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Pharmacology - Fall 2024 > Ch 34 - Coagulation Disorders (MEDS) > Flashcards

Ch 34 - Coagulation Disorders (MEDS) Flashcards

1
Q

Coagulation Modifier Drugs

A

Anticoagulants
antiplatelet drugs
thrombolytic drugs (fibrinolytic)
hemostatic or antifibrinolytic drugs

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2
Q

Anticoagulants

A

-inhibit the action of the formation of clotting factors
- prevent clot formation

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3
Q

antiplatelet drugs

A

-inhibit platelet aggregation
-prevent platelet plugs

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4
Q

thrombolytic drugs (also known as)

A

fibrinolytic drugs

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5
Q

hemostatic or antifibrinolytic drugs

A

-promote blood coagulation

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6
Q

Drugs to treat thromboembolism

A

heparin
warfarin
aspirin
streptokinase

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7
Q

heparin (class, action, effect)

A

anticoagulant parenteral, inactivation of clotting factor, prevent venous thrombosis

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8
Q

warfarin (class, action, effect)

A

anticoagulant oral, decrease synthesis of clotting factors, prevent venous thrombosis

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9
Q

Aspirin (class, action, effect)

A

antiplatelet drug, decrease platelet aggregation, prevent arterial thrombosis

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10
Q

Streptokinase (class, action, effect)

A

thrombolytic drug, fibrinolysis, breakdown of thrombi

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11
Q

Heparin (MOA)

How much does heparin enhance this enzyme’s activity?

At what rate is the heparin consumed through this process?

A

anti-thrombin III (via conformational change)

1000x enhancement

Heparin is not consumed by this process, only acts as a catalyst.

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12
Q

Heparin MW

A

5,000-30,000 MW

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13
Q

Heparin extracted from?

A

porcine intestinal mucosa and bovine lung

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14
Q

LMW Heparin (meds)

A

enoxaparin (lovenox)
dalteparin (fragmin)
tinzaparin (innohep)

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15
Q

LMW heparin (factor target)

A

more specific for factor Xa (less effect on thrombin)

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16
Q

Transient thrombocytopenia (heparin)

A

HIT

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17
Q

Heparin monitor

A

aPTT

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18
Q

Prothrombin time

A

assess the function of the extrinsic system and common pathway of coagulation cascade

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19
Q

aPTT

A

-measures activity of the intrinsic system and common pathway
-phospholipid added to induce intrinsic pathway.

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20
Q

Heparin reversal

A

Protamine sulfate

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21
Q

Fondaparinux (Arixtra)

Selective for?
Uses?

A

-synthetic
-pentasaccharide molecule of heparin
-less bleeding risk (useful for HIT)
-selective for factor X (not as effective)

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22
Q

Direct thrombin inhibitors

A

Dabigatran (pradaxa)
melagatran
argatroban
bivalirudin (angiomax)
hirudin (Lepirudin)

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23
Q

bind only to thrombin active site (3)

A

argatroban, melagatran, dabigatran (pradaxa)

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24
Q

Warfarin

A

100% oral availability
protein binding 99%
long half life: 36 hrs

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25
Q

Warfarin (MOA)

A

blocks the y-carboxylation of several glutamate residues (vit. K dependent)

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26
Q

Therapeutic range for warfarin

A

Normal INR = 0.8-1.2
target INR= 2-3

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27
Q

Warfarin (reversal)

A
  • stop drug
    -large dose of Vit. K
  • FFP
  • factor IX concentrates
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28
Q

Fibrinolytics

A

-lyse thrombi
- catalyze the formation of serine protease plasmin

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29
Q

streptokinase

A

synthesized by streptococci

30
Q

Urokinase

A

synthesized by kidneys
lyses the thrombus form within

31
Q

t-PA

A

tissue plasminogen activator

32
Q

t-PA MOA

A

recombinant forms (alteplase)
- activates plasminogen that is bound to fibrin

33
Q

Aspirin

A

COX1 selective platelet, inhibition of TXA2 synthesis (bleeding time), platelet change(shape, granule release, aggregation)

34
Q

clopidogrel and ticlopidine

A

Plavix and Ticlid reduce platelet aggregation with no effects on prostaglandin metabolism
- TTP associated with ticlopidine

35
Q

plavix and ticlid MOA

A

Irreversibly inhibit ADP receptors on platelets.

36
Q

Abciximab

A

monoclonal antibody GP IIb/IIa Inhibitor

37
Q

Vitamin K

A

fat souble, confers activity on prothrombin
- factors VII, IX and X

38
Q

Desmopressin acetate

A

-increases factor VIII activity
-Hemophilia A & von Willebrand Disease

39
Q

Aminocaproic acid (uses)

A

-adjunctive hemophilia therapy
-bleeding from fibrinolytic therapy
-intracranial aneurysms
-post surgical bleeding

40
Q

TXA

A

(tranexamic acid)

41
Q

TXA MOA

A

-antifibrinolytic
- inhibits plasminogen–>plasmin

42
Q

What occurs with platelet GP 1a & 1b receptor activation?

A

ADP, Thromboxane, & Serotonin are released & cause platelets to use GP IIb/IIIa receptors & fibrin to stick together.

