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Pharm 2 > Hematology > Flashcards

Hematology Flashcards

1
Q

What are the three main components of Virchow’s Triad?

A
  1. Hypercoagulable state
  2. Vascular wall injury
  3. Circulatory stasis
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2
Q

What is the number one reason people are on anticoagulation?

A

Atrial fibrillation

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3
Q

What is released from damaged cells after damage occurs outside the blood vessels?

A

Thromboplastin

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4
Q

What does thromboplastin activate?

A

Factor VII

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5
Q

Trauma to the blood itself or exposure of the blood to collagen activates what factor?

A

XII (XIIa)

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6
Q

XIIa activates what factor?

A

XI-XIa and XIa activates IX-IXa

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7
Q

Xa, when complexed on the platelet surface with Va and factor IV, converts ______ to _____?

A

Prothombin (II) to thrombin (IIa

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8
Q

IIa converts _____ to _____ ?

A

fibrinogen (I) to fibrin (Ia)

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9
Q

MOA of Heparin?

A

Acts as a catalyst to markedly accelerate the rate at which ATIII (heparin cofactor) neutralizes thrombin (II) and Factor Xa

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10
Q

What is heparin made out of?

A

Porcine intestinal mucosa (no longer made out of bovine)

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11
Q

T/F: Heparin induces a confirmational change in the ATIII that makes the reactive site less accessible to the protease?

A

False; makes it more accessible to the protease

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12
Q

Uses of heparin?

A
  1. Px and tx of VTE
  2. Px and tx of postop DVT and PE
  3. Tx of emboli from afib or heart valves
  4. Dx and tx of DIC
  5. Px and tx periph arteral embolism
  6. During arterial or cardiac surgery
  7. Unstable angina, non-Q wave MI, acute MI, PCI
  8. Complications of pregnancy
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13
Q

At what plasma concentration of heparin is Thombin (IIa), IXa, and Xa inhibited rapidly by ATIII?

A

0.1 to 1 unit/ml

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14
Q

Does heparin act on bound or unbound factors?

A

Unbound. It does not break down clots that have already been formed

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15
Q

Onset of action of heparin IV? Heparin SQ?

A

IV= immediate

SQ=1-2 hours

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16
Q

How is half life related to dose of heparin?

A

The more you give the longer the half life
100u/kg=1 hr
400u/kg=2.5 hrs
800u/kg=5 hrs

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17
Q

How is heparin metabolized?

A

Cleared by the reticuloendothelial system and then excreted by the kidneys

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18
Q

What type of cells is the reticuloendothelial system comprised of?

A

Phagocytes

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19
Q

Does heparin cross the placenta?

A

No

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20
Q

What are reasons for heparin resistance?

A
  1. Increased concentration of Factor VIII
  2. Accelerated clearance of the drug with massive PE
  3. Inherited ATIII deficiency
  4. Acquired ATIII deficiency
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21
Q

What are examples of causes for acquired ATIII deficiency?

A
  1. Cirrhosis
  2. Nephrotic syndrome
  3. DIC
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22
Q

Are patients with inherited or acquired ATIII deficiency more likely to have normal response to heparin?

A

Inherited ATIII Deficiency patients.

Acquired ATIII deficiency patients will require 2 units FFP and/or ATIII concentrate administration

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23
Q

What is the risk of bleeding with heparin?

A

1-33%

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24
Q

What are the 4 issues with heparin toxicity?

A
  1. Bleeding
  2. Thrombocytopenia (HIT)
  3. Abnormal LFTs
  4. Risk of osteoporosis and spontaneous vertebral fractures
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25
Q

Does HIT occur immediately after heparin adminstration?

A

No; 7-14 days after initiation of full dose or low dose heparin therapy (includes heparin flush solution)

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26
Q

Type I or II HIT due to heparin dependent antiplately IgG antibodies?

A

Type II HIT.

Type I is direct or nonimmunogenic effect on platelets

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27
Q

If patient previously exposes to heparin, can thrombocytopenia occur earlier or later?

A

Occur earlier

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28
Q

MOA of Protamine Sulfate?

A

Acts as heparin antagonist by complexing with strongly acidic and anionic heparin to form a stable salt. The complexes are removed by the reticuloendothelial system

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29
Q

Onset and duration of Protamine sulfate?

