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Anesthesia Pharm > Hemostasis (Pathophysiology) > Flashcards

Hemostasis (Pathophysiology) Flashcards

1
Q

When there is a disruption to blood vessels’ endothelial lining…

A

the breach in vessel-wall integrity can be caused by spontaneous plaque disruption, trauma, or iatrogenic reasons such as venous access or surgical intervention.

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2
Q

Vessel-wall injury initiates…

A

an extraordinary chain of events that causes the cessation of bleeding with the formation of a clot, and then followed by clot dissolution.

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3
Q

Hemostasis =

A

= is the process by which the body maintains the delicate balance between bleeding and clotting.

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4
Q

Steps of Hemostasis

A

Primary and secondary

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5
Q

Steps of Primary Hemostasis

A
  1. Adhesion of platelets to damaged vascular wall
    - von Willebrand’s factor (factor VIII:vWF)
  2. Activation of platelets
    - requires thrombin (factor IIa)
  3. Aggregation of platelets
    - requires ADP and thromboxane A2
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6
Q

Secondary Hemostasis

A

Production of Fibrin

requires extrinsic, intrinsic, and final common pathways

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7
Q

Platelets (gen info)

A
  • The normal platelet count is 150,000–400,000 cells per microliter
  • Approximately 33% of the platelet pool is sequestered in the spleen
  • Platelets have an average life-span of 8–12 days
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8
Q

Steps of Platelet Adhesion

A

Steps of Adhesion= 1st step of primary hemostasis

  1. Vascular endothelium tissue is damaged and exposes the subendothelium
  2. endothelial cells synthesized and released Von Willebrand’s factor
  3. One end of von Willebrand’s factor attaches to platelets’ Gp1b receptor, while the other end attaches to the subendothelial layer of damaged tissue
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9
Q

von Willebrand’s Disease (gen info)

A
  • This is the most common inherited coagulation defect
  • Most often, von Willebrands disease is a result insufficient synthesis of vWF within endothelial cells
  • Patients with von Willebrand’s disease often have an increased bleeding time despite a normal platelet count and normal clot retraction
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10
Q

von Willebrand’s Disease Treatment

A
  • First line therapy = DDAVP (desmopressin) releases stores of endogenous vWF and is effective in 80% of patients
  • Second line therapy = cryoprecipitate or factor VIII concentrate
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11
Q

Activation of Platelets

A

2nd step in primary hemostasis

  1. Thrombin (factor IIa) activates the platelet
  2. The activated platelet synthesizes and releases thromboxane A2 and ADP.
  3. Both thromboxane A2 and ADP promote platelet aggregation
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12
Q

Normal PLT activation

A
  1. Thrombin activates the platelet
  2. When the platelet is activated, phospholipase converts phospholipids to arachidonic acid
  3. Cyclooxygenase converts arachidonic acid to prostaglandin G2 (PGG2)
  4. PGG2 is metabolized to PGH2
  5. PGH2 is converted to a variety of prostaglandins and thromboxane A2
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13
Q

Aspirin and NSAID MOA:

A

Aspirin and nonsteroidal anti-inflammatory drugs interfere with cyclo-oxygenase, thus inhibiting the synthesis of thromboxane A2.

  • Aspirin irreversibly inhibits cyclooxygenase for the life- time of the platelet, which is approximately 8–12 days
  • NSAIDs reversibly inhibit cyclooxygenase for 24–48 hours
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14
Q

Aggregation of PLT

A

3rd step of primary hemostasis

  1. Thromboxane A2 and ADP uncovers fibrinogen receptors
  2. Fibrinogen attaches to its receptors, thereby linking platelets to each other.
  3. At this point, the clot is still water-soluble and friable
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15
Q

Production of Fibrin

A
  • After platelets aggregate, fibrin is woven into platelets and cross-linked.
  • Cross-linked fibrin is insoluble in water, thus the fibrin clot is now stable.
  • Cross-linking of fibrin strands requires coagulation factor XIII.
  • The final steps in fibrin production involve the extrinsic, intrinsic and final common pathways.
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16
Q

Extrinsic Pathway

A
  • The extrinsic pathway is initiated in response to damage occurring outside the blood vessel.
  • The coagulation factors of the extrinsic pathway are III (also known as tissue factor or thromboplastin) and VII.

“For 37 cents you can purchase the extrinsic pathway.”

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17
Q

Intrinsic Pathway

A
  • The intrinsic pathway is initiated by damage inside the blood vessel.
  • The coagulation factors of the intrinsic pathway are XII, XI, IX, and VIII.

“If you cannot buy the intrinsic pathway for $12, you can get it for $11.98.”

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18
Q

Final Common Pathway

A
  • The coagulation factors of the final common pathway are X, V, II, I and XIII.
  • Fibrin cross-linking occurs in the presence of factor XIII.

