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203 Cards in this Set
- Front
- Back
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what are the 3 cell types derived from pluripotent stem cells
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proerythrocyte, myeloid stem cells, lymphoid stem cell
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myeloblast cell line is derived from what, and differentiates into what 3 cells lines?
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derived from myeloid stem cells, goes to neutrophils, eosinophils, and basophils
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monoblast cell line is derived from what, and generates what cells?
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derived from myeloid stem cells, goes to monocytes
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megakaryoblasts are derived from what? And generate what?
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derived from myeloid stem cells, and go to megakaryocytes and ultimatley platelets
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what 3 cell lines are derived from myeloid stem cells?
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myeloblast, monoblast, and megakaryoblast
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lymphoid stem cells differentiate into what cell lines?
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to lymphoblasts and then to B and T cells and to Plasma and activated T cells
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what is the WBC differential in terms of highest concentration to lowest?
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Neutrophils Lmphocytes, monocytes, eosinophils, Basophils (Neutrophiles Like Making Everything Better)
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Survival time of erythrocyte
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120 days
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Define anisocytosis, poikilocytosis, reticulocytosis
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RBCs varying sizes, varying shapes, immature erythrocytes
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what are the granulocytes
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basophils, eosinophils, neutrophils
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Describe morphology and features of: Basophils
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Bilobed nucleus with dense basophilc granules contain heparin, histamine, leukotrienes. Found in blood- mediates allergic reaction- binds IgE
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Describe morphology and features of: mast cells
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similar to basophils- connective tissue, granules contain histamine, heparin, eosinophil chemotactics, binds IgE- mediates type I allergic reaction- Chromium Na helps prevent mast cell degranulation (Asthma)
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Describe morphology and features of: eosinophils
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bilobed nucleus with eosinophilic granules. Defens helminth and protazoan infections (MBP)- produces histamine and arylsulfatase
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Describe morphology and features of: neutrophils
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multilobed nucleus with azurophilic granules. Myeloperoxidase. 40-70% WBCs, lysosomes contain bactericidal lysozyme
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Describe morphology and features of: monocytes
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large kidney shaped nucleus, frosted glass cytoplasm--> differentiates into macs in tissue
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Describe morphology and features of: macrophages
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only in tissues- ameboid bacteria. Activated by gamma- interpheron and is an APC. Secrete IL1 IL-2, TNF-alpha
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Describe morphology and features of: dendritic cells
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professional APCs express MHC II and Fc receptor on surface. Main inducers of primary Ab respnse- called Langerhans cells in skin
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Describe morphology and features of: lymphocytes
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Round dense nucleus
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Describe morphology and features of: b cell
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matures in marrow, migrates to lymphoid tissue. CD19/CD20
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Describe morphology and features of: t cell
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originates in marrow, matures in thymus.
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Describe morphology and features of: plasma cell
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off-center nucleus with cloack-face chromatin distribution, abundant RER and golgi. Multiple myeloma is plasma cell neoplasm.
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5 causes of eosinophilia:
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NAACP Neoplastic, Asthma, Allergic processes, Collagen vascular disease, Parasites
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what is the common intersection in the coagulation cascade (extrinsic and intrinsic)
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X to Xa
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what test tests the intrinsic pathway?
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PTT
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what test tests the extrinsic pathway?
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PT (PeT Extrinsic)
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what are the vitamin K clotting factors: and what is the effect on PT, PTT
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2,7,9,10, C, S, prolonged PT, PTT (2 and 10 are common)
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what are the factors in the intrinsic pathway?
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XII, XI, IX, VIII, X, II (prothrombin) --> thrombin (Ia), I (fibrinogen) ---> Ia (fibrin) clot
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what are the factors in the extrinsic pathway?
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VII + tissue factor, X, II (prothrombin) --> thrombin (Ia), I (fibrinogen) ---> Ia (fibrin) clot
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tPa does what?
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cleaves plasmin from plasminogen which cleaves clots
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antithrombin III inactivaes what factors?
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thrombin (Iia), Ixa, Xa, Xia- this is activated by heparin
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what does protein C do? What activates protein C
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thrombomodulin activates protein C (with protein S) -->activated protein C --> inactives Va, and VIIIa.
