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Spr24 Assess Ex1&2 - Cornelius > Blood Disorders (Exam II) > Flashcards

Blood Disorders (Exam II) Flashcards

1
Q

What is the most common hereditary bleeding disorder?

A

vWF disorder

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2
Q

What are the S/S of vWF disorder?

A
  • Easy bruising
  • epistaxis
  • menorrhagia
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3
Q

What would lab values be for someone with vWF deficiency?

A
  • Normal PT & aPTT
  • Bleeding time is prolonged
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4
Q

What are the treatments for vWF deficiency?

A
  • Desmopressin (DDAVP)
  • Cryoprecipitate
  • Factor VIII
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5
Q

How does DDAVP work in regards to treatment of von Willebrand deficiency??

A

Stimulates vWF release from endothelial cells

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6
Q

What is the dose for DDAVP?

A

0.3 mcg/kg in 50 mL over 15-20 mins (Do not bolus)

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7
Q

What is the onset & duration of DDAVP?

A
  • Onset: 30mins
  • Duration: 6-8hrs
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8
Q

What are side effects of DDAVP?

A
  • HA
  • rubor/flushing
  • hypertension? hypotension?
  • tachycardia
  • hyponatremia
  • water intoxication (excessive water retention)
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9
Q

What is the most major side effect of DDAVP?

A

Hyponatremia

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10
Q

Someone that gets DDAVP needs to be on what to prevent water intox and hyponatremia?

A

Fluid restriction 4-6hrs before & after DDAVP

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11
Q

What blood product can be utilized for vWF disease if the patient is unresponsive to DDAVP?

A

Cryoprecipitate

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12
Q

1 unit of Cryo raises the ____ level by ___?

A

Fibrinogen by 50 mg/dL

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13
Q

What is a potential risk factor with cryoprecipitate?

A

Increased risk of infection (not submitted to viral attenuation)

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14
Q

What is Factor VIII concentrate made of?

A

Pool of plasma from a large number of donors.

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15
Q

What stage of surgery is Factor VIII given?

A

Preop or intraop

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16
Q

When should DDAVP be given prior to surgery?

A

60mins before Sx

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17
Q

What blood product poses an increase risk for infection? Why?

A
  • Cryoprecipitate
  • Not sent for viral attenuation
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18
Q

Pts with coagulopathies undergoing neuraxial anesthesia are at increased risk for what?

A
  • Hematoma
  • Nerve compression
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19
Q

What are the anesthesia considerations for someone with vWF deficiency?

A
  • Avoid trauma (particularly airway)
  • avoid IM sticks
  • avoid arterial lines (if feasible)
  • avoid spinals
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20
Q

How does heparin work?

A
  • Inhibition of Thrombin (needed to convert fibrinogen to fibrin)
  • Antithrombin III activation
21
Q

What labs are monitored with heparin?

A

PTT &/or ACT

22
Q

What is the mechanism of action of Coumadin?

A

Inhibition of vitamin K-dependent factors.

23
Q

Which factors are vitamin-K dependent?

A

II, VII, IX & X

24
Q

What is the onset for Vitamin K reversal of coumadin?

A

6-8hrs

25
Q

What drugs/products can be given to reverse coumadin faster than Vit K?

A
  • Prothrombin complex concentrates
  • Factor VIIa
  • FFP
26
Q

What is the mechanism of action for fibrinolytics (UK, streptokinase & tPA)?

A

Convert plasminogen → plasmin, which cleaves fibrin ⇒ lysis of clot

27
Q

How do tranexamic acid (TXA) and aminocaproic acid work?

A

Inhibit conversion of plasminogen to plasmin (prevents lysis of clot)

28
Q

What is the best way to treat DIC?

A

Treat the underlying cause

29
Q

What will labs show for someone in DIC?

A
  • ↓Platelet count
  • Prolonged PT, PTT & TT.
  • ↑ fibrin degradation products
30
Q

When is antifibrinolytic therapy given to someone in DIC?

A

Trick question, it shouldn’t. Can lead to catastrophic thrombotic complications

31
Q

What is factor V?

A
  • Protein for clotting, plays role in prothrombin → thrombin.

Activated protein C inactivates factor V thus stopping clot growth.

32
Q

What is Factor V Leiden?

A

Genetic mutation where Activated protein C cannot stop factor V Leiden thus => excessive fibrin.

33
Q

What does Activated Protein C do?

A

Inactivates factor V when enough fibrin has been made.

34
Q

Who is usually tested for Factor V Leiden?

A

Pregnant women. Especially ones with unexplained late stage abortions

35
Q

What anticoagulant medications could someone with Factor V Leiden be put on?

A
  • Warfarin
  • LMWH & UFH
36
Q

What is the hallmark sign of HIT?

A

Plt count <100,000

thrombocytopenia

37
Q

HIT results in ____ activation and potential____?

A

platelet; thrombosis

risk thombosis 30-75%

38
Q

What is heparin replaced with when HIT is diagnosed?

A

Agratroban, bivalirudin, lepirudin (direct-thrombin inhibitors)

39
Q

What is Fondaparinux & when is it used?

A
  • A synthetic Factor Xa inhibitor
  • used to treat VTE in HIT
40
Q

Serum Na+ of 120 mEq/L CNS changes? EKG changes?

A

CNS: confusion, restless

EKG: widened QRS

41
Q

Serum Na+ of 115 mEq/L CNS changes? EKG changes?

A

CNS: somnolence, nausea

EKG: Elevated ST, widened QRS

42
Q

Serum Na+ of 110 mEq/L CNS changes? EKG changes?

A

CNS: seizures, coma

EKG: Vtach or Vfib

43
Q

How does Factor VIII compare to cryo in terms of infection?

A

Undergoes viral attenuation, poses less infection risk

44
Q

What should be confirmed before surgery in vWF disorder pt?

A

Normalized bleeding time and improved F VIII levels

45
Q

Rapid reversal of heparins anticoagulant effect by?

A

Protamine (+ polypeptide)

46
Q

What benefits does LMWH have compared to UFH?

A
  • fewer effects on platelet function
  • reduced risk of HIT
47
Q

How would you describe DIC?

A

systemic coagulation activation leading to excess clotting ⇒ exhaustion of platelets and coagulation factors

48
Q

When would you often see thrombocytopenia in HIT?

A

5-14 days after initial therapy

Spr24 Assess Ex1&2 - Cornelius (26 decks)

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