Brainscape's Knowledge GenomeTM

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


See full index

Anti-Thrombotics > Anti- Thrombotics > Flashcards

Anti- Thrombotics Flashcards

1
Q

3 Categories of Antithrombolitics

A

Anticoagulants
Prevent new clot formation and extension (getting bigger)

Fibrinolytics
Break up existing clots

Antiplatelets
Interfere with platelet activity

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

2 Types of Thrombi

A

Red thrombus

White thrombus

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

White Thrombus

A

Platelet rich

Forms in the arteries

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

Red Thrombus

A

Fibrin and RBC rich

Forms in the veins

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

What does TXA2 do?

A

vasoconstriction and platelet activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does vWF do?

A

takes collagen fibers and adds platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does fibrinogen do?

A

forms bridges between the platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does thrombin (F IIa) do?

A
  • converts fibrinogen to fibrin which makes it stable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which factors does thrombin (F IIa) activate?

A

5 and 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the final result of the coagulation cascade?

A

fibrin seals the platelet plug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Targets of antiplatelet drug therapy?

A

TXA2
ADP
GPII B/ IIIaR

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

Coagulation cascade is broken down into 3 pathways:

A 
Intrinsic pathway
Activated by \_\_\_damaged cells
Extrinsic pathway
Activated by \_\_damaged blood vessel walls 
Common pathway
Converge onto the common pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Extrinsic pathway review 3 steps

A

Tissue Trauma leads to 3 key step:
Damaged endothelium releases tissue factor
Tissue factor binds to factor 7
Tissue factor 7 activates factor 10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

5 Steps for the Intrinsic pathway

A

STEP 1- Damaged cells release Poly Q
STEP 2- Poly P activates Pre kallikrein, factor 12
Step 3- factor 12a activates factor 11
STEP 4- Factor 11 activated factor 9 and 8
Step 5- factor 9&8 activates factor 10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Common pathway review

A

Intrinsic & Extrinsic end with 10a
10a converts prothrombin(factor 2) to thrombin(factor 2a)
Factor 2a converts fibrinogen to fibrin
Fibrin is the ultimate goal that Is necessary to form a stable clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Targets of anticoagulant drug therapy?

A

Factors 2, 7, 9, 10 are sites of many anticoagulant drugs
Warfarin affects factor 2,7,9,10
Factors 2a and 10a are sites of things like heparin and enoxaparin and fondaparinux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

4 Different Factors

A

7- extrinsic pathway
9- intrinsic pathway
2a= thrombin, common pathway
10a= start of common pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Different laboratory tests measure clotting ability of different pathways of the cascade

A

Prothrombin time (PT)
Can vary from hospital to hospital
Measures activity of factors II, VII, IX, X
International normalized ratio (INR)
Same as PT, but standardized worldwide
Partial thromboplastin time (PTT)
Measures activity of factors II, V, VII, IX, X, XI, XII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Indirect thrombin inhibitors to know

A

Unfractionated heparin (UFH)
Low molecular weight heparin
Enoxaparin (Lovenox®)
Fondaparinux (Arixtra®)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Normal activity of antithrombin

A

Binds factors IIa, IXa, Xa, XIa, and XIIa to inactivate them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Unfractionated heparin

A

Inhibits factors X and II
Administered as continuous infusion for ACS and warfarin bridging (acute VTE treatment)
Administered as subcutaneous injection for VTE prophylaxis

Monitoring
aPTT (goal level is 2-2.5 X control; approx. 60-80 seconds)

Adverse effects
Bleeding
Heparin induced thrombocytopenia
Osteoporosis long term treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Heparin induced thrombocytopenia (HIT)

A

Antibody-mediated adverse effect of heparin
Strongly associated with venous and arterial thrombosis

Treatment
Stop heparin and treat with a IV direct thrombin inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Low molecular weight heparins

A

Enoxaparin (Lovenox®)
Dalteparin
Tinzaparin

Inhibit factors X and II, but mostly factor X
Administered as subcutaneous injections for ACS, warfarin bridging (acute VTE treatment), and VTE prophylaxis
Monitoring
Not routinely done, Anti-Xa level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Choosing between UFH and enoxaparin

A 
Both are used for ACS, acute VTE treatment, and VTE prophylaxis
Heparin has a shorter half-life (1.5 vs. 7 hrs.)
Enoxaparin has a more predictable dose-response curve
Enoxaparin doesn’t require routine monitoring and subcutaneous 
Therapeutic anticoagulation (ACS, VTE treatment) requires heparin to be given by continuous IV infusion
Enoxaparin accumulates in renal dysfunction– cannot be used with pts with severe renal dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Fondaparinux (Arixtra®)

A

Synthetic pentasaccharide that inhibits factor Xa
Administered as a subcutaneous injection for acute VTE treatment and for VTE prophylaxis

Monitoring
Not routinely done, Anti Xa level
Adverse effects
Bleeding
Not for patients with renal dysfunction (CrCl < 30 mL/min)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How are indirect thrombin inhibitors reversed?

A

First, discontinue indirect thrombin inhibitor
Protamine sulfate, given by IV infusion
Max dose 50 mg/10 minutes (don’t need)

Heparin dose
1 mg/100 units heparin in the body
Enoxaparin dose
1mg/mg enoxaparin in the body (~60% effective)
Not effective to reverse fondaparinux
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

2 Oral direct Xa inhibitors

A

Rivaroxaban (Xarelto®)

Apixaban (Eliquis®)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Direct thrombin inhibitors (DTIs)

A

Action is independent of antithrombin

Intravenous
Bivalirudin (Angiomax®)
Argatroban

Oral
Dabigatran (Pradaxa®)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Intravenous DTIs

A

Bivalirudin (Angiomax®)
ACS undergoing percutaneous coronary intervention
Anticoagulation in patients with HIT
Argatroban
Anticoagulation in patients with HIT
Coronary angioplasty in patients with HIT
Administration: continuous IV infusion
Monitoring: aPTT
Adverse effect: bleeding
Reversal agent: none (give supportive care and blood products)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Oral DTI Dabigatran (Pradaxa®)

A 
Prevention of stroke and systemic embolism in patients with nonvalvular atrial fibrillation and DVT prophylaxis and treatment 
Accumulates in renal dysfunction
Reduce dose if CrCl 15-30 mL/min(don’t need these 2)
Do not use if CrCl < 15 mL/min
Monitoring: none
Adverse effects
Bleeding
GI upset
Reversal agent: none (use dialysis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Warfarin (Coumadin ®)

A

Inhibits factors II, VII, IX, X and proteins C and S(natural anticoagulants in the body)
Vitamin K antagonist

Uses
DVT/PE treatment
Prevention of stroke in patients with atrial fibrillation or heart valve replacement

Monitoring
INR

Adverse effects
Bleeding, bruising

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Warfarin MOA

A

Vit K used as precursors for factors that can be activated

Warfarin blocks the Vit K from becoming activating and being used

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Warfarin Dosing

A

Start low
5 mg po daily
2.5 mg if > 75 yrs., hepatic insufficiency, critically ill

Adjust based on WEEKLY dose
If INR < goal X 2, increase weekly dose 10%
If INR > goal X 2, decrease weekly dose 10%

34
Q

International Normalized Ratio (INR)–> Warfarin Monitoring

A

Goal 2 – 3
DVT/PE/atrial fibrillation
Bioprosthetic valve usually 3 months tx
Goal 2.5 – 3.5
Mechanical mitral valve, any mechanical valve with risk factors (HF, afib, MI, embolism)
Pts with predisposition (Factor V Leidon, Protein C/S Deficiency, etc.) who had clotting event when INR 2 - 3

35
Q

6 problems with Warfarin

A

Slow onset and offset (about 5 days)
Dietary interactions (avoid high Vit K)
Need for routine monitoring INR checked 1-3 months
Dose response variability
Narrow therapeutic index balance btw bleeding and clotting is very small
Drug interactions

36
Q

Monitoring for HIT

A

Monitoring for HIT
Platelets fall > 50% from baseline with nadir > 20,000
Platelets start to fall on day 5-10 of therapy
Thrombosis occurs while on heparin
Rule out other causes of thrombocytopenia
Drug causes: antibiotics and other antiplatelets

37
Q

Adverse effects of Low Molecular Weight Heparins

A

Adverse effects
Bleeding
Not for patients with severely reduced renal function (CrCl < 20 mL/min); reduce dose for CrCl 20-30 mL/min

38
Q

Apixaban (Eliquis®)

A

VTE prophylaxis after hip/knee replacement surgery

Prevention of stroke and systemic embolism in patients with nonvalvular atrial fibrillation

39
Q

Rivaroxaban (Xarelto®)

A

VTE prophylaxis and treatment

Prevention of stroke and systemic embolism in patients with nonvalvular atrial fibrillation

40
Q

Problems with Warfarin (6)

A

Slow onset and offset (about 5 days)
Dietary interactions (avoid high Vit K)
Need for routine monitoring INR checked 1-3 months
Dose response variability
Narrow therapeutic index balance btw bleeding and clotting is very small
Drug interactions

41
Q

Reversal of Warfarin

A

When warfarin is stopped, it takes about 5 days to return to baseline
With Vitamin K, it takes about 1 day

