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198 Cards in this Set
- Front
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- 3rd side (hint)
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What is the normal order of the WBC w/diff?
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neutrophils
lymphos monos eos basos |
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What is the vWF receptor?
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Gp1b
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What is the fibrinogen receptor?
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GpIIb/IIIa
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What cell type do platelets derive from?
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megakaryocytes
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What types of granules do platelets contain?
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dense granules: ADP and Ca2+
alpha-granules: vWF, fibrinogen |
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In what condition do you see hypersegmented poly's?
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B12/folate deficiency
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What does a monocyte look like?
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kidney shaped nucleus (one)
"frosted glass" cytoplasm |
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What do eosinophils look like?
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bilobate nucleus
packed with large eosinophilic granules of uniform size |
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What do eosinophils contain?
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major basic protein
histaminase arylsulfatase (help limit rxn following mast cell degranulation) |
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What are the causes of eosinophilia?
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NAACP:
neoplastic asthma allergies collagen vascular disease parasites (invasive only) |
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What do basophils contain?
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heparin
histamine vasoactive amines leukotrienes (LTD-4) |
similar to mast cells
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What do mast cells contain?
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histamine
heparin eosinophil chemotactic factors |
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What are Landerhan's cells
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dendritic cells in the skin
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What does a plasma cell look like?
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off-center nucleus
clock-face chromatin distribution abundant RER well-developed golgi |
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what is the difference between anit-AB antibodies and anti-Rh antibodies?
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anti-AB are IgM so they can't cross the placenta while anti-Rh are IgG so they can.
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what is thromboplastin?
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tissue factor exposed in damaged endothelium that activated the extrinsic coagulation patheway by catalyzing factor VII conversion to VIIa
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What does plasmin do?
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activated complement cascade by converting C3 ==> C3a
helps degrade fibrin (anti-clotting factor) |
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What does Kallikrein do?
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activates plasmin (clot buster)
activates bradykin (pro-inflam cascade) |
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What is the difference between Hemophilia A and B?
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A - deficiency of factor VIII
B - deficiency of factor IX |
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Which factors does heparin-activated antithrombin (AT III) inhibit? What does it activate?
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Inhibits:
intrinsic pathway (XIIa, XIa, Xa, IXa) thrombin (IIa) extrinsic pathway (VIIa) Activates: kallikrein plasmin |
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What does tPA do?
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activates plasminogen ==> plasmin which then cleaves fibrin mesh so it is a potent thrombolytic agent
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What does Protein C do?
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when activated, cleaves and inactivates factors Va and VIIIa
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What is acanthocyte?
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aka spur cell - spiny RBC found in liver disease and abetalipoproteinemia
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In which conditions do you find basophilic stippling of RBCs?
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Thalassemias
Anemia of chronic disease Iron deficiency Lead poisoning |
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What do "bite cells" indicate?
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G6PD deficiency
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In which conditions do you find schistocytes?
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DIC
TTP/HUS traumatic hemolysis |
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In which condition do you find tear drop cells?
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bone marrow infiltration like myelofibrosis
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In which conditions do you find target cells?
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HALT:
HbC disease Asplenia Liver disease Thalassemia |
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In which conditions do you find Heinz bodies?
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alpha-thal
G6PD deficiency |
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In which conditions do you find Howell-Jolly bodies?
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functional hyposplenia or asplenia (sickle cell, eg)
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What is HbH and when is it found?
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when Hg is made of four Beta-chains in alpha-thal
shows up differently on elecrophoresis severe anemia but still compatible with life |
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What are the findings on electrophoresis for Beta-thalassemia?
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no HbA
inc. HbA2 (two alpha, two delta) inc. HbF (two alpha, two gamma) |
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How does lead poisoning cause anemia?
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inhibits ferrochelatase and ALA dehydratase ==> dec. heme synthesis
Inhibits rRNA degradation ==>basophilic stippling |
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What causes sideroblastic anemia?
