Heme Onc USMLE
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| how does circulation and hemoglobin compensate for anemia | incrsd CO (incrsd HR and SV); R shift of Hb curve (incrsd 2,3 DPG)
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| when transfuse | <7g/dl (if no cardiopul dz)
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| clinical findings anemia | pallor, esp conjunctiva, hypotension and tachycardia
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| how much does 1 unit packed RBCs incrs Hb | 1 pt
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| 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)
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| 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
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| what does cryoprecip contain? When do you use it? | factor 8 and fibrinogen; give for HemoA, DIC (decrsd fibrinogen), and VWD
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| how much does 1 unit of platelets alter plt count | 10,000
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| when give whole blood | only for massive blood loss
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| 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
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| 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
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| delayed transfusion rxns: sympt, tx | sympt: F, jaundice, anemia; tx: none (self-limited)
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| causes of microcytic anemia (4) | anemia of chronic dz, Fe defic anemia, sideroblast (incl Lead), thalassemia
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| causes of macrocytic anemia (3) | vit B12, folate defic, liver dz
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| causes of normocytic anemia (5) | aplastic anemia, anemia of chronic dz, tumor, BM fibrosis, renal failure (decrsd EPO)
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| 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
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| key diffs bw anemia of chronic dz, sideroblast | both have high ferritin and low TIBC, but Fe is high in sideroblast
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| MC cause of anemia world wide? MC etiology of that cause? | MC is Fe defic anemia, MC etiology is menstrual (then GI)
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| why might infant get Fe defic anemia | too much human milk-low Fe
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| what pts need extra Fe | infants and adolescents bc they're growing, pregnant women
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| what will RDW show in Fe defic anemia | RDW (marker of variability in RBC size) will be abnml [nml in other microcytic anemias]
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| dx of Fe defic anemia | low ferritin [will also have incrsd TIBC and transferrin]
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| tx of Fe defic anemia | for menstruating women give trial of Fe suppl (FeSO3 oral); for others look for bleeding; r/o colon cancer
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| SE of oral FeSO3 | constipation and nausea
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| what use if need to give Iron by IV? | Fe dextran
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| should you transfuse Fe defic anemia | no
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| 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
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| 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
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| 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
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| causes of sideroblastic anemia | Lead exposure, Rx (chloramphenicol, INH, EtOH), collagen vascular dz
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| blood lab profile for sideroblast anemia | hi Fe, nml/decrsd TIBC, incrsd ferritin
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| tx sideroblastic anemia | consider pyridoxine (B6)
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| causes of aplastic anemia | MC: idiopathic, radiation, Rx (chloramphenicol, sulfa, carbamzepine, gold), viral (Parvo, Hep B, C, EBV, CMV, HIV, zoster)
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| clinical aplastic anemia | anemia-fatigue, dyspnea; decrsd plt: petichae, easy bruising; neutropenia: infxns
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| dx aplastic anemia | normocytic normochromic anemia, BM bx shows acellularity w decrsd progenitors of all the cell lines
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| tx of aplastic anemia | depends on cause but BM transplant, transfuse PRBC and plt if nec; immunosuppress
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| sources of B12 | meat and fish
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| 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)
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| 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
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| pt w dementia always consider | B12
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| positive Babinski | when touch underside of foot the foot goes UP (not down like nml), a UMN sign
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| dx B12 defic | megaloblastic anemia w hypersegment PMN; B12<100
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| if B12 unclear, what measure? What would folate defic show? | methylmalonic and homocysteine (will be incrsd); in folate only homocysteine will be incrsd
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| 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]
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| tx B12 defic | IM cyanobalamin (b12) q 1 month
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| 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
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| clinical folate defic | same as B12 exc w/o neuro
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| tx folate defic | oral folate daily
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| 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)
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| 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]
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| general lab values in hemo anemia | decrsd haptoglobin, incrsd LDH and indirect bili (w jaundice),
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| if chronic hemo anemia what clinical exam findings | splenomegaly, lymphadenopathy, stones
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| features of sickle cell by organ system/problem: hemo anemia | jaundice, pigmented gallstones, high output CHF, aplastic crisis w Parvo B19
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| 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
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| 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
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| features of sickle cell by organ system/problem: ID | infxns (asplenia), esp S Pneu and H Flu, Salmonella osteomyelitis
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| name 3 organ system/problem features of sickle cell | hemo anemia, vaso occlusive problems, ID
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| dx sickle cell | PBS shows sickled cells but need electrophoresis for dx
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| factors that can ppt sickle | decrsd O2 w hi altitude, acidosis, hypoxia, decrsd temp, infxn, dehydration
