Clotting

Question 1

what happens during primary hemostasis?

Answer 1

activation of platelets

Question 2

What happens when blood vessels are damaged?

Answer 2

They activate platelets and release
*ADP
*Epinephrine
*Collagen
*Thrombin
*Prostaglandins
*Thromboxane synthase

Question 3

what is secondary hemostasis?

Answer 3

Formation of the fibrin clot

Question 4

How is the fibrin clot activated

Answer 4

From the intrinsic or extrinsic pathway

Question 5

How is the intrinsic pathway activated

Answer 5

activated as a result of blood trauma or vessel damage ( damage happens inside)

Question 6

How is the extrinsic pathway activated

Answer 6

stimulated by traumatized tissue or vascular wall (damage happens outside)

Question 7

Both intrinsic and extrinsic pathways result in activated

Answer 7

factor X.

Question 8

Activated factor X converts inactive prothrombin to

Answer 8

active thrombin

Question 9

Thrombin cleaves inactive fibrinogen to

Answer 9

fibrin

Question 10

Fibrin monomers aggregate creating a cross-linked .

Answer 10

clot

Question 11

what is the factor chain for the intrinsic pathway

Answer 11

12-> 12a-11-> 11a->9,->9a= 8a-> 10->10a

Question 12

what is the factor chain for the extrinsic pathway

Answer 12

…

Question 12

Clotting is limited to the injured site by

Answer 12

antithrombin III.

Question 13

Antithrombin III binds to…

Answer 13

thrombin and inactivates it.

Question 14

what is mechanism 2 of clot control?

Answer 14

The evolving fibrin clot traps surrounding thrombin in it. This thrombin is inactivated.

Question 15

what is mechanism3 of clot control?

Answer 15

thrombomodulin/thrombin complex which activate protein c

Question 16

what happens when protein c is activated?

Answer 16

Activated protein C complexes with protein S

Question 17

what is plasminogen?

Answer 17

an inactive plasma compound

Question 18

what happens when tPA is released from healing tissue

Answer 18

• The plasminogen is activated and becomes plasmin.
• The plasmin dissolves the clot and inactivates other factors in the clotting cascade

Question 19

heparin’s MOA

Answer 19

Potentiates the action of antithrombin III
Increases the affinity of antithrombin III for thrombin by a factor of 1000
- Increased action of antithrombin III results in excess binding of thrombin. - No thrombin available to cleave fibrinogen
No new clots are formed. *Also inhibits some other clotting factors in the cascade
*Half-life 1 to 2 hours

Question 20

what is heparin used for

Answer 20

DVT, PE prophylaxis.. helps the clot not get bigger

Question 21

heparin monitoring is done how?

Answer 21

PTT (in patient), outpt ask about bleeding

Question 22

LMWH

Answer 22

Dalteparin (Fragmin®) *Tinzaparin (Innohep®) *Enoxaparin (Lovenox®) *Fondaparinux (Arixtra®)

Question 23

Heparin adverse effects

Answer 23

bleeding- (bruising, in urine, gums, vomit, stool)
peripheral neuropathy
priapism- erection sustained > 4 hrs
heparin induced thrombocytopenia

Question 24

Heparin drug interactions

Answer 24

*Digoxin, tetracycline, antihistamines, IV nitroglycerin decrease effect of heparin *NSAID, ASA, dipyridamole, dextran and hydroxychloroquine will potentiate heparin.

Question 25

what labs are checked for heparin

Answer 25

PTT platelet H/H

Question 26

Thrombin inhibitors examples and what do they do?

Answer 26

*Argatroban (Novastan®), dabigatran (Pradaxa®) Inhibits thrombin induced reactions *Fibrin formation, activation of factors V, VIII, XIII, and protein C, and platelet activation

Question 27

Argatroban Indication and dosing?

Answer 27

Dosing –2 mcg/kg/min–Indication *Prevention and treatment of thrombosis in heparin induced thrombocytopenia

Question 28

Dabigatran (Pradaxa®) indicated for, dose?

Answer 28

oral Indicated for stroke and embolic risk reduction in nonvalvular a-fib 150 mg BID with normal renal function –75 mg BID Cr Clearance 15–30 mL/min

Question 29

When converting from warfarin to dapigatran, overlap________ based on renal function

Answer 29

1–3 days

Question 30

When converting from dabigatran to warfarin, time delay ______ based on renal function

Answer 30

12–24 hours

Question 31

Bivalirudin (Angiomax®) is what?