A

Rapid onset 5 min or less and duration around 2 hours

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30
Q

Protamine has no effect on reversing LMWH?

A

False; if emergency reversal is needed, protamine will neutralize about 65% of Anti-Xa activity of LMWH

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31
Q

If heparin was given within 30-60mins, what is the dose of protamine reversal?

A

0.5-0.75mg/100u Heparin

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32
Q

If heparin was given 2 hours ago or more, what is the dose of protamine reversal?

A

0.25-0.375mg/100u Heparine

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33
Q

If heparin infusion is stopped, what is the dose of protamine reversal?

A

25-50mg

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34
Q

If heparin reversal is needed immediately following heparin administration for surgery, what is the protamine reversal dose?

A

1-1.5mg/100u heparin

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35
Q

How should protamine be administered?

A

Slow IV 10mg/ml over 1-3 mins.

Up to 50mg/10min maximum

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36
Q

What are adverse effects to rapid IV injection of protamine sulfate?

A

Acute Histamine related- hypotension, bradycardia, pulmonary hypertension, transient flushing, dyspnea.

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37
Q

Hypersensitivty reaction for protamine can result in what?

A
  1. Uticaria
  2. Angioedema
  3. Acute Pulmonary Hypertension
  4. Anaphylactoid Reaction
  5. Anaphylaxis
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38
Q

What four things predispose a patient to having a hypersensitivity reaction to protamine administration?

A
  1. Fish allergy
  2. Previous protamine reversal of heparin
  3. NPH Insulin
  4. Previous vasectomy
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39
Q

What are examples of insulin that predispose patients to protamine hypersensitivity reactions?

A

Humulin N and Novolin N

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40
Q

What is heparin rebound?

A

Re-anticoagulation after protamine administered

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41
Q

When does heparin rebound typically occur?

A

Usually 8-9hours after protamine administration (has been reported 30min-18hours after CPB).

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42
Q

What can overdose of protamine cause?

A

Protamine overdose may result in bleeding d/t it having anticoagulant and anti-platelet effects when given alone or in excess of heparin dose.

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43
Q

What has a higher risk of thrombocytopenia- Heparin or Low-molecular weight heparin?

A

Heparin

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44
Q

What lab value would indicate HIT?

A

PLT <100K

45
Q

T/F

HIT is reversible with stopping heparin

A

True

46
Q

What is the name of the thrombotic complication that can occur in a minority of patients with HIT?

A

White clots (HITTS)

basically arterial thrombosis with PLT-Fibrin clots

47
Q

What 3 drugs are LMWH?

A 
Dalteparin Sodium (Fragmin®)
Enoxaparin Sodium (Lovenox®)
Tinzaparin Sodium (Innohep®)
48
Q

What is the MOA of LMWH?

A

Inhibition of Factor Xa by antithrombin.

They do have some Factor IIa inhibition effect.

49
Q

According to the JAMA article, does LMHW reduce rate of VTE?

A

No

Other target sites, such as PLT, may be needed to be blocked

50
Q

What lab value should be monitored with LMWH’s?

A

Anti-Xa levels

51
Q

T/F

aPTT and PT relatively insensitive with LMWH therapy.

A

True

52
Q

What are the adverse effects with LMWH’s?

A

Thrombocytopenia (<1%)

Do not use in patients with HIT

Decrease dose in patients with chronic renal insufficiency

53
Q

How is Fondaparinux (Arixtra) different from LMWH’s?

A

No effect on Factor IIa or PLT function

Can give Arixta if pt has hx of HIT (no risk of HIT b/c the rate of thrombocytopenia is so low)

54
Q

T/F

Hemodialysis will help with bleeding complications from dabigatran, but not with xarelto and eliquis

A

True

55
Q

Out of coumadin, xarleto, eliquis, and dabagratan (pradaxa), which one’s pre-op cessation time is not half-life related?

A

Coumadin

this is the reason coumadin has a longer cessation time than the other ones.

56
Q

Out of coumadin, xarleto, eliquis, and dabagratan (pradaxa), which one is dependent on kidney function?

A

Dabagratan

57
Q

What are two specific antidotes for dabigatran?