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what is the result of Factor V Leiden mutation?
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resistance to activated protein C--> increase PT PTT
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how do you monitor heparin efficacy and safety? Tx for overdose?
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PTT, IV protamine sulfate
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how do you monitor warfarin efficacy and safety? Tx for overdose?
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PT, Vitamine K
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describe the formation of platelet plug. 3 main steps
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platelet adhesion to exposed basement menbrane (requires vWF), Aggregation - TXA2 released by platelets (increase agg) or PGI2 and NO released by endothelial cells (decr. Aggregation), swelling and ADP and Ca+ release to strengthen plug via fibrin deposition
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what factor released by plateless increases aggregation?
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TXA2 (ASA blocks)
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what factor released by endothelial cells decreasses aggregation?
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PGI2 (prostacyclin) and NO
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what are mechanisms of drugs to block platelet aggregation?
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block vWF with receptor antagonist, ASA blocks TXA2, ticlopigine and clopidogrel block platelet ADP receptors, tissue factor antagonists, thrombin inhibitors
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blood goup of universal recipient
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AB (no abs against others)
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blood group of universal donor
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O (no surface antigens)
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disease(s) with RBC disorder: spherocytes
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herditary spherocytosis, autoimmune hemolysis
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disease(s) with RBC disorder: helmut cell, schistocyte
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DIC, traumatic hemolysis
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disease(s) with RBC disorder: bite cell
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G6PD deficinecy
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disease(s) with RBC disorder: teardrop cell
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myeloid metaplasia with myelofibrosis
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disease(s) with RBC disorder: acanthocyte
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spiny appearance seen in abetalipoproteinemia
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disease(s) with RBC disorder: Target cell
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HbC disease, Asplenia, Liver diseas, thalassemia HALT
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disease(s) with RBC disorder: poikilocytes
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TTP/HUS, microvascular damage, DIC
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disease(s) with RBC disorder: burr cell
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TTP/HUS, microvascular damage, DIC
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disease(s) with RBC disorder: basophilic stippling
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Thalassemias, Anemia of chronic disease, Iron deficiency, Lead poisoning TAIL
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define aplastic anemia
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pancytopenia with severe anemia, neutropenia, and thrombocytopenia caused by failure of multipotent myeloid stem cells.
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causes of aplastic anemia:
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radiation, chloramphenicol, alkylating agents, antimetabolites, viral agents (parvoB19, HIV, EBV), fanconi's anemia, post hepatitis.
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pathologic features of aplastic anemia
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pancytopenia with normal cell morphology, hypocellular BM with fatty infiltrate.
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most common mutation for sickle cell anemia
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single aa replacement in B-chain from GLU to VAL.
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complications in HbS homozygotes
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aplastic crisis (parvoB19) autosplenectomy, encapsulated infections, salmonella osteomuelitis, vaso-occlusive crisi, renal papillaru necrosis, splecin sequestration crisis.
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treatment fro HbS
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hydroxyurea (increase HbF) and bone marrow transplant
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crew cut on skull x-ray is due to marrow expansion from increased erythropoiesis in what diseases?
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HbS, and thalassemias
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what populations is alph-thalassemia prevelant in?
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Asia and Africa
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what populations is beta-thalassemia prevelant in?
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Mediterranean
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what is the makeup of HbH?
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alpha thalassemia with B4 tetramers because you only have 1 good copy of alpha globin
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what is the makeup of Hb Barts?
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get gamma4 tetramers, lack all 4 alpha genes and results in hydrops fetalis and intrauterin fetal death
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beta-thalassemia minor:
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heterozygote - beta chain underproduced. - fetal increased
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beta-thalassemia major:
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homozygote- no beta gene- severe anemia requiring blood transfusions and cardiac failure due to secondary hemochromatosis. Fetal increased
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common findings in all hemolytic anemias
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increase serum bilirubin (jaundice, pigmented gallstones), increase reticulocytes (marrow compensation)
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antibodies in cold vs warm autoimmune anemia
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cold = IgM (triggered by cold, mycoplasma pneumoniae, mononucleosis), warm= IgG (SLE, CLL, drugs)
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direct coombs test:
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anti-Ig AB added to patient's RBCs --> agglutinate if RBCs are coated with Ig
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indirect coombs test
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normal RBCs added to patient's serum --> agglutinate if serum has anti-RBC surface Ig
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autoummine hemolytic anemia test:
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Coombs
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hereditary spherocytosis test:
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osmotic fragility test - coombs is negative
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defect causing hereditary spherocytosis
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intrinsic- spectrin or ankyrin defect- cells are small and round - increase MCHC and RDW.
