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Normal Platelet count 400,00-150,00/microliter
Thrombocytopenia <100,000/microliter
Pseudothrombocytopenia false low cause by EDTA, cold, or hard venipuncture.
Bleeding time Plt f(x)', nl 7.5-25 minutes, elevated in thrombocytopenia too. NOT in Factor deficiencies!!!
Aggregation studies Indicated for normal plt count, elevated bleeding time; aggregation: epi, adp, collagen; Adhesion: ristocetin
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.
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)
Congenital Amegakaryocytic Autosomal recessive; Plt GF receptor mutation. Megakaryocytes die without GF. Tx is BM transplant
Diseases that decrease the production of Plts Rubella, HIV
Drugs that suppress Plt productions Thiazide diuretics, Diethylstillberstrol, ethanol, and tolbutamide
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
Plt aggregation thrombocytopenia(drugs) Protamine, Heparin(early)
ITP - General Autoimmune; ab to 2,3, ba or 1b; Spleen destruction, virally self-limiting in child; chronic and non resolving in adults(spontaneous);
ITP - Manifestations Manifest: petechiae, bruises, epistaxis, gums, GI bleed and hematuria(less common), IC hemmorrhage(rare).
ITP - Diagnosis CBC: thrombocytopenia, all others nl; large plts, possible anemia(blood loss), Evan's Syndrome: autoimmune hemolutic anemia w/ reticulocytes and spheocytes.
ITP - management Predinsone 1-2mg/kg/24hrs; splenectomy, Ig 1g/kg; refractory: danazol, chemo
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
TTP - Manifestations Anemia: fatigue, pale, SOB on excertion; Bleeding: petechiae, purpura, pallor; Neurolgoical symptoms: headache.
TTP - Diagnosis CBC: anemia, reticulocytes, schistocytes, thrombocytopenia; inc. bilirubin(hemolysis); LDH elevated but less than expected(hemolysis); coag test normal.
TTP - management plasmapharesis, FFP, predisone,
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
HUS - Manifestation anemia; bleeding, renal failure; rare neurologic manifestations
HUS - Diagnosis Hemolytic anemia, thrombosytopenia(less severe TTP); LDH elevated; coombs test: -; coag: norm.
HUS - syndrome Children: self-limiting; pallative; Adult: plasmapharesis, FFP.
Plt destruction non immune mediated Preggers pre-eclampisa: low plt, htn, edmea, proteinuira; Hemolysis elevated liver enzyme and low plts
Causes of Hypersplenism(thrombocytopenia) Tumor, anemia, malaria, tb, portal hypertension, leukemias/omas
Bernard-Soulier Syndrome - general autosomal recessive - deficient 1b
Bernard-Soulier Syndrome - manifestations Sever bleeding
Bernard-Soulier Syndrome - Diagnosis thrombocytopenia; large plts, bleeding time prolonged; ristoceiten: abn; adp: ok;
Bernard-Soulier Syndrome - management Plt transfusions(no cure)
Glandzman Thrombasthenia - General autosomal recessive, deficient 2b3a,
Glandzman Thrombasthenia - manifestations mucosal and surgical bleeding(not as severe as BSS)
Glandzman Thrombasthenia - diagnosis bleeding time: abn; ritoceiten: ok; adp: abn
Glandzman Thrombasthenia - managment plt transfusion(no cure)
Vonwillebrand disease - general autosomal dominant; defective vWF most common bleeding disorder
Vonwillebrand disease - manisfestations spontaneous bleeding; menorrhagia
Vonwillebrand disease - diagnosis Low vWF; Plt count: ok; bleeding time: ok; plt aggr: normal; abnormal aPTT(<25%); decrease Factor 8
Vonwillebrand disease - treatment DDAVP(vasopressin stim endo to dump out vWF for: Type 1,3); FFP, cryoprecipitate.
