Module 2 exam 1 lecture 4

Question 1

how is the clot dissolved once BV is healed

Answer 1

fibrinolytic pathway

Question 2

major step of fibrinolytic pathway

Answer 2

activation of plasminogen to plasmin

Question 3

What is plasminogen

Answer 3

a circulating inactive enzyme

Question 4

plasminogen is activated by

Answer 4

TPA (tissue plasminogen activator)

Question 5

What does plasmin do?

Answer 5

binds to plasmin clot and breaks it down

Question 6

indication of thrombolytic drugs

Answer 6

dissolve clots, acute MI, stroke

Question 7

What does TPA do?

Answer 7

BInds fibrin and activates plasminogen that is bound to fibrin clot. Breaks down 100X more rapidly

Question 8

3 drugs that dissolve blood clots (TPAs)

Answer 8

Alteplase
reteplase
tenecteplase

Question 9

alteplase structure and MOA`

Answer 9

recombinant human TPA
binds fibrin

Question 10

Reteplase structure and MOA

Answer 10

shorter (truncated, removed aa from protease domain) no fibrin binding domain, less fibrin specific.

Question 11

TEnecteplase structure and MOA

Answer 11

Point mutation in protease domain that increases ability to bind fibrin. longer t1/2

Question 12

summarize how a clot is broken down

Answer 12

Plasminogen binds to fibrin clot, T-PA (altepase or tenecteplase) will bind to clor and plasminogen and activate it to plasmin

Question 13

Which TPA is different in terms of function? why?

Answer 13

Reteplase. It has no fibrin binding domain so it cleaves plasminogen whether it is bound to the clot or not

Question 13

How are TPA drugs cleared

Answer 13

renally and hepatically

Question 13

ROA for alteplase, reteplase, tenecteplase? t1/2?

Answer 13

IV for all
alteplase- 5-10 min
reteplase- 13-16 min
tenecteplase- 90-130 min

Question 13

Adverse effects of TPAs

Answer 13

Bleeding

Question 14

How do we stop bleeding caused by TPAs?

Answer 14

Antifibrinolyctic agents

Question 15

Name antifibrinolytic drugs

Answer 15

Aminocaproic acid (EACA)
Tranexamic acid

Question 16

Which aa are aminocaproic acid and tranexamic acid based on?

Answer 16

Lysine

Question 17

Which antifibrinolytic drug is more potent

Answer 17

Tranexamic acid is 10x more potent than aminocaproic acid

Question 18

How do tranexamic acid and aminocaproic acid work?

Answer 18

Prevent binding of plasminogen and plasmin to fibrin, sparing clots and preventing hemorrhage.

Question 19

inhibitors of platelet function are normally given iin PCI, why?

Answer 19

PCI is catheterization through BV. This will cause endothelial damage and induce platelet aggregation. Inhibitors of platelet function stop this.

Question 20

What does heparin inhibit

Answer 20

antithrombin 3

Question 21

MOA of heparin

Answer 21

accelerates binding of antithrombin 3 to thrombin (factor 2a) and factor Xa

Question 22

What does thrombin do when activated?

Answer 22

cleaves fibrinogen to fibrin

Question 23

heparin inhibits conversion of

Answer 23

prothrombin to thrombin and fibrinogen to fibrin

Question 24

LMWH drugs

Answer 24

Enoxaparin Palteparin

Question 25

LMWH MOA difference from heparin MOA

Answer 25

Inactivate Xa, but has little inactivation at thrombin due to short chains

Question 26

time required to get peak anticoag effect from warfarin

Answer 26

2-3 days

Question 27

warfarin MOA

Answer 27

Warfarin inhibits gamma-carboxylated factors (II,VII, IX and X). They must be depleted

Question 28

Which compound targets the binding of platelets to fibrinogen

Answer 28

eptifibatide (prevents crosslinking of platelets)

Question 29

Name an antibody that binds to GPIIb/IIIa receptors

Answer 29

Abciximab

Question 30

Protease activated receptor (PAR) is cleaved by what molecule in coagulation cascade

Answer 30

factor IIa (thrombin)

Question 31

protein C and S are dependent of which vitamin?

Answer 31

K

Question 32

What might cause deficiency in prothrombin (factor II) or in factor x

Answer 32

liver disease or vit K