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173 Cards in this Set
- Front
- Back
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Chediak-Higashi Syndrom
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inborn defect of phagolysosome formation
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Types of Inflammation (3)
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Acute, Chronic, Granulomatous
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Morphologic Patterns of Inflammation
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Serous, Fibrinous, Suppurative, Ulcer
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Endothelial cell contraction mediated by ___, ___, ___
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histamine, bradykinin, and leukotrienes
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Prothrombin G20210A
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3’ prothrombin gene mutation leads to 3-fold increase of venous thrombosis
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Most common clotting disorder
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Factor V Leiden
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Most common bleeding disorder
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VWF deficiency
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____ _ deficiency associated with neonatal purpura fulminans
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Protein C Deficiency
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Type III Protein S deficiency
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normal but reduced unbound form
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Acquired Protein C deficiency caused by ___
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Warfarin
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Major inhibitor of thrombin and Factor Xa
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ATIII
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Inherited Thrombophilic disorders (6)
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AT III deficiency
Protein C deficiency Protein S deficiency Factor V Leiden 3’ Prothrombin mutation Dysfibrinogenemia |
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Ristocetin is used to evaluate ___
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VWF function
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VWF has central role in ___
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TTP
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Weibel-Palade bodies
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store VWF
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_-___ present with DIC
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D-Dimers
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_____ is caused by a lack of receptor for VWF
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Bernard-Soullier
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____ is caused by a lack of fibrinogen receptor
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Glanzmann’s thrombasthenia
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____ mutations associated with PV, ET, and PMF
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JAK2
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___ and ___ produced to keep platelets moving
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NO and PGI2
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Apaf-1 binds to ___
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cytochrome c
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High PARP-1 activation favors ___
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necrosis
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Aspirin ____ binds COX1
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irreversibly
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___ only express COX1
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platelets
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____ mainly only express COX2
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endothelial cells
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___ inhibits gastric secretion
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COX1
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___ regulates renal flow
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COX1 and COX2
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____ regulates salt and H2O homeostasis
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COX1 and COX2
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Induce uterine contraction
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COX1 and COX2
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labile cells
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highly proliferative tissues
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stable cells
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tissues that divide at low rates
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Anti___ inhibits keloid formation
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TGFB
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___ stimulates angiogenesis
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VEGF
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____ treats pressure ulcers
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PGDF
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Hyperemia is an ____ process
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active
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Congestion is a ___ process
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passive
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Virchow’s triad
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Endothelial Injury
Abnormal Blood Flow Hypercoagulability |
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New capillary channels formed as part of repair process for thrombi
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Recanalization
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White infarcts due to __ occlusion
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arterial
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Red infarcts due to (3)
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Venous infarct, Dual blood supply, reperfusion
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____ test for mutagenesis
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Ames test; initiator (+) vs. promoter (-)
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Composition of solid tumor includes ____ and ____
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neoplastic cells and stroma
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3 routes of metastases
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1. Lymphatic
2. Hematogenous 3. Direct seeding |
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Grading of tumors (3)
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Differentiation, Rapid growth, Invasion (capsular, vascular, neural)
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Red Cell diameter
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8 um
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Hemoglobin has _ chains (_ alpha and _ beta)
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4
2 alpha 2 beta |
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EPO produced by ___
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kidneys
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Identify reticulocytes with ___ stain
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Wright stain (blue), supravital (nucleic acid stain)
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Corrected Retic Count
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Retic x (Actual Hct/ Ideal Hct)
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Pica and Spoon nails indicated
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Fe deficiency
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MCHC increased with ___
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Mean Corpuscular Hemoglobin Concentration;
spherocytosis |
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RDW
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RBC distribution width
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Dacrocyte sign of ___
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extramedullary hematopoiesis (tear drop cell)
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Leptocyte sign of
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too much membrane (target cell)
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Microcytic anemia
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Fe deficiency, Thalassemia
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Basophilic stippling
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Ribosomal RNA aggregates
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Pappenheimer bodies
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abnormal Fe accumulation
