Input: Mean corpuscular hemoglobin average mass of hemoglobin per RBC Mean corpuscular hemoglobin concentration concentration of hemoglobin in a give volume of pack RBCs These define chromicity [Name the erythropoesis steps]

Output: MCH MCHC


Input: Red cell distribution width SD of red cell size/MCV indicates the variation in size of RBCs Normal is 11.5-14.5 Low is never bad [Name the erythropoesis steps]

Output: RDW


Input: Increased RDW [Name the erythropoesis steps]

Output: Anisocytosis


Input: Immature RBCs, about 1% of circulation normally Still have ribosomes [Name the erythropoesis steps]

Output: Reticulocyte


Input: With worsening anemia, reticulocytes are extruded from bone marrow earlier RPI - reticulocyte production index Greater than 2 is a adequate response to an anemia [Name the erythropoesis steps]

Output: Anemia affect on reticulocytes Measured by?


Input: Pale, jaundice, cold skin Fatigue, SOB, syncope Low BP, rapid HR, breathing, heart murmur [Name the erythropoesis steps]

Output: Anemia sings and symptoms


Input: transferrin -- protein that binds Fe in blood transferrin iron binding capacity transferrin saturation Fe/TIBC normal -- 20-50% [Name the erythropoesis steps]

Output: Transferrin TIBC TS


Input: Protein that stores many atoms of Fe [Name the erythropoesis steps]

Output: Ferritin


Input: Decreased oral intake Decreased absorption gastritis, bypass, bacterial overgrowth, celiac, antacids, tea, spinach Increased loss (bleeding) [Name the erythropoesis steps]

Output: Iron deficiency anemia causes


Input: Exogenous EPO depletion of stores Hemolytic anemia leading to iron loss into urine [Name the erythropoesis steps]

Output: Weird causes of iron deficiency anemia


Input: Eating weird stuff Symptom of iron deficiency pagophagia--ice amylophagia - starch geophagia--dirt [Name the erythropoesis steps]

Output: Pica


Input: Iron deficiency anemia Dyspagia Esophageal webbing Atrophic glossitis Angular cheilosis Koilonychia (spoon nails) [Name the erythropoesis steps]

Output: Plummer-Vinson syndrome


Input: Microcytic Hypochromic Anisocytosis RPI <2, Fe, TS, Ferritin all down, TIBC up [Name the erythropoesis steps]

Output: Iron deficiency anemia smear and labs


Input: Microcytic anemia Basophilic stipling creating a ring Hypochromic Dimorphic populations [Name the erythropoesis steps]

Output: Sideroblastic anemia smear


Input: Congenital ALA deficiency Pyridoxine/copper deficiency Lead, ETOH, chloremphenicol, isoniozid RA, myeloma, myelo/lymphoproliferative diseases [Name the erythropoesis steps]

Output: Sideroblastic anemia causes


Input: Remove toxins Treat with pyridoxine Transfusions [Name the erythropoesis steps]

Output: Treating sideroblastic anemia


Input: Sideroblastic anemia of any MCV Disrupts both heme and globin synthesis Increased iron and sideroblasts in marrow [Name the erythropoesis steps]

Output: Lead poisoning blood stuff


Input: Anemia Lead line in gums Motor neuropathy -- lead palsy Autonomic neuropathy -- ileus/abdominal pain - lead colic [Name the erythropoesis steps]

Output: Lead poisoning symptoms


Input: Quantitative disorder of globin synthesis Not enough is made (Hemoglobinopathies are qualitative) [Name the erythropoesis steps]

Output: Thalessemias


Input: Minor: one mutation in beta globin gene microcytic anemia, usually normal longetivity Major: two mutations, marked hemolysis, extramedullary hematopoesis (facial bones, hepatospenomegaly, cardiac failure) [Name the erythropoesis steps]

Output: Beta thalassemia


Input: Splenectomy Transfusions Chelation Bone marrow transplant [Name the erythropoesis steps]

Output: Thalessemias treatment


Input: Iron deficiency Sideroblastic (lead poisoning) Thalassemias, hemoglobinopathies 1/3 anemia of chronic disease [Name the erythropoesis steps]

Output: Microcytic anemias


Input: Low reticulocyte -- hyproliferative with decreased production High reticulocyte -- destruction of blood cells (reticulocyte) [Name the erythropoesis steps]

Output: Major categories of normocytic anemias


Input: Hypoplastic states 2/3 of the anemias of chronic disease aplastic anemia others (renal, endocrine disease) [Name the erythropoesis steps]

Output: Normocytic anemias with a low reticulocyte


Input: Hemolytic states Autoimmune Drug-induced Mebraneopathies (hereditary spherocytosis, PNH) Enzymopathies Hemoglobinopathies Microangiopathic hemolytic anemias [Name the erythropoesis steps]

Output: Normocytic anemias with a high riticulocyte count


Input: Normo/microcytic Normochronmic Associated with diseases w/ inflammation, infection, malignancy [Name the erythropoesis steps]

Output: Anemia of Chronic Disease


Input: Acute phase protein -- produced during inflammation Decreased iron absorption in intestine Decreased iron release from macrophages Direct inhibition of erothropoesis [Name the erythropoesis steps]

Output: Hepcidin


Input: Low iron Low TIBC High ferritin [Name the erythropoesis steps]

Output: Iron studies in anemia of chronic disease


Input: Treat underlying disease [Name the erythropoesis steps]

Output: Treatment of anemia of chronic disease


Input: Absent hematopoetic precursors in bone marrow Pancyotopenia including normocytic anemia Most dangerous are leukopenia and thrombocytopenia [Name the erythropoesis steps]

Output: Aplastic anemia


Input: Primary - idiopathic, Fanconi's Secondary -- radiation, chemotherapy (alkylators), chloremphenicol, antiepileptics, nifedipine, benzene, parvovirus, EBV, hepatitis (non-A, non-B, non-C) [Name the erythropoesis steps]

Output: Causes of aplastic anemia


Input: Remove cause (stop radiation, meds) Transfusions Anti-thymocyte or antilymphocyte globulin Cylcosporin, cyclophosphamide Stem cell transplant [Name the erythropoesis steps]

Output: Aplastic anemia treatment


Input: Hypoplastic, normocytic anemia with low reticulocyte count Caused by underproduction of erythropoetin [Name the erythropoesis steps]

Output: Renal disease mechanism of causing anemia


Input: Hypothryoidism Panhypopituitarism Low testosterone [Name the erythropoesis steps]

Output: Endocrine causes of anemia


Input: Metaplasia of the bone marrow--replacement with fibroblasts Smear: teardrops, nucleated red cells, early white cells Usually with large spleen (extramedullary hematopoesis) Not possible to get aspirate from bone marrow, need to core [Name the erythropoesis steps]

Output: Primary myelofibrosis


Input: Infiltration of the bone marrow by fibrosis, tumor, granuloma Smear: teardrops, nucleated red cells, early white cells Look for a cancer [Name the erythropoesis steps]

Output: Myelophthistic anemia


Input: Binds to heme in vasculature Preventing iron use by bacteria Heme-haptoglobin is taken up and disposed of by macrophages Used to monitor levels of intravascular hemolysis [Name the erythropoesis steps]

Output: Haptoglobin


Input: Transfusion reactions G6P deficiency w/ oxidative stress Paroxysmal nocturnal hemolysis Infection (clostridial sepsis, severe malaria) Microangiopathy (aortic stenosis, artifical valve leak) [Name the erythropoesis steps]

Output: Causes of intravascular hemolysis


Input: Fragment of a red blood cell [Name the erythropoesis steps]

Output: Shistocyte


Input: Signs-- Pallor, fatigue, tachycardia Jaundice Blood tinged urine, plasma Labs-- Decreased haptoglobin, increased LDH Decreased RBC, hemoglobin, hct Increased bilirubin Increased reticuloucyte count [Name the erythropoesis steps]

Output: Intravascular hemolysis Clinical signs Labs


Input: Membrane defects Defective hemoglobin Enzyme deficiencies [Name the erythropoesis steps]

Output: Extravascular hemolysis Intrinsic causes


Input: Liver disease Hypersplenism Inflections (malaria) Oxidant agents (nitrites, dapsone) Autoimmune hemolytic anemia Intravenous immune globulin infusion [Name the erythropoesis steps]

Output: Extravascular hemolysis extrinsic causes


Input: Signs- Pallor, tachycardia, fatigue, jaundice Labs- decreased RBC, hemoglobin, HCT increased bilirubin increased reticulocyte count [Name the erythropoesis steps]

Output: Extravascular hemolysis Clinical Signs Labs


Input: Haptoglobin will be decreased in intravascular Hemoglobinuria or hemoglobinemia in intravascular only [Name the erythropoesis steps]

Output: Differentiating between extravascular and intrasvascular hemolysis


Input: Antibodies to RBC antigens can be auto or cross reactive Distinguished from others by Coombs test [Name the erythropoesis steps]

Output: Autoimmune hemolytic anemias


Input: Direct -- anti Ig antibodies are added to a tube of whole blood -- agglutination reveals that there were antibodies stuck to the RBC Indirect -- Donor RBCs are added to patient serum, then anit Ig Abs are added, agglutination means that there were anti-RBCs-Abs in serum [Name the erythropoesis steps]

Output: Coombs test


Input: Idiopathic SLE, RA, sjorgen's CLL, lymphomas Drug induced (methyldopa) [Name the erythropoesis steps]

Output: Warm type autoimmune hemolytic anemias


Input: Drug induced Transfusion reactions [Name the erythropoesis steps]

Output: Warm type alloimmune hemolytic anemias


Input: Idiopathic Infections (mycoplasma pneumonia, mononuclesosis) Lymphomas Paroxysmal noctural hematuria [Name the erythropoesis steps]

Output: Cold type autoimmune hemolytic anemias


Input: Antibodies coat RBC Splenic macrophages Fc receptors bind antibody Fragment red cell Producing spherocyte [Name the erythropoesis steps]

Output: Spherocyte formation


Input: Underlying condition Splenectomy Steroids Immunosuppresion Anti-CD20 (rituximab) Folic acid [Name the erythropoesis steps]

Output: Treating autoimmune hemolytic anemias


Input: Genetic disorder, usually autosomal dominant Spectrin deficiencies result in less membrane stability Splenic macrophages chomp of bits of cells Anemia with high MCHC, extravascular hemolytic anemia Splenectomy [Name the erythropoesis steps]

Output: Hereditary spherocytosis Cause Labs Treatment


Input: High mean corpuscular hemoglobin volume Hereditary spherocytosis or acquired hemolytic anemias [Name the erythropoesis steps]

Output: Increased MCHC


Input: Paroxysmal Nocturnal Hemoglobinuria Acquired mutation in a hematopoetic stem cell making blood cells glycophosphatidylinositol deficient and complement vulnerable Acidity increases liklihood complement mediated intravascular hemolysis - this happens at night [Name the erythropoesis steps]

Output: PNH Cause and pathophys


Input: Wake up with blood tinged urine Anemia Thrombosis Smooth muscle dystonia Decreased quality of life Can have problems with other lines [Name the erythropoesis steps]

Output: PNH Symptoms


Input: Transfusion Fe and folate supplements Eculizmab (anti-complement antibody) Stem cell transplant [Name the erythropoesis steps]

Output: PNH treatment


Input: Deficiency of glucose-6-phosphate dehydrogenase X-linked (affected males or female mosaics w/ mutation in RBCs) Extravascular hemolysis either after stress or all the time Hemoglobin oxidize to methHbg--sulfHbg--Heinz bodies [Name the erythropoesis steps]

Output: GP6D deficiency


Input: Infections Ketoacidosis Fava beans Drugs sulfonamides quinine and quinidine primaquine, cholorquine acetylsalicilic acid vitamin K chloremphenicol [Name the erythropoesis steps]

Output: GP6D oxidative stress triggers


Input: Heinz bodies cannot make it through the splenic sinus space and that part of the cell gets chopped off [Name the erythropoesis steps]

Output: Bite cells with Heinz bodies


Input: G6PD 400 million [Name the erythropoesis steps]

Output: Most common enzyme deficiency in the world?


