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68 Cards in this Set

  • Front
  • Back
Microcytic anemia
- hypohchromic (MCV < 80)
- decreased serum iron and ferriton, increased TIBC
- Thalassemias, lead poising, sideroblasitc anemias
B12 and folate deficiencies
- both associated w/ hypersegmented PMN's
- B12 assocated w/ nerological problems
Macrocytic Anemia
- hyperhchromic (MCV < 80)
- megaloblastic - vitatmin B12/ folate def
- drugs that block DNA synthesis (sulfa, AZT)
Normocytic anemia
- 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
RBC hemolysis lab indicators
- decreased serum haptoglobin, increased serum LDH
- Direct coomb's test is sued to distinguish b/c immune and non-immune hemolysis
Aplastic anemia pahtopys
- pancytopenia characterized by sever anemia, neutropenia, thrombocytopenia
- casued by descturction of MMSC's w/ inadequate production of differentiated cell lines
Aplastic anemia causes
- radiation
- benzene
- chloramphenicol
- alkylating agents
- antimetabolites
- viral (pB19, EBV, HIV)
- Fanconi's anemia
- idopathic (immune-mediated 1o stem cell defect)
- may follow accute hepatitis
Aplastic anemia symptoms
- fatigue
- malise
- pallor
- pupuria
- mucosal bleeding
- petechiae
- infection
Aplastic anemia treatment
- withdrawal of offending agent
- allogenic BM transplant
- RBC and paltelet transfusion
- G-CSF or GM-CSF (both GFs)
Hereditary spherocytosis pathophysiology
- EV hemolysis due to spectrin or ankryn defect
- small RBC's w/ no central pallor -> less membrane
- increased MCHC, RDW, and reticulocytes
Hereditary spherocytosis diagnosis and associated diseases
- diagnose w/ osmotic fragility
- associated w/ gallstones, splenomegaly, anemia, and jaundice
- distinguish from warm Ab hemolysis w/ DAT test (is coomb's negative)
Sickle Cell Anemia pathophys
- 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
Sickle Cell Anemia complications
- aplatic crisis (from pB19)
- autosplenectomy
- increased risk of encapsulated oranism infection
- salmonella osteomyelitis
- painful crisis (vaso-occlusive)
- spleinc sequestration crisis
alpha thalassemia
- 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
beta thalassemia
- 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
DIC pathophysiology
activation of coagulation cascades -> microthrombi and global compensation of platelets, fibrin and coagulation factors
DIC causes
- obstetric complications #1
- gram neg species
- transfusion
- trauma
- malignancy
- acute pancreatitis
- nephrotic syndrome
DIC lab findings
- increased PT
- increased PTT
- increased fibrin split products (D-dimers)
- decreased platelet count
- helmet shaped cells
- schistocytes on blood smear
platelet abnormalities
- 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)
Coagulation factor defects
- 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
lab findings for qualitative platelet defects
- increased bleeding time
lab findings for thrombocytopenia
- increased bleeding time
- decreased platelet count
lab findings for Hem A
- increased PTT
lab findings for Hem B
- increased PTT
lab findings for vWD
- increased bleeding time
- increased PTT
lab findings for DIC
- increased bleeding time
- increased PT
- increased PTT
- decreased platelet count
Hodgkin's lymphoma
- 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
nodular screening hodgkin's lymphoma
- only one more common in women - most common one
- RS low, lymphocytes high so prognosis excellent
mixed cellularity hodgkin's lymphoma
RS high, lymphocytes high, so prognosis intermediate
lymphocyte predominant hodgkin's leukemia
- in males <35
- RS low, lymphocytes high, so prognosis excellent
lymphocyte depleted hodgkin's leukemia
- in older males w/ disseminated disease
- RS high, lymphocytes low, so prognosis poor - very rare
Non-hodgkin's lymphoma
- ass w/ HIV or immunosup
- multiple, peripheral nodes - extranodal involvement common - noncontiguous spread
