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Pharm Test 3 > Blood Drugs > Flashcards

Blood Drugs Flashcards

1
Q

Goal of normal blood hemostasis

A

§ Prevent prolonged hemorrhage
§ Prevent spontaneous thrombosis

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2
Q

Stages of hemostasis

A
  1. vasospasm
  2. platelet response
  3. coagulation phase
  4. clot dissolution (fibrinolysis)
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3
Q

what is the vasospasm stage of hemostasis? how does it work?

A

Stage 1

§ Immediate; restricts blood flow
§ Sympathetics and local factors eg. thromboxane
§ Myogenic properties of vessel wall

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4
Q

what is the platelet response stage of hemostasis and how does it work?

A

Stage 2

§ Within seconds; forms initial plug
§ Platelets adhere to exposed collagen of damaged endothelium, and each other
§ Platelet plug releases chemical mediators (TXA2, 5-HT and ADP)
> recruit more platelets
> promote vasoconstriction
> initiate the coagulation cascade

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5
Q

what is the coagulation phase of hemostasis and how does it work?

A

Stage 3

§ Occurs thru sequential conversion of inactive proteins into catalytically active proteases
§ Tissue factor-factor VIIa pathway is main initiator
§ Result—conversion of soluble fibrinogen to insoluble fibrin—net of organized protein around platelet plug
§ Result of coagulation phase is clot proper (thrombus)

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6
Q

what is the clot dissolution phase of hemostasis and how does it work?

A

Stage 4
(Fibrinolysis)
§ Wound healing and restoration of blood flow
§ Dissolution of clot by proteolytic actions of plasmin bound to clot—process of fibrinolysis

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7
Q

— Excessive bleeding may be caused by…..

A
  • Platelet deficiency
    > Thrombocytopenias (quantitative consumption) —
    >von Willebrand’s (qualitative disorder)
  • Clotting factor deficiency
    > Single factor eg. hemophilia (VIII, IX)
    > Multiple factors ie. vitamin K deficiency
  • Fibrinolytic hyperactivity
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7
Q

— Excessive bleeding may be caused by…..

A
  • Platelet deficiency
    > Thrombocytopenias (quantitative consumption) —
    >von Willebrand’s (qualitative disorder)
  • Clotting factor deficiency
    > Single factor eg. hemophilia (VIII, IX)
    > Multiple factors ie. vitamin K deficiency
  • Fibrinolytic hyperactivity
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8
Q

treatments for hemorrhagic diseases

A
  • Vitamin K
  • Other agents (DDAVP, Protamine sulfate, antifibrinolytics)
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9
Q

what two natural forms of vitamin K exist?

A

— Vitamin K1: phytonadione (foods)
— Vitamin K2: menaquinone (intestinal bacteria)

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10
Q

mechanism of action of vitamin K for hemorrhagic diseases? how should it be administered and is it safe? what does it require for intestinal absorption?

A
  • Confers biological activity: factors II, VII, IX, X; post-translational modification

-Vitamin K1 available for oral and parenteral use
* Intravenous route—best to avoid; anaphylaxis possible
* IM route- hematoma possible; SC recommended route

-Fat soluble vitamin; considered very safe
* Requires bile salts for intestinal absorption

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11
Q

mechanism of action of vitamin K for hemorrhagic diseases? how should it be administered and is it safe? what does it require for intestinal absorption?

A
  • Confers biological activity: factors II, VII, IX, X; post-translational modification

-Vitamin K1 available for oral and parenteral use
* Intravenous route—best to avoid; anaphylaxis possible
* IM route- hematoma possible; SC recommended route

-Fat soluble vitamin; considered very safe
* Requires bile salts for intestinal absorption

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12
Q

uses of vitamin K for hemorrhagic diseases

A

— Vitamin K deficiency
— >Rodenticide toxicity
— >Dicumoral toxicity (sweet clover poisoning)

— Warfarin overdosing

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13
Q

what is desmopressin acetate used for? how is it administered?

A

hemorrhagic disease
* Transiently increases von Willebrand activity in mild von Willebrand disease
* Used prophylactically to control capillary bleeding during surgery
* Available as injectable or nasal spray (can be given SC)

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14
Q

what is protamine sulfate? what is it used for and what is its use in cases of hemorrhagic disease?

A
  • Low molecular weight strongly basic (cationic) protein produced by recombinant technology
  • Used to treat heparin overdoses
    > binds to heparin neutralizing its anticoagulant effects
    > More effective against large molecular weight heparin molecules in unfractionated heparins versus the low molecular weight heparins
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15
Q

how should we administer protamine sulfate? what do we need to keep in mind in terms of dosing?