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Normocytic anemia
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Sickle cell, hemolytic anemia, bleeding
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Macrocytic anemia
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Megaloblastic anemia (B12 and folate deficiency), myelodysplastic synrome
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Iron distribution
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70% Hb, 25% storage (ferritin and hemosiderin)
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Intestinal entry protein
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DMT1
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Fe transport protein
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Ferroportin
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Fe carrier protein
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Transferrin
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Fe storage protein
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Ferritin
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Hepcidin expression increased by ____ and __ _____
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inflammation, Fe overload
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Hepcidin expression decreased by __ ____
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Fe deficiency
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Folate needed for conversion of ____ to _____
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dUMP to dTMP
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__ binds B12 and transports through bowel
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IF
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IF made by ______
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parietal cells
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Absence of IF leads to ____ ____
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Pernicious anemia
(B12 deficiency) |
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____ B12 deficiency symptoms not corrected with folate
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Neurological
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Folate deficiency affects ___ to ____
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serine --> glycine
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Oncogenes (RAS, EGFR, MYC) cause disease through ___ mutations
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dominant
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Tumor suppressor genes cause disease through ____ mutations
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recessive
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Myc on Chromosome _
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8
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RB1 regulates __ to __ phase
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G to S
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Hb a-globin genes on chromosome __
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16
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Hb B-globin genes on chromosome __
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11
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Embryonic Hb
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zeta2 epsilon2
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Fetal Hb
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alpha2 gamma2
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Adult Hb
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alpha2 beta2 (A) and
alpha2 delta2 (A2) |
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Alpha Thal --> excess __ chains
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Beta
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Beta Thal --> excess __ chains
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Alpha (precipitate)
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Genetic basis of Sickle Cell
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GAG--> GTG (Glu-->Val)
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Log Jam model
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Hb S molecules sickle in small terminal vessels
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Sickle cell complications
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Acute Chest syndrome
Splenic sequestration crisis Aplastic crisis Vaso-occlusive crisis |
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Treatment for SCD
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inducers of fetal gamma globin
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Normal germinal center markers
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CD10+ BCL6+ BCL2-
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Normal Mantle zone
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CD10- BCL6- BCL2+
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Best predictor for lymphoma behavior
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immunophenotype
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Immature B cell marker
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TdT, CD19
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Mature B cell marker
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CD19, CD20
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Immature T cell markers
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TdT, CD1a, cCD3
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Lymphoma immunophenotypes
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CD3 (T) OR CD19(B)
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Burkitt mutation
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t(8,14)-->myc + Ig heavy chain
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Follicular lymphoma mutation
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t(14,18)- overexpresses BCL2
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Howell Jolly bodies
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residual nuclear material in target cells with dysfunctional spleen
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Proteins that bind free Hb and Heme
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Haptoglobin, hemopexin, albumin
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Microangiopathy indicated by ___
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shistocytes
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Direct Coombs test
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antisera recognizing ABs to RBC surface
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Indirect Coombs test
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anti-RBC ABs in serum
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Autoimmune hemolytic anemia distinctive feature
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spherocytosis
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Warm reactive antibodies due to ___
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IgG
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Cold antibodies due to ___
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IgM
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RBC membrane disorders due to ____
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spectrin, Band3, ankyrin
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G6PD deficiency
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sex linked hereditary hemolytic anemia, Heinz bodies present
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Heinz bodies
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membrane adherent aggregates of irreversibly oxidized globin
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Follicluar lymphoma treatment
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Rituxan (rituximab)
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Paratrabecular aggregates in marrow
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Follicular lymphoma
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Follicular lymphoma proliferation rate
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low
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Richter’s transformation
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CLL/SLL--> DLBCL
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Smudge cells
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CLL
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CD5 expressed on B cells
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CLL
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Zap 70 indicator
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CLL
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MALT mutation
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t(11,18)
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Flame cells associated with ___ ____
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Multiple Myeloma;
IgA expressing plasma cells |
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Mott cells associated with ____
