Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Cardio MT2 > MT2_6_Anticoagulant Pharma > Flashcards

MT2_6_Anticoagulant Pharma Flashcards

(78 cards)

Start Studying
1
Q

Red thrombus is made of

White thrombus is made of

A

fibrin and RBCs

platelets

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

Arterial thromboses develop in an ____that usually develops on top of an _______ and causes a __

A

artery
arthersclerotic plaque
Myocardial infarct

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

Describe the mechanism of blood coagulation (primary vs secondary)

A

vasoconstriction, then platelet plugging activating fibrin clot formation

clotting factors then come in because platelets are not enough fix the problem..occurs via the coagulation cascade

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

In the coagulation cascade, what is the goal?

A

to make thrombin (factor 2A) which converts soluble fibrinogen to insoluble fibrin (to make a stable thrombus)

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

What are the three pathways of the cascade?

A

extrinsic: quick fix, less thrombin (responds to factor 3)
intrinsic: tissue damage inside, takes longer, makes a lot of thrombin
common: both extrinsic and intrinsic converge at factor 10, which converts 10 to 10a, prothrombin to thrombin, then fibrinogen to fibrin

fibrin + platelets = thrombus

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

Indirect Anticoags

Direct Coags

A

Indirect: heparin, fonda, warfarin (activates antithrombin for anticaog. activity)

Direct: desirudin, bivalirudin, argatroban, dabigatran

Direct 10a: rivaroxaban apixaban, edoxaban, betrixaban

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

What is heparin dependent on, and does it have fibrinolytic activity?

A
  • dependent on AT

- does not have fibrinolytic activity..will prevent clots from forming but not break them down

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

How is anticoagulation achieved with heparin?

Long chain inhibits…and short chain inhibits…

A
  • binding of UFH + AT = complex catalyzing inactivation of factor 2a (thrombin) and 10a

2a, 10a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Heparin has a __onset and __half life. It is excreted very little in the ___ therefore__. It is metabolized by the ___, and safe to use in ___ (population)

A 
quick
short
kidney
safe in renally impaired patients
liver/reticuloendothelium system
pregnant women
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the dose for treating acute coronary syndrome?

DVT/PE?

Prophylaxis VTE?

A

60u/kg, then 12u/kg/hr

80u/kg, then 18u/kg/hr

5000U q8-12h SQ

can be used in bridge therapy in patients on warfarin

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

What is used to monitor heparin? (two things) When to measure?

A

aPTT, measures speed of fibrin clot..normal is 30 seconds..therapeutic range is 1.5-2.5x control

  • measure at baseline then q6hours..warfarin may prolong aPTT
  • Anti10a levels, which measure’s heparin’s ability to inhibit factor 10a
  • therapeutic range is .3-.7, measure q6hours after heparin initiation/change
  • useful for patients w inflammation or lupus inhibitor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is CI in the use of heparin? (3)

Side effects?

A
  • CI: hypersensitivity to pork, bleeding, severe thrombocytopenia
  • bleeding
  • heparin induced thrombocytopenia
  • osteoporosis, vertebral fractures, alopecia, priapism purple toe syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

In type 2 HIT (heparin induced thrombocytopenia), When does it occur, what happens, and the most common complication?

A

5-10 days after heparin

can cause life and limb threatening thrombotic complications

not marked by bleeding, most common is VTE (DVT/PE)

platelet count drops, development of thrombus

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

• _ is released from activated
platelets, binds heparin and promotes__ by
moderating effects of heparin‐like molecules
•_ formed directly against complexes of
_ factor
• Antibodies bind to PF4‐heparin complexes on platelet
surface and induce platelet activation
• ___releases procoagulant platelet
microparticles, causes platelet consumption and
thrombocytopenia
• Thrombin is generated: producing venous and arterial
thrombosis of HIT

A

PF4, coagulation
IgG, heparin bound platelet
platelet activation

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

Major presentations of HITII?

A

DVT/PE, can result in a stroke, MI, and venous limb gangrene

Skin lesions at injection sites

acute systematic reactions following IV hep bolus (fever, flushing, etc.)