42
Q

Clinical Pearls for reversing warfarin with Vit K

A

Vitamin K is well absorbed, so the oral route is preferred in cases of supratherapeutic INR with no major bleeding
Subcutaneous and intramuscular vitamin K injections are associated with erratic absorption – do not use!
Intravenous vitamin K 10 mg should always be diluted with 50 mL NS and administered over 10-30 minutes
Avoids risk of hypersensitivity reaction

43
Q

Novel oral anticoagulants

A

Direct thrombin inhibitor
Dabigatran (Pradaxa ®)

Factor Xa inhibitors
Rivaroxaban (Xarelto®)
Apixaban (Eliquis®)

44
Q

Advantages of new oral anticoagulants

A

Faster onset and offset
No routine monitoring
Few drug and food interactions
Predictable dose-response

45
Q

Disadvantages of new oral anticoagulants

A

Limited clinical experience
Renal excretion
No antidote
Likely more $$

46
Q

List of anticoagulants

A

Unfractionated heparin- ITI, both IV and subc
Enoxaparin- ITI, renal dose adjustment
Fondaparinux-ITI
Bivalirudin-
Argatroban
Dabigatran- renal dose adjustment
Rivaroxaban- block factor 10a, renal dose adjustment
Apixaban- block factor 10a
Warfarin- blocks vit k which then inhibit the factors
IV and oral

47
Q

Main Anti platelets (6)

A 
Clopidogrel
Prasugrel
Aspirin
Dipyridamole
Eptifibatide
Cilostazol
48
Q

Thienopyridine antiplatelets (2)

A

All work by inhibiting the platelet ADP receptor

Clopidogrel (Plavix®)
Prasugrel (Effient®)

49
Q

Clopidogrel (Plavix®) Uses and Adverse Reactions

A

Uses
ACS and secondary MI prevention
Secondary stroke prevention
Peripheral arterial disease

Adverse effect
Bleeding

50
Q

Prasugrel (Effient®) Uses and Adverse Effects

A

Uses
ACS and secondary MI prevention

Do not use in patients with previous stroke/TIA
Do not use in patients > 75 years old
Unless patient has DM or previous MI

Adverse effect
Bleeding

51
Q

ASA uses and Adverse Effects

A

Uses
CAD (primary and secondary prevention)
Acute coronary syndrome
**Prevention of stroke in patients with atrial fibrillation
Peripheral arterial disease
Acute stroke treatment and secondary stroke prevention

Adverse effects
GI upset
Bleeding

52
Q

Dipyridamole uses and adverse effects

A

Uses
Given as an extended release (ER) formulation with aspirin for PAD and secondary stroke prevention

Adverse effect
Headache (10%)
Usually goes away after several days

53
Q

Dipyridamole MOA

A

Inhibits phosphodiesterase (PDE)—-accumulation of cAMP and cGMP—-prevents platelet activation

54
Q

GP IIb/IIIa inhibitors

A

Eptifibatide (Integrilin®)

55
Q

Eptifibatide (Integrilin®) uses and adverse Effects

A

Use
ACS during PCI(percutaneous coronary intervention) in conjunction with heparin therapy

Adverse effect
Bleeding

Requires Renal Dose Adjustment**

56
Q

Cilostazol (Pletal®) uses and Adverse Effects

A

Use
PAD with intermittent claudication (IC)
NOT for patients with CAD or heart failure

Adverse effects
Headache
GI upset

57
Q

Cilostazol (Pletal) MOA

A 
Inhibits phosphodiesterase (PDE)-------accumulation of cAMP---prevents platelet activation
Causes local vasodilation
58
Q

Fibrinolytics

A

Lyse thrombi by converting plasminogen to plasmin

Tissue type plasminogen activator (t-PA, Alteplase®)
Available as recombinant IV drug therapy

59
Q

Goals of Therapy for ACS

A

Restoration of coronary blood flow to prevent MI expansion (STEMI/NSTEMI) or MI (UA)
Prevention of death and other complications
Relief of chest discomfort

60
Q

Treatment of STEMI

A

Immediate primary PCI (< 90 mins)

Fibrinolytic therapy if no PCI (< 30 mins)
Alteplase
Reteplase
Tenectaplase

61
Q

2 Treatment Options for NSTEMI/ UA

A

Option 1: Early invasive strategy
Patients who are high risk get PCI

Option 2: Conservative strategy
Patients who are low risk are managed medically
See if symptoms resolve
Undergo stress testing

62
Q

Anticoagulant therapy for MI

A

Patients undergoing fibrinolysis (STEMI only)
Enoxaparin administered for 7 days
Patients getting primary PCI
Heparin continuous infusion discontinued after PCI
(also give GP IIb/IIIa inhibitor X 12-18 hrs after PCI)
Bivalirudin continuous infusion discontinued after PCI
Patients getting medical management
Heparin continuous infusion X 48 hours