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hereditary deficiency in delta-aminolevulinic acid sythase ==> defect in heme synthesis
also alcohol and lead |
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What is the tx for sideroblastic anemia?
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give pyridoxine (B6) therapy
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what do the iron studies in sideroblastic anemia show?
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inc. iron
normal TIBC inc. ferritin |
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What are the signs of lead poisoning?
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Lead lines on gingivae and epiphyses of long bones
Encephalopathy Basophilic stippling Abdominal colic sideroblastic anemia Wrist and foot drop |
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What is the tx for lead poisoning?
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EDTA and dimercaprol
succimer for kids |
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What are the neurological sx in B12 deficiency?
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peripheral neuropathy
posterior column degeneration (de. vibration/proprioception) Later corticospinal tract degeneration (spasticity) Dementia |
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What are the causes of non-megaloblastic macrocytic anemia?
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Liver disease
Alcoholism reticulocytosis Congenital deficiencies of purine/pyrimidine synthesis Drugs: 5-FU, AZT, hydroxyurea |
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What is the pathophys of anemia of chronic disease?
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inflammation ==> inc. hepcidin ==> dec. release of iron from macrophages
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What are the pathologic features of aplastic anemia?
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pancytopenia (anemia, neutropenia, thrombocytopenia)
normal cell morpho hypocellular bone marrow with fatty inflitration |
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What causes aplastic anemia?
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radiation and drugs
viral agents (B19, EBV, HIV, HCV) fanconi's anemia (inheritied defect in DNA repair) idiopathic (immune-mediated or primary stem cell defetc, may follow acute hep) |
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Which drugs cause aplastic anemia?
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benzene
chloramphenicol alkylating agents antimetabolites |
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Aplastic anemia sx
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faituge
malaise pallor purpura mucosal bleeding petechiae infection |
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Aplastic anemia tx
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allogeneic bone marrow transplantation
RBC and platelet transfusion G-CSF or GM-CSF |
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Hereditary spherocytosis findings:
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splenomegaly
aplastic crisis (B19 infection) howell-jolly bodies (if splenectomy) small, round RBCs with no central pallor |
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Hereditary spherocytosis labs:
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positive membrane fragility test
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Hereditary spherocytosis tx
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splenectomy (cuz they are usually removed prematurely by spleen even though they are functioning properly)
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What is the pathophys of anemia in G6PD deficiency?
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hereditary defect in G6PD ==? dec. glutathione ==> inc. RBC susceptibility to oxidant stress
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G6PD deficiency findings
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hemolytic anemia following oxidant stress (e.g. sulfa drugs, infections, fava beans)
back pain hemoglobinuria a few days after stress |
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G6PD deficiency labs
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blood smear shows RBCs with Heinz bodies and bite cells
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Pyruvate kinase defiency causes:
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heymolytic anemia of newborn
can't make enough ATP via the anaerobic pathway so RBC's die |
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Where is the mutation in sickle cell anemia?
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point mutation at position 6 of the beta chain (Glu ==> Val)
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Sickle cell tx
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hydroxyurea (inc. HbF)
bone marrow transplant |
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Paroxysmal nocturnal hemoglobinuria pathophys
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defect in decay-accelerating factor makes RBCs more vulnerable to complement activation and subsequent destruction.
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PNH findings
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red pee in the morning
inc. urine hemosiderin |
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what is the difference between direct and indirect Coomb's test?
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in direct, you are adding anti-Ig antibody to the patient's RBCs
in indirect you are adding patient's serum to normal RBC's |
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Warm agglutinin hemolytic anemia is caused by/associated with?
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anti-IgG
SLE CLL alpha-methyldopa |
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Cold agglutinin hemolytic anemia is caused by/associated with?
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anit-IgM
CLL M. pneumo mono |
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What causes microangiopathic anemia?
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DIC
TTP-HUS SLE malignant HTN |
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What causes macroangiopathic anemia?
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prosthetic heart valves
aortic stenosis malaria babesia |
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What is transferrin?
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molecule that transports iron in the blood
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What is ferritin?
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Molecule that stores iron
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What is TIBC?
