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reticulocyte index formula
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reticulocyte index formula
(pt. hct x %Reticulocytes)/ (45%)

where 45% represents the normal hematocrit
hereditary or acquired deficiencies in heme synthesis
porphyria
anemia is a decrease in...
hemoglobin
platelets are also called
thrombocytes
lifespan of platelets
8-10 days
lymphocytes
Image: lymphocytes
Monocytes
Image: Monocytes
hematocrit equation
RBCxMCV= HCT x 10
what does the reticulocyte count tell us
if the bone marrow is working properly and making RBCs
where are RBCs made
bone marrow
Reticulocyte index for hypoproliferative anemias is usuallyless than 2reticulocyte index for hemolytic anemias have an index of3+target cells are found inthalassemia liver disease aspleniaartifacts of old bloodechinocytesoften see teardrop cells in...megaloblastic anemiabasophilic stippling is seen inlead poisoning thalassemiared cells have nonucleusseen in thalassemia, hemoglobinopathies, iron deficiency, and other hyperchromatic states seen with obstructive liver disease and after splenectomytarget cellsare most common in myeloproliferative diseases (myelofibrosis), megaloblastic anemias, and thalassemiateardrop cellslook like they have the flu? make sure to rule outcarbon monoxide poisoningsickle cell anemia: mutated...b-hemoglobinin alpha-thalassemia, excess b-chains form weak tetramers....with oxygen binding properties more like myoglobin than normal hemoglobinHbHheme synthesis is regulated by...ALA synthaseincreases heme synthesisbarbituratesdecreases heme synthesishemin, glucosehas similar symptoms to porphyria because it inhibits ALA dehydrates and ferrochelastaselead poisoningmajor symptoms of acute intermittent porphyrianeurovisceralacute intermittent porphyria is due....mutationPBG deaminasemessed up heme synthesisporphyriaabdominal pain port wine urine polyneuropahty psychologicalal issuesacute intermittent porphyriaacute intermittent porphyria treatmentglucose and heme/heminporphyria cutanea tarda is caused by inhibition/deficiency in...UPG III decarboxylaseshould not be prescribed for patients with a porphyriabarbiturateshemolytic anemia specific signjaundicethalassemia major specific signbone deformitiessickle cell disease specific signleg ulcerssevere vitamin B12 deficiency specific signneurological signslevels are significantly reduced or absent in intravascular hemolysishaptoglobinhaptoglobin is only relevant inintravascular hemolysispeptic ulcer disease is most often associated to this type of anemiairon deficiencyrisk of IV ironanaphylaxisdecreased ferritin (increased hepcidin)= ....iron absorptiondecreaseddecreased ferropotin= decreased...iron absorptiondecreased hepcidin=....ferropotinincreaseddecreased hepcidindemand iron deficiency hypoxiaincreases hepcidiniron intake inflammationHemoglobin electrophoresis confirms the diagnosis of what 2 types of anemia?thalassemia sickle cellB4 tetramer=HbHchronic hemolytic anemia --/-a thalassemiaHbH diseasepresentation mimics vitamin B12 deficiencyCopper Deficiencymost common cause of vitamin B12 deficiency autoimmune destruction of gastric parietal cells (deficiency in intrinsic factor)pernicious anemiaB12 is absorbed by...made by...intrinsic factor, parietal cellsantiparietal cell antibodies-- indication ofpernicious anemiacomplication of b12 therapy-....therefore must monitor....hypokalemia potassium (K+) levelsin acute chest syndrome (sickle cell anemia) treatment=urgent exchange blood transfusion (Hb is passed through to dilate HbS and relieve symptoms)prevention of sickle cell disease crises:....which increases HbF and deceases number of criseshydroxyureain PNH (hemolytic anemia) acquired defects in the myeloid stem cell results in absence of...which further impacts CD55/CD59GPI anchorsymptoms of PNHdark urine (morning) hemolysis pancytopenia thrombosis (most common cause of death)classic triad=PNHclassic pentad=TTPwarm antibody hemolytic anemia is...mediated and associated with extravascular hemolysisIgGcold antibody hemolytic anemia is...mediated and associated with intravascular hemolysisIgMfava beans impactG6PD deficiencyacute hemolysis with G6PD with...moth ballsgive...to give coagulation factorsplasmagive mainly for the fibrinogen and vWFcryoprecipitatehemoglobin level indicator of when you should start transfusing blood (if symptomatic)7fibronyltic cascade is primarily through the action of...plasminplasminogen is activated by...(which is why a deficiency would cause you to clot compared to bleed)XIIais an example of immune decreased platelet survival (auto-antibody)ITP (immune thrombocytopenia purpura)ITP auto-antibody against...gpIIb/IIIathe body's inappropriate response to many activating events (initially thrombotic and then turns into hemorrhagic)DICtwo major triggers for DICinappropriate release of tissue factor widespread injury to the endotheliumdefect in lately adhesion, autosomal recessive inherited defect of glycoprotein Ib (receptor for vWF)bebrnard-soulier syndromedifference between ITP and Glanzmann thromastheniaGlanzmann thromasthenia : defect or deficiency in gpIIb/IIIa ITP: autoantibody against gpIIb/IIIAmay be seen in patients with vWD (particularly type 3) because it serves as a stabilizing protein in the circulation (so without vWF, it is likely to degrade)Factor VIIIthrombotic disorders are commonly described by...Virchow's triadpatient's immune system has formed an antibody specific against heparinheparin-induced thrombocytopeniapreviously called lupus anticoagulant syndrome clinical manifestations: recurrent thrombosis, repeated miscarriages, cardiac valve vegetations and thrombocytopenia antibodies have specificity to phospholipids/phospholipid-protein complexantiphospholipid syndromeantiphospholipid syndrome (lupus anticoagulant syndrome) prolongesaPTTin antiphospholipid syndrome (lupus anticoagulant syndrome) you are more at risk for...than...clotting, bleeding5-15% of normal patients (no history of clotting) will have a laboratory detectable....antiphospholipid antibodymore recent thrombi may respond to fibronoyltics more readily (reason there is a time frame for tPA use-- want to use tPA before...crosslinks the clot)Factor XIII...main clinical outcome is downstream infarction of tissue (coronary and cerebral-- causing heart attacks/strokes)arterial thrombusmain clinical outcome is congestion and edema (lower pressure system, just causes a backup)venous thrombusdisrupts laminar flowdyskinetic contractionare prone to embolization (brain, kidney, spleen are common targets)cardiac thrombimost commonly noticed in the superficial and deep veins of the lower extremitiesvenous thrombosismore likely to embolize to the lungs, therefore more clinically seriousdeep vein thrombosis (DVT)most coagulation testing is done on....plasma samplessodium citratedeals with mainly plateletsprimary hemostasisis the anticoagulant used in samples submitted for CBC (when doing a platelet quantitation test)EDTAplatelet quantitation: occasionally, EDTA in the sample may induce platelets clumping resulting in.... giving low platelet counts which are inaccuratepseudothrombocytopeniaperformed on whole blood quick and dirty way to measure platelet activity (adhere/aggregate)PFA-100in a PFA-100, the platelets are being told to adhere and aggregate on a..membrane cartridgePFA-100: the time to block the aperture is called the....and prolongation of this indicates platelet dysfunctionclosure timeare platelets being impacted by antiplatelet drugs performed on whole blood trying to get the platelets to react with fibrinogen on cartridges (most common= aspirin and PRU-- p2Y12)VerifyNowtells you how active vWF isristocetin cofactor assayPT and aPTT are test that testsecondary hemostasis (coagulation cascade)commonly used to monitor patients on warfarinPTPT (when looking at warfarin patients) is normalized byINRadd these in to kickstart PTphospholipids + tissue factoradd these in to kickstart aPTTphospholipidscommonly used to monitor patients on heparin therapyaPTTpreferred test for monitoring heparinAnti-Xa assay/heparin assaydecrease in heparin=... in Factor Xaincreasetests for fibrinogen activitythrombin time (TT)is a breakdown product of a fibrin clot previously cross linked with factor XIIIa (stable clot)D-dimerpositive D-dimer indicatesDICupwards to 30% are new mutationshemophilia Aexcessive circumcision site bleeding is commonhemophiliamost adverse effect of hemostasis medicationsincreased risk of bleedingmajor limiting factor in warfarin's useintracranial bleedsdirect thrombin inhibitor (DOAC)dabigatrandirect Xa inhibitor (DOAC)rivaroxabanoften avoided in patients who are pregnant and those that have mechanical heart valvesDOACsin a patient with a mechanical heart valve, what anticoagulant would you dosewarfarinbinds to antithrombin and increases its activity by 1000xheparinreverses effect of heparinprotamineall heparin derivatives can decrease....activityFactor Xaonly longer heparin derivatives can decrease...activityFactor IIadoes not have a specific drug reversal agentbivalirudinuse this for the following: venous thromboembolism and pulmonary embolism atrial fibrillationanticoagulantsroutine oral antiplatelet drugaspirintwo most commonly used oral antiplatelet drugsaspirin, P2Y12bind ADP and inhibit them from activating more plateletsP2Y12 (clopidogrel, ticagrelor)eptifibbatide inhibitsglycoprotein IIb/IIIause these for: myocardial infarctionsantiplatelet drugsused for thrombus dissolution or acute pulmonary embolism (Active ischemic stroke, NEVER USE FOR A HEMMORHAGIC STROKE)tPApatient with thrombocytopenia and giant platelets, think..ITPwarfarin has an increased risk of....compared to DOACsintracranial hemorrhageused after myocardial infarctionsaspirin...are unlikely to present later in lifehemophiliaselevated D-dimer, low fibrinogen, thrombocytopenia, schistocytes, increased aPTT, PT thinkDICincreased aPTT but not bleedingFactor XII deficiency antiphospholipid syndrome (do not treat if asymptomatic)in TTP, your D-dimer would benormalITP is an antibody againstGpIIb/IIIaPathological activation of coagulation cascade Widespread microthrombi resulting in infarct and ischemia Consumption of platelets and factors results in bleeding especially from IV sites and mucosal surfaces (bleeding from body orifices)DICalmost always secondary (decreased fibrinogen, increased PT, aPTT), increased D-dimer (from split products), schistocytes, treat underlying causeDICPNH is an example ofintravascular hemolysis diseaseselevated D-dimer is an indicator offibronylysisA...is performed when a mixing study does not correct (and indicates an inhibitor is present) in which a large excess of phospholipids are added to the sample to see if the prolongation correctslupus anticoagulant test (aPTT based)a prolonged closure time in a PFA-100 test indicatesplatelet dysfunctionThrombin time is a clot assay that tests for...activityfibrinogenDIC leads to widespread activation and consumption of ... because of widespread exposure of TF and subendotheliumcirculating plateletsoccur when systemic platelet activation reduce platelet life span leading to thrombocytopenia and ultimately bleeding.thrombotic microangiopathies (TMA)manifests as recurrent thromboses, repeated mmiscarriages, cardiac valve vegitations, and thrombocytopenia.antiphospholipid syndromeare antibodies with phospholipid specificity that prolong aPTT because of how they affect in vitro test, though patients are more likely to clot than bleed:clot/bleed.lupus anticoagulants

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