to test that knowledge 1. If the plug contains only platelets it is called what? 2. If it containd RBC ot is called what

1. white thrombus 2. red thrombus

what are the roman numerics for the following clotting factors fibrinogen prothrombin tissue factor/thromboplastin Von Willibrands factor

fibrinogen- I prothrombin- II tissue factor/thromboplastin III Von Willibrands factor VIII:vWF

Coag ppt Flashcards by Dwayne Thibeault

4 statges of hemostasis

HUGE SLIDE BUT THE BASIS AND INTRO INTO ALL THAT FOLLOWS

VASCULAR CONSTRICTION- limits the flow of blood to the area of injury
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)
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.
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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test that knowledge

initial phase if hemostasis

vascular constriction

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to test that knowledge

platelets become activated by what?

thrombin

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what is responsible for stimulating platelet clumping

fibrinogen

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activated platelets release what?

(6)

ADP

TXA₂

Serotonin

Phospholipids

Lipoproteins

other proteins

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which protein released by activated proteins, activates additional platelets

TXA₂

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what forms to entrap the plug to insure stability

Fibrin mesh (clot)

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If the plug contains only platelets it is called what?
If it containd RBC ot is called what

white thrombus
red thrombus

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dissolution of the clot occurs through the action of what?

plasmin

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

1+1=?

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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

keep this we’ll expand

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Physiology, pathophysiology, and pharmacology of hemostasis

what is the patho for adhesion of platelets

Damage to endothelial surface → subendothelial collagen exposure
production/release of vWF form endothelial cells
vWF anchors platelets to subendothelial collagen vascular wall

vWF= Von Willebrad factor

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

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

Hint expand your 1st pic

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What is the most common inherited coagulation defect

Von Willebrands Disease

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what is tx for Von Willebrands disease

DDAVP- it releases vWF from endothelial cells

Give FFP

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Physiology, pathophysiology, and pharmacology of hemostasis

patho of the activation of plateletes

prothrombin → thrombin (IIa) which activates platelets
Shape changes and realease of mediators (TXA₂ and ADP)
TXA₂ and ADP promote platelet aggregation

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

prothrombin → thrombin (IIa) which activates platelets
Shape changes and realease of mediators (TXA2 and ADP)
TXA2 and ADP promote platelet aggregation

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Physiology, pathophysiology, and pharmacology of hemostasis

What is the patho for aggregation of platelets

TXA₂ and ADP “uncover” fibrinogen receptor (GPIIb/IIIa)
this allows fibrinogen (I) to bind to the receptor and further aggregate platelets

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TXA2 and ADP “uncover” fibrinogen receptor (GPIIb/IIIa)
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

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

the cross linkage requires fibrin stabilizing factor __2__

fibrin
XIII

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mechanism of action aspirin and NSAID’s

COX 1 inhibition: reduction in TXA₂

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

liver

tissue factor or thromboplastin (III)- released from traumatized cells
Ca++(IV)- diet
vWF (VIII:vWF)- vascular endothelial cells

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whhat are the vit K dependent factors

II
VII
IX
X
protein C
Protein S

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what are the roman numerics for the following clotting factors

fibrinogen
prothrombin
tissue factor/thromboplastin
Von Willibrands factor

fibrinogen- I
prothrombin- II
tissue factor/thromboplastin III
Von Willibrands factor VIII:vWF

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tissue factor/thromboplastin (III) comes from where?

Vascular wall and extravascular cell memerane; released from traumatized cells

clotting cascade TISSUE FACTOR PATHWAY (Extrinsic) (Factor III)

* 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_

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

what is the primary physiologic initiator of coagulation (in the extrinsic pathway)

tissue factor

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

PT test

how to remember the Extrensiv pathway

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

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

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

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

PTT

how to remember the intrinsic pathway

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

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

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

how to remember the clotting cascade common pathway?

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

Hemostasis: in short 5 steps down and dirty

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

What is antithrombin III

produced in the liver and neutralizes the final common pathway _IIa & Xa_ and intrinsic factors _IX, XIa, & XIIa_

antithrombin III 1. strongly inhibits what factors and 2. partially inhibits what factors

1. final common pathway IIa and Xa 2. intrinsic IXa, XIa & XIIa

antithrombin III os a required cofactor for what?