Answer 31

A Thrombin inhibitor.

Question 32

Bivalirudin (Angiomax®) indicated for?

Answer 32

Indicated for PCI or PCTA Used concomitantly with aspirin

Question 33

What is the reversal agent for Pradaxa?

Answer 33

Idarucizumab(Praxbind®)

Question 34

what do factor Xa direct inhibitors do

Answer 34

Act directly upon thrombin without using antithrombin III as a mediator

Question 35

what do factor Xa indirect inhibitors do

Answer 35

Acts through antithrombin III

Question 36

Factor Xa Inhibitors are used for

Answer 36

–Prophylaxis of venous thrombosis –Arterial thrombosis –Thrombotic CVA –Cancer-related thromboembolism

Question 37

*Indirect Xa inhibitors meds

Answer 37

Fondaparinux (Arixtra®), idraparinux–Sulodexide (Vessel Due®), dermatan sulfate

Question 38

Direct Xa inhibitors

Answer 38

–Apixaban (Eliquis®), otamixaban, rivaroxaban (Xarelto®)

Question 39

Apixaban

Answer 39

*Indicated for nonvalvular a-fib and stroke risk reduction *Prophylaxis of DVT/PE following hip or knee surgery

Question 40

Rivaroxaban

Answer 40

Indicated for–Stroke and systemic embolism reduction in nonvalvular a-fib –Treatment of DVT, PE, and risk reduction 6 months post dx–DVT prophylaxis for knee and hip surgical patients

Question 41

Warfarin MOA

Answer 41

Inhibits the conversion of prothrombin to thrombin Interferes with hepatic synthesis of vitamin k Half life of 42 hrs

Question 42

Dosing of warfarin

Answer 42

Begin @ 5-15 mg/day for 2-5 days

Question 43

Warfarin adverse effects

Answer 43

Bleeding Anorexia, nausea, vomiting, diarrhea, abd cramps Adrenal insufficiency Agranulocytosis Hepatotoxicity

Question 44

Warfarin drug interactions

Answer 44

Protein binding effect

Question 45

Lab eval for Warfarin

Answer 45

PT/INR H/H

Question 46

Warfarin contraindications

Answer 46

Sever liver or kidney disease( no erythropoietin) Uncontrolled bleeding GI ulcers Malignant hypertension Pregnancy

Question 47

Glycoprotein IIb/IIa inhibition effect what part of clotting

Answer 47

Primary clotting

Question 48

Glycoprotein IIb/IIa examples

Answer 48

Abciximab, eptifibatide, tirofiban Used in cath lab, unstable angina

Question 49

Dipyridamole/ASA (Aggrenox) MOA

Answer 49

Inhibits ADP receptors that activate platelets in the first place - twice as effective as ASA alone for TIA but higher cost

Question 50

Clopidogrel (plavix) MOA

Answer 50

Blocks ADP receptor 75 mg once daily After stents CVA prophylaxis

Question 51

Plaviz adverse effects

Answer 51

Chest pain, edema, hypertension Headache dizziness Rash pruritus purpura Arthralgia and back pain Neutropenia, agranulocytosis in <1% of patients

Question 52

Plavix interactions

Answer 52

Substrate of cytochrome p450 2c19 Cyp2c19 inhibitors can decrease efficacy PPI’s are inhibitor (except pantoprazole protonix, fluoxetine(Prozac), ketoconazole(nizoral)

Question 53

Plavix lab eval

Answer 53

H/H WBC diff Platelets LFT as indicated

Question 54

Prasurgrel (Effients)

Answer 54

More effective then plavix but more bleeding risk Less dependent on 2c19 for metabolism

Question 55

Who should you not give effient to

Answer 55

Prior stroke or TIA Over the age of 75

Question 56

ASA MOA

Answer 56

Arachidonic acid is derived from membrane phospholipid Cyclooxygenase acts on the acid and converts to PGH2

Question 57

PGH2 acts in 2 ways

Answer 57

Promotes and inhibits clotting

Question 58

ASA inhibits action of

Answer 58

Cyclooxygenase