Input: Autosomal recessive 2nd most common enzyme deficiency Rigid cells are sequestered by spleen and hemolyzed [Name the erythropoesis steps]

Output: Pyruvate kinase deficiency


Input: Hapten Innocent bystander - drug combines with plasma protein and sticks to RBCs becoming an antigen (quinidine) Anitgenic - drug induces Ab production that cross reacts with a platlet [Name the erythropoesis steps]

Output: Drug induced hemolytic anemias 3 kinds


Input: Opathies -- qualitative disorders, hemoglobin does not function appropriately Thalaseemias -- quantitative disorders, not enough hemoglobin [Name the erythropoesis steps]

Output: difference between thalassemias and hemoglobinopathies


Input: Valine for glutmine in Beta globin chain S hemoglobin is more likely to aggregate, creating structural problems in RBCs [Name the erythropoesis steps]

Output: Sickle cell anemia mutation


Input: Sickle cells lives only 10-20 days Some destroyed intravascularly, most in spleen [Name the erythropoesis steps]

Output: Sickle cell anemia RBC destruction


Input: Anemia Aplastic episodes (parvovirus) Delayed growth Pigment gallstones Vasooculusion -Avascular hip necrosis, priapism, pain, acute chest, stroke Leg uclers etc [Name the erythropoesis steps]

Output: Sickle cell clinical manifestation


Input: Infection Dehydration Oxygen deprivation (altitude, operations, OB delivery) Cold Heavy exercise [Name the erythropoesis steps]

Output: Precipitating factors of sickle cell crisis


Input: 2 million Americas 1 in 5000 African Americans Homozygous - 0.3-1.3% African Americans Heterozygous - 8% of African Americans [Name the erythropoesis steps]

Output: Prevalence of sickle cell anemia


Input: Heterozygotes - typically wildtype, sometimes small renal infarcts can lead to hematuria Homozygotes - variable, from infant crises to almost normal [Name the erythropoesis steps]

Output: Sickle cell disease penetrance


Input: Hemoglobin electrophoresis Trait -- some S and some A Disease -- just S and no A [Name the erythropoesis steps]

Output: Sickle cell diagnosis


Input: Prophylaxis with hydration, oxygenation, warmth, vaccines Crisis -- oxygen, hydration, analgesiacs Hydroxyurea- increase hemoglobin Stem cell transplant [Name the erythropoesis steps]

Output: Sickle treatment


Input: Increased MCV Increasd reticulocyte production DNA synthesis abnormalities Others [Name the erythropoesis steps]

Output: Macrocytic anemias


Input: Anemias where problem is DNA synthesis, end up with mature cytoplasm, immature nuceli Macrocytic anemia B12 deficiency, folate deficiency, drug induced, some hereditary [Name the erythropoesis steps]

Output: Megaloblastic anemias


Input: EPO Hydroxurea, methotrexate, 5FU, capecitabine Azt Phenytoin, valproic acid omezoprole, rantindin trimethoprim-sulfamethoxazole [Name the erythropoesis steps]

Output: Drugs causing megaloblastic, macrocytic anemias


Input: Colbalomine Cannot be produced by body Animal products (meat, milk, eggs) only dietary source Needs intrinsic factor to be absorbed [Name the erythropoesis steps]

Output: B12


Input: Decreased oral intake (vegans, alcohol) Decreased absorption deficiency in intrinsic factor pancreatic insufficiency gastrectomy, ileal resection gastritis crohn's disease neomycin, metformin, proton pump inhibitors [Name the erythropoesis steps]

Output: B12 deficiency


Input: Macrocytic anemias Ovalocytes Hypersegmented PMNs Demyelination of spinal cord loss of some sensations (deep touch, vibration, ataxia, reflex abnormalities) [Name the erythropoesis steps]

Output: B12 deficiency anemias


Input: Determining where B12 deficiency is coming from Have to first give an IM shot to avoid deprived tissues from sucking up all the B12 Then give radioactive B12 by mouth, with oral intrinsic factor, give antibiotics and try again (absorptive issue) Looking for B12 in urine [Name the erythropoesis steps]

Output: Schilling's Test


Input: leafy greens, beans, fortified grains Needed for thiamine synthesis and DNA replication/repair [Name the erythropoesis steps]

Output: Folate sources


Input: Macrocytic, megaloblastic anemia Ovalocytes Hypersegmented PMNs Same as B12 deficiency histologically but lacks the spinal cord part [Name the erythropoesis steps]

Output: Folate deficiency symptoms


Input: Treatment of b12 deficiency with folate will treat anemia but not spinal cord degeneration [Name the erythropoesis steps]

Output: Why not just give folate?


Input: Decreased oral intake (alcoholics, poor diet, overcooked foods) Decreased absorption (celiacs, bowel disease) Drugs (methotrexate, trimethoprim, phenytoin) Increase utilization (pregnancy, lactation, chronic hemolysis, exfoliative dermatitis) [Name the erythropoesis steps]

Output: Folate deficiency causes


Input: Reticulocytosis alone can cause increased MCV [Name the erythropoesis steps]

Output: Reticulocytes in macrocytic anemias


Input: MMA- increased with B12 deficiency and normal with folate Homocysteine - increased with both Can also test for serum folate level [Name the erythropoesis steps]

Output: Labs to differentiate between folate and B12 deficiency


Input: Malignant change in hemotopoetic stem cell Myeloid precursors in bone marrow are dysplasic Inadequate blood cell production Can become an actue leukemia (30-40%) Chromosomal changes important [Name the erythropoesis steps]

Output: Myelodysplastic disorders


Input: Hypocelluarlarity in periphery can be anemia, bicytopenia, pancytopenia Hypercellularlity in bone marrow [Name the erythropoesis steps]

Output: MDS counts


Input: Idiopathic Radiation Chemotherapy Benzene [Name the erythropoesis steps]

Output: Etiology of MDS


Input: Supportive-transfusions, growth factors, iron chelation (prevent transfusion toxicity) 5-Azacytadine Lenalidomide Chemo Stem Cell transplant [Name the erythropoesis steps]

Output: MDS treatment


Input: 90% of alcoholic have increased MCV Can be b12, folate deficient Liver disease results in lipids deposited into cell membrane Acetaldehyde may have direct effect on RBCs [Name the erythropoesis steps]

Output: Alcoholics and MCV


Input: Macrocytic Ovalocyte, hypersegmented PMNs Acanthocytes Target cells [Name the erythropoesis steps]

Output: Alcoholic blood smear


Input: Star like cells, out pouchings in membrane from fat deposition from failing liver [Name the erythropoesis steps]

Output: Acanthocytes


Input: Rements of DNA in circulating RBCs Splenectomy, sickle cell [Name the erythropoesis steps]

Output: Howell-Jolly bodies


Input: Hyposegement PMNs Seen in MDS [Name the erythropoesis steps]

Output: Pleger-Huet cells


Input: Too few white blood cells [Name the erythropoesis steps]

Output: Neutropenia define


Input: Too many white blood cells [Name the erythropoesis steps]

Output: Neutrophilia define


Input: Blast Promyelocyte Myelocyte This are dividing and differentiating [Name the erythropoesis steps]

Output: PMN precursors in the proliferation compartment of the bone marrow


Input: Metamyelocyte Band Neutrophil [Name the erythropoesis steps]

Output: PMN precursors in the differentiation compartment of the bone marrow


Input: 50% circulating and 50% marginated [Name the erythropoesis steps]

Output: Distribution of neutrophils in peripheral blood


Input: G-CSF Myeloid precursor proliferation Induction of myeloid maturation Protection from apoptosis Enhancement of PMN function [Name the erythropoesis steps]

Output: Growth factor most important in PMN development


Input: 8-12 days in bone marrow maturong 3-6 hours circulating 2-3 days in tissue [Name the erythropoesis steps]

Output: Lifespan of a PMN


Input: 20% Myeloid precursors 75% storage pools 3% marginating pool 2% circulating pool [Name the erythropoesis steps]

Output: WBC Distribution


Input: Acute - demargination Chronic -- changes in production and release from storage pools [Name the erythropoesis steps]

Output: Pathogenesis of increased white blood cell counts


Input: Defect in production Increased margination Increase sequestration [Name the erythropoesis steps]

Output: Pathogenesis of decreased white blood cell counts


Input: Neutrophils -- 35-65% Bands -- 1-5% Monos - 4-8% Eosin/basos - 1-2% Lymphocytes 20-50% [Name the erythropoesis steps]

Output: Normal differential


Input: T cells - 85% 2/3 CD4 1/3 CD8 B cells - 15% [Name the erythropoesis steps]

Output: Normal lymphocyte % distribution


Input: Absolute Neutrophil Count WBC X (% segs (PMNs) + % bands) [Name the erythropoesis steps]

Output: ANC


Input: 1500-6300 [Name the erythropoesis steps]

Output: Normal ANC


Input: Rises with decreasing number of neutrophils With ANC less than 1000, manage fever as outpatient ANC<500, admit and manage with IV antibiotics ANC <200 -- fungals and opportunistic a problem [Name the erythropoesis steps]

Output: Risk of infection with low neutrophils


Input: Most common is autoinfection Gram negatives -- can rapidly progress to sepsis Fungal/mucor -- related to the duration, not depth of neutropenia [Name the erythropoesis steps]

Output: Neutropenic infections sources/types


Input: Take low grade fever seriously There may be no symptoms [Name the erythropoesis steps]

Output: Symptoms of infection in neutropenia patient?


Input: Chemotherapy Infection Drugs, toxins Immune mediated Hypersplenism Idiopathic [Name the erythropoesis steps]

Output: Causes of acquired, extrinsic neutropenia


Input: Anything overwhelming typhoid, influenza, varicella, CMV, HIV, EBV, dengue, yellow fever, rubella Mechanism -- consumption, bone marrow suppression, egress, circulating antibodies [Name the erythropoesis steps]

Output: Infections causes neutropenia


Input: Antimicrobials - penicillin, cephs, vanco, bactrim Antihistamines - H2 blockers, cimetidine, rantidine Anticonvulsants Antipsychotics Procanimide Mechanism -- bone marrow suppression, maturation arrest, anti-neutrophil antibody production [Name the erythropoesis steps]

Output: Drugs that can induce neutropenia


Input: Tumor Sarcoidosis Tuberculosis [Name the erythropoesis steps]

Output: Neutropenia caused by bone marrow infiltration by


Input: B12. folate deficiency results in ineffective myelopoesis [Name the erythropoesis steps]

Output: Nutritional deficiency causing neutropenia


Input: Sequestration, immune, and infiltrative effects Cirrohsis with portal HTN Felty syndrome Gaucher's disease Chronic hemolysis (hereditary spherocytosis, malaria) [Name the erythropoesis steps]

Output: Hypersplenism Causes, mechanism of causing neutropenia


Input: Hypersplenism Leukopenia Rheumatoid arthritis [Name the erythropoesis steps]

Output: Felty syndrome


Input: Leukemia MDS Myeloproliferative disorders Aplastic anemia -- also extrinsic -- immune mediated [Name the erythropoesis steps]

Output: Neutropenia acquired, intrinsic causes


Input: Low ANC <1500, up 35% of those with incidentally discovered neutropenia More common in African Americans (5%) Much more common in Africans (50%) [Name the erythropoesis steps]

Output: Idiopathic or Chronic benign neutropenia


Input: Autosomal dominant (ELA2) 15-30 day cycles of neutropenia [Name the erythropoesis steps]

Output: Cyclic neutropenia


Input: > than 10^7 PMN/ml Causes: stress, infection, inflammation [Name the erythropoesis steps]

Output: Neutrophilia


Input: Smoking Obesity [Name the erythropoesis steps]

Output: Most common etiologies for neutrophilia in the community


Input: Moderate leukocytosis (15 - 20 x 10^9) Demargination of neutrophils Mature forms only Prednisone, epinephrine, excercise, seizures [Name the erythropoesis steps]

Output: Shift neutrophilia


Input: Severe leukocytosis >50 x 10^9 cell/L Demargination and increased production Mature and young forms in periphery Infection, inflammation, metastatic cancer, GCSF [Name the erythropoesis steps]

Output: Leukomoid reaction


Input: Early forms of white and red blood cells in periphery, nucleated RBCs, tear drops Seen with myelophthysic (marrow infiltration) and myelofibrosis [Name the erythropoesis steps]

Output: Leukoerythrobastic reaction


Input: Large increase in young forms -- acute Increase in all forms with shift toward young - chronic [Name the erythropoesis steps]

Output: Leukemia on differential


Input: AD (ELA2 and others) Multiple subtypes with static neutropenia [Name the erythropoesis steps]

Output: Sever congenital neutropenia


Input: AR Infantile agranulocytosis Presents with multiple severe infections [Name the erythropoesis steps]

Output: Kostmann congenital neutropenia


Input: AR (LYST gene) Neutropenia, giant lysosomes, oculocutaneous albinism, lymphoma like syndrome Failure in phagolysosome formation (lyso enzymes do not get to phagosome) Treated with chemo, steroids, transplant [Name the erythropoesis steps]

Output: Chediak-Higashi


Input: Inherited Problem with neutrophil chemotaxis Presents with dermatitis, pulmonary/sinus infections, staph, candida High IgE and IgD May use prophylaxis with antibiotics [Name the erythropoesis steps]

Output: Hyper IgE syndrome


Input: Inherited Problem w/ PMN rolling and adhesion Presents with neutrophilia, recurrent pus-less infections staph and fungal infections 75% mortality by age 5 with no treatment [Name the erythropoesis steps]

Output: Leucocyte adhesion deficiency


Input: Inherited Problem with neutrophil microbial activity -- lacks H202, superoxide burst Presents with recurrent pyogenic infections (staph, seratia, fungi) Managed with longerterm antibiotic prophylaxis [Name the erythropoesis steps]

Output: Chronic granulomatous disease


Input: Inherited Usually not clinical problems unless diabetic --- then candidal infections [Name the erythropoesis steps]

Output: Myeloperoxidase deficiency


Input: Myelodysplastic disorders [Name the erythropoesis steps]

Output: Major cause of acquired neutrophil dysfunction?


