Parenteral anticoagulation (I/V) Amboss Flashcards

1
Q

Unfractionated heparin (UFH). What drug?

A

Heparin

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2
Q

What is heparin administration for prophylaxis?

A

subcutaneous

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3
Q

What is heparin administration for therapeutic?

A

continuous intravenous infusion (therapeutic administration requires infusion pump)

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4
Q

Heparin monitoring?

A

aPTT and platelet count

including PLT baseline before treatment is started

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5
Q

Heparin clearance?

A

Clearance: hepatic (preferred agent for patients with renal insufficiency)

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6
Q

Heparin’s antidote?

A

Protamine sulfate

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7
Q

Charge of heparin?

A

negative

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8
Q

protamine sulfate charge?

A

positive

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9
Q

Why protamine sulfate binds heparin?

A

positively-charged protein that can neutralize negatively-charged heparin by forming inactive complexes

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10
Q

What drug is preferred for renal insufficiency?

A

Heparin - because its clearance is hepatic, not renal

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11
Q

What to monitor when use heparin in order to detect HIT?

A

platelets must be continuously monitored during heparin therapy and a baseline should be established before commencing treatment

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12
Q

Low molecular weight heparin (LMWH) drugs?

A

enoxaparin, dalteparin, tinzaparin, nadroparin, certoparin

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13
Q

LMWH. Administration?

A

Subcutaneous

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14
Q

LMWH. Monitoring?

A

Anti-factor Xa activity can be assessed in specific cases; not generally recommended –>
Only necessary in specific cases, e.g., patients with renal failure, underweight/overweight, as there is a risk of accumulation or underdosing. Anti-factor Xa activity needs to be checked 4 hours after administration (follow-up necessary as drug level is only consistent after several administrations)

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15
Q

LMWH. Clearance?

A

renal

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16
Q

Why LMWH not suitable in renal insufficiency?

A

Clearance: renal (contraindicated for patients with renal insufficiency)

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17
Q

LMWH antidote? What scope of reversal?

A

protamine sulfate (partial reversal –> Protamine antagonizes 50% of the effect of LMWH)

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18
Q

Synthetic heparin. What drug?

A

fondaparinux

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19
Q

Fondaparinux. Administration?

A

subcutaneous

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20
Q

Fondaparinux. Monitoring?

A

Same as heparin:
Not generally recommended;
Anti-factor Xa activity can be assessed in specific cases (Such cases include conditions with increased coagulability (e.g., chronic kidney disease, anemia, thrombocytopenia).

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21
Q

Fondaparinux. Antidote?

A

Possibly activated prothrombin complex concentrates (aPCC)

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22
Q

Heparinoid (glycosaminoglycan). What drug?

A

danaparoid

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23
Q

Heparinoid (glycosaminoglycan). All other same with administration and monitoring and antidote as in heparin/fondaparinux.

A

.

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24
Q

Direct thrombin inhibitors. Drugs?

A

I/v argatroban, bivalirudin, desirudin

p/o dabigatranas

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25
Q

Direct thrombin inhibitors. Monitoring?

A

not recommended

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26
Q

Direct thrombin inhibitors. Antidote?

A

Possibly aPCC and/or antifibrinolytics (e.g., tranexamic acid) - if no reversal agent available

Dabigatran: idarucizumab (monoclonal antibody)

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27
Q

Heparin mechanism?

A

Enhances the activity of antithrombin –> and it leads to decreased action of IIa and Xa. (IT’S INDIRECT INHIBITION!!!!! NES DIRECTLY AFFECT ANTITHROMBIN, NOT IIa and Xa).

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28
Q

Heparin mechanism. Xa inhibition?

A

antithrombin III potentiation → inhibition of factor Xa → decreased activation of prothrombin → ↓ thrombin→ ↓ fibrinogen activation → ↓ fibrin

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29
Q

Heparin mechanism. IIa inhibition?

A

Thrombin (factor IIa): UFH binds antithrombin III and thrombin simultaneously at two distinct binding sites → antithrombin III and thrombin held by heparin in close proximity (complex formation) → ↑ thrombin inhibition → ↓ fibrinogen activation → ↓ fibrin

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30
Q

Heparin half life?

A

SHORT - therefore anticoagulant effect quickly ceases once administration is stopped

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31
Q

LMWH mechanism?

A

LMWH: binds to antithrombin III → inhibition of factor Xa → decreased conversion of prothrombin → ↓ thrombin

aka PREDOMINANTLY acts on Xa

32
Q

Fondaparinux mechanism?

A

Only binds to antithrombin III → selective inhibition of factor Xa

Aka acts only on Xa.

33
Q

LMWH versus fondaparinux mechanism?

A

LMWH: PREDOMINANTLY acts on Xa

Fondaparinux: ONLY on Xa

34
Q

Heparin versus fondaparinux. Bioavailability?

A

Fondaparinux has better bioavailability than heparin

35
Q

Heparin versus fondaparinux. Half life?

A

Fondaparinux has 2-4x longer half time than heparin.

Heparin has short half life –> effec ceases quicly once administration is stopped.

36
Q

Direct thrombin inhibitors. Mechanism?

A

Directly inhibit thrombin (freely circulating and in association with clots)

Act independently from antithrombin

37
Q

!!!!!!!The effect of most parenteral anticoagulants (except for direct thrombin inhibitors) depends on native antithrombin. In patients with antithrombin III deficiency (e.g., due to nephrotic syndrome), this effect is reduced.

A

.

38
Q

If patient has nephrotic syndrome and reduced ATIII, what effect of parenteral anticoagulants?

