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| Normal Platelet count | 400,00-150,00/microliter
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| Thrombocytopenia | <100,000/microliter
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| Pseudothrombocytopenia | false low cause by EDTA, cold, or hard venipuncture.
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| Bleeding time | Plt f(x)', nl 7.5-25 minutes, elevated in thrombocytopenia too. NOT in Factor deficiencies!!!
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| Aggregation studies | Indicated for normal plt count, elevated bleeding time; aggregation: epi, adp, collagen; Adhesion: ristocetin
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| May-Hegglin Anomlay | Autosomal Dominant(MYH9:non-muscle myosin in heaveychain IIa; allows for normal plt size); Thrombocytopenia(spleen destruction), large plt, mild to mod. bruise, bleeding in surgery, High mean plt volume.
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| Wiskott-Aldrich Syndrome | x-linked; Thrombosytopenia(small plt); assoc. with immunodeficiency(no IgM) and eczema(1st indicator); severe bleeding w/ surgery, trauma, and mense. (rare)
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| Congenital Amegakaryocytic | Autosomal recessive; Plt GF receptor mutation. Megakaryocytes die without GF. Tx is BM transplant
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| Diseases that decrease the production of Plts | Rubella, HIV
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| Drugs that suppress Plt productions | Thiazide diuretics, Diethylstillberstrol, ethanol, and tolbutamide
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| Immune mediated thrombocytopenia(drugs) | Procainamide, Quinidine, Heparin(late): abs to plt factor 4 heparin complex on plt surface 3-5 days after first admin, less likely with LMW hep
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| Plt aggregation thrombocytopenia(drugs) | Protamine, Heparin(early)
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| ITP - General | Autoimmune; ab to 2,3, ba or 1b; Spleen destruction, virally self-limiting in child; chronic and non resolving in adults(spontaneous);
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| ITP - Manifestations | Manifest: petechiae, bruises, epistaxis, gums, GI bleed and hematuria(less common), IC hemmorrhage(rare).
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| ITP - Diagnosis | CBC: thrombocytopenia, all others nl; large plts, possible anemia(blood loss), Evan's Syndrome: autoimmune hemolutic anemia w/ reticulocytes and spheocytes.
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| ITP - management | Predinsone 1-2mg/kg/24hrs; splenectomy, Ig 1g/kg; refractory: danazol, chemo
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| TTP - General | (lymphomas and SLE) Immune mediated thrombocytopenia. ab against vW cleaving protease (adamts13). Long vW shred RBC, consume and consume plts and gets stuck in microvascular
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| TTP - Manifestations | Anemia: fatigue, pale, SOB on excertion; Bleeding: petechiae, purpura, pallor; Neurolgoical symptoms: headache.
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| TTP - Diagnosis | CBC: anemia, reticulocytes, schistocytes, thrombocytopenia; inc. bilirubin(hemolysis); LDH elevated but less than expected(hemolysis); coag test normal.
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| TTP - management | plasmapharesis, FFP, predisone,
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| HUS - Pathogenesis | Thrombocytopenia; endotheliacell dysfunction(e.coli invasion releases agglutinating factor; infancy and childhood;Micorangiopathic hemolytic anemia; thrombocytopenia(consume; renal failure(most common cause in child);Elevated LDH out of proportion;Coag:nl
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| HUS - Manifestation | anemia; bleeding, renal failure; rare neurologic manifestations
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| HUS - Diagnosis | Hemolytic anemia, thrombosytopenia(less severe TTP); LDH elevated; coombs test: -; coag: norm.
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| HUS - syndrome | Children: self-limiting; pallative; Adult: plasmapharesis, FFP.
