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Pharmacology > Anticoagulant Therapy > Flashcards

Anticoagulant Therapy Flashcards

1
Q

Steps of hemostasis 5

A

Vasoconstriction, plt plug, activate clotting cascade, fibrin clot forms, clot retracting and lysis

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2
Q

Primary hemostasis

What it is

A

Occurs sec-min, plt plug in response to injury. Subendothelial collagen that is exposed attracts platelets

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3
Q

Primary hemostasis: promoted by which pro coagulants, causes what to occur

A

VWF, factor 8, ADP

Localized vasoconstriction

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4
Q

Primary hemostasis

What adhered plt do 3

A

Activate to pseudopod shape and release TXA2.
Plt degranulate, releasing chemicals.
Plt aggreg begins, using fibrinogen and VWF

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5
Q

Agents released in degranulation and their roles

5

A

Serotonin and histamine: vasoconstrict. Thromboxane: vasoconstrict and degranulate plt. ADP- adherence and degranulation, cases plt stickiness. Clotting factors 5a, 8a, 9a. Plt factor 4 enhances clot formation

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6
Q

Extrinsic pathway: starts with what, where it connects to final common pathway

A

Thromboplastin. Converts factor 7 to factor 7a. To factor 10. To factor 10a where it connects to intrinsic pathway.

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7
Q

Intrinsic pathway: process start and where it becomes common

A

Collagen, goes from factor: 12 to 12a, 11 to 11a, 9 to 9a, 10 to 10a where it connects

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8
Q

Final common pathway

A

10a to prothrombin becomes thrombin, fibrinogen becomes fibrin

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9
Q

Secondary hemostasis

Process and what it forms

A

Min to hrs. Fibrin clot formation, stabilizes plt plug. End of coag cascade where factors converted to each active form

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10
Q

Which end of hemostasis humans tilt slightly towards

A

More towards coagulation vs anticoagulation

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11
Q

Arterial thrombosis: 3

A

MI, arterial thrombosis, CVA

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12
Q

Venous thrombosis

A

DVT and PE

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13
Q

Natural anticoagulants

What they are and their role 5 total

A

Once coag process activated they regulate process

Prostacyclin, antithrombin 3, heparin, protein c, protein s

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14
Q

What happens in clot retraction and lysis

A

After clot forms it retracts (fibrin strands shorten). Plt trapped in mesh, have actinomyosin like proteins. Begins in mins and most protein free in an hr

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15
Q

Lysis is carried out by what, mediated by what, activated by what
Process

A

Carried by fibrinolytic sys, mediated by plasmin, activ by coagulation and inflammation substances. Plasmin splits fibrin and fibrinogen into FDPs

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16
Q

Oral antiplt aggregation

5

A

Aspirin, ticlopidine, clopidogrel, prasugrel, ticagrelor

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17
Q

IV antiplt therapy 3

A

Abciximab, eptifibatide, tirofiban

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18
Q

Aspirin: what class, moa

A

Cox inhibitor, prevents form of TXA2 and degranulation of platelets. Action is irreversible and for plt life, 10-14d

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19
Q

Aspirin: indication. Dose.

A

Prevention of recurrent ischemic events: stroke, mi, symptomatic pad. 80 mg, 325 mg if active mi

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20
Q

Aspirin: precautions 5

A

Children (Reyes swelling in liver/brain after virus), pregnant, cv disease (bb/ace/diuretic med fx from prostaglandin inhib, mediates vasodil), asthmatics (leukotrienes), inc bleeding w other anticoags (tx- plt)

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21
Q

Ticlid

Name, moa

A

Thienopyridine, blocks ADP receptor on plt and inhib fibrinogen binding

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22
Q

Ticlid
Indication
Use restricted due to which SE

A

Prevents recurrent ischemic events esp if ASA intolerant

Neutropenia, TTP, GI upset, teratogenesis

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23
Q

Plavix

Name and moa

A

Thienopuridine- irreversibly blocks ADP receptor on plt and inhibits fibrinogen binding

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24
Q

Plavix

Indication

A

Recurrent ischemic events: stroke prevent, recent ACS, post PCI

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25
Q

ACS triggers

5

A

HLD, HTN, tobacco use, chronic inflammatory response, infection

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26
Q

Clopidogrel

Which therapy preferable

A

Clopidogrel > aspirin. Dual preferred

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27
Q

Clopidogrel

Precautions

A

Metab by CYP2C19, poor metab, req inc dose. Inhib CYP450. Dose adjust for renal or hepatic disease. Use w other anticoags.