A

idarucizumab, ciraparantag

58
Q

T/F

Giving too much coumadin initially can result in VTE formation

A

True

B/C Coumadin inhibits proteins C& S first (natural anticoagulants) before inhibiting factors 2,7,9,10

59
Q

What is the relationship b/w Vit K and factors II, VII, IX, and X?

A

These factors are biologically inactive. Vit K activates them via a carboxylation reaction.

60
Q

If giving Vit K for coumadin reversal, how long does it take before the body makes new factors II, VII, IX, and X?

A

24 hours

61
Q

What is the most common anticoagulant used?

A

Heparin

62
Q

Is heparin’s MOA direct or indirect? Is it reversible or irreversible?

A

Indirect (it is a catalyst of ATIII)

Reversible

63
Q

Does heparin cross the placenta?

A

No, hence it is the SAFEST anticoagulant to give to pregnant pts

64
Q

T/F

With HIT, you have a risk of clots even though it results in in thrombocytopenia

A

True

will see drop in PLT levels and clumping of pts (slide 17)

65
Q

What is the pathophysiology of HIT?

A

PLT’s have PF4 which binds with heparin. IgG complex recognizes heparin/PF4 and binds it up, results in a large complex

66
Q

Anaphylactoid reaction from protamine is due to ____ activation

A

compliment

67
Q

what is the DOA of protamine?

A

2 hrs (at best)

68
Q

T/F

Fondaparinux has the same risk of spinal and epidural hematoma as LMWH

A

True

69
Q

What are two unique features of Betrixaban (Bevyxxa)

A

Can only give PO and it is only used in the hospital setting

70
Q

T/F

Danaparoid Sodium (Orgaran) has no risk of HIT

A

FALSE

still has a risk of HIT, buts very low.

71
Q

Why do patients with massive PE’s have increased resistance to heparin?

A

the PE causes activation of the reticuloendothelial system, speeds up metabolism of heparin

72
Q

When evaluating HIT, is it more beneficial to look at PLT level or how fast PLT levels are dropping?

A

How fast PLT’s drop.

HIT could be present if there is a rapid drop in PLT’s (ex. 300K to 150K)

73
Q

If a patient has ARF or is on dialysis, what is the best oral Xa inhibitor to give them?

A

Edoxaban (Savaysa)

74
Q

Does oral Xa inhibitors have a reversal agent?

A

Previously no, but two reversal agents are Andexanet and Ciraparantag

75
Q

Which drugs is Andexanet alpha approved for?

A

rivaroxabam (Xarelto) and apixaban (Eliquis)

76
Q

Which drugs is Ciraparantag approved for?

A

Xa inhibitors, IIa inhibitors, Fondaparinux, and heparin

77
Q

MOA of Andexanet alpha

A

Reverses Factor Xa inhibitors- recombinant human Factor Xa (basically just giving more Xa, will bind up inhibitors)

Binds COMPETITIVELY to Factor Xa inhibitors for complete reversal

78
Q

MOA of Ciraparantag

A

Binds to anticoagulants through a hydrogen bond

79
Q

What is the only direct thrombin inhibitor that has a reversal agent?

A

dabigatran

agatraban and hirudin analogs do not

80
Q

Hirudin analogs binds ______ to the active catalytic and substrate-recognition sites of both ______ and ______ thrombin (Factor IIa).

A
  • irreversibly
  • circulating
  • clot bound
81
Q

When are hirudin analogs indicated?

A

for thrombosis assoc. with HIT

82
Q

What is a disadvantage of hirudin analogs?

A

Because they come from a natural products, Antihirudin antibodies form n~40% of patients and may be associated with an increased anticoagulant effect of
lepirudin.

83
Q

What is the only oral direct thrombin inhibitor?

A

dabigatran (pradaxa)

this is not a Xa inhibitor even though it has “xa” in its name

84
Q

What are the 2 reversal agents for dabigatran?

A

Idarucizumab (Praxibind) and Ciraparantag

85
Q

If bleeding or toxicity occurs, what are 2 major benefits of dabigratan compared to the other direct thrombin inhibitors?

A
  • It has reversal agents

- Hemodialysis will help remove dabigatran, whereas HD has no benefit with the other direct thrombin inhibitors

86
Q

How long will dabigatran (Pradaxa) reversal occur after administration of Idarucizumab (Praxibind)?