43
Q

What do Collagen and vonWillebrand factor interact with once exposed by injury?

A

GP 1a & 1b receptors on the Platelet.

44
Q

What two things are exposed by an endothelial cell injury?

A

Collagen & vWF

45
Q

What is Virchow’s Triad?

A

Endothelial Injury
Stasis
Hypercoagulability

46
Q

Which drugs inhibit fibrinolytic activity? How?

A

Aminocaproic & Tranexamic Acid inhibit fibrinolysis by preventing the conversion of plasminogen to plasmin.

47
Q

What is Tranexamic acid used for?

A

Decreasing bleeding in Trauma, heavy menstruation, & epistaxis.

48
Q

What links platelets together to form the platelet plug?
What receptors are used to accomplish this?

A

Fibrinogen
GP IIb/IIIa receptors on the platelet.

49
Q

How does Plavix (clopidogrel) compare in efficacy to aspirin?

A

Well. 8.7% reduction in ischemic events vs aspirin only.

50
Q

How does t-PA differ from other fibrinolytics?

A

t-PA preferentially activates plasminogen that is bound to fibrin avoiding systemic fibrinolysis and focusing on formed thrombus.

51
Q

Where do Monoclonal antibody anti-platelet
drugs work?
Name the prototypical drug of this class.

A

-Targeting of IIb/IIIa receptors on platelet, thus preventin platelets from adhering to each other using fibrin.
-Abciximab

52
Q

Differentiate streptokinase & urokinase.

A

Urokinase is synthesized by the kidneys & streptokinase is synthesized by streptococci. Both break down clots directly via catalyzation of plasminogen into plasmin

53
Q

How do virtually all fibrinolytic drugs work?

A

Catalyze the formation of Plasminogen into plasmin.

54
Q

What reversal is available for all the -aban drugs? (apixaban, rivaroxaban, etc.)
How do these drugs work?

A

No reversal is available.
Inhibition of Factor Xa & Thrombin

55
Q

What is the consequence of warfarin’s rate of protein binding?

A

Warfarin protein binding rate (99%) can antagonize binding of other drugs.
ex. Phenytoin can be displaced by warfarin thus causing phenytoin toxicity.

56
Q

The goal of warfarin therapy is reduction of prothrombin activity by ______ %.

A

25%

57
Q

What toxicity is seen with warfarin overdosing?

A

-Bleeding
-Hemorrhagic disorder of fetus & birth defects
-Cutaneous necrosis

58
Q

What is the delay in onset of action of warfarin?
What does this mean clinically?

A

8-12 hours till effect is seen
Wean off of heparin & on to warfarin slowly.

59
Q

Which direct thrombin inhibitors bind to both active & substrate sites of thrombin?

A

Hirudin & Bivalirudin

60
Q

Which direct thrombin inhibitors bind only to thrombin active sites?
What animal do we derive these drugs from?

A
  • Argatroban, Melagatran, & Dabigatran
  • Direct thrombin inhibitors derived from leeches.
61
Q

Who is more prone to hemmorrhage associated with heparin toxicity?

A

Elderly women & renal failure patients

62
Q

With what heparin is the risk of HIT (heparin-induced thrombocytopenia) higher?
What is the basic pathophysiology of HIT?

A

-Unfractionated.

-Transient ↓PLTs (platelets) due to antibodies binding to heparin-PLT complex and immune system destruction of PLTs.

63
Q

Which heparin is more specific for factor Xa?
What does this mean for its efficacy?

A
  • LMW heparin (enoxaparin)

-Less anticoagulative efficacy due to no binding on thrombin itself.

64
Q

Differentiate unfractionated heparin, LMW heparin, & Fondaparinux.

A

Unfractionated Heparin = ↑ Antithrombin III activity, binds to ATIII, Xa, & Thrombin.

LMW Heparin = Binds to Xa, & ATIII

Fondaparinux = binds to ATIII only (via pentasaccharide sequence)

65
Q

What drugs are indirect thrombin inhibitors?

What is their MOA?

A

Unfractionated & fractionated forms of heparin

Enhances anti-thrombin activity, inactivation of factor Xa, & inhibition of thrombin.

66
Q

What is the prototypical oral antiplatelet drug & its generalized MOA?

What is the goal of therapy with this drug?

A

Aspirin - ↓ platelet aggregation

Goal = ↓ arterial thrombosis

67
Q

What is the prototypical oral anticoagulant drug & its general MOA?

What is the goal of therapy with this drug?

A

Warfarin = ↓ synthesis of clotting factors

Goal = ↓ venous thrombosis

68
Q

What is the prototypical parenteral anticoagulant drug & its general MOA?

What is the goal of therapy with this drug?

A

Heparin = inactivation of clotting factors

Goal = ↓ venous thrombosis

69
Q

Differentiate anticoagulants & antiplatelets.

A

Anticoagulants - Inhibit action or formation of clotting factors thus preventing clot formation.

Antiplatelets - Inhibit platelet aggregation thus preventing platelet plugs.

70
Q

Abiciximab - monoclonal antibodies

A

antibody class

target IIb/IIIa

anti-aggregation result

acute coronary syndromes treatment

Pharmacology - Fall 2024 (14 decks)

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