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Experiment

QuestionAnswer
Gouty attacks are caused by ___ crystals that deposit in a ___ or ___. MONOSODIUM URATE, JOINT, KIDNEY
CML & Gout go together b/c ___ from increased ___ can't be salvaged so they're broken down into ___. PURINES, CELL TURNOVER, URIC ACID
Dysplasia is abnormal ___ of ___ or ___ GROWTH, ORGANS, CELLS
Myelodysplastic Disorder is ___: dysplasia of ___ & other elements in ___, which may take form of ___ or of abnormal ___ (which may precede ___ leukemia). PRE-LEUKEMIA, MYELOCYTES, BM, MYELOSUPPRESSION, PROLILFERATION, MYELOGENOUS
Hyperleukocytosis is treated by ___ + ___ to bring down ___. LEUKAPHERESIS, HYDROXYURIA, WBC CT
Acute Gout is treated with ___ or ___. COLCHICINE, INDOMETHACIN
Colchicine causes diarrhea because it's an ___ agent that effects ___ like ___. ANTI-MITOTIC, RAPIDLY DIVIDING CELLS, GI EPITHELIUM
Colchicine is given for gout because it lowers ___ => less ___ metabolism. NEUTROPHILS, PURINE
CNS Leukemia happens when ___ spread outside the blood into the CNS. Sx include: ___, ___, ___, ___, ___, ___. WBC PRECURSORS; HA, WEAKNESS, SEIZURES, VOMITING, POOR BALANCE, BLURRY VISION
CNS Leukemia is treated the same as ___ - ___ + ___. Sx decrease as ___ returns to normal. HYPERLEUKOCYTOSIS, LEUKAPHERESIS, HYDROXYUREA, WBC CT.
If Colchicine causes too much diarrhea, switch to ___ & treat dehydration with ___ & ___. ALLOPURINOL, FLUIDS, K+
Urate deposition in Gout is c/b increased ___ concentration d/t either ___ or ___ of ___. URATE, OVERPRODUCTION, UNDEREXCRETION, URATE
Crystals form in Gout when ___ ___ in the blood. MONOSODIUM URATE, SUPERSATURATION
Tophi are ___ masses of ___ crystals in ___ ___. NODULAR, MONOSODIUM URATE, SOFT, TISSUE
Gouty Arthritis develops when crystals cause ___ leading to ___. This causes ___ recruitment, which ___ crystals, causing damage to ___. This releases ___ (O2 metabolites) in the joint, which damage the joint surface causing ___ & ultimately ___. TISSUE DAMAGE, INFLAMMATION, PMN, PHAGOCYTOSE, PHAGOSOME MEMBRANE, LYSOSOMAL ENZYMES, INFLAMMATION, ARTHRITIS
The symptoms of Gout include: ___, usually ___ most commonly affecting the ___. ___ onset, ___ (typically nocturnal). Local postinflammatory ___ (___), & ___ (___). PAIN, MONOARTICULAR, MCP JOINT, ACUTE, FEVER, DESQUAMATION (SKIN PEELING), PRURITIS (ITCHY)
Gout is diagnosed by ___ on blood analysis. Definitive Dx = aspiration of ___ needles, but this is quite painful. HYPERURICEMIA, NEGATIVELY BIREFRINGENT
Acute pain in gouty attacks is caused by rapid ___ (either ___ or ___) in ___ concentration in a joint. Loose ___ irritate ___ causing an ___. CHANGE, INCREASE, DECREASE, URATE, CRYSTALS, SYNOVIUM, INFLAMMATORY RESPONSE
The 3 stages of Gout are: ___ Stage, ___ Stage, ___ Stage. ACUTE, INTERCRITICAL, CHRONIC
The Acute Stage of Gout includes: Joint ___ & ___. Pain peaks within ___ day(s). Mostly affects ___ joint. SWELLING, PAIN, 1, MCP
The Intercritical Stage of Gout includes: ___ between ___. The patient is ___. TIME, ATTACKS, ASYMPTOMATIC
The Chronic Stage of Gout includes: ___ symptoms of ___ & ___ in the affected joints. PERSISTENT, SORENESS, ACHING
Imatinib mesylate is a ___ inhibitor that inhibits ___. PROTEIN TYROSINE KINASE (PTK), BCR-ABL TK
Imatinib works by inhibiting ____ by inducing ___ & preventing ___. BCR-ABL TK, APOPTOSIS, CELL PROLIFERATION
