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Blood Drugs Flashcards

1
Q

what are the goals of normal hemostasis

A

1) prevent prolonged hemorrhage
2) prevent spontaneous thrombosis

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2
Q

what are the 4 stages of hemostasis

A

1) vasospasm (vasoconstriction)
2) platelet response
3) coagulation
4) fibrinolysis (clot dissolution)

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3
Q

what are some prothrombogenic factors

A
  • vasoconstriction
  • platelet activators
  • procoagulants
  • fibrinolytic inhibitors
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4
Q

what are some antithrombogenic factors

A
  • vasodilators
  • platelet inhibitors
  • anticoagulants
  • fibrinolytic activators
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5
Q

what happens during vasospasm (stage 1 of hemostasis)

A
  • immediate vasoconstriction mediated by myogenic properties of the vessel wall (recoil)
  • release of sympathetics and local factors such as thromboxane
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6
Q

what happens during the platelet response

A

platelets adhere to exposed collagen in the damaged endothelium and to each other; the platelet plug then releases factors to recruit more platelets, promote vasoconstriction and initiate coagulation (TXA2, 5-HT and ADP)

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7
Q

what happens during the coagulation phase (phase 3) of hemostasis

A

sequential conversion of inactive proteins into active proteases, resulting in conversion of soluble fibrinogen to insoluble fibrin and formation of a net -> clot proper

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8
Q

what is the main initiator of coagulation

A

tissue factor -> factor VIIa

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9
Q

what happens during fibrinolysis

A

dissolution of the clot proper (thrombus) by proteolytic actions of plasmin

occurs once wound has healed to restore blood flow

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10
Q

what can cause excessive bleeding

A
  • platelet deficiency (thrombocytopenia, VWD)
  • clotting factor deficiency (single factor such as hemophilia or multiple factors such as vitamin K deficiency)
  • fibrinolytic hyperactivity
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11
Q

hemophilia can involve what clotting factors

A

VIII and IX

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12
Q

what are the 2 forms of vitamin K and which is used pharmacologically

A

Vitamin K1: phytonadione (food)
Vitamin K2: menaquinone (intestinal bacteria)

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13
Q

what is the MoA of vitamin K1

A

post-translationally modifies coagulation factors II, VII, IX, X

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14
Q

how is vitamin K1 absorbed

A

fat soluble -> uses bile salts for intestinal absorption

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15
Q

what are the routes for vitamin K1 administration and which is recommended?

A

IV, IM, SQ

SQ recommended as safest. IM causes hematoma formation and IV associated with anaphylaxis

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16
Q

what are the uses of vitamin K1

A

1) vitamin K1 deficiency (rodenticide toxicity, sweet clover poisnoning aka dicumoral toxicity)

2) warfarin overdose

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17
Q

what is the MoA of desmopressin acetate (DDAVP)

A

transiently increases Von Willebrand activity

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18
Q

what are the uses of desmopressin acetate (DDAVP)

A
  • treatment of mild von Willebrand disease
  • transiently reduces capillary bleeding during surgery (prophylactic)
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19
Q

what are the routes of administration of desmopressin acetate

A

nasal and injectable

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20
Q

what is the caveat for using desmopressin acetate during surgery

A

lasts 2hrs, repeated doses have a reduced effect

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21
Q

what is the MoA of protamine sulphate

A

binds to and neutralizes heparin; better against high molecular (unfractioned) heparin