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indirect measure of transferring
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What is %transferrin saturation?
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Fe/TIBC
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Acute intermittent porphyria pathophys
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deficient in porphobilinogen deaminase so porphobilinogen, delta-ALA and uroporphyrin accumulate
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Acute intermittent porphyria sx
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painful abdomen
red wine-colored urine polyneuropathy psych disturbances *often precipitated by druge |
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Porphyria cutanea tarda pathophys
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deficiency in uroporphyrinogen decarboxylase so uroporphyrin accumulates
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Porphyria cutanea tarda tx
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tea-colored urine
blistering cutaneous photosensitivity |
most common porphyria
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What does PT test?
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function of extrinsic pathway - factors I, II, V, VII and X
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What does PTT test?
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function of all factors except VII and XIII (intrinsic pathway)
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What kind of coagulation pathway defect is Hemophilia?
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intrinsic pathway so inc. PTT
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What is Bernard-Soulier disease?
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defect in platelet plug formation
dec. Gp1b which binds to vWF lower platelet count inc. bleeding time |
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What is Glanzmann's thrombasthenia
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defect in platelet plug formation
dec. GpIIb/IIIa ---> platelets don't stick to each other inc. bleeding time but platelet count is normal |
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Idiopathic thrombocytopenic purpura pathophys
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dec. platelet survival due to anti0GpIIb/IIIa antibodies causing peripheral platelet destruction
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Idiopathic thrombocytopenic purpura findings
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inc. megakaryocytes
dec. platelet count inc. bleeding time |
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Thrombotic thrombocytopenic purpura
pathophys |
dec. platelet survival due to deficiency of ADAMTS13 ==> dec. degradation of vWF multimers ==> inc. platelet aggregation and thrombosis
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Thrombotic thrombocytopenic purpura symptoms
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neurologic and renal symptoms
fever thrombocytopenia microangiopathic hemolytic anemia |
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vonWillebrand's disease tx
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DDAVP (desmopressin) rleases vWF stored in endothelium
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vonWillebrand's disease pathophys
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coagulation defect: vWF carries factor VII so inc. PTT (intrinsic pathway)
platelet plug defect: dec. vWF means platelets can't stick to endothelium (inc. BT) |
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What are the coagulation disorders?
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Hemophilia A/B
Vit. K deficiency |
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What are the platelet disorders?
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Bernard-Soulier disease
Glanzmann's thrombasthenia ITP TTP |
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What are the hereditary thrombosis (hypercoagubility) syndromes?
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Factor V Leiden
Prothrombin gene mutation ATIII deficiency Protein C or S deficiency |
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What is Factor V Leiden disease?
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production of mutant factor V that cannot be degraded by protein C --> hereditary hypercoagulability
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What is Protein C or S deficiency?
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dec. ability to inactivate factors V and VII ==> hypercoagulable
inc risk of skin necrosis with hemorrhage following administration of warfarin |
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What is a Reed-Sternberg cell?
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distinctive tumor giant cell seen in hodgkin's disease
binucleate or bilobes with 2 halves as mirror images (owl eyes) CD30+ and CD15+ B cell origin |
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What determines a good prognosis in Hodgkin's lymphoma?
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inc. lymphocyte-to-RS ratio
more reed-steinberg relative to lympohcytes = worse disease (usually found in older males with disseminated disease) |
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Who gets Burkitt's lymphoma?
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young adults and adolescents
it is a non-hodgkin's lyphoma |
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What is the genetic defect in Burkitt's lympoma?
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t(8;14) c-myc gene mext to heavy chain Ig gene (14)
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Burkitt's histology
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"starry-sky" appearance of sheets of lymphocytes with interspersed macrophages
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Which is the most common adult non-Hodgkin lymphoma?
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Diffuse large B-cell lymphoma
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What is Mantle cell lymphoma?
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A CD5+ non-Hodgkin's lymphoma with a poor prognosis found in older males
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What is the genetic defect in Mantle cell lymphoma?
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t(11;14)
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What is follicular lymphoma?
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It is a type of non-hodgkin's lymphoma found in adults that has an indolent course and is difficult to cure
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What is the genetic defect in follicular lymphoma?
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t(14;18) bcl-2 gene (inhibits apoptosis)
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What is Adult T-cell lymphoma?
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An aggressive type of non-hodgkins lymphoma found in adults in Japan, West Africa and the Carribean that is caused by HTLV-1
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What is mycosis fungoides/sezary syndrome?
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a type of indolent non-hodgkin's lymphoma found in adults presenting with cutaneous patches/nodules
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What are Bence Jones proteins?
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Ig light chains in urine of multiple myeloma patients
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Where do you see rouleaux formation?
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RBC's stacked like poker chips found in multiple myeloma
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When do you get an M spike on electrophoresis
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Too many monoclonal IgM due to multiple myeloma
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What are the sx/findings in multiple myeloma?
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hypercalcemia
renal insufficiency anemia bone lytic lesions (punched out) |
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What other condition is multiple myeloma associated with?
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primary amyloidosis
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Who gets ALL?
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kids
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How does ALL present?
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bone marrow involvement in childhood or mediastinal mass in adolescent males
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What are the markers of ALL?
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TdT+ (marker on pre-B and T cells)
CALLA+ |
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What is the translocation in ALL?
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t(12;21)
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Who gets CLL?
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adults >60
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What are the findings in CLL?
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often asymptomatic
smudge cells on PBS warm antibody autoimmune hemolytic anemia |
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Who gets Hairy cell leukemia?
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the elderly
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What are the findings in hairy cell leukemia?
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mature b-cell tumor
cells have filamentous hair-like projections stain TRAP+ |
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What are the findings in AML?
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auer rods
tons of circulating myeloblasts on PBS |
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AML tx
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all-trans retinoic acid (vitamin A) induces differentioation of myeloblasts
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What is the translocation in CML?
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philadelphia chromosome
t(9;22) bcr-abl |
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What are the findings in CML/how does it present?
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myeloid stem cell proliferation
inc. neutrophils, basophils, metamyelocytes splenomegaly blast crisis (AML/ALL progression) very low leukocyte alkphos |
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CML tx
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imatinib (anti-bcr-abl antibody)
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Age ranges for the leukemias (ALL, AML, CML, CLL)
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ALL = <15
AML = >60 CML = 30-60 CLL = >60 |
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What are Auer bodies?
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peroxidase-positive cytoplasmic inclusion in granulocytes and myeloblasts commonly seen in the M3 type of AML (release of them during tx could cause DIC)
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What is Langerhans cell histocytosis?
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proliferative disorders of dendritic (langerhans) cells.
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what are lab/microscopic findings in Langerhans cell histocytosis?
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defective cells express S-100 and CD1a.
birbeck granules "tennis rackets" on EM |
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What is polycythemia vera?
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chronic myeloproliferative disorder in which RBCs, WBCs and platelets are all increased due to a JAK2 mutation
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What is essential thrombocytosis?
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chronic myeloproliferative disorder in which platelets are all increased due to a JAK2 mutation
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What is myelofibrosis?
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chronic myeloproliferative disorder in which RBC's are decreased due to fibrotic obliteration of bone marrow
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What is JAK2 and what is it associated with?
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JAK2 is involved in hematopoietic growth factor signaling.
mutatons are implicated in myeloproliferative disorders other than CML |
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What is appropriate absolute polycythemia?
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inc. in RBC mass due to lung disease, congenital heart disease or high altitude (epo is inc.)
O2 sat. is dec. |
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What is inappropriate absolute polycythemia?
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inc. RBC mass due to ectopic epo production
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what is polycythemia vera?
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inc. RBC mass due to RCC, wilms' tumor, cyst, HCC or hydronephrosis
(epo will be dec due to neg. feedback) |
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Lepirudin, bivalirudin MOA/uses
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hirudin derivatives that directly inhibit thrombin
used as an alternative to heparin in patients with HIT |
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What does aminocaproic acid do?