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

HIT II Diagnosis? (4Ts)

A

Thrombocytopenia (platelets less than 100,000 or 50% of baseline)

Timing of thrombocytopenia relative to heparin exposure (normal is 5-10 days, rapid is 24 hours, and delayed is 3-6 weeks which is more severe)

Thrombosis or other sequalae or HIT (VTE, skin lesions, systematic)

Other causes of thrombocytopenia (drugs, sepsis, etc.)

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

So, what to give patients with type I HIT? DC and give DIRECT thrombin inhibitors

A
  • argatroban
  • bivalirudin
  • fonda (not in patients with platelets less than 100,000)
  • warfarin (only when greater than 150000)

confirm with a HIPA assay,Hep PF4 ElISA assay, C-serotonin assay

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

What happens if a patient bleeds on heparin?

A

due to short half life, a reversal agent is not needed, so just stop the infusion.

Protamine sulfate is usually used in a bleed

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

Why would I use heparin? Why not?

A
  • good for bleeding risk, surgical candidate, quick onset and offset, and good for patients with bad kidneys
  • variation in response, does not affect fibrin 2a and 10a, so does not lyse the clot, HIT/osteo, intensive monitoring
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why would low molecular weight heparins be preferred? (4)

A

reduced binding to plasma proteins gives more predictability regarding dose response

also, less monitoring, less HIT, SQ (so can be used outpatient)

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

Similar to UFH, LMWH requires___

The shorter chain allows for more ____

A

Antithrombin

selectivity to 10a (not 2a)

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

LMWH half life?
Renal excretion?
Protein Binding
Protamine Reversal

A

4 hours (longer than UFH)

Renally excreted therefore adjust

does not bind to heparin binding proteins

partial reversal

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

For enoxaparin (LMWH) what are the main indications?(4)

A

VTE prophylaxis

  • ab surgery, VTE prophylaxis (40mgSQ q24)
  • hip/knee: 30mg sq q12
  • crcl less than 30 (30mg sq q24)

VTE treatment

UA/NSTEMI/STEMI MI

Heart Valves

  • 1mg/kg sq q12h or 1.5mg sq q24
  • for crcl less than 30, 1mg/kg sq q24
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

When a patient is on a LMWH, what do you monitor?

A
  • Hgb, Hct, platelets, bleeding

- anti 10 a sometimes…only if patient is obese, renal insufficiency, pregnant.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Enox CI
- pork allergy, bleeding
26
BBW for Enox
epidermal or spinal hematomas in patients getting LMWH + anesthesia...can result in paralysis
27
What is the MOA of warfarin? It is an __antagonist It inhibits the ___ subunit of ___to reduce regeneration of vitamin K It inhibits the synthesis of clotting factors ______
- vitaminK C1...VKORC1 7, 9, 10, 2 (SNTT)
28
What are the main indications for warfarin?
- all purpose anticoag - VTE A fib, a flutter - thrombus - prosthetic heart valves - Thrombophilia antiphospholipid syndrome
29
The onset of anticoagulation for warfarin is ___ Peak effect is ___ INR may increase in ___
- 1-3 days - 5-7 days - 36-72 hours basically, it has a long onset
30
warfarin has R and S enantiomers. S has more anticoagulant effect, but more DDIs. How is it metabolized?
Through CYP2C9 - 2*: decrease by 30% - 3* decrease by 80% - therefore decrease the dose of warfarin R is through 3A4, 1A2
31
What are the variables that contribute to warfarin dose response variations?
- DDIs - dietary vitamin K - genetic polymorphisms for CYP2C9, VKORC1 (AA phenotype) - hepatic congestion, impairment
32
What are some of the drugs that will potentiate warfarin's effect (therefore more bleeding?)
- thyroid supplements - antibiotics/fungals - amiodarone - cimetidine, allopurinol, fluoxetine, apap, alcohol
33
What are some of the drugs that will decrease warfarin's effect?
rifampin CBZ barbituates ethanol
34
When counseling a patient about vit K and diet, what do you say?
- consistency with diet | - foods that contain high vitamin k include greens, cauliflower, soybeans
35
What to monitor for with warfarin?
- PT/INR - Hbg/Hct, platelets - LFT, urinalysis, stool, pregnancy monitor INR daily then reduce over time
36
What is the most common INR goal?
2-3 (mechanical aortic valve with Low risk) 2.5-3.5 (mechanical mitral valve, mechanical aortic valve w high risk factors) e.g. a fib, low ejection fraction , mechanical valve with systemic embolism.. basically anything w mechanical valve with a high risk
37
starting dose for warfarin?
less than 5mg/day in the first 1-2 days then titrate based on INR
38
Dr. wants rapid anticoagulation. What to recommend?
- UFH/LMWH bridge | - overlap with parental anticoag for 5 days, target INR higher than 2 for 2 days before dc the parental heparin
39
How long does it take for warfarin to achieve full anticoag effect?
- 4-5 days due to the half lives of all the clotting factors
40
When do bleeds usually occur on warfarin (INR?) what to do if there is a bleed?
- INR >5 - Vit K (phytonadione) (large doses can make patients resistant for up to one week) - PO more preferred, but INR will drop in 1-2 days, give when INR is greater than 10 - IV is faster in 12 hours - SQ not preferred.
41
When is PCC4 (Kcentra) used? | BBW?
for serious bleeds, INR greater than 2 - contains factors SNTT, protein C, protein s - see decline in 10 min , recheck INR in 30 min BBW: THROMBOTIC EVENTS RISK
42
Major s/e of warfarin?
- skin necrosis, blue toe(days 3-8) | - limb gangrene in HIT (don't initiate warfarin until platelets greater than 150)
43
Pregnant women taking warfarin. What to do?
-X - DC! has teratogenic effects!!!! use heparin instead D: pregnancy w mechanical heart valves - in these patients, avoid in the 1st trimester and close to delivery (38 weeks), use LMWH or UFH instead
44
What is the main factor involved in thrombus formation?
factor 2a activates platelets and clotting factors, stabilizes clots, and converts soluble fibrinogen to insoluble.
45
Advantages of direct thrombin inhibitors includes binding___to thrombin, so no antithrombin is needed. DTIs inhibit both ____and___ bound thrombin. There are little interactions with plasma proteins so effects is more___. Is used for ___
directly thrombin and fibrin predictable HIT
46
how do DTI''s work?
- binds directly to the active site and/or exosite to block enzymatic activity.
47
What are the 2 uses or desirudin?
- post op and VTE prophylaxis - given SQ, renal adjust less than 30 - not very popular
48
How does bivalirudin differ from desirudin?
- reversible and bivalent, binding is weaker. reversibility contributes to decreased bleeds and safety
49
What are the main indications for bivalirudin?
- ACS (UA, NSTEMI, STEMI) undergoing PCI - HIT dose IV bolus .75mg/kg then 1.75 mg/kg/hr
50
Onset/offset of bivalirudin?Renally adjust?
immediate, and coagulation returns to baseline 1 hour after dc - if crcl is less than 30, adjust to .25-1 mg/kg/hr IV inf.
51
What happens when a patient bleeds on bivalirudin? What to monitor?
- hemodialysis, 4 factor PC, and FFP | - monitor aPTT q2 hours
52
How does argatroban bind? | How does it compare to other DTIs?
