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68 Cards in this Set
- Front
- Back
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Microcytic anemia
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- hypohchromic (MCV < 80)
- decreased serum iron and ferriton, increased TIBC - Thalassemias, lead poising, sideroblasitc anemias |
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B12 and folate deficiencies
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- both associated w/ hypersegmented PMN's
- B12 assocated w/ nerological problems |
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Macrocytic Anemia
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- hyperhchromic (MCV < 80)
- megaloblastic - vitatmin B12/ folate def - drugs that block DNA synthesis (sulfa, AZT) |
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Normocytic anemia
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- accute hemorrhage
- enzyme defects (G6PD def, PK def) - RBC membrane defects (sperocytosis) - BM disorders (aplastic anemia, leukemia) - hemoglobinopathies (SCD) - autoimmune hemolytic anemia - ACD (anemia of chromic disease) w/ decreased TIBC, increased ferritin and iron storage |
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RBC hemolysis lab indicators
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- decreased serum haptoglobin, increased serum LDH
- Direct coomb's test is sued to distinguish b/c immune and non-immune hemolysis |
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Aplastic anemia pahtopys
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- pancytopenia characterized by sever anemia, neutropenia, thrombocytopenia
- casued by descturction of MMSC's w/ inadequate production of differentiated cell lines |
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Aplastic anemia causes
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- radiation
- benzene - chloramphenicol - alkylating agents - antimetabolites - viral (pB19, EBV, HIV) - Fanconi's anemia - idopathic (immune-mediated 1o stem cell defect) - may follow accute hepatitis |
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Aplastic anemia symptoms
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- fatigue
- malise - pallor - pupuria - mucosal bleeding - petechiae - infection |
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Aplastic anemia treatment
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- withdrawal of offending agent
- allogenic BM transplant - RBC and paltelet transfusion - G-CSF or GM-CSF (both GFs) |
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Hereditary spherocytosis pathophysiology
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- EV hemolysis due to spectrin or ankryn defect
- small RBC's w/ no central pallor -> less membrane - increased MCHC, RDW, and reticulocytes |
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Hereditary spherocytosis diagnosis and associated diseases
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- diagnose w/ osmotic fragility
- associated w/ gallstones, splenomegaly, anemia, and jaundice - distinguish from warm Ab hemolysis w/ DAT test (is coomb's negative) |
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Sickle Cell Anemia pathophys
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- HbS - val for glu in B chain
- low O2 or dehydration causes more sickling - hetero's malaria resistant - crew cut on skull x-ray due to marrow expansion |
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Sickle Cell Anemia complications
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- aplatic crisis (from pB19)
- autosplenectomy - increased risk of encapsulated oranism infection - salmonella osteomyelitis - painful crisis (vaso-occlusive) - spleinc sequestration crisis |
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alpha thalassemia
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- 1 of 4 genes for the alpha chain makes it underproduced
- no compensatory increase of other chains - HbH (B4-tetramers, lacks 3 A genes - Hb Barts (y4-tetramers, lacks all 4 genes) leads to hydrops fetus and IU death |
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beta thalassemia
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- common in mediteranians
- minor is hetero - so B is underproduced - in major it's absent - fetal Hb is compensatory, but inadequate - results in major anemia, cardiac failure due to 2o hemochromatosis - marrow expansion -> skeletal deformaties |
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DIC pathophysiology
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activation of coagulation cascades -> microthrombi and global compensation of platelets, fibrin and coagulation factors
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DIC causes
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- obstetric complications #1
- gram neg species - transfusion - trauma - malignancy - acute pancreatitis - nephrotic syndrome |
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DIC lab findings
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- increased PT
- increased PTT - increased fibrin split products (D-dimers) - decreased platelet count - helmet shaped cells - schistocytes on blood smear |
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platelet abnormalities
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- MM bleeding, petechiae, purpuria, prolonged bleeding time
- casued by ITP (anit-platelet Ab's and inc megakaryoctyes) - also TTP (schistocytes), drugs, and DIC (inc fibrin split products) |
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Coagulation factor defects
(macrohemprrhage) |
- hemathrosis (bleeding into joints), easy bruising
- protoned PT (F 2,5,7,10) - prolonged PTT (all factors except 7 and 13) - inclueds hemophilia A (7 def), B (9 def) and vWD (vWF def) most common |
