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pharm- pace > Clotting > Flashcards

Clotting Flashcards

1
Q

what happens during primary hemostasis?

A

activation of platelets

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2
Q

What happens when blood vessels are damaged?

A

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

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3
Q

what is secondary hemostasis?

A

Formation of the fibrin clot

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4
Q

How is the fibrin clot activated

A

From the intrinsic or extrinsic pathway

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5
Q

How is the intrinsic pathway activated

A

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

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6
Q

How is the extrinsic pathway activated

A

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

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7
Q

Both intrinsic and extrinsic pathways result in activated

A

factor X.

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8
Q

Activated factor X converts inactive prothrombin to

A

active thrombin

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9
Q

Thrombin cleaves inactive fibrinogen to

A

fibrin

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10
Q

Fibrin monomers aggregate creating a cross-linked .

A

clot

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11
Q

what is the factor chain for the intrinsic pathway

A

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

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12
Q

what is the factor chain for the extrinsic pathway

A

…

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12
Q

Clotting is limited to the injured site by

A

antithrombin III.

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13
Q

Antithrombin III binds to…

A

thrombin and inactivates it.

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14
Q

what is mechanism 2 of clot control?

A

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

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15
Q

what is mechanism3 of clot control?

A

thrombomodulin/thrombin complex which activate protein c

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16
Q

what happens when protein c is activated?

A

Activated protein C complexes with protein S

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17
Q

what is plasminogen?

A

an inactive plasma compound

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18
Q

what happens when tPA is released from healing tissue

A
  • The plasminogen is activated and becomes plasmin.
  • The plasmin dissolves the clot and inactivates other factors in the clotting cascade
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19
Q

heparin’s MOA

A

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

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20
Q

what is heparin used for

A

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

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21
Q

heparin monitoring is done how?

A

PTT (in patient), outpt ask about bleeding

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22
Q

LMWH

A

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

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23
Q

Heparin adverse effects

A

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

24
Q

Heparin drug interactions

A

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

25
Q

what labs are checked for heparin

A

PTT
platelet
H/H

26
Q

Thrombin inhibitors examples and what do they do?

A

*Argatroban (Novastan®), dabigatran (Pradaxa®)

Inhibits thrombin induced reactions *Fibrin formation, activation of factors V, VIII, XIII, and protein C, and platelet activation

27
Q

Argatroban Indication and dosing?

A

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

28
Q

Dabigatran (Pradaxa®) indicated for, dose?

A

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

29
Q

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

A

1–3 days

30
Q

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

A

12–24 hours

31
Q

Bivalirudin (Angiomax®) is what?

A

A Thrombin inhibitor.

32
Q

Bivalirudin (Angiomax®) indicated for?

A

Indicated for PCI or PCTA
Used concomitantly with aspirin

33
Q

What is the reversal agent for Pradaxa?

A

Idarucizumab(Praxbind®)

34
Q

what do factor Xa direct inhibitors do

A

Act directly upon thrombin without using antithrombin III as a mediator

35
Q

what do factor Xa indirect inhibitors do

A

Acts through antithrombin III

36
Q

Factor Xa Inhibitors are used for

A

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

37
Q

*Indirect Xa inhibitors meds

A

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

38
Q

Direct Xa inhibitors

A

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

39
Q

Apixaban

A

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

40
Q

Rivaroxaban

A

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

41
Q

Warfarin MOA

A

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

42
Q

Dosing of warfarin

A

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

43
Q

Warfarin adverse effects

A

Bleeding
Anorexia, nausea, vomiting, diarrhea, abd cramps

Adrenal insufficiency
Agranulocytosis
Hepatotoxicity

44
Q

Warfarin drug interactions

A

Protein binding effect

45
Q

Lab eval for Warfarin

A

PT/INR
H/H

46
Q

Warfarin contraindications

A

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

47
Q

Glycoprotein IIb/IIa inhibition effect what part of clotting

A

Primary clotting

48
Q

Glycoprotein IIb/IIa examples

A

Abciximab, eptifibatide, tirofiban

Used in cath lab, unstable angina

49
Q

Dipyridamole/ASA (Aggrenox) MOA

A

Inhibits ADP receptors that activate platelets in the first place

  • twice as effective as ASA alone for TIA but higher cost
50
Q

Clopidogrel (plavix) MOA

A

Blocks ADP receptor
75 mg once daily

After stents
CVA prophylaxis

51
Q

Plaviz adverse effects

A

Chest pain, edema, hypertension
Headache dizziness
Rash pruritus purpura

Arthralgia and back pain
Neutropenia, agranulocytosis in <1% of patients

52
Q

Plavix interactions

A

Substrate of cytochrome p450 2c19
Cyp2c19 inhibitors can decrease efficacy

PPI’s are inhibitor (except pantoprazole protonix, fluoxetine(Prozac), ketoconazole(nizoral)

53
Q

Plavix lab eval

A

H/H
WBC diff
Platelets
LFT as indicated

54
Q

Prasurgrel (Effients)

A

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

55
Q

Who should you not give effient to

A

Prior stroke or TIA
Over the age of 75

56
Q

ASA MOA

A

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

57
Q

PGH2 acts in 2 ways

A

Promotes and inhibits clotting

58
Q

ASA inhibits action of

A

Cyclooxygenase

pharm- pace (18 decks)

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