“The final common pathway can be purchased at the five (V) and dime (X) for 1 (I) or 2 (II) dollars on the 13th (XIII) of the month”

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19
Q

Hemophilia A

A

(factor VIII:C deficiency)

  • Sex-linked recessive genetic disorder that is carried by the female member and affects males almost exclusively.
  • The second most inherited coagulation disorder

males cannot pass on to their sons

If a son has Hemophilia A it came from the mother

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20
Q

Hemophilia A Treatment

A

Fresh frozen plasma (FFP) and cryoprecipitate both contain factor VIII in low concentrations.

•The preferred replacement source is factor VIII concentrate, a pooled plasma product that is treated to inactivate HIV and hepatitis viruses.

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21
Q

Hemophilia B

A

Christmas disease; factor IX deficiency)

Treated with concentrated preparations of factor IX.

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22
Q

Antithrombin

A

Antithrombin is made in the liver and neutralizes final common pathway factors and some intrinsic factors by forming complexes with them.

Activated antithrombin:

  • strongly inhibits thrombin (factor IIa) and Xa.
  • partially inhibits factors IXa, XIa, XIIa.
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23
Q

Antithrombin is a required cofactor for…?

A

HEPARIN

• Heparin binds to antithrombin III. When heparin is attached to antithrombin, the rate of the thrombin-antithrombin reaction increases 1,000-fold or more.

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24
Q

Acquired antithrombin deficiency states are common with…

A
  • Cirrhosis of the liver.
  • Nephrotic syndrome.

An antithrombin deficiency is the most common reason a patient is unresponsive to heparin.

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25
Q

Heparin: Class and MOA

A

Class

•Anticoagulant

MOA

  • Heparin forms a complex with antithrombin III, increasing its activity 1,000 times
  • Inhibits thrombin (IIa) and factor Xa
  • Depresses factors IXa, XIa, and XIIa
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26
Q

Heparin: Use, Route, and Dose

A

Clinical Use: DVT prophylaxis, PE, Acute coronary syndrome

Route: IV, SQ

Dosing

•SQ: 5,000 units for DVT prophylaxis

27
Q

Heparin Onset and DOA

A
  • Onset: rapid
  • DOA: 3 – 6 hours
28
Q

Heparin Metabolism and Elimination

A

Metabolism

•Liver metabolism

Elimination

•Heparin-protamine complexes eliminated via reticuloendothelial system

29
Q

Heparin Considerations

A
  • Check PTT levels
  • HIT
  • Bleeding
30
Q

Protamine: Class and MOA

A

Class

•Heparin antidote

MOA

• Combines with heparin to form inactive compound w/ no anticoagulant effects

31
Q

Protamine: Use, Route, & Dose

A

Clinical Use: Reversal of heparin

Route: IV

Dosing

•Based on amount of heparin given

•Give @ <5mg/min (risk of anaphylaxis with bolus’!!!!)

•Typically 1 mg will reverse 100 U of heparin

32
Q

Protamine Onset and DOA

A
  • Onset: 5 min
  • DOA: 2 hours
  • E1/2t: shorter than heparin, so heparin rebound (bleeding) may occur
33
Q

Protamine Metabolism and Elimination

A

• Metabolized and eliminated by the reticulo endothelial system

34
Q

Protamine Considerations

A
  • Derived from salmon semen
  • Anticoagulant effect
  • Releases histamine
  • Hypotension
  • Pulmonary HTN
  • Circulatory collapse- gross vasodilation- no tone
  • Facial flushing
  • Bronchoconstriction
35
Q

Tranexamic Acid (TXA) Class and MOA

A

Class

•Antifibrinolytic agent

MOA

•TXA is a synthetic reversible competitive inhibitor to the Lysine receptor found on plasminogen. The binding of this receptor prevents plasmin (activated form of plasminogen) from binding to and ultimately stabilizing the fibrin matrix.

36
Q

TXA Use and Route

A

Clinical Use

•TXA is given intravenously to prevent or reduce bleeding and the need for transfusion

Route

•IV, PO

37
Q

TXA Dose

A

•1 gram over 10 minutes. May repeat a 1 gram dose during the next 8 hours, but do not exceed a total of 2 grams.

38
Q

TXA Metabolism and Elimination

A

Metabolism

•Small portion metabolized by the liver

Elimination

•Renally excreted (large portion unchanged)

39
Q

TXA Considerations

A

•rapid infusion may cause hypotension

40
Q

TXA Contraindications

A

• Known allergy to TXA, intracranial bleeding, history of venous or arterial thromboembolism or active thromboembolic disease.

41
Q

Fibrinolysis - components

A

Plasminogen & Plasmin

  • Plasminogen is synthesized in the liver and circulates in the blood
  • During clot formation, plasminogen is incorporated into the growing thrombus
42
Q

Plasminogen Activators

A
  1. Tissue-type plasminogen activator (tPA)
  2. Urokinase-type plasminogen activator (uPA)
  3. Streptokinase
43
Q

Tissue-type plasminogen activator (tPA)

A

• tPA is produced by endothelial cells and released into the circulation.

