Quantitative Platelet Issue.


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Group quantitative issue of platelets as indicated by essential ... Disarranges of Hemostasis. Essential. Skin. petechiae. purpura. ecchymoses. Mucous layers. nose ...
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Quantitative Platelet Disorders LabM 419 Clinical Coagulation Fall 2009 ©C. Calvo, MS, MT(ASCP), SH(ASCP) – UW, 2009.

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Learning Objectives – Upon fulfillment of required perusing, after watchful study, and tailing this address the understudy will have the capacity to: Define the key terms dark bolded or emphasized on pages 630 – 649 of the course message. Contrast clinical side effects and coagulation profiles of the quantitative platelet issue talked about in address with thickening element insufficiency issue. Clarify the essential pathophysiologic procedures of thrombocytopenia. Arrange quantitative scatters of platelets as indicated by essential pathophysiologic etiology. Portray immunologic and non-immunologic instruments by which drugs initiate thrombocytopenia. Give particular case to outline. Clarify the pathophysiology of and perceive the lab test outcomes\' profile connected with Thrombotic Thrombocytopenic Purpura (TTP), Immune Thrombocytopenic Purpura (ITP), Heparin-Induced Thrombocytopenia (HIT), Neonatal Alloimmune Thrombocytopenia (NAIT), and hemolytic-uremic disorder. List lab tests helpful in recognizing and separating the platelet issue distinguished in target 6. Contrast the serotonin discharge and the immunoassay test for HIT. Separate intense and ceaseless resistant thrombocytopenia. Recognize neonatal isoimmune from neonatal immune system thrombocytopenia. Look at and contract essential and receptive thrombocytosis. Decipher lab information, associate it with patient data, and orchestrate learning of the quantitative platelets issue to accurately react to test addresses and comprehend topic related contextual analyses.

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Checkpoint Primary Hemostasis It\'s about vasculature It\'s about platelets It\'s about keeping up blood in a liquid state inside the veins and averting inordinate blood misfortune after vascular harm Bottomline Platelet Abnormalities – QUANTITAIVE OR QUALITATIVE bring about draining Graphic got to URL http://www.uv.es/~vicalegr/CLindex/CLvasculitis/vasleu11.jpg , 2005.

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Primary Skin petechiae purpura ecchymoses Mucous layers nose drains sclera gums Secondary Tissues Joints Clinical Manifestations Primary v.s. Auxiliary Disorders of Hemostasis http://heme-coag.uthscsa.edu/wwwbleed97/22apet.gif

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Identify the reason for draining physical exam therapeutic history Prescribe proper treatment Important data Age of onset more youthful = acquired etiology umbilicus/circumcision draining optional hemostasis issue Severity and industriousness of indications Family History acquired condition Health status optional reasons for draining harm liver malady Drug history ibuprofen anticoagulants chemotherapeutics Exposure to poisons modern specialists pharmaceuticals Physician\'s Eye View

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Laboratory Perspective Platelet checks Function test Bleeding time Aggregation thinks about Coagulation ponders Prothrombin time (PT) Activated fractional thromboplastin time (aPTT) Thrombin time (TT) Fibrinogen (Fi)

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Inherited Abnormal amalgamation of subendothelial connective tissue parts Telangectasia Ehlers-Danlos Marfan Syndrome Rare Limited Lab Test Importance Acquired Abnormal cells Scurvy Paraproteins Amyloidosis Multiple myeloma Vasculitis contaminations Drugs Primary clinical manifestaton : Purpura Common Vascular-based Disorders

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Platelet-Associated Disorders Quantitative – Numbers diversion Increased = thrombocytosis >450K/m l Decreased = thrombocytopenia <100K/m l http://www.mcl.tulane.edu/classware/pathology/Krause/ET/RM1.html http://lifesci.rutgers.edu/~babiarz/Histo/Blood/Smear2.jpg http://www.ispub.com/xml/diaries/ijid/vol3n2/vivax-fig1.jpg

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Bleeding Clinical Correlation - PLT Numbers BT prolongation corresponding to PLT tally IF no confounding elements. Realistic got to URL http://home13.inet.tele.dk/gloerud/red_l.gif , 2004.

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Significant Lab Data in Defects of Primary Hemostasis

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Thrombocytopenia

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Congenital – absence of satisfactory BM Megakaryocytes Fanconi Anemia Wiskott-Aldrich Syndrome Bernard Soulier Syndrome May-Hegglin Anomaly Rare, Autosomal Dominant Dohle Bodies Big PLTS PLT Aggregation = NL Acquired – smothered or inadequate megakaryopoiesis Neonatal Hypoplasia Viral contamination (CMV) In utero drug presentation Chlorothiazide Tolbutamide Drugs Chemotherapy Alcoholism Interferon Estrogen Chloramphenicol B12 insufficiency Impaired or Decreased PLT Production

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Increased Platelet Destruction Categories Immune-interceded pulverization ITP Acute Chronic Alloimmune Drug-initiated Non-invulnerable demolition/utilization DIC Thrombotic Thrombocytopenic Purpura (TTP) Hemolytic Uremic disorder (HUS) Dilution or Distribution Disorders Thrombocytopenia comes about when creation and substitution of PLTS can\'t stay aware of rate of devastation

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Immune (Idiopathic) Thrombocytopenic Purpura = ITP Cause - antibodies against viral epitopes or antibodies against platelet layer glycoproteins IIb-IIIa or Ib-IX, and are of the IgG sort RES framework clears sharpened PLTs Acute – youngsters Viral Infection <20K/m l checks 1 – 3 weeks post disease Spontaneous reductions normal Treatment no particular treatment IVIG PLT transfusions Splenectomy Chronic – grown-ups PLT antibodies 30-80K/m l tallies Remissions uncommon 2/3rds recuperate Treatment IVIG Prednisone Splenectomy Graphic got to URL http://z.about.com/d/pediatrics/1/G/N/Q/bruises.JPG , 2007.

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Clinical Picture – Acute/Chronic ITP

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Neonatal Alloimmune Thrombocytopenia (NAIT) Analogous to HDN Mom needs PLT-particular Ag that hatchling acquired from father HPA – 1a: found on GPIIIa (Caucasian populaces) HPA-3a: found on GPIIb (Asian populaces) Fetal Ags may go into maternal flow Maternal IgG AB cross placenta and assault fetal PLTs Diagnosis by rejection Need to perceive early and treat properly NAIT – Autoimmune form : ITP or SLE in mother is essential – latent AB exchange from mother – embryo is accidental target

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Rare Develops 1 week after PLT-containing product(s) transfusion AB – preformed Anamnestic safe reaction AB target = HPA-1a Affected populace all the more frequently multi-parous ladies Previously transfused men Post-Transfusion Purpura Graphic got to URL http://www.coldbacon.com/mdtruth/pics/hsp.jpg , 2009.

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Immune Drug-Induced ITP Drugs of Interest Analgesics Salicylates Acetaminophen Antibiotics Cephalothin Penicillin Rifampin Sulfa Drugs Quinidine Sedatives Phenobarbital Meprobamate Carbamazepine Oral hypoglycemics Chlorpropamide Heavy Metals Bismuth Mercury Insecticides Figure 43-04. Immunoglobulin ties a platelet layer antigen or antigen and medication blend. Macrophage Fc receptors tie the Fc bit of the immunoglobulin. This may bring about platelet evacuation and thrombocytopenia. (From Rapaport SI: Introduction to Hematology, second ed. Philadelphia: JB Lippincott, 1987:489.) Graphic got to URL http://coursewareobjects.elsevier.com/objects/elr/Rodak3e/IC/jpg/Chapter43/043004.jpg , 2008.

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Heparin Induced Thrombocytopenia Common reaction of UFH Therapy (1-5% patients) Delayed onset with at no other time heparin-introduction Follows resistant reaction rate: manifestations @ 7-10 days Acute onset with past presentation Symptoms @ 1 – 3 days Graphic got to URL http://coursewareobjects.elsevier.com/objects/elr/Rodak3e/IC/jpg/Chapter43/043005.jpg , 2008 .

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Type I Benign Mild, transient thrombocytopenia Counts > 100K Counts come back to "ordinary" if heparin is proceeded with Type II Clinically huge Moderate –severe thrombocytopenia Counts < 100K Counts come back to typical just if heparin is suspended Heparin Induced Thrombocytopenia

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HIT Testing Figure 43-06. The serotonin discharge measure for heparin-prompted thrombocytopenia (HIT). Giver platelets in platelet-rich plasma are marked with tritiated (3H) serotonin, washed, and suspended in patient plasma. Heparin in helpful and immersing measurements is added to 2 aliquots. Arrival of radioactive serotonin in the restorative aliquot in mix with no discharge in the supra-helpful framework shows HIT. Realistic got to URL http://coursewareobjects.elsevier.com/objects/elr/Rodak3e/IC/jpg/Chapter43/043006.jpg , 2008.

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HIT Testing Figure 43-07. Protein immunoassay for HIT. The strong stage target antigen is a complex of PF4 and heparin or a heparin surrogate. Antiheparin/PF4 in patient serum ties the antigen and is bound by catalyst marked antihuman immune response, a sandwich measure. The compound catalyzes the arrival of a chromophore from its substrate. Realistic got to URL http://coursewareobjects.elsevier.com/objects/elr/Rodak3e/IC/jpg/Chapter43/043007.jpg , 2008.

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Non-Immune PLT Destruction CAUSES PLT introduction to non-endothelial surfaces Mechanical heart valve Activation of coagulation DIC PLT utilization by endovascular damage TTP HUS

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Thrombotic Thrombocytopenic Purpura (TTP) Graphics got to URL http://evolvels.elsevier.com/area/default.asp?id=1138_ccalvo7_0001 ,, http://www.coolhealthtips.com/coolimages/causes.jpg , & URL http://www.childrenshospital.org/az/Site1209/Images/ei_1884.gif 2008.

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TTP Mechanism ULVWF multimers are ordinarily processed by von Willebrand cutting protease , ADAMTS 13. In TTP, the nonappearance of ADAMTS13 permits arrival of ULVWF, activating platelet enactment. TTP, thrombotic thrombocytopenic purpura; ULVW, strangely extensive von Willebrand variable. " A D isintegrin-like A nd M etallprotease with T hrombo S pondin\' Graphic got to URL http://evolvels.elsevier.com/segment/default.asp?id=1138_ccalvo7_0001 , 2008.

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TTP Clinical Presentation Abdominal torment Visual imperfections Heart disappointment Headaches Seizures Confusion Renal brokenness Jaundice Graphic got to UR

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