Brainscape's Knowledge GenomeTM

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


See full index

IHO Week 6 > Thrombolytics, Anticoagulants and Anti-Platelet Drugs > Flashcards

Thrombolytics, Anticoagulants and Anti-Platelet Drugs Flashcards

1
Q

What is the principle complication of anticoagulant therapy?

A

BLEEDING!!

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

When do we interfere with hemostasis?

A
  • Treat bleeding disorders due to deficiencies and disease, etc.
  • Prevention and treatment of thrombosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the thrombosis that we prevent and treat?

A
  1. Venous thrombosis (life threatening, esp. in lung)
    - Inherited disorders characterized by tendency to form thrombi
    - Increased risk due to prolonged bed rest, surgery, cancer, atrial fibrillation, etc.
  2. Arterial thrombosis
    - Platelet activation is central
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the therapeutic uses of thrombolytics, anticoagulants and anti-platelet drugs?

A
  • Venous thromboembolism
  • Unstable angina
  • Acute myocardial infarction
  • Stroke
  • Prevent thrombosis during angioplasty and cardiopulmonary bypass
  • Etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the stages of clot formation?

A
  1. Platelet
  2. Activated platelet
  3. Fibrinogen
  4. Fibrin clot
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the four stages of hemostasis?

A

Phase I: Vascular constriction limits the flow of blood to the area of injury
Phase II: Platelets become activated and aggregate at the site of injury, forming a temporary, loose platelet plug (Primary Hemostasis)
Phase III: A fibrin mesh (also called the clot) forms and entraps the plug (Secondary Hemostasis)
Phase IV: The clot is dissolved in order for normal blood flow to resume following tissue repair

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

Do platelets have COX2?

A

NO

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

Can platelets make more COX?

A

NO

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

Can endothelial cells make more COX?

A

YES

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

Why don’t the other NSAIDs work well as anti-platelet agents?

A

NSAIDs are irreversible!! Aspirin is not!

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

What new anti-platelet drugs will be coming?

A
  • Inhibitors of PAR-1, the major thrombin receptor on platelets (Vorapaxar - indicated for reduction of thrombotic cardiovascular events in pts. with history)
  • Reversible inhibitors of ADP receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What helps convert fibrinogen to fibrin?

A

Thrombin!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What enzyme converts prothrombin to thrombin (IIa)

A

Xa

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

How does Fibrinogen become Fibrin?

A

Fibrinogen (little molecule) sticks to platelets — (thrombin - IIa) –> Fibrin (crosslinked fibrinogen)

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

What does Antithrombin do and how does it relate to treatment?

A
  • Antithrombin inactivates thrombin!

- We want to make antithrombin work better so we can get rid of thrombin and stop the fibrin clot from forming

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

What test can you use to measure the intrinsic pathway?

A

aPTT

17
Q

How does the aPTT work?

A
  • Recalcified plasma normally clots in 2-4 minutes
  • If you add negatively charged PL and particulates, Factor XII is activated and it clots faster –> activated partial thromboplastin time
  • If the aPTT is prolonged (and PT normal), then the person is considered to have a defect in the intrinsic pathway
  • Normal PTT times require the presence of the following coagulation factors: I, II, V, VIII, IX, X, XI & XII
18
Q

What drug is PTT used to monitor?

A

Heparin!

19
Q

What factors does Heparin affect?

A

Factor II & X

20
Q

What tests do you use to measure the extrinsic pathway?

A

PT and derived INR

21
Q

How does PT and derived INR work?

A
  • Recalcified plasma clots in 12-14 seconds if you add thromboplastin (TF + phospholipids)
  • If PT is prolonged (and aPTT normal), then the person has a defect in the extrinsic pathway
  • PT measures factors I (fibrinogen), II (prothrombin), V, VII, and X
22
Q

What is Factor I?

A

Fibrinogen

23
Q

What is Factor II?

A

Prothrombin

24
Q

If aPTT and PT prolonged. . .

A

. . .there is a defect in the common pathway

25
Q

Why do you need to give heparin early on while warfarin is taking effect?

A

You need to give Heparin early on so that coagulation is controlled while warfarin taking effect. Protein C and S are inhibited before Factors 2, 7, 9 and 10 - this makes blood hypercoagulable before the INR starts to increase. Warfarin has a narrow therapeutic index.

26
Q

What is the more active form of Warfarin?

A

S- form (it’s metabolized by different cytochromes than R- isoform)

27
Q

What affects the susceptibility of vitamin K reductase (VKORC1) to warfarin-induced inhibition?

A

Polymorphisms in the C1 subunit of vitamin K reductase (VKORC1). These polymorphisms can influence warfarin dosage requirements [affect warfarin pharmacodynamics]

28
Q

What other polymorphisms can affect warfarin pharmacokinetics?

A

Common genetic polymorphisms in CYP2C9 can influence warfarin metabolism – 30% are slow metabolizers

29
Q

How can polymorphisms influence dosage?

A

Differences like these can require anywhere from 20-70% or more change in dosage in different people.

30
Q

What’s importnat to know about warfarin??

A

MANY MANY DRUG INTERACTIONS

31
Q

What are pharmacokinetic properties?

A

Absorption, Distribution, Elimination (what body does to drug)

32
Q

What is a pharmacodynamic property?

A

Site of action (what drug does to the body)

33
Q

What are pharmacokinetics?

A
  • Absorption, distribution, metabolism, and elimination (ADME)
  • For oral anticoagulants pharmacokinetic drug interactions are primarily due to:
  • –Enzyme induction
  • –Enzyme inhibition
  • –Reduced plasma protein binding
34
Q

What are pharmacodynamics?

A
  • Biochemical or physiological effects of drugs and their mechanism of action
  • Individuals vary in the magnitude of their response to the same concentration of drug
  • For oral anticoagulants, pharmacodynamic drug interactions are primarily due to:
  • –Reduced clotting factor synthesis
  • –Competitive antagonism with Vitamin K
  • –Hereditary resistance to oral anticoag.
35
Q

What do you do if a patient has BLEEDING side effect from TOO MUCH WARFARIN?

A
  • Stop the drug
  • Add Vitamin K
  • -Phytonadione (vitamin k1)
  • -Or prothrombin complex concentrates
  • -Or recombinant factor VIIa
  • -Or. . .

IHO Week 6 (16 decks)

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