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| Plt destruction non immune mediated Preggers | pre-eclampisa: low plt, htn, edmea, proteinuira; Hemolysis elevated liver enzyme and low plts
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| Causes of Hypersplenism(thrombocytopenia) | Tumor, anemia, malaria, tb, portal hypertension, leukemias/omas
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| Bernard-Soulier Syndrome - general | autosomal recessive - deficient 1b
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| Bernard-Soulier Syndrome - manifestations | Sever bleeding
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| Bernard-Soulier Syndrome - Diagnosis | thrombocytopenia; large plts, bleeding time prolonged; ristoceiten: abn; adp: ok;
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| Bernard-Soulier Syndrome - management | Plt transfusions(no cure)
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| Glandzman Thrombasthenia - General | autosomal recessive, deficient 2b3a,
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| Glandzman Thrombasthenia - manifestations | mucosal and surgical bleeding(not as severe as BSS)
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| Glandzman Thrombasthenia - diagnosis | bleeding time: abn; ritoceiten: ok; adp: abn
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| Glandzman Thrombasthenia - managment | plt transfusion(no cure)
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| Vonwillebrand disease - general | autosomal dominant; defective vWF most common bleeding disorder
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| Vonwillebrand disease - manisfestations | spontaneous bleeding; menorrhagia
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| Vonwillebrand disease - diagnosis | Low vWF; Plt count: ok; bleeding time: ok; plt aggr: normal; abnormal aPTT(<25%); decrease Factor 8
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| Vonwillebrand disease - treatment | DDAVP(vasopressin stim endo to dump out vWF for: Type 1,3); FFP, cryoprecipitate.
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| Vonwillebrand disease - type 1 | most common; decrease in vWF
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| Vonwillebrand disease - type 2a | qualitative abnormality in protein that prevents multimer formation
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| Vonwillebrand disease - type 2b | qualitative abnormality in protein causing rapid clearance of large multimeric forms
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| Vonwillebrand disease - type 3 | autosomal recessive disorder in which vWF is nearly absent
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| Intrinsic Coagulation | F12-(kalkerin)>F12a; F11-(F12a)>F11a; F9-(F11a)>F9a; F10-(plt, ca, F9a, F8)>F10a; F2-(plt, ca, F10a, F5)> thrombin; Fibrinogen-(thrombin)>fibrin; F13-(thrombin)>F13a->cross links fibrin
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| Extrinsic Coagulation | F7-(thromboplastin)>F7a; F10-(plt, ca, F7a)>F10a; F2-(plt, ca, F10a, F5)> thrombin; Fibrinogen-(thrombin)>fibrin; F13-(thrombin)>F13a->cross links fibrin
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| PTT | Intrinsic pathway of coagulation; most sensitive to abnormals before F10 activation; heparin monitoring. Cephalin (negatively charged surface activates F11 and 12); Normal: 28-30s
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| PT | Extrinsic pathway of coagualtion; sensitive to fibrinogen, prothrombin, F5, F7, and F10. Tissue factor added to whole plasma; INR=pt/control; normal=1.
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| Hemophilia A - general | X-linked(30% mutations), most common hereditary dx of serious bleeding; deficient F8; 5-75%: mild bleeding, 1-5%:moderate; <1%: severe(hematuria)
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| Hemophilia A - manifestations | easy bruising/bleeding/spont, hemarthroses
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| Hemophilia A - Diagnosis | Bleeding time: ok, PTT: prolonged; PT: normal; F8: low
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| Hemophilia A - treatment | F8 concentrates (recombinant)
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| Hemophilia B - general | x-linked; F9 deficient(christmas factor); 1/3 quality, 2/3 quanity.
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| Hemophilia b - manifestations | easy bruising/bleeding/spontaneous; hemarthroses
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| Hemophilia B - Diagnosis | bleeding time: ok; ptt:prolonged; pt:ok; low F9
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| Hemophilia B - Treatment | F9 concentrations
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| Hemophilia C - general | Autosomal recessive; ashkenazi jews, F11 deficient
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| Hemophilia C - diagnosis | bleeding time: ok; PTT: prolonged; pt: ok; F11: low
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| Hemophilia C - manifestations | mild bleeding: post op
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| Hemophilia C - Treatment | FFP as needed
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| Afribrinogenemia | rare, variable, in presentation, replace with FFP
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| F12 deficiency | prolonged ptt; not associated with increased bleeding
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| Bleeding caused Liver disease | vitamin K defendant factors are reduced; increase fibrinolysis; Alpha2-antiplasmin is not longer made(inhibits plasmin); give FFP
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| Vitamin K deficiency | acquired defect leading to bleeding; intake from diet(leafy green veggies); intestinal bct; Abs kills bct, wardarin and coumadin inhibit vitamin K metabolism.
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| DIC - general | consumption of coagulation proteins that causes excessive bleeding caused by sepsis, tissue injury, OB complication, cancer. 50-60% die
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| DIC - Manifestations | Consumption of coag factors and activation of D-Dimer(Accelerates plasminogen->plasmin; bleeding; micro thrombosis
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| DIC - Diagnosis | Hypofibrinogenemia; elevated fibrin degradative products(D-Dimer); thrombocytopenia; PT and PTT:prolonged
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| DIC - management | Prevention(ab); heparin(stops the consumption of clotting factors).
