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173 Cards in this Set

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Chediak-Higashi Syndrom
inborn defect of phagolysosome formation
Types of Inflammation (3)
Acute, Chronic, Granulomatous
Morphologic Patterns of Inflammation
Serous, Fibrinous, Suppurative, Ulcer
Endothelial cell contraction mediated by ___, ___, ___
histamine, bradykinin, and leukotrienes
Prothrombin G20210A
3’ prothrombin gene mutation leads to 3-fold increase of venous thrombosis
Most common clotting disorder
Factor V Leiden
Most common bleeding disorder
VWF deficiency
____ _ deficiency associated with neonatal purpura fulminans
Protein C Deficiency
Type III Protein S deficiency
normal but reduced unbound form
Acquired Protein C deficiency caused by ___
Warfarin
Major inhibitor of thrombin and Factor Xa
ATIII
Inherited Thrombophilic disorders (6)
AT III deficiency
Protein C deficiency
Protein S deficiency
Factor V Leiden
3’ Prothrombin mutation
Dysfibrinogenemia
Ristocetin is used to evaluate ___
VWF function
VWF has central role in ___
TTP
Weibel-Palade bodies
store VWF
_-___ present with DIC
D-Dimers
_____ is caused by a lack of receptor for VWF
Bernard-Soullier
____ is caused by a lack of fibrinogen receptor
Glanzmann’s thrombasthenia
____ mutations associated with PV, ET, and PMF
JAK2
___ and ___ produced to keep platelets moving
NO and PGI2
Apaf-1 binds to ___
cytochrome c
High PARP-1 activation favors ___
necrosis
Aspirin ____ binds COX1
irreversibly
___ only express COX1
platelets
____ mainly only express COX2
endothelial cells
___ inhibits gastric secretion
COX1
___ regulates renal flow
COX1 and COX2
____ regulates salt and H2O homeostasis
COX1 and COX2
Induce uterine contraction
COX1 and COX2
labile cells
highly proliferative tissues
stable cells
tissues that divide at low rates
Anti___ inhibits keloid formation
TGFB
___ stimulates angiogenesis
VEGF
____ treats pressure ulcers
PGDF
Hyperemia is an ____ process
active
Congestion is a ___ process
passive
Virchow’s triad
Endothelial Injury
Abnormal Blood Flow
Hypercoagulability
New capillary channels formed as part of repair process for thrombi
Recanalization
White infarcts due to __ occlusion
arterial
Red infarcts due to (3)
Venous infarct, Dual blood supply, reperfusion
____ test for mutagenesis
Ames test; initiator (+) vs. promoter (-)
Composition of solid tumor includes ____ and ____
neoplastic cells and stroma
3 routes of metastases
1. Lymphatic
2. Hematogenous
3. Direct seeding
Grading of tumors (3)
Differentiation, Rapid growth, Invasion (capsular, vascular, neural)
Red Cell diameter
8 um
Hemoglobin has _ chains (_ alpha and _ beta)
4
2 alpha
2 beta
EPO produced by ___
kidneys
Identify reticulocytes with ___ stain
Wright stain (blue), supravital (nucleic acid stain)
Corrected Retic Count
Retic x (Actual Hct/ Ideal Hct)
Pica and Spoon nails indicated
Fe deficiency
MCHC increased with ___
Mean Corpuscular Hemoglobin Concentration;
spherocytosis
RDW
RBC distribution width
Dacrocyte sign of ___
extramedullary hematopoiesis (tear drop cell)
Leptocyte sign of
too much membrane (target cell)
Microcytic anemia
Fe deficiency, Thalassemia
Basophilic stippling
Ribosomal RNA aggregates
Pappenheimer bodies
abnormal Fe accumulation
Normocytic anemia
Sickle cell, hemolytic anemia, bleeding
Macrocytic anemia
Megaloblastic anemia (B12 and folate deficiency), myelodysplastic synrome
Iron distribution
70% Hb, 25% storage (ferritin and hemosiderin)
Intestinal entry protein
DMT1
Fe transport protein
Ferroportin
Fe carrier protein
Transferrin
Fe storage protein
Ferritin
Hepcidin expression increased by ____ and __ _____
inflammation, Fe overload
Hepcidin expression decreased by __ ____
Fe deficiency
Folate needed for conversion of ____ to _____
dUMP to dTMP
__ binds B12 and transports through bowel
IF
IF made by ______
parietal cells
Absence of IF leads to ____ ____
Pernicious anemia
(B12 deficiency)
____ B12 deficiency symptoms not corrected with folate
Neurological
Folate deficiency affects ___ to ____
serine --> glycine
Oncogenes (RAS, EGFR, MYC) cause disease through ___ mutations
dominant
Tumor suppressor genes cause disease through ____ mutations
recessive
Myc on Chromosome _
8
RB1 regulates __ to __ phase
G to S
Hb a-globin genes on chromosome __
16
Hb B-globin genes on chromosome __
11
Embryonic Hb
zeta2 epsilon2
Fetal Hb
alpha2 gamma2
Adult Hb
alpha2 beta2 (A) and

alpha2 delta2 (A2)
Alpha Thal --> excess __ chains
Beta
Beta Thal --> excess __ chains
Alpha (precipitate)
Genetic basis of Sickle Cell
GAG--> GTG (Glu-->Val)
Log Jam model
Hb S molecules sickle in small terminal vessels
Sickle cell complications
Acute Chest syndrome
Splenic sequestration crisis
