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Pharmacology Exam 4 > Procoagulants & Anticoagulants > Flashcards

Procoagulants & Anticoagulants Flashcards

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1
Q

How is major bleeding defined and examples?

A

by how it affects patient: intracranial, intraspinal, intraocular, mediastinal.

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2
Q

What are the risk factors for bleeding while on anticoagulation?

A

anti-coagulation effect, increased age, female, Hx GI bleed, use of ASA along with other anticoagulation

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3
Q

What are the triple As?

A

Primary hemostasis: platelet adhesion, activation, and aggregation

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4
Q

What is Adhesion dependent on?

A

von Willebrand’s factor (vWF) aka Factor VIII:v

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5
Q

What does vWF do?

A

acts as a bridge, one end attaches to platelet and the other to the damaged tissue

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6
Q

Where is vWF made?

A

synthesized and released from endothelial cells (not made in liver)

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7
Q

What connects the platelet to the endothelium via vWF?

A

Gp1B

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8
Q

What is the MOA of Desmopressin (DDAVP)?

A

stimulates a large release of vWF from the endothelium, will shorten bleeding time in patients with mild forms of hemophilia A or VWD.

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9
Q

When can you use Desmopressin?

A

in Type 1 & 3, qualitative disease. DDAVP doesn’t work in type 2

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10
Q

What’s the IV dose of DDAVP?

A

0.3mg/kg over 15-30 min to avoid hypotension. slow infusion. (can release local vasoactive mediators causing hypotension)

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11
Q

What can increase MI postop in CV patients two-fold?

A

desmopressin

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12
Q

What’s the MOA of activation?

A

thrombin combines with a thrombin receptor on the platelet surface and platelet changes shape and releases mediators that promote aggregation.

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13
Q

What are the important mediators in activation?

A

ADP and thromboxane A2

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14
Q

What acts on ADP?

A

plavix

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15
Q

What acts on thromboxane A2?

A

aspirin

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16
Q

When should you stop plavix preop?

A

7-10 days preop. Noncompetitive drug that has to live out life of platelets

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17
Q

What’s the MOA of thienopyridine derivatives?

A

antiplatelet effect from inhibition of adenosine diphosphate-induced platelet aggregation. inhibits P2y12 receptor on the platelet

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18
Q

Where does plavix affect hemostasis?

A

at binding

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19
Q

What are examples of thienopyridine derivatives?

A

ticagrelor, clopidogrel, prasugral

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20
Q

What is different about ticagrelor from the other thienopyridine derivatives?

A

ticagrelor is reversible and not a prodrug. clopidogrel and prasugral are prodrugs and irreversibly bind so require metabolism to work

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21
Q

How is thromboxaine A2 formed?

A

phospholipids–>phospholipase A2–>Arachidonic acid–>cyclo-oxygenase–>prostaglandin A2–>Prostaglandin H2–>Thromboxane A2. (Arachidonic acid breaks off from phospholipids and converts with cox to prostaglandin)

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22
Q

What is the MOA of cyclooxygenase inhibitors?

A

inhibit platelet cycooxygenase and prevent synthesis of thromboxane A2 (at activation)

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23
Q

What inhibits platelet cyclooxygenase?

A

low-dose aspiring (60-325 mg/d)

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24
Q

What are some examples of cyclooxygenase inhibitors?

A

ASA, NSAIDs, Celebrex

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25
When should you stop ASA preop?
7-10 days stop, restart 24h post surgery
26
T/F, a clot is still water-soluble after the triple As.
True
27
What do ADP and Thromboxane A2 uncover?
fibrin receptors GPIIb/IIIa
28
What does fibrin do?
links platelets together
29
What is the MOA of GPIIb/IIIa inhibitors?
inhibit platelet aggregation by interfering with platelet-fibrin receptors
30
What are examples of GPIIb/IIIa inhibitors?
abciximab, eptifibatide, tirofiban
31
When do you stop GPIIb/IIIa inhibitors prior to surgery?
eptifibatide(integrilin)/tirofiban(aggrastat) DC 8 hours preop, abciximab (reopro) DC 24-48hours preop
32
Where does aspirin act in the clotting cascade?
between vWF and TxA2
33
Where does plavix act in the clotting cascade?
between ADP and GPIIb/IIIa activation
34
Where do GPIIb/IIIa inhibitors act?
between GPIIb/IIIa activation and platelet aggregation
35
What is the key player in secondary hemostatsis?
fibrin
36
What is involved in fibrin production?
extrinsic, intrinsic, and final common pathway. incorporating all 13 clotting factors
37
When do clots become stable.
secondary hemostasis, after platelet aggregation fibrin is woven into platelets and they are cross-linked making them insoluble in water/stable
38
Which clotting factors are made in the liver?
(10 of them)I fibrinogen, II prothrombin, V proaccelerin, VII proconvertin, VIII antihemophilia, IX christmas factor, X stuart prower factor, XI plasma thromboplatin antecedent, XII Hageman factor, XIII fibrin-stabilizing factor
39
Which clotting factors are NOT made in the liver?
(3 of them) III thromboplastin--vascular wall/extravascular cell membranes, IV Calcium--diet, VIII vWF--vascular endothelial cells
40
What clotting factors are dependent on Vit K?
(4 of them) II prothrombin, VII proconvertin, IX Christmas Factor, X Stuart Prower Factor
41
What factor is missing in the clotting factors?
VI, there isn't one
42
What initiates the extrinsic pathway?
initiated in response to injury occuring outside the blood vessel
43
What factors are involved in the extrinsic pathway?
Factor III and VII
44
What leads to the release of Factor III?
damage to the vessel
45
What is the primary physiologic initiator of coagulation?
thromboplastin
46
What activates Factor VII?
Factor III
47
What is the beginning of the final pathway?
Factor VII and Factor III and calcium on the surface of platelet activate Factor X
48
How does coumadin work?
binding the vitamin K receptors in the liver and competitively inhibiting Vitamin K
49
What does coumadin do?
depress production of Vit K dependent clotting factors II, VII, IX, X, blocks classic extrinsic pathway and final common factors
50
What does coumadin do to PT?
prolong it
51
What assesses extrinsic pathway?
PT and INR
52
When do you DC coumadin preop?
very surgery/surgeon dependent but generally 5 days preop. still assess INR, possible bridging or reversal needed
53
Where does heparin work?
intrinsic pathway
54
What initiates the intrinsic pathway?
injury to INSIDE of blood vessel
55
What factors are part of the intrinsic pathway?
XII, XI, IX, VIII
56
Describe intrinsic pathway
trauma to vessel activates XII, XIIa activates XI, XIa activates IX, IXa combines on platelet surface with activated VIII:C and calcium which activates X (beginning of final common pathway)
57
What triggers the final common pathway?
activated factor X occurring from either extrinsic or intrinsic pathway complexes on platelet surface with factor V and calcium to convert factor II to thrombin IIa.
58
What does thrombin IIa do?
converts fibrinogen (factor I) to fibrin
59
What are the factors in the final common pathway?
X, V, II, I, XIII
60
What forms a stable clot in the final common pathway?
Factor XIII and fibrin Ia cross-linking occurs and forms stable clot
61
What is the main player in anticoagulation?
antithrombin III
62
Where is AT3 made and what does it do?
made in liver and neutralizes final common pathway factors II and X and intrinsic factors IX, XI, and XII by forming complexes with them.
63
What does heparin do to AT3?
increases it
64
What types of patients have AT3 deficiencies?
cirrhosis and nephrotic syndrome.
65
How does heparin work?
increasing effectiveness of AT3 >1000 fold | interferes with intrinsic pathway
66
What's the #1 reason a patient is unresponsive to heparin?
AT3 deficiency
67
How do you treat someone deficient in AT3?
FFP
68
What assesses the intrinsic pathway?
aPTT and ACT
69
What ACT level is adequate heparinization for cardiac pump cases?
>450
70
What does larger MW unfractionated heparin do?
catalyze inhibition of factor IIa and Xa
71
When do you DC unfractionated heparin preop?
4-6 hours preop
72
What's the differences with LMWH?
smaller MW catalyzes inhibition of only factor Xa, less protein bound, irreversibility with protamine, prolonged 1/2 life, lack of monitoring by anticoagulant response
73
What are examples of LMWH?