44
Q

Urokinase-type plasminogen activator (uPA)

A
  • Found in limited amounts in the blood.
    • Urokinase is the most widely used thrombolytic agent for intra-arterial infusion into the peripheral arterial system and grafts.
45
Q

Streptokinase

A

• Streptokinase is produced by β-hemolytic Streptococci.

46
Q

Plasmin Inhibition

A

Aprotinin (Trasylol) inhibits plasmin. By inhibiting plasmin, fibrin break- down is slowed

(aprotinin is an anti-fibrinolytic agent).

Aprotinin is used during cardiac surgery to decrease intraoperative blood loss

47
Q

What prevents the breakdown of Fibrin?

A

Epsilon aminocaproic acid (Amicar, EACA) and tranexamic acid prevent the breakdown of fibrin by preventing displacing the plasmin from fibrin.

Amicar may be beneficial in the control of hemorrhage.

48
Q

Complex Disorders of Coagulation

A

Complex disorders of coagulation are those in which there is an abnormality of more than one component of the hemostatic mechanism. Such as:

  • disseminated intravascular coagulopathy (DIC)
  • liver disease
  • uremia
  • multiple transfusions.
49
Q

Disseminated intravascular coagulation (DIC)

A

DIC is a manifestation of an underlying disease process

There is no pathogenomic laboratory test for DIC

50
Q

Conditions that can cause or contribute to DIC

A
  • Sepsis.
  • Hemolysis (massive); transfusion reaction.
  • Ischemia.
  • Brain trauma.
  • Hypotension/hypoperfusion.
  • Obstetrical emergencies
51
Q

Manifestations of Acute DIC in surgical patients

What often precipitates it?

A
  • Bleeding, with oozing from tubes, wounds, and vascular access sites are typical manifestations of DIC.
  • Shock, ischemia and infection are the most common precipitating factors for acute DIC in surgical patients.
52
Q

Laboratory abnormalities reflect…

A

Laboratory abnormalities reflect consumption of clotting factors and enhanced fibrinolysis

  • Decreased platelets, factors I, II, V, VIII and XIII
  • Increased fibrin degradation (split) products.
53
Q

Coagulation abnormalities associated with liver disease

A

Liver disease is the “Most common cause of an isolated high PT”

Defects in coagulation:

  1. Formation of the platelet plug
  2. Formation of fibrin clot on the surface of the platelet
  3. Fibrinolysis
54
Q

How does the platelet plug form in the patient with liver disease?

A
  • Thrombocytopenia from hypersplenism (hypersplenism keeps PLTs in the spleen, so they are lower in the blood)
  • Platelet dysfunction from elevated fibrin degradation (split) products
55
Q

Formation of fibrin clot on the surface of the platelet (for liver patient)

A
  • Synthesis of all coagulation factors except VIII is decreased
  • Elevated fibrin degradation (split) products interfere with fibrin polymerization.
56
Q

Fibrinolysis (for patient with liver disease)

A

• Increased lytic activity due to poor clearance of tPA.

57
Q

Coag disorder with liver disease: Treatment?

A

• Replace clotting factors with:

  • fresh frozen plasma
  • cryoprecipitate
  • vitamin K as needed.
58
Q

Coagulation abnormalities associated with renal failure

A

Uremia related coagulation problems:

  1. Platelet Dysfunction
  2. Fibrinolytic system is impaired
59
Q

Platelet Dysfunction (in regards to renal failure)

A
  • Platelet adherence to subendothelial collagen is impaired.
  • Platelet synthesis of thromboxane A2 is impaired.
  • Platelets have low levels of ADP and fibrinogen.
  • Platelet transfusion is ineffective; the transfused platelets rapidly become abnormal.
  • **Remember that they’ll have a normal platelet count, but a prolonged bleeding time. They have enough platelets, but they’re just dysfunctional.
60
Q

Coag disorders with Renal failure: Treatment

A
  • Adequate dialysis and elevation of hematocrit
  • Cryoprecipitate may correct the bleeding problem
  • DDAVP may correct the bleeding problem
61
Q

Coagulation abnormalities associated with massive blood transfusion.

A
  • Transfused blood is deficient in platelets and coagulation factors V and VIII.
  • Diffuse bleeding during massive transfusion is generally caused by thrombocytopenia.
62
Q

Coagulation abnormalities associated with massive blood transfusion: Treatment

A
  • Platelet transfusion to correct thrombocytopenia.
  • Fresh frozen plasma, which supplies all coagulation factors.
  • Cryoprecipitate is a primary source of factor I (fibrinogen), factor VIII, and factor XIII.
63
Q

Which pathway does Warfarin work on?

A

Extrinsic pathway

Anesthesia Pharm (18 decks)

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