underlying conditions can precipitate DIC?

A
  • trauma
    * amniotic fluid embolus
  • malignancy
    * sepsis (except urosepsis)
  • incompatible blood transfusion
37
Q

What lab results will you see with DIC?

A
  • Reduction in Platelets
  • Prolonged PT/PTT and thrombus time (TT)
  • Elevated concentration of fibrin degradation products
38
Q

How do you manage and treat DIC patients?

A
  • alleviating underlying conditions
  • blood component transfusions to replete coagulation factors and platelets.
39
Q

What medication/therapy is counterindicated in DIC d/t potential for catastrophic throbotic complications?

A
  • Antifibrinolytic
40
Q

What are the 2 most common Prothombotic Disorders?

A
  • Factor V Leiden
  • HIT
41
Q

When is Factor V Leiden typically discovered?

A
  • After multiple miscarriages
  • DVTs (with/without anticoagulants)
  • Late fetal loses.
42
Q

What is Factor V in the body?

A
  • protein C for normal clotting
  • when body produces enough fibrin, Activated Protein C inactivates Factor V
  • Stops the Clot from growing larger.
43
Q

Describe Factor V Leinden

A
  • Mutations in genes for Factor V
  • Factor V Leiden is an abnormal version of Factor V that is resistent to Activated Protein C.
  • Activate C is not able to stop Factor V Leiden from making more fibrin.
44
Q

Factor V Leiden: Anesthesia Implications

A
  • increased risk of developing DVT
  • Pts are on anticoags
45
Q

What are the most common anticoagulations?

A
  • warfarin
  • unfractioned heparin
  • LMWH
46
Q

Describe HIT (Heparin Induced Thrombocytopenia)

A
  • autoimmune-mediated drug reaction occuring in 5% of people after exposure to unfractioned heparin or LMWH.
47
Q

In HIT, when does thrombocytopenia typically occur? And what is the hallmark finding?

A
  • 5-14 days after intitial therapy
  • decrease in plt < 100,000
  • potential for arterial and venous thromboses.
48
Q

If someone developes HIT, what are their chances of developing a thrombosis?

A
  • Absolute Risk of 30 -75%
49
Q

If your patient developes a clot after starting heparin, what could be the problem?

A
  • Patient has deveolped HIT.
50
Q

What should you start the patient on if they have developed HIT to reduce the risk of thrombis?

A

Direct Thrombin Inhibitor
* bivalirudin
* lepirudin
* argatroban

51
Q

What is Fondaparinaux?

A
  • Primary Therapy for HIT
  • Treat VTE
  • Synthetic Factor Xa inhibitor
52
Q

After someone develops HIT, how long will it take for the heparin immune complexes to be completely out of their system?

A
  • 30 - 60 days.

Health Assessment (7 decks)

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