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Heme Onc USMLE

QuestionAnswer
how does circulation and hemoglobin compensate for anemia incrsd CO (incrsd HR and SV); R shift of Hb curve (incrsd 2,3 DPG)
when transfuse <7g/dl (if no cardiopul dz)
clinical findings anemia pallor, esp conjunctiva, hypotension and tachycardia
how much does 1 unit packed RBCs incrs Hb 1 pt
if want infuse PRBC faster what do you do? What do you not do? DO mix w NS, do NOT mix with Ringer's lactate (the Ca++ will cause coag in the line)
what does FFP contain? When do you use it? How monitor? contains all clotting factors but no RBC/WBC/Plts; give for incrsd PT/PTT, coagulopathy, defic of clotting factors if can't wait for vitK; f/u with PT/PTT
what does cryoprecip contain? When do you use it? factor 8 and fibrinogen; give for HemoA, DIC (decrsd fibrinogen), and VWD
how much does 1 unit of platelets alter plt count 10,000
when give whole blood only for massive blood loss
types of transfusion rxns: cause and when occur 1) intravasc/acute from ABO mismatch; 2) extravasc/delayed occurs 3-4 wks later from minor RBC Ag mismatch
acute transfusion rxns: sympt, cxns, tx sympt: F, N/V, back/flank pain, chest pain, dyspnea; cxns: hypovol shock, DIC, ARF w hemoglobulinuria; tx: stop transfusion aggressive fluids to prevent hypovolemic shock and ARF
delayed transfusion rxns: sympt, tx sympt: F, jaundice, anemia; tx: none (self-limited)
causes of microcytic anemia (4) anemia of chronic dz, Fe defic anemia, sideroblast (incl Lead), thalassemia
causes of macrocytic anemia (3) vit B12, folate defic, liver dz
causes of normocytic anemia (5) aplastic anemia, anemia of chronic dz, tumor, BM fibrosis, renal failure (decrsd EPO)
key diffs bw anemia of chronic dz, Fe defic anemia Fe decrsd in both anemia of chronic dz (ACD) and Fe defic, but ferritin hi and TIBC low in ACD and vice versa in Fe defic
key diffs bw anemia of chronic dz, sideroblast both have high ferritin and low TIBC, but Fe is high in sideroblast
MC cause of anemia world wide? MC etiology of that cause? MC is Fe defic anemia, MC etiology is menstrual (then GI)
why might infant get Fe defic anemia too much human milk-low Fe
what pts need extra Fe infants and adolescents bc they're growing, pregnant women
what will RDW show in Fe defic anemia RDW (marker of variability in RBC size) will be abnml [nml in other microcytic anemias]
dx of Fe defic anemia low ferritin [will also have incrsd TIBC and transferrin]
tx of Fe defic anemia for menstruating women give trial of Fe suppl (FeSO3 oral); for others look for bleeding; r/o colon cancer
SE of oral FeSO3 constipation and nausea
what use if need to give Iron by IV? Fe dextran
should you transfuse Fe defic anemia no
name types of thalassemias b chain: thal major (homozyg) and thal minor (MC); a chain (4 loci): a thalassemia trait (2 loci mutated), Hb H dz (3 loci), all 4
describe clinical present of b thalassemia types 1) thal major: severe anemia w massive hepatosplenomegaly, expansion of BM distorts bones, death w/in first yrs; dx: incrsd Hb F w microcytic hypochromic anemia; thal minor: asympt w mild mycrocytic hypochrom anemia
describe clinical present of a thalassemia types a thal trait: often AA, mild microcytic hypochrom anemia; HbH: hemolytic anemia, splenomegaly, signif microcytic hypochromic anemia; all 4: fatal at birth (hydrops fetalis) or shortly after
causes of sideroblastic anemia Lead exposure, Rx (chloramphenicol, INH, EtOH), collagen vascular dz
blood lab profile for sideroblast anemia hi Fe, nml/decrsd TIBC, incrsd ferritin
tx sideroblastic anemia consider pyridoxine (B6)
causes of aplastic anemia MC: idiopathic, radiation, Rx (chloramphenicol, sulfa, carbamzepine, gold), viral (Parvo, Hep B, C, EBV, CMV, HIV, zoster)
clinical aplastic anemia anemia-fatigue, dyspnea; decrsd plt: petichae, easy bruising; neutropenia: infxns
dx aplastic anemia normocytic normochromic anemia, BM bx shows acellularity w decrsd progenitors of all the cell lines
tx of aplastic anemia depends on cause but BM transplant, transfuse PRBC and plt if nec; immunosuppress
sources of B12 meat and fish
causes of B12 defic MC malabsorb: MC pernicious anemia, poor diet (EtOH, strict veget), terminal ileum (Crohns), gasterctomy, bugs eating B12 (Diphyllobothrim latum-fish tape worm, blind loop syndrome w bac overgrowth)
