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Pharm 2 > Hematology > Flashcards

Hematology Flashcards

1
Q

Damage outside of blood vessels triggers release of Thromboplastin (III) from damaged cells

A

Extrinsic Pathway

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2
Q

Trauma to the blood itself or exposure of the blood to collagen in a traumatized blood vessel wall activates factor XII (XIIa).

A

Intrinsic Pathway:
IXa when complexed on the platelet surface with activated factor VIII:C (VIII:Ca) and Ca++ activates factor X (Xa).

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3
Q

Common Pathway?

A

Activated factor X (Xa) when complexed on the platelet surface with activated factor V (Va) and calcium (factor IV) on the platelet surface, converts prothrombin (factor II) to thrombin (IIa).
IIa converts fibrinogen (I) to fibrin (Ia), and in the presence of factor XIII, cross-linking occurs.

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4
Q

What does Heparin do?

A

Accelerates Anti Thrombin III (ATIII) which neutalizes thrombin (IIa) and Factor Xa.

Essentially it only binds to newer baby unbound clotting factors.

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5
Q

Heparin MOA

A

Increase the rate of Thrombin - ATIII reaction at least 1000 fold.

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6
Q

Uses of Heparin

A

-prophylaxis VTE, DVT, PE Tx
-A-fib, new heart valves
-tx of peripheral artery embolism
-CV surgery
-complications in pregnancy

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7
Q

Heparin metabolism

A

Reticuloendothelial system of the LIVER. Does Not cross the placenta.

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8
Q

Heparin Dose for VTE

A

5,000 units bolus then 1200-1600 units/hr

Keep aPTT 1.5-2.5 times normal level

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9
Q

What does aPTT measure? (Heparin monitoring)

A

Measures activity of the INTRINSIC and COMMON pathways time to clot formation

has issues with results

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10
Q

Anti-Xa (IU/mL) measure?
(Heparin monitoring)

A

More direct measurement of Heparin concentrations

has less factors that can affect levels but results may vary between labs

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11
Q

ACT (seconds) (activated clotting time) measure?
(Heparin monitoring)

A

-Whole blood sample
-measures INTRINSIC pathway
-used in procedures with significant Heparin use
-has good linear dose response

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12
Q

Issues that may lead to a prolonged baseline aPTT

A

-Intrinsic clotting factor pathway deficiency (8,9,11,12)
-Leukemia
-Meds (warfarin, DOACs)
-DIC
-Liver disease
-recent pregnancy or miscarriage
-polycythemia
-lupus

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13
Q

What is Heparin resistance and how is it caused?

A

-Requires high doses: > 35,000 units/day
-Due to increase in Factor VIII (8), ATIII deficiency, massive PE
-Acquired AT III deficiency in patients with cirrhosis, nephrotic syndrome or DIC, ECMO tx

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14
Q

Treatment for Heparin resistance?

A

Administer 2 units FFP to provide AT III

Check both aPTT and Anti-Xa

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15
Q

Heparin Toxicity presentation/symptoms

A

-Bleeding (major bleeds in 1-11.5% of pts.)
-Thrombocytopenia (HIT)
-abnormal LFTs
-infrequent risk of osteoporosis
-rare hyperkalemia d/t aldosterone suppression and natriuresis

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16
Q

What is HIT and how is it caused?

A

-< 100,000 drop from baseline
-Heparin dependent antiplatelet IgG antibodies (Type II HIT)
Direct, non-immunogenic platelet effect

-5-15 days after start of treatment
Earlier with previous exposure

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17
Q

Risks of getting HIT?

A

-1-15% with heparin (any dose)
-5% with heparin flush
-10x lower risk with LMWH

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18
Q

HIT Treatment

A

-Stop heparin products

-Administer non-heparin anticoagulants to prevent thrombosis

-Add allergy to the chart
-PROTAMINE SULFATE (ANTEDOTE)

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19
Q

How is Protamine Sulfate dose determined?

A

Determined by the dose of heparin, route of heparin administration and time elapsed since the heparin was administered.

1 mg Protamine : 100 units heparin

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20
Q

Protamine hypersensitivity reaction to….

A

fish
pre-treat with corticosteroid and antihistamine

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21
Q

LMWH MOA

A

Inhibition of Factor Xa by antithrombin.

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22
Q

Do not use ______ in patients with HIT

A

LMWH

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23
Q

Synthetic indirect specific inhibitor of Factor Xa only

A

Fondaparinux (Arixtra)

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24
Q

DOAC drug names

A

Oral Xa Inhibitors

Rivaroxaban (Xarelto ®)
Apixaban (Eliquis ®)
Edoxaban (Savaysa ®)
Taking over warfarin
XA

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25
Q

How long to hold Oral Xa inhibitor before surgery w/ low-mod bleed risk and high bleed risk?

A

1 day- low/mod
2/day- high

Apixaban, Edoxaban, Rivaroxaban

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26
Q

Dabigatran preop monitoring?

