Blood Disorders (3) Flashcards

1
Q

What does vWF play a critical role in?

A

platelet adherence/adhesion

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2
Q

What is the most common hereditary bleeding disorder?

A

vWF disorder

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3
Q

Symptoms of vWF:

A
  • easy bruising
  • recurrent epistaxis
  • menorrhagia
  • patients are usually unaware until questionaire/surgery
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4
Q

Classification of Inherited vonWillebrand disease:

A
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5
Q

Diagnosis for vWF disease:

A
  • PT and aPTT are often normal in patients with vWD
  • BT is prolonged
  • hematologist to analyze labs
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6
Q

Treatment for vWF disease:

A
  • Correct the deficiency of vWF
  • Use desmopressin
  • By the transfusion of the specific factor
  • Cryoprecipitate
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7
Q

Dose for DDAVP:

A

IV dose = 0.3 mcg/kg in 50 mL of normal saline over 15 to 20 minutes

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8
Q

What is DDAVP?

A

A synthetic analogue of vasopressin and stimulates the release of vWF by endothelial cells

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9
Q

The maximal effect of DDAVP:

A

The maximal effect is in 30 minutes and lasts from 6 to 8 hours

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10
Q

Side effects of DDAVP:

A
  • headache
  • rubor
  • hypotenstion
  • tachycardia
  • hyponatremia
  • water intoxication
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11
Q

For patients getting DDAVP, how can you decrease water intoxication, hyponatremia, and consequent seizures?

A

The administration of water, orally or intravenously, should be restricted for 4-6 hours after the use of the drug

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12
Q

CNS and ECG changes for serum Na of 120 meq/L:

A

CNS: confusion and restlessness
ECG: Widening of QRS

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13
Q

CNS and ECG changes for serum Na of 115 meq/L:

A

CNS: somnolence and nausea
ECG: Elevated ST segments, widened QRS

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14
Q

CNS and ECG changes for serum Na of 110 meq/L:

A

CNS: seizures and coma
ECG: Vtach or Vfib

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15
Q

What is a risk of giving cryoprecipitate?

A

Increase risk of infection/reaction because it’s not submitted to viral attenuation

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16
Q

How much does 1 unit of cryo raise fibrinogen?

A

50 mg/dL

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17
Q

Anesthesia considerations for patients with vWF disease:

A
  • general anesthesia
  • undergoing neuroaxial block = increased risk of developing a hematoma and compression of neurological structures
  • avoid traumas (intubating)
  • arterial puncture is not recommended
  • laryngeal trauma during intubation may cause hematoma - postop obstruction of the airways
  • avoid IM
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18
Q

Characteristics of heparin:

A
  • negatively charged, CHO containing glucuronic acid residues
  • inhibits thrombin
  • heparin derives its anticoagulant effect by activating antithrombin III
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19
Q

How do you monitor heparin intraop?

A

PTT and ACT

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20
Q

Reversing heparin:

A

Heparin’s anticoagulant effect is rapidly reversible by protamine (+ polypeptide forming a stable complex neutralizing heparin)

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21
Q

Which heparin is more effective for VTE prophylaxis?

A

LMWH is more effective compared to UFH

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22
Q

LMWHs have a more predictable ______ ______, fewer effects on ______ ______, and a reduced risk for ___.

A

Pharmacokinetic response;
platelet function;
HIT (heparin induced thrombocytopenia)

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23
Q

MOA of coumadin:

A

Interferes with hepatic synthesis of vitamin-k dependent coagulation factors (II, VII, IX, X)

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24
Q

What are the vitamin k dependent coag factors?

