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Principles III > Coag ppt > Flashcards

Coag ppt Flashcards

1
Q

4 statges of hemostasis

HUGE SLIDE BUT THE BASIS AND INTRO INTO ALL THAT FOLLOWS

A
  1. VASCULAR CONSTRICTION- limits the flow of blood to the area of injury
  2. PLATELETS become ACTIVATED by thrombin and aggregate at the site if injury (temp loose PLATELET PLUG). Fibrinogen is responsible for stimulating platelet clumping (platelets bind to collagen that becomes exposed following rupture of the endothelial lining of vessles)
  3. Activated platelets release ADENOSINE-5’-DIPHOSPHATE (ADP) and TXA2 (which activates additional platelets), SEROTONIN, PHOSPHOLIPIDS, LIPOPROTEINS, and other proteins important for the coagulation cascade. Activated platelets change their shape to accomodate the formation of the plug.
  4. to insure stability of the initial loose platelet plug, a FIBRIN MESH (CLOT), forms and entraps the plug. if the plug contains only platelets it is termed WHITE THROMBUS, if red blood cells are present it is called RED THROMBUS.

The clot must be dissolved in order for normal blood flow to resume following tissue repair. the dissolution of the clot occures through the action of PLASMIN

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2
Q

test that knowledge

initial phase if hemostasis

A

vascular constriction

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3
Q

to test that knowledge

platelets become activated by what?

A

thrombin

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4
Q

to test that knowledge

what is responsible for stimulating platelet clumping

A

fibrinogen

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5
Q

to test that knowledge

activated platelets release what?

(6)

A

ADP

TXA2

Serotonin

Phospholipids

Lipoproteins

other proteins

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6
Q

to test that knowledge

which protein released by activated proteins, activates additional platelets

A

TXA2

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7
Q

to test that knowledge

what forms to entrap the plug to insure stability

A

Fibrin mesh (clot)

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8
Q

to test that knowledge

  1. If the plug contains only platelets it is called what?
  2. If it containd RBC ot is called what
A
  1. white thrombus
  2. red thrombus
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9
Q

to test that knowledge

dissolution of the clot occurs through the action of what?

A

plasmin

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10
Q

Whooooo made it time for an easy question to make you feel smart again!

1+1=?

A

2

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11
Q

picture time

now that you feel better. draw me a pic representation of what you want your edothelial layer to look like with a break and blood in the middle

A

keep this we’ll expand

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12
Q

Physiology, pathophysiology, and pharmacology of hemostasis

what is the patho for adhesion of platelets

A
  1. Damage to endothelial surface → subendothelial collagen exposure
  2. production/release of vWF form endothelial cells
  3. vWF anchors platelets to subendothelial collagen vascular wall

vWF= Von Willebrad factor

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13
Q

you now know the adhesion of plateletes draw it!!!

  1. Damage to endothelial surface → subendothelial collagen exposure
  2. production/release of vWF from endothelial cells
  3. vWF anchors platelets to subendothelial collagen vascular wall

Hint expand your 1st pic

A
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14
Q

What is the most common inherited coagulation defect

A

Von Willebrands Disease

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15
Q

what is tx for Von Willebrands disease

A

DDAVP- it releases vWF from endothelial cells

or

Give FFP

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16
Q

Physiology, pathophysiology, and pharmacology of hemostasis

patho of the activation of plateletes

A
  1. prothrombin → thrombin (IIa) which activates platelets
  2. Shape changes and realease of mediators (TXA2 and ADP)
  3. TXA2 and ADP promote platelet aggregation
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17
Q

now that you know the patho for activation of platelets draw it!!!

  1. prothrombin → thrombin (IIa) which activates platelets
  2. Shape changes and realease of mediators (TXA2 and ADP)
  3. TXA2 and ADP promote platelet aggregation
A
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18
Q

Physiology, pathophysiology, and pharmacology of hemostasis

What is the patho for aggregation of platelets

A
  1. TXA2 and ADP “uncover” fibrinogen receptor (GPIIb/IIIa)
  2. this allows fibrinogen (I) to bind to the receptor and further aggregate platelets
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19
Q
  1. TXA2 and ADP “uncover” fibrinogen receptor (GPIIb/IIIa)
  2. this allows fibrinogen (I) to bind to the receptor and further aggregate platelets

yep your going to draw it!!! try putting all of the drawings together

A
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20
Q

After platelets aggregate , __1__ is woven into plateets and cross-linked (water soluble >stable)

the cross linkage requires fibrin stabilizing factor __2__

A
  1. fibrin
  2. XIII
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21
Q

mechanism of action aspirin and NSAID’s

A

COX 1 inhibition: reduction in TXA2

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22
Q

All procoagulants (clotting factors) are produced in the ___1___, with the exception of what 3? and where are they produced?