Imatinib works on ___ lines & “___” cells that are ___. Also inhibits ___ proteins of ___ & ___ factor. It has little effect on ___ hematopoietic cells because it’s designed for ___. BCR/ABL SC, FRESH LEUKEMIC, PH+, TK RECEPTOR, PDGF, SC, NORMAL, BCR/ABL
MOA of Imatinib: ___ is the energy & ___ source for the ___ enzyme. Imatinib blocks the ___ pocket where ___ binds. ATP, PHOSPHATE, KINASE, KINASE, ATP
Imatinib should be used in the ___ stage of CML. In ____ stages, ___ mutations ___ the effectiveness. EARLY, LATER, FURTHER, DAMPEN
___% of patients on imatinib achieve _____. ~75, COMPLETE CYTOGENIC REMISSION
CML Pathogenesis: BCR/ABL translocation => ___ TK activity. Net effect is ___ cell division & ___ of apoptosis. CONSTITUTIVE, UNREGULATED, INHIBITION
CML differs from other MPDs in the following ways: ___kD BCR-ABL translocation. Chrom ___ gets a new ___ end from Chrom ___. Chrom ___ is shortened into the ___ chrom. 210, 22, 3’, 9, 22, PHILADELPHIA
Clinical course of CML is ____: ___ phase, ____ phase, & ___. TRIPHASIC, CHRONIC, ACCELERATED, BLAST CRISIS
___% of CML patients are diagnosed during ___ phase. 85, CHRONIC
Chronic phase typically lasts ___ depending on ___. 2-10 YRS, TREATMENT
The hallmark of Chronic phase is ___ production of ___. UNCONTROLLED, MATURING GRANULOCYTES
In Chronic Phase, you see peripheral blood ___ of myeloid precursors. ___ WBCs – mainly ___. Also ___ of non-functioning ___ in ___% of patients. LEUKOCYTOSIS, >25, 000, PMNS, THROMBOCYTOSIS, PLATELETS, 50
“Left Shift” is proliferation of ___ cells. ___ cells are on the L, ___ cells are on the R (arbitrary). MATURING, IMMATURE, MATURE
Signs of Chronic Phase seen on PE are ___ d/t ___ hematopoiesis, & occasionally ___ or ___. SPLENOMEGALY, EXTRAMEDULLARY, HEPATOMEGALY, ADENOPATHY
Other lab findings during Chronic Phase include: abnormally low ___, hypercellular ___, dominance of ___ tissue (esp. ___). LEUKOCYTE ALKALINE PHOSPHATASE, BM, HEMATOPOIETIC, GRANULOPOIESIS
Sx during Chronic Phase: gradual onset of ___, ___, ___, ___, ___. FATIGUE, ANOREXIA/EARLY SATIETY, WT LOSS, LUQ DISCOMFORT, EXCESSIVE SWEATING
CML is diagnosed by identifying ___ . PH+ CHROMOSOME
Accelerated Phase is essentially a ___ to ___. TRANSITION, BLAST CRISIS
___ all patients go through ___ Phase. At least ___% go straight to ___ without evidence of ___. NOT, ACCELERATED, 20, BLAST CRISIS, ACCELERATED PHASE
In Accelerated Phase ___ differentiation is progressively impaired. ___ counts are more difficult to control with ___ meds. Development of increasing degrees of ___ unaccounted for by ___ or ___. ___ & ___ may not be controllable. PMN, WBC, MYELOSUPPRESSIVE, ANEMIA, BLEEDING, CHEMO, SPLENOMEGALY, ANEMIA
Blast Crisis resembles ___. ___ or ___ fail to differentiate. It can be ___ if initial diagnosis occurs in this phase. ACUTE LEUKEMIA, MYELOID BLASTS, LYMPHOID BLASTS, MISDIAGNOSED
During Blast Crisis ___ count is greatly increased (>___%) in blood smear or BM. Extramedulary infiltration of ___, ___, ___, & ___. BLAST, 30, LN’S, SKIN, SUB-Q TISSUE, BONE
The most common physical findings in Blast Crisis include ___, ___, & ___. SUB-Q NODULES, HEMORRHAGIC SKIN LESIONS, LYMPHADENOPATHY
Blast Crisis is exacerbated by ___. SMOKING
Once entering Blast Crisis a patient is estimated to survive ___. 3-6 MONTHS
The DDx of CML includes essentially any myeloproliferative disorder (MPD): ___, ___, ___, ___. POLYCYTHEMIA VERA, REACTIVE LEUKOCYTOSIS, ESSENTIAL THROMBOCYTOSIS, ANGIOGENIC MYELOID METAPLASIA.