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inhibits the conversion of plasminogen to plasmin
used in tPA/streptokinase overdose |
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What do tPA/streptokinase do to PTT, PT, and bleeding time?
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inc. PT
inc. PTT no effect on bleeding time |
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What does aspirin do to PTT, PT, and bleeding time?
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inc. bleeding time
no effect on PT or PTT |
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Aspirin MOA
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acetylates and irreversibly inhibits COX-1/2 thereby preventing the conversion of arachadonic acid to TXA2
dec. TXA2 means less platelet aggregation |
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Clopidogrel, ticlopidine MOA
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inhibit platelet aggregation by irreversibly blocking ADP receptor. inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa expression
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Ticlopidine toxicity
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neutropenia
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Clopidogrel, ticlopidine clinical uses
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acute coronary syndrome
coronary stenting to dec. the incidence or recurrence of thrombotic stroke |
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Abciximab MOA
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monoclonal antibody that binds to the glycoprotein receptor IIB/IIIA on activated platelets, preventing aggregation
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Methotrexate MOA
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folic acid analog that inhibits dihydrofolate reductase ==> dTMP ==> dec. DNA and protein syn
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Methotrexate clinical use
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cancers: leukemias, lymphomas, choriocarcinoma sarcomas
abortion, ectopic preg. RA, psoriasis |
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Methotrexate toxicity
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myelosuppression (reversible with leucovorin)
macrovesicular fatty change in liver mucositis teratogenic |
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5-FU MOA
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pyrimidine analog bioactivated to 5F-dUMP which covalently complexes with folic acid, inhbiting tymidylate synthase ==> dec. dTMP => dec. DNa and protein syn
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5-FU clinical use
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colon cancer and other solid tumors
basel cell carcinoma (topical) synergy with MTX |
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5-FU toxicity
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myelosuppresion which is NOT reversible with leucovorin ("rescue" is with thymidine)
photosensitivity |
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6-MP MOA
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purine analog ==> dec. de novo purine synthesis
activated by HGPRTase |
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6-MP clinical use
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leukemias, lymphomas (not CLL or hodgkin's)
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6-MP toxicity
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bone marrow, GI, liver
metabolized by xanthine oxidase so worse with allopurinol |
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6-TG MOA
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same as 6-MP (dec. de novo purine synthesis)
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6-TG clinical use
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acute lymphoid leukemia
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6-TG toxicity
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bone marrow depression, liver
can be given with allopurinol |
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Cytarabine (ara-C) MOA
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pyrimidine antagonist ==> inhibition of DNA polymerase
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Cytarabine (ara-C) clinical use
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AML
ALL high-grade non-Hodgkin's lymphoma |
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Cytarabine (ara-C) toxicity
|
leukopenia
thrombocytopenia megaloblastic anemia |
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Dactinomycin MOA
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intercalates in DNA
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Dactinomycin clinical use
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Wilm's tumor
Ewing's sarcoma rhabdomyosarcoma (childhood tumors) |
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Dactinomycin toxicity
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myelosuppression
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Doxorubicin (adriamycin), daunorubicin MOA
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generate free radicals
noncovalently intercala in DNA ==> breaks DNA ==> dec. replication |
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Doxorubicin (adriamycin), daunorubicin clinical use
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Hodgkin's lymphomas
myelomas sarcomas solid tumors (ovary, breast, lung) |
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Doxorubicin (adriamycin), daunorubicin toxicity
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cardiotoxicity
myelosuppression alopecia toxic to tissues with extravasation |
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Bleomycin MOA
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induces free radical formation, which causes breaks in DNA strands
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Bleomycin clinical use
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tisticular cancer
hodgkin's lymphoma |
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Bleomycin toxicity
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pulmonary fibrosis
skin changes minimal myelosuppression |
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Etoposide (VP-16), teniposide MOA
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inhibits topoisomerase II ==> inc. DNA degradation
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Etoposide (VP-16), teniposide clinical use
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small cell lung cancer
prostate cancer testicular cancer |
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Etoposide (VP-16), teniposide toxicity
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myelosuppression
GI irritation alopeica |
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Cyclophosphamide MOA
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covalently cross-links DNA at guanin N-7
*requires bioactivation by liver |
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Cyclophosphamide clinical use
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Non-hodgkin's lymphoma
breast and ovarian carcinomas (also immunosppressants for anti-rejection) |
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Cyclophosphamide toxicity
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myelosuppression
hemorrhagic cystitis (partially prevented with mesna) |
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Nitrosoureas (carmustine, lomustine, semustine, sretozocin) MOA
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require bioactivation
cross BBB ==> CNS |
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Nitrosoureas (carmustine, lomustine, semustine, sretozocin) clinical use
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brain tumors (including glioblastoma multiforme)
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Nitrosoureas (carmustine, lomustine, semustine, sretozocin) toxicity
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CNS toxic - dizziness, ataxia
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Busulfan MOA
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alkylates DNA
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Busulfan clinical use
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CML
also used to ablate patient's bone marrow before transplant |
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Busulfan toxicity
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pulmonary fibrosis
hyperpigmentation |
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Vincristine, vinblastine MOA
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alkaloids that bind tubulin in M-phase and block polymerization of microtubules so that mitotic spindle cannot form
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Vincristine, vinblastine clinical use
|
Hodgkin's lymphoma
Wilm's tumor choriocarcinoma |
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Vincristine, vinblastine toxicity
|
neurotoxicity (areflexia, peripheral neuritis)
paralytic ileus bone marrow suppression (vinblastine) |
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Paclitaxel MOA
|
hyperstabilize polymerized microtubules in M-phase so that mitotic spindle can not break down (anaphase can't occur)
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Paclitaxel clinical use
|
breast and ovarian cancers
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Paclitaxel toxicity
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myelosuppression
hypersensitivity |
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Cisplatin, carboplatin MOA
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cross-link DNA
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Cisplatin, carboplatin clinical use
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testicular
bladder ovary lung |
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Cisplatin, carboplatin toxicity
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nephrotoxicity
acoustic nerve damage |
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Hydroxyurea MOA
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inhibits ribonucleotide reductase ==> dec. DNA synthesis (S-phase specific)
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Hydroxyurea clinical use
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melanoma
CML sickle cell disease (inc. HbF) |
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Hydroxyurea toxicity
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bone marrow suppression
GI upset |
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Prednisone MOA (in cancer)
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may trigger apoptosis, may even work on nondividing cells
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Prednisone clinical use (in cancer)
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CLL
Hodgkin's lymphomas (mart of MOPP) auto-immune diseases |
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Prednisone toxicity
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Cushingoid
immunosuppression cataracts acne osteoporosis HTN peptic ulcers hyperglycemia psychosis |
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Tamoxifen, raloxifene MOA
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SERMs - receptor antagonists in breast and agonists in bone. block the binding of estrogen to estrogen receptor-positive cells
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Tamoxifen, raloxifene clinical use
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breast cancer
prevention of osteoporosis |
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Tamoxifen, raloxifene toxicity
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tamoxifen = inc. risk of endometrial carcinoma via partial agonist effects. also "hot flashes"
raloxifene does not have this effect |
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Trastuzumab MOA
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aka Herceptin
monoclonal antibody against HER-2 (erb-B2). helps kills breast cancer cells that express HER-2 through antibody mediated cytotoxicity |
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Trastuzumab clinical use
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metastatic breast cancer
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Trastuzumab toxicity
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cardiotoxicity
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Imatinib MOA
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aka Gleevec
philadelphia chromosome bcr-able tyrosine kinase inhibitor |
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Imatinib clinical use
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CML
GI stromal tumors |
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Imatinib toxicity
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fluid retention
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Rituximab MOA
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monoclonal antibody again CD20, which is found on most B-cell neoplasms
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Rituximab clinical use
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non-hodgkins lymphomas
RA (w/MTX too) |
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