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6_20 StepUp CT Hem

CT and Heme

four types of SLE 1) spontaneous, 2) discoid (skin lesions w/o other involvement), 3) Rx induced, 4) ANA -
characteristics of ANA - SLE Ro (SS-A) +, has arthritis, Raynauds, subacute cutaneous Lupus, risk of neonatal Lupus
key features of neonatal Lupus born to Ro (SS-A) + women, skin lesions w cardiac anomalies incl heart block (AV), tGA, and valve/septal anomalies
3 MC sympt in Lupus malar rash (1/3), joint pain (90%), fatigue (common)
what steps in screening for Lupus ANA should be + (but not specific), then check dsDNA and Sm Ab; if ANA - should check Ro (SS-A) and La (SS-B) which is + in ANA - SLE
describe LE (lupus erythemosus) prep ANAs bind nuclei damaged cells creating LE bodies
name some of the other connective tissue dzs that can be ANA + RA, scleroderma, Sjorgens, polymyositis and dermatomyositis
describe features of SLE by organ system: mucocutaneous, CVS, pulmon, hemo, renal, GI mucocutaneous: malar rash, discoid rash, photosensitivity, Reynauds, oral uclers; CVS: pericarditis, myocarditis, Libman-Sacks endocarditis; pulmon: pleuritis (MC); heme: hemolytic anemia, decrsd WBC and plts, + lupus anticoag; renal: proteinuria, cell ca
name all immunol/Ab abnml in SLE ANA, dsDNA & Sm Ab (specific), Ro & La (in ANA -, assoc neonatal SLE), anti His (Rx SLE), VDRL/RPR syph, anticardiolipin and lupus anticoag,
tx SLE NSAIDs, local or systemic steroids +/- hydroxychloroquine
name GN grading for SLE, which is MC and which assoc w renal failure I=min, II=mesangial, III=focal prolifer, IV=diffuse prolifer (40%, renal failure is common), V=membranous; note: GN usu present at dx
describe anti-phospholipid syndrome and what dzs it's assoc w recurrent arterial or venous thrombosis, recurrent fetal loss, decrsd plts, livedo reticularis (purplish lace-like rash on LE)
name HLAs assoc w SLE, Sjorgen, RA, ankylosing spondylitis, Reitiers, psoriatic arthritis SLE=DR2,3; Sjorgen=DR2; RA=DR4; ankylosing spondylitis, Reitiers, psoriatic arthritis=B27
what's the MC presenting sympt of scleroderma Reynauds
what dz is commonly found w Scleroderma Sjorgens (20%)
key Abs for scleroderma CREST or limited=anti-centromere; diffuse=anti-Scl70 (or topoisomerase?)
CREST stands for Calcinosis digits, raynauds, esophageal, sclerodactyly, telangiectasia (digits, nails)
describe skin involvement in scleroderma subtypes, how relate to dz progression in limited only extremities and head and neck are involved (not trunk), whereas diffuse has widespread skin involvemnet; amt skin involvement can predict dz
what need to monitor in scleroderma esophageal motility w Ba swallow and PFTs (MC cause of death is pulmon)
describe sympt unique to diffuse scleroderma ILD, peripheral edema, polyarteritis and carpal tunnel, fatigue, mscle involvement, + visceral involvement of lungs, heart, GI, kidney
describe pathophys of Sjorgen lymphocytes invade lacrimal and salivary glands
describe 2 types of Sjorgens primary w/o another connective tissue dz, 2ry w RA, sclero, SLE, polymyositis
what Ab + in Sjorgens in 50% Ro (SS-A) and La (SS-B) are + [not specific]; note: SS-A at risk for neonatal SLE
tx Sjorgens drops pilocarpine and eye
what Ab + in mixed connective tissue dz; describe the dz anti-UI-RNP; overlap of dzs but don't nec occur simultaneously
pts who present w RA usu women 20-40
describe arthritis and key radiographic findings of RA symmetrical inflamm polyarthritis w hot, swollen joints, MC PIP, MCP, wrists NOT DIP; radiographic: periarticular osteoporosis, bony erosion, pannus (cartilage is like granulomatous tissue) + ulnar deviation, swan neck, and boutenierre deformities
key findings accompany RA C1, C2 cervical instability, pl eff common, pericarditis, episcleritis, rheum nodules
kids w uveitis, inflamm arthritis, RF -…what dz? RA (often RF isn't + and in pauciarticular)
tx of RA; tx of OA tx RA=NSAIDs (pain) + combo of MTX, hydroxychloroquine, sulfsalazine (Dz modifying Rx); tx OA=acetaminophen (since no inflamm component, or NSAIDs but concern PUD with long term use) can give joint steroids
MC cause of arthritis osteoarthritis
key findings of OA on radiography joint space narrowing, osteophytes, sclerosis of subchondral bone, subchondral cysts; Bouchards=PIP and Heberdens DIP
name of genetic syndrome assoc w gout Lesch Nyhan defic in hypoxanthine guanidine phosphoryibosyltrxse
joint aspirate of gout v pseudogout v RA all will have WBC>5,000, gout has needle shaped - birefringent, pseudogout has wkly + rod/rhomboid
what rheum dz can MTX be used for, and what are SE; and what must you monitor RA; SE incl GI upset, oral ulcers, bone marrow suppression, hepatocell injury, interstitial pneumonitis **give folate and monitor LFTs and renal
tx acute gout NSAIDs (indomethacin) and colchicine [not ASA makes worse, not acetaminophin bc doesn't have anti-inflamm prop]