Input: >1500 cells/ul for 6 weeks, severe is >5000 Most common - atopic in developed nations, parasites in developing Primary - clonal disease of myeloid lineage Secondary- infections, allergies, toxins, reactive to lymphomas [Name the erythropoesis steps]

Output: Eosinophilia causes Most common? Types?


Input: Human infection by roundworms of dogs Dogs as pets suggestive of this potential cause of eosinophilia [Name the erythropoesis steps]

Output: Toxocaria canis


Input: Dysregulation of normal eosinophil production signaling Eosins must invade organs and cause end organ damage Sometimes reversible with treatment Steroids are used Must rule out cancers, other causes [Name the erythropoesis steps]

Output: Hypereosinophilia syndrome


Input: Monocytes Precursors to macrophages, DCs [Name the erythropoesis steps]

Output: Cell line to return first after chemotherapy


Input: Infection Autoimmune, connective tissue disorders Granulomatous disease (sarcoid, ulcerative colitis, etc) [Name the erythropoesis steps]

Output: Monocytes elevated in


Input: Hematologic malignancies Chronic myelomonocytic leukemia Acute monocytic leukemia [Name the erythropoesis steps]

Output: Highest monocyte counts seen in?


Input: ALC < 1000 cell/ul (going to be mostly T helper cell loss, as that is most of the cells) Suseptible to viral, fungal, mycobacterial, atypical infections Congenital, meds, infectious, hematologic malignancies (esp Hodgkin's), starvation [Name the erythropoesis steps]

Output: Lymphopenia Define, suseptibilities, etiologies


Input: HIV TB Malaria [Name the erythropoesis steps]

Output: Infectious causes of lymphopenia


Input: corticosteroids immune-suppressive chemo xrt [Name the erythropoesis steps]

Output: Medication causes of lymphopenia


Input: >4000 cells/ul Acute infection--pertussis, EBV, hepatitis Chronic infection - brucellosis, TB, syphillis Hypersensitivity rxn to drug Cancer - lymphomas, leukemias [Name the erythropoesis steps]

Output: Lymphocytosis define, causes


Input: Based on clonality B cells -- use flow to check kappa:lamba ratio (should be 70:30) T cells -- PCR/southern blot looking at t cell receptor Vastly altered kappa:lambda ratio - light chain restriction [Name the erythropoesis steps]

Output: Deciding whether a lymphocytosis is malignant or not?


Input: Recurrent bacterial infections (esp systemic) Infections at unusual sites (osteomyelitis) Unusual pathogens Chronic gingivitis, aphthous ulcers [Name the erythropoesis steps]

Output: Signs concerning for chronic neutropenia


Input: Congenital lymphocytopenia [Name the erythropoesis steps]

Output: Wiskott-Aldrich


Input: Giant cells Multinucleate or biolobed nuceli Bone marrow aspirates of Hogdkin's disease [Name the erythropoesis steps]

Output: Reed-sternberg cell


Input: 1. Vasoconstriction 2. Formation of platelet plug 3. Thrombus formation via coagulation cascade 4. Termination of thrombus formation by control mechanisms 5. Removal of clot by fibrinolysis [Name the erythropoesis steps]

Output: Five stages of hemostasis


Input: Intact endothelium is antithrombotic Prostacylin and NO secreting keeps plts from aggregating [Name the erythropoesis steps]

Output: Role of endothelium in steady state


Input: Anucleate 150k-400k is normal Life 7-10 days Alpha, dense, glycogen granules [Name the erythropoesis steps]

Output: Platelets General description


Input: Primary plug Provide reactive phospholipid surface for coagulation cascade [Name the erythropoesis steps]

Output: Platelets role in coagulation


Input: Pro/anti-coagulation factors vWF, fibrinogen, Factor V, Protein S, platelet factor 4, ADP, Ca2+ [Name the erythropoesis steps]

Output: Alpha granules of platelets


Input: Bridging protein in platelet adhesion to subendo Factor VIII chaperon to site of injury Made by endothelial cells and megakaryocytes monomers that are modified to multimers Stored in --Weibel-Palade in endo, alpha granules in plt Cleaved in plasma to smaller multimers by ADAMTS13 [Name the erythropoesis steps]

Output: vWF


Input: Bridging protein platelet aggregation [Name the erythropoesis steps]

Output: Fibrinogen in thrombus formation


Input: Vasoconstriction, reducing blood flow and allows procoagulant factors to bind Platelets aggregate Coagulation cascade initation [Name the erythropoesis steps]

Output: Result of vascular endothelial damage


Input: Exposure to subendothelial collagen and matrix proteins Thrombin, collagen -- potent activators Activation results in degranulation, shape change, TxA2 secretion (vasoconstriction) [Name the erythropoesis steps]

Output: Platelets are activated by? and activation results in?


Input: Platelets bridging to surface GPIb-IX (also IIb/IIIa) binds to vWF whcih connect to subendothelial collagen [Name the erythropoesis steps]

Output: Adhesion define and mechanism


Input: Platelet to platelet bridging GPIIb/IIIa changes conformation with activation Resulting in high affinity for fibrinogen [Name the erythropoesis steps]

Output: Platelet aggregation Define, mechanism


Input: Lack of GP1b-IX-V receptor Bleeding disorder [Name the erythropoesis steps]

Output: Bernard-Soulier syndrome


Input: Deficiency in GPIIb/IIIa receptor Bleeding disorder [Name the erythropoesis steps]

Output: Glanzmann thrombasenia


Input: Primary hemostasis Collagen-vWF-activated plts-fibrinogen-other activated plts TxA2 production and vasoconstriciton Not enough--coagulation cascade occurs on plt surface to convert fibrinogen to fibrin [Name the erythropoesis steps]

Output: Platelet plug


Input: Thrombin Which convert fibrinogen to fibrin Fibrin polymerizes around platlets and stabilizes Creating the secondary hemostatic plug [Name the erythropoesis steps]

Output: Outcome of the coagulation cascade


Input: ADP ATP Ca Serotonin [Name the erythropoesis steps]

Output: Dense granules of platelets


Input: ADP Epi Collagen Thrombin Serotonin Thromboxane A2 [Name the erythropoesis steps]

Output: Agonists of platelet aggregation


Input: Exposure of phosphatidyl serine and phosphatidyl ethanolamine to platelet surface Allows coagulation factors to bind [Name the erythropoesis steps]

Output: Platelet factor 3 activity


Input: Defect in platelet factor three Bleeding disorder [Name the erythropoesis steps]

Output: Scott syndrome


Input: Amplification cascade Zymogen conversion to active serine proteases Protease actives subsequent zympogen [Name the erythropoesis steps]

Output: Coagulation cascade generally


Input: ALL VIII is also made in endothelial cells vWF is made only megakaryocytes and endothelial cells [Name the erythropoesis steps]

Output: Factors synthesized in liver


Input: Vascular endothelial cell injury induces tissue factor production by monocyte or vascular endothelium Circulating factor XII complexes with TF and is activated [Name the erythropoesis steps]

Output: First step in coagulation cascade


Input: Activates X to Xa Activates IX to IXa Which activates X to Xa In the presence of VIII [Name the erythropoesis steps]

Output: Action of TF/XII complex


Input: Vastly accelerates the conversion of X to Xa Carried in circulation by vWF Necessary cofactor, along with calcium, for IX to bind to platelet membrant [Name the erythropoesis steps]

Output: Factor VIII


Input: Converts II to IIa (prothrombin to thrombin) In the presence of V [Name the erythropoesis steps]

Output: Factor X


Input: Secreted by platelets when the are activated, therefore it is at the site of injury Helps hold IIa and X close together on platelet phospholipid membrane ---prothrombinase complex Vastly increases conversion to thrombin [Name the erythropoesis steps]

Output: Factor V


Input: Converts fibrin to fibrinogen Converts XI to XIa, which converts IX to IX---thrombin burst--amplifies signal Also activates V and VIII Regulates (prevents breakdown and then activates anticoagulation) [Name the erythropoesis steps]

Output: Thrombin role in thrombosis


Input: Helps crosslink fibrin into strong sheets [Name the erythropoesis steps]

Output: XIIIa


Input: 1. Hemodilution of of activated factors by systemic circulation 2. Hepatic clearance -- activated factors are metabolized 3. Endogenous anticoagulants 4. Fibrinolysis [Name the erythropoesis steps]

Output: Cessation Coagulations 4 things


Input: Antithrombin Protein C/protein S Tissue factor pathway inhibitor Protein Z [Name the erythropoesis steps]

Output: Endogenous anticoagulants


Input: Made by liver, endothelial cells Binds and inactivates Xa and IIa Activity vastly increased by heparin [Name the erythropoesis steps]

Output: Antithrombin


Input: With cofactor protein S Inactivates Va and VIIIa Activated by thrombin after thrombomodulin has changed its conformation After thrombomodulin binding (on endothelial surface) thrombin cannot activate coagulation factors [Name the erythropoesis steps]

Output: Activated protein C


Input: Made by endothelial cells Binds to and inactivates Xa Xa/TFPI inactivate TF/VIIa complex [Name the erythropoesis steps]

Output: Tissue Factor Pathway Inhibitor


Input: Plasminogen made by liver and circulates Plasminogen binds to fibrin Plasminogen activated to plasmin by TPA/UPA Plasmin cleaves fibrin into degradation products like D-dimers [Name the erythropoesis steps]

Output: Fibrinolysis process


Input: Major inhibitor of plasmin Deficiencies result in bleeding disorders [Name the erythropoesis steps]

Output: Alpha-2-antiplasmin


Input: Major inhibitor of tPA Stored in platelets Deficiencies result in bleeding disorders [Name the erythropoesis steps]

Output: Plasminogen activator inhibitor-1


Input: Plasma Blue top tube Citrate is the anticoagulant -- binds Ca making it unable to be a cofactor for coagulation cascade [Name the erythropoesis steps]

Output: Testing for coagulation? What tube?


Input: Purple top EDTA (anticoagulant) [Name the erythropoesis steps]

Output: Testing for cellular blood elements? What tube


Input: Usually not until under 10K [Name the erythropoesis steps]

Output: Platelet count where spontaneous bleeding is a problem


Input: EDTA sometimes results in platelet clumping Automated counter returns low platelet count that is artifactual Look at the smear! or run again with a blue top tube [Name the erythropoesis steps]

Output: Psuedothrombocyptopenia


Input: 10 plts on a 100x field = 150K 20 = 300K [Name the erythropoesis steps]

Output: Platelets on smear


Input: Measures the platelet/blood vessel wall interaction How long does it take a person to stop bleeding? Hopefully less than 9 minutes. Not great at predicting surgical bleeding, operator dependent [Name the erythropoesis steps]

Output: Bleeding time


Input: In vitro test of plt fnc (adhesion and aggregation) How long does it take for stimulated platelets to occlude an aperture Collagen/ADP-- tests for vWF Collagen/epi -- tests for aspirin, other dysfunction [Name the erythropoesis steps]

Output: PFA-100


Input: Will increase time without their necessarily being a functional deficit [Name the erythropoesis steps]

Output: Thrombocytopenia and platelet function studies?


Input: Time to clot when (TF + phospholipid + Ca) are added to citrated plasma "Extrinsic pathway" Prolonged by deficiencies in VII, X, V, II, I DHMC--12.2-14.8 sec [Name the erythropoesis steps]

Output: PT


Input: Standardization of PTs based on analysis of the thromboplastin reagent based on a WHO standard Normal INR - 1 Normal for anticoagulates 2-3 [Name the erythropoesis steps]

Output: INR


Input: partial thromboplastin time Citrated plasma + Ca + phospholipid + contact activator glass, cellite, kaolin, ellagic acid "Intrinsic pathway" test Prolonged by Deficiencies in-- HMWK, pre-kalikrein, XII, VIII, IX, XI X, V, II [Name the erythropoesis steps]

Output: PTT


Input: Deficiencies in HMWK, pre-kalikrein, XII [Name the erythropoesis steps]

Output: Prolong aPTT with no risk of bleeding


Input: Factor VII deficiency, polymorphism, inhitor Early liver disease or Vit K deficiency Early warfarin [Name the erythropoesis steps]

Output: Prolonged PT and normal PTT


Input: Hemophilia -- A (def in VIII), B (IX), C (XI) vWF disease Inhibitor of intrinsic pathway Heparin HMWK, pre-kal, XII deficiencies [Name the erythropoesis steps]

Output: Prolonged PTT and normal PT


Input: Common pathway/multiple factors effected Severe liver disease Therapeutic warfarin Consumptive coagulopathy Hemodilution Sever Vit K deficiency Low fibrinogen or dysfunctional fibrinogen Direct thrombin inhibitors [Name the erythropoesis steps]

Output: Prolonged PT and PTT


Input: 50:50 ratio of patient and pooled normal plasma correction of prolonged clotting studies indicates factor deficiency --if prolongs again after time-- likely VIII inhibitor persistence indicates inhibitor [Name the erythropoesis steps]

Output: Mixing study


Input: How much factor is there compared to normal pooled plasma? normal considered 50-150% except XII: 30-150% [Name the erythropoesis steps]

Output: Coagulation factor assays


Input: Exogenous thrombin added to plasma Time to clot Detect fibrinogen abnormalities hypo, dys, heparin, thrombin inhibitors [Name the erythropoesis steps]

Output: Thrombin clotting time


Input: Fibrin breakdown product Elevated in acute thrombosis Also DIC, cancer, infection, surgery, inflammation [Name the erythropoesis steps]

Output: D-dimer


Input: Decreased production Increased consumption Sequestration in spleen [Name the erythropoesis steps]

Output: Quantitative platelet disorders


Input: Autoantibodies against platelets Self-limited in kids with viral infections Chronic and requiring immune suppression in adults [Name the erythropoesis steps]

Output: Autoimmune thrombocytopenia like ITP


Input: Immune mediated Quinine -- low plts and bleeding Heparin -- HIT, low plts and clotting [Name the erythropoesis steps]

Output: Medication induced thrombocytopenia


Input: microangiopathic hemolytic anemia thrombocytopenia fever neurologic changes renal failure Clotting Failure of ADAMT13 to cleave vWF resulting in too many large vWFs (autoimmune or medication induced) Treat with plasma exchange, immunosuppression) [Name the erythropoesis steps]

Output: Thrombocytopenia thrombotic purpura (TTP)


Input: Similar to TTP hemolysis, elevated liver enzymes, low platelets [Name the erythropoesis steps]

Output: HELLP in pregnancy


Input: Splenomegaly Enlarged spleen can have 90% of plts (normal sized has 30%) Happens in myeloproliferative disorders, portal hypertension, portal/hepatic thrombosis [Name the erythropoesis steps]

Output: Thrombocytopenia 2/2 sequestration


Input: Leukemia, MDS, aplastic anemia Bone marrow infiltration Virus (HIV, heps are toxic to megakary) Toxins (alcohol, xrt, chemo, meds) Nutritional deficiencies (B12, folate) Hereditary (rare) [Name the erythropoesis steps]

Output: Thrombocytopenia 2/2 decreased production


Input: Lysosomal storage disorder glucocerebrosidase builds up Bone marrow fills with fat not hematopoetic cells [Name the erythropoesis steps]

Output: Gaucher's disease


Input: Usually medication aspirin, NSAIDs, anticoagulants SSRIs, herbal supplements Uremia (circulating toxin) MDS, myeloproliferative disorders Cardiopulmonary bypass [Name the erythropoesis steps]

Output: Acquired plt function disorders


Input: Absent alpha granules [Name the erythropoesis steps]

Output: Gray plt disorder


Input: Elevated uPA in plt granules Granule contents degraded [Name the erythropoesis steps]

Output: Quebec platelet syndrome


Input: Less ADP released Hermansky-Pudlack Chediak-Higashi [Name the erythropoesis steps]

Output: Delta granule disorders


Input: Defect in assembling coagulation factors on plt surface [Name the erythropoesis steps]

Output: Scott syndrome


Input: Most common inherited bleeding disorder 1% of population had deficiency Autosomal dominant Levels vary between normal individuals Type O blood has less [Name the erythropoesis steps]

Output: vWF epidemiology


Input: Low levels of activity 70-80% of affected [Name the erythropoesis steps]

Output: vWF deficiency Type 1


Input: Normal levels Reduced activity -- abnormal molecule or reduced number of high molecular weight multimers 20-30% of affected [Name the erythropoesis steps]

Output: vWF deficiency Type 2


Input: Absent vWF factor and factor VIII activity Rare [Name the erythropoesis steps]

Output: vWF deficiency type 3


Input: Due to autoantibody Rare [Name the erythropoesis steps]

Output: Acquired vW disease


Input: Ranges in severity Mucocutaneous predominates (mennorhagia, epistaxis, easy brusing, GI bleeding, oralpharyngeal) Hemarthroses rare Excessive bleeding with trauma, surgery Long bleeding with minor cuts Worse with aspirin [Name the erythropoesis steps]

Output: Bleeding phenotype of vWD


Input: PT, TCT are normal PTT may be normal or prolonged (2/2 factor VII effect) Prolonged bleeding time, PFA-100 Abnormal aggregation on ristocetin test (1,2,3 are slow to aggregate, 2b is fast) [Name the erythropoesis steps]

Output: Lab testing in vWF


Input: Gain of function Hyperaggregation at low ristocetin doses Plts normal but thrombocytopenia common (pseudo vWD is a gain of funciton in GPIb) [Name the erythropoesis steps]

Output: vWD type 2b


Input: DDAVP (desmopressin, synthetic vasopressin) Stimulates release of vWF Good in 1 and mild 2, BAD in 2b Factor replacement Anti-fibrinolytics to stabilize clots Contraceptive for mennorhagia Avoid aspirin [Name the erythropoesis steps]

Output: vWD treatment


Input: Hemo A - VIII deficient -- X-linked Hemo B - IX deficient -- X-linked --christmas disease Hemo C - XI deficient-- AR Parahemophilia - V deficient - AR [Name the erythropoesis steps]

Output: Hemophilas Deficiency and inheritance


Input: menorrhagia [Name the erythropoesis steps]

Output: Symptom of female carriers with hemophila a or b


Input: 80% A and 20 % B Mild: 5-40% factor, bleed with trauma/surg, may have normal aPTT Mod: 2-5% factor, may bleed spontaneous, prolonged aPTT Severe: 0-1%, spontaneous bleeding common, prolonged aPTT [Name the erythropoesis steps]

Output: Hemophila A/B subtypes


Input: May be delayed because primary hemostasis is fncal Hemarthroses common -- target joint Muscle hematomas CNS bleeds Bleeding after trauma, dental work, etc Hematuria [Name the erythropoesis steps]

Output: Hemophila bleeding phentype


Input: Markedly reduced thromin burst [Name the erythropoesis steps]

Output: Effect on hemophila on coagulation cascade


Input: aPTT prolongs with factor less than 30% Corrects with mixing Specific factor levels low PT normal, PFA normal [Name the erythropoesis steps]

Output: Labs in hemophila


Input: Treat with recombinant factor replacement (mild VIII may respond to DDAVP) Either for acute bleeding or Prophylaxis 3x/week to keep trough level >1% -- only considered in severe [Name the erythropoesis steps]

Output: Treatment of hemophila


Input: Joint destruction (arthropathy) HIV/Hep C -80% of severe hemophiliacs in 80s, 50% of all -no HIV since 1986 Inhibitors to missing factors these antibodies can complicate treatment -might have to bypass using VIIa [Name the erythropoesis steps]

Output: Complications of hemophila


Input: Autoantibody to factor VIII Bleeding disorder in previously healthy 1/million/yr Mostly idiopathic and in the elderly, sometimes w/ cancer, post partum [Name the erythropoesis steps]

Output: Acquired hemophilia


Input: factor eight inhibitor bypass agent treats acquired hemophilia [Name the erythropoesis steps]

Output: FEIBA


Input: Typically delay (12-24 hrs later) Mucocutaneous, GU Rare hereditary -- quebec plt disorder, alpha-2-antiplasmin, pai-1 deficiency, More commonly acquired -- cancer, liver disease, DIC, prostate surgery [Name the erythropoesis steps]

Output: Fibrinolytic bleeding disorders


Input: Prolonged PT and PTT Increased D-dimers (may look like DIC) [Name the erythropoesis steps]

Output: Labs in fibrinolytic bleeding disorders


Input: Supportive plasma infusions Anto-fibrinolytic drugs (epsion aminocaproic acid, tranexamic acid) [Name the erythropoesis steps]

Output: Treating fibrinolytic bleeding disorders


Input: Over anti-coagulation [Name the erythropoesis steps]

Output: Most common cause of bleeding due to vit K deficiency


Input: Dietary -- poor intake, malabsorption, alcoholism Meds - antibiotics, salicyates, herbs, vitamins a and e, comarins [Name the erythropoesis steps]

Output: Causes of vit K deficiency


Input: Prolonged PT and PTT, correct with mixing Normal plt studies Low II, VII, IX, X with preserved V [Name the erythropoesis steps]

Output: Labs in Vit K deficiency


Input: Oral Vit K - IV only in emergency b/c rare anaphylaxis - substantial restorate at 24 hours add FFP in emergencies, will temporarily correct [Name the erythropoesis steps]

Output: Treatment of Vit K deficiency


Input: Problems with synthesis of coagulants and anticoagulants Bleeding is the result usually, although clotting can also happen [Name the erythropoesis steps]

Output: Liver disease


Input: INR is part of the liver disease end stage assessment Low factors levels including V but not VIII PT/INR may not accurately predict bleeding [Name the erythropoesis steps]

Output: Liver disease and coagulation labs


Input: Transplant Supportive hemostatic treatments don't really work but...Vit K, FFP [Name the erythropoesis steps]

Output: Treatment of coagulopathy of liver disease


Input: Disseminated intravascular coagulation Insult results in excessive thrombin generation Activating both coagulation and anticoagulation Results in clotting and bleeding Insults-- infections, cancer, trauma, brain injury, snake bite, burns, etc [Name the erythropoesis steps]

Output: DIC


Input: Bleeding at surgical, IV sites Purpura fulminans -skin necrosis, usually with infection --> amputation Thromboses -- micro w/ end organ damage common, large venous/arterial less Sometimes asymptomatic-- usually with cancer pts [Name the erythropoesis steps]

Output: DIC presentation


Input: Prolonged PT and PTT Elevated D-dimers Decreased fibrinogen Decreased plts Anemia RBC schistocytes Endogenous anticoagulants low (antithrombin, C, S) [Name the erythropoesis steps]

Output: Lab evidence of DIC


Input: Treat underlying cause Support with plasma (factors), cryoprecipitate (fibrinogen), and plts RBCs Heparin will stop, but with high risk of bleeding [Name the erythropoesis steps]

Output: Treating DIC


Input: Mutated bone marrow cells that divide but do not mature normally Dysfunctional cells with premature apoptosis Hypercellular bone marrow the peripheral cytopenias [Name the erythropoesis steps]

Output: MDS general idea


Input: Acute leukemia High grade lymphoma [Name the erythropoesis steps]

Output: Cells proliferate quickly but are arrested at immature level of differentation


Input: Chronic leukemia Myeloproliferative disorders [Name the erythropoesis steps]

Output: Cells proliferate and mature normally but accumulate because of additional divisions or problems with cell death regulation


Input: Normally less than 5% 5-19% -- myelodysplasia >20% -- acute leukemia [Name the erythropoesis steps]

Output: Increased number of myeloblasts in bone marrow


Input: Asymptomatic -- on CBC Cytopenia symptoms -- infections, fatigue, bleeding 15% have autoimmune disorders incidence increases with age primary is idiopathic, secondary due to mutagenic insult [Name the erythropoesis steps]

Output: Presentation of MDS


Input: Microcytic anemia-- most common Multiple cytopenias common Smear -- macrocytes, acanthocytes, elliptocytes, nucleated RBCs, pseudo-pelger-huet, hypogranulated neutrophils [Name the erythropoesis steps]

Output: Lab findings in MDS


Input: Thrombocytosis in common [Name the erythropoesis steps]

Output: MDS with 5q minus


Input: Hypercellular with at least one dysplastic lineage Megakaryocytes dysplasia -- clustered cells, micromegakaryocytes, abnormal disorder Erythroid -- delayed nuclear to cytoplasmic maturation, erythroid hyperplasia with megaloblastiod hyperplasia -ringed sideroblasts can be seen [Name the erythropoesis steps]

Output: Bone marrow biopsy in MDS


Input: Cytopenias PMNs -- hypogranular, segemental abnormalities Erythrocytes -- macrocytes, ovalocytes, anisopolkicytosis, basophilic stipling, nucleated froms Plts - large, hypogranular Monocytes - monocytosis [Name the erythropoesis steps]

Output: Peripheral findings of MDS


Input: Refractory anemia +/- ringed sideroblasts Refractory anemia with multiple lineage dysplasia +/- ringed sideroblasts 5q- syndrome [Name the erythropoesis steps]

Output: MDS subtypes with less than 5% blasts


Input: Good prognosis, lower risk of progression to AML [Name the erythropoesis steps]

Output: 5q minus in MDS prognostics


Input: Multiple cytogenetic abnormalities Changes in 5 or 7 that are not 5q- secondary mds almost always has these bad markers [Name the erythropoesis steps]

Output: Poor cytogenic prognostics in MDS


Input: Number of basts Number of cytopenias Karyote Worst - 5 months median survival, best -- 5 years median survival [Name the erythropoesis steps]

Output: Prognostic scale in MDS


Input: Treat when symptomatic Supportive w/ transfusions, growth factors, immunomodulatory agents, demethylating chemotherapy, induction chemotherapy Bone marrow transplant is only cure [Name the erythropoesis steps]

Output: Treatment of MDS


Input: Sick at presentation with acute Immature cells seen in bone marrow and peripheral blood in acute, mature in With chronic, bone marrow function until late stages [Name the erythropoesis steps]

Output: Difference between acute and chronic leukemias in presentation


Input: Infection Fatigue, dyspnea Bruising, bleeding DIC, bone pain, myeloid sarcoma/chloroma, organomegaly, CNS/gingival, cutaneous infilitration [Name the erythropoesis steps]

Output: Symptomatic presentation of AML


Input: Bone marrow biopsy w/ >20% blasts -hypercellular, monotonous population Determine lineage with cytochemical/flow Determine cytogenetics [Name the erythropoesis steps]

Output: Diagnosing AML


Input: Myeloperoxidase + sudan black --granulocyte Butyrate esterase--monocytic PAS - lymphocytic [Name the erythropoesis steps]

Output: Cytochemical stains to determine linease


Input: CD34 [Name the erythropoesis steps]

Output: Surface marker for hematologic stem cells


Input: CD33 CD33+, CD34+ [Name the erythropoesis steps]

Output: Surface marker for myeloid lineage? Surface profile of myeloid leukemia


Input: CD3, CD4 [Name the erythropoesis steps]

Output: Surface markers for t cell lineage


Input: C19, CD20, CD22 [Name the erythropoesis steps]

Output: Surface markers for a b cell lineage


Input: t (8;12) t (15;17) -- m3 inversion (16) - M4Eo [Name the erythropoesis steps]

Output: Favorable karyotypes in AML


Input: Any 5 or 7 changes (including 5q) Trisomy 8 Monsomy 7 [Name the erythropoesis steps]

Output: Bad karyotypes in AML


Input: NPM1 [Name the erythropoesis steps]

Output: Good prognosis mutations in AML


Input: FLT3 KIT P53 [Name the erythropoesis steps]

Output: Poor prognosis mutations in AML


Input: AML w/ recurrent genetic abnormalities AML w/ multilineage dysplasia AML/MDS that is therapy related AML, NOS divided into M0-7 based on histology [Name the erythropoesis steps]

Output: Classification of AMLs


Input: Age ECOG h/o previous hematologic malignancy Cytogenetics [Name the erythropoesis steps]

Output: Prognostics in AML


Input: AML w/ recurrent genetic change 10% of AML Younger adults, some kids Generally favorable prognosis RUNX1-CBFA2T1 fusion protein represses transcription of genes related to differentiation -- differentiation block - AML Associated with extramedullary disease (skin, cns, myeloid sarcs) [Name the erythropoesis steps]

Output: t (8;12) AML1/ETO


Input: AML with recurrent genetic changes Eosinophils affected Generally good prognosis CBFbeta/MYH11 fusion protein blocks transcription of differentiation related genes -- differentation block -- AML [Name the erythropoesis steps]

Output: inv(16)(p13;q22) AML


Input: AML with recurrent cytogenetic changes Differentiation block is at promyelocyte stage 5-8% of AML Most are t (15;17) -- 95% creating PML/RARalpha fusion others are also RARalpha mutants Large granules with Auer rods Extremely prone to clotting Responsive to all-trans retinoic acid [Name the erythropoesis steps]

Output: Acute Promyelocytic Leukemia (M3)


Input: Subtype of acute promyelocytic leukemia Appear agranular or hypogranular Butterfly or bilobed nuclei High WBC count [Name the erythropoesis steps]

Output: Microgranular Acute Promeylocytic Leukemia


Input: AML with recurrent genetic changes Approximately 5% of AMLs, associated with topoisomerase inhibitors Mixed Lineage Leukemia gene involved in multiple translocations (9;11), (11,19) Intermediate prognosis [Name the erythropoesis steps]

Output: AML w/ 11q23 (MLL) abnormalities


Input: Bad prognosis Severe pancytopenia in elderly >50% dysplasia in at least 2 cell lines Can arise from MDS or not [Name the erythropoesis steps]

Output: AML w/ multiple dysplastic lines


Input: Generally poor prognosis 1) with ionizing radiation or alkylating agents (cyclophosphamide, chlorambucil) --presents as MDS years later 2) with topoisomerase 2 inhibitors (often associated with 11q23 changes) --presents as overt leukemia, sometimes as soon as 12 months out [Name the erythropoesis steps]

Output: AML, therapy related


Input: Minimally differentiated No myeloid maturation Blasts vary in size with 1-2 nucleoli myeloperoxidase, sudan back, PAS, NSE--negative No granules No Auer rods [Name the erythropoesis steps]

Output: AML -- M0


Input: Arrest at myeloblast stage Blasts vary in size w/ 1-2 nucleoi >3% are MPO, sudan black + Can have granules, Auer rods [Name the erythropoesis steps]

Output: AML -- M1


Input: AML with Maturation 30-45% of all AML >10% pros, myelos, neutrophils in marrow usually have granules and Auer rods [Name the erythropoesis steps]

Output: AML-- M2


Input: Mixed monocyte/granulocyte population 15-25% of AML >20% blats >20% neutrophils + precursors >20% monocytes + precursors [Name the erythropoesis steps]

Output: M4: Acute Myelomonocytic leukemia


Input: 80% of cells in monocytic lineage monoblast, promonocyte, monocytes Gingival infiltration, extramedullary disease are clinical features [Name the erythropoesis steps]

Output: M5: Acute Monoblastic leukemia


Input: Rare Erythroleukemia >50% erythroid precursors in marrow >20% of myeloblasts are non-erythroid Pure erythroid leukemia 80% of precursors are erythroid [Name the erythropoesis steps]

Output: M6: Acute Erythrocytic leukemia


Input: Can get bone marrow fibrosis Two ages Infants, kids <3 w/ downs -- good prognosis t (1,22) Older adult usually de novo, occasionally MDS [Name the erythropoesis steps]

Output: M7: Acute Megakaryocytic leukemia


Input: Treat infections Check cardiac fnc (adriamycin) Manage leukostasis Manage hyperuricemia Tumor lysis syndrome DIC [Name the erythropoesis steps]

Output: Initial stabilization concens in AML


Input: Goal -- remission w/ fewer than 5% blasts in marrow Myeloablative doses of chemotherapy resulting in transfusion dependent cytopenia for 3 weeks 70% remission 5-20% complications stop treat 15-% - resistant disease Followed by 3-4 doses of consolidation and/or autologous transplant Allogenic transplant used in high risk patients [Name the erythropoesis steps]

Output: Treatment of AML


Input: Granules in acute promyelocytic leukemia contain procoagulants TF activates factor VII Cancer procoagulant activates factor X 10-20% die of hemorrhagic events [Name the erythropoesis steps]

Output: APML and DIC


Input: t (15,17) with PML/RARalpha fusion protein APMLs respond to high doses of all trans retinoic acid these doses push through the mutant retinoic acid receptor to progress differentiation normally ATRA shortens DIC, with chemo puts 80-90% in remission [Name the erythropoesis steps]

Output: APML and ATRA


Input: Potentially fatal syndrome occuring in 20% of APML patients treated with ATRA Fever, edema, pulmonary infiltrates, respiratory distress Usually in first 3 weeks, unclear etiology Stop ATRA temporarily, give steroids [Name the erythropoesis steps]

Output: Retinoic acid syndrome


Input: Probably due to white cell maturation Can cause leukostasis [Name the erythropoesis steps]

Output: Hyperleukocytosis in ATRA treatment


Input: Second line therapy Induces differentiation and apoptosis through interaction with PML/RARalpha fusion product [Name the erythropoesis steps]

Output: APML and arsenic


Input: Increase numbers in one or more cell lines, clonal marrow expansion Extramedullary hematopoesis w/ hepatosplenomegally Hypercatabolism (fevers, night sweats, weight loss) Loss of sensitivity to growth factors Predisposition to develop AML [Name the erythropoesis steps]

Output: Characteristics of myeloproliferative disorders


Input: Activating tyrosine kinase mutations [Name the erythropoesis steps]

Output: Mutations often seen in myeloproliferative disorders


Input: Must be t(9;22) Present with fevers, chills, weight loss, early satiety, splenomegaly [Name the erythropoesis steps]

Output: Chronic myeloid leukemia Genetics Presentation


Input: Bone marrow -- hypercellular w/ increased myeloid:erythroid ratio Peripheral-- immature myeloid cells, but few blasts [Name the erythropoesis steps]

Output: CML Bone marrow Smear


Input: Elevated WBC and plts early, low late Maybe elevated LDH [Name the erythropoesis steps]

Output: CML labs


Input: t(9;22) creates fusion product BCR-ABL BCR-ABL is an unregulated tyrosine kinase that stimulates proliferation [Name the erythropoesis steps]

Output: CML pathogenesis


Input: Chronic phase - Counts/spleen easily controlled with hydroxyurea, pts well, can be cured with stem cell transplant (3 years) Acute -- counts more difficult to control with hydroxyurea, spleen grows, constitutional symptoms reappear (1 yr) Blast -- AML/ALL - like, unresponsive to therapy/transplant, (3-6 months) [Name the erythropoesis steps]

Output: Natural history of CML prior to TKIs


Input: First line with dasatinib -- BCR-ABL tyrosine kinase inibitor Monitor-- counts, t(9;22) by fish, Bcr-ABL mRNA by RT-PCR With treatment fail, try other BcrABL TKs...then stem cell transplant [Name the erythropoesis steps]

Output: Current treatment for CML


Input: Remission at 1 yr [Name the erythropoesis steps]

Output: Important prognostic in CML


Input: Increased hemoglobin, red cell mass -this can fall late Low serum EPO Presence of Jak2 mutation Hypercellular mone marrow No other reason for the high red cells [Name the erythropoesis steps]

Output: Polycythemia Vera Diagnosis


Input: Median age 60 sweats, fatigue, weight loss, HA, visual disturbances, abd pain, thrombosis, puritis, erythromelalgia (neurovascular peripheral pain) splenomegally (70%), plethora (70%), haptomegally (40%) [Name the erythropoesis steps]

Output: Polycythemia Vera Presentation


Input: Poor prognosis if untreated, good w/ Treatment of choice -- phlebotomy (to Hct-40) to the point of iron depletion and decreased proliferation Can develop resistant AML/ALL or meylofibrosis [Name the erythropoesis steps]

Output: Polycythemia Vera Treatment and prognosis


Input: plts consistently >450K increased/weird megakaryocytes in BM Not CML, inflammation, iron deficiency [Name the erythropoesis steps]

Output: Essential Thrombocythemia Diagnosis


Input: 50% have JAK2 mutation, others have MPL (myeloproliferatie leukemia virus gene-- the thrombopoetin receptor) [Name the erythropoesis steps]

Output: Essential Thrombocythemia Genetics


Input: HA, lightheadedness, syncope, atypical chest pain, visual changes, mild splenomegaly Some clot, some bleed [Name the erythropoesis steps]

