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blood thinners Flashcards

1
Q

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

A

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

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2
Q

Coagulation involves what?

A

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

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3
Q

Arterial thrombosis usually consists of what?

A

Arterial thrombosis usually consists of a platelet-rich clot

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4
Q

antihemostatic agent drug classes

A

anticoagulents and platelet inhibitors

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5
Q

whats an example of a fibrinolytic?

A

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

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6
Q

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

A

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

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7
Q

The cascade consists of ___ interrelated pathways

A

The cascade consists of two interrelated pathways

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8
Q

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

A

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

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9
Q

Drugs acting within the intrinsic pathway

inhibit the activity of what?

A

coagulation factors

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10
Q

what does the extrinsic pathway lead to?

A

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

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11
Q

whats most important about the intrinsic pathway?

A

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

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12
Q

how can intrinsic cascade start?

A

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

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13
Q

what are the three pathways?

A

intrinsic
extrinsic
common

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14
Q

2 antagonists

A

vitamin k and coagulation factor

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15
Q

which of the 2 antagonists is an indirect drug

A

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

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16
Q

vitamin k antagonist

A

coumadin (warfarin)

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17
Q

indication for coumadin

A 
anticoagulation
dosing (2-10 mg) 1 tab qd
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18
Q

most widely prescribed anticoagulant in usa

A

coumadin

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19
Q

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

A

moa of coumadin

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20
Q

which coagulation factors are inhibited by vitamin k?

A

7, 9, 10

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21
Q

warfarin is important because?

A

it can affect both pathways?

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22
Q

trauma activates what pathway

A

extrinsic

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23
Q

damaged surface (vessel) activates what pathway?

A

intrinsic

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24
Q

are vitamin k and potassium the same thing?

A

no

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25
Q

whats the christmas factor?

A

9

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26
Q

11 –> 9 –> 8 are wat?

A

3 hemophilias

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27
Q

9 and 8 are associated with what disease?

A

x linked disease

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28
Q

11 is associated with what?

A

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

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29
Q

if you have an infection what pathway is activated?

A

intrinsic????

isolation of microbes –> enhanced bf for leukocytes –> all liked to inflammation process

30
Q

vitamin k epoxide reductase regenerates what?

A

new vitamin k

31
Q

if we cut off vitamin k what happens?

A

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

32
Q

ADVERSE EFFECTS

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

A

coumadin adverse effects

33
Q

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

A

coumadin serious adverse effects

34
Q

what ocular disease do we treat tetracycline with?

A

MGD; gram positive

35
Q

WHAT If pt is taking coumadin and tetracycline?

A

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

36
Q

name 2 coagulation factor antagonists

A
  • Enoxaparin [Lovenox®, Xaparin®, Clexane®]

* Rivaroxaban [Xarelto®]

37
Q

indication for enoxaparin

A

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

38
Q

how is enoxaparin administered?

A

injection

39
Q

enoxaparin moa

A

binds to antithrombin 3 and accelerates its activity; inhibiting thrombin and factor (xa)

*acts as a stimulant for antithrombin and and antagonist to coagulation

40
Q

whats heparin used for?

A

in hospital settings

41
Q

heparin sequence

A

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

42
Q

lmw heparin sequence

A

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

43
Q

why is lmwh preferred over regular heperin?

A

yes because heperin has an unpredictable response due to its length

44
Q

is lmwh activity predictable?

A

yes

45
Q

pros of lmwh

A

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

46
Q

can heperin be used outside of hospital settings

A

yah its better than enoxaparin

47
Q

adverse effects of enoxaparin

A

hemorrhage and fever

48
Q

serious adverse effects of enoxaparin

A

anemia

49
Q

Platelet aggregation inhibitors decrease what?

A

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

50
Q

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

A

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

51
Q

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

A

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

52
Q

platelet aggregation inhibitors inhibit cox-1, block

which receptors?

A

platelet aggregation inhibitors inhibit cox-1, block

adp receptors or GP 11b/111a receptors

53
Q

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

A

TXA2 activation

54
Q

where does COX1 act in inflammation pathway?

A

stops arachidonic acid from turning into TXA2

55
Q

pgi2

A

antiinflammatory involving inhibitition of platelets and vasodilator

56
Q

2 platelet inhibitor drug classes

A
  • Adenosine Receptor Blockers

- Glycoprotein IIb/IIIa Receptor Antagonists

57
Q
  • Clopidogrel [Plavix®]
  • Ticlopidine [Ticlid®]
  • Prasugrel [Effient®]
  • Dipyridamole [Persantine®]
A

adenosine receptor blockers

58
Q

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

A

clodipogrel

59
Q

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

A

thrombotic event prophylaxis

60
Q

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

A

moa of clopidogrel

61
Q

irriversible inhibition is shown in what drugs?

A

NSAID and clopidogrel/ticlopidine

62
Q

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


A

adverse effects of clopidogrel

63
Q

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


A

clopidogrel drug interactions

64
Q

mab

A

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

65
Q

caution: ocular disease

A

clopidogrel

66
Q

Abciximab [ReoPro®]

• Eptifibatide [Integrilin®]

A

gp 2b/3a receptor antagonists

67
Q
  • 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)

A

abciximab

68
Q

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

A

moa of abciximab

69
Q

Common: hemorrhage, hypotension, dizziness, headache

A

adverse effects of abciximab

70
Q

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

• Ophthalmic NSAIDs (Additive)

A

drug interactions of abciximab

71
Q
  • recent surgery or trauma

- uncontrolled hypertension

A

abciximab contraindications

systemic pharm (16 decks)

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