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Howell-Jolly bodies present after splenectomy: disorder?
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hereditary spherocytosis
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increase urine hemosiderin: diseas?
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paroxysmal nocternal hemoglobinuria
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defect in paroxysmal nocternal hemoglobinuria
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membrane defect--> increase sensitivity of RBCs to the lytic activity of complement (impaired synthesis of GP I anchor in RBC membran)
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Microangiopathic anema: caused by what diseases and what finding on smear?
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DIC/ TTP/HUS/ SLE, malignant hypertension- schistocytes (helmet cells) on smear
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Causes of DIC
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Sepsis (gram -), trauma, obstetrics, acute Pancreatitis, Malignancy, Nephrotic syndrom, Transfusions : STOP Making New Thrombi!
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findings in DIC (lab)
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increase PT, PTT, fibrin split products (D-dimer), decrease platelet count. Helmet shaped cells and schistocytes on smear
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findings in microhemorrhage:
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platelet abnormalities- mucous membrane bleeding, epistaxis, petechia, purpura, increase bleeding time
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findings in macrohemorrhage:
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coagulation factor defects- hemarthrosis (bleeding into joints), easy bruising, increase PT and/or PTT
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defect in Hemophilia A
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factor VIII
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defect in hemophilia B
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facttor IX
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defect in von Willebrand's disease
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mild- most common bleeding disorder, deficiency of vWF--> defect of platelet adhesion and decrease factor VIII survival
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hemorrhagic disorders with: platelet: down BT: up PT: - PTT:-
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thrombocytopenia and Bernard-Soulier diseas (defect in platelet adhesion)
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hemorrhagic disorders with: platelet: - BT: - PT: - PTT: up
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hemophilia A/B
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hemorrhagic disorders with: platelet: - BT: up PT: - PTT: up
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vWB disease
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hemorrhagic disorders with: platelet: down BT: up PT: up PTT: up
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DIC
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hemorrhagic disorders with: platelet: - BT: - PT: up PTT: up
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Vitamine K deficiency
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hemorrhagic disorders with: platelet: - BT: up PT: - PTT:-
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Glanzmann's thrombasthenia = defect of platelet aGgegration (decrease GP Iib and IIIa)
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levels for bleeding in thrombycytopenia or platelet count:
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Thrombo <100,0000 platelets 15-20,000
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Reed sternberg cells are necessary for the diagnosis of what disease?
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Hodkin's disease- but not sufficient- giant tumor cell with binucleate or bilobed with mirror images (owls eyes).
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features of Hodgkin's lymphoma
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Reed-sternberg cells, localized single group of nodes (vs non-hodgkins), B-signs- low fever, night sweats, weight loss, mediastinal lymphadenopathy- 50% cases with EBV- young and old. Good prognosis if increase lymphocytes and decrease RS
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features of non-hodgkins's lymphoma
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HIV and immunosuppression, multiple peripheral nodes (vs hodgkin's), majority involve B cells, no hypergammaglobulinema, fewer signs and peak incidence 20-40 years.
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most common type of Hodkin's lymphoma
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nodular sclerosing (65-75%) excellent prognosis (RS+, Lymphs +++) young adults
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bence jones protein = what disease
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multiple myeloma
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what type of Ig do multiple myelomas produce
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IgG 55%, IgA 25%.
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most common primary tumor arising within bone in elderly?
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multiple myeloma
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what disease is associated with a monoclonal spike (M protein) on serum protein electrophoresis?
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multiple myeloma
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what disease has RBCs stacked on blood smear?
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multiple myeloma
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what are the findings in multiple myeloma?