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28
Q

Clopidogrel
Toxicities- most common in who
Tx

A

Inc risk of bleeding (mostly in elderly, underwt, and prev hx stroke/tia). Stop drug (at least temporarily), transfuse plt

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29
Q

Prasugrel (effient)
Comparison to clopidogrel
Popular w who

A

Greater prev of plt agg, reduced risk of MI/in stent thrombosis. Greater risk of bleeding and greater # of fatal events. In clopidogrel non responders

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30
Q

Prasugrel precautions: 5

Dont use when

A

Active bleed, prev stroke/TIA, underwt, older than 75 y/o (dec dose), 4x greater risk of bleed in cv surgery than clopidogrel
Dont use pre cardiac cath

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31
Q

Ticagrelor (brillianta)
MOA
Comparison to clopidogrel

A

Blocks ADP receptors from diff binding site (allosteric)
Greater reduction of death rates post MI r/t vascular causes (MI/stroke). Higher rate of non procedure related bleed and higher fatal intracranial hemorrhage

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32
Q

Ticagrelor
Indication
How its always given

A

Prevent recurrent ischemic events post MI (stroke, ACS, post PCI).
Dual therapy w ASA unless ASA contraindicated

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33
Q

Ticagrelor
Precautions: 4
Contraindications: 2

A

Prec: Hepatic dysfunc, ASA >100mg/d, hold 5 days before surgery, BID dosing compliance issue
Contra: active bleed, hx intracranial hemorrhage

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34
Q

GIIb/IIIa inhibitors
MOA
Uses
3 drugs

A

Blocks IIbIIIa receptor preventing fibrinogen binding. Use: ACS, PCI. Reopro, integrillin, agrastat.

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35
Q

GPIIbIIIa Inhibitors: Abciximab
Indication
If used w heparin do what
2 other defining traits

A

ACS w planned PCI. W hep keep aptt 60-85 sec. most expensive drug, most prolonged effects

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36
Q

GPIIbIIIa: eptifibatide
Indications
Gtt rate based on

A

ACS and/or PCI bolus then gtt. Drip rate based on creatinine level

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37
Q

GP IIB IIIA
Toxicities which/what
Interactions w

A

Bleeding: abciximab (reverse w plt), eptifibatide and tirofiban (d/c drug)
Other antiplt and anticoag drugs potentiate effects

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38
Q

Antiplt therapy post STEMI
What is usually given
What for PCI/stent pts
Fibrinolysis pts

A

ASA as mono lifetime therapy for CAD/prior MI to prevent repeat.
PCI- dual therapy w ASA and other antiplt for one year
Fibrin- ASA for life and at least 14d of clopidogrel

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39
Q

Antiplt peri op
When to d/c and restart
Pt high risk for cv events should do what

A

D/c 7-10 days before. Resume next day post op if hemostasis achieved.
Risk: continue ASA continue through OR, clopidogrel stopped at least 5d before

40
Q

Heparin (unfrac)
What’s in it
MOA

A

Heterogeneous mix of polysaccharide chains.

Activ antirhombin III: inc inhib of thrombin IIa and Factor Xa by 1000 fold

41
Q

Unfrac hep

Uses

A

DVT prophylaxis, VTE tx, ACS, when warfarin started or contraindicated

42
Q

Unfrac hep

DVT prophylaxis dose

A

5000 units sq q8. Poor kidney less frequently. Q12 if neurosurgery and ESRD

43
Q

Unfrac hep

IV infusions based/adjustments

A

Weight based bolus and infusion. Adjusted on aPTT or anti Xa values q6hrs until stable then QD

44
Q

Unfrac hep
Interactions
Drawback of drug

A

Inc risk of bleeding when used w other anticoags/antiplt.

Variable anticoag effects, inability to inhibit clot bound thrombin

45
Q

Unfrac hep

Toxicities

A

Bleed: stop gtt, reverse w protamine. Benign thrombocytopenia or HIT

46
Q

HIT

What it is, type 1

A

Non immune mediated. Benign. Mild plt drop usually within 4d of start of hep tx. Not progressive or assoc w thrombosis

47
Q

HIT type 2

A

Immune mediated. Typical onset. Follows heparin exposure (prophylactic or full), reduce ct to <150k or dec 50% from baseline pre heparin. 5-14d after exposure

48
Q

HIT

Occurs more in who. Typical plt ct.

