Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CPT > Anticoagulants > Flashcards

Anticoagulants Flashcards

You may prefer our related Brainscape-certified flashcards:
NASM ® CPT flashcards
1
Q

What do all anti-coagulant drugs do?

A
  • Prevent thrombus formation and thrombus from growing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is an endogenous inactivator of many clotting factors?

A
  • Antithrombin III
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Why is regulation of the coagulation cascade essential?

A
  • Prevents solidification of all blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is the coagulation cascade regulated?

A
  • Coagulation factors are present in the blood as zymogens
  • Lots of intrinsic inhibitors of this pathway incl. antithrombin III
  • Vascular endothelium regulates many mediators critical for balance in coagulation cascade
  • Ca2+ is an important co-factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the different types of heparins?

A
  • Unfractionated heparins (large - 7-30 kDa)
  • Low molecular weight heparins (1-6 kDa)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What do heparins do to prevent coagulation?

A
  • Enhance antithrombin III activity
  • To varying degrees
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which clotting factors does heparin inhibit?

A
  • Xa
  • Thrombin IIa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Outline the pharmacokinetics of unfractionated heparins?

A
  • Fast onset of action
  • Half-life is 30 minutes at low dose or 2 hours at higher doses
  • Mixed elimination (unpredictable)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How is unfractionated heparin administered?

A
  • I.V. bolus and infusion
  • Given s.c. for prophylaxis with low bioavailability
  • I.V. administration allows us to tightly control administration - can easily stop infusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the mechanism of action of unfractionated heparin?

A
  • Binds to ATIII increasing its activity
  • Accelerates interaction of antithrombin with thrombin IIa and factor Xa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Give some examples of low molecular weight heparin

A
  • Dalteparin
  • Enoxaparin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is low molecular weight heparin administered?

A
  • Almost always subcutaneously
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Outline the pharmacokinetics/pharmacodynamics of low molecular weight heparin

A
  • Bioavailability >90%
  • Half life is ~2 hours +
  • Typically ~15 polysaccharides which are absorbed more uniformly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the mechanism of action of low molecular weight heparins?

A
  • Enhances ATIII activity
  • Inhibits factor Xa
  • Do not inactivate thrombin (LMWH is too short)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is fondaparinux?

A
  • Synthetic pentasaccharide
  • Selectively inhibits Xa by enhancing ATIII
  • S.c.
  • Half life is 18 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Compare the use of UFH vs LMWH

A
  • UFH is used when pt has moderate renal impairment
  • Or when very fine control is needed
  • LMWH can be used in most situations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Compare the metabolism of UFH vs LMWH

A
  • UFH is dose dependent
  • Protein binding, depolymerisation, desulfation (1st and 0 order)
  • LMWH exhibits rapid or slower renal excretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Compare the monitoring of UFH vs LMWH

A
  • UFH is unpredictable - monitor with activated partial thromboplastin time (dosed in standard units)
  • LMWH generally doesn’t need monitoring (U/kg dosing)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are some indications for use of heparins and fondaparinux?

A
  • Prevention of VTE e.g. perioperative prophylaxis with LMWH
  • DVT and PE
  • Acute coronary syndromes with DAPT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Can heparins be given during pregnancy?

A
  • Yes
  • Do not cross placenta
  • Monitor with caution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Outline how heparins are used to treat DVT and PE

A
  • Given as the initial treatment prior to oral agents in some
  • Given long-term in some patient groups
  • Treat cancer related VTE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Outline how heparins are used to treat ACS

A
  • Dual antiplatelet therapy
  • Given short term
  • Reduce recurrence/extension of coronary artery thrombosis post STEMI
  • UFH is given during percutaneous coronary intervention
  • Fondaparinux given following NSTEMI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are some adverse drug reactions of heparins?

A
  • Bruising and bleeding
  • E.g. intracranial, at site of injection, GI, epistaxis
  • Heparin induced thrombocytopenia
  • Hyperkalaemia (inhibition of aldosterone secretion)
  • Osteoporosis (rare)
24
Q

What is heparin induced thrombocytopenia?

A
  • Autoimmune response - normally delayed
  • Antibodies to heparin platelet factor 4 complex
  • Depletion of platelets
  • Results in thrombosis
25
Q

What are some contraindications of heparins?

A
  • Clotting disorders
  • Renal impairment (LMWH and fondaparinux)
26
Q

What are some DDIs of heparin?

A
  • Other antithrombotic drugs
  • ACEi/ARB
  • K+ sparing diuretics
27
Q

How is UFH monitored?

A
  • Activated partial thromboplastin time (aPTT) when using therapeutic i.v. doses of UFH
  • Dose is titrated/adjusted against this value
28
Q

How is LMWH monitored?

A
  • Much more predictable in its action
  • Requires little monitoring
29
Q

How do we reverse heparin’s action?