A
  1. liver
  • tissue factor or thromboplastin (III)- released from traumatized cells
  • Ca++(IV)- diet
  • vWF (VIII:vWF)- vascular endothelial cells
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23
Q

whhat are the vit K dependent factors

A
  • II
  • VII
  • IX
  • X
  • protein C
  • Protein S
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24
Q

what are the roman numerics for the following clotting factors

  • fibrinogen
  • prothrombin
  • tissue factor/thromboplastin
  • Von Willibrands factor
A
  • fibrinogen- I
  • prothrombin- II
  • tissue factor/thromboplastin III
  • Von Willibrands factor VIII:vWF
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25
Q

tissue factor/thromboplastin (III) comes from where?

A

Vascular wall and extravascular cell memerane; released from traumatized cells

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26
Q

clotting cascade TISSUE FACTOR PATHWAY (Extrinsic)

(Factor III)

A
  • Damage occurs from outside of blood vessel → triggers release of tissue factor
  • Tissue factor comes in contact with factor VII
  • Complexed with Ca++ on platelet → activates factor X
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27
Q

clotting cascade TISSUE FACTOR PATHWAY (Extrinsic)

  • Damage occurs from outside of blood vessel → triggers release of tissue factor
  • Tissue factor comes in contact with factor VII
  • Complexed with Ca++ on platelet → activates factor X

put this whole cascasde into a picture

A
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28
Q

what is the primary physiologic initiator of coagulation

(in the extrinsic pathway)

A

tissue factor

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29
Q

the tissua factor pathway (extrinsic pathway) is measured by what?

A

PT test

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30
Q

how to remember the Extrensiv pathway

A

you can buy the extrinsic pathway for $0.37 (III, VII)

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31
Q

Clotting cascade Contact activation pathway (Intrinsic)

A
  • Initiated when there is trauma to the vessel itself or exposure of blood to collagen
  • Activation of XII→ XI→IX when complexed with platelet surface with factor VIII:C and Ca++ → factor X
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32
Q

Clotting cascade Contact activation pathway (Intrinsic)

  • Initiated when there is trauma to the vessel itself or exposure of blood to collagen
  • Activation of XII→ XI→IX when complexed with platelet surface with factor VIII:C and Ca++ → factor X

make it into a diagram

A
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33
Q

the contact activation pathway (Intrinsic) is measured by what?

A

PTT

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34
Q

how to remember the intrinsic pathway

A

you can buy the intrinsic pathway for $12 (XII) or $11.98 (XI, IX, VIII)

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35
Q

clotting cascade Final common pathway

A
  • Activatio startes with X -> V -> II -> I -> XIII
  • Thrombin converts finbrinogen (I) to fibrin and in the pressence of XIII, fibrin cross-linking occurs
  • the new clot is formed now
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36
Q

clotting cascade Final common pathway

  • Activatio startes with X -> V -> II -> I -> XIII
  • Thrombin converts finbrinogen (I) to fibrin and in the pressence of XIII, fibrin cross-linking occurs
  • the new clot is formed now

now since we know everything put it all together in one big ass diagram that encompasses the final common pathway

A
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37
Q

how to remember the clotting cascade common pathway?

A

the common pathway can be purchased at 5 (V) or 10 (X) for 1 (I) or 2 (II) dollars on the 13th (XIII) of each month

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38
Q

Hemostasis: in short

5 steps down and dirty

A
  1. vasoconstriction
  2. formation on platelet plug
  3. activation of coagulation cascade
  4. Formation of blood clot
  5. Clot retraction and dissolution (fibrinolysis)
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39
Q

What is antithrombin III

A

produced in the liver and neutralizes the final common pathway IIa & Xa and intrinsic factors IX, XIa, & XIIa

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40
Q

antithrombin III

  1. strongly inhibits what factors

and

  1. partially inhibits what factors
A
  1. final common pathway IIa and Xa
  2. intrinsic IXa, XIa & XIIa
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41
Q

antithrombin III os a required cofactor for what?

