blood thinners

Question 1

Thrombotic disorders such as acute myocardial infarction, deep vein thrombosis, pulmonary embolism, and acute ischemic stroke are treated with what drugs?

Answer 1

Thrombotic disorders such as acute myocardial infarction, deep vein thrombosis, pulmonary embolism, and acute ischemic stroke are treated with drugs such as anticoagulants and *fibrinolytics

Question 2

Coagulation involves what?

Answer 2

Coagulation involves both cellular (platelet) and protein-based (coagulation factors) components

Question 3

Arterial thrombosis usually consists of what?

Answer 3

Arterial thrombosis usually consists of a platelet-rich clot

Question 4

antihemostatic agent drug classes

Answer 4

anticoagulents and platelet inhibitors

Question 5

whats an example of a fibrinolytic?

Answer 5

TPA (tissue plasminogen activator) - utilized in hospital setting; used for pt with MI

Question 6

The coagulation process culminates in the generation of thrombin which stimulates what?

Answer 6

The coagulation process culminates in the generation of thrombin which stimulates conversion of fibrinogen to the glycoprotein fibrin

Question 7

The cascade consists of ___ interrelated pathways

Answer 7

The cascade consists of two interrelated pathways

Question 8

Drugs acting within the extrinsic pathway (which is most important in vivo) affect the synthesis of what?

Answer 8

Drugs acting within the extrinsic pathway (which is most important in vivo) affect the synthesis of vitamin K- dependent coagulation factors

Question 9

Drugs acting within the intrinsic pathway

inhibit the activity of what?

Answer 9

coagulation factors

Question 10

what does the extrinsic pathway lead to?

Answer 10

rapid accummulation of thrombin (which is last step to convert fibrin)
*most efficacious part

Question 11

whats most important about the intrinsic pathway?

Answer 11

minor role in clot activation and is more important in inflammation pathways (tissue injury)

Question 12

how can intrinsic cascade start?

Answer 12

blood vessel injury –> subendothelial tissue factor in bv –> leads to activation of factor 7 –> starts intrinsic cascade

Question 13

what are the three pathways?

Answer 13

intrinsic
extrinsic
common

Question 14

2 antagonists

Answer 14

vitamin k and coagulation factor

Question 15

which of the 2 antagonists is an indirect drug

Answer 15

vitamin k antagonist –> cofactor that combines with decarboxylase enzyme –> carboxylation (activation) of tissue coagulation factors –> vitamin k is oxidized (not useful)–> vitamin k epoxide reductase –> reduces vitamin k back to original state

Question 16

vitamin k antagonist

Answer 16

coumadin (warfarin)

Question 17

indication for coumadin

Answer 17

anticoagulation
dosing (2-10 mg) 1 tab qd

Question 18

most widely prescribed anticoagulant in usa

Answer 18

coumadin

Question 19

Inhibits vitamin K-dependent coagulation factor synthesis (II, VII, IX, X, proteins C and S)

Answer 19

moa of coumadin

Question 20

which coagulation factors are inhibited by vitamin k?

Answer 20

7, 9, 10

Question 21

warfarin is important because?

Answer 21

it can affect both pathways?

Question 22

trauma activates what pathway

Answer 22

extrinsic

Question 23

damaged surface (vessel) activates what pathway?

Answer 23

intrinsic

Question 24

are vitamin k and potassium the same thing?

Answer 24

no

Question 25

whats the christmas factor?

Answer 25

9

Question 26

11 --> 9 --> 8 are wat?

Answer 26

3 hemophilias

Question 27

9 and 8 are associated with what disease?

Answer 27

x linked disease

Question 28

11 is associated with what?

Answer 28

hemophelia type c (autosomal recessive) --> found in isolated pops

Question 29

if you have an infection what pathway is activated?

Answer 29

intrinsic???? isolation of microbes --> enhanced bf for leukocytes --> all liked to inflammation process

Question 30

vitamin k epoxide reductase regenerates what?

Answer 30

new vitamin k

Question 31

if we cut off vitamin k what happens?

Answer 31

neither pathways are able to generate fibrin clots, because prothrombin depends on vitamin k

Question 32

ADVERSE EFFECTS | • Common: Bleeding/bruising, headache, dizziness, pruritus, edema, dermatitis, fever, paresthesias, alopecia

Answer 32

coumadin adverse effects

Question 33

SERIOUS CV: syncope, vasculitis, hemorrhage, cholesterol embolism • Hematology: anemia

Answer 33

coumadin serious adverse effects

Question 34

what ocular disease do we treat tetracycline with?

Answer 34

MGD; gram positive

Question 35

WHAT If pt is taking coumadin and tetracycline?

Answer 35

pt will bleed to death because tetracycline will impair metabolism of drug

Question 36

name 2 coagulation factor antagonists

Answer 36

* Enoxaparin [Lovenox®, Xaparin®, Clexane®] | * Rivaroxaban [Xarelto®]

Question 37

indication for enoxaparin

Answer 37

Post-op DVT prophylaxis*, Unstable Angina DOSING [30-40mg*] • 30mg SC bid; 40mg

Question 38

how is enoxaparin administered?

Answer 38

injection

Question 39

enoxaparin moa

Answer 39

binds to antithrombin 3 and accelerates its activity; inhibiting thrombin and factor (xa) *acts as a stimulant for antithrombin and and antagonist to coagulation

Question 40

whats heparin used for?

