Introduction Coagulation Disorders Hemostasis Management Extrinsic Pathway Intrinsic Pathway...

Introduction

Coagulation Disorders

Hemostasis Management

Extrinsic Pathway

Intrinsic Pathway

Medications

Labs

Clinical Application

Summary

QUIZ

Coagulation Disorders (Coagulopathy)

Presented by:Nardalyn Johnson, RN

MSN StudentAlverno College

April 22, 2010

In collaboration with:Jim Molnar, APRN – Preceptor

Jan Theis, APRN

MSN 621 Instructors:Patricia Bowne

Luanne Wielichowski

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INTRODUCTION

The Interventional Radiology (IR) department multidisciplinary team works with patients who have various types of coagulation disorders.

Hemostasis management is complex due to the wide array of patient co-morbidities and demographics.


Malloy, P.C., Grassi, C. J., Kundy, S., Gervais, Miller, D. L., Osnis, R. B. et al. (2009). Consensus Guidelines for

Periprocedural Management of Coagulation Status and Hemostasis Risk in Percutaneous. Society of Interventional Radiology.

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• Objectives– Review importance of hemostasis management

in IR – Review coagulation disorders– Review the coagulation cascade (intrinsic and

extrinsic pathways)– Identify common lab tests– Identify common medications that can affect

hemostasis– Focus on clinical application of hemostasis in IR

Special Note:– Whenever you see an underlined word, move the

curser over the underlined word to view more information


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A group of conditions that cause an individual to experience either:

Excessive bleeding

Excessive Clotting


Wellcome Images

Porth, C.M., 2005. Pathophysiology, 7th edition. Lippincott.

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A 49 yr old male Presents to IR for placement of a permCath to initiate dialysis. He returns to IR the following day due to excessive bleeding

during dialysis.

BP 159/75 HR 76 Temp 97.8Lab: INR 1.8 (0.9 – 1.3)

Case Study

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Why Does the IR multidisciplinary team need

to be concerned about patients with clotting or

bleeding disorders?

Hemostasis management


Click the diagram to reveal the answer

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Hemostasis

Definition: Hemostasis is the process of stopping blood loss.

This process occurs via the hemostatic mechanism known as blood coagulation

It is regulated by “activators” and “inhibitors”.

If Normal

If Abnormal

Seals blood vessels and prevents blood loss and

hemorrhage

Causes inappropriate bloodclotting or excessive bleeding

Nowak, T.J., Handford, G. A. (2004). Pathophysiology: Concepts and Applications for Health Care Professionals. (3rd Ed). McGraw-Hill. NY

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• Prevents cancellation of IR procedures due to appropriate pre-op procedure not done

• Prevents excessive bleeding pre, intra, or post procedure

• Decreased risk for post-procedural thrombosis

• Achieves hemostasis pre, intra, and prior to discharge

• Helps with healing

• Provide appropriate patient education

• Identify new protocols for patients with coagulation disorders

• Early identification of at risk patients pre-procedure

Why is Hemostasis Management Important?

http://www.vascularsolutions.com/company-info/contact

Nursing Outcomes

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Hemostasis management for patients undergoing percutaneous image-guided procedures can be complex due to the wide range of procedures and equally wide range of patient demographics and co-morbidities.

Some patients are on special medications that increase their risk for bleeding or have internal stents or other devices that predispose them to forming clots.

Microsoft clipart

Microsoft clipart

Malloy, P.C., Grassi, C. J., Kundy, S., Gervais, Miller, D. L., Osnis, R. B. et al. (2009). Consensus Guidelines for

Periprocedural Management of Coagulation Status and Hemostasis Risk in Percutaneous. Society of Interventional Radiology.

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Five Stages for Achieving HemostasisClick each box along the pathway to reveal the steps

Move the curser over the underlined word to view more information

A Closer Look at “Hemostasis process”

Vessel spasm

Formation of platelet plug, platelet adhesion, & aggregation

Formation of fibrin clot and activationof intrinsic or extrinsic coagulation cascade

Clot retraction

Clot dissolution


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Clot retraction normally occurs within ____time

after a clot is formed


5 to 10 minutes 8 to 10 hours

2 to 4 hours 20 – 60 minutes

Clot retraction: is when the blood clot becomes smaller, squeezing serum from the clot and joining the edges of the broken vessel

Incorrect… This is abnormal and

could be due to low platelet

count

CORRECT!This is key

for hemostasis

NO…….This is not enough time and you are at risk for bleeding

TRY AGAIN…….It begins shortly after formation

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Factor Name Roman Numeral Fibrinogen I

Prothrombin II

Tissue Factor III

Calcium IV

Preaccelerin V

Proconvertin VII

Antihemophilic Factor VIII

Christmas Factor IX

Stuart-Prower Factor X

Plasma thromboplastin antecedent XI

Hageman Factor XII

Fibrin-stabilizing Factor XIII

The Intrinsic and Extrinsic Coagulation Cascade

The coagulation cascade is one component of the hemostasis process. For coagulationto work successfully, we need both the “Intrinsic pathway” and the “extrinsic pathway.” Both pathways are interrelated and link to form the common pathway.

Here is a list of Factors that help to build the coagulation cascade

Sometimes you will see them referenced by their original name. Othertimes you will see only the roman numeral references.


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Damaged Tissue Blood vessel damage

The Extrinsic Pathway The Intrinsic Pathway

Tissue Factor (III)

Proconvertin(VII)

Ca2+

Factor X

ProthrombinActivator

Thrombin

Fibrinogen (I) Fibrin (monomer)

Fibrin (polymer)

A Closer Look at “Normal Coagulation Cascade”

Factor XII(from activePLT)

Plasma thromboplastin antecedent (XI)

Cascade reaction

Factor VFactor III

Ca 2+PF3

Prothrombin (II)Cross-linked Fibrin mesh

Factor XIII

RBC & PLT get caught in meshForming blood clot

See step-by-step explanation on next slide

Return to Calcium (Ca 2+)

Slide created by Nardayn Johnson

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The extrinsic pathway gets initiated when there is damage to blood vessels or surrounding tissue (usually a fast process).

Factor III is released in response to damaged tissue which then

activates Factor VII with the help of calcium ions.

The intrinsic pathway (a slower process) is then activated when factor XI gets activated by Factor XII from active platelets.

Activated factor XI and factor VII cause a cascade reaction which leads to the activation of factor X.

Activated Factor X with the help of calcium ions, Factor III, Factor V, and PF3 activates prothrombin activator which then converts prothrombin to thrombin.

Next, thrombin converts fibrinogen to fibrin which forms a loose mesh.

Fibrin along with factor III forms a denser network of mesh fibers which can trap RBC & PLT forming a successful clot.

The Coagulation Cascade Explained(See previous slide)


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Blood coagulation requires systematic activation of coagulation factors controlled by activators and inhibitors.

It is vital to promoting healing after a patient undergoes any percutaneous imaging procedure.

The Intrinsic and Extrinsic Coagulation Cascade

Microsoft clipart


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The Intrinsic pathway

A slow ProcessBegins in the blood itself

The Extrinsic pathway

A faster ProcessBegins with damage to blood vessel or surrounding tissue

The Intrinsic vs. Extrinsic Coagulation Cascade

Need both for Hemostasis

The activation of one procoagulation factor/enzyme leads to the activation of the next factor, similar to a domino effect.

“Most of the inactive procoagulation factors are present in the blood all the time.” (Porth, 2005)

Damage to tissue

Extrinsic pathwayGets activated

Small amount of Thrombin formed

Stimulus to Intrinsicpathway

Formation of moreThrombin

Produce large Amount of Fibrin

CoagulationSuccessful

+

Return to Protein C


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CASE STUDY:

Recall the 49 yr old male who presented to IR for placement of a permCath to initiate dialysis.

He returned to IR the following day due to excessive bleeding problems during dialysis.