clinical B12 defic sore tongue (stomatitis, glossitis), neuropathy (unlike folate): demyelination of posterior columns, corticospinal and spinocerebellar leading to loss of position/vibratory, ataxia, UMN (incrsd DTR, Babinski), dementia
pt w dementia always consider B12
positive Babinski when touch underside of foot the foot goes UP (not down like nml), a UMN sign
dx B12 defic megaloblastic anemia w hypersegment PMN; B12<100
if B12 unclear, what measure? What would folate defic show? methylmalonic and homocysteine (will be incrsd); in folate only homocysteine will be incrsd
describe Schilling test give unlabeled B12 IM, give oral radiolabeled B12 and measure urine and plasma B12 to see how much is absorbed; repeat w IF and if that returns absorption to nml then its pernicious anemia [otherwise its malabsorption]
tx B12 defic IM cyanobalamin (b12) q 1 month
causes of folate defic get from green leafy veg so MC is inadequate intake (tea and toast diet, EtOH), incrsd demand (preg, hemolysis), MTX, phenytoin, hemodialysis
clinical folate defic same as B12 exc w/o neuro
tx folate defic oral folate daily
2 types of hemo anemias and subtypes 1) factors external to RBC (MC): immune, mechanical; 2) intrinsic RBC defects: Hb related (sickle cell, HbC, thalassemia), membrane (hereditory spherocytosis, paroxys nocturnal hemoglob), enzyme (G6PD, pyruv kinase)
2 types of where hemolysis occurs and lab/PBS findings 1) intravascular (w/in circulation): schistocytes, decrsd haptoglobin; 2) extravascular (reticuloendo system, usu spleen): spherocytes, helmet [but overlap in those findings]
general lab values in hemo anemia decrsd haptoglobin, incrsd LDH and indirect bili (w jaundice),
if chronic hemo anemia what clinical exam findings splenomegaly, lymphadenopathy, stones
features of sickle cell by organ system/problem: hemo anemia jaundice, pigmented gallstones, high output CHF, aplastic crisis w Parvo B19
features of sickle cell by organ system/problem: vaso oclusive painful bone (MC, mltpl sites, 2-7d), hand-foot dactilitis MC how dz presents, avascular necrosis (esp hip), acute chest (mltpl infarcts infiltrate, chest pain, hypoxia), splenomegaly->asplenic/not palp later, acute abd, renal pap necrosis, leg ulcers
describe splenic sequestration syndrome, in what dz occurs pooling of blood in spleen causes splenomegaly and hypovol shock, seen in SC (in kids when spleen still fxnl) and thalassemia
features of sickle cell by organ system/problem: ID infxns (asplenia), esp S Pneu and H Flu, Salmonella osteomyelitis
name 3 organ system/problem features of sickle cell hemo anemia, vaso occlusive problems, ID
dx sickle cell PBS shows sickled cells but need electrophoresis for dx
factors that can ppt sickle decrsd O2 w hi altitude, acidosis, hypoxia, decrsd temp, infxn, dehydration
tx of SC hydroxyurea (incrs Hb F), folate for hemo anemia, vaccine S Pneu, H Flu, Neisseria mening + PCN prophyl 4mos-6yo; hi fluid intake
tx of SC painful crisis hydration, morphine, suppl O2
cause, dx, tx of here spherocytosis AD spectrin defect, dx: osmotic fragility, tx: splenectomy (bc extravasc hemolysis by macrophages in spleen)
causes of spherocytosis hereditary, G6PD, autoimmune hemo anemia, hypethermia, ABO incompatibility
types of G6PD and how present mild: AA, anemia w infxn, or Rx (sulfa, antimalarials like primadine), severe: Mediterranean severe hemo anemia after fava beans
dx G6PD incl PBS PBS: bite cells (where Heinz bodies bitten away by macro in spleen), Heinz bodies, decrsd NADPH formation, after crisis check G6PD levels
tx G6PD avoid Rx, fava, fluids
types of autoimmune hemo anemia and dx warm AIHA (MC): IgG bind RBC at warm temp leads to extravasc hemolysis in spleen; cold AIHA: IgM causes complement activ, intrasc hemolysis and sequester in liver; dx: + Coombs=warm AIHA, + cold agglutin=cold AIHA
causes of difft types AIHA warm=idiopathic (MC), or 2ry to lymphoma, CLL, SLE, methyldopa; cold=1ry often elderly idiopathic, or 2ry to mycoplas pneu or mono (EBV)
tx AIHA usu none, but warm AIHA=steroids, splenectomy if not responding, can try immunosuppress (azathioprine, cyclophosph); cold=avoid cold, chemotherap can help, NOT steroids
describe defic and type of hemolysis in paroxysmal nocturnal hemoglobulinuria (PNH) defic in anchor proteins cause complement-mediated lysis of RBC, WBC, plt and chronic intravasc hemolysis
