6.1 - Blood Flashcards

1
Q

What kind of drug is acetylsalicylic acid?

A

Antiplatelet Drug
–> Inhibits cyclooxygenase enzymes (COX) that produce thromboxane A2, resulting in:
Reduction of platelet aggregation and prolonged bleeding time

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2
Q

What are the functions of ADP and thromboxane A2?

A

Substances that stimulate the activation and aggregation of platelets to form a plug

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3
Q

What are the adverse effects of acetylsalicylic acid?

A

Most common are gastric irritation (Heartburn), and risk of gastric ulceration

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4
Q

What is low dose (81mg/day) aspirin used for?

A

Used to prevent complications related to thromboses
–> Also effective in circumstances where there is an increased risk of arterial thrombosis (such as during angioplasty)

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5
Q

What kinds of drugs are clopidogrel, prasugrel, and ticagrelor?

A

ADP Receptor Antagonists
–> decreases platelet aggregation results in inhibition of ADP released from activated thrombocytes
–> Used to prevent thrombus formation (e.g., following angioplasty)

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6
Q

Which clotting factors are vitamin K dependent?

A

II, VII, IX, X

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7
Q

What is antithrombin III?

A

An anticoagulant in our body responsible for inactivation of factors:
Xa
IIa (thrombin)
IXa
XIa
XIIa

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8
Q

Which test will measure the speed of the intrinsic pathway?

A

aPartial Thromboplastin Time

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9
Q

What test measures the speed of the extrinsic pathway?

A

Prothrombin Time

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10
Q

How do anticoagulants work?

A

They reduce the ability of blood to form clots.

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11
Q

What is heparin?

A

Anticoagulant
–> Activates ATIII, resulting in inactivation of Xa, IIa, XIIa, XIa, and IXa.

Results in reduced coagulation

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12
Q

How is heparain administered?

A

IV
–> Effective immediately

Sub-Q
–> 1-2 hours

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13
Q

Administration of heparin requires close monitoring using which test?

A

Activated partial thromboplastin time aPTT OR Anti-Factor Xa

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14
Q

How is the dose of heparin adjusted?

A

aPTT/ newer way: Anti-Factor Xa
With a goal of obtaining a coagulation time of 1.5-2.5 times the normal value of this patient

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15
Q

What are the clinical uses of heparin?

A

–> Prevention or treatment of venous and arterial clots (DVT, PE, Acute coronary syndrome)
–> During extracorporeal circulation (Bypass, hemodialysis)

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16
Q

What are the adverse effects of heparin?

A

Bleeding
–> Nose, gums, bruising, petechiae
–> Menorrhagia, GI bleed, hematuria
–> HypoTN, tachycardia, Decreased LoC
–> Headache, confusion, change in vision
–> Abdominal or pelvic pain

–> Heparin-induced thrombocytopenia
–> Osteoporosis

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17
Q

What is heparin induced thrombocytopenia?

A

An immune reaction to heparin that results in platelets being pulled from the blood stream.

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18
Q

How can heparin toxicity be treated?

A

Protamine

19
Q

What kinds of drugs are delteparin and enoxaparin? What are its advantages?

A

Low molecular weight heparin
–> Acts more on factor X than on II (2-4x more selective)

–> More predictable anticoagulant response and fewer hemorrhagic complications

20
Q

What is fondaparinux? How is it administered?

A

A indirect specific factor Xa inhibitor
–> activates ATIII specifically such that is only increases desctruction of factor Xa
–> s.c.

21
Q

What kind of drugs are apixaban and rivoroxaban?

A

Direct factor Xa inhibitors
–> inhibits Xa specifically by binding directly to it
–> p.o.

22
Q

How does warfarin work? What is its route of administration and onset of action?

A

Oral anticoagulant
–> Vit K antagonist, decreasing synthesis of factors II, VII, IX, X
–> Treatment requires 3-4 days before it has reached full efficacy as only newly synthesized factors will be affected

23
Q

Which test is used to monitor levels of warfarin therapy? What are the normal and therapeutic goal ranges for this test?

A

Prothrombin Time (INR)
INR = pt’s PT / ave pop PT

Normal range: 0.8-1.2
Therapy aim: 2.0-3.5

24
Q

What is warfarin used for?

A

Long-term prophylaxis of thrombosis
–> a-fib, mechanic heart valves

25
Q

What are the adverse effects of warfarin?

A

–> Bleeding, bruising
–> Can cross placenta; known teratogen
–> Very sensitive to dietary vitamin K intake (Vit K reduces warfarin’s efficacy)
–> Multiple drug-drug interactions, and other drugs that affect CYP levels or compete for binding to plasma proteins

26
Q

How do you treat warfarin toxicity?

A

–> Vitamin K (p.o./i.v.)
–> Prothrombin complex concentrate (II, VII, IX, X)
–> Fresh-frozen plasma

27
Q

What kind of drug is dabigatran? Why would you use it instead of warfarin?

A

A direct thrombin inhibitor (p.o)
–> Not sensitive to vit K intake, fewer drug-drug interactions like warfarin. Therefore more predictable and less frequent monitoring is required.

28
Q

What are the adverse effects of dabigatran?

A

bleeding & dyspepsia

29
Q

How do you treat toxicity due to dabigatran?

A

idarucizumab

30
Q

What are the clinical uses of fribin/thrombolytics?

A

MI, PE, ischemic stroke

31
Q

What is tPA?

A

Tissue plasminogen activator
–> thrombin/fibrinolytic

32
Q

What is tenecteplase?

A

A synthetically modified tPA

33
Q

What is streptokinase?

A

a thrombin/fibrinolytic of bacterial origin

34
Q

What is the mechanism of action of thrombolytics?

A

Increase conversion of plasminogen to plasmin, which destroys fibrin within blood clots.

35
Q

What are the adverse effects of thrombolytics?

A

Plasmin can destroy pre-existing clots and promote recurrence of bleeding at sites of recently healed injury - this is especially problematic if this leads to intracranial hemmorhage

36
Q

What is something to be aware of when administering streptokinase?

A

Due to its bacterial origin, pt’s often mount an immune response against the enzyme of the first use. Therefore, it can usually only be used once.

37
Q

What kind of drug is tranexamic acid?

A

An antifibrinolytic
–> Reduces fibrinolysis by inhibiting binding of plasminogen to fibrin

38
Q

Why would you use an antifibrinolytic such as tranexamic acid?

A

Reduce bleeding
–> Menorrhagia
–> Hemophilia
–> During some surgery

39
Q

What are the adverse effects of antifibrinolytics such a tranexamic acid?

A

Thromboembolic events and allergic skin reactions.

40
Q

Which coagulation factors are associated with the intrinsic pathway? Which test tests their efficacy?

A

XII, XI, IX, VIII
–> aPartial Thromboplastin Time

Cascade to activate factor X –> II (thrombin) –> I (fibrin)

41
Q

Which factors are associated with the extrinsic pathway? Which test tests their efficacy?

A

Tissue factor & factor VII
–> Tested with Prothrombin Time

Cascade to activate factor X –> II (thrombin) –> I (fibrin)

42
Q

What are the adverse effects of clopidogrel?

A

–> Must be activated by CYO 2C19 (so may not be activated enough in slow metabolizers)
–> Agranulocytosis
–> Bleeding

43
Q

What are the adverse effects of prasugrel?

A

–> Must be activated by hepatic enzymes (so may not be fully activated by slow metabolizers)
–> Bleeding

44
Q

What are the adverse effects of ticagrelor?

A

Bleeding