A

Factors II, VII, IX, X

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25
Reversal for coumadin:
Vitamin K reverses coumadin anticoagulation - takes 6-8 hours to correct
26
More rapid reversal for coumadin:
- Prothrombin complex concentrates (very expensive) - Recombinant factor VIIa and FFP - Cryo
27
What is MOA of fibrinolytics?
Act by converting plasminogen to plasmin which cleaves fibrin (breaking up clots)
28
What are common fibrinolytics?
* Tissue plasminogen activator (tPA) * Streptokinase (SK) * Urokinase (UK)
29
What are anti-fibrinolytic agents?
* Tranexamic acid * E-aminocaproic acid * Aprotinin
30
What is the MOA of anti-fibrinolytics?
Inhibits conversion of plasminogen to plasmin (No clot breakdown)
31
What is a wierd S/E of TXA?
Loss of color vision
32
What is DIC?
Disseminated Intravascular Coagulopathy: Systemic activation of the coagulation system simultaneously leads to thrombus formation and exhaustion of platelets and coagulation factors
33
What underlying disorders may precipitate DIC?
* Trauma * Amniotic fluid embolism * Malignancy * Sepsis * Incompatible blood transfusions
34
What do you target when treating DIC?
Target the source
35
What causes the bleeding aspect of DIC?
Depletion of platelets and coag factors
36
What causes multiorgan failure associated with DIC?
Intravascular fibrin deposition→ Thrombosis of small and midsized vessels with organ failure
37
What labs are reduced with DIC?
Platelets
38
What labs are increased with DIC?
* PT * PTT * TT (thrombin time) * elevated concentrations of soluble fibrin degradation products
39
_________ therapy is usually contraindicated in DIC.
Antifibrinolytic → potential for catastrophic thrombotic complications
40
What is used to treat DIC?
* Blood component transfusions→ need to replete coagulation factors and platelets consumed in the process
41
What is the apache score used for?
Sepsis grading
42
What are 2 examples of Prothrombotic disorders?
* Factor V Leiden * HIT
43
When the body is working normally, What inactivates Factor V to stop the clot from growing larger?
Activated Protein C
44
What is Factor V Leiden?
An abnormal version of Factor V * Resistant to activated protein C * Activated protein C cant stop Factor V Leiden from making more fibrin
45
What causes Factor V Leiden? When is it common to discover this condition?
* Genetic mutation of Factor V *Commonly discovered with pregnancy (inflammatory state)→ Causes late fetal loses
46
What medication do you put someone on with Factor V Leiden?
Lovenox at home
47
If a patient with factor V leiden has a fetal lose, what is the typical anesthesia plan?
DNC under GA * Lovenox makes neuraxials high risk*
48
Factor V Leiden is associated with increased risk of ______ developement.
DVT (with or without PE)
49
What are common anticoagulant options for patient with Factor V Leiden?
* Warfarin * Unfractionated heparin * LMWH (lovenox)
50
Most Factor V Leiden are silent until ___________.
Pregnancy
51
What are common presentations of factor V Leiden?
* DVT * Repeated missed abortions * Recurrent late fetal losses
52
Why might prophylactic anticoagulation be indicated in some cases of Factor V Leiden?
Prevent venous or placental thrombosis→ Improved placental blood flow is likely to lead to better pregnancy outcomes
53
What is HIT?
Heparin induced thrombocytopenia: * Autoimmune-mediated drug reaction after exposure to unfractionated heparin or (rare) LMWH
54
What percent of patients experience HIT after heparin exposure?
as many as 5%
55
When does HIT occur?
5-14 days after initial therapy
56
What is the hallmark finding for HIT?
PLT count <100,000
57
How can HIT cause potential for venous and arterial thromboses?
Platelet activation
58
Evidence suggests that HIT Is mediated by ______ _________.
Immune complexes
59
Which immune complexes are thought to mediate HIT?
* IgG antibody * Platelet factor 4 (PF4) * Heparin
60
Patients are who develop HIT have a substantially higher risk for ____________.
Thrombosis (30-75%)
61
How do activate platelets behave during HIT?
62
HIT should be considered for any patient experiencing __________ or __________ during or after heparin administration.
Thrombosis or Thrombocytopenia
63
What is the first step if HIT is suspected?
D/C heparin (including unfractionated, heparin catheters, heparin flushes, LMWH)
64
What can you give if heparin is d/c d/t concern for HIT?
Must give alternative AC→ Direct thrombin inhibitor (Bivalirudin, Lepirudin, Argatroban)
65
What is an example of a synthetic factor Xa inhibitor?
Fondaparinaux
66
PF4/Heparin immune complexes clear from the circulation within ___ months.
3
67
T/F: Patients who have experiences HIT should avoid future exposure to unfractionated heparin
True