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lab findings for qualitative platelet defects
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- increased bleeding time
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lab findings for thrombocytopenia
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- increased bleeding time
- decreased platelet count |
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lab findings for Hem A
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- increased PTT
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lab findings for Hem B
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- increased PTT
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lab findings for vWD
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- increased bleeding time
- increased PTT |
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lab findings for DIC
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- increased bleeding time
- increased PT - increased PTT - decreased platelet count |
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Hodgkin's lymphoma
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- presence of Reed-Sternberg cells (CD30+ and CD15+ B)
- localized, single groups of nodes, extranodal rare, contiguous spread - constitutional signs - low grade fever, night sweats, weight loss - 50% ass. w/ EBV - more common in men - if increased lymphocytes and decreased RS, good prognosis |
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nodular screening hodgkin's lymphoma
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- only one more common in women - most common one
- RS low, lymphocytes high so prognosis excellent |
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mixed cellularity hodgkin's lymphoma
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RS high, lymphocytes high, so prognosis intermediate
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lymphocyte predominant hodgkin's leukemia
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- in males <35
- RS low, lymphocytes high, so prognosis excellent |
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lymphocyte depleted hodgkin's leukemia
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- in older males w/ disseminated disease
- RS high, lymphocytes low, so prognosis poor - very rare |
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Non-hodgkin's lymphoma
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- ass w/ HIV or immunosup
- multiple, peripheral nodes - extranodal involvement common - noncontiguous spread - maojory involves B cells - no hypergammaglobulins - peak incidence 20-40 yrs |
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small lymphocytic lymphoma - non-hodgkin's lymphoma
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- adults
- B cells - like CLL w/ focal mass; low grade |
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follicular lymphoma - non-hodgkin's lymphoma
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- adults
- B cells - blc-2 is invoved in apoptosis - most common, difficult to cure - indolent course |
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diffuse large cell - non-hodgkin's lymphoma
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- usually older adults, but 20% in kids
- 80% B, 20% T (mature) - agressive but half curable |
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lymphoblastic lymphoma - non-hodgkin's lymphoma
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- kids most often
- immature T cells - commonly presents w/ ALL and mediastinal mass - very agressive |
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Burkett's lymphoma - non-hodgkin's lymphoma
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- kids most often
- B cells - t (8;14) c-myc gene moves next to heavy chain IG gene (14) - starry sky appearance (sheets of lymphocytes w/ macrophages) - ass w/ EBV - jaw lesions big in africa - sporatic form in pelvis or abdomen |
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Leukemia - general stuff
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- increased # of circulating leukocytes in blood
- BM infiltrates of leukemic cells - marrow failure -> amenia, infection, and hemorrhage - infiltrates common in liver, spleen, and LN's common |
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ALL leukemia
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- children
- lymphoblasts - most responsive to therapy - may spread to CNS and testes |
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AML leukemia
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- auer rods
- myeloblasts - adults |
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CLL leukemia
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- older adults
- lymphadenopathy - hepatosplenomegaly - few symptoms - indolent course - increased smudge cells in peripheral blood smear - warm Ab autoimmune hemolytic anemia - similar to SLL |
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CML leukemia
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- ass w/ philadelphia chromosome (t[9;22])
- myeloid stem cell prolif - presents w/ increased neutrophils & metamyelocytes - may accelerate to AML (blast crisis) - v low leukocyte alkaline phoshatase |
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acute leukemia
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- blasts predominate, kids or elderly, short and drastic course
- ALL - lymphoblasts - AML - myeoblasts |
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chronic leukemia
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- more mature cells, midlife age, longer and better course
- CLL - lymphocytes (non-Ab producing B cells) - CML - myeloid stem cells |
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Multiple myeloma - overview and symptoms