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IgG, or IgA, bence jones , M protein spike, hypercalcemia with destructive bone lesions. Renal insufficiency, increase infections and anemia. Associated with primary amyloidosis and punched-out lytic bone lesions on X-ray
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findings of a leukemoid reaction:
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increas with left shift (80% bands) and increase leukocyte alkaline phosphatase
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what type of lymphoma is burkitts
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non-hodgkin's lymphoma
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which non-hodgkin's lymphomas are more common in children?
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burkitts (b cell) and lymphoblastic lymphoma (t cell, most common in children)
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most common non-hodgkin's lymphoma in children? Adults?
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children = lymphoblastic, adults= follicular lymphoma
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starry sky appearance (sheets of lymphs with interspersed macs), associated with EBV, jaw lesions in endemic form in africa, pelvis in sporadic form: disease?
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burkitt's lymphoma
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chromosomal translocation: t(9,22)
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philadelphia CreaML cheese (CML) bcr-abl
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chromosomal translocation: t(8:14)
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Burkitt's lymphoma (c-myc activation)
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chromosomal translocation: t(14:18)
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Follicular lymphomas (bcl-2 activation)
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chromosomal translocation: t(15:17)
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M3 type of AML (responds to all-tans RA)
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children, lymphoblasts, TdT, most respnsive to therapy, may spread to CNS and testes: disease?
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ALL
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auer rods, myeloblasts, adults
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AML
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older adults, lymphadenopathy, Hsmegaly, few symptoms, increase smudge cells in peripheral bloos smear, warm antibody hemolytic anemia, similar to ALL: disease?
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CLL
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defined by philadelphia chromosome, myeloid stem cell proliferation, increase neutrophils and metamyelocytes, splenomegaly, may accelerate to AML. Very low leukocyte alkaline phosphatase.
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CML
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Ages of the 4 main leukemias:
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<15 = ALL, 5-40=AML, 30-60= CML, >60= CLL
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what are auer rods?
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peroxidase positive cytoplasmic inclusions in granulocytes and myeloblasts. Acute promyelocytic leukemia. Treatment of AML M3 can release auer rods leading to DIC
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Histiocytosis X: features:
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langerhans cells infiltrate lung. Birbeck granules (tennis racket on EM) affects young adults, worse with smoking
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MOA of heparin:
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catalyzes the activation of antithrombin III, decrease thrombin and Xa. Follow PTT
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Aes for heparin
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bleeding, thrombocytopenia, osteoporosis, drug-drug. Overdose tx w/ protamine sulfate (positive charge binds )
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MOA for lepirudin, bivalirudin=
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hirudin derivatives that directly inhibit thrombin. Alternative to heparin for patients with HIT
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MOA warfarin
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interferes with synthesis and gamma-carboxylation of vitamin K clotting factors. Metabolized by cytochrome p-450, effects extrinsic pathway (increase PeT) long 1/2 life
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AE's for warfarin
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bleeding, teratogenic, skin/tissue necrosis, drug-drug
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which passes placenta: warfarin or heparin
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warfarin duh
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4 thrombolytics
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streptokinase, urokinase, tPA (alteplase), APSAC (anistreplase)
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MOA of thrombolytics in general
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direct/indirect conversion of plasminogen to plasmin which cleaves thrombin and fibrin clots. Increase PT, PTT no change in platelet count.
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Toxicity of thrombolytics:
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bleeding- contraindicated in pts with active bleeding, history of intracranial bleeds, recent surgery, severe hypertension. Tx toxicity with aminocaproic acis, inhibitor of fibrinolysis.
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MOA of ASA
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acetylates and irreversibly inhibits COX-1/2 to prevent conversion of arachidonic acid to thrombaxane A2. bleeding time increased. No effect on PT or PTT
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clinical use of ASA
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antipyretic, ,analgesic, anti-inflammatory, anti-platelet
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Aes for ASA
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gastric ulceration, bleeding, hyperventilation, Reye's syndrome, tinnitus (CN VIII)
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MOA for clopidogrel or ticlopidine
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the clopids= inhibit platelet aggregation by irreversibly blocking ADP receptors on platelet. Inhibit fibrinogen binding by preventing glycoprotein Iib/IIIa expression
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clinical use of clopidogrel
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acute coronary syndrom, coronary stenting, decrease incidence or recurrence of thrombotic stroke.