Output: Essential thrombocythemia presentation


Input: Low risk -- <60, no h/o thrombosis, plts <1000K No treatment High risk Hydroxyurea, sometimes aspirin, anagrelide Usually normal life span, rarely get clotting complication, AML, ALL, myelofibrosis [Name the erythropoesis steps]

Output: Essential thrombocythemia Treatment and prognosis


Input: Collage fiber deposited in bone marrow Anemia -- can be severe w/ teardrop cells Increased, abnormal megakaryoctes in BM Plts, WBC can be up or down [Name the erythropoesis steps]

Output: Primary myelofibrosis Diagnosis


Input: Worse with Hgb<10 WBC<4 or >30 Plts <100 Monocytes >1.0 range is from 175 months to 26 months COD: transformation to MDS, AML, bleeding, infection [Name the erythropoesis steps]

Output: Primary myelofibrosis Prognosis and COD


Input: Stem cell transplant is curative Hydoxyurea, transfusions, splenectomy [Name the erythropoesis steps]

Output: Primary myelofibrosis Treatment


Input: Fever Weight loss Night sweats [Name the erythropoesis steps]

Output: Systemic symptoms of lymphoma


Input: Direct kills of organisms or infected cells Modulation of immune response through helper and suppressor Ts [Name the erythropoesis steps]

Output: Function of T cells


Input: Produce antibodies Antigen present to T cells [Name the erythropoesis steps]

Output: Function of B cells


Input: Maturation to competence: thymus and marrow Differentiation and antigen driven replication: lymph nodes, spleen, MALT, others LN in aggregate is the largest [Name the erythropoesis steps]

Output: Locations of maturation and differentiation of lymphocytes


Input: Capsule Subcapsular sinus: afferent lymph enters this space Cortex with follicles Paracortex Medulla with cords and sinuses Medullary vessels: artery and vein [Name the erythropoesis steps]

Output: Seven divisions of lymph node


Input: Small B cells Virgin or recirculating memory cells [Name the erythropoesis steps]

Output: Primary lymphoid follicle


Input: Antigenic stimulation for differentiation Creates germinal center with follicular dividing cells Surrounded by mantle of transient small lymphocyytes [Name the erythropoesis steps]

Output: Secondary lymphoid follicle


Input: Primary and secondary follicles --for stimulation and differentation/proliferation Medullary cords, plasma cells release Igs into efferent lymph [Name the erythropoesis steps]

Output: Sites of B cell homing


Input: Paracortex [Name the erythropoesis steps]

Output: Site of T cell homing


Input: Blood into Lymph node Surveilling for presentation of specific antigen Leave through efferent lymphatics [Name the erythropoesis steps]

Output: Normal lymphocyte circulation


Input: Small round blue dots Round nucleus Clumped chromatin Small/not visible nucleous [Name the erythropoesis steps]

Output: Small lymphocytes appearance


Input: T or B Virgin or effector or memory [Name the erythropoesis steps]

Output: Small lymphocytes identities


Input: Primary follicles Mantle zones of secondary follicles Medullary cords [Name the erythropoesis steps]

Output: Where are B cells in LN?


Input: Paracortex A few in the germinal center [Name the erythropoesis steps]

Output: Where are T cells in LN?


Input: Replicating population Small and large (based on comparison with macrophage nucleus Expanding the number of antigen specific cells [Name the erythropoesis steps]

Output: Noncleaved cells in lymph node


Input: Post mitotic plasma or memory cell precursors Look a lot like lymphocytes but are irregularly folded and cleaved Nonproliferating [Name the erythropoesis steps]

Output: Small cleaved cells


Input: Bigger version of small cleaved Replicaiton potential not clear [Name the erythropoesis steps]

Output: Large cleaved cells


Input: Follicular cells Non cleaved, large cleaved [Name the erythropoesis steps]

Output: Cells of the germinal center


Input: Proliferating large cell outside of germinal center of lymph node May be B or T Looks like dividing cell: vesicular chromatin, nulceoli visible [Name the erythropoesis steps]

Output: Immunoblast


Input: To T cells - interdigitating reticulin cells To B cells - dendritic reticulin cells [Name the erythropoesis steps]

Output: APCs in LNs


Input: Main cell of medullary sinus Abundant pale cytoplasm, oval nucleus, one nucleolus A few in germinal center [Name the erythropoesis steps]

Output: Macrophages in lymph node


Input: Proliferation in one or all of lymph node zones based on stimulus Not cancer [Name the erythropoesis steps]

Output: Reactive hyperplasia


Input: Type of reactive hyperplasia Expansion of germinal centers (can go into paracortex, medullary areas Collagen vascular disease Systemic toxo Syphillus [Name the erythropoesis steps]

Output: Follicular hyperplasia Define Associated with


Input: A reactive hyperplasia Paracortical expansion Skin disease, viruses, drug reactions [Name the erythropoesis steps]

Output: Interfollicular hyperplasia


Input: Expansion of macrophages in the sinus Indicative of adjacent cancer or infections [Name the erythropoesis steps]

Output: Sinus histiocytosis


Input: Dominant cell type (or transformed cell type) Stage Patient's health status [Name the erythropoesis steps]

Output: Factors predicting lymphoma course


Input: Divides lymphoma into low, intermediate, high grades Clinical Based on clinical history, dominant cell type, "follicularity"-- do the cells form normalish LNs [Name the erythropoesis steps]

Output: Working Formula and lymphoma?


Input: Cell of origin: B vs T/NK vs Hog Peripheral vs precursor [Name the erythropoesis steps]

Output: WHO lymphoma classification


Input: Is most of the disease in the lymph organs or the bone marrow/blood? [Name the erythropoesis steps]

Output: Leukemia vs lymphoma


Input: Monoclonal light chain CD19 CD20 CD5 CD10 negative [Name the erythropoesis steps]

Output: IHC profile in B cell small lymphocytic lymphoma


Input: Monoclonal light chain CD19 CD20 CD10 CD5 negative [Name the erythropoesis steps]

Output: IHC profile in B cell small cleaved lymphoma


Input: CLL follicular marginal zone MALT [Name the erythropoesis steps]

Output: Indolent lymphomas, name some


Input: Slowly progressive Difficult to cure Goals of chemo are extension of life with good quality Only cure is allogenic HSCT [Name the erythropoesis steps]

Output: Indolent lymphomas general course, treatment goals


Input: Grow rapidly Can be rapidly fatal Immediate aggressive treatment with the goal of cure [Name the erythropoesis steps]

Output: Aggressive lymphomas general course, treatment goals


Input: ALL, Burkitt's [Name the erythropoesis steps]

Output: Aggressive lymphomas name some


Input: diffuse large cell peripheral T cell mantle cell [Name the erythropoesis steps]

Output: Intermediately aggressive lymphomas name some


Input: I -- involvement of a single LN region II - multiple regions on same side of diaphragm III - disease on both sides of the diaphragm IV - multifocal extranodal involvement or regionally distant extrnodal invovlement A or B (symptoms) [Name the erythropoesis steps]

Output: Staging in Lymphoma


Input: Night sweats Fever Greater than 10% weight loss [Name the erythropoesis steps]

Output: B symptoms


Input: Originates from large replicating cells of germinal center and paracortex Oval/cleaved cells with nucleoli and vesicular chromatin Diffiuse infiltration of LN CD19/20 positive May overexpress bcl-2/6 [Name the erythropoesis steps]

Output: Diffuse large B cell lymphoma Pathology


Input: Intermediate aggressiveness lymphoma 30-40% cure rate [Name the erythropoesis steps]

Output: Diffuse large B cell lymphoma prognosis


Input: Children or adults (median age 64) Present with an enlarging, painless mass in lymph node region Diffuse or localized [Name the erythropoesis steps]

Output: Diffuse large B cell lymphoma presentation


Input: Age (>60 bad) Stage (III or IV) LDH elevation Poor performance status Extranodal involvement [Name the erythropoesis steps]

Output: Prognostics in diffuse large B cell lymphoma


Input: For localized: chemo + xrt Advanced: Anthracycline based chemo R-CHOP used -- rituxin, cyclophosphamide, adriamycin, vincristin, prednisone Rituxin increases OS by 10% [Name the erythropoesis steps]

Output: Diffuse large B cell lymphoma treatment


Input: Chemo + autologous transplant Transplant helps up cure rate by 20% [Name the erythropoesis steps]

Output: Relapsed large B cell lymphoma treatment


Input: Cancer of small cleaved cells of germinal center Clumped chromatin, irregular nuclear profile Retain follicular structure of LN but monotonous cells More large cells -- worse grade [Name the erythropoesis steps]

Output: Follicular lymphoma pathology


Input: t(14;18) bcl-2 overexpression CD19, 20, 10, bcl2+ CD5, cyclinD1 - [Name the erythropoesis steps]

Output: Follicular lymphoma IHC/molecular changes


Input: Most common of indolent lymphomas 22% of NH lymphomas Disease of adults >40 Typically presents as stage III or IV [Name the erythropoesis steps]

Output: Follicular lymphoma epi


Input: No curable 7-10 years, but highly variable Transformation to large cell has more aggressive course Prognosis as FLIPI score based on: Age >60, elevated LDH , stage III/IV, >4 LN sites, hemoglobin <12 [Name the erythropoesis steps]

Output: Follicular lymphoma prognosis


Input: treat with gentle chemo including rituximab when bulky, painful adenopathy organ system invovlement cytopenias severe B symptoms high FLIPI score [Name the erythropoesis steps]

Output: When to treat follicular lymphoma


Input: Origin is post germinal center memory B cell CD20+, CD5-, CD10- Arising in muscosal tissue of GI tract, tear duct, salivary gland, lung [Name the erythropoesis steps]

Output: Marginal zone lymphoma pathology


Input: Indolent Curable [Name the erythropoesis steps]

Output: Marginal zone lymphoma prognosis


Input: MALT lymphoma Extranodal marginal zone B cell lymphoma [Name the erythropoesis steps]

Output: Marginal zone lymphoma AKA


Input: Same as follicular Watch and wait until meets criteria [Name the erythropoesis steps]

Output: Marginal zone lymphoma treatment paradigm


Input: Marginal zone lymphoma arising from gastric mucosa Usually with H pylori infection H pylori antigens drive T cell activation, B cell clonal proliferation -->lymphoma Can be cured with H pylori antibiotic treatment Presents like a peptic ulcer [Name the erythropoesis steps]

Output: Gastric MALT lymphoma


Input: Unique cytoplasmic projections CD19, 20, 103 + CD 5, 10 negative In bone marrow looks like fried egg Trap IHC (tartrate acid phosphotase) [Name the erythropoesis steps]

Output: Hairy cell leukemia pathology


Input: Indolent lymphoma Cytopenias, fatigue, weight loss Splenomegaly [Name the erythropoesis steps]

Output: Hairy cell leukemia presentation


Input: 80% cure rate with Purine analog cladribine Rituxin for refractory/relapsed [Name the erythropoesis steps]

Output: Hairy cell leukemia treatment and prognosis


Input: Origin: small noncleaved cell of germinal center t(8;14) results in upregulation of myc oncogenes [Name the erythropoesis steps]

Output: Burkitt's lymphoma pathogenesis


Input: Diffuse infiltration of lymph node Small round cells with vesicular chromatin and nucleoli Lots of ineffective mitosis = macrophages = "starry sky" 19, 20, 10+, 5- [Name the erythropoesis steps]

Output: Burkitt's lymphoma pathology


Input: Highly aggressive High LDH, rapid doubling time Presents with bulky disease can involve CNS, bone marrow, extranodal sites [Name the erythropoesis steps]

Output: Burkitt's general features


Input: Sporadic Immunocompromised Endemic [Name the erythropoesis steps]

Output: Burkitt's subtypes


Input: Africa Jaw disease EBV related [Name the erythropoesis steps]

Output: Endemic Burkitt's


Input: AIDS associated Abdominal masses, marrow, lymph nodes 30% are EBV positive [Name the erythropoesis steps]

Output: Immunocompromised Burkitt's


Input: Children and young adults Abdominal masses, marrow, LNs 30% are EBV positive [Name the erythropoesis steps]

Output: Sporadic Burkitt's


Input: Live only weeks if not treated 80-90% cure early stage, 60-80% with advanced stage [Name the erythropoesis steps]

Output: Burkitt's course


Input: High LDH CNS involvement Bone marrow involvement Tumors >10 cm Immunocompromised Burkitt's [Name the erythropoesis steps]

Output: Poor prognostics in Burkitt's


Input: Origin: lymphocyte of inner mantle zone Looks like cleaved cell Nodal involvement either diffuse or expansion of mantle zone [Name the erythropoesis steps]

