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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
ACS triggers | 5
HLD, HTN, tobacco use, chronic inflammatory response, infection
26
Clopidogrel | Which therapy preferable
Clopidogrel > aspirin. Dual preferred
27
Clopidogrel | Precautions
Metab by CYP2C19, poor metab, req inc dose. Inhib CYP450. Dose adjust for renal or hepatic disease. Use w other anticoags.
28
Clopidogrel Toxicities- most common in who Tx
Inc risk of bleeding (mostly in elderly, underwt, and prev hx stroke/tia). Stop drug (at least temporarily), transfuse plt
29
Prasugrel (effient) Comparison to clopidogrel Popular w who
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
30
Prasugrel precautions: 5 | Dont use when
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
31
Ticagrelor (brillianta) MOA Comparison to clopidogrel
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
32
Ticagrelor Indication How its always given
Prevent recurrent ischemic events post MI (stroke, ACS, post PCI). Dual therapy w ASA unless ASA contraindicated
33
Ticagrelor Precautions: 4 Contraindications: 2
Prec: Hepatic dysfunc, ASA >100mg/d, hold 5 days before surgery, BID dosing compliance issue Contra: active bleed, hx intracranial hemorrhage
34
GIIb/IIIa inhibitors MOA Uses 3 drugs
Blocks IIbIIIa receptor preventing fibrinogen binding. Use: ACS, PCI. Reopro, integrillin, agrastat.
35
GPIIbIIIa Inhibitors: Abciximab Indication If used w heparin do what 2 other defining traits
ACS w planned PCI. W hep keep aptt 60-85 sec. most expensive drug, most prolonged effects
36
GPIIbIIIa: eptifibatide Indications Gtt rate based on
ACS and/or PCI bolus then gtt. Drip rate based on creatinine level
37
GP IIB IIIA Toxicities which/what Interactions w
Bleeding: abciximab (reverse w plt), eptifibatide and tirofiban (d/c drug) Other antiplt and anticoag drugs potentiate effects
38
Antiplt therapy post STEMI What is usually given What for PCI/stent pts Fibrinolysis pts
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
39
Antiplt peri op When to d/c and restart Pt high risk for cv events should do what
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
Heparin (unfrac) What's in it MOA
Heterogeneous mix of polysaccharide chains. | Activ antirhombin III: inc inhib of thrombin IIa and Factor Xa by 1000 fold
41
Unfrac hep | Uses
DVT prophylaxis, VTE tx, ACS, when warfarin started or contraindicated
42
Unfrac hep | DVT prophylaxis dose
5000 units sq q8. Poor kidney less frequently. Q12 if neurosurgery and ESRD
43
Unfrac hep | IV infusions based/adjustments
Weight based bolus and infusion. Adjusted on aPTT or anti Xa values q6hrs until stable then QD
44
Unfrac hep Interactions Drawback of drug
Inc risk of bleeding when used w other anticoags/antiplt. | Variable anticoag effects, inability to inhibit clot bound thrombin
45
Unfrac hep | Toxicities
Bleed: stop gtt, reverse w protamine. Benign thrombocytopenia or HIT
46
HIT | What it is, type 1
Non immune mediated. Benign. Mild plt drop usually within 4d of start of hep tx. Not progressive or assoc w thrombosis
47
HIT type 2
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
HIT | Occurs more in who. Typical plt ct.
UF > LMWH. Surgery > medical > obstetric
49
HIT Typical onset Delayed Rapid
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
HITT What it is Which is more common
Thrombocytopenia w thromboembolism, 10-25% of cases | Venous 4x more common
51
HITT Venous Arterial Mortality, amputation
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
HIT lab testing | ELISA: what it measures, s/s
Measures IgG antibody to heparin PF4 complex. Easy to do. Sens 90% spec 80%
53
HIT lab testing | SRA: what it detects, availability, s/s, dont do what
Plt activation. Not readily available. 95%. Confirmatory test. Dont delay tx waiting for result
54
HIT clinical management
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
Lmwh | What it is, action, uses
Saccharide chains, 5k daltons Binds w antithrombin III, inhibits factor 10a DVT prophylaxis, ACS, VTE tx
56
LMWH Dose depends on Dose effects checked how
Indication of prophylaxis/tx/ACS | Not routinely monitored, can check anti xa levels
57
LMWH Precautions: 4 Tx if bleed
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
Fondaparinux (Arixtra) What it is MOA What it doesnt affect
Synthetic factor 10a inhib. Binds w anti-thrombin 3 to potentiate xa inhibition 300x. No direct effect on 2a (thrombin)
59
Arixtra indications
ACS, PE/DVT prophylaxis, DVT tx
60
Arixtra Contraindications Tx of bleeding
Cr cl <30 ml/min, spinal anesthesia/lumbar puncture | No known reversal, FFP doesnt work. D/c drug
61
IV direct thrombin IIa inhib Don't require what Examples 6, which is reversible
Antithrombin 3 | Hirudin, lepirudin, desirudin, hirulog, argatroban (reversible), bivalirudin