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toxicity of ticlopidine
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neutopenia
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MOA for abciximab
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mab binds glycoprotein receptor Iib/IIIa on activated platelets, preventing aggregation
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toxicity of abciximab
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bleeding , thrombocytopenia
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3 cancer drugs that work at protein level:
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tamoxifen, vinca alkaloids (inhibit microtubule formation), paclitaxel- inhibits microtubule disassembly
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cell cycle specific cancer drugs:
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antimetabolites (MTX, 5-FU, 6-MP), etoposide, bleomycin, vinca alkaloids, paclitaxel
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cell cycle non-specific cancer drugs:
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alkylating agents, antibiotics (dactinomycin and doxorubicin)
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which cancer drugs work during S phase?
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antimetabolites, etoposide
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which cancer drugs work during M phase?
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vinca alaloids and taxols
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which cancer drugs work during G2 phase?
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etoposide and bleomycin
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MOA methotrexate
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S-phase specific antimetabolite. Folic acid analog inhibits dihydrofolate reductase, resulting in decreased dTMP- DNA, protein synthesis
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Toxicity of methotrexate:
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myelosuppression which is reversible with leucovorin (folinic acid). Macrovascular fatty change in liver. Mucositis
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MOA 5-fluorouracil 5-FU
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S-phase antimetabolite. Pyrimidine analog activated to 5F-dUMP, which covalently complexes folic acid - inhibts thymidylate synthase, resulting in decrease dTMP.
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Toxicity of 5-FU
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myelosupression which is NOT reviersible with leucovorin, photosensitivity. Rescue with thymidine
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MOA 6-mercaptopurine 6-MP
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blocks de novo purine synthesis. Activated by HGPRTase
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Toxicity of 6-MP
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bone marrow, GI, Liver. Metabolized by xanthine oxidase- thus increase toxicity with allopurinol
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MOA cytarabine, toxicity:
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inhibits DNA polymerase; leukopenia, thrombocytopenia, megaloblastic anemia
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MOA cyclophosphamide
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alkylating agent, covalently x-link DNA at guanine N-7. requires bioactivation by liver
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toxicity cyclophosphamides ifosfamide
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myelosuppression, hemorrhagic cyctitis which can be partially prevented with mesna
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MOA/toxicity nitrosoureas
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alkylating DNA. Require bioactivation, cross BBB--> CNS where is can cause dizziness, ataxia
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MOA/toxicity cisplatin, carboplatin
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act as alkylating agents; nephrotoxic and acoustic nerve damage
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MOA/toxicity busulfan
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alkylates DNA; pulmonary fibrosis, hyperpigmentation
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MOA doxorubicin
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generates free radicals and noncovalently intercalate in DNA (breaks in DNA to decrease replication)
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Toxicity doxorubicin
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cardiotoxic, myelosuppression and alopecia. Toxic extravasation?
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Dactinomycin MOA/toxicity/uses (actinomycin D)
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intercalates DNA; myelosupression; Wilm's, Ewing's sarcoma, rhabdomyosarcoma Actinomycin D for childhood tumors that ACT out
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MOA bleomycin
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free radicals cause breaks in DNA strands
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toxicity bleomycin
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pulmonary fibrosis, skin changes, minimal myelosuppression
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MOA hydroxyurea- uses/ AE's?
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inhibits Ribonucleotide Reductase -->decrease DNA synthaesis (S-phase specific); melanoma, CML, sickle cell; bone marrow suppression, GI upset
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Etoposide MOA
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G2-specific agent inhibits topo II and increases DNA degredation.
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Toxicity Etoposide
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myelosuppression, GI upset, alopecia
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MOA prednisone as cancer drug
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triggers apoptosis, even on nondividing cells
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Toxicity prednisone
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cushing-like, immunosuppression, cataracts, acne, osteoporosis, HTN, peptic ulcers, hyperglycemia, psychosis
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MOA tomoxifen, raloxifen
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receptor antagonist in breast, agonist in bone, block estrogen binding in ER+ cells
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Toxicity tomoxifen, raloxifen
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increase risk of endometrial carcinoma via partial agonist effect. "hot flashes". Raloxifen does not cause endometrial carcinoma because it is an endometrial antagonist
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MOA trastuzumab (herceptin) and toxicity
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mab against HER-2 through antibody-dependent cytotoxicity; cardiotoxic
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MOA/Uses/toxicity with imatinib (gleevac)
|
philadelphia chromosome brc-abl tyrosine kinase inhibitor; CML, GI stromal tumors; fluid retention
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MOA vincristine, vinblastine
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M-phase specific alkaloids that bind tubulin and block polymerization of microtubules.
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toxicity vincristine, vinblastine
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vincristine- neirotoxic, paryltic ileus, vinblastine - bone marrow suppression
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MOA paclitaxel, toxicity
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M-phase specific agent binds tubulin and hyperstabilize polymerized microtubules so that mitotic spindle cannot break down; myelosuppression, hypersensitivity
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C3 deficiency leads to increased susceptability of what organism?
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staph aureaus
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C6,7,8 deficiency leads to increased susceptability to which organism
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neisseia gonorrhea and menengitis
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blood smear: hyper segmented neutrophil
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folate/B12 deficiency
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blood smear: burr cells
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uremia
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blood smear: microspherocytes
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coombs hemolysis
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blood smear: schistocytes
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DIC/TTP/HUS
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blood smear: target cells
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liver disease, thalassemia
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blood smear: spur cells (acanthocytes)
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liver disease, abetalipoproteinemia
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blood smear: Howell-Jolly bodies
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asplenia
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blood smear: heinz bodies
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G6PD def.
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blood smear: teardrop cells
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myeloid metaplasia with myelofibrosis
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which microcytic anemia has low serum ferritin?
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Iron-deficiency anemia
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which microcytic anemia has low TIBC?
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anemia of chronic disease
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which microcytic anemia has high serum Fe
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sideoblastic anemia
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what disease produces heterophile antibodies directed against horse, sheep, bovine RBCs?
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EBV infectious mononucleolus
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B cell receptor for EBV?
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CD21
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what cells produce EPO?
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endothelial cells of peritubular capilaries
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what is the end product of heme degredation in the macrophage?
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uncobjugated bilirubin
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most common cause of sideroblastic anemia?
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alcohol- damages heme biosynthesis pathways in mitochondria
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most common cause of pyridoxine deficiency leading to sideroblastic anemia- and why?
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INH - B6 is a cofactor in ALA synthase which is the rate limiting step of what? You guessed it.
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lab finding in extravascular hemolysis:
|
increase unconjugated hyperbilirubinemia
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lab finding in intravascular hemolysis:
|
decrease haptoglobin, hemoglobinuria
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defect in PNH:
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loss of anchor for DAF (neutralizes complement attatched to RBCs). Occurs at night because resp. acidosis enhances complement attatchment
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PNH screen and confirmation tests
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sucrose hemolysis test, acidified serum test.
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leukoerythroblastic reaction: what is that? Most common cause?
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immature bone marrow cells enter ther peripheral blood. MCC = woman >50 = metastatic breast cancer = tear drop RBCs
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most common leukemia overall
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CLL
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most common metastasis to left supraclavicular node:
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stomach or pancreatic carcinoma
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most common malignant lymphoma
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NHL
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what is mycosis fungiodes?
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neoplasm of CD4+ Th cells, skin involvement
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anterior mediastinal mass + single group of nodes above diaphragm:
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nodular sclerosing hodgkin's lymphoma
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extrinsic system factor:
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VII
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intrinsic system factors:
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XII, XI, IX, VIII
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functions of vWF
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platelet adhesion- prevents degredation of VIII: C
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PGI2 function in hemostasis:
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vasodilator, inhibits platelet aggregation
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TXA2 function in hemostasis:
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vasoconstrictor, activates platelet aggregation
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serum vs plasma
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serum = spun down = no clotting factors
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4 steps to platelet sequence in hemostasis
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adhesion, release aggregating agents, synthesis of TXA2, temporary plug---(with clotting factors develops a stable plug)
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what is bleeding time testing?
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formation of temporary plug by platelets
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