A
  • Protamine sulphate
30
Q

How does protamine sulphate work?

A
  • Forms an inactive complex with heparin
  • Given IV
  • Dissociates heparin from AT III
  • Irreversible binding
  • Much greater effect with UFH than LMWH
  • No effect on fondaparinux
31
Q

Outline the mechanism of action of vitamin K antagonists

A
  • Inhibition activation of vitamin K dependant clotting factors
  • Inhibits conversion of vitamin K to active reduced form
  • Hepatic synthesis of certain clotting factors requires vitamin K as a co-factor for activation
32
Q

Which clotting factors require vitamin K for their synthesis?

A
  • II, VII, IX, X
33
Q

Give an example of a vitamin K antagonist

A
  • Warfarin
34
Q

Why is there a delay in onset of action of warfarin?

A
  • Circulating active clotting factors are present for several days
  • Must be cleared and replaced with non-carboxylated forms (inactive clotting factors)
35
Q

What is the half life of warfarin?

A
  • 36-48 hours
36
Q

What are some indications for use of warfarin?

A
  • VTE
  • PE
  • DVT and secondary prevention
  • AF patients where DOAC not suitable or already taking warfarin
  • Heart valve replacement
37
Q

How do we compensate for the slow onset of action of warfarin?

A
  • Heparin cover if anticoagulation is needed immediately
38
Q

What are the pharmacokinetics of warfarin?

A
  • Good GI absorption
  • 95% bioavailability when taken orally
  • Plasma concentration does not correlate directly with clinical effect
  • Mixture of two enantiomers which are metabolised differently
39
Q

What affects a patient’s response to warfarin?

A
  • CYP2C9 polymorphisms contribute to significant inter individual variability
  • Vitamin K intake
  • Alcohol
40
Q

What are the contraindications of warfarin?

A
  • Crosses placenta
  • Avoid in early post-partum period and following haemorrhagic stroke
41
Q

What are the adverse side effects of warfarin?

A
  • Bleeding
  • Epistaxis
  • Spontaneous retroperitoneal bleeding
42
Q

How do we reverse the action of warfarin?

A
  • Give vitamin K1
  • Prothrombin complex concentrate i.v.
  • Stop warfarin
43
Q

When do we need to stop warfarin?

A
  • Perioperative anticoagulation needs to be considered
  • Specific patient group and local guidelines will dictate
  • Bridging therapy with LMWH often required when initiating or temporarily stopping warfarin
44
Q

What are the DDIs of warfarin?

A
  • Drugs that inhibit hepatic metabolism, especially CYP2C9
  • E.g. amiodarone, clopidogrel, intoxicating dose of alcohol
  • NSAIDs and drugs that decrease GI absorption of vitamin K - displace warfarin from plasma albumin
  • Barbiturates, phenytoin, rifampicin, St Johns Wort - accelerate warfarin metabolism
45
Q

What does high INR mean?

A
  • More blood anticoagulated
46
Q

What does low INR mean?

A
  • Less blood anticoagulated
47
Q

Why does Warfarin require monitoring?

A
  • Huge variation in patient response
  • Keeping diet and lifestyle/medications stable is important
48
Q

What is INR?

A
  • International normalised ratio
  • Clotting time measured against a standard
  • Allows for standard corrected value comparable across all laboratories
49
Q

Give some examples of direct Xa DOACs

A
  • Apixaban
  • Edoxaban
  • Rivaroxaban
50
Q

What is the mechanism of action of direct Xa DOACs?

A
  • Inhibit both free Xa and Xa bound with ATIII
  • Do not directly affect thrombin (IIa)
  • Metabolised by liver
  • Excreted partly by kidneys
51
Q

Give an example of a direct IIa DOAC?

A
  • Dabigatran
52
Q

What is the mechanism of action of direct IIa DOACs?

A
  • Selective direct competitive thrombin inhibitor
  • Affects both circulating and thrombus bound thrombin (IIa)
53
Q

What are the benefits of DOACs?

A
  • Oral administration
  • Standard dosing
  • Little direct monitoring required
54
Q

Why might we choose to use warfarin over DOACs?

A
  • Requires patient monitoring
  • Improves adherence
  • An excuse to monitor patient and check INR
55
Q

What are the adverse side effects of DOACs?

A
  • Bleeding
  • Skin reactions
  • Caution in GI bleed risk groups
56
Q

What are the contraindications of DOACs?

A
  • Dabigatran contraindicated in low creatine clearance
  • Others are contraindicated at very low creatine clearance
  • Avoid in pregnancy and breastfeeding
57
Q

What are the DDIs of DOACs?

A
  • Less frequent interactions than warfarin but affected by CYP inhibitors and inducers
  • Plasma concentrations reduced by carbamazepine, phenytoin and barbiturates
  • Plasma concentrations increased by macrolides

CPT (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions