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Summer 1 > anticoags > Flashcards

anticoags Flashcards

1
Q

Explain thrombus formation

A

activated platelets adhere to vascular endothelium and express P-selectin
microparticles accumulate and bind to platelets and the p selectin
tissue factor leads to thrombin generation which leads to fibrin clot formation

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2
Q

What receptors are at the platelet membrane and what do they bind

A

GP Ia: binds collagen
GP Ib: binds vWF
GP IIb/IIIa: fibrinogen and other molecules

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3
Q

Explain the clotting mechanism at the site of vascular wall injury

A

Platelet membrane receptors bind clotting factors
Antiplatelet prostacyclin is released
Aggregating substances from degranulating platelet are released (ADP, thromboxane A2, and 5-HT)

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4
Q

What is hemostasis

A

maintains integrity of circulatory system after blood vessel injury
hemostatic clots stay localized to vessel wall and do not impair blood flow
pathologic clots causing VTE do result in impaired blood flow
-this is followed by fibrinolysis (clot degradation)

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5
Q

What are some clotting factors and what affects them

A

Prothrombin: heparin, dabigatran, warfarin
Proconvertin (factor VII): warfarin
PTC (factor IX): warfarin
Factor X: heparin, rivaroxiban, apixaban, edoxaban, warfarin
Protein C&S: warfarin
Plasminogen: thrombolytic enzymes, aminocaproic acid

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6
Q

What is the goal in treating with anticoags

A

prevent VTE in high risk by:
prevent thrombus extension and embolization
reduce recurrence risk
prevent long term complications (post thrombotic syndrome, chronic thromboembolic pulm HTN)

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7
Q

What are the different anticoag therapies available

A

Aspirin: anti-platelet
Warfarin: vitamin K antagonist
Heparin: antithrombin (inactivates factor Xa)
LMWH: indirect antithrombin w/ factor Xa inhibitor
Fondaparinux: indirect factor Xa inhibitor
DOAC: direct Xa inhibitors
Dabigatran: Direct thrombin inhibitor

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8
Q

What are Chest guidelines on patients with DVT of leg or PE and no cancer

A

for long term (first 3 months) anticoag therapy, Dabigatran, Rivaroxiban, apixaban, or edoxaban should be used over vitamin K antagonists

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9
Q

How do you incorporate initial parenteral anticoagulation

A

Give it before dabigatran and edoxaban
do NOT give it before rivaroxiban and apixaban
Overlap it with VKA therapy

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10
Q

How is heparin dosed

A

weight based! and admin as continuous IV infusion

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11
Q

How does heparin work

A

binds endothelial cells and macrophages, and plasma proteins
Neutralize platelet factor 4 released from active platelets
Reduce capacity of heparin-antithrombin comples to inhibit factor Xa bound to active platelets

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12
Q

What are the limitations of heparin

A

poor bioavailability at low dose
dose dependent clearance
variable anticoag response
reduced activity in vicinity of platelet rich thrombi
limited activity against factor Xa incorporated in the prothrombinase complex, and thrombin bound to fibrin

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13
Q

What are the ADE of heparin

A

MC: bleeding!
thrombocytopenia (PLT <100k or 50% decrease)
osteoporosis
elevated transaminases

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14
Q

How do you monitor heparin

A

activated PTT or anti-factor Xa level

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15
Q

How do you reverse heparin’s effect

A

IV protamine sulfate neutralized heparin
-mix of basic polypeptides isolated from salmon sperm that bind heparin with high affinity and result in protamine heparin complexes that are cleared

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16
Q

What are features of heparin induced thrombocytopenia

A

PLT levels fall 5-10 days after starting heparin
MC with unfractionated heparin, less common with LMWH
MC in surgical pts and those with cancer
VTE > ATE

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17
Q

How do you manage heparin induced thrombocytopenia

A

Stop heparin!!
Give a diff anticoag (lepirudin, argatroban, bivalirudin, fondaparinux, rivaroxiban)
Do not give PLT transfusions
Do not give warfarin until PLT count returns to baseline
Eval for thrombosis, esp. DVT

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18
Q

How does LMWH work

A

Same as heparin!

Binds AT-III which inactivates thrombin, factor IXa, Xa, and XIIa

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19
Q

What are LMWH agents

A

Enoxaparin (lovenox)
Dalteparin (fragmin): surgical prophylaxis, extended cancer VTE Tx
Fondaparinux (Arixta): AT-III mediated selective inhibition of factor Xa

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20
Q

What is the principle difference in the activity of UFH and LMWH

A

Relative inhibition of factor Xa and thrombin!
UFH: anti Xa:IIa ratio is 1:1
LMWH: anti Xa:IIa ratio is 4:1 - 2:1

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21
Q

What are advantages of LMWH

A

Predictable anticoag dose response= can be given subQ QD-BID as prophylaxis and Tx
Lower incidence of thrombocytipenia= safer for short or long term admin
Reduced need for routine monitoring: safer for extended admin

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22
Q

Initiating anticoag therapy with Lovenox is

A

Weight based!

but all basically 1mg/kg q12 hrs?

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23
Q

Initiating anticoag therapy with Fondaparinux is

A

weight based! <50 kg= 5mg qd. 50-100kg= 7.5mg qd

Start warfarin on 2nd day of Tx, but continue Fonda until INR >2 (at least 24 hours)

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24
Q

What meds are affected by pork allergy

A

Heparin

LMWH (EXCEPT fondaparinux!!)

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25
Q

What should Enoxaparin NOT be used in

A

patients with cancer

-it can be used as prophylaxis in hip/knee replacement, abd surgery, acute med illness, and DVT Tx

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26
Q

What should Dalteparin NOT be used in

A

DVT/PE treatment
Knee replacement surgery
-can be used in hip replacement, abd surgery, acute med illness, and VTE cancer prophylaxis

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27
Q

What are properties of heparins

A 
Large acidic polysaccharide polymers 
Parenteral admin
site of action: blood 
Onset: rapid, minutes 
MOA: binds AT-III and inactivates factor IXa, Xa, XII
Monitoring: aPTT for UFH
Antidote: protamine IV for UFH
Use: acute, over days 
Use in pregnancy: yes!
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28
Q

What are properties of warfarin

A 
Small lipid soluble molecule 
PO 
site: Liver 
Onset: slow (days); limited by halflives of normal factors 
MOA: interferes w/ synthesis of vitamin K dependent clotting factors (II, VII, IX, X) 
Monitor: PT/INR 
Antidote: vitamin K if Sx. plasma 
Use: chronic, wk-mo
Pregnancy: No! it is teratogenic*
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29
Q

What is warfarin also known as

A

rat poison!

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30
Q

What is the MOA of warfarin

A

Inhibits VK poxide reductase= interferes with synthesis of functional VK= No VK dependent clotting factors
-Used in VTE, PE, preventing clots in AFIB or cardiac valve replacement
PO has delayed onset and offset activity

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31
Q

What are ADE of Warfarin

A

Bleeding! can use VK to reverse effects
thrombosis early in therapy is 2/2 protein C deficiency
*Monitor PT/INR

32
Q

What drugs does warfarin interact with

A

CYP450 inducers: decreases effect

CYP450 inhibitors: increases effect

33
Q

What clotting protein does vitamin K block first

A

Factor VII!!! (4-6 hour half life)
Then protein C (9 hour half life)
Lastly Protein S (60 hr half life)

34
Q

What are some contraindications to warfarin

A 
Hypersensitivity 
Hemorrhagic tendencies 
recent eye surgery or CNS 
lumbar block anesthesia or traumatic surgery 
malignant HTN 
Adherence concerns (need to monitor)
35
Q

What are the DOACs

A

Apixaban (eliquis)
Betrixiban
Edoxaban
Rivaroxaban (xarelto)- most bioavailable (80%)
Dabigatran: prodrug! converted in liver to active form. most renally excreted drug (80%)

36
Q

How do DOACs work

A

Bind active site of Factor Xa and inhibit enzyme action
-Used for VTE, PE, preventing stroke in AFib pts
Fixed PO dose

37
Q

ADE of DOACs are

A

bleeding! no specific reversal agent

Do not need to monitor these patients or dose adjust, but can check factor Xa test

38
Q

What DOACs should NOT be used in VTE prophylaxis after orthopedic surgery

A

Dabigatran (pradaxa)

Edoxaban (also do NOT use this in extended VTE Tx; >6 months)

39
Q

What is important to note about administering Rivroxiban

A

When using for extended VTE Tx (>6 months), give the dose WITH food!
The only time you have the option, w/ or w/o food, is short term VTE prophylaxis after ortho surgery

40
Q

What DOAC is good to use in ESRD

A

Apixaban!

It has the lowest renal excretion, at only 25%

41
Q

What do current guidelines say about long term DVT and PE prevention

A

Full dose anticoag therapy is recommended for min. 3 months after DVT or PE
Patients at high risk may benefit from extended Tx
Low dose DOAC is safer than full dose traditional anticoag for extended Tx
*Consider low dose DOAC for patients requiring long term VTE prevention after 3-6 months of acute Tx

42
Q

What are reversal agents for DOACs

A

Dabigatran: Praxbind
Rivaroxiban, Apixaban, LMWH: Andexanet (FDA approved)
Ciraparantag: UFH, LMWH, Rivaroxaban, Apixaban, Edoxaban, Dabigatran

43
Q

What is the VTE treatment PO only strategy

A 
Day 0-7: Apixaban high dose 
Wk 2-6 mo: Apixaban med dose 
>6 months: Apixiban low dose 
OR 
Day 0-21: Rivaroxaban 15mg
Day 22->6 mo: Rivaroxaban 20mg
44
Q

What is the VTE Tx Switch strategy

A

Day 0-5: UFH, LMWH, or Fondaparinux

Day 5- >6mo: Dabigatran or Edoxaban

45
Q

What is the VTE Tx overlap strategy

A

Day 0-6: UFH, LMWH, or Fondaparinux

Day 0- >6mo: Warfarin PO daily

46
Q

What is appropriate duration of VTE Tx

A

Initial duration to effectively treat acute 1st episode of VTE: 3 months
This reduced recurrent VTE risk

47
Q

What is INR goal range for warfarin therapy

A

2-3

Except if with a mechanical valve: 2.5-3.5 (lifelong therapy)

48
Q

What is the way to remember the color of warfarin tabs

A 
Please Let Granny Brown Bring Peaches To Your Wedding 
Pink -1
Lavender -2
Green -2.5
Brown -3
Blue -4
Peach -5
Teal -6
Yellow -7.5 
White -10
49
Q

How do you start warfarin therapy

A

Day 1: 5mg
2-3 days later: if INR <1.5, continue at 5. >3, hold and recheck next day
5-7 days later: if INR <1.5, increase to 7.5-10. If >3, reduce to 0-.25mg

50
Q

How frequently do you check INR when initiating warfarin therapy

A

Every 2-3 days until INR in therapeutic range on 2 consecutive checks
Every week until 2+ checks in therapeutic range
Every 2 weeks until 2+ checks in therapeutic range
Every 4 weeks when dose is stable

51
Q

What is a basic way you can adjust warfarin dose based on INR (if goal is 2-3)

A

<1.5: increase 10-20% TWD
1.5-1.9: increase 5-10% total weekly
2-3: no change
3-1.4: decrease 5-10% total weekly
4.1-5: hold 1-2 doses and decrease 10% total weekly
-If goal is 2.5-3.5, hold 1-2 doses and decrease 10% if INR is 4.6-5

52
Q

How frequently do you check warfarin when maintaining warfarin therapy

A

After 1 week if starting or stopping interacting med, changing diet or activity level
Every 1-2 wks if 5-10% dose adjustment needed
Every 4 wks if maintained on same stable dose <3 mo.
Every 6-8 weeks if pt on same stable dose 3+ mo
Every 12 weeks if pt on same stable dose for 6+ mo

53
Q

What factors indicate warfarin sensitivity

A 
Increased INR response 
Baseline INR >1.5 
65+ y/o
ABW <45kg (actual < ideal)
Malnourished/NPO >3 days 
Hypoalbuminemia 
Chronic diarrhea 
Significant dug interactions 
Decompensated HF 
Increased bleeding risk 
Thrombocytopenia 
Cirrhosis/total bili >2.4 
Hx alcohol abuse 
ESRD 
GI bleed in past 30 days 
Surgery in the past 2 weeks 
IC bleed in past 30 days
54
Q

What are key concepts in managing warfarin

A

dose adjustments should be made on current total weekly dose
consider trends in INR when making management decisions
consider pt ht, wt, age with dose requirements
Consider repeating INR in same day if value is very diff. than expected
Consider no dose adjustments for INR on low end or high end, retest in 1-2 weeks
Consider no dose adjustments for INR above or below therapeutic range by 0.5 or less. retest in 1-2 wks
Monitor more frequently in first month of initiation
Consider extending monitoring more frequently in first 3 mo. of in-range INR
CoaguCheck XS machine is only accurate for INR 0.8-8

55
Q

If pt INR is 5-10 (supratherapeutic), how do you proceed

A

Recommend against use of VK
Hold 1-2 doses, check INR in 24 hrs
Resume lower dose when INR in range

56
Q

If pt INR is >10 (supratherapeutic), how do you proceed

A

Give VK 2.5-5mg
Hold 2 doses, check INR in 24 hrs
Repeat VK prn
Resume lower dose of warfarin when INR is in range

57
Q

Pearl on holding warfarin

A

Holding warfarin 1 dose drops INR by appx. 1

58
Q

How do you transition from LMWH to warfarin

A

Need min. 5 days of warfarin therapy and pt INR in goal range for min 24 hours before you can d/c Lovenox
day 1: initiate lovenox and warfairn
day 4: check INR. cont or adjust dose if needed
day 6: check INR. cont or adjust dose if needed
day 7: check INR. dc lovenox if INR in goal range for 24 hrs, or continue lovenox until it occurs

59
Q

What procedures are high risk for bleed

A 
heart valve replacement 
CABG 
neuro, urologic, head/neck, abd, or breast cancer 
laminectomy 
kidney biopsy 
transurethral prostate resection 
polypectomy, variceal Tx, biliary sphincterotomy, pneumatic dilation 
PEG placement 
EGD guided FNA 
multiple tooth extractions 
vascular and general surgery 
Any major op lasting >45 min
60
Q

How do you bridge therapy for high-mod risk of thromboembolism

A

4 days before surgery: dc warfarin
3 days before surgery: initiate LMWH
2 days before surgery: check INR
1 day before surgery: dc LMWH
1 day after surgery: resume warfarin
2 days after surgery: resume LMWH for low bleed risk procedure
3 days after surgery: resume LMWH for high bleed risk procedure

61
Q

How do you switch from warfarin to LMWH

A

dc warfarin and start Dabigatran or Eliquis when INR <2

dc warfarin and start Rivaroxaban when INR <3

62
Q

How do you switch rom LMWH to warfarin

A

Rivaroxaban: no data available
Dabigatran:
CrCl >50, start warfarin 3 days before dc dabigatran
CrCl 30-50, start warfarin 2 days before dc
CrCl 15-30, start warfarin 1 day before dc

63
Q

When should you assess patients on anticoags

A

Extended therapy: at periodic intervals (ex. yearly)
w/ leg DVT or PE on warfarin: maintain INR 2-3
w/ leg DVT or PE, no cancer, no DOAC: warfarin preferred

64
Q

Recommendations for pts with DVT

A

If home circumstance is adequate, initial Tx at home is better
Early ambulation is suggested over bed rest
Anticoag Tx alone is better than cath thrombolysis if DVT is acute and proximal LE
If acut and Sx leg DVT, do not use compression stockings

65
Q

What are the thrombolytics

A

Alteplase, Reteplase
Tenecteplase
Streptokinase
Urokinase

66
Q

How do thrombolytics work

A

convert plasminogen to plasmin which causes breakdown of clots
-Good for MI, DVT, PE, and ischemic stroke (t-PA)
Alteplase, Reteplase convert fibrin bound plasminogen targeting clots

67
Q

Indications for the use of fibrinolytics

A

Ischemic chest discomfort lasting 20+ min, onset <12 hours
ST elevation in 2 contiguous leads (2+mm in men, 1.5+mm in women in V2-3 -OR- 1+mm in all other leads)
New LBBB

68
Q

Absolute contraindications to fibrinolytics are

A 
active internal bleeding (not menses) 
previous IC hemorrhage
Ischemic stroke w/in 3 mo
known IC neoplasm 
known structural cerebral vascular lesion (AVM) 
suspected aortic dissection 
significant closed head/facial trauma w/in 3 mo
IC or intraspinal surgery w/in 2 mo 
severe uncontrolled HTN 
Use of streptokinase w/in 6 mo
69
Q

What should STEMI/NSTEMI management include

A 
*Aspirin! class 1 recc. for both 
Clopidogrel in addition to ASA is class 1 recc for both 
PCI in both is also a class 1 
Prasugrel added to ASA is a class I for both 
Can also add Ticagrelor, or Cangrelor to ASA therapy
70
Q

Warfarin and LMWH therapy recommendations in STEMI/NSTEMI include

A 
UFH is a class I in both 
Enoxaparin is a class I in both 
Bivalirudin is a class I for both
Fondaparinux is a class I for both
71
Q

What are fibrinolytic recommendations in STEMI/NSTEMI

A 
Fibrinolytic Tx: STEMI w/in 12 hrs, class I. NSTEMI, class III
GPI inhibitors: NSTEMI class I (for abciximab). STEMI class IIa (for abciximab) 
Nitroglycerin: class I for both
72
Q

Other pharm therapy for STEMI/NSTEMI

A 
BB: class I for both (PO). class III for IV 
CCB: NSTEMI class I. Diltiazem for NATEMI/AMI class III 
ACE-I: class I for both 
ARB: class I for both 
Aldosterone antag: class I for both 
Morphine: class IIb for both if CP persists after drug Tx 
Statins: class I for both
73
Q

Where do antiplatelet drugs work

A

ASA: inhibits thromboxane A2 synthesis by irreversibly inhibiting COX-1
Clopidogrel, prasugrel: irreversibly block P2Y12 (ADP receptor on PLT surface)
Cangrelor, ticagrelor: reversibly ind P2Y12 receptor
Abciximab, Eptifibatide, tirofiban: block fibrinogen and vWF binding to GP IIb/IIIa= inhibit final common pathway of platelet aggregation
Vorapaxar: targets PAR-1 (major thrombin receptor) and inhibits thrombin mediated platelet activation

74
Q

What are the direct thrombin inhibitors and how do they work

A

Bivalirudin, Desirudin, Argatroban
Bind thrombin’s active site and inhibit it’s enzymatic action
Used as anticoag in patients w/ heparin induced thrombocytopenia

75
Q

ADE of direct thrombin inhibitors

A

Bleeding!

monitor aPTT

76
Q

What is the best direct thrombin inhibitor

A

Bivalrudin! No renal or liver clearance, and shorter half life so easier to control
-Desirudin is renally cleared, Argatroban has hepatic metabolism

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