Vonwillebrand disease - type 1 most common; decrease in vWF
Vonwillebrand disease - type 2a qualitative abnormality in protein that prevents multimer formation
Vonwillebrand disease - type 2b qualitative abnormality in protein causing rapid clearance of large multimeric forms
Vonwillebrand disease - type 3 autosomal recessive disorder in which vWF is nearly absent
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
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
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
PT Extrinsic pathway of coagualtion; sensitive to fibrinogen, prothrombin, F5, F7, and F10. Tissue factor added to whole plasma; INR=pt/control; normal=1.
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)
Hemophilia A - manifestations easy bruising/bleeding/spont, hemarthroses
Hemophilia A - Diagnosis Bleeding time: ok, PTT: prolonged; PT: normal; F8: low
Hemophilia A - treatment F8 concentrates (recombinant)
Hemophilia B - general x-linked; F9 deficient(christmas factor); 1/3 quality, 2/3 quanity.
Hemophilia b - manifestations easy bruising/bleeding/spontaneous; hemarthroses
Hemophilia B - Diagnosis bleeding time: ok; ptt:prolonged; pt:ok; low F9
Hemophilia B - Treatment F9 concentrations
Hemophilia C - general Autosomal recessive; ashkenazi jews, F11 deficient
Hemophilia C - diagnosis bleeding time: ok; PTT: prolonged; pt: ok; F11: low
Hemophilia C - manifestations mild bleeding: post op
Hemophilia C - Treatment FFP as needed
Afribrinogenemia rare, variable, in presentation, replace with FFP
F12 deficiency prolonged ptt; not associated with increased bleeding
Bleeding caused Liver disease vitamin K defendant factors are reduced; increase fibrinolysis; Alpha2-antiplasmin is not longer made(inhibits plasmin); give FFP
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.
DIC - general consumption of coagulation proteins that causes excessive bleeding caused by sepsis, tissue injury, OB complication, cancer. 50-60% die
DIC - Manifestations Consumption of coag factors and activation of D-Dimer(Accelerates plasminogen->plasmin; bleeding; micro thrombosis
DIC - Diagnosis Hypofibrinogenemia; elevated fibrin degradative products(D-Dimer); thrombocytopenia; PT and PTT:prolonged
DIC - management Prevention(ab); heparin(stops the consumption of clotting factors).
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
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.
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.
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).
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.
Protein S deficiency Protein S acts as a cofactor for C. clotting is uncontrolled in this congenital disease.
Coumadin Disrupts vitamin K utilization; Vitamin K dependant Factors: 2,7(most effected),9, 10; oral admin; slow onset; Monitor w/ PT
Heparin Blocks thrombin, F10a, F9a, and F11a synergystically with antithromben III; IV or subq admin; fast onset; high variability except LMW; monitor with PTT
Thrombomodulin When thrombin is activated it binds to thrombomodulin and activates protein C+S to stop clotting; released by endothelium.
Petechiae <.5cm; usually from thrombocytopenia; not a functional problem.
Purpura >=5cm; superficial dermatological bleeding; can be problem with plts, or vascular abn;
Ecchymosis Subq bleeding
Hemorrhage blood loss from vascular
Integrin Blocks 2b3a, Iv admin
TPA catalyst for Plasminogen to plasmin; released by endothelial
Thromboxane A2 Arachadonic Acid from plts is turned into thromboxane A2 which causes plt aggregation and vasoconstriction. COX1>2 inhibition.
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.
COX-1 Inhibitors Stops Thomboxane A2, PGE2, and prostaglandin synthesis
COX-2 inhibitors stops PGI2 and prostaglandin synthesis.
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.
COX-1 Inhibitors Stops Thomboxane A2, PGE2, and prostaglandin synthesis
COX-2 inhibitors stops PGI2 and prostaglandin synthesis.
Types of Hemoglobin HbA(alph2, beta2) 96%; HbA2(alpha2. delta2) 3%; HbF: (alpha2, gamma2) fetal; HbS (SS) (alpha2, beta2mutation)
RBC count 4(women)-5(men)10x6/ul;
Hemoglobin 12-16 gm/dl, 14-17 gm/dl, women-men
Hematocrit (Hgx3)=;37%-47%, 40%-54%, women-men
Mean corpuscular Volume 87-103 ul
Mean corpuscular hemoglobin 26-24 pg/cell or .40-.53 fmol/cell
Mean corpuscular hemoglobin concentration 31-37 g/dl should be 1/3 of the cell
reticulocyte .5-2.5%, .5-1.5%, women-men
Decrese in quality of RBC's Hct: <37%, 40%; Hg: <12 gm/dl, <13.5 gm/dl
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.