dx PNH FC for CD55,59; also Ham's test of acidified serum or sugar water test
tx PNH prednisone, but many don't respond; BM transplant
describe HIT1, 2 HIT1=<48 hrs heparin directly causes plt aggreg; no tex; HIT2=heparin induces Ab mediated injury to plat 3-12d after heparin is started; must d/c heparin immed
describe 3 congenital dzs and 3 Rx that can cause decrsd plt production congenital rubella, Fanconis, Wiskott-Aldrich; Rx=EtOH, chloramphenicol, benzene
t/f: plt dzs cause hemarthosis f, plt dzs generally don't cause major bleeding into tissues and joints
describe 2 types of ITP, pts and tx acute: in kids, s/p viral, usu self-limited; chronic: women 20-40, no infxn, tx: steroids, IV Ig, splenectomy
lab findings of ITP plt <20,000, other labs nml; BM bx show incrsd megakaryocytes
contrast ITP and TTP ITP only decrsd plt, TTP no infxn, decrsd RBC, plt, hemolysis w ARF and CNS findings
describe presentation, PBS, and tx for TTP decrsd RBC, plt, hemolysis, ARF, CNS; PBS: schistocytes, nml PT, PTT; tx: plasmophoresis (**no plt!**)
compare HUS and HSP both hematuria in children, HUS: s/p E Coli diarrhea, w decrsd RBC, plt, ARF and hemolysis; HSP: s/p viral URI, nml RBC, decrsd plt, nml PBS
causes of decrsd plt in preg HELLP=hemo anemia, elev liver enz, low plt; fatty liver of preg: RF, decrsd plt, incrsd LFT, coag +/- DIC
name and describe defic in 2 inherited plt defects Bernard Soulie-defic in GPIB-IX; Glanzmann Thrombasthenia-defic in GPIIb-IIIa
how differentiate Bernard Soulier and Glanzmann Thrombasthenia both incrsd BT, Bernard Soulier: large plt and decrsd number that don't aggreg w ristocetin; Glanzmann Thrombasthenia: nml plt morph and number, do respond to ristocetin but not to ADP, thrombin, collagen
describe 3 types of VWD 1) MC is decrsd amt vWF, 2) qualitative problems vWF, 3) no vWF
describe lab profile of VWD nml plt number, incrsd BT that corrects w plasma, +/- incrsd PTT; decrsd vWF and factor 8
how does VWD do on ristocetin test decrsd response to ristocetin that corrects when nml plasma is added
tx VWD DDAVP (desmopresin) causes endothelial cells to secrete vWF; factor 8 concentrate for type 3 vWD and after major trauma or during surgery; also avoid ASA and NSAIDs
which factor is defic in HemoA? HemoB? HemoA=factor 8; HemoB=factor 9
how tx acute hemoarthoses pain=codeine (NOT ASA or NSAIDs), immobil joint and ice packs
which dzs incrs PTT? And what are their BTs? hemo (BT nml), vWF (incrsd BT), DIC (incrsd BT and PT, etc, etc)
which dzs incrs PT? And what are their BTs? vitK (nml BT), liver dz (nml BT, PTT may be incrsd), DIC (incrsd BT, PTT, etc)
which factors in PTT, what Rx affects? think hit pitt=intrinsic pathway (8,9,11,12), heparin incrs PTT
which factors in PT, what Rx affects? extrinsic=TF and factor 7, warfarin
what does thrombin time measure fibrinogen level
common causes of DIC MC: infxn, esp GN sepsis, obstetric cxns, major tissue injury (burns, trauma, sx), snake venom, shock/circ collapse
labs for DIC, PBS? incrsd PT, PTT, BT, TT, + fibrin split products, D-dimer, decrsd plt, fibrinogen; PBS: schistocytes
tx DIC plt transfusion, cryoprecip (gives clotting factors + fibrinogen, v FFP only gives clotting factors)
causes of vit K defic MC: critically ill NPO on broad spec Abx (since intestinal flora creates some of vitK), TPN (unless vit K added), malabsrob (small bowel dz, Crohns, IBD, obstructive jaundice)
how long take to reverse warfarin vit K replacement takes few days, so if severe bleeding give FFP
describe pathophysiol of Liver coag decrsd syn of clotting factors (all are made in liver exc vWF), cholestasis causes decrsd vitK absorb, hypersplenism from portal HTN causes decrsd plt
labs for liver coag and compare to DIC incrsd PT, +/- incrsd PTT, but unlike DIC TT, BT, and fibrinogen are nml
name 6 inherited hypercoag ATIII defic, anti phospholipid syn, prot C, S defic, factor V Leiden, prothrombin gene mutation, hyperhomocyteinemia
tx inherited hypercoag if >2 events, pt on permanent anti-coag w warfarin
2ry hypercoag states/risks malignancy (esp pancreas, GI, ovaries, lung), preg, OCP, post-op (esp ortho), nephrotic, PNH, CHF (blood stasis)
cxns assoc heparin HIT, osteoporosis, rebound hypercoag
