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185 Cards in this Set
- Front
- Back
Factors 8 and 5 are "accelerating factors" - what inhibits these? |
Protein C and Protein S |
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Why do you usually start warfarin with heparin? |
Because you're transiently hypercoagulable when you give someone warfarin - it breaks down protein C and protein S faster than it breaks down 2, 7, 9, and 10 |
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Kallikrein has two functions - makes plasmin from plasminogen (breaks down clots), and it makes bradykinin from HMWK (high molecular weight kininogen), and bradykinin has these three functions |
Vasodilator, increases vascular permeability, mediator of pain --> involved with inflammation |
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Factor 5 Leiden is a mutation |
makes it resistant to inactivation by protein C, so you increase coagulation |
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How do heparin and LMWHs differ in their mechanism of action? |
Heparin stimulates antithrombin to inactive thrombin and factor Xa AND binds to thrombin itself, but LMWH only stimulates antithrombin to inactivate factor Xa |
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What is the antidote for heparin? Warfarin? Thrombolytics? |
Protamine sulfate, FFP + Oral/IV vitamin K, aminocaproic acid |
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Fondaparinux |
synthetic Factor Xa inhibitor |
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In what situations are thrombolytics contraindicated? |
patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding disorder, severe hypertension |
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Which cytoskeleton protein in RBCs is responsible for them being flexible/bendy? |
Spectrin |
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Main cause of basophilic stippling? |
Lead poinsoning |
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Spiky RBCs - Burr cell aka Echinocyte vs acanthocyte |
Polycythemia vera, Essential thrombocytosis, myelofibrosis - all have JAK2 mutation where it's on all the time |
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Schistocytes seen with these conditions |
DIC, TTP, HUS |
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Which conditions can you have target cells with? |
THAL - Thalassemia, Hemoglobin C disease, Asplenia, Liver disease |
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Howel Jolly bodies seen in these patients |
Asplenic |
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Howel jolly bodies look like heinz bodies, but heinz bodies are found in patients who DO have a functioning spleen. Often found with bite cells as splenic macrophages try to bite off the heinz body. Who gets these? |
G6PD - oxidative damage to hemoglobin causes heinz bodies |
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Teardrop cells seen with |
Myelofibrosis |
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Sideroblastic anemia common with |
Lead poisoning |
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Incompatible blood type transfusions cause this type of hypersensitivity reaction |
Type II - antibody mediated. Circulating antibodies binding to cellular antigens |
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Anytime a pregnant mom is in any sort of trauma, when she's at 28 weeks, or three days post delivery, we give mom this to prevent erythroblastosis fetalis |
Anti Rh immunoglobulin to Rh- moms |
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Fetal hemoglobin has a lower affinity for ____ and a higher affinity for ____ |
2,3 DPG, Oxygen |
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Rate limiting enzyme of heme synthesis is |
aminolevulinic acid synthase (ALA synthase) - make ALA from glycine and succinyl CoA with B6 |
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What are the two types of porphyria to know? |
Acute intermittent porphyria and porphyria cutanea tarda. |
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What enzyme defect causes acute intermittent porphyria and what is the presentation? |
Acute is caused by uroporphyrinogen-1-synthase deficiency AKA porphobilinogen deaminase. Abdominal pain, very dark "port wine" urine, polyneuropathy and psychological disturbances. Precipitated by drugs (barbiturates, seizure drugs, firampin, metoclopramide) |
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Treatment of acute intermittent porphyria |
Glucose (or dextrose) and heme - inhibit ALA synthase |
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Symptoms of porphyria cutanea tarda and the enzyme implicated |
Porphobilinogen deaminase. Sx are blistering of skin, photosensitivity, tea colored urine and hypertrichosis (excessive hair growth). Associated with hepatitis, alcoholism, elevation of LFTs |
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Which two enzymes of heme synthesis are effected by lead poisoning? Symptoms? |
ALA dehydratase and ferrochelatase. Red cells have increased levels of protoporphyrin because of ferrochelatase inhibition. Sx include encephalopathy, memory loss, delirium, foot dorp/wrist drop, basophilic stippling, sideroblastic anemia, lead lines in X rays |
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Treatment of lead poisoning |
Succimer or EDTA |
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Which 4 tumors can cause polycythemia? |
Pheochromocytoma, Renal cell carcinoma, hepatocellular carcinoma, and hemangioblastoma (vascular CNS tumor) |
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Iron deficiency anemia + esophageal webs + atrophic glossitis |
Plummer Vinson syndrome |
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What are the microcytic anemias? |
Iron deficiency, thalassemias, lead poisoning, sideroblastic anemia, anemia of chronic disease sometimes but it's mostly normocytic |
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Normally, you have 4 alleles for alpha globin gene - 2 from mom and 2 from dad. What happens when 1 is mutated? 2? 3? 4? |
1 - nothing, 2 - alpha trait, 3 - Hemoglobin H disease (where beta globins pair up and make hemoglobin H), 4 - incompatible with life (hemoglobin Bart's forms - 4 gamma globins) |
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Instead of 4 alleles for alpha globin, for beta globin you only have 2. What causes beta globin minor vs major? |
Minor - 1 mutation decreases amount of B globin. Increased hemoglobin A2 (alpha globin + delta globin). Beta major has no beta globins, severe anemia requiring blood transfusions |
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"Hair on end" appearance on X ray in beta thalassemia |
Due to bone marrow hyperplasia - seen in sickle cell as well, often called a "crew cut" x ray |
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Hypersegmented neutrophils |
Megaloblastic anemias (folate, B12) |
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Folate or B12 - which one causes neurological deficits like peripheral neuropathy and dementia? |
B12 |
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Homocysteine increased in both folate deficiency and B12 deficiency, but ____ is increased in B12 and not folate |
Methylmalonic acid |
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Which megaloblastic anemia is NOT correctible by B12 or folate? |
Orotic aciduria - deficiency of UMP sytnhase which is part of pyrimidine synthesis |
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What are the etiologies of nonhemolytic normocytic anemia? |
Anemia of chronic disease, aplastic anemia, renal failure b/c low EPO |
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Hypocellular bone marrow with fatty infiltration, normocytic anemia |
Aplastic anemia |
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What causes aplastic anemia? |
Parvovirus B19 (particularly sickle cell patients) , EBV, HIV, radiation, benzene, chloramphenicol/cancer drugs |
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What are the different types of hemolysis? |
Intravascular and extravascular |
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What labs do you see with intravascular hemolysis? |
Increased LDH, decreased haptoglobin, increased unconjugated bilirubin |
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What can cause intravascular hemolysis? |
Autoimmune hemolytic anemia, paroxysmal nocturnal hemoglobinuria, mechanical destruction of RBCs (eg prosthetic heart valves, aortic stenosis) |
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What can cause extravascular hemolysis? |
Hereditary spherocytosis - spleen destroys these, G6PD deficiency, pyruvate kinase deficiency, hemoglobin C disease, sickle cell |
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Ankyrin, spectrin deficiency = |
Hereditary spherocytosis |
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Higher RDW (variability in size), increased MCHC |
Hereditary spherocytosis - increased MCHC = mean corpuscular hemoglobin conc is increased b/c you have same amount of hemoglobin in a smaller area |
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Osmotic fragility test |
Diagnostic test for hereditary spherocytosis |
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Treatment for hereditary spherocytosis? |
Splenectomy to stop anemia. You'll see howell jolly bodies after |
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Why does pyruvate kinase deficiency cause hemolytic anemia? |
because you can't do glycolysis and can't make ATP. RBCs swell and lyse |
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RBCs missing surface markers CD55 and CD59 |
Paroxysmal nocturnal hemoglobinuria - complement attacks RBCs and lyses them |
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Ham's test |
Test for paroxysmal nocturnal hemoglobinuria - Add acid and that lowers pH, activating complement, lyses RBCs |
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Hypoxemia, dehydration, acidosis can all cause |
Sickle cell crysis |
|
Salmonella osteomyelitis |
More common in sickle cell patients |
|
Renal papillary necrosis |
Sickle cell |
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Tx for sickle cell |
Hemoglobin F |
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Hemoglobin C disease mutation |
Lysine substitued for glutamic acid - not as bad as sickle cell. Hemoglobin C molecules form hexagonal crystals in the cell but don't make long polymers like sickle cell |
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Microangiopathic vs macroangiopathic anemia |
Macroangiopathic is due to prosthetic heart valves and aortic stenosis. Microangiopathic is due to DIC, TTP, HUS, malignant hypertension, lupus |
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What are the two types of autoimmune hemolytic anemia? |
Warm (IgG) and cold (IgM) agglutinins |
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Cold aggluctinins occur with these infections |
EBV or mycoplasma, as well as CLL |
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Warm agglutinins are seen in |
EBV, HIV, Lupus, CLL/non hodkin limphomas |
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Platelet plug formation goes in these three general steps |
Platelet adhesion, activation, aggregation |
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What makes von willebrand factor? What does vWF do? |
Endothelial cells lining vasculature and megakaryocytes. Stabalizes factor 8 and platelet adhesion to vessell wall and other platelets |
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Increaed PTT and increased bleeding time with this deficiency |
Von willebrand factor deficiency |
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vWF binds to subendothelial cartilage and |
GPIB on surface of platelet - platelet adhesion |
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What do activated platelets secrete? |
ADP, PDGF, serotonin, fibrinogen, lysosomal enzymes, Thromboxane A2, calcium, thrombin |
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What does thromboxin A2 do? What does ADP do? |
TXA2 - vasoconstriction and platelet aggregation. ADP triggers platelets to express GPIIb/IIIa receptor, which binds to fibrinogen released by platelets and forms cross links/ promotes aggregation |
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How does aspirin inhibit platelet function? |
Inhibits COX and irreversibly blocks arachidonic acid to TXA2 conversion (remember, TXA2 is important for platelet aggregation) |
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How does clopidogrel work? |
Binds ADP receptor and blocks it and prevents GPIIb/IIIa expression to block platelet aggregation |
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Abciximab, tirofiban, eptifibatide |
Block glycoprotein IIb/IIIa to prevent platelet aggregation |
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Autoantibodies to GPIIb/IIIa |
ITP - immune thrombocytopenia. |
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ADAMTS 13 deficiency - what is this disease? describe the pathophys |
This is TTP - thrombotic thrombocytopenic purpura. ADAMTS 13 normally cleaves vWF into usable units. If you have this deficiency, you get excessive platelet aggregation and activation and cause widespread thrombosis. Then because you're consuming all of these platelets, you get thrombocytopenia |
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What is the classic triad of HUS and what is the classic triad of TTP-HUS? |
HUS - hemoylsis, renal insufficiency (uremia), thrombocytopenia. TTP would be those three + neurological symptoms (confusion/headaches/seizure) and fever |
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E Coli 0157:H7 infection in children |
Associated with HUS |
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Defect of glycoprotein Ib, which binds vWF to subendothelial collagen |
Bernard Soulier syndrome - defect of platelet plug formation, platelet count is just slightly lower |
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Defect in glycoprotein IIb/IIIa |
Glanzmann thrombasthenia - platelet can't aggregate normally, but normal platelet count |
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Treatment of vWF disease? |
DDAVP - desmopressin. Increases release of vWF from endothelial cell stores |
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High D-dimer, low fibrinogen, prolonged PT, PTT, and bleeding time |
DIC |
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Causes of DIC |
STOP Making Thrombi - sepsis, trauma, obstretric complications, pancreatitis, malignancy, transfusion |
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Hodgkin lymphomas are usually confined to |
lymph nodes |
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Translocation 14;18 in some, lymphoma seen in elderly |
Large B cell lymphoma |
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Translocation 14;18 in most of these lymphomas |
Follicular lymphoma |
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Translocation t(8;14), activation of C-myc oncogene, starry sky appearance |
Burkitt lymphoma |
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HTLV-1 |
Adult T cell lymphoma |
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Mycosis fungoides - what is this and what can it progress to? |
Cutanoues T cell lymphoma that can progress to sezary syndrome |
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Long term celiac disease can cause this lymphoma |
intestinal T cell lymphoma |
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PAS+ leukemia, in children, very good prognosis |
ALL |
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Auer Rods |
AML. Stain positive for myeloperoxidase. If APL - treat with all trans retinoic acid |
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Acute leukemia shows a ton of ____ in marrow |
Blasts (either myeloblasts or lymphoblasts) |
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Chronic leukemia doesn't have a lto of blasts (<5 % blasts). Instead, myeloid (CML) or lymphoid mature cells (CLL) |
just know that |
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Smudge cells in this leukemia of elderly |
CLL |
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Philadelphia chromosome (9;22) always present |
CML |
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Pelger Huet Anomaly |
Cells that have two little lobes that look like sunglasses. Found in Myelodysplastic Syndrome - can progress to AML |
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What are the myeloproliferative disorders? What mutation do they have in common? |
Polycythemia vera, Essential thrombocytosis, myelofibrosis |
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JAK2 is a NON receptor tyrosine kinase |
just know that |
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Pruirits after hot shower, splenomegaly, hyperviscous blood, and low erythropoietin |
Polycythemia vera |
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Bone marrow with fibrosis infiltrate and teardrop shaped cells? Bone marrow for adipocyte infiltrate? |
Fibrosis - myelofibrosis. Fats - aplastic anemia |
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Malignancy of plasma cells |
Multiple myeloma |
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Anemia, renal insufficiency, back pain, hypercalcemia |
Multiple myeloma |
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Bence Jones proteins in urine |
Immunoglobulin light chains in urine found with multiple myeloma |
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Monoclonal antibody spike (M spike) on serum protein electrophoresis |
Multiple myeloma (remember, this is a plasma cell cancer making a ton of immunoglobulins, but makes just one type over and over, giving you that spike appearance) |
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Rouleaux formation |
multiple myeloma - RBCs stacked like coins |
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Multiple myeloma without bone lesions? monoclonal proliferation of IgM |
Waldenstrom macroglobulinemia |
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MGUS |
Monoclonal Gammopathy of Undetermiend significance - proliferation of plasma cells but no myeloma symptoms, but CAN progress to multiple myeloma |
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Solid tumor of plasma cells - can be solitary in bone or extramedullary in nose, and do not cause bone lesions |
Plasmacytoma |
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Which 4 cancers have psammoma bodies? |
Papillary thyroid cancer, serous papillary cystandenocarcinoma of the ovary, meningioma, malignat mesothelioma |
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Which cancers commonly metastasize to liver? |
Cancer Sometimes Penetrates Benign Liver - Colon, stomach, pancreas, breast, Lung |
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How does methotrexate work to prevent thymidine synthesis? |
It's an analog of folic acid that inhibits dihydrofolate reductase |
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What can you give with methotrexate to prevent myelosupression? What are other side effects of methotrexate? |
Leucovorin (aka folinic acid). Fibrotic lung disease and teratrogenicity are other side effects |
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5 fluorouracil also inhibits pyramidine synthesis like methotrexate, but inhibits this enzyme instead |
Thymidylate synthase - can't convert dUMP to dTMP |
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Leucovorin can't be used to treat myelosuppression you get with 5-fluorouracil - what can you use instead? |
Uridine |
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Methotrexate, 5 Fluorouracil, and hydroxyurea inhibit ____ synthesis. 6 mercaptopurine and mycophenolate inhibit ____ synthesis |
Pyrimidine, Purine |
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Toxicity of 6-mercaptopurine increases when patient is on |
Allopurinol, because it inhibits xanthine oxidase, which metabolizes 6-mercaptopurine |
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Cytarabine is pyrimidine analog - how does it work? |
Inhibits DNA polymerase |
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How does cyclophosphamide work? |
it's an alkylating agent - attaches an alkyl group to DNA, forming crosslink strands so DNA can't replicate |
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Which side effect can cyclophosphamide cause? This is due to its toxic metabolite acrolein. You can prevent this by giving mesna with cyclophosphamide |
cystitis |
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These anthracyclines are used to treat cancer |
Doxorubicin and daunorubicin |
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How do doxorubicin and daunorubicin work? |