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| Lupus Anticoagulant | Acquired/congential; an IgM or IgG produces prolonged PTT by binding phospholipid in the invitro assay; does not cause bleeding disorder unless second disorder exists
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| Acquired defects leading to hypercoagulable state | Cancer: some colon CA release pro-coagulable products; Estrogens: being older and smoking increase this; pregnancy: fibrinigen levels double in 3rd tri; anticardiolipin abs: autoimmune diseases, unknown reason.
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| Antithrombin III deficiency | congenital disorder causing a hypercoaguable state; Works synergistically with heparin to block thrombin, F10a, F9a, and F11a. end most common to F5 leiden.
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| Factor V Leiden | A defect on the F5 leiden does not allow C reactive protein to bind and deactivate it. This causes very large clots to form once they start(congenital).
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| Protein C defciency | Protein C binds F5 and F8 and in activates them to control the clotting process; clotting is uncontrolled in this congenital disease; can be quality or quanity.
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| Protein S deficiency | Protein S acts as a cofactor for C. clotting is uncontrolled in this congenital disease.
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| Coumadin | Disrupts vitamin K utilization; Vitamin K dependant Factors: 2,7(most effected),9, 10; oral admin; slow onset; Monitor w/ PT
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| Heparin | Blocks thrombin, F10a, F9a, and F11a synergystically with antithromben III; IV or subq admin; fast onset; high variability except LMW; monitor with PTT
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| Thrombomodulin | When thrombin is activated it binds to thrombomodulin and activates protein C+S to stop clotting; released by endothelium.
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| Petechiae | <.5cm; usually from thrombocytopenia; not a functional problem.
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| Purpura | >=5cm; superficial dermatological bleeding; can be problem with plts, or vascular abn;
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| Ecchymosis | Subq bleeding
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| Hemorrhage | blood loss from vascular
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| Integrin | Blocks 2b3a, Iv admin
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| TPA | catalyst for Plasminogen to plasmin; released by endothelial
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| Thromboxane A2 | Arachadonic Acid from plts is turned into thromboxane A2 which causes plt aggregation and vasoconstriction. COX1>2 inhibition.
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| PGI2 | Arachadonic Acid from endothelial cells is turned into PGI2 which causes decrease plt activation and vasodilation. COX2>1 inhibition. Less affected by COX-1 (high cox turnover)inhibition than Thromboxane A2.
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| COX-1 Inhibitors | Stops Thomboxane A2, PGE2, and prostaglandin synthesis
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| COX-2 inhibitors | stops PGI2 and prostaglandin synthesis.
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| PGI2 | Arachadonic Acid from endothelial cells is turned into PGI2 which causes decrease plt activation and vasodilation. COX2>1 inhibition. Less affected by COX-1 (high cox turnover)inhibition than Thromboxane A2.
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| COX-1 Inhibitors | Stops Thomboxane A2, PGE2, and prostaglandin synthesis
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| COX-2 inhibitors | stops PGI2 and prostaglandin synthesis.
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| Types of Hemoglobin | HbA(alph2, beta2) 96%; HbA2(alpha2. delta2) 3%; HbF: (alpha2, gamma2) fetal; HbS (SS) (alpha2, beta2mutation)
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| RBC count | 4(women)-5(men)10x6/ul;
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| Hemoglobin | 12-16 gm/dl, 14-17 gm/dl, women-men
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| Hematocrit | (Hgx3)=;37%-47%, 40%-54%, women-men
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| Mean corpuscular Volume | 87-103 ul
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| Mean corpuscular hemoglobin | 26-24 pg/cell or .40-.53 fmol/cell
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| Mean corpuscular hemoglobin concentration | 31-37 g/dl should be 1/3 of the cell
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| reticulocyte | .5-2.5%, .5-1.5%, women-men
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| Decrese in quality of RBC's | Hct: <37%, 40%; Hg: <12 gm/dl, <13.5 gm/dl
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| Iron metabolism | Stored in liver and Macrophages as ferritin(indicator of total body iron); heme iron absorption 10%, non-heme iron 1%; average daily absorption 1mg/day and daily loss equal each other.
