Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm II Unit II > Drugs Affecting Coagulation > Flashcards

Drugs Affecting Coagulation Flashcards

1
Q

Hemostasis is achieved in what three ways?

A

Vascular contraction (vasospasm)

Platelet adhesion, activation, aggregation

Fibrin formation and reinforcement of the platelet plug (coagulation)

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

What is the common point in the coagulation cascade, where the intrinsic and extrinsic pathways meet?

A

Factor Xa

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

Which factors are in the intrinsic pathway?

A

XII—>XIIa

XI —> XIa

IX —> IXa

X —> Xa (with VIIIa)

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

Which factors are in the extrinsic pathway?

A

III (TF) —> IIIa

VII —> VIIa-TF

X —> Xa

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

Heterogeneous mix of sulfates mucopolysaccharides (large negatively charged molecule)

A

Heparin

Action from a unique pentasaccharide

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

MOA for heparin

A

Activity is dependent on ANTITHROMBIN III

Mainly affects Xa and thrombin

Affects factors IXa, XIa and XIIa as well

Catalyst —> accelerates ATIII activity (x1000)

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

________ competes for binding to heparin and has immediate effect

A

Protamine sulfate

Works b/c it’s a large positive molecule (helps it bind to heparin’s large negative molecule)

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

What are the indications for Heparin use?

A

Anticoagulant for operations or IV catheters

Prophylaxis against thrombosis (DVT/PE)

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

***How is unfractionated heparin administered

A

Exclusively IV

Not IM —> hematoma

Onset of action is IMMEDIATE

Therapeutic target is PTT 2-2.5x normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the adverse effects of Heparin?

A

HEMORRHAGE (true of all anticoagulants)

Allergic reactions

Mild decrease in platelets

HEPARIN-INDUCED THROMBOCYTOPENIA (HIT)

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

What is the reversal agent for Heparin

A

Protamine sulfate (think heParin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Contraindications for heparin use

A

RENAL OR HEPATIC DYSFUNCTION

Don’t use in patients who are:
• Actively bleeding
• Hemophilia or other clotting disorders
• Hypersensitve
• During or after surgery of the brain, spinal cord, or eye
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the names for the Low Molecular Weight Heparins?

A

Enoxaprin

Fondaparinux (a synthetic pentasaccharide)

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

***LMW Heparin is similar to UFH except…

A

Main inhibitory action is on factor Xa (not much effect on thrombin

Can be injected subcutaneously***

Lower incidence of HIT

Protamine sulfate does not completely reverse LMWH and has NO EFFECT on fondaparinux***

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

Bivalirudin is a recombinant form of hirudin, a natural anticoagulant from …

A

Leeches

Highly specific direct inhibitor of thrombin (no AT III)

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

What drug is given as an alternative anticoagulant in patients with HIT?

A

Bivalirudin (IV only)

Can cause hypersensitivity (40%)

Use caution in liver patients

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

Direct inhibitor of thrombin given as an alternative in patients with HIT

A

Argatroban (think “thro(M)Ban”)

Cleared by the liver and given by continuous IV infusion

Use caution in patients with poor liver function

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

***ORAL direct inhibitor of thrombin

A

Dabigatran (Pradaxa)***

Used to prevent stroke in patients with non-valvular a fib

19
Q

***Direct thrombin inhibitor with predictable anticoagulant effects (so not monitored by PTT)

A

Dabigatran***

20
Q

Why does Dabigatran (Pradaxa) have a black box warning?

A

Avoid abrupt d/c without adequate alternative anticoagulant —> increased risk of thrombotic events

21
Q

What is the antidote for Dabigatran (Pradaxa)

A

Idarucizumab (Praxbind)

22
Q

What are the “XaBans”?

A

Direct inhibitors of Factor Xa

Rivaroxaban, Apixaban, Edoxaban, Betrixaban

ORAL

Used for DVT, PE, and future clots (prophylaxis)

23
Q

Rivaroxaban and Apixaban can be used in _______ patients, the other XaBans are for use in _______.