A

Heparin

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42
Q

Heparin binds to antithrombin III and enhances AT III by ______ x’s

A

1000

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43
Q

which anticoagulant drug is an inhibitor of clotting factor synthesis include what drug

A

Coumadin

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44
Q

Which anticoagulant drugs are known as a thrombin inhibitor

A

Heparin

Lepirudin (refludan)

45
Q

what are 3 ANTIcoagulant drugs

A
  1. coumadin
  2. Heparin
  3. Lepirudin (Refludan)
46
Q

name 8 anti-platelet drugs

A
  1. aspirin
  2. NSAIDs
  3. Ticlid
  4. Plavix
  5. Persantine
  6. Integrilin
  7. reopro
  8. aggrastat
47
Q

anti-platelet drugs

how does ASA work

A

inhibits cyclooxygenase: duration of action is life of platelet (due to covelent bond)

48
Q

anti-platelet drugs

how do NSAIDs work

A

same as ASA but depression of TXA2 is shorter 24-48 hours

49
Q

anti-platelet drugs

how do the drugs

ticlid

plavix

and

Persantine work

A

inhibit ADP

50
Q

anti-platelet drugs

how do the drugs

Integrilin

reopro

aggrastat work

A

Antifibrinogen receptor (GPIIb/IIIa)

51
Q

what are 2 thrombolytics currently in use

A
  1. tPa
  2. streptokinase
52
Q

what is an antifibrinolytic drug not in use due to fear of law suits

53
Q

what is an antifibrinolytic drug currently in use for CPB and acute hemmorrhage

54
Q

Anticoagulants

MOA: heparin

A
  • binds/activates ANTITHROMBIN III
  • which inhibits SERINE PROTEASES of the coag cascade
55
Q

Anticoagulants

Heparins response to injury

A
  • heparin is abundant in granules of the mast cells taht line the vasculature
  • in response to injury, heparin is released and inhibits coagulation
  • side note heparin is also present in basophils and liver
56
Q

Anticoagulants

MOA: Coumadin

A
  • inhibits the VITAMIN K dependent y-carboxylation reactions necessary to thr function of thrombin, and factors II, VII, IX and X as well as protein C
57
Q

antiplatelet drugs

MOA: ASA

A
  • inhibits the activity of cyclooxygenase, ASA reduces the production of TXA2
  • ASA also reduces endothelial cell production of PGI2 (an inhibitor of platelet aggregation and a vasodilator)
  • since endothelial cells regenerate active COX faster than platelets teh net effect of ASA is more in favor of endothelial cell-mediated inhibition of coagulation cascade
58
Q

antiplatelet drugs

MOA: Gylcoprotein IIb/IIIa inhibitors

(Repro, Integrilin, Aggrastat)

A
  • inhibits the integrin gylcoprotein IIb/IIIa receptor in the membrane of platelets, inhibits platelet aggregation
  • side note–used inACS in ACLS protocol
59
Q

is a thrombolytic agent an anticoagulant?

A

fuck no like is like saying you have a god damn dissecting aneurysm just not fucking possible

60
Q

Thrombolytic agents

MOA: tPa

A
  • Highly selective for degradation of fibrin in clots, it is extremly useful in restoring the patency of coronary arteries following thrombosis, in particular during short periods following MI
61
Q

Thrombolytic agents

MOA: Streptokinase

A
  • an enzyme from the streptococci bacterium
  • less selective than tPA, being able to activate circulating plasminogen as well as plasminogen to a fibrin clot
62
Q

what do all anticoagulants do? very basic

A

delay or prevent clotting

63
Q

do anticoagulants work on clots already formed?

A

NOOOOOOOOOOOOOOOOOOOO!!!!!! they have no effect on clots that have already formed

64
Q

what are 3 ex of anticoagulants that we frequently use?

A
  1. Heparin
  2. Enoxaparin (lovenox)
  3. COUMADIN
65
Q

Heparin can be fractionated into 2 parts using affinity chromatography with immobolized antithrombin what are the 2 and what do they do?

A
  • the high-affinity fraction is responsible for nearly all of the anticoagulant activity
  • the other fraction, low-affinity heparin, has virtually no anticoagulant activity
66
Q

low molecular weight heparin (LMWH) is prepared by what process

A

fractionation

67
Q

heparin in prepared form what?

A

bovine lung and bovine/ porcine intestine

68
Q

what is the duration of use of heparin?

69
Q

what is the only contraindication of heparin?

70
Q

pts with what d/o are receiving heparin and develop antibodies to antigens on platelets. and leads to thrombocytopenia

71
Q

down and dirty patho of hit (3 steps)

A

heparin antibodies -> platelet aggregation -> thrombocytopenia

72
Q

going off the last definition!! HIT is also called what?

A

HIPA

heparin induced platelet activation

73
Q

tx for HIT

A

D/C heparin

74
Q

steps to diagnose HIT?