Output: Mantle cell lymphoma pathology


Input: t(11:14) upregulates bcl-1 which increased cyclin D1 production [Name the erythropoesis steps]

Output: Mantle cell lymphoma pathogenesis


Input: Looks indolent, isn't 5 year survival 30-50% Allogenic HSCT can prolong but not cure Autologous may also help [Name the erythropoesis steps]

Output: Mantle cell lymphoma course


Input: Less common More likely to be extranodal With nodal involvement are usually bad, and not as responsive to therapy as B cell [Name the erythropoesis steps]

Output: T cell lymphomas


Input: Indolent T cell lymphoma of the skin Incurable with slow course [Name the erythropoesis steps]

Output: Mycosis fungiodes


Input: T cell lymphoma Can have a 2;5 translocation with ALK gene ALK gene is a positive prognostic [Name the erythropoesis steps]

Output: Anaplastic large cell lymphoma


Input: Reed-Sternberg cell a minor population but diagnostic altered B cell CD15 and 30 positive Spread continguously via lymphatics [Name the erythropoesis steps]

Output: Hogkins's disease pathology


Input: Less common than NH lymphoma Biomodal age: late adolescents and 60s [Name the erythropoesis steps]

Output: HD epi


Input: Nodular sclerosis - most common neck/mediastinum, fibrous capsule and bands of expanding cells Lymphocyte predominant - neck limited disease, young adults Lymphocyte depleted - oft retroperitoneal aggresive Mixed celluarlity - very aggressive [Name the erythropoesis steps]

Output: HD subgroups


Input: 80% cure rate Dependent on stage, bulk, subtype ESR can be used as a marker of activity [Name the erythropoesis steps]

Output: HD course


Input: Radiation only for some stage I Abreviated Chemo + radiation [Name the erythropoesis steps]

Output: Treatment of stage I/II HD


Input: ABVD chemo, anthracylcine based Concerns: secondary malignancies (breast, lung, MDS, sarcoma) Cardiac tox of anthracyclines [Name the erythropoesis steps]

Output: Treatment of advanced stage HD


Input: Disease that grows through treatment or recurs in 6 months Often rapidly progressive to death [Name the erythropoesis steps]

Output: Primary refractory HD


Input: Treated like a large cell But still not curable [Name the erythropoesis steps]

Output: Follicular lymphoma grade 3


Input: Rituxan, cytoxan, vincristine, prednisone Fludarabine [Name the erythropoesis steps]

Output: Follicular lymphoma chemo


Input: Makes a 20+ different upfront in combo Maintenance therapy can improve PFS by 2 years [Name the erythropoesis steps]

Output: Rituximab in follicular lymphoma


Input: xrt to stomach rituximab [Name the erythropoesis steps]

Output: If antibiotics do not work for gastric MALT?


Input: Origin: immature T cells of thymus Diffuse infilitration of thymus Disease of teenagers, boys>girls Aggressive and curable (70%) [Name the erythropoesis steps]

Output: Precursor T cell lymphomas


Input: B symptoms Pruitis Alcohol induced pain [Name the erythropoesis steps]

Output: Systemic symptoms of HD


Input: Negative PET after 2 cycles [Name the erythropoesis steps]

Output: Intratreament prognostic for HD?


Input: 60-160x increased risk of NHL 25-40% lifetime risk Mostly with <100 CD4s (except Burkitts) Burkitt's, diffuse large cell, primary CNS, primary effusional [Name the erythropoesis steps]

Output: HIV and NH lymphoma


Input: Increased risk of marginal and diffuse B cell Treating Hep C sometimes results in remission Thought to be due to chronic antigenic stimulation [Name the erythropoesis steps]

Output: Hep C and NH lymphoma


Input: Acute lymphoblastic lymphoma/ lymphoblastic leukemia Either T or B cell blasts Say lymphoma if its less than 25% blasts in marrow and there is a mass [Name the erythropoesis steps]

Output: ALL


Input: 75% of cases are in <6 yo 80-85% are B cells in kids Of adult leukemias, ALL is 20%, 75% are B cell [Name the erythropoesis steps]

Output: ALL epi


Input: Marrow symptoms -- fatigue, infection, bleeding T cell precursor ALL may present with mediastinal mass [Name the erythropoesis steps]

Output: ALL presentation


Input: Blasts in marrow and cytopenias is periphery Myeloperoxidase negative TdT positive, myelperoxidase negative T : CD3, 7 B: CD10, 19 Many cytogenetic abnormalities [Name the erythropoesis steps]

Output: Pathology of ALL


Input: Better in kids: 80% cure Adults: 40% cure [Name the erythropoesis steps]

Output: ALL outcomes


Input: Rapid resistance is a problem Use multidrug induction and then long consolidation CNS prophylaxis with XRT or intrathecal chemotherapy -25% CNS relapse without Many adults need allogenic transplant to survive [Name the erythropoesis steps]

Output: ALL treatment


Input: Indolent course, not curable [Name the erythropoesis steps]

Output: Chronic lymphocytic leukemia/ small lymphocytic lymphoma


Input: CD5+, CD19+, CD23+ Not much Ig or CD20 10-, cyclinD1- [Name the erythropoesis steps]

Output: CLL flow profile


Input: Asymptomatic Male (2:1) > 50 (median is 65) Lymphocytosis with small mature lymphocytes or Adenopathy [Name the erythropoesis steps]

Output: CLL presentation


Input: With B symptoms Cytopenias Bulky/painful adenopathy Organ involvement Progressive splenomegaly, hepatomegaly Lymphocyte doubling time < 1 year [Name the erythropoesis steps]

Output: CLL when to treat?


Input: Infections due to immunocompromise Autoimmune disease ITP or hemolytic anemia Rickter's transformation to diffuse large cell [Name the erythropoesis steps]

Output: Complications of CLL


Input: Median is 9 years Rai criteria - clinical Cytogenetics : 17p is p53 loss-- BAD Mutation status of IgVh: unmutated heavy chain indicates less mature cell = more aggressive Surface markers: CD38, Zap70-- bad [Name the erythropoesis steps]

Output: Prognosis of CLL


Input: Prednisone, cyclophosfamide, fludaribine Rituximab [Name the erythropoesis steps]

Output: Treatment of CLL


Input: Either a progression from CML or de novo Use imatinib [Name the erythropoesis steps]

Output: Philadelphia chromosome in ALL


Input: Seen on smear Fragile cell gets destroyed by process Characteristic of CLL [Name the erythropoesis steps]

Output: Smudge cell


Input: Not yet Remember early treatment has not been shown to help [Name the erythropoesis steps]

Output: Do we treat CLL based on cytogenetics?


Input: CD52 monoclonal antibody Use late in CLL Problems with infections [Name the erythropoesis steps]

Output: Alemtuzumab


Input: Nitrogen mustard Used in CLL (in combos) [Name the erythropoesis steps]

Output: Bendumustine


Input: BAD prognosis less than a year [Name the erythropoesis steps]

Output: CLL refractory to fludarabine


Input: Another CLL transformation Larger cells, less distinct nucleoli, less dense chromatin Refractory [Name the erythropoesis steps]

Output: Prolymphocytoid transformation


Input: Serum protein elctrophoresis Separates proteins by size [Name the erythropoesis steps]

Output: SPEP


Input: Increases in the beta and or gamma regions Spikes for monoclonal, more generalized increases for polyclonal [Name the erythropoesis steps]

Output: Ig increases will be seen on serum protein elctrophoresis as?


Input: Infection, inflammation, reactivity [Name the erythropoesis steps]

Output: Polyclonal expansion states?


Input: Malignancy [Name the erythropoesis steps]

Output: Monoclonal expansion states?


Input: Can see light chains here Bence-Jones proteins when found in urine [Name the erythropoesis steps]

Output: Urine electrophoresis


Input: Parallel runs of electrophoresis Stain for different heavy chains and light chains Can characterize the gammaglobinopahy [Name the erythropoesis steps]

Output: Serum immunofixation


Input: Monoclonal gammaglobinopathy of unclear significance No symptoms, no lytic lesions, plasma cells in marrow <10% 25% of patients will get a hematologic disorder Increasing prevalence with age (1% at 50, 8% at 80) [Name the erythropoesis steps]

Output: MGUS


Input: Neoplasm of plasma cells Mature cells that have undergone class switching CD38 and 138 positive Il-6 is growth factor [Name the erythropoesis steps]

Output: Multiple myeloma


Input: Typically complex Deletion 13 is bad [Name the erythropoesis steps]

Output: Multiple myeloma cytogenetics


Input: Intact antibody Free light chain Both [Name the erythropoesis steps]

Output: Mutiple myeloma Ig products


Input: C - hypercalcemia R - renal failure A - anemia B - bone lesions I - infections [Name the erythropoesis steps]

Output: Multiple myeloma symptoms


Input: Il-6 and other cytokines increase osteoclast activity Increased osteoclast activity results in hpercalcemia [Name the erythropoesis steps]

Output: Pathogenesis of lytic lesions in mutliple myeloma


Input: Nausea Fatigue Renal insufficiency Constipation Mental status change [Name the erythropoesis steps]

Output: Symptoms of hypercalcemia


Input: 2% of multiple myelomas, mostly Ms and As related CNS symptoms, CHF, renal insufficiency, bleeding Can be fatal [Name the erythropoesis steps]

Output: Hyperviscosity syndrome


Input: Solid tumor of plasma cells Can be painful [Name the erythropoesis steps]

Output: Plasmacytoma


Input: 60% IgGs 20% IgAs - worse prognosis Few IgDs Rest are light chains [Name the erythropoesis steps]

Output: Distribution in Igs of multiple myeloma


Input: SPEP, UPEP xrays CBC Bun Bone marrow biopsy [Name the erythropoesis steps]

Output: Workup for multiple myeloma


Input: >4 bad [Name the erythropoesis steps]

Output: B-2-microglobulin and prognosis in multiple myeloma


Input: Big M spike Lots of plasma cells in marrow Hypogammaglobinemia Plasmacytoma Lytic lesions/end organ damage [Name the erythropoesis steps]

Output: Diagnosis of multiple myeloma


Input: Smoldering myeloma [Name the erythropoesis steps]

Output: Worse than MGUS but not multiple myeloma


Input: Not curable 7 months untreated 3-5+ years with treatment Remission, relapse pattern Cytogenetics, staging can predict [Name the erythropoesis steps]

Output: Multiple myeloma prognosis


Input: Alkylating agents and prednisone Bortezomab/velcade - nfKB thalidomide, lanolidomide - immune modulatory ( decrease Il-6, induce apoptosis, disruption of BM microenvironment) Radiation to lytic, plasmacytomas Autologous transplant? [Name the erythropoesis steps]

Output: Multiple myeloma treatment


Input: IgM disease Post germinal center memory cell Ranging from gammopathy to lymphoplasmacytic lymphoma with IgM Hyperviscosity syndrome is a problem - plasmaphorese [Name the erythropoesis steps]

Output: Waldenstrom Macroglobemia


Input: Only symptomatic Rituxin Cytoxan, fludarabine, prednisone relvlimid, velcade also active [Name the erythropoesis steps]

Output: Waldenstroma Macroglobemia treatment


Input: 1% per year [Name the erythropoesis steps]

Output: Risk of progression from MGUS to multiple myeloma


Input: IgA or IgM Serum IgM protein size Abnormal FLC ratio [Name the erythropoesis steps]

Output: Increased chance of MGUS progression


Input: 1% of new cancers 14% of hematologic malig Increases with age AA > caucasians [Name the erythropoesis steps]

Output: Multiple myeloma epi


Input: Light chain deposition in tissues With or without myeloma Prognosis is months if cardiac involvement Treat like myeloma [Name the erythropoesis steps]

Output: Amyloid AL


Input: Sausage-link, tortous retinal veins [Name the erythropoesis steps]

Output: Fundoscopic with hyperviscosity syndrome


Input: Filtering out WBC from blood units Must be <5 million Makes CMV safe Reduces febrile non-hemolytic transfusion reactions, HLA alloimmunization [Name the erythropoesis steps]

Output: Leukoreduction


Input: O and AB [Name the erythropoesis steps]

Output: Most/least frequent blood type


Input: AB [Name the erythropoesis steps]

Output: Universal plasma donator


Input: Rh, Kell, Kidd, Duffy... Need exposure to have antibodies Pregnancy is one way to get exposed [Name the erythropoesis steps]

Output: Non-ABO antigens


Input: Hemolytic transfusion reaction Hemolytic disease of the newborn Extravascular hemolysis [Name the erythropoesis steps]

Output: Complications of incompatibility


Input: Forward -- what will clump patients red cells Reverse - what will patients serum clump [Name the erythropoesis steps]

Output: ABO forward and reverse typing


Input: Looking for non-ABO antibodies Antigens on plate well Plasma Anti-Ig tagged antibody [Name the erythropoesis steps]

Output: Solid phase antibody screen


Input: Tests for ABO Add a little of patient serum to proposed donor sample If it clumps...don't use it [Name the erythropoesis steps]

Output: Immediate spin cross matching


Input: Test for non ABO Add donor red cells to patient serum Add anti-Ig antibody Look for clumping [Name the erythropoesis steps]

Output: Anti-globulin cross matching


Input: Symptomatic anemia Usually not necessary if over 10 Usually necessary if under 7 [Name the erythropoesis steps]

Output: Transfusion indications


Input: Age 60-80, transfuse below 9 40-60, below 8 4 m - 40 years, below 7 Below 10 with age and recent MI [Name the erythropoesis steps]

Output: Gray area RBC transfusion recommendations


Input: Correction of low or dysfunctional platelets Prophylaxis: in hospital <5, out patient <20 Treatment of microvascular bleeding 2/2 uremia or plt harming drugs with Massive Transfusions [Name the erythropoesis steps]

Output: Platelet transfusion indications


Input: replacement of coagulation factors Prophy with abnormal coag studies Treat microvascular bleeding with abnormal coag studies THIS DOES NOT SEEM TO WORK [Name the erythropoesis steps]

Output: FFP indications


Input: 1 g/dl [Name the erythropoesis steps]

Output: How much does hemoglobin go up in response to 1 unit of PRBCs


Input: 10-30K [Name the erythropoesis steps]

Output: How much does plt ct go up in response to unit of plts


Input: More likely to have a fatal hemolytic transfusion reaction [Name the erythropoesis steps]

Output: Risk of contracting HIV vs fatal hemolytic transfusion rxn?