Heparin

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

1000

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

Coumadin

Which anticoagulant drugs are known as a thrombin inhibitor

Heparin Lepirudin (refludan)

what are 3 ANTIcoagulant drugs

1. coumadin 2. Heparin 3. Lepirudin (Refludan)

name 8 anti-platelet drugs

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

anti-platelet drugs how does ASA work

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

anti-platelet drugs how do NSAIDs work

same as ASA but depression of TXA₂is shorter 24-48 hours

anti-platelet drugs how do the drugs ticlid plavix and Persantine work

inhibit ADP

anti-platelet drugs how do the drugs Integrilin reopro aggrastat work

Antifibrinogen receptor (GPIIb/IIIa)

what are 2 thrombolytics currently in use

1. tPa 2. streptokinase

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

Aprotinin

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

amicar

Anticoagulants MOA: heparin

* binds/activates ANTITHROMBIN III * which inhibits SERINE PROTEASES of the coag cascade

Anticoagulants Heparins response to injury

* 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

Anticoagulants MOA: Coumadin

* 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

antiplatelet drugs MOA: ASA

* 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

antiplatelet drugs MOA: Gylcoprotein IIb/IIIa inhibitors (Repro, Integrilin, Aggrastat)

* inhibits the integrin gylcoprotein IIb/IIIa receptor in the membrane of platelets, inhibits platelet aggregation * * * side note--used inACS in ACLS protocol

is a thrombolytic agent an anticoagulant?

***_fuck no_*** like is like saying you have a god damn dissecting aneurysm just not fucking possible

Thrombolytic agents MOA: tPa

* 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

Thrombolytic agents MOA: Streptokinase

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

what do all anticoagulants do? very basic

delay or prevent clotting

do anticoagulants work on clots already formed?

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

what are 3 ex of anticoagulants that we frequently use?

1. Heparin 2. Enoxaparin (lovenox) 3. COUMADIN

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

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

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

fractionation

heparin in prepared form what?

bovine lung and bovine/ porcine intestine

what is the duration of use of heparin?

unlimited

what is the only contraindication of heparin?

HIT

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

HIT

down and dirty patho of hit (3 steps)

heparin antibodies -\> platelet aggregation -\> thrombocytopenia

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

HIPA heparin induced platelet activation

tx for HIT

D/C heparin

steps to diagnose HIT?

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)

of a pt has HIT what is wrong with each of teh folloing alternative therapies 1. LMWH 2. Danaparoid (a heparinoid) 3. Warfarin

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

heparin dosing prior to vascular occlusion

3000-7500 units IV

protamine reversal dose

25, 50, 100 mg 1-1.3 mg/100U heparin

protamine sulfat can be found where?

salmon sperm

1 mg protamine neutralizes \_\_\_mg heparin

1 mg

how fast do you want to administer heparin

5-10 min IV

how does protamine neutralize heparin

***_electrostatically_*** binds heparin protamine (+) + Heparin (-) = HP (~)

what will occur if protamine is given in absence of heparin

anticoagulation

SE of protamine

* antihemostatic * Hypotension (histamine release) * Pulm HTN or bronchoconstriction * Hypersensitivity * Fish allergy (not shell)

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

* 1 mg/50ml test dose over 10 min * steroid and antihistamine pretreatment * give slower

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

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

advantages of lovenox (LMWH) over heparin

* binds less avidly to proteins * More predictable anticoagulant response * better DVT protection * Longer elimination half-time

coumadin blocks conversion of _____ \_\_\_\_ _____ to _____ \_\_\_\_\_

vitamin K epoxide Vitamin KH2

what is coumadin used for

prosthetic heart valves afib cva prevention recurrent MI

what is the target INR while on coumadin?

2.0-3.0

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

* d/c 1-3 days b4 * elimination 1/2 time 24-36 hours

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

* Vit K * Fresh whole blood * FFP

platelets tell me what you know normal levels needs further workup increased risk of bleeding spont bleeding

* 200,000 - 400,000 (+/- 50,000) * \<100,000 * \<50,000 * \<20,000

PT detectsdefects in what what pathway?

extrinsic pathway

what coag test is indispensable for monitoring patients on oral anticoags

normal PT

10-12 sec

PTT or aPTT detects deficiency in clotting factors of what pathway

intrinsic

what coag test is most commonly used for monitoring heparin therapy

PTT, aPTT

levels of PTT, aPTT

normal 24-30 abnormal \>35

what are chelating agents

agents which bind Ca++ therby preventing activation of the coagulation cascade * _By many stages of teh total cascade require the availability of Ca++_

what is a comercial prothrombin time reagent

INR

activated clotting time (ACT) it is similar to what other test? Normal Values?

PTT 90-120

thrombin time measures what? screening tool for assessing what? Normal levels prolonged if what is occuring?

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

Fibrinogen Normal levels? less than what is asscoiated with bleeding low levels found in what d/o? increased levels found when?

* 200-400 * \<100 mg/ml * DIC * following sx or trauma

what is a more precise measurment for detection of fibrinolysis

fibrin degradation products (FDPs) or fibrin split products

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

plasmin

Normal level of FDPs or FSPs

\<5ug/ml

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

that they have an anticoagulant effect and actually inhibit clotting circulation

causes of DIC

trauma snake bite amniotic fluid imcompatable blood burns neoplasms

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

DIC

Coag ppt Flashcards

(109 cards)