A

R/A —> any patients (been around longer, so more studies)

Other XaBans —> patients with non-valvular afib or critically ill

24
Q

Avoid XaBans in patients with…

A

Liver Disease

Renal Failure

25
Q

***What is the antidote for Direct Inhibitors of Factor Xa (XaBans)?

A

Factor Xa decoy (Andexxa)***

26
Q

***What it’s the MOA for Warfarin

A

Inhibits reduction of vitamin K —> interferes with synthesis of factors II, VII, IX, X, and Proteins C & S***

Protein C&S have shorter 1/2 life so you start to see effect because of these factors first

27
Q

***Why do you have to start Warfarin in combo with heparin?

A

Because it takes 4-5 days to take full effect because it works by inhibiting clotting factor synthesis***

Peak effect after 48 hours, monitored by INR (2-3)

28
Q

Indications for Warfarin use

A

Prevent development of emboli —> DVT, thromboembolism

No effect on already formed thrombi

Given chronically*** (oral)

29
Q

**ADVERSE EFFECTS OF WARFARIN****

A

Hemorrhage, esp into the bowel

***Reversal of action is with VITAMIN K (takes time to work) or FRESH FROZEN PLASMA

Quickly reduces levels of Protein C (short half-life) —> increased chance for warfarin-induced thrombosis —> CUTANEOUS NECROSIS AND INFARCTION

Must co-administer with heparin for first 5 days

30
Q

Contraindications for Warfarin**

A

Pregnancy - Category X (crosses placenta, teratogenic)

Drug interactions (lots!)

31
Q

What are the four steps in Fibrinolysis?

A

1) tPA released from healthy endothelium
2) Circulating tPA is inactivated by PAI
3) If not bound, tPA cleaves plasminogen into plasmin
4) Plasmin degrades the fibrin threads of the clot into soluble degradation products and removes the clot

32
Q

What is the MOA for Fibrinolytic Agents?

A

Convert plasminogen to plasmin (lyses thrombus from within)

Given IV or intra-arterially for the lysis of clots, in MI, PE, DVT, or arterial thrombosis

Can cause serious bleeding (if so, give aminocaproic acid)

33
Q

**What are the Thrombolytics drugs?

A

Alteplase (Tissue plasminogen activator or t-PA)

Tenecteplase

These guys are CLOT-SELECTIVE

34
Q

How is Tenecteplase different from Alteplase?

A

Multiple point mutant of tPA (longer plasma half-life)

More fibrin specific and resistant to PAI-1 than standard tPA

Becoming the fibrinolytic agent of choice

35
Q

________ drugs directly activate plasminogen but are not clot-fibrin specific (so they do generalized systemic fibrinolysis

A

Urokinase drugs

Streptokinase and Anistreplase

OFF-MARKET**

36
Q

What drugs are useful in bleeding disorders AND reversal of fibrinolytic therapy?

A

Antifibrinolytics: Aminocaproic Acid, Tranexamic Acid

Completely inhibit plasminogen activation

DO NOT USE IN PATIENTS WITH DIC or GU BLEEDING

37
Q

**What is the MOA for Aspirin

A

IRREVERSIBLE INHIBITION of COX enzyme —> reduced prostaglandin synthesis (TXA2) —> reduced platelet aggregation

Lasts the life of the platelet (7-10 days)

38
Q

**Indications for Aspirin use

A

A single dose may prolong bleeding time for DAYS

May be useful in patients at risk for embolisms

SECONDARY PREVENTION OF CV EVENTS in patients with established CVD

39
Q

**What is the MOA for Clopidigrel, Ticlopidine, and Prasugrel?

A

IRREVERSIBLY BLOCKS THE ADP RECEPTOR ON PLATELETS —> reduced platelet aggregation

40
Q

How are Clopidigrel, Ticlopidine, and Prasugrel used?

A

***In patients who are allergic to aspirin (less GI bleeding)

To reduce thrombotic events following MI/stroke

**DOC for preventing thrombosis in patients undergoing placement of coronary stents

41
Q

Clopidigrel is metabolized in its active form by CYP2C19, so use with caution when…

A

Using drugs that impair CYP2C19 function like OMEPRAZOLE

42
Q

***What is the MOA for Abciximab, Eptifibatide, Tirofiban?

A

Inhibitors of GPIIb/IIIa receptor —> reduced platelet aggregation***

Abciximab is an antibody***
Eptifibatide and Tirofiban is an analog of carboxy end of fibrinogen

43
Q

*****Indications for GPIIb/IIIa receptor inhibitors

A

Combined with heparin for percutaneous coronary intervention

Given IV in patients undergoing ANGIOPLASTY, ATHERECTOMY, AND STENT PLACEMENT

44
Q

What is Vorapaxar?

A

Antagonist of the protease-activated receptor-1, the major thrombin receptor on human platelets

Potently inhibits thrombin-related platelet aggregation, used in prophylaxis in patients with previous MI or PAD

Given orally, long 1/2 life

Contraindicated in patients with Hx of stroke/TIA

Pharm II Unit II (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions