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63 Cards in this Set
- Front
- Back
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where is an uncommon place for sarcomas to metastasize?
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lymph nodes! sarcomas tend to use the blood stream to get around, carcinomas are all about going to lymph nodes.
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ataxia telagiectasia - what cancers are at increased risk by this disease?
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blood cancers! lymphoma/leukemia.
recall that this is an ATM mutation (DNA repair gene) |
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when talking about lymphoma, what's a good way to tell between large and small cell B cell lymphomas? quick review of which is in which category:
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small cell includes:
CLL/SLL Follicular (14:18t, BCL2) Mantle (11:14), up cyclin D/BCL1 Marginal (11:18t) Lymphoplasmocidic (high monoclonal IgM/hyperviscosity) Large: -Burkitt's (8:14t, starry sky, varouled cells, EBV) -Diffuse, Large Cell (BCL-6 mut, CHOP) The path book says the way to tell the difference is first to verify that it's B cell involved (cd19+, cd10+). Diffuse large cell tends to be LOCALIZED (weird, 'cause it's diffuse), often Waldeyr's Ring - small cell tends to be more WIDESPREAD, liver/spleen enlargement, lymph nodes all over screwed up. |
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what diseases involve hyperviscosity, and what are the associated symptoms?
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P vera and lymphoplasmocytic Lymphoma are both diseases of hyperviscosity. Typically see problems of dizziness/eye problems. Bleeding too.
multiple myeloma too. |
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What if you see lots of blasts of different lineages in bone marrow? And a c/somal deletion (either partial or complete?)
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often MYELODYSPLASIA (MDS) - often post-treatment for other blood cancers. Screwed up stem cells of various varieties. Remember that it's monosomy 5/7, trisomy 8.
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if the cancer in question is found to regress when H. pylori is treated, what are we likely talking about?
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a MALToma that is likely B cell cell in origin and small cell - MARGINAL zone. Marginal tumors are often related to autoimmune or infectious processes.
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how do you identify follicular lymphoma on slides? compared to nodular sclerosis and diffuse large B cell lymphoma?
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see a LN biopsy with follicles BACK TO BACK, still well organized. In contrast to Nodular Sclerosis HODGKIN's, which has fibrous bands between the follicles.
Also note that with follicular lymphoma, you'll see BUTTOCK cells in the peripheral blood smears. compared to DLBCL, don't see any follicles with DLBCL - just disorganized, ugly lymph nodes. Just for fun, compared to ALCL - the T cell version - there are TONS of weird, disorganized, shitty follicles without one dominant cell type. |
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what mutations should we associate with hereditary melanoma?
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p16 mutation.
note that the number of relatives with melanoma is the best predictor of disease risks, not the age of onset. mutation = 70% risk of melanoma. |
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What's LCA and where do you see it?
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leukocyte common antigen - seen on Burkitt's lymphoma!
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HIV lymphomas - where are they seen?
what causes body cavity lymphoma? |
they can be nodal or extranodal. Note that they're mid or high grade B cell lymphomas.
Extranodal common sites are the CNS and GI tract. Also liver, skin, cavity-based. body cavity can be HHV8 related, or EBV. |
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if you see RBC's in skin but not in vessels (extravascular invasion of RBC's) what disease should you think of?
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Kaposis Sarcoma!
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in AIDS patients, what can coccoidies give you? what should multinucleated giant cells make you think of?
what about microglial nodules? |
lung infiltrations.
multinucleated giant cells = MAC. microglial nodules = pathonumonic for AIDS DEMENTIA COMPLEX. |
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what do you see with JC virus?
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on EM, spaghetti and meatballs.
these are the crystaline forms of the virus (papovirus = JC). |
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in HIV disease, it's found that the Gp120/41 domains have homology with what, and what can this cause?
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MHC II - this ups the auto-destruction of CD4+ cells, driving disease progression.
Also note that CD4 cells die from apoptosis, from ADCC. |
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one ides for HIV treatment is to get the latent reservoirs to go lytic and express virus. how do we do that?
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Valproic Acid
or HDAC: Histone DeAcetylase! |
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viral loads and HIV diseases: where do you get Cryptococcus? Toxo? Mac? CMV? TB? PCP?
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Crypto and Toxo go together - less than 200, above 50.
Mac and CMV go together at less than 50. Don't forget that MAC can take weeks go grow out of culture. TB goes with KS get that at 200 to 500. PCP happens below 200. |
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what's a side effect of AZT we're supposed to remember?
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that you STOP FORMING RED BLOOD CELLS - and so get anemia. .
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what does a target RBC indicate?
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targetoid RBC's are indicicative of THALASEMIAS, especially Beta. Any congenital hemoglobinopathy. Liver disease. Maybe spleen disease.
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Though the distinction between lymphoma and leukemia is not always very clear, what's one definition?
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if greater than 4000 lymphocytes cells per uL are found in the blood, it's a leukemia.
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what conditions show up with microspherocytes? what about microcytic anemia?
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autoimmune hemolytic anemia and inherited spherocytosis (ankyrin gene screwed up)
microcytic anemia can be involved with IRON DEFICIENCY, or the inherited thalasemias. |
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what drug must be polyglutemated to stay inside cells?
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methotrexate.
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what is the heterophile antibody associated with?
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it's the usual EBV test, though it's not 100%.
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what's the identifying features of sarcomas?
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know OSTEOSARCOMA (osteoid), leiomyosarcoma (spindle cells have weird mitotic activity) from leiomyoma (spindle cells are benign looking, even).
All spindle sarcomas will have SPINDLE CELLS. |
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what do target cells indicate?
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hemoglobinopathies or liver disease -
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s-100 indicates what?
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neuroendocrine cells.
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What protein can mess with p53?
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MDM-2 has the power to inactivate p53, making MDM2 an oncogene.
Also note that p53 has the power to be DOMINANT NEGATIVE - meaning if a single copy is mutated, it can create a weird protein which inhibits normal p53 - this is, in effect, causing the "two hits" to happen with only ONE hit. |
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what does RB bind and do?
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RB binds E2F, which is a cell-cycle transcription factor that encourages cell growth. Also might interact with MYC, which has a similar action.
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if someone says inhibitory cell pathways, what should you think of?
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cip/kip, and Ink4/ARF (this is normally activated by p16
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what are the direct and indirect anti coagulants?
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what are the direct and indirect anti coagulants? direct = heparin and deravitives. strong acid, interaction with anti-thrombin
indirect = warfarin. warfarin = strong |
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what pro-coagulants can you given?
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thrombin and fibrin are drugs that can be given.
also, OXIDIZED CELLULOSE. |
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how do cancer cells get resistance, primarily?
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primary resistance - drug may simply not work on that cell.
acquired resistance - tumor cells used to be susceptible, not any more. can up DNA repair, MDR1 - P glycoprotein! - multidrug resistance gene. causes NATURAL DRUGS TO EFFLUX OUT. |
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antimetabolites - what's special about their activity?
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they have to be activated INSIDE cancer cells to be activated.
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what are capecitabine and gemcitabine?
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Capctabine - prodrug of 5-fu. Activated by liver.
Gemcitabine - kills ribonucleotide diphsphate rreductase (ribonucleotide reductase) - so no deoxy nucleotides = no DNA. |
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what's the main difference in indication for 5-fu and methotrexate?
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they're both antimetabolites, but have different cancers used on.
5fu only used on solid tumors, methotrexate can be used on both solid and blood cancers. |
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what's TAC? what other drug combos are used in this?
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what's TAC? used for breast cancer.
piclataxel (taxol) A = doxorubicin C = cyclophosphamide. also use CAF and CMF: cyclophosphamide, doxorubicin, and 5fu. cyclophosphamide, methotrexate, and 5-fu. |
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what's tumor lysis syndrome?
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seen in cancers that respond really well to drugs - like acute leukemias, high grade lymphomas. comes from high cellular turnover. also small cell lung cancer, testicular cancer.
HYPOcalcemia high LDH, phosphate, potassium. LOW CALCIUM. treat with hydration and allopurinol, maybe need dialysis. |
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what causes hyper-segmented polys?
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b12/folate, and MDS. Also some drugs like hydroxurea.
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TTP?
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thrombotic thrombocytopenia purpura - messed up von wily is too sticky and get little micro thromboli all over, get SCHISTOCYTES, MAHA, fever, renal, CNS problems.
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MCHC?
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goes up ONLY IN heredetary spherocytosis. Not up too much in warm acquired hemolysis.
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bite cell?
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G-6-P deficiency!!!!!
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what happens in spleen size when compared to kids?
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kids have BIG SPLEENS with sequestration crisis, adults have little tiny killed spleens.
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Do you see jaundice in the warm/cold acquired immune driven hemolytic anemias?
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yes - remember that these problems involve EXTRAVASCULAR hemolysis (warm = IgG = killed in spleen, cold = IgM = killed by complement fixation/liver.
INTRAVASCULAR hemolysis is seen in G6PD deficiency - note here you also get BITE CELLS. |
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if the prompt has a kid with bone lesions, what should you think of?
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langerhans cell hysteocytosis. don't know what this is yet, but lytic bone lesions are typically associated with multiple myeloma IN ADULTS (not kids).
kids also might have a rash. |
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what does someone with specifically high IgM concentrations in the serum probably have?
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waldenstrom macroglobulinemia. see TINY plasma cells in the marrow (multiple meloma has big normal-ish plasma cells, and has GAMMAopathy)
also, if it were multiple myeloma, the prompt would include something about bones or hypercalcemia. |
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presentation of large vs. small cell B cell lymphomas:
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large cells tend to be in one place (waldyer's ring), whereas small cell tends to involve wide spread lymphadenopathy.
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If you see a smear with huge platelets full of granules, what's the diagnosis?
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Bernard Soulier Syndrome. Unclear if we have to know this.
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Prothrombin Time and aPTT - what does having these times prolonged say about the platelet count? What are the typical values?
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they say NOTHING about the platelet count - these are for looking at the function of blood CLOTTING FACTORS. Bleeding time might have something to do with platelets?
normal PT = 10-15 seconds. normal PTT = 20-30 seconds. normal bleeding time is up to 9 minutes. |
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vimentin = what?
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sarcoma
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dysplasia pictures - what do they generally look like, and what's the definition?
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called NON NEOPLASTIC - disordered growth. see cells that are all pointed the wrong way, hyperchromatic.
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Signet rings are found in what?
while we're on the subject, what do liposarcomas have as a distinguishing figure? |
adenocarciomas that produce mucin INSIDE the cell. note that they can make mucin OUTSIDE the cell too, which causes the cells to "float"
LIPOSARCOMAS - they have flattened nuclei that are touching several fat vacoules, flattening the nuclei out. |
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remember what a carcinoid tumor looks like and what it can do?
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these are of neuroendocrine origin, so they can secrete active hormones/peptides.
the picture we've seen is a big clump of cells deep to the lumen of the intestine. usually low grade, well differentiated, not super dangerous. |
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What is TGF-beta? what about a quick review of what APC does?
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transforming growth factor beta. It's a tumor suppressor, stops cell cycle (think SMAD4-it's activated by TGF and suppresses).
It's mutated in all pancreatic cancers, most colon cancers. APC = a killer of BETA catenin, which goes on to activatee WNT. A, B, W. |
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in which of our acquired immune hemolytic anemias are RBC's cleared in the spleen?
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warm! warm = spherocytes = spleen.
remember in cold, the RBC's are covered by IgM which bind COMPLEMENT. |
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If you find someone who has a several week history of some form of anemia, what cells should you EXPECT To see in the blood smear? what if they're not there?
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Reticulocytes should begin to form in response to anemia within 4 days. If they're not there, expect APLASTIC anemia - maybe caused by DRUG exposure in normal people, or CHEMO, or B-19 in people with underlying congenital RBC issues.
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TTP should show what symptoms? How do you tell it from ITP?
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renal failure
MAHA headache/CNS problems fever thrombocytopenia. = thrombotic thrombocytopenic purpura. remember that TPP is caused by lack of the ADAM enzyme that normally cleaves up Von Wili into smaller bits - when it stays big, it causes little clots ALL over (sorta like DIC, but with schistocytes from the MAHA). idiopathic thrombocytopenic purpura = everything's normal, but not enough platelets around (see megakaryocytes raised in the BM to replace the ones that are dying, etc). recent infection antibodies may be killing the platelets. |
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what ethnicity is at most risk for serious alpha thalasemia?
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southeast asians and blacks. if there are NO alphas of the 4 possible, get double GAMMA dimers (bart's Hb). baby dies.
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in beta thalasemia, what kinds of inclusions are found in RBC's?
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alpha inclusions - you make lots of alphas and not enough betas, so they get hung up. Also can get targetoid cells.
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what is the process of a chemical carcinogen messing with someone?
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initiation, promotion, progression. I pro pro.
initiation is irreversible DNA damage, but not yet neoplastic. promoters - MUST BE METABOLICALLY ACTIVATED. Don't have to mutate, are MITOGENS, have to be around for awhile. Promote division, fixation of already acquired mutations. Progression - now IRREVERSIBLE, becoming MALIGNANT. Includes angiogenesis. remember that carcinogens HAVE TO BE ACTIVATED IN THE LIVER. |
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what can inactivate p53?
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MDM2
and HBx (the HBV protein), also ups insulin-like growth receptors. |
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what is the process of a chemical carcinogen messing with someone?
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initiation, promotion, progression. I pro pro.
initiation is irreversible DNA damage, but not yet neoplastic. promoters - MUST BE METABOLICALLY ACTIVATED. Don't have to mutate, are MITOGENS, have to be around for awhile. Promote division, fixation of already acquired mutations. Progression - now IRREVERSIBLE, becoming MALIGNANT. Includes angiogenesis. remember that carcinogens HAVE TO BE ACTIVATED IN THE LIVER. |
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what can inactivate p53?
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MDM2
and HBx (the HBV protein), also ups insulin-like growth receptors. |
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what do smear cells make you think of? what are the other key words for this?
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no such thing as smear cells.
SMUDGE cells are part of CLL. This is the most common ADULT leukemia. |
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what's choliocytic atypia?
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in carcionomas ,see HALOS around cells. ?
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