SE of colchicine GI (80%): N/V, abd cramps, severe diarrhea
prophylaxis for gout, when to give, what Rx give after 2 attacks, Rx: if <800mg/d urine uric acid then under secreting uric acid and give probenacid or sulfinpyrazone; if >800 then overproduction is the problem and give allopurinol
after gout attack what should you avoid to prevent more attacks thiazide and loop diuretcs (incrs uric acid in blood), EtOH, dietary purine [secrets says to alkanize urine and incrs fluids]
what type of crystals form in pseudo gout calcium pyrophosphate
MC organism causing septic arthritis; what does joint aspirate show S Aureus, but in young sexually active N Gonorrhea (which will have + cultue in only 1/4); joint aspirate will show >50,000 WBC and >70% PMN (v 5,000 WBC and 50-70%PMN in inflamm arthritis)
how is pseudogout treated esstly same as gout
clinical findings common to polymyositis and dermatomyositis symmetrical prox mscle wknss (trbl getting up from chair, climbing steps), myalgia (1/3), dysphagia (1/3)
what skin findings seen in dermatomyositis heliotrope rash, V sign, shawl sign, Gotton's papules=papular, eryth scaly lesions over knuckles
once dermatomyositis is dx what do you need to look for other malignancy
key markers and Abs in dermatomyositis/polymyositis CPK (mrkr dz severity), anti-synthetase (anti-Jo-1): abrupt onset, poor px; anti-signal recognition protein: cardiac, worst px; anti-Mi-2: best px
how is mscl bx different bw polymyositis and dermatomyositis polymyositis (and inclusion body)=endomysial inflamm and fibrosis; dermatomyositis=perivascular and perimysial
how is inclusion body myositis difft from polymyositis and dermatomyositis more common in elderly men, prox and distal wkness, no Abs, slight incrsd CPK, poor px and response to tx
who does polymyalgia rheumatica occur in, what else to look for? more elderly women, 10% have temporal arteritis
what are the muscles most often affects in polymyalgia rheumatica? neck, shoulder, pelvic girdle [also for myositis]
what is clinical dx for fibromylagia 11 of 18 points >3mos
what are key distinguishing features of fibormyalgia pain is constant, aching, aggravated by stress, cold, sleep deprivation and better w rest, warmth, and mild exercise; insomnia; anxiety depression
name the seronegative spondylarthropathies ankylosing spondylitis, reactive arthritis/Reiters, psoriatic arthritis
what are clinical findings of ankylosing spondylitis key is low back pain (bilateral sacroilitis) w limited motion, can have constitutional +/- uveitis
distinguishing features of reactive arthritis/Reitiers occurs after an enteric infxn (Salmonella, Shigella, Camp, Yersinia) or urethritis (ie Chlamydia); asymm arthritis progresses from 1 joint to another usu LE
classic Reiters characteristics arthritis, uveitis, urethritis after enteric or GU infxn +/- genital and oral ulcers like Behcets
name the large artery vasculitis Takayasu and temporal
name the med vessel arteritis (5) PAN, Kawasaki, Wegeners, Churg Strauss, microscopic polyangitis
name the small arteritis (3) HSP, hypersensitivity vasculitis, Behcets
key features temporal arteritis, what else to look for >50, women, new onset headache, temporal pain and jaw claudication; look for ophthalmic artery involvement and 40% hav polymyalgia rheumatica
key features of, dx, cxns of Takayasu young Asian women, involved Ao arch, pulseless; dx w arteriogram; cxns incl Ao anurysm and renal artery stenosis causing HTN
key features of, dx, tx of Churg Strauss palpable purpura in pt w asthma, Eos; dx by skin bx (Eos) and pANCA; tx: steroids but poor px
key features of, dx, tx of Wegeners hemoptysis, hematuria, bloody sinusitis; cANCA + (open lung bx confirms); tx=steroids and cyclophosph but poor px (death <1yr in most)
key features of, dx, tx of PAN assoc w Hep B, HIV, Rx rxns; can have bowel angina but no pul involvement; pANCA may be + but need bx for dx; steroids helps some; poor px
common present of Behcets young male 20s w painful oral and genital ulcers +/- uveitis, arthritis, eryth nodosum (but no prior infxn unlike Reiters)
dx, tx Behcets need bx, steroids
key features of, dx, tx of hypersensitivity vasculitis mostly skin involved w palpable purpura, macules, vesicles, usu LE; Rx ie PCN, sulfa or infxn; dx=bx; withdrawal agent and steroids
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, acute chest, splenomegaly as child that infarcts and becomes asplenic and not palpable 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
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
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, whereas NHL 2x as common and usu 20-40; spread: H localized dz in LN w contiguous spread, NHL mltpl peripheral LN, extranodal and non-contiguous spread; sympt: H has constitut symp; NHL assoc w HIV and immunosuppress, Hodgkins must
name Hodgkins lymph types in order of freq, pathology, and px 1) