Agents that affect the clotting system Flashcards

(73 cards)

1
Q

initial activation of platelets causes what?

A

platelet plugs

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2
Q

3 receptors on a platelet

A

thrombin
TXA2
ADP

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3
Q

which go on to further actuvate the platelet?

A

TXA2 and ADP

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4
Q

what inhibits platelet aggregation?

A

cAMP

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5
Q

what connects two platelets thus activating them?

A

fibrinogen

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6
Q

fibrinogen binds to what receptor on the platelet?

A

glycoprotein (GPllB/GPlllA) receptors

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7
Q

what is a clot mosty formed out of?

A

fibrin

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8
Q

all factors are circulating ______, when activated become ______

A

proteins,

proteolytic enzymes

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9
Q

all factors require _____ for synthesis?

A

vitamin K

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10
Q

clotting cascade main ion

A

Calcium

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11
Q

prothrombin ll —> _______

A

thrombin lla

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12
Q

thrombin lla does what?

A

activates platelets, factors Vll, Vlll, Xlll

converts fibrinogen to fibrin, and as we know fibrin forms clots

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13
Q

what stabilizes clots?

A

Xlll –> Xllla

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14
Q

to reverse clot formation

A

plasminogen –> plasmin –> clot lysis

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15
Q

to localize the clotting

A

antithrombin lll –> causes inactivation of thrombin, factors 9, 10, 11, 12

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16
Q

too much clotting called what?

A

thrombus

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17
Q

clotting in arteries?

A

called white thrombi- associated with artharosclerotic plaque
- platelets + fibrin strands

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18
Q

clotting in veins?

A

red thrombi, associated with pooling of blood in extremities.
rbc + fibrin

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19
Q

thromboembolus

A

piece of thrombus breaks off and travels through the blood stream

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20
Q

conditions for which anticoagulants are used?

A
  1. thromboembolic disease- prevents formation and extension of clots in venous system
  2. after most kinds of surgery
  3. during transfusions
  4. pt’s with heart disease- arrhythmias
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21
Q

thrombophlebitis

A

due to deep venous thrombosis

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22
Q

anticoagulants do what

A

prevent clot formation

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23
Q

what are some in vitro anticoagulants?

A

calcium chelators- citric acid, ETDA, EGTA,

all bind calcium, remove from cascade. DONT GIVE TO PEOPLE, they are in blood bags.

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24
Q

main anticoagulant

A

heparin

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25
heparin properties and location
located in mast cells strong negative charge large polymers 3-30 kd
26
heparin physiological effects
inhibits clotting by activating lipoprotein lipases.
27
heparin mechanism of action
binds to antithrombin lll, and increases its affinity for clotting factors by 1000x at low dose. also inhibits factor Xa., thus decrease thrombin.
28
does heparin lyse existing clots?
no
29
how is heparin administered?
IV or sublig. too big to be absorbed by gut. also too big to be passed by placenta.
30
onset of action of heparin is what?
fast, t 1/2 = 1 hours.
31
heparin is degraded by what?
heparinsase.
32
overdose of heparin treated with what?
protamine sulfate
33
long term use of heparin causes what?
osteoporosis thrombocytopenia (HIT) hypersensitivity.
34
low molecular weight heparins
enoxaparin dalteparin fondaparinux
35
does heparin have a predictable dose response?
no
36
low molecular weight heparins
``` 4-5 kd- still too big for oral longer t 1/2 though = 4 hours more effect on 10a less HIT, osteoporosis more predictable D-R ```
37
fondaparinux
t 1/2 = 17 hours acts only on 10a, given subling
38
SE of low molecular weight heparins
(more expensive) not reversed by protamine may cause spinal hematoma in pt's who have had spinal tap or anesthesia
39
what is used when pt has heparin induced thrombocytomepnia (HIT)
leech hirudin anticoagulant analogs- inhibits thrombin
40
3 analogs of leech hirudin
BAD bivalirudin argatroban desirudin.
41
main oral anticoagulant
warfarin
42
Mech of action of warfarin
inhibits an enzyme that recycles vitamin K. so you get a deficiency, vit. K is used to make many factors in the blood clotting cascade.
43
does warfarin break up existing clots or just prevents new ones?
prevents new ones from forming.
44
how long does it take warfarin to have an effect?
long time, t 1/2 life of factor X is 40 hours, prothrombin 60 hours
45
what do you have to worry about with taking warfarin?
any drug that effects P450 can effect concentrations (barbiturates induce P450) also monitor diet
46
can warfarin pass the placenta?
yes
47
anything that inhibits factors is a what
enzyme inhibitor
48
direct thrombin inhibitor
dabigatran
49
dabigatran
``` prodrug enzyme inhibitor direct inhibitor works fast. taken orally ```
50
dabigatran SE
hemorrhage
51
warfarin is a direct or indirect mechanism
indirect. induces vit K deficiency
52
Factor Xa inhibitors
rivaroxrudin | apixarudin
53
SE of factor Xa inhibitors
bleeding after spinal tap or spinal surgery
54
platelet inhibitors: thrombin receptor blocker
vorapaxar
55
contraindication of vorapaxar
pt's with history of inter cranial bleeding.
56
platelet inhibitors: ADP inhibitors
``` TIC TIC CLO PRA ticlopidine ticagrelor clopidogrel prasugrel ```
57
side affect of ticlopidine
neutrapenia- low neutraphils | agranulocytosis
58
platelet inhibitors: fibrinogen receptor inhibitors
abciximab tirofiban eptifibatide
59
fibrinogen general mechanisms, all given how? and SE
prevent platelet aggregation all IV all cause thrombocytopenia (lots of platelets)
60
COX inhibitors
aspirin
61
COX mechanism of action
inhibits thromboxane All synthesis by | cyclooxygenase inhibitor....decrease in platelet aggregation
62
phosphodiesterase inhibitors
cilostazol | dipyridamole
63
phosphodiesterase inhibitors mech of action
inhibit enzyme that breaks down cAMP, so increase in CMP
64
platelet count reducer
anagrelide
65
anagrelide mech of action
decrease platelet formation, maturation, and number
66
contraindications for all anticoagulants
bleeding disorders sever hypertension after surgery on eye, brain, spinal cord
67
thrombolytic agents
streptokinase urokinase Tissue plasminogen activator (TPA)
68
all thrombolytic agents are what? and work how
enzymes | convert plasminogen to plasmin
69
what does plasmin do
hydrolyzes fibrin
70
how are thrombolytic agents given
IV
71
hemostatic agents
aminocaproic acid | tranexamic acid
72
aminocaproic acid
enzyme inhibitor | inhibits plasminogen activation
73
tranexamic acid
more potent that aminocaproic, same mech of action.