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Multiple Myeloma; neoplastic plasma cells loaded with intracytoplasmic Ig
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Bence Jones protein
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Excess light chains from Multiple Myeloma extreted in urine
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Cast nephropathy
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cells aggregate in urine
SLE renal dysfunction |
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Rouleaux characteristic of _____
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multiple myeloma
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Amyloidosis associated with ___
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Multiple Myeloma oversecreted clonal serum Igs
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DLBCL morphologies (2)
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Centroblastic and Immunoblastic
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Starry sky pattern seen in ______
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Burkitt Lymphoma
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Characteristic Hodgkin lymphoma cell
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Reed-Sternberg Cell
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Philadelphia chromosome seen in ____
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CML
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Target of Imatinib (Gleevac)
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tyrosine kinase
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APL FAB M3 mutation
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t(15,17)
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APL M3 treated with
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retinoic acid
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Auer Rods seen in ___
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AML
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Cachexia syndrome
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fatigue, weight loss, mediated by TNF
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Log Kill Model
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constant fraction of cells killed at given dose
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Norton-Simon model
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cells killed related to growth rate of tumor
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Gompertzian model
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exponential growth can’t be sustained, repeated cycles can be successful
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Drug Resistance gene
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MDR
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Goldie-Coldman Hypothesis
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multiple agents should be given over shortest period
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Direct DNA agents
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Cisplatin (dna crosslink)
Cyclophosphamide (alkylating) Ifosphamide (alkylating) |
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Indirect DNA agents
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(nucleoside analogs)
5-FU Methotrexate |
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Anti-Mitotic agents
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Paclitaxel
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Chromatin remodeling inhibitors
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Doxorubicin
Topotecan (top1 inhib) Irinotecan (top1 inhib) |
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Tyrosine Kinase Agents
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Imatinib
Gefitinib (EGFR) |
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Monoclonal Abs Treatment
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Bevacizumab/ Avastin
Trastuzuman/ Herceptin |
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Immune modulators
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Interferon
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Hormonal Therapy
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Tamoxifen (estrogen)
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Radiation delivery methods
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External (EBRT)
Internal (brachytherapy) |
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Joint components
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Cartilage, Bone, Synovial tissue, muscle/tendon, Vascular endothelium, peripheral nerve
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RA MHC
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HLA-DR shared epitope
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Non-inflammatory Rheumatoid diseases
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Osteoarthritis and osteoporosis
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Primary PMN Rheumatoid disease
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Gout
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Primary B Cell Rheumatoid disease
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SLE
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Primary T Cell Rheumatoid disease
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Ankylosing spondylitis
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Infection Rheumatoid disease
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Septic arthritis, reactive arthritis, lyme arthritis
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Bone destruction in RA mediated by ___
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RANK
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Morning stiffness
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OA
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AS MHC
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HLA-B27
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Arthritogenic peptide hypothesis
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molecular mimicry of HLA-B27
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SLE MHC
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HLA-DR2/3
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SLE symptoms
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malar rash, discoid rash, photosensitivity, oral ulcers, arthritis, serositis, neurologic disorders, hematologic disorders, antinuclear Ab
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SLE ANAs
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Anti-dsDNA (specific for lupus)
Anti-smith Anti-RNP Anti-Ro/La |
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Infectious arthritis 2 categories
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Gonoccocal
Nongonoccocal |
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S. Aureus virulence factors (2)
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MSCRAMMs
Agr |
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Lyme disease molecular mimicry
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OspA(tick spit) and LFA-1a(knee)
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ParvoB19 Arthritis cause
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Antigen persistence
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Causes of hyperuricemia
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HGPRT deficiency
-Lesch-Nyhan (complete) and Kelley-Seegmiller(partial) |
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PAN symptom
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transmural infiltrate, fibrinoid necrosis, intimal proliferation
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2 ANCA pattersn
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c-ANCA-Wegener’s
p-ANCA- MPA |
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DMARDs
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Disease Modifying Antirheumatic Drugs-methotrexate and leflunomide
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Abatacept
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anti-CD80/86
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Tocilizumab
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Ab against IL-6 receptors
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Abs targeting TNF
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Adalimumab
Infliximab Etanercept Certolizumab |
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Scleroderma differential
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Diffuse or CREST
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Scleroderma MHC
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HLADQ7 and HLA DR5
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Scleroderma and SLE patients are both ____
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ANA +
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Scleroderma abnormal cytokines
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TGFB, IL4, IL1
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