63
Q

GP IIb/IIIa inhibitors

A

Eptifibatide
Abciximab

Only given to patients undergoing PCI who also get heparin as the anticoagulant

64
Q

Chronic antiplatelet therapy for MI– ASA

A

everyone gets this
325 mg PO daily X 1 month after bare metal stent
325 mg PO daily X 3-6 months after drug eluting stents
81 mg PO daily for life (all patients)

65
Q

Chronic antiplatelet therapy for MI–Clopidogrel (Plavix®)

A

some will get this or Prasugrel with the ASA
300-600 mg PO X 1 loading dose
75 mg PO daily X 1 year

66
Q

Chronic antiplatelet therapy for MI – Prasugrel

A

60 mg PO X 1 loading dose

10 mg PO daily X 1 year (reduce dose to 5 mg if < 60 kg)

67
Q

Treatment of acute VTE (Venous Thromboembolism)

Continuous heparin infusion

A

Continuous heparin infusion
Start immediately and continue X 5 days and until INR 2-3 on warfarin therapy

Monitoring
Check baseline aPTT
Check aPTT in 6 hours – adjust heparin dose based on aPTT result

68
Q

Treatment of acute VTE (Venous Thromboembolism)

Enoxaparin

A 
Enoxaparin (Lovenox®)
1 mg/kg subQ every 12 hours
1.5 mg/kg subQ every 24 hours
Can send the pt home with it
Do not need to dose it
Heparin has a shorter half life
69
Q

Warfarin for acute VTE

A

Duration of therapy
First occurrence: 3 months
Second occurrence: lifelong

Monitoring
INR Goal 2.5 (Range 2.0-3.0)

70
Q

Adjusting maintenance dose of warfarin

A

Adjust based on WEEKLY dose
If INR < goal X 2, increase weekly dose 10%-20%
If INR > goal X 2, decrease weekly dose 10%-20%

71
Q

Risk Factors for VTE

A

Most hospitalized patients have at least one risk factor for VTE

72
Q

4 meds used in Prevention of VTE

A

Unfractionated heparin

Enoxaparin
Discontinue at hospital discharge or up to21 days after surgery

Fondaparinux
Discontinue at hospital discharge or up to 21 days after surgery

Rivaroxaban

73
Q

Goals of therapy for stroke

A

Reduce neurologic injury to prevent mortality and long term disability
Acute ischemic stroke
Prevent stroke recurrence
Secondary stroke prevention

74
Q

Treatment of acute ischemic stroke includes only 2 medications

A

Intravenous t-PA (Alteplase®)
0.9 mg/kg over 1 hour (max 90 mg), with 10% given as initial bolus over 1 minute

Aspirin 325 mg PO daily
If IV t-PA given, wait 24 hours before starting aspirin

75
Q

Stroke Treatment Protocol

A

Activate stroke team
Treat as early as possible if within 4.5 hours of symptom onset
CT scan to rule out hemorrhage
Meet inclusion and exclusion criteria for t-PA
Administer t-PA 0.9 mg/kg over 1 hour (max 90 mg), with 10% given as initial bolus over 1 minute
Avoid all antithrombotic therapy (including aspirin) for 24 hours
Monitor patient closely for BP, response, and hemorrhage

76
Q

Antiplatelet therapy for secondary stroke prevention

A

Aspirin 81 mg or 325 mg PO daily
Clopidogrel (Plavix®) 75 mg PO daily
Aspirin plus ER (EXTENDED RELEASE) dipyridamole (Aggrenox®)
Warfarin for patients with cardioembolic stroke A-FIB that increases risk for clot into the heart

77
Q

Goals of therapy for Peripheral Arterial Disease

A

Improve walk distance
Improve pain free walking time
Improve quality of life
Prevent cardiovascular complications and death

Primary symptoms
Intermittent claudication
Cramping, fatigue, and discomfort while walking
Pain at rest

78
Q

Antiplatelet therapy for PAD (4 meds)

A

Aspirin 81-325 mg PO daily
Clopidogrel 75 mg PO daily
Patients who cannot take aspirin
Aspirin plus ER dipyridamole (Aggrenox®) 25-200 mg PO BID
Alternative to aspirin and clopidogrel
Cilostazol 100 mg PO BID
For patients with intermittent claudication

79
Q

CHADS2 Criteria

A 
previous stroke or TIA = 2 points
age > 75 = 1 point
HTN= 1 point
DM= 1 point
HF= 1 point

Between 2-6= high which means the recommended therapy is warfarin
1 is moderate risk which means the recommended therapy is warfarin/ asa
0 is low risk which means the recommended therapy is asa

80
Q

4 options for anticoagulation

A

Warfarin–Dosed to a goal INR of 2.5 (range 2.0-3.0)
Dabigatran
Rivaroxaban
Apixaban

Anti-Thrombotics (1 decks)

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