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| Ferritin lab value | 20-400 ng/ml
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| Iron Deficiency - general | Microcytic-hypochromic anemia; causes: chronic bleeding 2-4ml/day, medications(aspirin), dietary causes, pregnancy. clinical findings when hg is 7-8 gm/dl.
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| Iron deficiency - Manifestations | Classic manifestations: pale, weakness, SOB, fatigue, brittle nails, paraesthesia, sore tongue, decrease appetite, weight loss, increase HR, decrease BP, Pica, cheilosis(more with B deficiency).
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| Iron deficeincy - diagnosis | total iron: decreased; Ferritin(can be normal if inflammatory disease): decresed; TIBC: increased(liver compensation); % sat: decreased; MCV: decreased; MCHC: decreased
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| Iron Deficeincy - management | oral iron: ferrous sulfate 325 mg TID = 150mg/day pure Fe(up to 10mg absorbed)4-6wks 1/2 normal, 2 mo. normal, continue 3-6 mo to replenish; Parenteral iron: only if intol. to GI absorb.can cause anaphylaxis, IM= stain; Packed RBC best 1ml=1mg Fe
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| Anemia of Chronic Disease - general | Microcytic-hypochromic anemia; causes: CHF, cancer, IBD, liver disease; RBC survival reduced; BM fails to compensate; iron metabolism fails
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| Anemia of Chronic Disease - manifestations | manifestations relating to causative condition; classic manifestations: pale, weakness, SOB, fatigue, brittle nails, paraesthesia, sore tongue, decrease appetite, weight loss, increase HR, decrease BP, Pica, cheilosis(more with B deficiency).
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| Anemia of Chronic Disease - Diagnosis | Hct, hg, MCV, MCHC: decreased; reticulocytes; serum iron: low; TIBC: low(liver is not as active); Ferratin: increased or normal; % sat: decreased
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| Anemia of Chronic Disease - Management | nothing; treat chronic disease; EPO 30,000units/wk
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| Alpha Thalassemias - General | Microcytic-hypochromic anemia; gene deletion (reduced alpha chain syn.); hereditary; asian and chinese descent
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| Alpha Thalassemias - manifestations | 3 genes normal: heme normal, carrier; 2 genes normal: alpha trait(form of minor); 1 gene normal: Hg H disease; chronic hemolytic anemia(variable severity) pallor, splenomegaly; 0 genes normal:still born, hydrop fetalis
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| Alpha Thalassemias(trait or minor) - Diagnosis | Trait or minor(mild anemia): hct:28-40%, MCV:60-75; MCHC: dec.; RBC: normal, inc.; Target cells:yes; Electropharesis: normal
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| Alpha Thalassemias(Hg H disease) - Diagnosis | hct:22-32%, MCV:60-70; MCHC: dec.; Target cells:yes; Electropharesis: abn
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| Beta Thalassemia - general | Microcytic-hypochromic anemia; point mutations-premature chain termination resulting in reduced or absent beta-globin chain synthesis; Mediterranean; hetero: minor; homo: major; severe anemia develops at 6 months requiring transfusions(fetal hg)
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| Beta Thalassemia minor - manifestations | modest anemia
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| Beta Thalassemia Major - manifestations | severe anemia
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| Beta Thalassemia minor - Diagnosis | MCHC, MCV: decreased, target cells, basophilic stippling, reticulocyte: normal or increased
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| Beta Thalassemia major - Diagnosis | sever poikilocytosis, MCV, MCHC: decreased, target cells, basophilic stippling
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| Beta Thalassemia minor - management | no treatment
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| Beta Thalassemia major - management | regular transfusion schedule(hemaochromatosis if to much iron); folate; splenectomy; iron chelation(deferipone; Bm transplant
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| Alpha Thalassemia (trait) - management | no treatment
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| Alpha Thalassemia (Hg H disease) - management | folate; avoid iron
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| Sideroblastic Anemia - general | Microcytic-hypochromic Anemia; hereditary/hetero/acquire; hemoglobin syn. disorders; fails to incorporate heme into protoporphyrin; iron accumulates
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| Sideroblastic Anemia - manifestations | Classic anemia manifestations: pale, weakness, SOB, fatigue, brittle nails, paraesthesia, sore tongue, decrease appetite, weight loss, increase HR, decrease BP, Pica, cheilosis(more with B deficiency).