what factor does heparin work on, how does that compare w LMWH heparin activ antithrombin that inihibits thrombin and factor Xa; LMWH just acts on factor Xa
how give and monitor LMWH can only ive SC, can't monitor PT, PTT (doesn't affect)
contraindications for giving heparin hx of HIT, active bleeding, hemophilia or decrsd plt, sever HTN, recent sx on eyes, spine, brain
how reverse heparin can give protamine, otherwise takes 4 hrs after d/c heparin; give FFP if severe bleeding
how start person on warfarin if need acute anticoag start heparin, once PTT nml start warfarin, continue heparin >4d, then once INR therapeutic on warfarin, d/c heparin
how long does it take warfarin to have an effect 4-5d
who do you not give warfarin to EtOH (risk of intracranial bleed when they fall), someone pregnant (teratogenic)
how long does it take to reverse warfarin give vitK and takes 4-10hrs if liver nml
pt population who get Multiple myeloma usu >50, more often AA
key features of MM (3) 1) skel: osteolytic lesions esp back, ribs, jaw, pathol fractures, 2) renal failure and Bence Jones proteins, 3) infxns
dx criteria for MM >10% if abnml plasma cells in BM + 1 of following: M protein in urine or serum, lytic bone lesions
labs of MM incrsd Ca++, incrsd serum protein from Ig, incrsd ESR [can get pancytopenia later with BM invasion]
tx and px of MM tx if sympt or adv dz: chemo w alkylating agents or radition if not responsive to chemo or disabling pain, poor px (2-4yrs w tx); if transplant do peripheral blood stem cell transplant rather than BM transplant
describe Waldenstrom's Macroglobulinemia, how its difft from MM, tx IgM produced causes hyperviscosity, no bone lesions; tx: chemotherapy and plasmaphoresis for hyperviscosity
describe MGUS, pt pop, how its difft from MM, tx usu in elderly and asx finding; IgG <3.5, <10% plasma cells in BM and Bence Jones <1g/d; <20% develop MM in 10-15yrs; tx: none
compare Hodgkins and NHL in terms of age, spread, sympt, and assoc findings age: Hodgkins bimodal, NHL 2x as common and usu 20-40; spread: H local dz in LN w contig spread, NHL mltpl periph LN, non-contiguous spread; sympt: H has constitut symp; NHL assoc w HIV and immunosuppress, Hodgkins must have Reed Sternberg cells
name Hodgkins lymph types in order of freq, pathology, and px 1) Nod scleros: lots lymph, few RS bands of collagen encircle pools of RS; excellent px; 2) Mixed Cell: lots lots RS, lots lymph, intermed px; 3) lymph predom: lots lymph, few RS, excellent px; 4) lymph deplete: few RS>lymph, old men dissemin dz, poor px
Hodgkins staging (Ann Arbor) I: single LN, II: at least 2 LN same side diaphragm, III: both sides diaphragm, IV: extra lymph
NHL staging I: single LN of 1 extralymph, II: at least 2 LN same side diaphragm or localized LN w contiguous extra LN, III: LN both sides diaphragm, IV: dissemin at least 1 extra lymph organs
name 2 low grade NHL, pts, cell type, progression/px/tx 1) small lymphocytic, in elderly adults, B cell, like CLL, indolent eventually wide spread LN; 2) follicular (MC): adults, B cell, presents painless peripheral LAD, may transform to diffuse large cell; t(14,18); localized (15%) can cure w radiotherapy
name 1 intermediate NHL, pts, cell type, progression/px/tx diffuse large cell, usu older adults but 20% kids, 80% B cell, presents as large extranodal mass, locally invasive, 85% cure w CHOP
name 2 high grade NHL, pts, cell type, progression/px/tx 1) lymphoblastic: usu children, T cell, aggressive w rapid dissemin, may progress to T cell ALL, may respond to combo tx; 2) Burkitts usu children, B Cell, African: jaw bone, EBV, American: abd organs; t(8,14); grave, tx aggressive chemo can cure 50%
describe mycosis fungoides T cell skin cancer, eczematoid skin diseem to LN blood, organs, <2 yrs if dissemin, if limited to skin can be curable w radiation and topical chemo; characteristic cribiform lymphocytes
describe Sezary syndrome involves skin and blood stream, considered maybe a late stage Mycosis fungoides
which are HIV lymphomas often Burkitts or diffuse large cell, very poor px
name Rx in CHOP Cyclophosphamide, Hydroxydaunomycin (doxyrubicin), oncovin (vincristine), prednisone
describe overall px for different grades of NHL low grade-cure is rare, survival 5-7yrs, intermed grade: 50% cure w aggressive tx, survival 2yrs; ~70% cure w aggressive tx otherwise survival is months
how dz NHL need LN bx
key features of AML mostly adults, don't respond as well to tx as ALL, Auer rods, DIC, can get skin nodules
how tx Hodgkins if <IIIA radiotherapy, if IIIB and above chemo
how dx AML, ALL need BM bx
key features of ALL the leuk most responsive to tx, MC malignancy in children <15, assoc Downs and radiation, can have testicular and CNS involvement
features of poor px ALL <2yo, >9yo; WBC>50,000
lab values of tumor lysis syndrome incrsd K, phosphate and uricemia
tx/px for AML and ALL ALL: kids >75% complete remission (v 40% adults) and often responsive when relapse; AML: BM transplant best hope
key features of CLL MC leuk in >50, usu pts >60; least aggressive, prolonged indolent course, warm AIHA, chemo has little effect on survival but used to decr sympt and infxns, often fludarabine and cholambucil
tx of CLL chemo has little effect on survival but used to decr sympt and infxns, often fludarabine and cholambucil
dx of CLL PBS often dx: absolute leukocytosis w small mature lymphocytes and smudge cells
key features of CML usu >40yo, chronic course until blast crisis, Phila chromo(9,22), decrsd LAP
tx CML if Phila chromo (bcr-abl tyr kinase) can use Gleevec (imatinib)
how tell leukomoid rxn v CML leukomoid has no splenomegaly, incrsd LAP and hx of infxn
CLL staging Rai staging: 0=lymphocytosis, 1=lympho + LAD, 2=lympho + splenomeg, 3= lympho + anemia, 4=lympho + decrsd plts
cutoffs for polycyth vera dx must have: RBC >36men, >32 women; O2 Sat>92, splenomegaly PLUS any 2 of: decrsd plts, incrsd WBC, LAP>100, incrsd B12
sympt of polycythemia vera mostly due to hypervisc: HA, dizziness, pruritis, visual impair, HTN; tx=repeated phlebotomy meylosuppression w hydroxyurea or IFN
how is esstl thrombocytosis defined, tx? >600K, tx=anagrelide + ASA
tx for acute intermittent porphyria hematin
what give during blast crisis for tumor lysis syndrome give allopurinol to prevent hyperuricemia and renal insuffic
key factors for ALL usu children (3-5yo), lymphoblasts, rapid progression, can have bone pain (medulla expansion) pancytopenia (bleeding, fever, anemia), radiation, Downs **most responsive to therapy
key factors for AML >30yo, myeloblasts, pancytopenia (bleeding, fever, anemia), Auer rods, DIC **M3 AML (acute promyelo leuk) good prog bc responds to all-trans retinoic acid
key factors for CML 30-50yo, myeloid stem cells, WBC>50,000, Phila chromo, blast crisis (accelerates to AML), splenomegaly, low leukocyte alk P
key factors for CLL >50yo, lymphocytes, male, lymphadenopathy, lymphocytosis, infxns, smudge cells, splenomegaly
generally how difft acute and chronic leukemias acute: blasts on smear, in children or elderly, short drastic course; chronic: more mature cells, midlife, longer less devastating course
common clinical features of leuk BM failure leads to anemia, infxn (loss WBC), hemorrhage (loss platelets); leukemic cells infiltrate spleen (splenomegaly), liver, LNs
Phila chromo, what's it assoc w t(9;22), (bcr-abl) CML
t(8;14) assoc w, clinical presentation Burkitts lymphoma; c-myc moves to Ig heavy chain gene, starry sky lots lympho w interspersed macro, assoc Africa, EBV, jaw
t(14;18) assoc w Follicular lymphoma (small cleaved cell B cell type), bcl2 activ, MC non-Hodg lymphoma
t(15;17) assoc w M3 type AML which is responsive to all-trans retinoic acid
t(11;22) assoc w Ewings sarcoma
name the types of Hodgkin's lymph (4), prevalence, blood smear, prognosis Nodul scleros (MC, lots lymph, good prognosis); mixed (**lots RS**, many lymph, intermediate prognosis); lymphocyte predmoinant (lots lymphs, good prog) lymph dplete (rare, few lymphs with RS high relative to lymphs, older males dissem dz poor prog)
describe nodular sclerosing lymph, prevalence, blood smear, prognosis MC, lots lymph, good prognosis
describe mixed cellularity lymphoma, prevalence, blood smear, prognosis 25% **lots Reed Stern**, many lymph, intermediate prognosis
describe lymphocyte predmoinant lymph, prevalence, blood smear, prognosis 6% lots lymphs, good prog usu <35yo males
describe lymphocyte depleted, prevalence, blood smear, prognosis rare, some lymphs, RS high relative to lymphs, poor prognosis, seen in older males w disseminated dz
what do Reed Sternberg cells look like? Cell markers? large cells w predominant nucleoli on polymorphic background, CD30+ CD15+ B cell
key diff bw NHL and Hodgkins lymphoma HL: RS cells, localized single grp of nodes, not extranodal involvement, continuous spread; constitutional symptoms, mediastinal lympadenopathy, bimodal age; NHL also HIV/immunosuppress, B cell, peak 20-40yo
what are the B cell NHLs? T cell NHLs? B cell: small lymphocytic lymphoma, follicular, diffuse large, Burkitts; T cell: lymphoblast lymph, diffuse large (mature T cells)
name types of NH lymph (5); cell type, children v adults small lymphocyt lymphoma, adults B cell; follicular small cleaved cell adults B cell t(14;18) w bcl2 expression, MC; diffuse large cell adult B cell 80%, T cell 20%; lymphoblastic lymphoma, children usu immature T cells; Burkitts, children, B cell t(8;14)
describe small lymphocytic lymphoma (age, cell type, key features, prog) NHL, adults, B cell, like CLL w focal mass, low grade
describe follicular lymphoma (age, cell type, key features, prog) NHL small cleaved cell adults B cell t(14;18) w bcl2 expression; MC; difficult to cure, indolent
describe diffuse large cell lymphoma (age, cell type, key features, prog) NHL, adult, B cell 80%, T cell (mature) 20%, aggressive but up to 50%
describe lymphoblastic lymphoma (age, cell type, key features, prog) NHL, children usu immature T cells, commonly presents w ALL and mediastinal mass, aggressive
describe Burkitts lymphoma (age, cell type, key features, prog) NHL, B cell, children, t(8;14) c-myc moves to Ig heavy chain gene, starry sky lots lympho w interspersed macro, assoc EBV, jaw lesion in Africa endemic form, or pelvis or abd in sporadic form
clinical present multiple myel, blood character destructive bone lesions, hi Ca++, renal insuff, infx, anemia; M protein (monoclonal Ig), Bence Jones protein in urine (Ig light chain); PBS: rouleau formation
what can appear like multiple myeloma Waldenstroms macroglobulinemia, M spike, but its IgM and no lytic lesions
what virus is assoc w T cell leuk its caused by HTLV-1
how difft myeloblasts from lymphoblasts myeloblasts are larger w more cytoplasm, conspicuous nucleoli, often w granules and 50% Auer rods **myeloperoxidase +
what is the most common presenting symptom of lymphomas? lymphadenopathy
pathology of bands of collagen enveloping pools of RS cells nodular sclerosing
which Hodgkins occurs more freq in women nodular sclerosing
describe Hodgkins staging Ann Arbor staging: I=1 LN, 2= >1 LN on same side of diaphragm; 3=both sides diaphragm; 4=extra lymph sites; A=no symptoms; B=fever, wgt loss, night sweats (worse px)
Hodgkins diagnosis LN bx, CXR and CT (to detect LN involvement), BM bx to see if BM involved, lab (lymph, ESR can indicate dz)
Hodgkins tx, px I, II, IIIA: radiotherapy alone, IIIB, IV: chemo; chemo and radiotherapy in combo cures 70%
relative freq of Hodgkins and NHL NHL 2x as common
when do you bx a suspicious LN? if >1cm for >4wks that can't be attributed to infxn
NHL staging extent of dz (Ann Arbor same as Hodgkins staging); Ann Arbor staging: I=1 LN, 2= >1 LN on same side of diaphragm; 3=both sides diaphragm; 4=extra lymph sites; A=no symptoms; B=fever, wgt loss, night sweats (worse px)
what are the low grade NHLs small lymphocytic lymphoma, follicular small cleaved cell adults B cell t(14;18) w bcl2 expression, MC
which NHL usu presents w painless peripheral LAD follicular
which NHL is closely related to CLL small lymphocytic lymp
which NHL are considered intermediate grade? High grade? intermediate: diffuse, large-cell; high grade: lymphoblastic and burkitts
describe mycosis fungoides; pathology, presentation, px T cell lymph of skin that dissem to LN, blood; presents w eczematoid skin lesions; cribiform shape of lymphocytes; if just skin can be cured (radiation, topical chemo) if dissem <2 yrs
describe overall px for NHLs of difft grades low grade-cure is rare, median survival 5-7yrs; intermediate 50% cure w aggressive tx, median survival 2 yrs; high grade 70% cure w aggressive tx, without tx survival is mos
what does CHOP therapy consist of cyclophosphamide, hydroxydaunomycin (doxorubiciin), oncovin (vincristine), prednisone
what's the MC leuk >50yo CLL
overall px CLL good, it's the least aggressive, (survive longer than acute leuk or CML), pts usu die of other causes
PBS of CLL almost all WBC are mature small lymphocytes, w smudge cells
what lymphoma often presents w large extranodal mass diffuse, large cell lymphoma (a NHL)