A

Bleed risk and CrCl (kidney function)

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27
Q

Oral Xa reversal?
(cannot measure INR)

A

D/C medication, mechanical compression, surgical hemostasis, transfusion support (blood products, activated charcoal)

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28
Q

Oral Xa Reversal?

A

Andexanet alpha (Andexxa)

Ciraparantag- pending since 2016

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29
Q

How does Andexxa work?

A

Reverses Factor Xa inhibitors- recombinant human Factor Xa
Binds competitively to Factor Xa inhibitors for complete reversal

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30
Q

Andexxa dosing
(Xa inhibitor reversal agent)

A

Low Dose
Initial IV bolus: 400 mg at 30 mg/min
Follow Infusion: 4 mg/min for up to 120 min

High Dose
IV Bolus: 800 mg at 30 mg/min
Infusion: 8 mg/min for up to 120 min

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31
Q

Andexxa Chart

A
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32
Q

Name Direct Thrombin Inhibitors

A

Argatroban, Hirudin Analogs (Bivalirudin, Lepirudin), Dabigatran

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33
Q

Argatroban MOA and Use

A

Small molecule.
Highly selective and reversible direct thrombin inhibitor (Factor IIa).

Used for the prevention and treatment of thrombosis in patients with HIT or HITTS (no reversal agent)

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34
Q

Hirudin Analogs indicated for?

A

Indicated for thrombosis associated with HIT

35
Q

How do Hirudin analogs work?

A

Binds irreversibly to the active catalytic and substrate-recognition sites of both circulating and clot-bound thrombin (Factor IIa).
No Reversal agent.

36
Q

Dabigatran reversal?
(Direct Thrombin inhibitor)

A

Idarucizumab (Praxbind )

37
Q

MOA of Warfarin

A

Indirect anticoagulant that alters the synthesis of blood coagulation factors II, VII, IX, and X by interfering with the action of vitamin K

38
Q

Warfarin characteristics. How long does it take to work?

A

No effect on normal factors already in the blood when the drug is started.

Slowing down the future, not immediate effect
Can take up to 5 days to build up

39
Q

Warfarin Toxicity antidote and treatment?

A

Antidote is Vitamin K1, but takes up to 24 hours for the synthesis of new fully carboxylated

For immediate hemostatic competence: FFP 10-20ml/kg

40
Q

Vitamin K recommendation

A

Oral Vit. K recommended for most situations.
I.V. for serious or life-threatening bleeds.
NEVER S.Q.

41
Q

Warfarin toxicity plan?

A

Look at INR and look at condition, pick intervention

42
Q

Warfarin preoperative management?

A

Goal INR is < 1.5

Begin holding at least 5 days prior to procedure
Restart based on bleeding risk within 24 hours at pre-op dose unless

43
Q

Bridge Therapy recs DOAC and Warfarin?

A

Most DOAC DO NOT require bridge therapy as they are only held 24-48 H prior to procedure.

Warfarin has several different recommendations based on bleeding risk and thromboembolism risk.

44
Q

A-fib guidelines for bridging?

A

Afib 2019 guidelines only support bridging if the patient is VERY high risk of stoke (mech valve, recent stroke,etc)

45
Q

CHEST 2022 bridging rec

A

If Warfarin is used for mechanical heart values, atrial fibrillation, or VTE, no bridge therapy is recommended for most patients.

46
Q

What is CHA2DS2-Vasc

A

CLOT RISK SCORING, FOR A-FIB PATIENTS WITH STROKE RISK

47
Q

How long to hold bridge therapy if using a LMWH?

A

24 hours pre-procedure if using LMWH

At least 4 hours pre-procedure if using UFH

48
Q

Name the Thrombolytic Agents

A

”ASEs”

Alteplase
Reteplase
Tenecteplase
Streptokinase
Urokinase

49
Q

How do Thrombolytic Agents work?

A

t-PA binds to fibrin and plasminogen and converts bound plasminogen to plasmin WHICH BREAKS CLOTS

50
Q

Thrombolytic Agent Uses

A

-Lysing thrombi during treatment of acute MI.
-Treatment of P.E.
-Treatment of venous thrombosis.
-Open occluded I.V. catheters.

51
Q

What happens with Thrombolytic Agent Toxicity

A

Major toxicity is hemorrhage due to:
Lysis of fibrin in “physiological thrombi” at sites of vascular injury.

52
Q

Do Thrombolytics have reversal agent?

A

No. Fibrinolytic activity can last for 7-24 hours after discontinuation of the drug

53
Q

What does Sodium Citrate do?

A

Binds free Calcium(FACTOR IV) in blood

54
Q

Dextran Use?

A

Water-soluble glucose polymer (polysaccharide).

Expansion of intravascular volume.
Prevent thromboembolism by decreasing blood viscosity.

55
Q

Epsilon Aminocaproic Acid (Amicar®): Pro-coagulant

A

Inhibitor of fibrinolysis by indirect inhibition of plasmin’s anti-platelet effects.