A
  • Give IV slowly to avoid adverse reactions that can include collapse
  • Accurate dosing needed; high doses can produce anticoagulant effects
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16
Q

what substance lyses fibrin and fibrinogen? where does it attach to fibrin?

A
  • Plasmin lyses fibrin and fibrinogen
    > Attaches to fibrin via lysine binding sites
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17
Q

what is aminocaproic acid? what does it do? what are its uses

A

fibrinolytic inhibitor

  • Synthetic agent similar to lysine; blocks lysine binding site so that plasmin cannot bind to cause lysis
  • Competitively inhibits plasmin action on fibrin
  • Incomplete lysis can lead to thrombi formation

Uses:
* Bleeding from fibrinolytic therapy
* Adjunct therapy-hemophiliacs

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18
Q

what is a thrombus? what does red vs white mean?

A

“blood clot proper”
-Red thrombus - fibrin rich, large # RBCs; venous —
-White thrombus - platelet rich; arterial

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19
Q

what is a thromboemboli?

A

migration of thrombus in body

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20
Q

what are the 3 contributors to thrombosis?

A

endothelial injury
abnormal blood flow
hypercoagulability

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21
Q

Pathogenesis of thrombosis requires prothrombic factors such as:

A

Local vessel injury
Circulatory stasis
Altered blood coagulability
>Hyperactivity of hemostatic mechanisms —
>Hypoactivity of fibrinolytic mechanisms

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22
Q

drug classes used to treat thrombosis

A

Systemic anticoagulants
Antithrombotic drugs —
Fibrinolytic drugs

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23
Q

what would an ideal systemic anticoagulant do?

A

Prevent pathologic thrombosis
Allow normal response to vascular injury and limit bleeding

24
Q

what is heparin? where does it come from?

A

Systemic anticoagulant
-Mixture of sulfated mucopolysaccharides
-Isolated from mast cells: bovine lung/porcine GI mucosa

25
Q

mechanism of action of heparin

A

Enhances (accelerates 100-fold) the action of Antithrombin III (AT-III) >forms heparin-ATIII complex

AT- III inhibits activated clotting factors especially thrombin (IIa) and Xa—acts as a “suicide substrate”

26
Q

primary use of heparin and other uses, generally (no specific diseases)

A

Primarily used in the initial treatment of thrombosis and thromboembolic disease
- Rapid onset of action renders it useful as an “acute anticoagulant” >Oral anticoagulant usually given concurrently
-Prevents new thrombus formation only!! —
>Does not lyse existing thrombus

27
Q

what are some diseases where heparin would be useful?

A

-Feline cardiomyopathies
-DIC, venous thrombosis, pulmonary thromboembolism
-Canine IMHA
-Equine laminitis

28
Q

adverse effects of heparin? how can we neutralize an overdose?

A

-Bleeding tendencies
-Monitor aPTT; 1.8-2.5X normal mean aPTT
-Protamine sulfate can neutralize heparin in overdose

29
Q

what are low molecular weight heparins and how are they made? what is the most commonly used of these?

A

Are fractioned from standard (unfractionated) heparin or chemically
synthesized
-Enoxaparin is the most common low molecular weight heparin

30
Q

what clotting factors does enoxaparin inactivate well? what does it not do that unfractionated heparins can?

A

— Enoxaparin inactivates Xa well, but not thrombin (factor IIa)

31
Q

what are advantages of low molecular weight heparins over unfractionated heparins?

A

Being used more commonly due to advantages over unfractionated heparin

  • Less bleeding tendencies possible
  • Protamine sulfate is less active against LMW heparins —
  • Less risk of thrombocytopenia
  • Improved pharmacokinetics– can give subcutaneous
  • Longer half-life
32
Q

what is warfarin? how does it work?

A

-Oral anticoagulant by antagonizing vitamin K actions
-Reduces clotting factors (II, VII, IX and X); factor VII has shortest half-life
-Clotting time not affected until existing factors used

33
Q

how is warfarin administered?

A

Injectable and oral formulations available

34
Q

what is the traditional use for warfarin in veterinary medicine? is it still used?

A

Was used as an oral chronic preventative anticoagulant, but less use in veterinary medicine now with availability of other drugs
- Dosing usually begun with heparin administration

35
Q

what should we monitor while administering warfarin?

A

Monitor using international normalized ratio (INR) —
> patient PT/mean normal PT for the lab
> increase INR value to 2.0-3.0

36
Q

adverse effects of warfarin?