Input: Red blood cells [Name the erythropoesis steps]

Output: Hemolytic transfusion reactions are reactions against?


Input: Plasma proteins Anaphylactic Anaphylactoid Allergic [Name the erythropoesis steps]

Output: Hypersensitivity transfusion reactions are against what? types?


Input: Febrile transfusion reactions Alloimmunization Transfusion related acute lung injury Graft vs host disease Immunomodulation [Name the erythropoesis steps]

Output: Transfusions complications related to WBCs


Input: Reaction against platlets [Name the erythropoesis steps]

Output: Post transfusion purpura


Input: 3-3.5% [Name the erythropoesis steps]

Output: Risk of some type of transfusion reaction?


Input: Stop the transfusion Evaluate and treat patient Send labs (bili, haptogloben, cbc) also on transfused blood Check for clerical errors Collect first urine [Name the erythropoesis steps]

Output: What to do when a transfusion rxn happens?


Input: Antibodies in plasma recognize antigens on red cells Phagocytes are activated Systemic activation of immune response [Name the erythropoesis steps]

Output: Pathogenesis of acute hemolytic transfusion reaction


Input: Antibody titers Antibody class Antigen concentration on cells Antigen position on cells Number of cells transfused [Name the erythropoesis steps]

Output: Factors effecting extent of hemolytic transfusion reaction


Input: Fever, chills - Il-1, 6, TNFalpha Shock, inflammatory response- complement (C3a, 5a), bradykinin DIC -- coagulation cascade, thrombin Kidney failure [Name the erythropoesis steps]

Output: Components of hemolytic transfusion reaction and mediators


Input: Hypotension - acute tubular necrosis Immune complex glomerulonephritis DIC -glomerular capillary thrombosis Free Hgb-- leads to tissue damage and ischemia [Name the erythropoesis steps]

Output: Pathogenesis of kidney failure in hemoytic transfusion reaction


Input: Can be asymptomatic Fever, chills Pain at iv site Red urine DIC Back (kidney) pain N/V Hypotension [Name the erythropoesis steps]

Output: Signs and symptoms of acute immune hemolysis


Input: 6% die 41% have morbility but survive 47% have no adverse effects [Name the erythropoesis steps]

Output: Outcomes of ABO mismatch transfusions


Input: 50% administrative errors 30% technical errors [Name the erythropoesis steps]

Output: What is responsible for fatal transfusion reactions?


Input: Occur 5-14 days later Either a primary response to antigen or amnestic response with a latent population of memory cells Fever, chills, signs of extravascular hemolysis New alloantibody seen in serum Rarely needs treatment [Name the erythropoesis steps]

Output: Delayed hemolytic transfusion reactions


Input: Non intially With transfusion, antibodies made Antibodies attach to RBCs (direct Coombs positive) More antibodies made, cells begin to lyse (direct and indirect positive) All cells destroyed, antibodies in blood (indirect positive, direct negative) [Name the erythropoesis steps]

Output: Explain antibodies in delay hemolytic transfusion reaction


Input: New antibodies detectable after transfusion but not hemolysis [Name the erythropoesis steps]

Output: Delayed serologic transfusion reaction


Input: Reaction to plasma proteins Happens 1-3% of time Uticaria, flushing, puritis, wheezing dyspnea [Name the erythropoesis steps]

Output: Allergic transfusion reactions


Input: Stop transfusion Give antihistamine Give steroids Give albuterol by neb [Name the erythropoesis steps]

Output: Treating allergic transfusion reactions


Input: Reaction to IgA or other plasma protein Occurs 1 in 20K or 50K Dyspnea, larygneal edema, cynanosis, n/v/d, hypotension, shock, deah [Name the erythropoesis steps]

Output: Anaphylactic or analphylactoid transfusion reactions


Input: Stop transfusion, eval patient Give epinepherine, antihistamines, steroids Support respiration and BP [Name the erythropoesis steps]

Output: Treating anaphylactic or analphlactoid transfusion reaction


Input: IgA deficiency 1 in 700 May have antibodies against all IgAs or a subtype that they are missing Allergies to products that can be in blood (penicillin) [Name the erythropoesis steps]

Output: Increased susceptibility to anaphylacic transfusion reaction


Input: Autologus Wash cells, plts Use IgA deficient donors [Name the erythropoesis steps]

Output: What do you do when a patient who has known anti-IgA needs a transfusion


Input: Reaction to WBCs Increase of 1C or 2F, chills, rigors, HA, n/v Happens in 1% of RBCs, more in plts -- less with leukoreduced [Name the erythropoesis steps]

Output: Febrile transfusion reaction


Input: Stop transfusion Rule out hemolysis Give antipyretics Steriods meperdine [Name the erythropoesis steps]

Output: Treating ferbile transfusion reaction


Input: Classic -- recipients antibodies attack antigens on donor WBCs Immune complex -- recipients antibodies react with antigens/proteins in donor and stimulate macrophages Cytokines -- donor macrophages produce cytokines in storage, which are transfused in [Name the erythropoesis steps]

Output: Mechanisms of febrile transfusion reaction


Input: transfusion related acute lung injury Donor antibodies, recipient cells, host actors = bilateral lung infiltrates Like ARDS but only 10% mortality [Name the erythropoesis steps]

Output: TRALI


Input: Donor antibodies lead to complement activaiton--->C5a ---> PMNs that activate and damage pulmonary vascular bed (also other vasculatures probably) [Name the erythropoesis steps]

Output: Pathophysiology of TRALI


Input: multiparous women recipients of multiple transfusions [Name the erythropoesis steps]

Output: Donors at risk for causing TRALI


Input: [1] element [2]

Output: a substance that cannot be broken down into other substances by chemical reaction

Biology Chapter 2: The Chemical Context of Life Flashcards - Cram.com


Input: [1] compound [2]

Output: a substance consisting of two or more different elements combines in a fixed ratio

Biology Chapter 2: The Chemical Context of Life Flashcards - Cram.com


Input: [1] essential element [2]

Output: a chemical element required for an organism to survive, grow, and reproduce

Biology Chapter 2: The Chemical Context of Life Flashcards - Cram.com


Input: [1] trace element [2]

Output: an element indispensable for life but required in extremely minute amounts

Biology Chapter 2: The Chemical Context of Life Flashcards - Cram.com


Input: [1] atom [2]

Output: the smallest unit of matter that retains the properties of that element

Biology Chapter 2: The Chemical Context of Life Flashcards - Cram.com


Input: [1] neutrons [2]

Output: a subatomic particle having no electrical charge (electrically neutral) with a mass of about 1.7x10^-24g. Found in the nucleus of an atom

Biology Chapter 2: The Chemical Context of Life Flashcards - Cram.com


Input: [1] protons [2]

Output: a subatomic particle with a single positive electrical charge, with a mass of about 1.7x10^-24g. found in the nucleus of an atom.

Biology Chapter 2: The Chemical Context of Life Flashcards - Cram.com


Input: [1] electrons [2]

Output: a subatomic particle with a single negative charge and a mass of about 1/2,000 that of a neutron or proton. One or more electrons move around the nucleus of an atom.

Biology Chapter 2: The Chemical Context of Life Flashcards - Cram.com


Input: [1] atomic nucleus [2]

Output: an atom's dense central core, containing protons and neutrons.

Biology Chapter 2: The Chemical Context of Life Flashcards - Cram.com


Input: [1] dalton [2]

Output: atomic mass unit 1.6605x10^-27g

Biology Chapter 2: The Chemical Context of Life Flashcards - Cram.com


Input: [1] atomic number [2]

Output: the number of protons in the nucleus of an atom unique for each element and designated by a subscript to the left of the elemental symbol

Biology Chapter 2: The Chemical Context of Life Flashcards - Cram.com


Input: core business requirements

Output: What is a core concern?

Spring Practice Chapter 5 Flashcards - Cram.com


Input: 1) code tangling. Having to handle multiple concerns as well as the core calculation logic at the same time. This will lead to poor code maintainability and reusability. 2) Code Scattering. Repeat the same statements (i.e. logging) multiple times in multiple modules to fulfill a single requirement. Later, if the logging criteria change, you would have to modify all of the modules. Moreover, it is also hard to ensure that the logging requirement will be implemented consistently. If you have missed a logging statement somewhere, the overall system logging will be inconsistent.

Output: What are the two main problems caused by non-modularised crosscutting concerns?

Spring Practice Chapter 5 Flashcards - Cram.com


Input: You can apply a design pattern called proxy to separate crosscutting concerns from core concerns. Proxy is one of the 23 GoF (Gang of Four) object-oriented design patterns, which belong to the “structural pattern” category. The principle of the proxy design pattern is to wrap an object with a proxy and use this proxy to substitute for the original object. Any calls that were made to the original object will go through the proxy first.

Output: What design pattern can you use to assist with implementing crosscutting concerns?

Spring Practice Chapter 5 Flashcards - Cram.com


Input: It supports creating a proxy dynamically for any object. Dynamic proxies are implemented with the Java Reflection API, so they can be used in a more general way than static proxies. For this reason, dynamic proxy is one of the core technologies used by Spring for its AOP implementation.

Output: What is a dynamic proxy?

Spring Practice Chapter 5 Flashcards - Cram.com


Input: The crosscutting action to take at a particular execution point is encapsulated in an advice

Output: What is an advice?

Spring Practice Chapter 5 Flashcards - Cram.com


Input: 1) Before Advice (before method execution) 2) After returning advice (After the method returns a result) 3) After throwing advice (After the method throws an exception) 4) Around advice (Around the method execution)

Output: What types of advices does Classic Spring AOP support?

Spring Practice Chapter 5 Flashcards - Cram.com


Input: Advices are written by implementing one of the proprietary advice interfaces

Output: How are advices written using the classic Spring AOP approach?

Spring Practice Chapter 5 Flashcards - Cram.com


Input: MethodBeforeAdvice

Output: In classic Spring AOP, what interface do you implement to use before advice?

Spring Practice Chapter 5 Flashcards - Cram.com


Input: AfterReturningAdvice

Output: What interface do you need to implement for after returning advice?

Spring Practice Chapter 5 Flashcards - Cram.com


Input: ThrowsAdvice

Output: What interface do you need to implement to handle throwing advice?

Spring Practice Chapter 5 Flashcards - Cram.com


Input: -ACTH -melanocyte stimulating hormone -somatotropic (growth and prolactin) -glycoprotein (FSH and LH-testosterone stimulation) -TSH (thyroid stimulating) [Anterior pituitary located...]

Output: anterior pituitary secretes...

Pathophysiology Chapters 17, 18, 28, 29, 30, 25, 26, 27, 33, 34, 35 Flashcards - Cram.com


Input: stimulates uterus contractions and ejection of milk [Anterior pituitary located...]

Output: oxytocin

Pathophysiology Chapters 17, 18, 28, 29, 30, 25, 26, 27, 33, 34, 35 Flashcards - Cram.com