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N221 exam 1 and 2 > Anticoagulation Meds > Flashcards

Anticoagulation Meds Flashcards

1
Q

Anticoagulation

A

Suppression of clot formation from getting bigger

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2
Q

Stage one: coagulation

A

Platelet plug formation:
platelet aggregation starts when platelets come in contact with collagen at the site of damaged blood vessels

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3
Q

Stage two: coagulation

A

Production of fibrin to reinforce the platelet plug

Clotting cascade begins when clot factors turn into their active forms

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4
Q

How do we prevent excess clotting?

A

Body has antithrombin III

*protein that binds with clotting factors and inhibits their activities “turning off” clotting cascade

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5
Q

Arterial thrombosis

A

Local issue

Platelets will adhere to a damaged arterial wall

The platelets released ADP and TXA2 attracting additional platelets forming the plug

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6
Q

Venous thrombosis

A

Systemic issue

Develops at sites where blood flow is stagnant
*this intiates coagulation cascade leading to production of fibrin
The fibrin traps RBCs and platelets forming a thrombus

Thrombi have tails and may break off causing an emboli (systemic issue)

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7
Q

Two main med routes for anticoagulation

A

IV/SQ:
-heparin (IV,SQ, po not common)
-enoxaparin (Lovenox)

PO:
-warfarin (Coumadin)
-dabigatran (Pradaxa)

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8
Q

Heparin (how it works)

A

Binds with antithrombin II increasing ability to interact with inactive thrombin

Helps antithrombin III inactivate clot factors

Heparin only suppresses formation of further fibrin and clost

Injection is quick acting but PO could take days to work

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9
Q

Why does Heparin free floating amount vary hour to hour

A

Bind with many different elements

So continuous monitoring is imperative

The half-life is short : 1.5hrs

So you have to stop it and check 1.5 hrs later

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10
Q

Reasons for heparin use

A

PE
anticoagulant for pregnancy
DVT
Open heart surgery
Renal dialysis
Post-op for DVT prevention
DIC
AMI
Stroke

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11
Q

Heparin SE/AR

A

SE:
Hemorrhage
Osteoporosis (long term use)(years)

AR:
Heparin-induced thrombocytopenia (decreased platelets)
Hypersensitivity reactions (made from animal tissue)

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12
Q

Heparin warnings/cautions

A

Extreme caution for pt showing likelihood of bleeding profusely:
*hemophilia=trouble clotting
*increased capillary permeability
*dissecting aneurysm
*peptic ulcer disease
*severe HTN
*spontaneously threatened abortion
*severe disease of kidney/liver

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13
Q

Heparin antidote

A

Protamine sulfate

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14
Q

Labs to monitor for heparin

A

Monitor the aPTT

Normal = 40secs

Therapeutic: 1.5-2 times normal or 60-80secs

Evaluate q4-6 hours

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15
Q

LMWHs
Low-molecular-weight heparins

A

Can be utilized at home and doesnt require as much monitoring after lab values level out

Ex: enoxaparin (Lovenox)

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16
Q

Warfarin (anticoagulation)

A

warfarin (Coumadin)
ORAL

Supppresses coagulation by acting as an antagonist to VIT K therfore inhibiting clot factors and prothrombin
Bc of this the antidote to Caoumadin OD or high blood levels is VIT K

17
Q

warfarin use

A

Delay action

Will not work on clotting factors already existing in body
Must wait until these clotting factors dissipate
(6hrs —2.5days)

May take t days to reach therapeutic effects and may be seen 2-5 days upon discontinuing the med

DOC for long-term suppression of clotting
*usually start on heparin and then get slowly switched to warfarin for at home use

18
Q

Warfarin lab test

A

Monitor PT

INR should be the ultimate lab determination of warfarin therapy

Normal INR <1.1

Therapeutic levels 2-3 but can be 3-4.5 in others

Takes 5-6 days for the INR to adjust to dose

19
Q

Warfarin drug reactions

Which drug heparin or warfarin more likely to bleed

When to check blood for iv and sq

A

It has alot of them

More likely to bleed on coumadin than heparin

Draw labs 5 hrs after iv injection and 24 hrs after SQ injection or youll get a false reading

20
Q

Warfarin SE/AR

A

SE:
Hemorrhage
Red-orange color urine

AR:
Fetal hemorrhage and teratogenesis (if crosses placenta)
Alopecia

21
Q

Other PO anticoagulants

A

Dont require labs but too expensive for insurances to pay

Direct thrombin inhibitors

Do not require PT/INR testing

DVT and PE prevention

A-fib clot formation prevention

22
Q

Antiplatelets

A

Prevent clot from happening

Suppress platelet aggregation

Platelet cores are the bulk of the arterial thrombus

23
Q

3 groups of anti-platelets

A

Aspirin

ADP receptor antagonists

GP llb/llla receptor antagonists

24
Q

Asprinin

A

Suppresses platelet aggregation by inhibiting COX 1&2

Mainly used for prophylaxis for AMI

Low dosage (81mg) sufficient but up to 325mg can be utilized

Enteric-coated to prevent gastric problems

25
Q

ADP
Adenosine Diphosphate Receptor antagonists

A

Irreversible blockade of ADP receptors on platelet surface prevent aggregation

26
Q

Meds within the ADP class

A

Clopidogrel (Plavix) (usually taken during AMI)

ticlopidine (Ticlid) (post AMI)

Same precautions as ASA

27
Q

Glycoprotein GP llb/llla receptor antagonists

A

Super aspirins

Most effective anti-platelet drugs

Administered IV and combined with ASA and low-dose heparin

TX is very expensive

28
Q

What does GP llb/llla do

A

Reversble blockade of platelet GP llb/llla receptors

Inhibits the final step in platelet aggregation

Utilized in short-term to prevent ischemic. Events in pt with acute coronary syndrome (ACS)(cardiac event) and those undergoing PTCA

29
Q

Thrombolytic meds how they work
(Antiplatelets)

A

Break apart existing clots

Utilized with AMI and stroke therapy

30
Q

Thrombolytic medications
Antiplatelets

A

Streptokinase (animal product so can cause allergic reactions)

tPA (Alteplase) synthetic so no allergic reactions (most common)

31
Q

Thrombolytics absolute and relative contraindications

A

GI bleed
Hypertension
Recent interal bleed
CVA
Head surgery
Recent trauma
Arteriovenous malformation
Cerebrovascular disease
CPR in last 10 days
Left heart thrombus
Pericarditis
Subacute bacterial endocarditis

N221 exam 1 and 2 (11 decks)

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