A

UF > LMWH. Surgery > medical > obstetric

49
Q

HIT
Typical onset
Delayed
Rapid

A

Typical- 66%, 5-14d
Delayed- 3-5%, 2-6 wks
Rapid- 25-30%, hrs to days. D/t residual circulating antibodies from heparin exposure past 100 days

50
Q

HITT
What it is
Which is more common

A

Thrombocytopenia w thromboembolism, 10-25% of cases

Venous 4x more common

51
Q

HITT
Venous
Arterial
Mortality, amputation

A

V: DVT, PE, venous limb gangrene, dural sinuous thrombosis
A: cerebral infarct, limb ischemia, skin necrosis, MI, mesenteric ischemia, adrenal/renal/spinal artery infractions
30% mort, 25% amp rate

52
Q

HIT lab testing

ELISA: what it measures, s/s

A

Measures IgG antibody to heparin PF4 complex. Easy to do. Sens 90% spec 80%

53
Q

HIT lab testing

SRA: what it detects, availability, s/s, dont do what

A

Plt activation. Not readily available. 95%. Confirmatory test. Dont delay tx waiting for result

54
Q

HIT clinical management

A

Stop all drugs known to cause thrombocytopenia. Stop heparin start non hep anticoag (argatroban). Look for hx heparin exposure. Look for hep sources in flush bags/catheters/prophylactic SQ

55
Q

Lmwh

What it is, action, uses

A

Saccharide chains, 5k daltons
Binds w antithrombin III, inhibits factor 10a
DVT prophylaxis, ACS, VTE tx

56
Q

LMWH
Dose depends on
Dose effects checked how

A

Indication of prophylaxis/tx/ACS

Not routinely monitored, can check anti xa levels

57
Q

LMWH
Precautions: 4
Tx if bleed

A

Pregnant (monitor anti xa), obese (wt based dosing), not recc if cr cl <30 ml/min (if no alt reduce dose by 1/2), dont use for spinal surgery pts or w epidurals. Protamine, 60% reversal

58
Q

Fondaparinux (Arixtra)
What it is
MOA
What it doesnt affect

A

Synthetic factor 10a inhib. Binds w anti-thrombin 3 to potentiate xa inhibition 300x. No direct effect on 2a (thrombin)

59
Q

Arixtra indications

A

ACS, PE/DVT prophylaxis, DVT tx

60
Q

Arixtra
Contraindications
Tx of bleeding

A

Cr cl <30 ml/min, spinal anesthesia/lumbar puncture

No known reversal, FFP doesnt work. D/c drug

61
Q

IV direct thrombin IIa inhib
Don’t require what
Examples 6, which is reversible

A

Antithrombin 3

Hirudin, lepirudin, desirudin, hirulog, argatroban (reversible), bivalirudin

62
Q

Direct thrombin inhib

Uses and which specifically for each use 2

A

HIT (argatroban, lepirudin)

PCI (bivalirudin)

63
Q

Direct thrombin inhib

Toxicities, which

A

Bleeding. Lepirudin and desirudin can only be used once d/t anaphylaxis risk

64
Q

Direct thrombin inhib
Interactions
Tx of bleeding

A

Inc bleeding w other anticoags, thrombolytics, or antiplt.

Stop gtt, may respond to combo of: factor 7, FFP, and cryo

65
Q

Warfarin

MOA

A

Interferes w production of vit k dep clotting factors (2, 7, 9, 10). Interferes w carboxylation of natural anticoags protein c and protein s

66
Q

Warfarin

Indications: 4

A

Prevention of thrombosis/embolism in: dvt, afib, mechanical heart valves. Long term tx of vte

67
Q

Warfarin
Dose based on what
INR goal. High risk pts (which 3), goal of what

A

Inr. 2-3. Mechanical valve, previous thrombus, anti-phospholipid syndrome. 2.5-3

68
Q

Warfarin
Overlap w LMWH for how long
Duration of therapy for ___ DVT and PE how long

A

1-2 days

Uncomplicated, 3 months

69
Q

Warfarin
Toxicities: 3
Interactions: 4 that increase effect

A

Bleeding, birth defects, cutaneous necrosis

Inc effect from: amio, cimetidine, tyelenol, phenylbutazone

70
Q

Warfarin
Decreased effect from 5
Precautions 2

A

Sucralfate, cholestyramine, spironolactone, barbiturates, vitamin k foods
Concomitant anti plt therapy and/or nsaid use

71
Q

Warfarin
Sub therapeutic inr:
Super therapeutic inr w/o bleeding:
Reversal/tx of bleeding:

A

Continue same dose, re-check 1-2 weeks
Hold next dose, check in 1 week
Vitamin k oral or iv, ffp

72
Q

Periop warfarin
When it needs to be held
When resumed
Do what for high risk pts

A

5 days before OR to normalize INR. Resume 12-24 hrs postop if hemostasis achieved.
Bridge w heparin until 4-6 hrs of surgery

73
Q

Novel oral anticoags
Also known as what
Where they work
Contraindicated in who and why 2

A

Direct oral anticoags. Enzymatic activity of thrombin and factor 10a. Prosthetic heart valves (greater thrombosis risk) and pregnancy (lack of clinical evidence)

74
Q

Oral direct thrombin inhibitor
Dabigatran (Pradaxa)
MOA
Uses: 4

A

Inactivates circulating and clot bound thrombin (factor Iia). Stroke and embolism prevention in NON-VALVULAR afib. Prevents DVT after hip or knee replacement surgery. Tx PE/DVT.