A defect in which pathway would cause bleeding problems?

Extrinsic Pathway

Try Again. This is not be most correct response

Intrinsic PathwayTry Again

There’s a better answerThink about the procedure performed


Both

Correct!

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Jim Molnar, 2010 – (Preceptor)

Molnar. J. (2010). Thrombolytics. Froedtert hospital Radiology Department.

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Abnormality in the clotting process can result if there is a problem with one or more factors (Porth, 2005).

This can lead to inappropriate activation at any point along the pathway depending on the factor(s)causing the problem (Nowak, 2004).




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• Calcium plays a key role in the coagulation cascade. It is “required in all but the first two steps of the clotting process.” (Porth, 2005)

• 3 types of calcium (calcium salts, protein bound, and ionized calcium)• **ionized calcium** aid in coagulation cascade

• Calcium = Factor IV

• Only need a small amount so patients with calcium deficiency will not necessarily exhibit any significant effect on coagulation cascade.

• If calcium gets inactivated when it is removed from the body, then blood will not clot.Think about the EDTA tubes that you use to collect blood. They contain chelating agent thatinactivates Ca++ that prevents the blood from clotting.

Ca2+

Calcium (ionized)

View coagulation pathway

Why are Ca 2+, Vitamin K, Protein C, and Platelets Important?


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VITAMIN K

FUNCTION OF VITAMIN K: Needed by liver to produce clotting factors Needed to produce clotting Factors such as VII, IX, X and to synthesize Protein C Helps to regulate calcium…keeping it in your bones and out of your blood

Watch patients who are taking warfarin as it can decrease clotting by interfering with vitamin K and increase risk for excesses bleeding after a procedure You do not need much—just enough to prevent you from bleeding to death Older patients will need more vitamin K

Is a fat soluble vitamin andwithout it your blood will not clot


http://www.hemophilia.org/NHFWeb/MainPgs/MainNHF.aspx?menuid=176&contentid=378&rptname=bleeding

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Protein C

A special anticoagulant protein. Activated Protein C functions as an anticoagulant, limiting clot formation (down regulates the coagulation cascade). Resistance to activated Protein C prevents Protein C from cleaving to Factor V and/or VIII.

You need the help of vitamin K to help build Protein C.

Do not confuse this with “C-reactive protein.” This is produced in the liver and is a

bi-product of inflammation.


View Positive feedback


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You found out during testing that JT has a Protein C deficiency.

This deficiency predisposes him to __________?

Venous Thrombosis

Click here


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Why are Platelets important for Hemostasis?

Platelets are very important in hemostasis management

You need enough to prevent excessive bleeding, but too many can be problematic because they cause hypercoagulation

Some patients may have internal stents or other devices that predispose them to forming clots

Cancer patients who have decreased platelet count are at increased risk for bleeding

Wellcome Images

King, K. W. (2010). Platelet Activation and von Willebrand Factor (vWF). IU School of Medicine.

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Why are Platelets important for Hemostasis?

CASE STUDY

KLS presents to IR for permCath evaluation due to poor blood flow. This is his third visit to IR in one mouth.

KLS requests a new catheter because he believes something is wrong with the current catheter.

Lab tests prior to procedure reveal:INR=1.0 (0.9-1.3), Plt = 654 (150-350), PTT 24 (25-33)

You change the catheter, but two weeks later he is back again. It makes no sense to keep changing the catheter. It appears his bodyis forming thrombi around the catheter causing decreased blood flow.

Medical Decision: In addition to performing a catheter stripping procedure, he is started on Aspirin 325 mg by mouth MWF to help decrease platelet aggregation. Aspirin would help to decrease platelet aggregation.

Microsoft clipart

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Medications that Affect Coagulation Cascade

Some patients are on special medications that increases their risk for bleeding

Thombolytics (tPA)

Anticoagulants (heparin, warfarin)

Anti-platelet agents (ASA, Plavix, ticlid)

These medications can complicate a procedure if not managed appropriately.