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| Sideroblastic Anemia - diagnosis | Ringed sideroblasts(nucleated RBC with iron in cytoplasm) and inc. iron in BM; MCV: variable; MCHC: dec.; iron: inc.; % sat. inc.; can be caused due to decrease in B6(malnourished).
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| Vitamin B12 Deficiency - general | Macrocytic-normochromic anemia; B12(colbalamin) is a cofactor for homosycteine->methionine, methylmolanic acid->succybyl CoA; in animal protein; transported by Transcobalamin(1,2,3); causes: lack of intrinsic, dietary, iatrogenic(surgery), age(atrophy)
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| Vitamin B12 Deficiency - manifestations | Slow onset(liver storage:2000-5000mcg, lose 3-5 mcg/day); hg 7-8gm/dl=classical signs; neurological: methylmelonic build-up; lat. adn post columns of SC demyelination(proprio, vibe, fine, integrate) irreversible;
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| Vitamin B12 Deficiency - diagnosis | Hg, Hct: dec.; MCV: inc.; MCHC: ok; aniso-poikilo-cytosis; hypersegmented neutrophil(mean lobe: >4); reticulocyte: dec.; BM: blasts(may affect all cells); Vit B12(transcobalamin 2): dec.; Methylmalonic: inc.; schilling: radio active B12 urine test;
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| Vitamin B12 Deficiency - treatment | 1000mg q day x 7days, then weekly then monthly
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| Folic acid deficiency - general | folic acid is important to DNA syn.; causes: dietary; body store 5000mcg; 50-100 mcg/day;
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| Folic acid deficiency - manifestations | similar to classic manifestations; No neurological like B12
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| Folic acid deficiency - diagnosis | HG, Hct: dec.; MCV: inc.; nomral; MCHC: ok; aniso-poikilo-cytosis; macro-ovalocyte;hypersegmented neutrophil(mean lobe: >4); folate: dec.; B12: ok
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| Folic acid deficiency - treatment | folic acid
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| Aplastic Anemia - general | Normocytic/normochromic anemia; bone marrow hypoplasia; erythrocyte stem cells: underdeveloped, defective, absent; causes: radiation; medication; autoimmune; Fanconi: genetic aplastaic with early onset; idiopathic: 80% are >50yo
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| Aplastic Anemia - manifestations | Classic as RBCs get low; deficiency of all cells(plts and WBCs)
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| Aplastic Anemia - diagnosis | pancytopenia; MCV, MCHC: ok; BM: hypocellular
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| Aplastic Anemia - treatment | whole blood transfusions; severe: BM transplant
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| Sickle cell Anemia - general | Normocytic/normochromic anemia; autosomal recessive; point mutation(T->A): Glutamine to valine; 8% of African americans have 1 gene;
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| Sickle cell pathophysiology | In low po2, acidic environments RBCs with high levels of Hbs(HBa and HBf are inhibitory)go into the deoxy, sickle form, this causes permanent membrane damage; The more damage the stickier they get and the less likelihood of returning to the normal shape
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| Sickle cell anemia - manisfestations | Chronic hemolytic anemia, jaunidce, pigmented gallstones, slpenomegally(child); infartion:kidney, heart, liver, lungs, GI, spleen; classic signs
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| Sickle cell anemia - diagnosis | Hct: 20-30%; sickled: 5-50%; reticulcytes:10-25%; WBCs: inc.; hyposplenism; Bilirubin: inc.; electrophoresis: abn
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| Sickle cell anemia - treatment | Avoid dec. po2, dehydration; pain control, Hydroxyurea: 500-750 mg/day (stimulates fetal hemoglobin)
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| Herditary spherocytosis - general | autosomal dominant-variable severity(defective spectrin); disorder of red cell membrane; chronic hemolytic anemia(spleen); decrease surface to volume ratio(no biconcave shape)
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| Herditary spherocytosis - manifestations | Classic signs
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| Herditary spherocytosis - diagnosis | Hct, Hg, MCV: decreased; MCHC: increased(onlt anemia with microcytosis and hyperchromia); reticulocytes; spherocytes; bilirubin
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| Herditary spherocytosis - treatment | no cure, folic acid; splenecotomy
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| Glucose-6-phophate Dehyrdrogenase Deficiency | x-linked recessive; 10-15% African American males; G6PD is important in GSH synthesis which protects Hg from oxidative denaturation(Heinz bodies); aspirin, sulfas, and nitrates bind G6PD; reticulocytes and bilirubin inc.(hemolysis); avoid triggers
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