Findings indicative of CML are no ___, decreased ___, normal ___ with 0-few ___ RBCs. ____ = definitive Dx. LAP (LEUKOCYTE ALKALINE PHOSPHATASE), HEMATOCRIT, RBC MORPHOLOGY, NUCLEATED, BCR/ABL
Other MPDs differ from CML in the following ways: WBC ct usually <___/uL. Usually no ___. Elevated ___. Most important: no ____! 50,000, SPLENOMEGALY, LAP, BCR/ABL GENE
Polycythemia Vera is a ___ from multipotent ___. There’s increased BM production of ___, ___, & ___ cells, but ___ are produced in greatest excess, so ___ & ___ are also very high. You’ll also see ___, ____, ____, & high ___. NEOPLASM, ERYTHROID, GRANULOCYTIC, MEGAKARYOCYTIC, RBC’s, HEMATOCRIT & HEMOGLOBIN, SPLENOMEGALY, LEUKOCYTOSIS, THROMBOCYTOSIS, TOTAL BLOOD VOLUME
Reactive Leukocytosis is associated with ___. It differs from CML in the following ways: WBC count usually <___/uL. Usually no ___. Elevated ___. Most important: no ___! INFECTION, 50,000, SPLENOMEGALY, LAP, BCR/ABL GENE
In Essential Thrombocytosis ___ don’t fXn properly => excessive ___. It’s the ___ common MPD & c/b a mutation in ___. ___ are greatly +++ed with no alternative cause. ___ levels are normal, ___ are often greatly elevated, & often a mild increase in ___. PLATELETS, BLEEDING, LEAST, JAK2 KINASE, PLATELETS, HB, MEGAKARYOCYTES, PMNs
Angiogenic Myeloid Metaplasia, a.k.a. ___ is a ___ disorder that leads to chronic ___ & ___ hyperplasia. ___ fibrosis is caused by abnormal ___ levels. ___, ___, & severe ___ morphology changes are also seen. CHRONIC IDIOPATHIC MYELOFIBROSIS, HEMATOPOIETIC SC, MYELOPROLIFERATION, MEGAKARYOCYTIC, BM, GROWTH FACTOR, ANEMIA, SPLENOMEGALY, RBC
CML is diagnosed by increased ___ & significant ___ of ___ progenitor cells (w/ decreased ___ & ___). Presence of ___ or ___. WBC, L-SHIFT, MYELOID, PROMYELOCYTE, BLASTS, PH+ CHROMOSOME, BCR/ABL GENE
Ph+ chromosome occurs by ___ translocation between the ___ arms of chromosomes ___ & ___. The translocation occurs in a ___ SC. RECIPROCAL, LONG, 9, 22, PLURIPOTENT
___% of CML pts are Ph+. 95
ABL is a ___ on chromosome ___. (___ = long arm). ABL = ___, which is the name of a leukemia ___ with a similar ___. It encodes a non-receptor ___ (c-ABL). PROTO-ONCOGENE, 9q, q, ABELSON, VIRUS, PROTEIN, PTK
BCR = “___”. It’s located on chromosome ___. It’s named for the point at which the ___ breaks in ___ translocation. BCR protein is involved in ___, ___, ___, ___. BREAKPOINT CLUSTER REGION, 22q, CHROMOSOME, CML, OLIGOMERIZATION, SERINE KINASE ACTIVITY, GUANINE NUCLEOTIDE EXCHANGE, GTPase ACTIVITY
The BCR/ABL fusion protein is a ___kD protein made when both genes are translated into a single ___ with no ___. It’s found on the ___ side of the cell membrane. It has a ___ active ___ region. 210, PROTEIN, STOP CODON, CYTOPLASMIC, CONSTITUTIVELY, TYROSINE KINASE