A

— -Bleeding tendencies; can combat with Vitamin K1
— -Serious bleeding requires fresh blood/plasma
— -Warfarin crosses the placenta; don’t use in pregnancy

37
Q

is it better to use warfarin or heparin during pregnancy? why?

A
  • Heparin does not cross the placenta so use it
  • Warfarin crosses the placenta; don’t use in pregnancy
38
Q

what is an important selective factor Xa inhibitor? how does it work and how fast?

A

Rivaroxaban
- Inactivate factor Xa directly
- Does not interact with ATIII and no thrombin activity
- Fairly quick anticoagulant activity

39
Q

advantage of rivaroxaban over warfarin/heparins

A

Predictable pharmacokinetics and a fixed dosage can be used without monitoring as with warfarin or heparins

40
Q

route of admin for rivaroxaban

A

oral

41
Q

adverse effect of Rivaroxaban and how to possibly mitigate

A

Bleeding can occur
> Reversing agents are available but limited data in veterinary patients

42
Q

primary use of Rivaroxaban in vet med

A

Being used more in veterinary medicine
- Use primarily in dogs with IMHA thus far

43
Q

common systemic anticoagulants

A

heparin
low molecular weight heparins
warfarin
selective factor Xa inhibitors

44
Q

common antithrombotic drug? how does it work?

A

Aspirin (Less commonly used with clopidogrel available)
-cyclooxygenase inhibitors-

Irreversibly binds (acetylates) cyclooxygenase-1
-COX-1 selective over COX-2 at low doses; selectivity lost at higher doses
-Prevents TXA2 production in platelets reducing platelet aggregation
-Other NSAIDs can inhibit cyclooxygenase-1 but not irreversibly; hence a shorter duration of action

45
Q

what animal metabolizes aspirin poorly? what do we need to do as a result?

A

— Cat metabolizes aspirin poorly; 2X weekly dosing used

46
Q

what does aspirin prevent?

A

Prevents thrombus and re-thrombosis formation
>Feline cardiomyopathy
>Heartworm disease
>Equine laminitis and navicular diseases

47
Q

adverse events related to aspirin use?

A
  • Renal damage
  • Bleeding tendencies
  • Gastrointestinal ulceration
48
Q

types of antithrombotic drugs?

A

-cyclooxygenase inhibitors- (Aspirin)
-ADP Inhibitors- (Clopidogrel)

49
Q

what is clopidogrel and how does it work?

A

Antithrombotic Drugs -ADP Inhibitors-

-Reduce platelet aggregation by inhibiting ADP pathways
* Act as P2Y12 (aka P2YADP) receptor antagonists; prevent binding of ADP to receptors
- May be synergistic with aspirin as work by different mechanisms of action —
- Clopidogrel is irreversible inhibitor of the P2Y12 receptor

50
Q

how is clopidogrel activated? what are drugs like this called?

A

Clopidogrel is a “prodrug”—must be activated by liver P450 metabolism

51
Q

what is clopidogrel mainly used for?

A

Clopidogrel is routinely used for thromboembolic concerns in cats (HCM) and in dogs (mainly IMHA)

52
Q

is clopidogrel safe?

A

fairly safe

53
Q

how do fibrinolytic drugs work? what are two common examples?

A

-Fibrinolytics rapidly lyse thrombi by activating plasmin from clot bound plasminogen
> Studies have shown that interventional angioplasty is superior to these agents in human medicine for myocardial infarction

Tissue Plasminogen Activators

54
Q

what are tissue plasminogen activators? how do they work? what are their properties and route of admin?

A

-Are proteases that bind fibrin
-Can preferentially activate clot bound plasminogen —
>Limits activation of systemic plasmin

  • Fairly short half-life necessitates constant rate infusion
55
Q

uses of tissue plasminogen activator

A

Thromboembolic therapy for canine pulmonary thromboembolism and feline saddle thrombis

56
Q

adverse effects of tissue plasminogen activator

A
  • Reperfusion injury
  • Bleeding tendencies
57
Q

what is erythropoietin? how is it made? how does it work and what does it do?

A

Drug used in anemia

Growth Factor
* Glycoprotein made by kidney in response to hypoxia
-Prepared by recombinant technology (rHuEPO)
-EPO receptor is member of JAK/STAT superfamily
-Stimulates proliferation-differentiation of red cell progenitors and release of reticulocytes

58
Q

result of erythropoietin use? what should we take with it?

A
  • Increase in hematocrit and hemoglobin in 2-4 weeks
  • Iron supplementation is advised with EPO therapy

Pharm Test 3 (16 decks)

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