Lovenox, dalteparin
74
When do you stop LMWH preop?
12 hours preop
75
What is the MOA of direct thrombin inhibitors?
bind to thrombin in varying degrees
76
What are examples of direct thrombin inhibitors?
bivalrudin, argatroban, lepirudin, desirudin, ximelagatran, dabigatran
77
When do you DC direct thrombin inhibitors?
bivalrudin/argatroban 4-6h Lepirudin, Desirudin 24h Ximelagatran, Dabigatran 48h
78
What coagulation factors make up Prothrombin Complex Concentrates (PCC)?
II, VII, IX, X
79
What are PCCs used for in other countries?
coumadin reversal
80
What are examples of PCCs?
KCENTRA, octaplex, FEIBA, profilnine, Bebulin
81
What is bebulin for?
indicated for the prevention and control of bleeding episodes in adult patients with hemophilia B (factor IX deficiency or Christmas disease)
82
What does bebulin contain?
factor IX, II, X, and low amounts of factor VII
83
What are the Vit K dependent clotting factors?
factor IX, II, X
84
Where does Apixaban (eliquis) work?
final common pathway, anti Xa
85
What is the main FDA use for Eliquis?
VTE prophylaxis, also afib
86
What is the reversal in trial for eliquis?
FEIBA (factor eight inhibitor bypass activity)
87
When do you stop eliquis preop?
1-4 days preop
88
Is there any lab screening for eliquis?
No
89
What is the dose of eliquis?
8mg bid, 2.5mg if old or little, VTE prophylaxis 2.5mg bid
90
Where does Xarelto (rivaroxaban) work?
final common pathway, anti Xa
91
What is Xarleto used for/dosing?
VTE prophylaxis 10mg qd, AF 20mg qd unless old or decreased CrCl then 15mg qd, VTE treatment 15mg bid x21 days then 20mg qd
92
What lab can be screened for Xarelto?
PT
93
What is the reversal in trial for Xarelto?
PCCs, ?FEIBA
94
When do you stop Xarelto?
1-4 days preop
95
Where does Edoxaban (savaysa) work?
anti Xa
96
What is Edoxaban for/dosing?
AF 60 mg qd, VTE treatment 60mg qd, 30 mg qd if old or decreased Cr Cl
97
What labs do you screen with Edoxaban?
PT/INR
98
What reversal is in trial for Edoxaban?
PCCs, FEIBA
99
When do you stop Edoxaban?
1-4 days preop
100
Where does Dabigatran (pradaxa) work?
anti-IIa
101
What are the indications/doses for pradaxa?
AF 150 mg bid, VTE prophylaxis 220mg qd
102
What lab do you screen with pradaxa?
aPTT
103
What is the reversal for pradaxa?
dialysis, now can add PCCs/FEIBA
104
When do you stop pradaxa preop?
3-5 days
105
Which NOAC can cause increased GI bleed?
Pradaxa
106
In general when should NOACs be stopped preop?
3-5 half lives, 2-5 days depending on drug and CrCl
107
What is the main player in fibrinolysis?
Plasmin
108
What is the inactive form of plasmin formed in the liver and circulating in the blood?
plasminogen
109
T/F. Plasminogen is incorporated into all clots when they form.
True, but its not active
110
What converts plasminogen to plasmin?
tissue type plasminogen activator (tPA) and urokinase type plasminogen activator (uPA)
111
What does plasmin do?
breaks down fibrin in the clot and splits products. clot buster
112
What are anti-fibrinolytic agents?
lysine analogs, competitively inhibit the activation of plasminogen to plasmin
113
What types of patients were anti-fibrinolytics studied in?
cardiac and orthopedic
114
What were the results of studying anti-fibrinolytics?
all seemed to decrease blood loss but not proven to decrease transfusion rate or mortality. major outcome in CV was CT output postop day 1
115
What are 2 types of anti-fibrinolytics?
Tranexamic Acid, Amicaproic acid
116
Which is proven to decrease transfusions? TXa or Amicar?
Txa.
117
What are some effects of Txa?
decreases transfusions, can inhibit plasmin at high levels, causes seizures, can give orally for heavy menstrual bleeding
118
What does Aprotinin do?
inhibit plasmin so fibrin breakdown is slow and bleeding is decreased.
119
When is Aprotinin used?
primarily cardiac bypass cases especially reops to decrease postop bleeding
120
What are the risks of aprotinin?
primary allergic reaction after first dose or severe anaphylaxis after 2nd. can also worsen renal function
121
What is protamine made of?
salmon semen
122
What is the MOA of protamine?
inhibits platelets and serine proteases involved with coagulation
123
What is protamine used for?
reverse unfractionated heparin through neutralization reaction (acid-base)
124
What is the dose of protamine?
1mg per 100u of heparin, or give based on circulating heparin level
125
What are the adverse reactions of protamine?
anaphylaxis, acute pulm vasoconstriction, RV failure, hypotension. GIVE SLOW
126
What are common herbal medications that affect coagulation?
3 g's: garlic, ginkgo, ginseng
127
What does garlic do?
inhibit platelet aggregation possibly irreversibly, increased fibrinolysis, antihypertensive activity. DC 7days
128
What does ginkgo do?
inhibit platelet-activating factor. DC 36h
129
What does ginseng do?
lowers blood glucose, increase prothrombin and activated partial PTs in animals. DC 24h

Pharmacology Exam 4 (7 decks)

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