BCR/ABL fusion protein causes increased ___, decreased ___, disturbed interaction with the cell’s ___. PROLIFERATION, APOPTOSIS, ECM
The increased proliferation caused by BCR/ABL is increased cell cycle entry of ___ cell lines & ___ cells in the absence of ___. This causes these cell lines to become independent of ___ for ___ & ___. HEMATOPOIETIC, PRIMARY, GROWTH FACTORS, CYTOKINES, SURVIVAL, PROLIFERATION
Decreased apoptosis caused by BCR/ABL is caused by the ___ that activates downstream ___ to prevent ___. TYROSINE KINASES, KINASE, APOPTOSIS
BCR/ABL causes disturbed interaction w/ the cell’s ECM by activating several proteins associated with ___ structure & function. CYTOSKELETAL
The 1st line drugs for CML before imatinib were ___ + ___ (___) or ___. INTERFERON α (INF), CYTOSINE ARABINOSIDE (CYTARABINE – CA), HYDROXYUREA
Treating CML using INF & CA is problematic because they are very ___ chemotherapy. They are ___ with heavy ___ (<___% imatinib vs ___% for INF). BROAD SPECTRUM, NONSPECIFIC, SEs, 1, 25
The advantage of imatinib over INF is that more patients achieve complete ___ (absence of ___) with imatinib. ___% imatinib vs ___% INF. CYTOGENIC RESPONSE, PH+, 76, 14
Colchicine works by binding ___, a ___ protein causing its ___. This disrupts cellular fxns like the mobility of ___, thus decreasing their ___ to the ___. TUBULIN, MICROTUBULAR, DEPOLYMERIZATION, GRANULOCYTES, MIGRATION, AFFECTED AREA
Probenecid is a ___ agent. It is a weak ___ acid that promotes ___ of ___ by inhibiting the ___ in the ___ that mediates ___ reabsorption. URICOSURIC AGENT, ORGANIC, RENAL CLEARANCE, URIC ACID, URATE-ANION EXCHANGER, PROXIMAL TUBULE, URATE
Allopurinol blocks ___, which is helpful because when that is inhibited, circulating ___ derivatives (___ & ___) are more ___ & less likely to ___. It also causes feedback inhibition of ___ synthesis. XANTHINE OXIDASE, PURINE, XANTHINE, HYPOXANTHINE, SOLUBLE, PRECIPITATE, PURINE
Oxypurinol is a ___ of ___ that also inhibits ___. METABOLITE, ALLOPURINOL, XANTHINE OXIDASE
RN reductase or ___ reductase is the ___ in ___ synthesis. RIBONUCLEOTIDE, RATE-LIMITING ENZYME, DNA
SNoW DRoP Southern blot: DNA, Northern blot: RNA, Western blot: Protein
In the past, hydroxyurea was used in CML when the patient was ___ or did not ___ to ___. RESISTANT, RESPOND, INF
In CML, hydroxyurea ___ the disease, but does not ___. It holds cells in ___ & is lethal to those in ___. MANAGES, CURE, G1, S PHASE
Hyperleukotic syndrome is treated with ___ + ___ as the 1st step in treatment. Then ___ is added while ___ is tapered as ___ lower. LEUKAPHORESIS, HYDROXYUREA, IMATINIB, HYDROXYUREA, WBCs
Rational Drug Design is a way of creating drugs based on their ___ - usually a ___ in a ___ or ___ pathway. BIOLOGICAL TARGET, MOLECULE, SIGNALING, METABOLIC
Rational Drug Design is developed using ___ at ___ resolution to understand structures of ___ so ___ can be designed & ___ minimized. X-RAY CRYSTALLOGRAPHY, ATOMIC, RECEPTOR COMPLEXES, LIGANDS, DRUG RESISTANCE
Dasatinib is a drug that more effectively ___ BCR/ABL ___ than ___. INHIBITS, KINASE, IMATINIB
Gleevec resistance may occur by ___ of the Bcr/Abl gene &/or increased ___ due to increased ___, &/or ___ of bcr/abl ___ resulting in high levels of ___ activity even in the presence of ___. AMPLIFICATION, EFFLUX, MULTI-DRUG RESISTANCE PTN, ALTERATIONS, AAs, KINASE, IMATINIB
Dasatinib's ___ allows for activity in the majority of ___ stages of __ & ___. CHEMICAL STRUCTURE, IMATINIB-RESISTANT, CML, PH+ ALL
Dasatanib isn't a substrate for ___ (a.k.a. ___). This means it can have increased ___ in ___ cells that highly express ___. MULTI-DRUG RESISTANT PROTEIN, P-GLYCOPROTEIN, CONCENTRATION, HEMATOPOIETIC CELLS, P-GLYCOPROTEIN
Dasatanib also targets many other ___. This may contribute to the ___ response. KINASES, CYTOGENIC
There may not be ___ btn dasatinib & imatinib, as studies have ID’ed several ___ that confer resistance to ___ but not ___. X-RESISTANCE, BCR/ABL MUTATIONS, DASATINIB, IMATINIB
In CML, hydroxyurea specifically binds ___ catalytic subunit – highest [] during ___. Esp in ___ this leads to ___ of cells at ___ causing apoptosis. Immediate inhibition of ___ synth – no effect on ___ or ___ synth. M2, S PHASE, RAPIDLY DIVIDING CELLS, ACCUMULATION, G1/S PHASE, APOPTOSIS, DNA, RNA, PTN
___ is the only curative Tx for CML. 1st & 2nd line Txs = ___ & ___ for leukocytosis. Older chemotherapeutic agents are no longer used unless newer treatments do not work. Hydroxyurea is still used for WBC >___ before primary Tx is started. BM TRANSPLANT, TK INHIBITORS, HYDROXYUREA, 100,000
Hematologic Response – normalization of ___ in ___, not necessarily in ___. WBC CT, BLOOD, BM
Cytogenic Response – reduction in or the elimination of the ___ expressing the ___. # OF CELLS, PH+ CHROMOSOME
Leukapheresis: use ___ to rapidly & safely lower WBC counts in pts w/ WBC >___ cells/uL. May ctrl ___ in ___ phase CML. ___ & ___ – used to alleviate ___ Sx. Used in emergencies like ___ or ___. Also in ___ who need to avoid ___ drugs. CELL SEPARATOR, 300,000, BLOOD CTS, CHRONIC, EXPENSIVE, CUMBERSOME, ACUTE, PULM FAILURE, STROKE, PG WOMEN, TERATOGENIC
INF has ___ & ___ activity. Suppresses CML ___ cells & allows normal SCs to reconstitute the ___. Tx of choice after ___ – given after ___ response. Used in pts too old for ___ or who don’t have a ___. ANTI-TUMOR, IMMUNOMODULARY, PROGENITOR, BM, IMATINIB, HEMATOLOGIC, BM TXPLT, MATCHED DONOR
With INF, cytogenic response tested every __. Goal = ___. Pts w/ ___ should stay on maintenance therapy as long as ___ continues. ___ noted in most pts, ___ noted in ___% pts. Usually started at low doses due to heavy toxicity. 3-6 MOS, 100% REMISSION, MINIMAL RESIDUAL DISEASE (MRD), PARTIAL REMISSION, COMPLETE, 27
Hydroxyurea is an ___ of ___ synthesis – most common ___ used for hematologic remission. INHIBITOR, DEOXYNUCLEOTIDE, MYELOSUPPRESIVE AGENT
When giving hydroxyurea monitor ___ & ___ ct ea ___ & adjust dose accordingly. Less ctrl of ___ manifestations req's more F/Us. Most pts achieve ___ remission w/in ___. Has low ___, but rarely => ___ remission. WBC, PLT, 2-4WKS, HEMATOLOGIC, HEMATOLOGIC, 1-2MOS, TOXICITY, CYTOGENIC
Busulfan (___)is an ___ agent used to keep ___ <___cells/uL. Difficult to maintain numbers b/c ___ effects occur much later & persist longer. Not used anymore b/c long-term use causes ___ & ___. MYLERAN, ALKYLATING, WBCs, 15,000, MYELOSUPPRESSIVE, PULM FIBROSIS, HYPERPIGMENTATION
___ AKA Bone marrow transplant is the only ___ treatment for CML. Recommended w/in ___ of DX or after ___ of ___ therapy w/o good ___ response. HEMATOPOIETIC (STEM) CELL TRANSPLANTATION, CURATIVE, 1YR, 1YR, INF, CYTOGENIC
BM TXPLT cures CML by initial ___ then long-term ___ from donor’s ___. Alloimmune effect called “___”. Recurring ___ disease after transplantation can usually be reversed w/o more ___ by infusion of ___from ___ – can => long term remission in ___% pts. CYTOREDUCTION, IMMUNE CTRL, IMMUNE SYSTEM, GRAFT VS LEUKEMIA, CHRONIC PHASE, CHEMO, T LYMPHS, INITIAL DONOR, 50-70
BM TXPLT Should be considered early in pts <___. It's better for pts in ___. Most difficult part is ___ – only ___ have HLA matched siblin. ___ HLA match donor = best possible match. Complications inc. ___, ___ and ___. 40Y, CHRONIC PHASE, FINDING DONOR, 1/3, 6/6, GRAFT VS HOST DISEASE, VENO-OCCLUSIVE DISORDERS, TRANSPLANTATION-RELATED INFECTIONS.
Dasatinib, AKA ___ is used in pts resistant to ___. It's ___ competitive, dual specific ___ & ABL kinase inhibitor. ___ fold potency against BCR/ABL compared to imatinib. Approved as a ___ line Tx for CML; being evaluated as ___ line. SEs: ___ & ___. SPRYCEL, IMATINIB, ATP, SRC, ABL, 100-300, 2ND, 1ST, MYELOSUPPRESSION, GI TOXIC EFFECTS
Nilotinib is a ___ inhibitor. It has ___ fold potency compared w/ ___. Better ___ for ___ pocket. Currently in clinical trial. TK, 20-30, IMATINIB, TOPOGRAPHICAL FIT, KINASE
Microtubules are attached to ___ & pull on ___ in ___. They are used in ___, ___, & ___. SPINDLES, CHROMOSOMES, MEIOSIS, MITOSIS, CYTOKINESIS, VESICULAR TRANSPORT
Microfilaments: ___ filaments of the ___. They're found in the ___ of all ___ cells. They're linear polymers of ___ – flexible & strong, & highly versatile: ___, ___, changes in ___. Also contractile ___ like tensile platform for ___ in muscle contraxn. THINNEST, CYTOSKELETON, CYTOPLASM, EUKARYOTIC, ACTIN, CELL CRAWLING, AMOEBOID MVMT, CELL SHAPE, MOLECULAR MOTORS, MYOSIN,
Created by: 16813610