56
Q

Amicar: USE?
PRO-COAGULANT

A

-Treatment of excessive bleeding
-Systemic hyperfibrinolysis is associated with surgical complications
-Allows completion of surgery after stopping oozing in patients with cirrhosis
-Reduces bleeding and transfusion requirements after CPB

57
Q

Tranexamic Acid (TXA) MOA
PRO-COAGULANT

A

Competitive inhibitor of several plasminogen binding sites leading to inhibition of fibrinolysis, also reduced plasmin activity.
Uses: Bleeding prophylaxis for surgery, trauma, etc

58
Q

What is RAPLIXA

A

Spray dried fibrin sealant to control bleeding during surgery when standard surgical techniques, such as suture, ligature, or cautery are ineffective or impractical.
MOA: Purified human plasma-derived fibrinogen and thrombin.

59
Q

NovoSeven RT(Coagulation factor VIIa (Recombinant) USE

A

Hemophilia A or B.
Patients with congenital factor VII deficency.

Works in the extrinsic pathway.

60
Q

NovoSeven RT off-label uses….

A

Warfarin-induced bleeding that cannot wait reversal with FFP or Vit. K.
Spontaneous intracranial hemorrhage.
Massive bleeding:

61
Q

NovoSeven RT complications

A

Most significant are thromboembolic:
Myocardial ischemia or infarction.
Cerebral ischemia or infarction.

62
Q

Platelet Function (1,2,3)

A
  1. Adhesion
  2. Activation
  3. Aggregation
63
Q

What happens with Adhesion?

A

vonWillebrand’s factor (Factor VIII:vWF) is manufactured and released from endothelial cells
-Factor VIII:vWF promotes platelet adhesion to damaged vascular walls

64
Q

Most common inherited coagulation defect?

A

vonWillebrand’s disease

65
Q

Activation:

A

Thrombin (factor IIa) combines with the thrombin receptor on the platelet surface to activate the platelet
-Changes the shape of the platelet

66
Q

Thromboxane A-2 and ADP do what?

A

promote platelet aggregation

67
Q

Aggregation:

A

Thromboxane-A2 and ADP uncover fibrinogen receptors. Fibrinogen (factor I) attaches to the receptors linking the platelets to each other

68
Q

How does Aspirin inhibit platelet aggregation?

A

-Cyclo-oxygenase (COX) is rendered non-functional (
-Persists for the life of the platelet (8-12 days).

69
Q

How long does NSAIDs block thromboxane-A2 production?

A

temporary (approx. 24-48 hours).
Hold about 2 days prior to surgery

70
Q

Thienopyridine ADP-receptor Antagonists

A

Clopidogrel (Plavix®)
Prasugrel (Effient®)
Ticagrelor (Brilinta®) - reversible
Cangrelor (Kengreal®)

71
Q

Platelet Glycoprotein (GP IIb/IIIa) Receptor Inhibitors

A

Abciximab (ReoPro®)
Eptifibatide (Integrilin ®)
Tirofiban (Aggrastat ®)

72
Q

How early should you hold Clopidogrel (Plavix ®): P2Y12 inhibitor before surgery?

A

-Stop 5 days prior to surgery
Platelet aggregation and bleeding time return to baseline values within 5 days.

73
Q

Reversible P2Y12 inhibitors end in -

A

“-treglor”

74
Q

How long hold Ticagrelor (Brilinta)
before surgery?

A

3-5 days

75
Q

Cangrelor (Kengreal)

A

IV P2Y12 inhibitor

Reversible- platelet function returns to normal 1 hour after stopping infusion

76
Q

ADRs of P2Y12 Inhibitors

A

Bleeding
N/V
Rash and diarrhea
Thrombotic Thrombocytopenia Purpura
Severe neutropenia (low risk)

77
Q

Do P2Y12 inhibitors have reversal agents?

A

No!
-VerifyNow P2Y12:
Measures the percentage of platelet inhibition

78
Q

Aspirin perioperative recommendation?

A

Do not hold for non-cardiac surgery unless high bleeding risk. If held- </= 7 days

79
Q

Noncardiac Surgery P2Y12 (perioperative)

A

Clopidogrel: 5 days
Prasugrel: 7 days
Ticagrelor: 3-5 days

Resume </= 24 hours post op

80
Q

GIIb/IIIa Inhibitors Uses

A

Acute ischemic complications of percutaneous coronary intervention (PCI)
Unstable angina and non-Q wave MI

81
Q

DDVAP uses

A

-Hemostatic activity due to the increased release of vonWillebrand factor in patients with uremia, chronic liver disease and certain types of hemophilia
-Promotes platelet adhesiveness to the vascular endothelium

82
Q

DDAVP for DI?

A

Intranasally for the treatment of DI due to inadequate production of ADH by the posterior pituitary

83
Q

Clotting Cascade

A

Pharm 2 (5 decks)

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