A

Platelet count drops during or after heparin therapy

plt < 50% baseline or <100,000

no other cause of thrombocytopenia indentified

Clinical diagnosis of HIT

D/C all heparin

Assess risk of thrombosis

If indicated, initiate alternatinve therapy (anticoag)

75
Q

of a pt has HIT what is wrong with each of teh folloing alternative therapies

  1. LMWH
  2. Danaparoid (a heparinoid)
  3. Warfarin
A
  1. contraindicated -nearly 100% corss-ractivity to heparin- antibodies
  2. Has a rate of 10-15% cross-reactivity and is contraindicated
  3. takes several days for its onset of activity, and therefore althernatives must be used in conjunction
76
Q

heparin dosing prior to vascular occlusion

A

3000-7500 units IV

77
Q

protamine reversal dose

A

25, 50, 100 mg

1-1.3 mg/100U heparin

78
Q

protamine sulfat can be found where?

A

salmon sperm

79
Q

1 mg protamine neutralizes ___mg heparin

80
Q

how fast do you want to administer heparin

A

5-10 min IV

81
Q

how does protamine neutralize heparin

A

electrostatically binds heparin

protamine (+) + Heparin (-) = HP (~)

82
Q

what will occur if protamine is given in absence of heparin

A

anticoagulation

83
Q

SE of protamine

A
  • antihemostatic
  • Hypotension (histamine release)
  • Pulm HTN or bronchoconstriction
  • Hypersensitivity
  • Fish allergy (not shell)
84
Q

how do you give protamine oif pt is at risk w/ hypersensitivity

A
  • 1 mg/50ml test dose over 10 min
  • steroid and antihistamine pretreatment
  • give slower
85
Q

lovenox (LMWH) is derived from what?and how?

A

heparin by chemical depolymerization to yeild 1/3 the size of heparin (WM” 4K to 5K daltons)

86
Q

advantages of lovenox (LMWH) over heparin

A
  • binds less avidly to proteins
  • More predictable anticoagulant response
  • better DVT protection
  • Longer elimination half-time
87
Q

coumadin blocks conversion of _____ ____ _____ to _____ _____

A

vitamin K epoxide

Vitamin KH2

88
Q

what is coumadin used for

A

prosthetic heart valves

afib

cva prevention

recurrent MI

89
Q

what is the target INR while on coumadin?

90
Q

when do you want to d/c coumadin prior to sx and why that time frame

A
  • d/c 1-3 days b4
  • elimination 1/2 time 24-36 hours
91
Q

if your pt is takinf coumadin and is having emergency sx what 3 things can you give to help reverse it?

A
  • Vit K
  • Fresh whole blood
  • FFP
92
Q

platelets tell me what you know

normal levels

needs further workup

increased risk of bleeding

spont bleeding

A
  • 200,000 - 400,000 (+/- 50,000)
  • <100,000
  • <50,000
  • <20,000
93
Q

PT detectsdefects in what what pathway?

A

extrinsic pathway

94
Q

what coag test is indispensable for monitoring patients on oral anticoags

95
Q

normal PT

96
Q

PTT or aPTT

detects deficiency in clotting factors of what pathway

97
Q

what coag test is most commonly used for monitoring heparin therapy

98
Q

levels of PTT, aPTT

A

normal 24-30

abnormal >35

99
Q

what are chelating agents

A

agents which bind Ca++ therby preventing activation of the coagulation cascade

  • By many stages of teh total cascade require the availability of Ca++
100
Q

what is a comercial prothrombin time reagent

101
Q

activated clotting time (ACT)

it is similar to what other test?

Normal Values?

A

PTT

90-120

102
Q

thrombin time

measures what?

screening tool for assessing what?

Normal levels

prolonged if what is occuring?

A
  • conversion of fibrinogen to fibrin
  • end stage of coag cascade
  • 10-12
  • low fibrinogen, elevated fibron degradation products, heparin tx
103
Q

Fibrinogen

Normal levels?

less than what is asscoiated with bleeding

low levels found in what d/o?

increased levels found when?

A
  • 200-400
  • <100 mg/ml
  • DIC
  • following sx or trauma
104
Q

what is a more precise measurment for detection of fibrinolysis

A

fibrin degradation products (FDPs) or fibrin split products

105
Q

FDPs or FSPs are produced when fibrin is split by what?

106
Q

Normal level of FDPs or FSPs

107
Q

the presence of FSPs or FDPs means that they have what effect

A

that they have an anticoagulant effect and actually inhibit clotting circulation

108
Q

causes of DIC

A

trauma

snake bite

amniotic fluid

imcompatable blood

burns

neoplasms

109
Q

what is the diffuse consumptive coagulopathy that leads to formation of small clots in teh blood vessel, that eventually consumes clotting factors/ platelets

dissrupion of normal coagulation and increases in bleeding

Principles III (24 decks)

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