- reversible, small, univalent that binds to the active site | - lowest affinity for thrombin compared to other DTIs
53
Main indications for argatroban? - side effects? - CI's?
- HIT, PCI - bleeding, chest pain, dyspnea - for bleeding consider 4 factor PCC - CI in bleeding
54
Is onset immediate from argatroban? how is the drug metabolized?
- yes, extensively through the liver, therefore use caution when dosing!
55
What is the argatroban dosing for HIT?
- 2mcg/kg/min for hepatic issues, 0.2-0.5 mcg/kg/min no adjustment needed for renal impairment!!
56
How to monitor Argatroban?
- aPTT every 2-4 hours, and check aPTT after every rate change. then check every AM when 2x aPTT goal. - CBC, LFT, PT//INR (may increase w argatroban use)
57
How does dabigatran work?
- directly inhibits thrombin, reversibly binds to active site - oral, therefore highly lipiphillic and GI absorbable
58
What are the indications for dabigatrin? Dose?
nonvalvular a fib, VTE, 150mg BID (not for MI!) VTE prophylaxis: 110mg 1-4h, maintain at 220mg once daily
59
How is dabigatrin excreted? What is it a substrate of?
- renally - Pgp efflux transporter, so avoid use (rifampin, amiodarone, clarithromycin, verapamil, quinidine) avoid use w CrCl less than 50
60
Common side effects of Dabigatran? CI BBW Reversal agent?
- s/e: GI bleeding, dyspepsia, gastritis - BBW: premature d/c increases risk of thrombotic events - Epidermal/spinal hematomas in which patients are receiving anesthesia - idarucizumab
61
Name the indirect and direct 10a inhibitors What are these agents approved for?
- indirect: fonda (SQ) - direct (rivaroxaban, apixaban, edoxaban, betrixaban PO) - both indirect and direct are approved for VTE, direct NOT of ischemic heart disease
62
How does Fonda work? Indications? Excretion? CI?
- with antithrombin, it irreversibly binds to antithrombin, neutralizing it - VTE prophylaxis, treatment, and ACS - renal - CrCl less than 30 - anti10a can be monitored, but mainly only in peds, obese, pregnant, renal failure
63
BBW of fonda | CI
epidermal/spinal hematomas + anesthesia CI: severe renal impairment less than 30 - body weight less than 50kg - active major bleeding, bacterial endocarditis, thrombocytopenia
64
Main indications for rivaroxaban? Must take with...
- nonvalvular fib, VTE treatment and prophylaxis | - FOOD to increase BA
65
How is rivaroxaban metabolized?Excreted Avoid use when..
- liver, excreted in urine avoid use if CrCl is less than 15-30,mod/severe hepatic impairment (B, C) and strong 3A4 inducers/inhibitors
66
SE of rivaroxaban | BBW?
- bleeding (reversal agent: adexanet alfa), 4factor PCC - premature dc increase risk of thrombotic events - epidermal/spinal hematoma
67
Indications for apixaban? | Metabolism? Excretion
- nonvalvular fib, VTE treatment and prophylaxis - cyp 3A4/5 PGP (avoid in inhibitors--cins, roles) - excreted in urine
68
SE CI BBW for apixaban
- bleeding, reversal (andexanet) - severe bleeding - premature DC/epidermal, spinal hematomoas
69
Indications for edoxaban?
- valvular fib, VTE TREATMENT ONLY no prphylaxis (given at least 5 days after with IV anticoag)
70
Edoxaban is Metabolized by... Excreted in .... Dialysis?
- cyp 3A4, pgp - renally excreted - only one where dialysis is not effective in removing from blood....less protein binding
71
For nonvalvular afib, edoxaban should not be used when CrCL is...
greater than 95 or less than 15 (for fear of underexposure to the drug, resulting in increased risk of ischemic stroke)
72
Edoxaban SE, CI, and BBW?
- SE: bleeding - CI: Bleeding - BBW: premature dc, epidermal/spinal hematomas
73
Indications for Betrixaban? (BED) How long does it last? Avoid use in...
VTE prophylaxis in hospitalized patients anticoag effect may persist more than 73 hours after discontinuing avoid use in hepatic impairment
74
S/E of betrixaban? CI? BBW
- bleeding - CI in bleeding - premature discontinuation increases the risk of thrombotic events, and the anticoag effect may persist for at least 72 hours - BB: epidermal or spinal hematomas
75
What are the monitoring parameters for rivaroxaban, apixaban, edoxaban, betrixaban?
- PT and aPTT can detect the drug in the plasma, anti 10a, to see the accumulation of the drug, not used for dose adjustments
76
What is the reversal agent for factor 10a?
- andexanet | - only rivaroxban and apixaban are approved for reversal
77
What are the advantages of direct oral anticoags?
rapid onset/offset fewer DDI than warfarin predictable PK lack of regular monitoring
78
Disadvantages of DOACs? - warfarin is the __ - med __ - Uncertainty in __ - Avoided in - DDIs - $$
- warfarin is the standard of care - adherence concerns - uncertainty about dosing (renal dysfunction, extremes in body weight) - avoided in dialysis patients - DDI's Pgp transport utilized and extensive hepatic metabolism

Cardio MT2 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions