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Pharm 2 > Anticoagulants > Flashcards

Anticoagulants Flashcards

1
Q

Do anticoagulants have a high or low Vd?

A

low because you want it to stay in the blood

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2
Q

What is hemostasis?

A

the cessation (ending) of blood loss from a damaged vessel

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3
Q

What is hemostasis for?

A

-prevent blood loss
-prevent thrombosis (clot blocks vein or artery)
-aid in clot removal

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4
Q

what are the similarities between antiplatelet and anticoagulant drugs?

A

-they are both present in hemostasis
-they both are used in stroke prophylaxis and acute coronary syndromes

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5
Q

What are some differences between antiplatelet and anticoagulant drugs?

A

-antiplatelets only work on platelets = weaker = safer
-antiplatelets can be used for stroke treatment, not anticoagulants
-anticoagulants can be used for heart valve replacement = triggers immune response = clotting

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6
Q

What are the three componenets of hemostasis?

A

-blood vessels
-platelets
-coagulation factors

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7
Q

What are the steps of primary hemostasis?

A

goal: aggregation

vasoconstriction -> platelet aggregation -> clotting -> go to area to be clotted -> combine with fibrin to cement mesh and create clot

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8
Q

what are the steps of secondary hemostasis?

A

goal: coagulation

thrombin -> fibrin -> combine with aggregated platelets to form clot

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9
Q

Does primary and secondary hemostasis occur simultaneously or sequentially?

A

simultaneously

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10
Q

How is a platelet plug formed?

A

damaged vessel or capillary -> immediate reflex -> vasoconstriction -> exposed collagen promotes platelet adherence -> degranulation and release cytoplasmic granules -> contain serotonin (vasoconstrictor), ADP and thromboxane A2 -> ADP attracts platelets -> thromboxane promote aggregation, degranulation and vasoconstriction -> positive feedback loop and platelet plug is formed

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11
Q

What are the three basic mechanisms that promote hemostasis?

A
  1. immediate vasoconstriction
  2. exposed collagen promote platelet adherence = degranulate and release granules with serotonin, ADP and Thromboxane
  3. serotonin, ADP and thromboxane promote more platelet adhesion and aggregation and vasoconstriction
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12
Q

What are the steps in coagulation?

A
  1. damaged tissue -> release factor 3 -> activate factor 7 with Ca (extrinsic)
  2. active platelets -> release factor 12 -> activates factor 11 (intrinsic)
  3. factor 7 and 11 activate reactions that activate factor 10
  4. factor 10, 3, 5, Ca, and PF3 (platelet thromboplastic factor) -> activate prothrombin activator -> converts prothrombin to thrombin -> converts fibrinogen to fibrin
  5. fibrin loose mesh + factor 12 -> covalent crosslinks -> dense fiber aggregation -> catches RBC and platelets -> blood clot
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13
Q

What does thrombin do?

A

changes fibrinogen to fibrin

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14
Q

What are the characteristics of a resting platelet?

A

-round shape
-inactive GP 2b/3a receptors

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15
Q

what does prostacyclin do

A

vasodilation

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16
Q

what are the characteristics of an activated platelet?

A

-oblong shape
-activated GP 2b/3a receptors

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17
Q

what does cAMP do?

A

inhibits the release of calcium

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18
Q

What do GP 2b/3a receptors do?

A

-important to blood clot formation
-signaling and binding to fibrinogen

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19
Q

What activates GP 2b/3a receptors?

A

release of calcium in the platelet

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20
Q

What three things activate calcium release within platelets?

A

-thrombin
-thromboxane A2
-ADP

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21
Q

What are two clotting factor diseases and what causes them?

A

-hemophilia: recessive X-linked genetic disorder; no functional factor 8 and 9
-Von Willebrand disease: genetic lack of vWF

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22
Q

What are some characteristics of platelets?

A

-no nucleus
-contain remnants of ER (have Ca2+)
-produced from megakaryocytes

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23
Q

What are the three steps of the platelet response?

A

-adhesion
-activation
-aggregation

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24
Q

What are the three receptors responsible for platelet adhesion and what are their functions?

A
  1. GP1a = binds to exposed collagen
  2. GP2b/3a = promotes aggregation
  3. GP1b = binds to vWF
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25
Q

What is vWF?

A

-a blood glycoprotein
-promotes hemostasis and platelet adhesion

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26
Q

What are three things that activate COX-1 in platelet activation?

A

-arachidonic acid
-collagen
-thrombin

27
Q

What component is the most important to activate the platelets?

A

overdose of calcium

28
Q

What does COX-1 activate in platelet activation?

A

thromboxane A2 which activates GP 2b/3a which promotes aggregation

29
Q

What three things act on platelets to promote aggregation?

A

-ADP
-Thrombin
-TxA2

30
Q

What are the two pathways for coagulation and what are its key players?

A

-intrinsic pathway: factor 11
-extrinsic pathway: factor 7

31
Q

What parts of the coagulation cascade require calcium

A

-both intrinsic and extrinsic
-some of the last steps too

32
Q

What is the order of mediators and factors in the intrinsic pathway?

A

charged surface -> 12a -> 11a -> 9a -> 10a -> thrombin (2a) -> thrombin-fibrin clot

33
Q

What is the order of mediators and factors in the extrinsic pathway?

A

-tissue damage -> tissue factor (3) -> 7a -> 10a -> thrombin -> thrombin-fibrin clot

34
Q

What factors act on factor 10a?

A

-factor 7, 9, 8,11

35
Q

**List the indirect thrombin inhibitors

A

-unfractionated heparin
-Low molecular weight heparin
-rivaroxiban
-fondaparinux

36
Q

Why is unfractionated heparin only given IV or SC?

A

-because IM can lead to hematoma = blood in the muscle

37
Q

What is another name for thrombin?

A

-factor 2a

38
Q

What part exactly binds to antithrombin 3?

A

pentasaccharide sequence in the polysaccharide chain of the thrombin inhibitor drug

39
Q

How is heparin removed from the body?

A

-cleared by macrophage/monocyte system
-inactive metabolites and left over parent drug excreted into urine

40
Q

What are some differences between UFH and LMWH?

A

-LMWH can be given SC
-LMWH has better bioavailability (90% vs 30%)
-LMWH has less bleeding = safer = less monitoring
-LMWH has longer half life (4-6h)
-UFH only has t1/2 of 0.5-1h

41
Q

Why does LMWH have a better bioavailability than UFH?

A

because it has short chains so it is easier to go to the blood and less is lost in transport

42
Q

What are the three main complications of heparin therapy and how are they treated?

A

-bleeding -> protamine sulfate
-osteoporosis -> 3-6mo treatment
-heparin-induced thrombocytopaenia (HIT) -> depends

43
Q

What are the types of HIT and how are they different?

A

-HIT 1: 10% of pt; non-immune; benign
-HIT 2: 0.5-1% of pt; immune related; can lead to venous or arterial thrombosis

44
Q

high risk HIT: how it occurs?

A

platelets contain PF4 -> when injured platelets release PF4 -> if heparin is present, body makes heparin antibodies -> heparin binds to heparin IgG -> binds to PF4 -> increases platelet activation -> platelet to fibrin/thrombin ration off -> excessive coagulation -> collapses veins -> may lead to dead tissue

45
Q

What is the difference between indirect and direct thrombin inhibitors?

A

-indirect: requires antithrombin; no effect on thrombin in clots because antithrombin cannot reach the thrombin
-direct: can bind to thrombin in clots; displaces from clots

46
Q

What does thrombin do in the presence of an indirect inhibitor if it is trapped in a clot?

A

-indirect inhibitors do not displace the thrombin from the clot, so the thrombin will continue to make fibrin and activate platelets

47
Q

Where is a lot of Vitamin K stored in the body?

A

the liver

48
Q

What factors require vitamin K for their creation?

A

factor 2, 7, 9, 10

49
Q

What are the issues with warfarin?

A
  1. its abs is decreased in the presence of cholestyramine
  2. pt has hypoproteinemia (low protein) = no protein to bind to warfarin = increases Vd and shortens half life
  3. antibiotics decrease K+ because remove gut flora = excessive effects of warfarin
  4. eating vit K rich foods = work against warfarin
  5. other drugs that inhibit or increase the metabolic effects of CYP2C9 will affect warfarin effects
50
Q

Where in the body does warfarin work?

A

the liver

51
Q

What is warfarin-induced skin necrosis caused by?

A

-due to inhibition of protein C = results in clotting

52
Q

What is the target of warfarin?

A

Vitamin K enzyme

53
Q

What is the target of dabigatran?

A

thrombin

54
Q

What interacts with dabigatran?

A

P-glycoprotein

55
Q

What is the target of rivaroxaban?

A

Factor 10a

56
Q

What interacts with rivaoxaban?

A

-CYP3A4
-P-glycoprotein

57
Q

What is the target of apixaban?

A

-factor 10a

58
Q

What interacts with apixaban?

A

-CYP3A4
-P-glycoprotein

59
Q

What are three laboratory tests done to monitor the affects of anticoagulants?

A

-Partial Thromboplastin Time (aPTT)
-Prothrombin Time (PT)
-International Normalized Ratio (INR)

60
Q

What is the standard for blood clotting?

A

-blood clots in 4-8 min in test tube
-recalcified plasma clots in 2-4min

61
Q

How does Partial Thromboplastin time work?

A

-measures intrinsic pathway
-normal pt: if you add phospholipids to recalcified blood -> clotting in 26-33 seconds
-if clotting time doesn’t shorten -> intrinsic pathway not working
-if clotting takes shorter time -> excessive amount of factors

62
Q

How does Prothrombin Time work?

A

-measures extrinsic pathway
-normal pt: add phospholipids and thromboplastin to recalcified blood -> clots in 12-14 sec
-if clotting takes longer = extrinsic not working
-if clotting is immediate = excess factors/overactive

63
Q

How does INR work?

A

-prothrombin ratio
-goal: INR 2-3
-INR = patients PT (s)/mean normal PT (s)
-ISI = relative sensitivity of PT compared to WHO standard

Pharm 2 (11 decks)

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