A

10 mins

87
Q

How long after a procedure can direct thrombin inhibitors be resumed?

A

as soon as adequate hemostasis has been achieved

she stressed this in the lecture

88
Q

For direct thrombin inhibitors, how many life-lives need to pass before it is safe to proceed with surgery

A

2 half-lives (usually 1-2 days)

holding med for at least 1 day is safe to proceed for minor procedures

2-4 days for major procedures

hold times for these meds are based on kidney function and type of procedure

89
Q

If a patient accidentally took a direct thrombin inhibitor within 2 hours prior to surgery, what can be done?

A

give activated charcoal

90
Q

When would agatroban be a good choice?

A

Used for the prevention and treatment of thrombosis in patients with HIT or HITTS

91
Q

What is lab monitoring goal for agatroban?

A

Goal: aPTT 1.5 to 3 times baseline (<100 sec.)

Will see increases in EVERYTHING (aPTT, ACT, PT, and TT)

92
Q

T/F

Dabigatran has no CYP3A4 interactions, only PgP interactions

A

True

93
Q

If a pt is on a DOAC and bleeding, when is the only time a reversal agent is recommended?

A

Life threatening, critical organ, or major bleeding not responding to maximal supportive effort

94
Q

If a pt is on a DOAC and not bleeding, when is the only time a reversal agent is recommended?

A

Only when an invasive procedure cannot be safely performed while anticoagulated and cannot be delayed

Trauma and drug overdose are not reasons to give a reversal agent for DOAC’s

95
Q

Why are DOAC reversal agents given cautiously?

A

b/c once anticoagulation is reversed, it is even harder to get them re-anticoagulated again

96
Q

Coumadin decreases the total amount of each Vit. K dependent coagulation factor made by the liver by ____ %.

In addition, the factors made are _______ resulting in diminished biological activity (10-40% normal).

A

30-50%

undercarboxylated

You DO NOT want completely block all the Vit K factors, only decrease them slightly

97
Q

What route of Vit K administration is recommended?

A

PO

98
Q

What route of Vit K administration is never recommended (according to Emily)?

A

SQ

99
Q

Does coumadin have a lot of drug interactions? What drugs are of most concern for interaction?

A

YES! (Emily said to file coumadin along with digoxin, amiodarone, diltiazem as a drug that has many interactions)

  • Antibiotics
  • Acetaminophen (causes an interaction with 2D1)
  • Supplements (the ones that begin with “g”)
  • NSAIDS and other blood thinners
  • Seizure meds
100
Q

Bridge therapy is recommended for what medication?

A

Coumadin only. No need for oral direct thrombin inhibitors bc you only need to hold them for a day or two

101
Q

T/F

There is no reduction in thromboembolic events and increased risk of bleeding with bridge therapy

A

True

Only bridge if pt is very high risk (slide 61)

102
Q

Indwelling neuraxial catheters should be removed ____ hours after the last heparin dose and after evaluating the patient’s coagulation status.

A

2-4 hrs

103
Q

T/F

ASA and NSAIDs do not appear to be associated with an increased risk of epidural hematoma.

A

True

104
Q

For LMWH use, Needle placement should occur at least _____hours after last LMWH dose. High doses of LMWH require a delay of at least ____ hours.

A

10-12 hours
24 hours

remembering 12 hour increments makes it easy to remember

105
Q

For LMWH…If epidural cath inserted, it should be done ____ hours prior to any dose of postoperative LMWH (single daily dosing) and ____ hours for twice daily dosing

A

6-8hours

24 hours

106
Q

Removal of epidural catheter should be done ____ hours before any dose of LMWH

A

2-4hours

107
Q

Removal should occur ____ hours after any dose of LMWH and __ hours before a subsequent dose.

A

10-12 hours

2 hours

108
Q

D/C DOAC prior to neuraxial procedures ___ days for dabigatran and 3-5D for Xa inhibitors

A

4-5 days
3-5 days

4 days is easier to remember

109
Q

How soon after surgery can DOAC’s be restarted?

A

24 hours for low-bleed risk and 72 hours for high-bled risk

Pharm 2 (19 decks)

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