75
Q

Pradaxa

Lower dose for who: 3

A

Bleeding, elderly, mod-severe renal impairment

76
Q

Pradaxa

Comparison to warfarin based on 2 doses

A

Higher dose- superior to warf in reduction of stroke and embolism w no diff in major bleed. Lower dose non inferior for prevention w a 20% relative risk reduction for major bleed

77
Q

Dabigatran

Advantages 4

A

No routine monitoring needed, predictable pharmacokinetics. Less influenced by diet and drugs. Peak action 1 hr (fast). Short 1/2 life 12-24h in pts w normal renal func

78
Q

Dabigatran
Disadvantages 3
Use what for which cases of bleeding

A

High cost and BID dosing. May req adjustment for renal ins and obesity. No antidote, Fab used if life threat bleed. Non specific pro coagulant agents pt complex conc or factor 7a also can be used in serious bleed.

79
Q

Dabigatran
Disadvantages
2

A

No assay for monitoring of effect. No long term data, some fatal bleed cases

80
Q

No parental versions avail for which inhibitor, moa

A

Direct factor 10a, inactivate circulating and clot bound 10a

81
Q

Xarelto
Class
Uses 3

A

Direct factor 10a inhibitors. Uses: stroke and systemic embolism prevention in non-valvular afib, prevent dvt post hip/knee replacement, tx pe/dvt

82
Q

Xarelto

Comparison to warfarin

A

Non inferior for preventing stroke or embolism. Overal bleed risk about same, decreased risk of intracranial and fatal bleed w rivaroxaban

83
Q

Rivaroxaban

Advantages 5

A

No routine monitoring needed/predictable kinetics, less influenced by diet/drugs,QD, rapid peak 2-4h, short 1/2t 7-11h

84
Q

Rivaroxaban
Disadvantages
3

A

High cost, not rec for VTE proph/tx or secondary prevention w impaired creatinine clearance. No current antidote. Praxbind/10a decoy under investigation, shown to reduce 10a inhibitor activity

85
Q

Rivaroxaban
What for bleeding
No data on

A

Non specific pro coagulant agents (pt complex or 7a) can be used for fatal bleed. No long term data

86
Q

Apixaban
Class
Uses 3

A

Direct factor 10a inhib. Stroke/systemic embolism prevention in non valvular afib, prevent dvt after hip/knee replacement, tx pe/dvt

87
Q

Apixaban
Comparison to ASA in who
Comparison to warfarin

A

Benefit over ASA if not candidate for warfarin.

Superior to warf for prevention of stroke/embolism. Decrease in bleeding risk, ICH, and mortality

88
Q

Apixaban

Advantages 4

A

No routine monitoring needed/predictable, less influence by diet/drugs, fast peak 3h, short 1/2 life 12h

89
Q

Apixaban
Cons
3

A

High cost/bid dose. Dose adjust for age, weight, renal func. No antidote. Praxbind under investigation

90
Q

Apixaban
Use what in serious bleed
No what

A

Pt complex concentrate/factor 7a

No assay to monitor, no long term data

91
Q

Aripazine

What it is and what it does

A

Reversal for oral dabigatran, apixaban, rivaroxaban, sq lovenox, sq fondaparinux

92
Q

Fibrinolytics

Action

A

Plasminogen activators convert plasminogen to plasmin which causes fibronolysis

93
Q

Fibrinolytics

Uses 3

A

Acute STEMI, acute ischemic stroke (within 6 hrs of symptom onset, tpa, urokinase (de-clog CVL, pe)

94
Q

Fibrinolytics

Absolute contraindications 6

A

Previous hemorrhagic stroke, ischemic stroke last 3 months, known intracranial tumor, active internal bleed, suspected aortic dissection, significant closed head/facial trauma last 3 months

95
Q

Fibrinolytics

Relative contraindications 5

A

Severe uncontrolled htn 180/110, severe chronic htn hx, current use anticoags/inr >2.5, known bleeding disorder, non compressible vascular puncture

96
Q

Fibrinolytics

5 more relative contraindications

A

Trauma in 2-4 wks (cpr too), surgery last 3 weeks, recent 2-4 internal bleed, pregnancy, streptokinase- allergy or prior exposure (5d-2yrs)

Pharmacology (19 decks)

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