Microsoft clipart

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Anticoagulants


Two commonly used drugs in the US are:

Warfarin (Coumadin) Heparin

Vitamin K antagonist

Decrease production ofFactors II, VII, IX, X

Prevent thrombosis

Activate anti-thrombin III

Blocks thrombin

Warfarin: is “prescribed to ~2 million newpatients per Year in US” (USA Today, 2010).Therefore, your chance of having a patient on this medication is high.

E.g. prescribed to patients with history ofDVT, PE, prosthetic heart valve etc. Anticoagulants help with hemostasisby preventing inappropriate blood clotting in vessels.

They chip away at clot making it smaller

Prevents thrombosis in veins

Close hemostasis management is important pre, intra, and post procedure to prevent excessive bleeding complications.

Remember labs: INR, PT

Heparin - released from tissue basophils and inactivates thrombin.

Sternberg, S. (2010). Gene test cuts complications from blood thinner warfarin. USA Today.

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Warfarin (Coumadin) HeparinDeceases prothrombin & other procoagulation factors

Found naturally in body

Vitamin K antagonist Increase availability of antithrombin III which decrease formation of fibrin

36-72 hr to take effect

Oral prescription available IV/SC preparation only

Microsoft clipart Microsoft clipart

Huber, C. (2007). Anticoagulant Therapy Management. Cedar Rapids Healthcare Alliance.http://en.wikipedia.org/wiki/Anticoagulant

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Why Give Heparin by IV or SC preparation Versus taking it by mouth?

Answer

It is unable to cross membrane of GI Tract

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A patient scheduled for central line placement in IR with a recent history of Pulmonary Emboli (PE)

Anticoagulant medication: Warfarin 4 mg by mouth dailyRecent lab: INR 2.1 (0.9-1.3)

Which of the following instructions should be given to the patient?

a) Hold Warfarin 3 days before procedure Initiate Lovenox therapy Hold AM dose of Lovenox prior to procedure Recheck INR prior to procedure

b) Hold Warfarin 7 days before procedure Initiate Lovenox therapy Hold AM and PM dose of Lovenox prior to procedure Recheck INR prior to procedure

c) Hold Warfarin 5 days prior to procedure

X NoOnly need 3 days

X Try Again

Correct Due to different half live of preformed clotting factors

Click on the correct response:

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Article Published by USA Today 3/16/2010 Title: Gene Test Cuts Complication from Blood Thinner

Warfarin

Points from article:

It takes time for a doctor to settle on a safe and effective dose when prescribing warfarin.

“Roughly 1 in 5 patients are hospitalized for bleeding within six months of starting the drug. Others develop a life-threatening blood clot.”

“Warfarin is the second-greatest cause of hospitalization due to drug complication.”

“Warfarin is prescribed to 2 million new patients in the USA each year.”

Genetic tests can be used to personalize warfarin treatment and decrease the rate of hospitalization.

See full article at: http://www.usatoday.com/news/health/2010-03-16-warfarin-gene_N.htm


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Thombolytics (tPA)


TB reported to IR for tunneled catheter evaluation with a report from the dialysis center of poor blood flow.

Medical decision: tPA catheterPost evaluation: Catheter flush & aspirate w/o difficulty

A protein that breaks down blood clot

CatalysesPlasminogen

Plasmin

FibrinDegradation

A clot-busting medication

Important for cell migration and tissue healing

Increase activity = increase bleeding

Decreased activity = thrombosis

tPA

FMLH Radiology

Thrombolytic drug. Retrieved March 19, 2010 from http://en.wikipedia.org/wiki/Thrombolytic_drug

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Anti-platelet agents


Suppress platelet aggregation

Prevent thrombosis in arteries whileanticoagulants (Warfarin & heparin,

Prevent thrombosis in veins

Inhibit COX enzyme

Decrease Platelet Synthesis of TXA2

Decrease Pathway in platelet activation

Two commonly used drugs in the US are:

Aspirin (ASA) Ticlid

Blocks ADP receptor on platelet

surface

Prevent Thrombusformation

Antiplatelet. Retrieved March 19, 2010 from http://en.wikipedia.org/wiki/Antiplatelet_drug


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Some Important Labs You Need to Know About

If the procedure is invasive, hemostasis status should be assessed and closely monitored. Tests needed will be based on the procedure you will perform.

Tests for Hemostasis--Needed Pre-Invasive Procedures

INR (.09-1.3)

Assess problems with extrinsic or common pathwayClotting factors I, II, V, VII, X Be aware of patients on anticoagulant therapy and patients with liver disease

PT (10-13) Same as INR

aPTT (25-33)

Assess problems with intrinsic pathway Deficiency in Factor VIII, IX, XI. Assess patients on heparin therapy or have history of von Willebrand disease

Platelet count (150-250)

Used to diagnose bleeding disorder e.g. DIC, thrombocytopenia Abnormally low platelet count increase risk for excessive bleeding

FMLH Radiology

Malloy, P.C., Grassi, C. J., Kundy, S., Gervais, Miller, D. L., Osnis, R. B. et al. (2009). Consensus Guidelines for Periprocedural Management of Coagulation Status and Hemostasis Risk in Percutaneous. Society of Interventional Radiology.

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Functions of the Liver

Most clotting Factors are produced in the liver

Factor Name Roman Numeral Source Fibrinogen I Liver

Prothrombin II Liver * * Tissue Factor III Damages cells

Calcium IV Gut and bone

Preaccelerin V Liver and platelet

Proconvertin VII Liver * *

Antihemophilic Factor VIII Platelets and endothelium

Christmas Factor IX Liver * *

Stuart-Prower Factor X Liver * *

Plasma thromboplastin antecedent XI Liver

Hageman Factor XII Liver

Fibrin-stabilizing Factor XIII Liver

* * Dependent on vitamin K for synthesis in liver

Microsoft clipart


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What Happens if the Liver is Damaged?

Tissue DamageLiver Damage

DecreaseClotting Factor

Synthesis

Depletion ofClotting Factors

Hypocoagulation

Compromise Bile synthesis

Shortage of Vitamin K

Decrease clotting Factor synthesis

Liver disease (e.g. liver cancer, cirrhosis, fibrosis, hepatitis) will decrease the synthesis of all liver dependent clotting factor

Your body will take longer to clot, thereby increasing the risk for bleeding

INR lab - Will be elevated with severe liver damage

Wellcome Images


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Case Study

Patient with increased liver function test present to IR for liver biopsy

History of ESRD, kidney transplant, on immunosuppression,basal cell carcinoma, fatty liver

Lab: Liver fn panel, Plt 99 (150-350) Hgb 7.2 Stat type & cross

IR medical team decision: 2 units packed RBC ordered, 1 unit infused prior to

procedure

What happens if the Liver is Damaged?

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Role of Inflammation & Effects on Coagulation

• Inflammation is a biochemical and cellular process that occurs in vascularized tissues

• Inflammation in the liver will affect coagulation

Tissue

Damage

Liver Damage

DecreaseClotting Factor

Synthesis

Depletion ofClotting Factor

Hypocoagulation

Inflammation

Wellcome Images


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chronic inflammatory process (outside the liver) can trigger the clotting cascade.

Clotting causes damage through lack of perfusion (ischemia) to vital organs, such as the liver, kidneys, heart which would then activates the clotting cascade which increase clotting.

Role of Inflammation & Effects on Coagulation

Decrease activity of natural anticoagulant mechanism

Hypercoagulation

Chronic Inflammation

Impairs Fibrinolytic system

Esmon, C. T. (2005). The interactions between inflammation and coagulation . British Journal of Haematology. 131(14) 417-430.

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Which of these Factors is not synthesized in the liver?

a) Prothrombin (Factor II)

b) Antihemophilic Factor (Factor VIII)

c) Hageman Factor (Factor XII)

d) Stuart-Prower Factor (Factor X)

X Incorrect

X No

X Try Again

CorrectSource: Platelets and endothelium

Click on the correct response:

What happens if the Liver is Damaged?

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•The stress response protects the individual from threats to homeostasis.• Trauma as a result of percutaneous image-guided procedures can induce the stress response

Stress Adaptation Response & Effects on Coagulation

Case Study

50 yr old Male presents to IR for treatment with drug eluting bead chemoembolization

Diagnosed with neuroendocrine cancer w/liver metastasisHad multiple hypertensive crises recently

BP 133/65 R=18 HR 72 wt=245#

The patient is at risk of a hypertensive crisisMed requested = Alpha blockade

Medication ordered = phentolamine (REGITINE) 5 mg

Reason: Phentolamine prevent stress response (hypertensive crisis) which may occur due to stress or due to a surgical procedure.

Hypertension damages the blood vessels thereby affecting the coagulation cascade

Microsoft clipart

Hehne, R. A. (2004). Pharmacology for Nursing Care. (5th Ed). Saunders. Missouri

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Role of Aging & Effects on Coagulation

Aging

**Defective VesselSupport Due to

Weakness in Connective Tissue

IncreaseBleeding Risk

Increased Vessel Fragility

Aging

Vitamin KDeficiency **

DecreasedClotting Factor

Synthesis by Liver

Hypocoagulation

** Older patients will need more vitamin K** With aging, the skin becomes thinner so tissues supporting underlying blood vessels are more fragile

Microsoft clipart

Toloza, E, (2005). Bruises. Department of Emergency Medicine, University of Texas at Houston School of Medicine.

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Role of Genetics & Effects on Coagulation

Deficiencies in clotting factors may be due to genetics

Factor VIII/IX Deficiency Hemophilia

Factor V Deficiency Owren’s Disease

Factor X DeficiencyStuart-Prower Factor Deficiency

Microsoft clipart

Taylor, A.K. (1997). Venous Thrombosis and the Factor V (Leiden) Mutation. The Mountain States Genetics Foundation (14).

For all Bleeding and Clotting Disorders. Retrieved March 8, 2010 from http://www.hemophilia.org/NHFWeb/MainPgs/MainNHF.aspx?menuid=176&contentid=378&rptname=bleeding


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Video Links

1. http://www.hopkinsmedicine.org/hematology/Coagulation.swf

A review of the coagulation cascade can be found at the following link

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List The Five Stages for Achieving HemostasisClick each box to reveal the correct response

A Closer Look at the “Hemostasis Process”

Vessel spasm

Formation of platelet plug, platelet adhesion, & aggregation

Formation of fibrin clotActivate intrinsic or extrinsic coagulation cascade

Clot retraction

Clot dissolution


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The Interventional Radiology (IR) department multidisciplinary team work with patients who have various types of coagulation disorders. Hemostasis management is complex due to the wide array of patient co-morbidities of patients undergoing percutaneous image-guided procedures in IR. This complexity is further complicated by the wide range of procedures and patient demographics.

Some patients are on special medications that increases their risk for bleeding or have internal stents or other devices that predispose them to forming clots.

The use of Thombolytics (tPA), anti-coagulants (heparin, warfarin), or anti-platelet agents (ASA, Plavix, ticlid) can complicate a procedure if notmanaged appropriately.

Medical interdisciplinary team understanding of the various coagulation disorders will assist in medical care to patients. This would include pre-op measures to prevent lengthy delays or costly cancellation of procedures.

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QUIZ

1. The process of stopping blood loss is known as?a) Coagulation cascadeb) Clot retractionc) Hemostasisd) Clot dissolution

2. For coagulation to work successfully we need these two pathways. Both pathways are interrelated and link to form the common pathway.

a) IR pathway AND clot retraction pathwayb) Intrinsic pathway AND Extrinsic pathwayc) Internal pathway AND External pathway d) None of the above

3. Calcium (Factor V) plays a key role in the coagulation cascade. It is “required in all but the first two steps of the clotting process. The type of calcium needed in the coagulation cascade is?

a) Calcium saltsb) Protein bound calciumc) Ionized calciumd) Unbound calcium

4. Identify two commonly used anticoagulant medication used in the US. They can affect hemostasis for patients undergoing percutaneous image-guided procedures in IR.

a) Warfarin AND Heparinb) Aspirin AND Ticlidc) Tissue plasminogen activator (tPA) AND Streptokinase (SK)d) Prednisone AND Dexamethasone

5. Identify the organ where most of the clotting factors are synthesized: ____________________

Click here to reveal the answers

Answers1. C 2. B3. C4. A5. LIVER

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References



Hehne, R. A. (2004). Pharmacology for Nursing Care. (5th Ed). Saunders. Missouri

Rayfield, S., Manning, L. (1998). Nursing made Insanely Easy. (2nd Ed). ICAN Louisiana


Huber, C. (2007). Anticoagulant Therapy Management. Cedar Rapids Healthcare Alliance.

Guyton, A.C., Hall, J.E. 2000. Medical Physiology. 10th edition. Saunders.

Malloy, P.C., Grassi, C. J., Kundy, S., Gervais, Miller, D. L., Osnis, R. B. et al. (2009). Consensus Guidelines for Periprocedural Management of Coagulation Status and Hemostasis Risk in Percutaneous. Society of Interventional Radiology.

Hemostasis. Retrieved March 24, 2010 from http://www.mhhe.com/biosci/esp/2002_general/Esp/folder_structure/tr/m1/s7/trm1s7_3.htm

Tissue Plasminogen Activator (tPA). Retrieved March 24, 2010 from http://www.americanheart.org/presenter.jhtml?identifier=4751

Symptoms of Coagulation Disorders. Retrieved March 24, 2010 from http://www.signsofbleeding.com/index.php?page=4

Tissue plasminogen activator. Retrieved March 19, 2010 from http://en.wikipedia.org/wiki/Tissue_plasminogen_activator

Coagulation Cascade. Retrieved March 12, 2010 from http://www.hopkinsmedicine.org/hematology/Coagulation.swf

Thrombophilia or Hypercoagulable States. Retrieved March 12, 2010 from http://www.peds.ufl.edu/residency/resources/hematology/th_states.pdf

Radiological Society of North America (2010). Radiology Info: the Radiology information for patients. Radiological Society of North America, Inc.

For all Bleeding and Clotting Disorders. Retrieved March 8, 2010 from http://www.hemophilia.org/NHFWeb/MainPgs/MainNHF.aspx?menuid=176&contentid=378&rptname=bleeding

Thrombolytic drug. Retrieved March 19, 2010 from http://en.wikipedia.org/wiki/Thrombolytic_drug


Molnar. J. (2010). Thrombolytics. Froedtert hospital Radiology Department.

Anticoagulants. Retrieved March 19, 2010 from http://en.wikipedia.org/wiki/Anticoagulant

Antiplatelet. Retrieved March 19, 2010 from http://en.wikipedia.org/wiki/Antiplatelet_drug

Ganda. K. (2005). The Clotting Pathway. TUFTSOPENCOURSEWARE ,Tufts University.

Toloza, E, (2005). Bruises. Department of Emergency Medicine, University of Texas at Houston School of Medicine.

Introduction



Extrinsic Pathway

Intrinsic Pathway

Medications

Labs


Summary

QUIZ

References

Taylor, A.K. (1997). Venous Thrombosis and the Factor V (Leiden) Mutation. The Mountain States Genetics Foundation (14).

mcGilvray,I. , Rotstein, O.D.(2001). Assessment of Coagulation in Surgical Critical Care Patients. Department of surgery, University of Toronto and Toronto General Hospital, Canada.

Esmon, C. T. (2005). The interactions between inflammation and coagulation . British Journal of Haematology. 131(14) 417-430.

Contact InformationNardalyn Johnson, [email protected]

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