{"id":368,"date":"2020-04-21T17:36:14","date_gmt":"2020-04-21T09:36:14","guid":{"rendered":"http:\/\/www.perthhaematology.com.au\/?page_id=368"},"modified":"2020-05-01T12:06:59","modified_gmt":"2020-05-01T04:06:59","slug":"platelet-function-tests","status":"publish","type":"page","link":"https:\/\/www.perthhaematology.com.au\/index.php\/platelets\/platelet-function-tests\/","title":{"rendered":"Platelet Function Tests"},"content":{"rendered":"\n<p class=\"wp-block-paragraph\"><strong><span class=\"has-inline-color has-vivid-cyan-blue-color\">PFA-200 :: Platelet Function Analyser<\/span><\/strong><\/p>\n\n\n\n<p class=\"wp-block-paragraph\">An automated analyser assesses primary haemostasis under shear stress.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">Two cartridges:<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li><strong>CEPI<\/strong>: collagen and epinephrine (adrenaline).<\/li><li><strong>CADP<\/strong>: collagen and ADP<\/li><\/ul>\n\n\n\n<p class=\"wp-block-paragraph\">Blood sample is aspirated through the cartridge membrane \u2013 leading to platelet activation and aggregation.&nbsp; The time to close the membrane aperture (closure time) is measured.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">Aggregation depends on adequate platelet numbers, and platelet functional ability (vWF, platelets GP Ib, GP IIb\/IIIa and fibrinogen).<\/p>\n\n\n\n<p class=\"wp-block-paragraph\"><strong>Variables affecting results:<\/strong><\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>Collection Time: Assay within 4 hours of collection.<\/li><li>Haematocrit: Anaemia increases closure time (Hct &lt;20%).<\/li><li>Platelet Count: Closure times increase as plate count&lt;100.<\/li><li>Blood group\/vWF levels<\/li><li>Drugs: Aspirin, NSAID, clopidogrel (variable)<\/li><li>Acquired platelet function defects: cardio-pulmonary bypass, liver disease, renal failure.<\/li><\/ul>\n\n\n\n<p class=\"wp-block-paragraph\"><strong>PFA-200 patterns<\/strong><\/p>\n\n\n\n<figure class=\"wp-block-table\"><table><tbody><tr><td><strong>Disorder<\/strong><\/td><td><strong>Col\/Epi<\/strong><\/td><td><strong>Col\/ADP<\/strong><\/td><\/tr><tr><td><strong>Aspirin\/NSAID<\/strong><\/td><td>\u2191<\/td><td>N<\/td><\/tr><tr><td><strong>Clopidogrel<\/strong><\/td><td>N\/\u2191<\/td><td>N\/\u2191<\/td><\/tr><tr><td><strong>vWD<\/strong><\/td><td>\u2191<\/td><td>\u2191<\/td><\/tr><tr><td><strong>Glanzmann\u2019s;&nbsp; Bernard Soulier<\/strong><\/td><td>\u2191<\/td><td>\u2191<\/td><\/tr><tr><td><strong>Storage Pool Defect<\/strong><\/td><td>\u2191<\/td><td>N (or \u2191)<\/td><\/tr><tr><td><strong>Macrothrombocytopathy<\/strong><\/td><td>\u2191<\/td><td>N<\/td><\/tr><tr><td><strong>Renal Failure, MPD, CABG<\/strong><\/td><td>\u2191<\/td><td>\u2191<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<p class=\"wp-block-paragraph\"><strong><span class=\"has-inline-color has-vivid-cyan-blue-color\">Platelet aggregation studies<\/span><\/strong><\/p>\n\n\n\n<p class=\"wp-block-paragraph\">Tests the ability of certain agonists (stimulants) to produce platelet clumping or aggregation.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">Patterns of abnormality can help identify the type of platelet defect.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">Common defect patterns:<\/p>\n\n\n\n<figure class=\"wp-block-table\"><table style='font-size:10px'><thead><tr><th>Disorder<\/th><th>Defect<\/th><th>Plat Count<\/th><th>Blood Film<\/th><th>ADP 2uM<\/th><th>ADP 5-10uM<\/th><th>Collagen 1ug\/mL<\/th><th>AA 100uM<\/th><th>Adrenaline 10UM<\/th><th>Risocetin 1.2mg\/mL<\/th><\/tr><\/thead><tbody><tr><td><strong>Aspirin\/NSAID<\/strong> <strong>&nbsp;<\/strong><\/td><td>Inhibit COX<\/td><td>N<\/td><td>N<\/td><td>1Y wave no 2y wave<\/td><td>1y<br>no 2y<\/td><td>\u2193absent<\/td><td>Absent<\/td><td>\u2193<\/td><td>N<\/td><\/tr><tr><td><strong>ADP antagonists (clopidogrel)<\/strong><\/td><td>Inhib ADP