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| 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
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| tx of SC painful crisis | hydration, morphine, suppl O2
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| cause, dx, tx of here spherocytosis | AD spectrin defect, dx: osmotic fragility, tx: splenectomy (bc extravasc hemolysis by macrophages in spleen)
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| causes of spherocytosis | hereditary, G6PD, autoimmune hemo anemia, hypethermia, ABO incompatibility
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| 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
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| 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
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| tx G6PD | avoid Rx, fava, fluids
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| 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
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| 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)
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| 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
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| 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
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| dx PNH | FC for CD55,59; also Ham's test of acidified serum or sugar water test
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| tx PNH | prednisone, but many don't respond; BM transplant
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| 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
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| describe 3 congenital dzs and 3 Rx that can cause decrsd plt production | congenital rubella, Fanconis, Wiskott-Aldrich; Rx=EtOH, chloramphenicol, benzene
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| t/f: plt dzs cause hemarthosis | f, plt dzs generally don't cause major bleeding into tissues and joints
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| 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
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| lab findings of ITP | plt <20,000, other labs nml; BM bx show incrsd megakaryocytes
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| contrast ITP and TTP | ITP only decrsd plt, TTP no infxn, decrsd RBC, plt, hemolysis w ARF and CNS findings
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| describe presentation, PBS, and tx for TTP | decrsd RBC, plt, hemolysis, ARF, CNS; PBS: schistocytes, nml PT, PTT; tx: plasmophoresis (**no plt!**)
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| 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
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| 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
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| name and describe defic in 2 inherited plt defects | Bernard Soulie-defic in GPIB-IX; Glanzmann Thrombasthenia-defic in GPIIb-IIIa
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| 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
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| describe 3 types of VWD | 1) MC is decrsd amt vWF, 2) qualitative problems vWF, 3) no vWF
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| describe lab profile of VWD | nml plt number, incrsd BT that corrects w plasma, +/- incrsd PTT; decrsd vWF and factor 8
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| how does VWD do on ristocetin test | decrsd response to ristocetin that corrects when nml plasma is added
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| 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
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| which factor is defic in HemoA? HemoB? | HemoA=factor 8; HemoB=factor 9
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| how tx acute hemoarthoses | pain=codeine (NOT ASA or NSAIDs), immobil joint and ice packs
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| which dzs incrs PTT? And what are their BTs? | hemo (BT nml), vWF (incrsd BT), DIC (incrsd BT and PT, etc, etc)
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| 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)
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| which factors in PTT, what Rx affects? | think hit pitt=intrinsic pathway (8,9,11,12), heparin incrs PTT
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| which factors in PT, what Rx affects? | extrinsic=TF and factor 7, warfarin
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| what does thrombin time measure | fibrinogen level
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| common causes of DIC | MC: infxn, esp GN sepsis, obstetric cxns, major tissue injury (burns, trauma, sx), snake venom, shock/circ collapse
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| labs for DIC, PBS? | incrsd PT, PTT, BT, TT, + fibrin split products, D-dimer, decrsd plt, fibrinogen; PBS: schistocytes
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| tx DIC | plt transfusion, cryoprecip (gives clotting factors + fibrinogen, v FFP only gives clotting factors)
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| 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)
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| how long take to reverse warfarin | vit K replacement takes few days, so if severe bleeding give FFP
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| 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
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| labs for liver coag and compare to DIC | incrsd PT, +/- incrsd PTT, but unlike DIC TT, BT, and fibrinogen are nml
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| name 6 inherited hypercoag | ATIII defic, anti phospholipid syn, prot C, S defic, factor V Leiden, prothrombin gene mutation, hyperhomocyteinemia
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| tx inherited hypercoag | if >2 events, pt on permanent anti-coag w warfarin
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| 2ry hypercoag states/risks | malignancy (esp pancreas, GI, ovaries, lung), preg, OCP, post-op (esp ortho), nephrotic, PNH, CHF (blood stasis)
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| cxns assoc heparin | HIT, osteoporosis, rebound hypercoag
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| 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
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| how give and monitor LMWH | can only ive SC, can't monitor PT, PTT (doesn't affect)
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| contraindications for giving heparin | hx of HIT, active bleeding, hemophilia or decrsd plt, sever HTN, recent sx on eyes, spine, brain
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| how reverse heparin | can give protamine, otherwise takes 4 hrs after d/c heparin; give FFP if severe bleeding
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| 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
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| how long does it take warfarin to have an effect | 4-5d
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| who do you not give warfarin to | EtOH (risk of intracranial bleed when they fall), someone pregnant (teratogenic)
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| how long does it take to reverse warfarin | give vitK and takes 4-10hrs if liver nml
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| pt population who get Multiple myeloma | usu >50, more often AA
