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MLAB 1227: Coagulation Keri Brophy-Martinez

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Title: MLAB 1227: Coagulation Keri Brophy-Martinez


1
MLAB 1227 CoagulationKeri Brophy-Martinez
  • Coagulation Disorders
  • Secondary Hemostasis
  • Part Two

2
Acquired Coagulation Disorders
  • Two or more factors generally affected, more
    complicated
  • Bleeding from multiple sites
  • More common than hereditary disorders
  • Classification
  • DIC
  • Primary Fibrinogenolysis
  • Liver Disease
  • Vitamin K Deficiency
  • Acquired Pathologic Inhibitors

3
1. DIC Disseminated Intravascular Coagulation
  • Consumption Coagulopathy
  • As fibrin is formed, clotting proteins and
    naturally occurring inhibitors and platelets are
    consumed faster than they are made
  • Thrombo-hemorrhagic disorder
  • Clotting and lysing occurring in blood vessel, at
    the same time
  • Life threatening
  • Bleeding is the most apparent characteristic
  • Initiating events are thrombotic, where material
    enters circulation
  • Occurs due to lack of the negative feedback
    mechanism
  • Affects young and elderly

4
DIC Triggers
  • Obstetric usually due to major tissue damage
    such as retained dead fetus, abruptio placentae,
    or placenta previa
  • Acute leukemias Promyelocytic increase number
    of granules released into circulation as cells
    break down
  • Intravascular hemolysis ex transfusion
    reaction
  • Massive trauma (especially crushing injuries),
    burns, surgical procedures
  • Heat stroke
  • Snake venoms
  • Septicemias and infections viral, bacterial,
    rickettsial, fungal, protozoan (especially gram
    negative that release endotoxins)
  • Tumors foreign tissues and cells
  • Prosthetic devices heart valves, aortic
    balloon, peritoneal shunting
  • Vascular disease damaged endothelial lining

5
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6
Course of DIC
7
DIC How Does It Occur?
  • Step 1 Out of control clotting
  • Causes widespread fibrin deposits in vessels of
    tissues and organs
  • Subsequent event Hemorrhage
  • Clotting proteins consumed at a high rate
  • Causes multiple factor deficiencies, especially
    fibrinogen group
  • Platelets caught in thrombi and removed

8
DIC How Does It Occur?
  • Step 2 Triggers Fibrinolytic system to remove
    fibrin
  • Results in
  • Circulating degradation products (FDPs) that
    interfere with platelet function normal clot
    formation
  • Degradation of Factor V VIII

9
DIC How Does It Occur?
  • Step 3 Uncontrolled plasmin and thrombin enter
    circulation
  • Why?
  • Inhibitors such as AT have been depleted

10
DIC How Does It Occur?
  • Step 4 Appearance of Symptoms
  • Bleeding from multiple sites
  • Petechiae
  • Purpura
  • Occlusions in organs
  • Oozing from needle puncture sites
  • Shock

11
Lab Features of DIC
  • Platelet count decreased
  • (40-75 x 109/L)
  • PT increased
  • PTT increased
  • Fibrinogen decreased
  • FDP /D-dimer positive
  • Most helpful in diagnosis
  • AT decreased
  • RBC fragments present

12
DIC
  • Treatment
  • Goal is to treat the underlying condition
  • Remove the triggering process treat with
    antibiotics, antineoplasms, remove dead tissue,
    treat the diseases or conditions
  • Heparin to prevent or limit further coagulation
  • Replace factors, platelets give FFP

13
2. Primary Fibrinogenolysis
  • Similar to DIC
  • Plasminogen is inappropriately activated to
    plasmin
  • Plasmin circulates overwhelming the antiplasmin
    inhibitors and degrading fibrinogen and factors
    V,VIII, XIII
  • No thrombin is generated
  • Liver disease is a common trigger

14
3. Liver Disease
  • Affects all proteins made in the liver that
    function in fibrin formation, fibrinolysis and
    inhibition.
  • Patients show minimal bleeding, except in severe
    cases
  • Lab features
  • Increased
  • PT,PTT
  • Decreased
  • Platelets

15
4. Vitamin K Deficiency
  • Liver cells able to make precursor protein but
    the calcium binding site is nonfunctional
  • Causes
  • Malabsorptive syndromes
  • Sprue
  • Obstruction in biliary tract
  • Ingestion of vitamin K inhibitors- like warfarin
  • Antibiotic therapy
  • Kills off normal flora in gut which made vitamin K

16
5. Acquired Pathologic Inhibitors
  • Develop in patients with certain disease states
    and others with no underlying conditions
  • Circulating anticoagulants which may develop
    against any clotting factor
  • Classed as immunoglobulins
  • Either IgG or IgM
  • Can be alloantibodies or autoantibodies

17
Types of Inhibitors
  • Directed towards a single coagulation factor
  • Seen in patients with inherited factor
    deficiencies that have had replacement therapy
    for bleeding complications
  • Less commonly seen in healthy people and those
    taking certain drugs
  • Rare, except Factor VIII IX
  • How do we find them?
  • Interfere with clotting factor activity
  • PTT prolonged, other tests normal
  • Mixing study test will still be prolonged

18
Types of Inhibitors
  • Lupus Inhibitor/Anticoagulant
  • Seen in patients with autoimmune diseases, drug
    reactions, but also in normal patients
  • Autoantibodies interfere with phospholipid-depende
    nt reagents used in PTT tests
  • Patients have no bleeding problems (though some
    have an increase risk of thrombosis)
  • In vitro, any coag test using a phospholipid
    reagent will be falsely prolonged (PT, PTT)
  • Coag studies must be performed using reagents
    that do not contain phospholipids

19
Comparison of Acquired Disorders
Test DIC Primary Fibrinogenolysis Severe Liver Disease Vitamin K Deficiency Factor Inhibitor Lupus Anticoagulant
Platelet Count Dec Normal Dec Normal Normal Normal
PT Inc Inc Inc Inc Normal, except VII inhibitor Normal
APTT Inc Inc Inc Inc Inc Inc
Fibrinogen Dec Dec Dec Normal Normal Normal
D-dimer Inc Normal Normal Normal Normal Normal
Plasminogen Dec Dec Normal-dec Normal Normal Normal
Antithrombin Dec Normal Dec Normal Normal Normal
Blood Smear Fragments Normal Macrocytes Targets, acanthocytes Normal Normal Normal
20
References
  • McKenzie, Shirlyn B., and J. Lynne. Williams.
    "Chapter 32." Clinical Laboratory Hematology.
    Boston Pearson, 2010. Print.
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