chp 22

hemostasis

Coordinated process that limits blood loss after vessel injury. A balance between clot formation with clot removal.

Normal hemostasis

oVessel spasm: Vascular constriction reduces blood flow

oPlatelet plug: Adhere to the injured vessel wall to form a temporary plug

oCoagulation cascade: Produces a fibrin mesh

oClot retraction: Clot squeezed to join edges of the broken vessel

oClot dissolution: Fibrinolysis removes the clot after repair

When regulation fails

↓ clotting à bleeding; ↑ clotting àthrombosis

coagulation factors

Plasma proteins

oMost coagulation factors are produced by the liver

oMany circulate in an inactive form

oVitamin K is required to produce factors II, VII, IX, and X

oVitamin K also supports production of proteins C and S

Other essential components

oCalcium: factor IV, required for several coagulation reactions

ovon Willebrand factor: supports platelet adhesion and carries factor VIII

oPlatelets: provide a surface for coagulation reactions

Key point

oCoagulation requires these and an intact vessel wall

step 1 : vascular contriction

What happens:

oVessel injury triggers contraction of vascular smooth muscle

oReduced blood flow limits initial blood loss

Important signals:

oLocal nerve reflexes

oEndothelin released by injured endothelial cells

oThromboxane A₂ released by activated platelets

step 2: primary hemostasis

How platelets are produced

o1. Thrombopoietin is released by the liver and kidneys to stimulate platelet production in the bone marrow

o2. Megakaryocytes develops in in the bone marrow

o3. Platelets enter circulation when megakaryocytes break into cytoplasmic fragments

o4. Old platelets are removed from circulation after approximately 7–10 days by the spleen and liver

Clinical connection

oLow platelet count: Impaired platelet plug formation, petechiae, easy bruising, mucosal bleeding, prolonged bleeding

oHigh platelet count: ↑ risk for inappropriate clot formation

Platelet plug formation

oAdhesion: Platelets bind to exposed collagen through von Willebrand factor.

oActivation: Platelets change shape and release ADP and thromboxane A₂.

oAggregation: Activated platelets bind to one another through fibrinogen bridges.

oResult: A temporary platelet plug forms at the site of injury

step 3: coagulation

Pathway

o1. Tissue factor and contact activation begin separate pathways

o2. Both pathways activate factor X

o3. Factor Xa helps convert prothrombin to thrombin

o4. Thrombin converts fibrinogen to fibrin

o5. Fibrin strands stabilize the platelet plug

Key concept

oCoagulation strengthens the platelet plug with fibrin mesh

Nursing connection

oPT/INR evaluates the extrinsic pathway

oaPTT evaluates the intrinsic pathway

step 4 and 5

Clot retraction

oPlatelets contract & clot pulls the edges of the vessel together

oSerum is expelled as the clot becomes more compact

Fibrinolysis

oEndothelial cells release tissue plasminogen activator

otPA converts plasminogen to plasmin

oPlasmin breaks down the fibrin mesh

oThe clot is removed after vessel repair

why thrombosis occurs

Three conditions promote inappropriate clot formation

Virchow’s triad:

• Endothelial injury

• Atherosclerosis

• Smoking

• DM

• Trauma or surgery

Abnormal blood flow

oVenous stasis

oImmobility

oHeart failure

oTurbulent arterial flow

Hypercoagulability

o↑ platelet activation

o↑ coagulation activity

o↓ anticoagulant activity

oMalignancy or estrogen exposure

thrombocytosis

Definition

oPlatelet count above approximately 450,000/µL

oA count above 1,000,000/µL represents extreme thrombocytosis

Why it matters

oMore platelets may ↑ platelet-rich thrombus formation

oRisk depends on the cause and the patient’s condition

oExtreme thrombocytosis may also be associated with bleeding

Possible causes

oChronic inflammation, iron deficiency, infection

oSplenectomy, myeloproliferative disorders

Clinical findings to monitor

oHeadache or visual changes

oChest pain or shortness of breath

oUnilateral limb swelling or pain

oNeurologic changes

oUnusual bruising or bleeding

Key point

oA high platelet count does not automatically mean thrombosis, but it requires evaluation of the cause and the patient’s symptoms

platelet disorders

Thrombocytopenia

oPlatelet count below 150,000/µL

oCommon mechanisms include:

§Decreased bone marrow production

§Increased platelet destruction

§Increased platelet consumption

§Splenic sequestration

Platelet dysfunction

oPlatelet count may be normal

oPlatelets do not adhere, activate, or aggregate normally

oMedications, inherited disorders, kidney disease, and systemic illness may impair function

thrombocytopenia

Decreased production

oBone marrow failure or infiltration

oChemotherapy or other marrow-suppressing medications

oViral infections such as HIV or hepatitis C

oNutritional deficiencies

Increased destruction

oImmune thrombocytopenia

oDrug-induced immune thrombocytopenia

oAutoimmune disease

Increased consumption

oDisseminated intravascular coagulation

oThrombotic thrombocytopenic purpura

oHemolytic uremic syndrome

Splenic sequestration

oEnlarged spleen retains more platelets

oMay occur with liver disease and portal hypertension

Clinical connection

oThe mechanism helps guide the laboratory evaluation and treatment plan

Skin findings

oPetechiae

§Pinpoint red, purple, or brown spots

oPurpura

§Larger areas of non-blanching bleeding under the skin

oEcchymoses

§Larger purple or blue bruises

Other findings

oEpistaxis, gingival bleeding, heavy menstrual bleeding, blood in urine or stool, prolonged bleeding from minor injuries

hemophilia

Mechanism

oDeficiency or dysfunction of factor VIII in hemophilia A and factor IX in hemophilia B

oBoth are usually inherited in an X-linked recessive pattern

Clinical findings

oBleeding into joints à chronic damage if recurrent, muscle hematomas, prolonged bleeding after procedures or injury

Nursing priorities

oPrevent trauma, use bleeding precautions

oAvoid aspirin and NSAIDs

oAdminister prescribed factor replacement

oMonitor joints for swelling, warmth, pain, and decreased movement

von willebrand disease

Mechanism

oInherited deficiency or dysfunction of von Willebrand factor

oImpaired platelet adhesion at the site of vessel injury

oReduced stabilization of factor VIII

Clinical findings

oFrequent nosebleeds

oEasy bruising

oGingival bleeding

oHeavy menstrual bleeding

oProlonged bleeding after dental work or surgery

Typical laboratory pattern

oPlatelet count is usually normal

oPT is usually normal

ovon Willebrand factor testing is needed for diagnosis

oFactor VIII levels may be reduced

Treatment depends on the type and severity

oDesmopressin for responsive patients

ovon Willebrand factor replacement

oAntifibrinolytic therapy for selected mucosal bleeding

Takeaway

ovon Willebrand disease affects both platelet adhesion and factor VIII stability