describe difft parts of bone, and where bone tumors commonly arise epiphysis=very end of bone--giant cell (benign soap bubble); metaphysis=bone neck--osteochondroma (benign), osteosarcoma (malignant); diaphysis=middle bone--chondrosarcoma, Ewings
describe osteochondroma, incidence/clinical course, location most common benign, often incidental finding on metaphysis (neck of bone)
describe osteosarcoma, incidence/clinical course, location malignant w poor px, metaphysis
describe osteosarcoma appearance, assoc w other dzs Codman's trianlge (periosteum elevates), sunburst; assoc w Pagets, familial rb
describe chondrosarcoma, clinical course, location malignant, diaphysis in medulla
describe Ewing's sarcoma, incidence/clinical course, location malignant in diaphysis, aggressive in boys15 but responds to chemo
describe Ewing's sarcoma, appearance, assoc small blue cell onion ring, t11;22
how difft chondrosarcoma v osteosarcoma chondro=diaphysis in medulla, osteo=metaphysis w Codman's triangle, sunburst
what's the MC malignant bone tumor multiple myeloma (Rouleaux RBC, lytic lesions, hi Ca++, anemia, low WBC w infxn, mono Ab spike and Bence jones proteins, bone pain)
epiphyseal tumor w multinucleated giant cells--what dx? giant cell tumor
cancers assoc w rb gene retinoblastoma, osteogenic sarcoma
lots of colon polyps, think what dz? Cancer? familial polyposis, they always become cancer
gardner's syndrome--describe findings? Cancer? familial polyposis, (they always become cancer) + osteomas, soft tissue tumors
turcot's syndrome--describe findings? Cancer? familial polyposis, (they always become cancer) + CNS tumors
peutz-jegher's syndrome--describe findings? Cancer? perioral freckles, non cancerous polyps; increased risk of non colon cancer (no incrsd risk of colon cancer)
which syndromes w colon polyps have risk of colon cancer? Which don't? cancerous: familial polyposis, gardner's, turcot's; non cancerous: peutz-jeghers [but they're at risk for non-colon cancers]
what cancers assoc w von Hippel Lindau hemangioblastoma of Cb, RCC [they also have kidney, liver cysts]
what 2 syndromes carry higher risk of skin cancer albinism, xeroderma pigmentosa
tuberous scleorsis assoc w which cancers renal angiomyolipomas, cardiac rhabdomyomas
what cancer is assoc w rubber/dye industry? bladder
what environmental risk factors are assoc w bladder cancer? smoking, aniline dyes (rubber/dye industry), schistomiasis
what environmental risk factors are assoc w liver cancer? EtOH, vinyl chloride [liver angiosarcomas], aflatoxins (Africa)
EtOH is assoc w which ENT cancers? oral, pharynx/larynx, eso
benzene is assoc w which cancer leukemia
clear cell cancer of cervix and vagina is assoc w? in utero diethylstilbestrol (DES)
what clinical syndromes can an apical (Pancoast) lung cancer cause? Horners (unilateral ptosis, miosis, anhydrosis); SVC syndrome; unilateral diaphragm paralysis from phrenic nerve; hoarseness from recurrent laryngeal
describe Horner's syndrome unilateral ptosis, miosis, anhydrosis from cancerous involvement of cervical sympathetic chain
what paraneoplastic syndromes are seen w lung cancer (4), and which type? Cushings=(ACTH production), small cell; SIADH=small cell; HyperCa (PTH-like hormone production)=squamos; Eaton-Lambert (MG-like that spares ocular; mscls stronger w use v MG)=small cell
what does AFP stand for? What cancers does it screen for? alpha fetoprotein, liver (hepatocellular ca) and gonad (yolk sac)
what does CEA stand for? What cancers does it screen for? carcinoemryogenic antigen, colon pancreas, and other GI
what does PSA stand for? What cancers does it screen for? prostate specific antigen, screens for early prostate
what does acid phoshatase screen for? prostate cancer w extension outside of the capsule
what does HCG stand for? What cancers does it screen for? human chorionic gonadotropin, hydatiform moles and choriocarcinoma
what tumor marker used to screen for ovary cancer? CA-125
what cancers does S100 screen for? melanoma, CNS and nerve tumors
what tumor marker used to screen for pancreatic cancer? CA 19-9
what does CA 27-29 indicate? breast cancer
characteristics of sideroblastic anemia, causes little dots (basophilic stipling)=free Fe, ringed sideroblast found in bone marrow; caused by EtOH, lead poison, Rx isonazid