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| key features of MM (3) | 1) skel: osteolytic lesions esp back, ribs, jaw, pathol fractures, 2) renal failure and Bence Jones proteins, 3) infxns
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| dx criteria for MM | >10% if abnml plasma cells in BM + 1 of following: M protein in urine or serum, lytic bone lesions
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| labs of MM | incrsd Ca++, incrsd serum protein from Ig, incrsd ESR [can get pancytopenia later with BM invasion]
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| 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
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| describe Waldenstrom's Macroglobulinemia, how its difft from MM, tx | IgM produced causes hyperviscosity, no bone lesions; tx: chemotherapy and plasmaphoresis for hyperviscosity
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| 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
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| 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
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| 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
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| Hodgkins staging (Ann Arbor) | I: single LN, II: at least 2 LN same side diaphragm, III: both sides diaphragm, IV: extra lymph
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| 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
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| 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
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| 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
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| 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%
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| 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
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| describe Sezary syndrome | involves skin and blood stream, considered maybe a late stage Mycosis fungoides
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| which are HIV lymphomas | often Burkitts or diffuse large cell, very poor px
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| name Rx in CHOP | Cyclophosphamide, Hydroxydaunomycin (doxyrubicin), oncovin (vincristine), prednisone
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| 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
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| how dz NHL | need LN bx
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| key features of AML | mostly adults, don't respond as well to tx as ALL, Auer rods, DIC, can get skin nodules
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| how tx Hodgkins | if <IIIA radiotherapy, if IIIB and above chemo
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| how dx AML, ALL | need BM bx
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| 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
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| features of poor px ALL | <2yo, >9yo; WBC>50,000
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| lab values of tumor lysis syndrome | incrsd K, phosphate and uricemia
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| tx/px for AML and ALL | ALL: kids >75% complete remission (v 40% adults) and often responsive when relapse; AML: BM transplant best hope
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| 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
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| tx of CLL | chemo has little effect on survival but used to decr sympt and infxns, often fludarabine and cholambucil
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| dx of CLL | PBS often dx: absolute leukocytosis w small mature lymphocytes and smudge cells
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| key features of CML | usu >40yo, chronic course until blast crisis, Phila chromo(9,22), decrsd LAP
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| tx CML | if Phila chromo (bcr-abl tyr kinase) can use Gleevec (imatinib)
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| how tell leukomoid rxn v CML | leukomoid has no splenomegaly, incrsd LAP and hx of infxn
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| CLL staging | Rai staging: 0=lymphocytosis, 1=lympho + LAD, 2=lympho + splenomeg, 3= lympho + anemia, 4=lympho + decrsd plts
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| 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
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| sympt of polycythemia vera | mostly due to hypervisc: HA, dizziness, pruritis, visual impair, HTN; tx=repeated phlebotomy meylosuppression w hydroxyurea or IFN
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| how is esstl thrombocytosis defined, tx? | >600K, tx=anagrelide + ASA
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| tx for acute intermittent porphyria | hematin
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| what give during blast crisis | for tumor lysis syndrome give allopurinol to prevent hyperuricemia and renal insuffic
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| 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
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| 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
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| key factors for CML | 30-50yo, myeloid stem cells, WBC>50,000, Phila chromo, blast crisis (accelerates to AML), splenomegaly, low leukocyte alk P
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| key factors for CLL | >50yo, lymphocytes, male, lymphadenopathy, lymphocytosis, infxns, smudge cells, splenomegaly
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| 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
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| common clinical features of leuk | BM failure leads to anemia, infxn (loss WBC), hemorrhage (loss platelets); leukemic cells infiltrate spleen (splenomegaly), liver, LNs
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| Phila chromo, what's it assoc w | t(9;22), (bcr-abl) CML
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|
||||
| 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
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|
||||
| t(14;18) assoc w | Follicular lymphoma (small cleaved cell B cell type), bcl2 activ, MC non-Hodg lymphoma
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|
||||
| t(15;17) assoc w | M3 type AML which is responsive to all-trans retinoic acid
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|
||||
| t(11;22) assoc w | Ewings sarcoma
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|
||||
| 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)
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|
||||
| describe nodular sclerosing lymph, prevalence, blood smear, prognosis | MC, lots lymph, good prognosis
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|
||||
| describe mixed cellularity lymphoma, prevalence, blood smear, prognosis | 25% **lots Reed Stern**, many lymph, intermediate prognosis
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|
||||
| describe lymphocyte predmoinant lymph, prevalence, blood smear, prognosis | 6% lots lymphs, good prog usu <35yo males
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|
||||
| describe lymphocyte depleted, prevalence, blood smear, prognosis | rare, some lymphs, RS high relative to lymphs, poor prognosis, seen in older males w disseminated dz
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|
||||
| what do Reed Sternberg cells look like? Cell markers? | large cells w predominant nucleoli on polymorphic background, CD30+ CD15+ B cell