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22
Q

what are the uses of protamine sulphate

A

heparin overdose

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23
Q

how is protamine sulphate given

A

IV slowly; accurate dose needed

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24
Q

why are accurate doses of protamine sulphate needed

A

too much causes anticoagulant effects

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25
plasmin lyses fibrin and fibrinogen by attaching to fibrin on __________
lysine binding sites
26
what is the MoA of aminocaproic acid (Amicar)
binds to the lysine binding site on fibrin and competitively inhibits plasmin
27
what are the uses of aminocaproic acid
to stop bleeding from fibrinolysis; as an adjunct therapy for hemophiliacs
28
a red thrombus is _______ rich and contains a large number of ______, it is _________ in origin a white thrombus is _______ rich and contains a large number of _________; it is __________ in origin
fibrin; RBCs; venous platelet; platelets; arterial
29
pathogenesis of thrombosis requires (3)
- local vessel injury - changes in blood flow (stasis or turbulence) - altered blood coagulability
30
what are the 3 drug classes of anticoagulants
1) systemic anticoagulants 2) antithrombotic drugs 3) fibrinolytic drugs
31
what is the MoA of heparin
binds to ATIII and forms a heparin-ATIII complex that inhibits activated Xa and IIa
32
what is the composition of heparin
mix of sulphated mucopolysaccharides isolated from mast cells
33
what are the uses of heparin
as an acute anticoagulant to initially treat thrombosis and thromboembolic disease
34
what is the caveat of heparin
only prevents new clot formation
35
what are some adverse effects of heparin and how can we mitigate this
- bleeding - monitor aPTT - can give protamine sulphate if overdose
36
what is Enoxaparin (Lovenox)
low molecular weight heparin
37
what are the advantages of Enoxaparin over regular unfractioned heparin
- less bleeding tendency - less risk of thrombocytopenia - improved pharmacokinetics: can give SQ, increased half life
38
how does Enoxaparin differ from heparin
Enoxaparin only inhibits Xa but not thrombin (IIa) making it less "effective" but safer
39
what is a disadvantage of Enoxaparin over heparin
protamine sulphate is not as effective at reversing an overdose of Enoxaparin vs heparin
40
what is the MoA of warfarin
inhibits Vitamin K factors II, VII, IX, X and stops clotting after existing factors are used
41
what are the uses of warfarin
in the past has been given as a chronic preventative anticoagulant and is commonly given as a first dose with heparin (works later)
42
what are adverse effects of warfarin
1) bleeding (combat with Vitamin K1) 2) crosses the placenta so cannot give to pregnant animals
43
how do we monitor warfarin therapy
international normalized ratio (INR) which is the patients PT/mean normal PT for the lab want to see 2.0-3.0
44
what is the MoA of rivaroxaban
selective Xa inhibitor
45
how does rivaroxaban differ from enoxaparin
rivaroxaban does not interact with ATIII, unlike enoxaparin rivaroxaban can be given orally
46
what is a main advantage of rivaroxaban
no monitoring required with a fixed dosage unlike with using heparins or warfarin
47
what is the main use of rivaroxaban at the moment
dogs with IMHA
48
what is the MoA of aspirin
inhibits COX-1 selectively (at low doses), preventing TXA2 production in platelets and therefore reducing platelet aggregation
49
what are the uses of aspirin
prevents thrombus formation and re-thrombus formation
50
what are some side-effects of aspirin
- bleeding - gastric ulceration - renal damage
51
what is the MoA of clopidogrel
Irreversibly inhibits the binding of ADP to its receptors (P2Y12 or P2YADP), resulting in impaired platelet aggregation
52
what is a consideration regarding the pharmacokinetics of clopidogrel
it is a prodrug and must be activated by P450 metabolism in the liver
53
what are the main uses of clopidogrel
for thromboembolic concerns in dogs with IMHA and cats with HCM
54
what is the MoA of t-PA
binds fibrin and preferentially activates clot-bound plasminogen
55
what are the uses of t-PA
thromboembolic therapy for canine pulmonary thromboembolism and feline saddle thrombus given as a CRI due to short half-life
56
what are adverse effects of t-PA
bleeding tendencies and reperfusion injury
57
what is the MoA of erythropoietin
stimulates proliferation-differentiation of RBC precursors and release of reticulocytes
58
what are the uses of EPO
- anemia of CKD - anemia of cancer
59
if you give EPO you should expect to see therapeutic results in
2-4 weeks
60
what are adverse effects of EPO
hypertension, seizures, therapeutic failure

Pharmacology & Anesthesiology (36 decks)

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