Aplastic crisis
Vaso-occlusive crisis
Treatment for SCD
inducers of fetal gamma globin
Normal germinal center markers
CD10+ BCL6+ BCL2-
Normal Mantle zone
CD10- BCL6- BCL2+
Best predictor for lymphoma behavior
immunophenotype
Immature B cell marker
TdT, CD19
Mature B cell marker
CD19, CD20
Immature T cell markers
TdT, CD1a, cCD3
Lymphoma immunophenotypes
CD3 (T) OR CD19(B)
Burkitt mutation
t(8,14)-->myc + Ig heavy chain
Follicular lymphoma mutation
t(14,18)- overexpresses BCL2
Howell Jolly bodies
residual nuclear material in target cells with dysfunctional spleen
Proteins that bind free Hb and Heme
Haptoglobin, hemopexin, albumin
Microangiopathy indicated by ___
shistocytes
Direct Coombs test
antisera recognizing ABs to RBC surface
Indirect Coombs test
anti-RBC ABs in serum
Autoimmune hemolytic anemia distinctive feature
spherocytosis
Warm reactive antibodies due to ___
IgG
Cold antibodies due to ___
IgM
RBC membrane disorders due to ____
spectrin, Band3, ankyrin
G6PD deficiency
sex linked hereditary hemolytic anemia, Heinz bodies present
Heinz bodies
membrane adherent aggregates of irreversibly oxidized globin
Follicluar lymphoma treatment
Rituxan (rituximab)
Paratrabecular aggregates in marrow
Follicular lymphoma
Follicular lymphoma proliferation rate
low
Richter’s transformation
CLL/SLL--> DLBCL
Smudge cells
CLL
CD5 expressed on B cells
CLL
Zap 70 indicator
CLL
MALT mutation
t(11,18)
Flame cells associated with ___ ____
Multiple Myeloma;
IgA expressing plasma cells
Mott cells associated with ____
Multiple Myeloma; neoplastic plasma cells loaded with intracytoplasmic Ig
Bence Jones protein
Excess light chains from Multiple Myeloma extreted in urine
Cast nephropathy
cells aggregate in urine
SLE renal dysfunction
Rouleaux characteristic of _____
multiple myeloma
Amyloidosis associated with ___
Multiple Myeloma oversecreted clonal serum Igs
DLBCL morphologies (2)
Centroblastic and Immunoblastic
Starry sky pattern seen in ______
Burkitt Lymphoma
Characteristic Hodgkin lymphoma cell
Reed-Sternberg Cell
Philadelphia chromosome seen in ____
CML
Target of Imatinib (Gleevac)
tyrosine kinase
APL FAB M3 mutation
t(15,17)
APL M3 treated with
retinoic acid
Auer Rods seen in ___
AML
Cachexia syndrome
fatigue, weight loss, mediated by TNF
Log Kill Model
constant fraction of cells killed at given dose
Norton-Simon model
cells killed related to growth rate of tumor
Gompertzian model
exponential growth can’t be sustained, repeated cycles can be successful
Drug Resistance gene
MDR
Goldie-Coldman Hypothesis
multiple agents should be given over shortest period
Direct DNA agents
Cisplatin (dna crosslink)
Cyclophosphamide (alkylating)
Ifosphamide (alkylating)
Indirect DNA agents
(nucleoside analogs)
5-FU
Methotrexate
Anti-Mitotic agents
Paclitaxel
Chromatin remodeling inhibitors
Doxorubicin
Topotecan (top1 inhib)
Irinotecan (top1 inhib)
Tyrosine Kinase Agents
Imatinib
Gefitinib (EGFR)
Monoclonal Abs Treatment
Bevacizumab/ Avastin
Trastuzuman/ Herceptin
Immune modulators
Interferon
Hormonal Therapy
Tamoxifen (estrogen)
Radiation delivery methods
External (EBRT)
Internal (brachytherapy)
Joint components
Cartilage, Bone, Synovial tissue, muscle/tendon, Vascular endothelium, peripheral nerve
RA MHC
HLA-DR shared epitope
Non-inflammatory Rheumatoid diseases
Osteoarthritis and osteoporosis
Primary PMN Rheumatoid disease
Gout
Primary B Cell Rheumatoid disease
SLE
Primary T Cell Rheumatoid disease
Ankylosing spondylitis
Infection Rheumatoid disease
Septic arthritis, reactive arthritis, lyme arthritis
Bone destruction in RA mediated by ___
RANK
Morning stiffness
OA
AS MHC
HLA-B27
Arthritogenic peptide hypothesis
molecular mimicry of HLA-B27
SLE MHC
HLA-DR2/3
SLE symptoms
malar rash, discoid rash, photosensitivity, oral ulcers, arthritis, serositis, neurologic disorders, hematologic disorders, antinuclear Ab
SLE ANAs
Anti-dsDNA (specific for lupus)
Anti-smith
Anti-RNP
Anti-Ro/La
Infectious arthritis 2 categories
Gonoccocal
Nongonoccocal
S. Aureus virulence factors (2)
MSCRAMMs
Agr
Lyme disease molecular mimicry
OspA(tick spit) and LFA-1a(knee)
ParvoB19 Arthritis cause
Antigen persistence
Causes of hyperuricemia
HGPRT deficiency
-Lesch-Nyhan (complete) and Kelley-Seegmiller(partial)
PAN symptom
transmural infiltrate, fibrinoid necrosis, intimal proliferation
2 ANCA pattersn
c-ANCA-Wegener’s
p-ANCA- MPA
DMARDs
Disease Modifying Antirheumatic Drugs-methotrexate and leflunomide
Abatacept
anti-CD80/86
Tocilizumab
Ab against IL-6 receptors
Abs targeting TNF
Adalimumab
Infliximab
Etanercept
Certolizumab
Scleroderma differential
Diffuse or CREST
Scleroderma MHC
HLADQ7 and HLA DR5
Scleroderma and SLE patients are both ____
ANA +
Scleroderma abnormal cytokines
TGFB, IL4, IL1