Generate free radicals and intercalate DNA |
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What side effect is very important to know about doxorubicin and daunorubicin? |
Dilated cardiomyopathy because of free radical damage (heart cells have deficiency of superoxide dismutase) |
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Bleomycin also generates free radicals - what side effect does this have? |
Pulmonary fibrosis - bisulfan and methotrexate also causes pulmonary fibrosis |
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Cisplatin and carboplatin cross link DNA. They can cause nephrotoxicity and ototoxicity. Which other drugs also have these side effects? |
Loop diuretics! So do aminoglycosides vand vanco |
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Fluroquinolones (eg ciprofloxacin) and etoposide both inhibit |
topoisomerase II |
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Pilocytic astrocytoma and medulloblastoma are the two most common brain tumors in children. You can differentiate them on imaging - how? |
neurotoxicity, peripheral neuritis |
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Vinblastine and vincristine block microtubule polymerization. Paclitaxel also works on microtubules but has a different mechanism of action |
They hyperstabalize microtubules so cells can't break down the microtubules to properly divide |
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Tamoxifen is an estrogen receptor antagonist in ____ but agonist in ___ |
breast, bone. It's a partial agonist in endometrium |
|
Tamoxifen increases your risk of |
endometrial cancer - because it's a partial agonist here. So it can be helpful in women who have endometrial cancer, but increases risk of endometrial cancer in women who DONT have it |
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Monoclonal antibody against HER-2 used to treat breast cancers that express HER-2 |
Trastuzumab |
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Antibody against CD20, used to treat lymphomas, leukemias, and sometimes rheumatoid arthritis |
Rituximab |
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tPA and other fibrinolytics can cause |
Reperfusion arrhythmias on arterial reopening due to rapid reperfusion (these are usually benign) |
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What does c-myc actually do? |
it's a transcription activator |
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Which chemotherapy drugs can cause nephrotoxicity, and what do you give to patients to minimize/prevent nephrotoxicity? |
Cisplatin - give amifostine (cytoprotective free radical agent) and hydration |
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What do you give to prevent doxorubicin induced cardiotoxcicity? |
Dexrazoxane - iron chelating agent |
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Angiogenesis is stimulated by these two growth factors |
VEGF and FGF (NOT EGF - epidermal growth factor) |
|
T(15;17) |
APL - acute promyelocytic anemia, subtype of AML. Auer rods. ATRA treatment |
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What is the MDR1 gene and what does it code for? |
It codes for P glycoproteink, an ATP dependent efflux pump that pumps drugs out of cells and induces resistance to chemo drugs |
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Hemorrhagic cystitis - side effect of which chemo drug and how can it be prevented? |
Cyclophosphamide. Give mesna (binds |
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Malaise, anorexia, anemia, weight loss and generalized wasting |
Cachexia - caused by TNF-alpha |
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Pulmonary fibrosis and skin discoloration are side effects of this chemo drug |
Bleomycin |
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How does heparin work? |
Increases antithrombin activity |
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What are the encapsulated bacteria that infect asplenic patients and what symptoms do they cause? |
Strep pneumoniae and H flu (pneumonias). Neisseiria meningitidis (meningitis), Salmonella (osteomyelitis), Klebsiella, E coli and Staph aureus also all can cause osteomyelitis |
|
Decreased warfarin efficacy with |
CP450 inducers |
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Patients with renal dysfunction (eg diabetics) can have excessive bleeding due to accumulation of uremic toxins in the blood. this causes a QUALITATIVE platelet disorder - what would you see on PTT, PT, paltelet count, and bleeding time? |
everything normal besides bleeding time |
|
What is a hemarthrosis? |
Bleeding into joints - common in hemophilia |
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Findings in DIC |
Prolonged PTT, PT. Thrombocytopenia/microangiopathic hemolytic anemia. Low fibrinogen. Elevated D dimer, Low factor 5 and 8. |
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How do you monitor/early identification of DIC? |
Fibrinogen levels |
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This protein is a regulator of G1 to S phase transition |
Retinoblastoma - Rb |
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Increased incidence of Burkitt lymphoma and nasopharyngeal carcinoma |
EBV or mycoplasma, as well as CLL |
|
Neoplastic cells in multiple myeloma secrete |
IL-1 and IL-6 - activate osteoclasts and causes bone resorption/hypercalcemia. |
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Amyloidosis and subsequent renal failure with this leukemia |
Multiple myeloma - renal failure due to plasa cell infiltration and deposition of amyloid |
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Patients who recieve more than one body blood volume of whole blood or packed RBCs over 24 hour period can have elevated blood levels of ____. This can chelate calcium/magnesium and cause paresthesias |
Citrate |
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Person over 50 with iron deficiency anemia - what do you have to rule out? |
Blood loss, especially from GI tract due to colon cancer |
|
Which antiretroviral drugs do not require activation via intracellular phosphorylation? |
NNRTIs - Neviparine, Efavirenz, Delaviridine |
|
These two drugs are HIV fusion inhibitors |
Enfuviritide (GP41), and Maraviroc (CCR-5) |
|
Integrase inhibitor (HIV drug) |
Reltegravir |
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What are the protease inhibitors used to treat HIV? |
____navir (just know that) - prevent maturation and assembly of the virus. |
|
What are common side effects associated with NNRTIs? |
Hepatic failure with encephalopathy - flu like, abdominal pain, jaundice, fever |
|
15% of oral radiolabeled B12 is excreted in the urine (normal > 5) - is this pernicous anemia or dietary deficiency of B12 if this person has anemia? |
Dietary deficiency |
|
Which drugs can cause G6PD flare ups? |
Dapsone, antimalarial drugs, and TMP SMX |
|
Blurry vision due to increased VEGF |
Wet macular degeneration - angiogenesis due to elevated VEGF. Treat with anti VEGF therapy (ranibizumab) |
|
This is the drug of choice for hairy cell leukemia. It is resistant to degradation by adeosine deaminiase |
Cladribine - purine analog of adenosine |
|
Hepatitis B can integrate into DNA but hep C can't because it's an RNA virus |
just know this |
|
Waxing and waning lymphadenopathy with T(14,18) and BCL-2 oncogene overexpression |
Follicular lymphoma - most common indolent non hodgkin lymphoma in adults |
|
direct factor Xa inhibitors increase PT and PTT but not |
thrombin time |
|
integrin mediated adhesion of cells to basement membrane and extracellular matrix involves integrins binding to |
fibronectin, collagen, laminin |
|
BCL-2 is an oncogene because |
it has anti apoptosis effects |
|
Argatroban mechanism of action |
direct thrombin inhibitor - binds to thrombin active sites |
|
Abciximab blocks this receptor |
GP IIb/IIIa |
|
Treating B12 deficiency with folate can actually |
worsen neurological defects |
|
What is Li Fraumeni syndrome? What mutation is it associated with |
P53 mutation - autosomal dominant. Predisposes you to a ton of cancers (sarcomas, tumors of breast, brain, adrenal cortex) |
|
Pilocytic astrocytoma and medulloblastoma are the two most common cerebellar tumors in children. You can differentiate them on imaging - how? |
Pilocytic will have solid and cystic features (black and white), where meduloblastoma will just be solid (black) |
|
Ependymomas present with |
Bad headache, paiplledema, vomitting, HYDROCEPHALUS - obstruct CSF flow |
|
Hemosiderin accumulation in patients with hemolytic anemia or thalassemia b/c these patients often require frequent blood transfusions |
Just know that |
|
Down sindryome patients more likely to have this leukemia |
ALL |
|
extramedullary hematopoiesis can cause skeletal abnormalities and liver/spleen growth |
Thin bony cortex, impaired bone growth and deformities as well as hepatosplenomegaly |
|
This selective COX 2 inhibitor has anti-inflammatory effects without bleeding/GI side effects associated with nonselective ones |
Celecoxib |
|
Gram negative bacterial sepsis can cause |
DIC --> can cause schistocytes |
|
Which RBC fragmentation would you see with DIC? |
Schistocytes b/c this would be microangiopathic hemolytic anemia |
|
Pure red cell aplasia is associated with |
Thymoma (thymic tumor) and parvovirus B19 |
|
ALL is the most common malignancy in children. Can be B cell or T cell ALL. T cell ALL often presents as a mediastinal mass and causes |
respiratory symptoms, dysphagia, or superior vena cava syndrome (compresses great vessels) |
|
Triad of acute renal failure, thrombocytopenia (prolonged bleeding time), and microangiopathic hemolytic anemia |
Hemolytic uremic syndrome (HUS) - often affects young children and associated with bloody diarrhea/shiga toxin |
|
Black pigmented gallstones common with |
chronic hemolytic anemia |
|
Rb, BRCA, P53, and APC are all anti oncogenes, that when mutated, can lead to cancer. K-ras rather is a |
proto oncogene |
|
Majority of nonselective NSAIDs have reverisble effects on cox. Aspirin has |
Irreversible effects on COX1 and2 |
|
Side effects of ganciclovir and zidovudine HIV drugs? |
Neutropenia and bone marrow supression |
|
ERB-B2 positive breast cancer |
Another name for Her2/neu). Indicates aggressive tumor that can respond to trastuzumab |
|
Prognosis of a tumor is directly related to the STAGE (eg invasion/penetration to nearby tissues) rather than grade (differentiation) |
Just know that |