- maojory involves B cells
- no hypergammaglobulins
- peak incidence 20-40 yrs
small lymphocytic lymphoma - non-hodgkin's lymphoma
- adults
- B cells
- like CLL w/ focal mass; low grade
follicular lymphoma - non-hodgkin's lymphoma
- adults
- B cells
- blc-2 is invoved in apoptosis
- most common, difficult to cure - indolent course
diffuse large cell - non-hodgkin's lymphoma
- usually older adults, but 20% in kids
- 80% B, 20% T (mature)
- agressive but half curable
lymphoblastic lymphoma - non-hodgkin's lymphoma
- kids most often
- immature T cells
- commonly presents w/ ALL and mediastinal mass
- very agressive
Burkett's lymphoma - non-hodgkin's lymphoma
- 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
Leukemia - general stuff
- 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
ALL leukemia
- children
- lymphoblasts
- most responsive to therapy
- may spread to CNS and testes
AML leukemia
- auer rods
- myeloblasts
- adults
CLL leukemia
- older adults
- lymphadenopathy
- hepatosplenomegaly
- few symptoms
- indolent course
- increased smudge cells in peripheral blood smear
- warm Ab autoimmune hemolytic anemia
- similar to SLL
CML leukemia
- 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
acute leukemia
- blasts predominate, kids or elderly, short and drastic course
- ALL - lymphoblasts
- AML - myeoblasts
chronic leukemia
- more mature cells, midlife age, longer and better course
- CLL - lymphocytes (non-Ab producing B cells)
- CML - myeloid stem cells
Multiple myeloma - overview and symptoms
- 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
Multiple myeloma - associated diseases and lab findings
- 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)
Hb basic structure
- 2a chains and 2b chains
- T is deoxy
- R is oxy
Hb structure regulation
inc Cl, H, COs, DPG, and Temp favor R over T (right shift)
- iron in Hb is in a oxidized state (fe 3+) - should be reduced
- when this happens it wont bind O2 as readily
C02 transport in blood
- 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
- 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)
varying erythrocyte size
varying erythrocyte size
- granulocytes - basophils, eosinophils, neutrophils
- nomonuclear cells - lymphocytes and monocytes
- defense against infection
- mediates allergic rxns
- bilobed nucleus
- basophilic granules w/ heparin and histamine
mast cell
- mediates allerigic rxns
- deganulation -> histamine, heparin, and eosinophil chemotactic release
- can bind IgE to membrane
- resemble basophils but found in tissue
progression of granulocytes
- myelobalst
- promyleocyte
- myleocyte
- megamyleocyte
- stab cell
- neutrophil, eosinophil, or basophil
progression of erythrocytes
- proerythocyte
- reticulocyte
- erythrocyte
progression of platelets
- megakaryoblast
- megakaryocytes
- bilobed nucleus
- packed w/ large eosinophilic granules
- defends against helminths and protazoa
- v. phagocytic for Ag-Ab complexes
- produces histaminase and arylsulfatase
causes eosinophilia
- neoplastic
- asthma
- allergic processes
- collagen vascular diseases
- parasites
- 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
- large, kidney shaped nucleus
- extensive frosted glass cytoplasm
- differentiases into macrophages once in tissues
- small, round, densly staining nucleus
- small amt of pale cytoplasm
- Bs produce Abs
- Ts manifest cellular immune response and regulate Bs and macrophages
plasma cell
- off center nucleus w/ clock face chromatin
- abundant RER, complex golgi
- come from B cells
- multiple myeloma is plasma cell neoplasm
- 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
- mediates cellular immune response
- matures in thymus
- diff into cytotoxic T cells (MHCI, CD8), helper T's (MHCII, CD4), and delayed hypersensitivity T cells
- phagocytize bacteria, cell debris, and senescent red cells
- long life in tissue
- activated by g-IFN
- can be an APC via MHC II