Altered HomeostasisAltered Blood Clotting

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Altered Homeostasis/Altered Blood Clotting
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Homeostasis

• Homeostasis is the regulation, formation,
  retraction and dissolution of a clot.
• Clot Formation/ Clot Lysing

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Normal Clotting 3 Components

• 1. Vascular response
• vasoconstriction, ? blood loss
• 2. Platelets
• Sticky, Adhesive blood components
• Platelet Aggregation
• 3. Plasma clotting factors
• Always circulating
• Become Active when stimulated/needed
• Roman Numerals I-XII ( pg. 724 in text)

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Homeostasis

• A Balance between Procoagulation Factors and
  Anticoagulation Factors
• Keeps blood in a viscous, flowing state
• Promotes Oxygen delivery to cells
• Altered Homeostasis.
• Too Much or Too Little
• Inherited States Vs Acquired States of Altered
  Homeostasis

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Altered Coagulation.

• Inherited
• Hemophilia
• von Willebrands disease
• Acquired
• D.V.T.
• P.E.
• Spontaneous Bleeding
• DIC

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Clotting Mechanisms

• Happens along one of two Pathways, then to Common
  pathway
• Follows through a Cascade or Staged Process

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Intrinsic Pathway

• Within the Vessel
• Begins with the rough surface created by a
  ruptured vessel
• Platelets adhere to the ruptured area
• Platelets disintegrate and release their
  coagulation factors into the plasma
• CA is critical

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Extrinsic Pathway

• Cellular tissue outside the vessel
• Tissue cell injury results in the release of
  Thromboplastin, a coagulation factor
• Thromboplastin , in the presence of CA reacts
  with the clotting factorts to form the extrinsic
  thromboplastin
• Extrinsic thromboplastin and other factors are
  necessary to convert prothrombin to thrombin

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Clotting Studies
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Disorders of Coagulation

• Hypercoagulation States
• Venous thromboembolism
• Pulmonary embolism
• Ischemic States
• Hypocoagulation States
• Excessive bleeding
• Thrombocytopenia
• Disseminated Intravascular Coagulation
• ( D.I.C.)

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Hypercoagulation States

• DVT, PE Most Common
• At Risk Patients can be I. D., Treated
  prophalactically
• Advanced age
• Prolonged immobility or paralysis
• Prior venous thromboembolism
• Cancer
• Surgery
• Obesity/Very Tall
• Varicose veins
• Known hypercoagulability disorder

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Triad of Events (Virchows Triad)

• Venous Stasis
• Venous Endothelial injury
• Hypercoagulability
• Venous Stasis--Alteration of Blood Flow
• Venous Endothelial Injury
• --alteration in Platelet and coagulation factors

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Venous Thromboembolism

• Serious, sometimes fatal
• Activated clotting factors and platelets
  accumulate in vein cusps
• A fibrin mesh is formed and occludes the vessel
• Pulmonary Embolism can result

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Thrombus Formation
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Pulmonary Embolism

• PE blocks pulmonary artery and chemically induces
  arterial and bronchoconstriction
• Lyses of these clots create secondary PEs
• Symptoms can mimic MI with pain, respiratory
  distress, impending doom, rapid, shallow
  breathing, dysrhythmias
• Can be life threatening 12 mortality rate
• PEs most frequently happen down the line ,
  Ex. 7-10 days Post Op

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Related Physiological Concepts

• Ischemia,
  a condition in which
  insufficient O2 is available to meet the
  metabolic demands of the tissue involved
• Heart, Brain, Mesenteric Artery

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Clinical Therapies Thrombosis/Embolism

• Prevention
• hydration
• positioning
• foot dorsiflexion
• compression devices
• Treat underlying cause
• Initiate anticoagulation therapy
• Be aware of Risk Factors, Risk Timeline

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Heparin

• Interferes with conversion of prothrombin to
  thrombin
• Monitor APTT, Baseline-then want Therapeutic at
  1.5-2.5 x Baseline
• Antidote Protamine Sulfate
• Adverse effects
• hemorrhage thrombocytopenia, allergy
• Short Term Therapy prevents further clotting
• Lovenox - a low molecular weight heparin

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Warfarin

• AKA Coumadin
• Oral therapy (P.O.)
• Monitor PT, INR- therapeutic at 1.5-2.5 X
  Baseline
• More long term therapy, still designed to prevent
  further clotting episodes
• Alters synthesis of Vitamin K dependent
  coagulation factors by the liver
• Antidote
• Vitamin K

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Antiplatelets

• Aspirin
• blocks adhesion of platelets to exposed collagen
  fibers
• Dipyramidole ( persantine)
• decreases platelet aggregation
• Dextran 40
• blocks coagulation factor activation
• coats the surface of platelets
• Plavix- new one

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Thrombolytic Therapy

• Clot Busters
• Urokinase, streptokinase, TPA, TNK
• Lyses clots
• Contraindications
• Risk hemorrhage

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Bleeding Clinical Therapies

• Prevention
• Arrest cause
• Replacement Fluids, Blood, Blood Components,
  Iron supplements
• Prevent tissue damage
• Maintain body image
• Labs Hct, Hgb, PT, APTT, Plt, electrolytes,
  ABGS, FSP

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ThrombocytopeniaNormal 150,000-400,000/mcl

• Decreased Platelet Production
• Increased Platelet Destruction
• Abnormalities of Platelet function

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Manifestations

• Petechiae
• Purpura Visual indicators, Skin Ecchymosis
• Prolonged bleeding after routine procedures
• Internal bleeding
• Bleeding time prolonged

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Nursing

• Discourage OTC meds
• Seek careepistaxis, petechiae, Assess for
  changes
• Acute Intervention
• prevent and control hemorrhage
• avoid SQ and IM injections
• platelet administration
• ITP
• corticosteroids, high dose IV immunoglobulin,Splen
  ectomyTransfusions

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Disseminated Intravascular Coagulation (D.I.C.)

• Results from abnormally initiated and accelerated
  clotting at the capillary level
• Subsequent decrease in clotting factors and
  platelets which may lead to uncontrollable
  hemorrhage
• Always caused by an underlying disease
• Labs Fibrin Split Products (FSP), D-Dimers
• Life threatening

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Disease States Associated With DIC

• Nonmalignant
• Infections Gm and -
• Viral Disorders HIV, Cytommegalovirus,
• Burns
• Crush injuries, necrotic tissue
• Obstetrical Complications
• Hemolytic Tx Reactions
• Massive Blood Tx
• Acute Liver disease,Hepatitis
• Intravascular prosthetic devises

• Malignant
• Leukemia
• Metatstic diseases
• Lung Cancer
• Breast Cancer
• Hepatic Cancer
• Colon Cancer
• Prostate Cancer
• Chemotherapy
• Radiation Therapy

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DIC Treatment

• Treat/Remove underlying cause
• Minimize further bleeding
• Nursing careful assessment mouth, wound and
  orifice care
• Heparin therapy by stopping thrombosis/bleeding
  cycle
• prevent further clotting
• Amicar-interferes w/ fibrinolysis
• Support of Oxygenation, Perfusion,
  Fluid/electrolytes through episode

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Homeostasis

• A balance
• Clot Formation/ Clot Lysing