Atnicoagulant, antiplatelet, thrombolytic

Question 1

2 stages of hemostasis

Answer 1

Formation of platelet plug

Reinforcement with fibrin

Question 2

Platelet plug formation

Answer 2

Platelet aggregation occurs when they come in contact with exposed collagen on damaged vessel.
Glycoprotein IIb/IIIa receptors on platelet surface form bridges with other platelets made of fibrinogen
Each IIb/IIIa receptor must first undergo activation, activation is from thromboxane A2, thrombin, collagen, platelet activation factor, ADP.
Aggregation allows for platelet plug to form, must be reinforced with fibrin to last

Question 3

Coagulation

Answer 3

Coagulation is the production of fibrin, which is a thread like protein that reinforces platelet plug. Fibrin is produced through two pathways, intrinsic and extrinsic

Question 4

Extrinsic factor from tissue factor (tissue thromboplastin) release

Answer 4

Tissue factor released from damaged epithelium.
TF activates VII turns into X
X causes conversion of prothrombin (factor II) to thrombin (factor IIa)
Thrombin causes 3 things to happen
Fibrinogen –> fibrin
Factor V –> Va
Factor VIII –> VIIIa

Question 5

Intrinsic pathway (contact activation pathway)

Answer 5

Blood exposed to collagen of vessel wall. Collagen causes factor XII to be converted to XIIa
XIIa activates XI which activates IX which activates X
X converted to Xa and clotting cascade is finished
Coagulation occurs with activation of X into Xa

Question 6

Inactivation of clots is achieved with

Answer 6

Antithrombin.

Question 7

Enzyme used to breakdown fibrin meshwork of clot

Answer 7

Plasmin. Produced through activation of plasminogen

Question 8

Fibrinolytic drugs work by

Answer 8

Converting plasminogen to plasmin

Question 9

3 main categories of fibrinolytics

Answer 9

Anticoagulants: disrupt coagulation cascade, thereby suppressing production of fibrin
Antiplatelets: Inhibit platelet aggregation
Thrombolytics: Promote lysis of fibrin, causing dissolution of thrombi

Question 10

Anticoagulants reduce

Answer 10

Formation of fibrin

Question 11

Anticoagulant mechanisms

Answer 11

Inhibition of synthesis of clotting factors, X and thrombin

Inhibition of clotting factors Xa and thrombin

Question 12

Heparin (unfractionated)

Answer 12

Suppresses formation of fibrin
Enhances antithrombin (helps antithrombin to inactivate clotting factors thrombin and factor X)

Question 13

Sources of heparin

Answer 13

Cattle lungs, pig intestines. Administered by rapid-acting anticoagulant administered IV or SQ

Question 14

Heparin therapeutic uses

Answer 14

Preferred during pregnancy when rapid anticoag required
PE, DVT, evolving stroke
Open heart surg, post op, renal dialysis
DIC
Adjunct to thrombolytic therapy

Question 15

LMW heparins

Answer 15

Heparin preparations composed of molecules that are shorter than those found in unfractionated heparin
For:
DVT after surg
TX of established DVT
Prevention of ischemic complications (UA, MI, STEMI)

Question 16

LMW pros and cons

Answer 16

SQ based on body weight
Antidote for protamine sulfate toxicity
Costs more than unfractionated
No monitoring after
Adverse effects include bleeding (less than unfractionated heparin, immune-mediated thrombocytopenia, severe neuro injury for pts undergoing spinal epidural anesthesia)

Question 17

Thrombocytopenia

Answer 17

Low levels of thrombocytes (platelets)

Question 18

Three common LMWs

Answer 18

Enoxaparin
Dalteparin
Tinzaparin

Question 19

Enoxaparin (lovenox)

Answer 19

LMW heparin, anticoag

Indications: STEMI

Question 20

Enoxaparin (lovenox) contras

Answer 20

Hypersens to heparins or pork
Active major bleeding
Bacterial endocarditis
Thrombocytopenia
Suspected intracranial bleeding

Question 21

Enoxaparin (lovenox) dose

Answer 21

IV - BLUE
75 or less - 30mg IV
Over 75 - withhold 
Adult SC (black)
75 or less 1mg/kg
Over 75 0.75mg/kg

Question 22

Warfarin is an

Answer 22

anticoagulant. Vit K antagonist.

Question 23

Warfarin works for

Answer 23

Blocks biosynthesis of factors VII, IX, X and prothrombin

It has a delayed onset

Question 24

Anticoagulants

Answer 24

Not useful in emergencies
Long-term prophylaxis of thrombosis
Prevention of thromboembolism (pts with prosthetic heart valves)
Prevention of thrombosis during a-fib

Question 25

Antiplatelet drugs 3 major categories

Answer 25

These drugs suppress platelet aggregation P2Y12 ADP receptor antagonist GP IIb/IIIa inhibitors Cyclooxygenase inhibitor (ASA)

Question 26

ASA effects

Answer 26

ASA is a nonselective cyclooxygenase (COX) inhibitor It reduces inflammation, fever and pain (COX 2 inhibition) Protects against MI and ischemic stroke (COX 1 inhibition)

Question 27

ASA antiplatelet effects

Answer 27

``` Suppresses aggregation by causing irreversible inhibition of COX 1 which makes TXA2. TXA 2 (thromboxane A2) in platelets promotes aggregation ```

Question 28

Class and indications for ASA

Answer 28

Antiplatelet, thromboxane A2 inhibitor | ACS

Question 29

ASA contras and dose

Answer 29

Hypersens, active GI bleed, asthmatic with hx of ASA,NSAID sensitivity Adult dose is 160mg PO

Question 30

Clopidogrel (plavix) blocks

Answer 30

P2Y12ADP receptors on platelet surface, preventing ADP-stimulated aggregation`

Question 31

Clopidogrel uses

Answer 31

Blockage of coronary artery stents Reduces thrombotic events in pts with acute coronary syndromes Prevents stenosis of coronary stents, also for secondary prevention of MI, ischemic stroke and other vascular events. Similar adverse effects as ASA

Question 32

Clopidogrel (plavix) class

Answer 32

Platelet inhibitor, P2Y12ADP receptor inhibitor | Indications STEMI-VHR protocol

Question 33

Clopidogrel (plavix) conras

Answer 33

Hyper sense Active bleed Liver dysfunction/jaundice, cirrhosis, alcoholism Suspected aortic dissection

Question 34

Clopidogrel (plavix) dose

Answer 34

75 or less 300mg PO | Over 75 75mg PO

Question 35

Ticagrelor (brilinta) class

Answer 35

Platelet inhibitor, P2Y12ADP receptor inhibitor

Question 36

Ticagrelor contras

Answer 36

Hypersens HX of intracranial hemorrhage Hepatic dysfunction Active bleeding

Question 37

Ticagrelor dose

Answer 37

180mg PO (given if getting PCI)

Question 38

VHR if 75 or less with TNK

Answer 38

TNK weight based dose Enoxparain 30mg IV - Blue Clopidogrel (plavix) 300mg PO Enoxaparin 1mg/kg sub q - black

Question 39

VHR if over 75 with TNK

Answer 39

TNK weight based dose NO IV enoxaparin Clopidogrel 75mg PO Enoxaparin (lovenox) 0.75mg/kg

Question 40

VHR for PCI

Answer 40

Enoxaparin 30mg IV Ticagrelor 180mg PO Enoxaparin 1mg/kg sub Q

Question 41

GP IIb/IIIa receptor antagonsits

Answer 41

Most effective antiplatelet drugs "super aspirin" Reversible blockade of platelet GP IIb/IIIa receptors Therapeutic uses include ACS and PCI

Question 42

Eptifibatide (integrilin)

Answer 42

Small peptide that causes reversible and highly selective inhibition of GP IIb/IIIa receptors For: ACS, PCI Antiplatelet effects reverse within 4 hours of stopping infusion

Question 43

Tenecteplase (TNK)

Answer 43

Variant of human tissue plasminogen activator (tPA, alteplase) Approved for acute MI only

Question 44

How to minimize bleeding risk

Answer 44

Minimize physical manipulation of pt Avoid subQ and IM injections Minimize invasive procedures Minimizes concurrent use of anticoags (heparin, warfarin, dabigatran) Minimize conccurent use of antiplatelet drugs (ASA, clopidogrel)

Question 45

Tenecteplase (TNKase) class

Answer 45

Thrombolytic, fibrinolytic | for STEMI

Question 46

Tenecteplase (TNKase) contras

Answer 46

Hypersen Active bleeding Brain tumor Ischemic CVA within 3 months Significant closed head/facial trauma within 3 months Intracranial or spinal surg within 2 months Suspected aortic dissection

Question 47

Teneceteplase (TNKase) dose

Answer 47

``` 30-50mg over 5 seconds <60k 30mg 60-70kg 35mg 70-80kg 40mg 80-90kg 45mg 90kg or more 50mg ```