blood serum characteristic of sideroblastic anemia hi Fe, hi ferritin, low TIBC, low saturation [v anemia chronic dz *low Fe*, high ferritin, low TIBC, low sat]
causes of normocytic anemia (w or w/o retic) w nml/incrs retic: acute blood loss, hemolytic, Rx; low retic: anemia of chronic dz, aplastic anemia, RF, cancer/dysplasia
causes of microcytic anemia (w or w/o retic) w nml/incrs retic: thalassemia, sickle cell; low retic: lead poison, sideoblastic, Fe defic, anemia of chronic dz
causes of macrocytic anemia (all have low retic) folate, B12, EtOH, liver dz/cirrhosis, Rx (methotrexate, phenytoin)
MC cause anemia in US Fe defic
lab values for Fe defic anemia low Fe, low ferritin, high TIBC, but low sat--trying to use all Fe it has (hi TIBC), anemia of chronic dz has Fe in cells (hi ferritin, also acute phase reactant) but not using it (low TIBC)
what's ferritin? TIBC? ferritin=iron-protein complex that regul Fe stores and transport (indicates body's Fe stores); TIBC=ability of transferrin to bind Fe (?body's ability to use Fe stores--Fe defic anemia body makes more transferrin to use all the little Fe)
hypersegmented PMN think folate defic
MC cause B12 defic, mechanism pernicious anemia; Abs ag parietal cells so they can't secrete intrinsic factor and/or ileum isn't able to absorb B12/IF
how tell diff thalassemia and Fe defic anemia? both are microcytic, hypochromic but in thalassemia Fe levels are nml (and don't give Fe supplement or will get Fe overload!); also look for target cells
spherocytes on PBS (peripheral blood smear) autoimmune anemia (incomplete destruction of RBCs); and spherocytosis (in which osmotic fragility test is abnl)
characteristics of anemia of chronic dz normocytic or microcytic, Fe and TIBC low (so %sat nml), ferritin is incrsd (Fe inside cells); in presence of dz w chronic inflamm, ie RA, Lupus, cancer, TB
how distinguish anemia of chronic dz from Fe defic anemia? ferritin is high in anemia of chronic dz (indicating that the body has Fe); ferritin is low in Fe defic anemia but TIBC high (body try to use all Fe it has)
how distinguish sideroblastic anemia from anemia of chronic dz and Fe defic anemia? sideroblastic has high Fe; (ferritin is high and TIBC low unlike Fe defic anemia (but like anemia of chronic dz)]
how B12 defic treated B12 intramuscular/parenteral injxn (can't be absorbed in gut)
describe Plummer-Vinson syndrome esophageal web causing dysphagia, Fe defic anemia, glossitis
Heinz bodies on peripheral blood smear (PBS) G6PD defic (inclusions in RBCs of denatured Hb)
target cells on peripheral blood smear (PBS) thalassemia, liver dz
Howell-Jolly bodies on peripheral blood smear (PBS) asplenia
echinocytes, incl burr cells and acanthocytes on peripheral blood smear (PBS) uremia
schistocytes, helemt cells on peripheral blood smear (PBS) intravascular hemolysis
tear-shaped RBC on peripheral blood smear (PBS) space occupying lesion in BM, ie myelofibrosis
peripheral blood smear (PBS) of CRF pt, mechanism? normocytic or microcytic, low retic, bc low EPO production
describe G6PD, cause X linked rec in Af Am and Mediterr, RBC enzyme, sudden hemolysis after fava beans, antimalarials, salicylates, sulfa Rx
how diagnose G6PD assay for RBC enzyme, but can't do it immediately following an attack (older RBC which show altered enz are destroyed already)
is PTT intrinsic or extrinsic? Which factors? intrinsic, factors 8,9,11,12
which monitor for heparin: PT or PTT? PTT (but LMWH doesn't require monitoring)
which monitor for warfarin: PT or PTT? PT
what is the mech of heparin activates antithrombin III, which inactivates thrombin (converts fibrinogen to fibrin)
what are the vit K dependent enzymes? 2,7,9,10, Prot C, S
what are the main causes of incrsd PTT hemo, vWF (also DIC and liver dz may or may not have PTT)
what are the main causes of incrsd PT? vit K, DIC, Liver dz
how difft hemo and vWF both have incrsd PTT, but hemo BT nml
how difft liver dz and DIC both incrsd PT, but DIC has incrsd BT and decrsd 8
how difft DIC and vWF both incsrd PTT, vWF has nml PT
how difft vitK and liver dz liver dz PT doesn't correct w vitK
how difft vitK and DIC vitK nml BT
how does Lupus effect PT, PTT Lupus anticoagulant incrs PT, but risk toward clotting
Created by: ehstephns on 2010-12-12



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