Ferritin lab value 20-400 ng/ml
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.
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).
Iron deficeincy - diagnosis total iron: decreased; Ferritin(can be normal if inflammatory disease): decresed; TIBC: increased(liver compensation); % sat: decreased; MCV: decreased; MCHC: decreased
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
Anemia of Chronic Disease - general Microcytic-hypochromic anemia; causes: CHF, cancer, IBD, liver disease; RBC survival reduced; BM fails to compensate; iron metabolism fails
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).
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
Anemia of Chronic Disease - Management nothing; treat chronic disease; EPO 30,000units/wk
Alpha Thalassemias - General Microcytic-hypochromic anemia; gene deletion (reduced alpha chain syn.); hereditary; asian and chinese descent
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
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
Alpha Thalassemias(Hg H disease) - Diagnosis hct:22-32%, MCV:60-70; MCHC: dec.; Target cells:yes; Electropharesis: abn
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)
Beta Thalassemia minor - manifestations modest anemia
Beta Thalassemia Major - manifestations severe anemia
Beta Thalassemia minor - Diagnosis MCHC, MCV: decreased, target cells, basophilic stippling, reticulocyte: normal or increased
Beta Thalassemia major - Diagnosis sever poikilocytosis, MCV, MCHC: decreased, target cells, basophilic stippling
Beta Thalassemia minor - management no treatment
Beta Thalassemia major - management regular transfusion schedule(hemaochromatosis if to much iron); folate; splenectomy; iron chelation(deferipone; Bm transplant
Alpha Thalassemia (trait) - management no treatment
Alpha Thalassemia (Hg H disease) - management folate; avoid iron
Sideroblastic Anemia - general Microcytic-hypochromic Anemia; hereditary/hetero/acquire; hemoglobin syn. disorders; fails to incorporate heme into protoporphyrin; iron accumulates
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).
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).
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)
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;
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;
Vitamin B12 Deficiency - treatment 1000mg q day x 7days, then weekly then monthly
Folic acid deficiency - general folic acid is important to DNA syn.; causes: dietary; body store 5000mcg; 50-100 mcg/day;
Folic acid deficiency - manifestations similar to classic manifestations; No neurological like B12
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
Folic acid deficiency - treatment folic acid
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
Aplastic Anemia - manifestations Classic as RBCs get low; deficiency of all cells(plts and WBCs)
Aplastic Anemia - diagnosis pancytopenia; MCV, MCHC: ok; BM: hypocellular
Aplastic Anemia - treatment whole blood transfusions; severe: BM transplant
Sickle cell Anemia - general Normocytic/normochromic anemia; autosomal recessive; point mutation(T->A): Glutamine to valine; 8% of African americans have 1 gene;
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
Sickle cell anemia - manisfestations Chronic hemolytic anemia, jaunidce, pigmented gallstones, slpenomegally(child); infartion:kidney, heart, liver, lungs, GI, spleen; classic signs
Sickle cell anemia - diagnosis Hct: 20-30%; sickled: 5-50%; reticulcytes:10-25%; WBCs: inc.; hyposplenism; Bilirubin: inc.; electrophoresis: abn
Sickle cell anemia - treatment Avoid dec. po2, dehydration; pain control, Hydroxyurea: 500-750 mg/day (stimulates fetal hemoglobin)
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)
Herditary spherocytosis - manifestations Classic signs
Herditary spherocytosis - diagnosis Hct, Hg, MCV: decreased; MCHC: increased(onlt anemia with microcytosis and hyperchromia); reticulocytes; spherocytes; bilirubin
Herditary spherocytosis - treatment no cure, folic acid; splenecotomy
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
Created by: bmg4