Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Experiment
| Question | Answer |
|---|---|
| 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
Popular USMLE sets