A

effect is reduced

LMWH, fondaparinux

39
Q

pentasaccharide molecules. what is this anticoagulant?

A

fondaparinux, ie synthetic heparin

40
Q

Parenteral anticoagulants. What main side effect?

A

Bleeding, drug interactions

41
Q

Parenteral anticoagulants.

UFH and LMWH. What side effect?

A

Allergic reactions

Heparin-induced thrombocytopenia: risk of type 2 HIT LMWH:UFH ≈ 1:10

Osteoporosis

Drug interactions (e.g., ASA, tetracycline)

42
Q

UFH and LMWH. Why is adverse osteoporosis?

A

Dose-dependent; therefore, switch to oral anticoagulants for long-term therapy. Osteoporosis is most likely related to increased osteoclastic activity, but decreased production of calcitriol is another potential cause

43
Q

Parenteral anticoagulants. What main side effect?

Fondaparinux?

A

Occasionally low platelet count

44
Q

Parenteral anticoagulants. What main side effect?

Heparinoid (glycosaminoglycan)

A

Asthma exacerbation (rarely)

45
Q

Parenteral anticoagulants. What main side effect?

Direct thrombin inhibitors

A

Allergic reactions, fever

46
Q

!!!!!Heparin treatment requires regular monitoring of the platelet count, especially for UFH, even before starting treatment.

A

.

47
Q

Thrombocitopenia in anticoagulants?

A

Treatment with heparin, especially UFH, can cause thrombocytopenia.

Thrombocytopenia may be immune-mediated heparin-induced thrombocytopenia (formerly known as type 2 HIT) or non-immune heparin associated thrombocytopenia (formerly known as type 1 HIT):

48
Q

Immune HIT. type?

A

Type 2 HIT

49
Q

Non-Immune HIT. type?

A

type 1 HIT

50
Q

Indications.

LOW-dose heparin?

A

DVT prophylaxis for prolonged bedrest, peri- and postoperative state, immobility

51
Q

Indications.

HIGH-dose heparin?

A

Immediate anticoagulation effect for:

  1. Atrial fibrillation
  2. DVT, acute arterial thrombosis, PE
  3. Acute coronary syndrome, MI
  4. Mechanical heart valve replacement
  5. VTE prophylaxis for patients with hemodialysis, heart-lung machine, etc.
52
Q

Indications.

Low molecular weight heparin?

A

Prophylaxis of DVT in orthopedic and abdominal surgery, prolonged immobility

Treatment of DVT

Acute coronary syndrome

53
Q

Indications.

Direct thrombin inhibitors?

A

AF, VTE, Type 2 HIT

54
Q

What anticoagulants have highest risk for HIT?

A

unfractionated heparin

55
Q

Which type of HIT has worse prognosis?

A

type 2 HIT has a worse prognosis than type 1 HIT

56
Q

What is BAD HIT?

A

Use direct thrombin inhibitors (Bivalirudin, Argatroban, Dabigatran) to treat the BAD HIT (heparin induced thrombocytopenia)

57
Q

Contraindication for parenteral anticoagulants?

A

Recent stroke
Uncontrolled hypertension
Active bleeding
HIT (except for direct thrombin inhibitors which can be used for anticoagulation in HIT)

58
Q

HIT. What anticoagulants can be used?

A

direct thrombin inhibitors

59
Q

Pregnancy and anticoagulations. Mechanism of hypercoagulability?

A

Physiological hypercoagulability (e.g., due to increased levels of clotting factors) leads to increased risk of thrombosis.

60
Q

What anticoagulants can be used in pregnancy?

A

UFH and LMWH

61
Q

Which anticoagulant has fewer side effects in comparison to other?

A

LMWH has fewer side effects.

62
Q

Patients with decreased renal function. Which cannot be used and why?

A

In severe renal failure: accumulation of LMWH → increased bleeding risk → adjust dose or switch to UFH

63
Q

Heparin Low-dose dosing frequency?

A

Low dose: subcutaneous administration every 8–12 hrs

64
Q

Heparin High-dose dosing frequency?

A

High dose: intravenous administration with bolus and continuous application via infusion pump

65
Q

LMWH dosing?

A

Dosage depends on specific drug used, indication, body weight, and kidney function; adjust to body weight and decreased kidney function.

66
Q

Effect of LMWH lasts for about ………

A

Effect of LMWH lasts for about 12 hours

67
Q

LMWH.

Monitoring of anti-factor Xa is only necessary in patients with decreased kidney function (and significant over- or underweight); anti-factor Xa activity is measured 4 hrs after administration

A

.

68
Q

Severe bleeding is more common in heparin or LMWH?

A

Heparin

69
Q

HIT is more common in heparin of LMWH?

A

Type 2 HIT is about 10-fold more common

70
Q

What to monitor if heparin is used therapeutically?

A

If used therapeutically, PTT levels have to be monitored frequently (target range: 1.5–2.5-fold prolongation)

71
Q

In what CcCl is contraindicated LMWH?

A

Contraindicated if renal function is poor (CrCl < 30mL/min)

72
Q

LMWH - No full antagonist available (only partial that binds 50proc)

A

.

73
Q

When to use heparin?

A

Emergencies and renal failure

74
Q

Patient has renal failure, what anticoagulant is used?

A

Heparin - for patients with advanced renal failure (e.g., in patients with severe renal insufficiency (CrCl < 30mL/min) or the elderly)

LMWH - contraindicated in <30ml/min

75
Q

LMWH use?

A

DVT prophylaxis, outpatient care (longer half-life → fewer injections)

Generally preferred to UFH (fewer side effects, easier handling) as long as there are no contraindications