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|
||||
| 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
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|
||||
| 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)
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|
||||
| 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)
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|
||||
| describe small lymphocytic lymphoma (age, cell type, key features, prog) | NHL, adults, B cell, like CLL w focal mass, low grade
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|
||||
| 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
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|
||||
| 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%
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|
||||
| describe lymphoblastic lymphoma (age, cell type, key features, prog) | NHL, children usu immature T cells, commonly presents w ALL and mediastinal mass, aggressive
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|
||||
| 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
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|
||||
| 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
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|
||||
| what virus is assoc w T cell leuk | its caused by HTLV-1
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|
||||
| how difft myeloblasts from lymphoblasts | myeloblasts are larger w more cytoplasm, conspicuous nucleoli, often w granules and 50% Auer rods **myeloperoxidase +
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|
||||
| what is the most common presenting symptom of lymphomas? | lymphadenopathy
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|
||||
| pathology of bands of collagen enveloping pools of RS cells | nodular sclerosing
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|
||||
| which Hodgkins occurs more freq in women | nodular sclerosing
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|
||||
| 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)
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|
||||
| Hodgkins diagnosis | LN bx, CXR and CT (to detect LN involvement), BM bx to see if BM involved, lab (lymph, ESR can indicate dz)
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|
||||
| Hodgkins tx, px | I, II, IIIA: radiotherapy alone, IIIB, IV: chemo; chemo and radiotherapy in combo cures 70%
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|
||||
| relative freq of Hodgkins and NHL | NHL 2x as common
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|
||||
| when do you bx a suspicious LN? | if >1cm for >4wks that can't be attributed to infxn
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|
||||
| 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)
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|
||||
| 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
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|
||||
| which NHL is closely related to CLL | small lymphocytic lymp
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|
||||
| which NHL are considered intermediate grade? High grade? | intermediate: diffuse, large-cell; high grade: lymphoblastic and burkitts
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|
||||
| 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
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|
||||
| 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
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|
||||
| what does CHOP therapy consist of | cyclophosphamide, hydroxydaunomycin (doxorubiciin), oncovin (vincristine), prednisone
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|
||||
| what's the MC leuk >50yo | CLL
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|
||||
| overall px CLL | good, it's the least aggressive, (survive longer than acute leuk or CML), pts usu die of other causes
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|
||||
| PBS of CLL | almost all WBC are mature small lymphocytes, w smudge cells
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|
||||
| what lymphoma often presents w large extranodal mass | diffuse, large cell lymphoma (a NHL)
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|
||||
| 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
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|
||||
| describe osteochondroma, incidence/clinical course, location | most common benign, often incidental finding on metaphysis (neck of bone)
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|
||||
| 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
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|
||||
| 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
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|
||||
| how difft chondrosarcoma v osteosarcoma | chondro=diaphysis in medulla, osteo=metaphysis w Codman's triangle, sunburst
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|
||||
| 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)
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|
||||
| epiphyseal tumor w multinucleated giant cells--what dx? | giant cell tumor
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|
||||
| cancers assoc w rb gene | retinoblastoma, osteogenic sarcoma
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|
||||
| lots of colon polyps, think what dz? Cancer? | familial polyposis, they always become cancer
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|
||||
| gardner's syndrome--describe findings? Cancer? | familial polyposis, (they always become cancer) + osteomas, soft tissue tumors
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|
||||
| turcot's syndrome--describe findings? Cancer? | familial polyposis, (they always become cancer) + CNS tumors
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|
||||
| peutz-jegher's syndrome--describe findings? Cancer? | perioral freckles, non cancerous polyps; increased risk of non colon cancer (no incrsd risk of colon cancer)
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|
||||
| 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]
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|
||||
| 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
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|
||||
| what cancer is assoc w rubber/dye industry? | bladder
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|
||||
| what environmental risk factors are assoc w bladder cancer? | smoking, aniline dyes (rubber/dye industry), schistomiasis
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|
||||
| what environmental risk factors are assoc w liver cancer? | EtOH, vinyl chloride [liver angiosarcomas], aflatoxins (Africa)
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|
||||
| EtOH is assoc w which ENT cancers? | oral, pharynx/larynx, eso
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|
||||
| benzene is assoc w which cancer | leukemia
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|
||||
| clear cell cancer of cervix and vagina is assoc w? | in utero diethylstilbestrol (DES)
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|
||||
| 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
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|
||||
| 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]
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|
||||
| 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
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|
||||
| 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)
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|
||||
| 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
🗑
|
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