Hemostasis Flashcards by Brandon Taylor

What are the 4 stages of hemostasis?

I: Primary
II: Secondary
III: Anticoagulation
IV: Fibrinolysis

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What are the 4 main stages of primary hemostasis?

1) adhesion
2) activation
3) aggregation
4) fibrin

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______ promotes platelet ADHESION.

von Willebrand factor (vIII)

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Where is vWF manufactured and released from?

endothelial cells

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vWF is the ligand for the _______ receptor found on the platelet.

GP1b

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What is the life span of a PLT?

8-12 days

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What is the normal value for PLT’s?

150,000-400,000 cells per mL

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What percent of the PLT’s can be found sequestered in the spleen?

33%

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What is the MOST common inherited coagulation defect?

vWF disease (vIII)
*the more common form is characterized by insufficient production of vWF by endothelial cells

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Why should you still suspect vWF disease in a pt with a normal PLT count and increased bleeding time?

they may have enough platelets, but it is the vWF that adheres the PLT to the injury site

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What is the 1st line treatment for vWF disease? How does it work?

D-amino D-arginine vasopressin (DDAVP, desmopressin)–> a non pressor analogue of arginine vasopressin causes release of endogenous stores of vWF
effective in 80% of cases

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What is the dosing for DDAVP for vWF?

0.3mcg/kg IV infusion for 10-20 minutes

PLT adhesion is increased within 30 minutes of injection and wears off at 4-6 hours

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What is the concern with DDAVP administration in vWF disease type 2B?

thrombocytopenia

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What is given to patients that do not respond to desmopressin for vWF disease?

cryoprecipitate or factor VIII concentrate (Humate-P)

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What factors does cryoprecipitate have?

factor VIII, I (fibrinogen), XIII

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What is needed to activate the PLT?

thrombin (activated factor II or IIa)

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What is synthesized and released from the activated PLT?

thromboxane A2 and ADP

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What is the role of thromboxane and ADP?

uncovers fibrinogen receptors on the platelet by conformational change—> it binds to the receptor activating signal transduction—> fibrinogen then attaches thereby linking other PLT’s to each other

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What is formed during aggregation?

platelet plug

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How strong is a PLT plug?

water soluble and friable

also called a white thrombus or white clot

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_______ aggregates platelets.

fibrinogen (factor I)

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What occurs in the PLT after the thrombin attaches?

it is activated–> phospholipase A2 liberates arachidonic acid–> cyclooxygenase converts arachidonic acid to prostaglandin G2–> PGG2 is metabolized to PGH2–> PGH2 is converted to a variety of prostaglandins and thromboxane A2

This is the arachidonic acid cascade.

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Name the arachidonic acid cascade.

phospholipase A2 liberates arachidonic acid–> cyclooxygenase converts arachidonic acid to prostaglandin G2–> PGG2 is metabolized to PGH2–> PGH2 is converted to a variety of prostaglandins and thromboxane A2

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What part of hemostasis does drugs like aspirin, NSAIDs, and Plavix effect?

platelet aggregation

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What is the fibrinogen receptor?

GPIIb/IIIa

Name common anti-fibrinogen receptor drugs.

Eptifibatide (integrilin) Abciximab (Reopro) Tirofiban (Aggrastat) Remember "EAT"

How many hours before surgery should the following drugs be discontinued? Eptifibatide (integrilin) Abciximab (Reopro) Tirofiban (Aggrastat)

Eptifibatide (integrilin)--> 24 hours Abciximab (Reopro)--> 72 hours Tirofiban (Aggrastat)--> 24 hours

How many hours before surgery should the following drugs be discontinued? Aspirin NSAIDs

Aspirin: 7-10 days (life of PLT) NSAID: 24-48 hours

How do the following drugs work? Eptifibatide (integrilin) Abciximab (Reopro) Tirofiban (Aggrastat)

They cap the fibrinogen receptor to prevent attachment of fibrinogen--> so no aggregation

Name 2 anti ADP drugs.

Clopidogrel (Plavix)--> anti ADP agent (life of PLT) | Ticlopidine (Ticlid)--> inhibits ADP induced fibrinogen aggregation

How many hours before surgery should the following drugs be discontinued? Clopidogrel (Plavix) Ticlopidine (Ticlid)

Clopidogrel (Plavix)--> 7-10 days (life of PLT) | Ticlopidine (Ticlid)---> 14 days

How does the drug Dipyridamole (Persantine) work? What is it commonly used for?

increases cAMP in pt's---> increased cAMP prevents aggregation of PLTs commonly used in combination with warfarin to treat prosthetic heart valves

What is the MOST common ACQUIRED blood clotting defect?

inhibition of cyclooxygenase production by aspirin or NSAIDs

There is no factor ______.

Where do platelets come from?

bone marrow--> thrombocytes

Secondary Hemostasis is all about the production of _____.

Fibrin

If it requires vitamin K it MUST be made in the ______.

liver

What are the vitamin K dependent factors?

II, VII, IX, X (procoagulants) and protein C & S (anticoagulants)

All procoagulant factors except _____, _______, and ______ are made in the liver.

vWF (VIII) made in endothelial cells, tissue factor (III) made in the tissues, and calcium (IV) from diet

______ is woven into platelets and crosslinked.

fibrin

How strong is a fibrin clot?

insoluble in water; stable also called a red clot or red thrombus

Cross-linking of fibrin strands requires coagulation factor _______. The final steps in fibrin production involve the ________ pathway.

XIIIa (fibrin stabilizing factor) | extrinsic, intrinsic, and final common pathways

________ gets converted into fibrin and creates a _____ bond after being stabilized by XIIIa.

fibrinogen covalent *cryo contains I, VIII, XIII--> helps stabilize fibrin

What is the Leroy Brown story of the extrinsic, intrinsic, and final common pathways?

Look man, I picked up 0.37 cents outside (EXTRINSIC) and I really want those potato wedges... I can't pay 12.00 but I can give you 11.98 (INTRINSIC)..... "No man".... Look fool, It's common on Friday the 13th to kill 1, 2, 5, 10 of you fools (COMMON)

What is the textbook answer for appropriate heparinization for cardiac surgery?

400-450

Warfarin (coumadin) interferes with the ______ pathway.

extrinsic

Prothrombin time (PT) and the International Normalized Ratio (INR) assess the _________ pathway.

extrinsic

Heparin interferes with the ________ pathway.

intrinsic

Partial thromboplastin time (PTT) and activated coagulation time (ACT) assess the ______ pathway.

intrinsic

What is the second MOST common INHERITED coagulation disorder?

hemophilia A So both are factor VIII 1) vWF 2) VIII:C hemophilia factor

What is the difference in hemophilia A and hemophilia B?

hemophilia A is from factor VIII:C, hemophilia B is from christmas factor IX deficiency

What is the most important clue to clinically significant bleeding disorders in an otherwise healthy patient?

THE HISTORY

What is the most common reason for coagulopathy in patients receiving massive blood transfusions?

Lack of platelets | *PLT's in stored blood are non functional after 1-2 days.... there is also dilution of factors V and VIII

What is the only acceptable clinical indication for transfusion of packed red blood cells?

to increase oxygen carrying capacity of blood

ALL procoagulants except ______ are present in fresh frozen plasma.

platelets

Cryoprecipitate contains factor _______, factor ______, and factor ______.

factor I (fibrinogen), factor VIII (both vWF and C), and factor XIII (fibrin stabilizing factor)

How is cryoprecipitate harvested?

from FFP as it is thawing

One unit of platelets will increase count by _______.

5,000-10,000/mm3

One unit of RBCs will increase Hct by ______% or ____g/dl.

3-4% or 1g/dl

1 cc/kg of RBCs will increase Hct by _____%.

Massive transfusion is defined as ___________.

one complete blood volume transfused within 24 hours

What is the role of antithrombin?

it binds thrombin (factor IIa) and factor Xa GREATLY it binds IX, XI, and XII to a LESSER extent removes them from circulation--> anticoagulating the blood

How does heparin work?

increases the effectiveness of antithrombin 1,000 fold or more

Where is antithrombin made?

the liver

Heparin binds to _______.

antithrombin III

Heparin increases the rate of thrombin-antithrombin reaction by _______.

1000 fold or more

Name 2 disease processes that can cause an acquired antithrombin deficiency state.

1) cirrhosis of liver | 2) nephrotic syndrome

What is the MOST common reason a patient can be unresponsive to heparin?

b\c they have an antithrombin deficiency

What is the appropriate ACT result indicating that a patient has been adequately heparinized before a CABG?

>400s if the ACT is low you can give FFP because FFP contains all coagulation and anticoagulation factors made by the liver--> including antithrombin

What pathway or pathways does heparin block?

classical intrinsic and final common pathway

What is the reversal for heparin?

protamine

How does protamine work to reverse heparin?

it is a positively charged substance that combines electrostatically with heparin, a negatively charged substance--> this is a neutralization reaction

Protamine reverses the action of heparin by ______.

neutralization

Warfarin (coumadin) binds to ______ receptors in the ______.

vitamin K receptors in the liver---> production of vit K dep factors (II, VII, IX, X) is depressed

What pathway is blocked with warfarin?

classical extrinsic and final common pathways

Recombinant hirudin, ximelagatran, and argatroban are direct _____ inhibitors.

thrombin

What two tests assess heparin?

PTT and ACT

Heparinization is adequate if the ACT is > _______ sec.

400-450 sec

What is the normal value? bleeding time

3-10min

What is the normal value? platelet

150-400,000 cells/ml

What is the normal value? prothrombin time (PT)

12-14 sec

What is the normal value? activated partial thromboplastin time (PTT)

25-35 sec

What is the normal value? activate coagulation time (ACT)

80-150sec

_______ is the body's clot buster.

plasmin

How does plasminogen (inactivated form of plasmin) get converted into plasmin? (2)

tpa and upa tissue type plasminogen activator urokinase type plasminogen activator

When a clot is formed, what is there all along that will assist in the destruction of the clot at a later time?

plasminogen is incorporated into the clot as it is formed

Plasminogen, the inactive form of plasmin, is synthesized in the ________ and circulates in the blood.

liver

Where is TPA made and what is its role?

its made in endothelial cells---> released when needed to convert plasminogen into plasmin

Aprotinin and Amicar (epsilon aminocaproic acid) work by _______.

inhibiting plasmin

When plasmin is inhibited, fibrin that is formed breaks down _______, so bleeding is _______.

slowly; decreased

What is the definitive test for DIC?

none

Name some conditions that contribute to or cause DIC?

sepsis, hemolysis, transfusion reaction, ischemia, hypotension, obstetrical emergencies (abruptio placenta, amniotic fluid embolism), acute DIC in surgical patients

What are some causes of acute DIC in surgical patients?

infection, shock, and ischemia are MOST common precipitating factors of acute DIC in surgical patients

What lab abnormalities reflect consumption of clotting factors and enhanced fibrinolysis that can be seen with DIC?

decreased--> PLTs, fibrinogen, prothrombin, levels of factors V-VIII-XIII increased--> fibrin degradation products

What is the most common cause of isolated high "PT"?

liver disease

What is the treatment for coagulation abnormalities associated with liver disease?

replace clotting factors with FFP, cryoprecipitate, and vit K as needed

Coagulation abnormalities can be associated with massive blood transfusion. What is deficient in transfused blood?

platelets, and factors V and VIII Treatment: platelet transfusion, FFP (supplies all coagulation factors), cryoprecipitate is a primary source of factor I (fibrinogen), VIII, and XIII

What clotting factor is considered the physiologic initiator of the coagulation cascade?

III (tissue factor or thromboplastin)

Antithrombin III inhibits what 5 clotting factors?

II, IX, X, XI, XII | II and X MOST profoundly inhibited

How does protamine work to reverse heparin? What kind of reaction is this?

combines electrostatically; neutralization

Name 3 substances that convert plasminogen to plasmin.

1) tpa 2) upa 3) streptokinase

When is aprotinin generally used in anesthesia? How does it work?

for repeat sternotomies and works by inhibiting plasmin

What is the BEST test for primary hemostasis, or platelet function?

standardized skin bleeding time

What are the typical manifestations of DIC?

bleeding, with oozing from tubes, wounds, and vascular access sites