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- monoclonal plasma cell (fried egg) cancer
- arises in marrow and produces large amounts of IgG - most common 1o tumor arising in adult bone - destructive bone lesions and hypercalcemia - renal insufficiency - increased infection rate - anemia |
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Multiple myeloma - associated diseases and lab findings
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- ass w/ 1o amyloidosis and punched out lytic bone lesions on s-ray
- you have Ig spike (M protein) on serum electrophoresis - Ig light chains in urine - blood smear shows RBCs stacked like poker chips (roleau formation) |
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Hb basic structure
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- 2a chains and 2b chains
- T is deoxy - R is oxy |
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Hb structure regulation
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inc Cl, H, COs, DPG, and Temp favor R over T (right shift)
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methemoglobinemia
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- iron in Hb is in a oxidized state (fe 3+) - should be reduced
- when this happens it wont bind O2 as readily |
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C02 transport in blood
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- it binds aa's in globin chain but not to heme
- favors T form to promote O2 unloading - must be transported from tissue to lungs |
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erythrocyte
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- anucleate, biconcave
- source of E (glucose) - 120 day survival - membrane contains Cl-bicarb antiport that does the physiologic Cl shift (lets RBCs transfer C02 to lungs) |
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anisocytosis
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varying erythrocyte size
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poikilocytosis
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varying erythrocyte size
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leukocyte
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- granulocytes - basophils, eosinophils, neutrophils
- nomonuclear cells - lymphocytes and monocytes - defense against infection |
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basophil
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- mediates allergic rxns
- bilobed nucleus - basophilic granules w/ heparin and histamine |
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mast cell
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- mediates allerigic rxns
- deganulation -> histamine, heparin, and eosinophil chemotactic release - can bind IgE to membrane - resemble basophils but found in tissue |
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progression of granulocytes
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- myelobalst
- promyleocyte - myleocyte - megamyleocyte - stab cell - neutrophil, eosinophil, or basophil |
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progression of erythrocytes
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- proerythocyte
- reticulocyte - erythrocyte |
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progression of platelets
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- megakaryoblast
- megakaryocytes |
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eosinophil
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- bilobed nucleus
- packed w/ large eosinophilic granules - defends against helminths and protazoa - v. phagocytic for Ag-Ab complexes - produces histaminase and arylsulfatase |
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causes eosinophilia
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NAACP
- neoplastic - asthma - allergic processes - collagen vascular diseases - parasites |
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neutrophil
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- accute inflam response cell
- 40-75% WBC's - large lysosomes (shperical azurophilic granules) w/ hydrolytic enzymes, lysozyme, myeloperoxidase, and lactoferrin - hypersegmented seen in B12 folate def |
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monocyte
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- large, kidney shaped nucleus
- extensive frosted glass cytoplasm - differentiases into macrophages once in tissues |
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lymphocyte
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- small, round, densly staining nucleus
- small amt of pale cytoplasm - Bs produce Abs - Ts manifest cellular immune response and regulate Bs and macrophages |
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plasma cell
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- off center nucleus w/ clock face chromatin
- abundant RER, complex golgi - come from B cells - multiple myeloma is plasma cell neoplasm |
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B-lymphocyte
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- part of humoral response
- made in BM, then go to LN follicles, white pulp of spleen, unencapsulated lymph tissue - diff into plasma cells when Ag i sencountered - is an APC via MHC II |
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T-lymphcyte
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- mediates cellular immune response
- matures in thymus - diff into cytotoxic T cells (MHCI, CD8), helper T's (MHCII, CD4), and delayed hypersensitivity T cells |
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macrophage
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- phagocytize bacteria, cell debris, and senescent red cells
- long life in tissue - activated by g-IFN - can be an APC via MHC II |