Answer 40

in hospital settings

Question 41

heparin sequence

Answer 41

heparin binds to antithrombin --> (thrombin + factor 10a) binds to heparin combo --> takes it out of activity

Question 42

lmw heparin sequence

Answer 42

lmwh --> binds to antithrombin --> combo binds to factor xa

Question 43

why is lmwh preferred over regular heperin?

Answer 43

yes because heperin has an unpredictable response due to its length

Question 44

is lmwh activity predictable?

Answer 44

yes

Question 45

pros of lmwh

Answer 45

half life is 4 hours, predictable response, 90% bioavailability, less frequent bleeding, hospital and outpatient

Question 46

can heperin be used outside of hospital settings

Answer 46

yah its better than enoxaparin

Question 47

adverse effects of enoxaparin

Answer 47

hemorrhage and fever

Question 48

serious adverse effects of enoxaparin

Answer 48

anemia

Question 49

Platelet aggregation inhibitors decrease what?

Answer 49

Platelet aggregation inhibitors decrease the formation or the action of chemical signals that promote platelet aggregation

Question 50

The platelet membrane GP IIb/IIIa receptor which is activated in the critical last phase of thrombus formation serves to what?

Answer 50

The platelet membrane GP IIb/IIIa receptor which is activated in the critical last phase of thrombus formation serves to bind adhesive proteins like fibrinogen

Question 51

• Platelet stimulating agents that lead to GP IIb/IIIa receptor activation include what?

Answer 51

• Platelet stimulating agents that lead to GP IIb/IIIa receptor activation include Thromboxane-A2, ADP, thrombin, serotonin, and collagen

Question 52

platelet aggregation inhibitors inhibit cox-1, block | which receptors?

Answer 52

platelet aggregation inhibitors inhibit cox-1, block | adp receptors or GP 11b/111a receptors

Question 53

membrane phospholipids --> arachidonic acid --> prostaglandin H2 --> thromboxane A2

Answer 53

TXA2 activation

Question 54

where does COX1 act in inflammation pathway?

Answer 54

stops arachidonic acid from turning into TXA2

Question 55

pgi2

Answer 55

antiinflammatory involving inhibitition of platelets and vasodilator

Question 56

2 platelet inhibitor drug classes

Answer 56

- Adenosine Receptor Blockers | - Glycoprotein IIb/IIIa Receptor Antagonists

Question 57

* Clopidogrel [Plavix®] * Ticlopidine [Ticlid®] * Prasugrel [Effient®] * Dipyridamole [Persantine®]

Answer 57

adenosine receptor blockers

Question 58

INDICATION • Acute Coronary Syndrome, Thrombotic Event Prophylaxis • DOSING [75 & 300mg] • 1 tab qd

Answer 58

clodipogrel

Question 59

whats the reason a patient will show up at our optometry office indicating use of clopidogrel?

Answer 59

thrombotic event prophylaxis

Question 60

CLINICAL PHARMACOLOGY • Antiplatelet Mechanism of Action • Prodrug: metabolized to active metabolite by the CYP450 enzyme CYP2C19* • Irreversible inhibition of platelet ADP receptors which normally trigger platelet activation and aggregation via downstream activation of the GPIIb/ IIIa complex

Answer 60

moa of clopidogrel

Question 61

irriversible inhibition is shown in what drugs?

Answer 61

NSAID and clopidogrel/ticlopidine

Question 62

• Common: hemorrhage, pruritus, cough, bronchitis, dizziness, headache SERIOUS ADVERSE EFFECTS • Hypersensitivity: Angioedema, SJS, TEN • Hematology: TTP 

Answer 62

adverse effects of clopidogrel

Question 63

• Evening Primrose Oil, Flaxseed, Omega-3 FA, NSAIDs (Additive) • Ketoconazole (Reduced metabolism/ activation) 

Answer 63

clopidogrel drug interactions

Question 64

mab

Answer 64

monoclonal antibody-drug that has been engineered; purified pool of ab that are monoclonal specific for an antigen

Question 65

caution: ocular disease

Answer 65

clopidogrel

Question 66

Abciximab [ReoPro®] | • Eptifibatide [Integrilin®]

Answer 66

gp 2b/3a receptor antagonists

Question 67

* INDICATION * An adjunct to percutaneous coronary intervention (PCI) for the prevention of cardiac ischemic complications * Unstable angina DOSING [Variable] • IV bolus (all at once-very rapid)

Answer 67

abciximab

Question 68

clinical pharm: antiplatelet moa Fab fragment: a chimeric human-murine mAB -binds to the GP 2b/3a receptor of human platelets and inhibits platelet aggregation -binds to the vitronectin (avb3) receptor on platelets and vessel wall endothelial and smooth muscle cells

Answer 68

moa of abciximab

Question 69

Common: hemorrhage, hypotension, dizziness, headache

Answer 69

adverse effects of abciximab

Question 70

Omega-3 & Omega-6 fatty acids, NSAIDs (Additive) | • Ophthalmic NSAIDs (Additive)

Answer 70

drug interactions of abciximab

Question 71

- recent surgery or trauma | - uncontrolled hypertension

Answer 71

abciximab contraindications