62
Direct thrombin inhib | Uses and which specifically for each use 2
HIT (argatroban, lepirudin) | PCI (bivalirudin)
63
Direct thrombin inhib | Toxicities, which
Bleeding. Lepirudin and desirudin can only be used once d/t anaphylaxis risk
64
Direct thrombin inhib Interactions Tx of bleeding
Inc bleeding w other anticoags, thrombolytics, or antiplt. | Stop gtt, may respond to combo of: factor 7, FFP, and cryo
65
Warfarin | MOA
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
Warfarin | Indications: 4
Prevention of thrombosis/embolism in: dvt, afib, mechanical heart valves. Long term tx of vte
67
Warfarin Dose based on what INR goal. High risk pts (which 3), goal of what
Inr. 2-3. Mechanical valve, previous thrombus, anti-phospholipid syndrome. 2.5-3
68
Warfarin Overlap w LMWH for how long Duration of therapy for ___ DVT and PE how long
1-2 days | Uncomplicated, 3 months
69
Warfarin Toxicities: 3 Interactions: 4 that increase effect
Bleeding, birth defects, cutaneous necrosis | Inc effect from: amio, cimetidine, tyelenol, phenylbutazone
70
Warfarin Decreased effect from 5 Precautions 2
Sucralfate, cholestyramine, spironolactone, barbiturates, vitamin k foods Concomitant anti plt therapy and/or nsaid use
71
Warfarin Sub therapeutic inr: Super therapeutic inr w/o bleeding: Reversal/tx of bleeding:
Continue same dose, re-check 1-2 weeks Hold next dose, check in 1 week Vitamin k oral or iv, ffp
72
Periop warfarin When it needs to be held When resumed Do what for high risk pts
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
Novel oral anticoags Also known as what Where they work Contraindicated in who and why 2
Direct oral anticoags. Enzymatic activity of thrombin and factor 10a. Prosthetic heart valves (greater thrombosis risk) and pregnancy (lack of clinical evidence)
74
Oral direct thrombin inhibitor Dabigatran (Pradaxa) MOA Uses: 4
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
Pradaxa | Lower dose for who: 3
Bleeding, elderly, mod-severe renal impairment
76
Pradaxa | Comparison to warfarin based on 2 doses
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
Dabigatran | Advantages 4
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
Dabigatran Disadvantages 3 Use what for which cases of bleeding
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
Dabigatran Disadvantages 2
No assay for monitoring of effect. No long term data, some fatal bleed cases
80
No parental versions avail for which inhibitor, moa
Direct factor 10a, inactivate circulating and clot bound 10a
81
Xarelto Class Uses 3
Direct factor 10a inhibitors. Uses: stroke and systemic embolism prevention in non-valvular afib, prevent dvt post hip/knee replacement, tx pe/dvt
82
Xarelto | Comparison to warfarin
Non inferior for preventing stroke or embolism. Overal bleed risk about same, decreased risk of intracranial and fatal bleed w rivaroxaban
83
Rivaroxaban | Advantages 5
No routine monitoring needed/predictable kinetics, less influenced by diet/drugs,QD, rapid peak 2-4h, short 1/2t 7-11h
84
Rivaroxaban Disadvantages 3
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
Rivaroxaban What for bleeding No data on
Non specific pro coagulant agents (pt complex or 7a) can be used for fatal bleed. No long term data
86
Apixaban Class Uses 3
Direct factor 10a inhib. Stroke/systemic embolism prevention in non valvular afib, prevent dvt after hip/knee replacement, tx pe/dvt
87
Apixaban Comparison to ASA in who Comparison to warfarin
Benefit over ASA if not candidate for warfarin. | Superior to warf for prevention of stroke/embolism. Decrease in bleeding risk, ICH, and mortality
88
Apixaban | Advantages 4
No routine monitoring needed/predictable, less influence by diet/drugs, fast peak 3h, short 1/2 life 12h
89
Apixaban Cons 3
High cost/bid dose. Dose adjust for age, weight, renal func. No antidote. Praxbind under investigation
90
Apixaban Use what in serious bleed No what
Pt complex concentrate/factor 7a | No assay to monitor, no long term data
91
Aripazine | What it is and what it does
Reversal for oral dabigatran, apixaban, rivaroxaban, sq lovenox, sq fondaparinux
92
Fibrinolytics | Action
Plasminogen activators convert plasminogen to plasmin which causes fibronolysis
93
Fibrinolytics | Uses 3
Acute STEMI, acute ischemic stroke (within 6 hrs of symptom onset, tpa, urokinase (de-clog CVL, pe)
94
Fibrinolytics | Absolute contraindications 6
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
Fibrinolytics | Relative contraindications 5
Severe uncontrolled htn 180/110, severe chronic htn hx, current use anticoags/inr >2.5, known bleeding disorder, non compressible vascular puncture
96
Fibrinolytics | 5 more relative contraindications
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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