receptor<\/td><td>N<\/td><td>N<\/td><td>Absent<\/td><td>Absent<\/td><td>N<\/td><td>N<\/td><td>N<\/td><td>N<\/td><\/tr><tr><td><strong>Glanzmanns\u2019s Thrombasthenia<\/strong><\/td><td>GpIIb\/IIIa receptor<\/td><td>N<\/td><td>N<\/td><td>Absent<\/td><td>Absent<\/td><td>Absent<\/td><td>Absent<\/td><td>Absent<\/td><td>N<\/td><\/tr><tr><td><strong>Bernard Soulier Syndrome<\/strong><\/td><td>GpIb-V-IX receptor<\/td><td>\u2193<\/td><td>Giant plats \u00ea plat<\/td><td>N<\/td><td>N<\/td><td>N<\/td><td>N<\/td><td>N<\/td><td>Absent<\/td><\/tr><tr><td><strong>vWD<\/strong><\/td><td>&nbsp;<\/td><td>N\/\u2193<\/td><td>N<\/td><td>N<\/td><td>N<\/td><td>N<\/td><td>N<\/td><td>N<\/td><td>\u2193<\/td><\/tr><tr><td><strong>Gray Platelet Syndrome<\/strong><\/td><td>\u03b1-granule defic<\/td><td>\u2193<\/td><td>Gray plats<\/td><td>N\/\u2193<\/td><td>N\/\u2193<\/td><td>N\/\u2193<\/td><td>N<\/td><td>N<\/td><td>N<\/td><\/tr><tr><td><strong>Dense Granule Deficiency<\/strong><\/td><td>\u03b4-granules<\/td><td>N<\/td><td>N<\/td><td>N<\/td><td>Absent<\/td><td>\u2193<\/td><td>N<\/td><td>No 2y wave<\/td><td>? 1Y only<\/td><\/tr><tr><td><strong>VWD Type IIb<\/strong><\/td><td>VWF protein<\/td><td>\u2193<\/td><td>&nbsp;<\/td><td>N<\/td><td>N<\/td><td>N<\/td><td>N<\/td><td>N<\/td><td>N&nbsp;&nbsp;<br>\u2191 0.5 risto<\/td><\/tr><tr><td><strong>Platelet type vWD<\/strong><\/td><td>Mutn GpIb receptor<\/td><td>\u2193<\/td><td>&nbsp;<\/td><td>N<\/td><td>N<\/td><td>N<\/td><td>N<\/td><td>N<\/td><td>N&nbsp;&nbsp;<br>\u2191 0.5 risto<\/td><\/tr><tr><td><strong>Renal Failure<\/strong><\/td><td>Acquired SPD<\/td><td>N\/\u2193<\/td><td>&nbsp;<\/td><td>N<\/td><td>\u2193<\/td><td>N\/\u2193<\/td><td>N\/\u2193<\/td><td>\u2193<\/td><td>N\/\u2193<\/td><\/tr><tr><td><strong>Liver Disease<\/strong><\/td><td>&nbsp;<\/td><td>N\/\u2193<\/td><td>&nbsp;<\/td><td>1Y only<\/td><td>1Y only<\/td><td>\u2193<\/td><td>?<\/td><td>1Y only<\/td><td>N\/\u2193<\/td><\/tr><tr><td><strong>Afibrinogenaemia<\/strong><\/td><td>&nbsp;<\/td><td>&nbsp;<\/td><td>&nbsp;<\/td><td>Absent<\/td><td>Absent<\/td><td>Absent<\/td><td>&nbsp;<\/td><td>Absent<\/td><td>&nbsp;<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<p class=\"wp-block-paragraph\">Strong agonists: collagen, thrombin, TXA2 \u2013 directly induce plat agg, TX synthesis and plat gran secretion.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">Weak agonists: ADP, Adren: Induce platn agg without secretion. (biphasic curve)<\/p>\n\n\n\n<p class=\"wp-block-paragraph\"><strong>Agonists:<\/strong><\/p>\n\n\n\n<figure class=\"wp-block-table\"><table><tbody><tr><td><strong>Agonist<\/strong><\/td><td><strong>Conc<\/strong><\/td><td><strong>Comment<\/strong><\/td><\/tr><tr><td>ADP<\/td><td>LD:1\u20135 uM HD 10uM<\/td><td>ADP binds ADP receptor on plat. Shape change \u2013 1y agg. 2y wave = ADP from plat storage grans. LD \u2013&gt; 1y only. 2y wave inhib by aspirin and NSAIDs. Clopidogrel inhibs P2Y1 receptor<\/td><\/tr><tr><td>Collagen<\/td><td>1, 4ug\/mL<\/td><td>Collagen binds GpVI and GpIa\/IIa inducing granule release, TX and GPIIb\/IIIa activn. Lag phase.<\/td><\/tr><tr><td>Ristocetin<\/td><td>LD: 0.5mg\/mL HD: 1.5-5mg\/mL<\/td><td>Ristocetin (not LD) cuases plats agglutination (not agg) via vWF abd GP1b-IX-V complex.<\/td><\/tr><tr><td>Adrenaline<\/td><td>5,10uM<\/td><td>Adrenaline blinds a2 recepotor on plat &#8212; Ca release. Similar to ADP agg. 1y , 2y wave with ADP released from grans. 2y wave inhib by aspirin,. NSAIDs.&nbsp; Variation in a receptor density \u2013 reduced agg.<\/td><\/tr><tr><td>Arachadonic Acid<\/td><td>500ug\/mL<\/td><td>AA is precursor to TXA2. Via cyclo-oxygenase and thromboxane synthase.&nbsp; TX is potent plat activator<\/td><\/tr><\/tbody><\/table><\/figure>\n","protected":false},"excerpt":{"rendered":"<p>PFA-200 :: Platelet Function Analyser An automated analyser assesses primary haemostasis under shear stress. 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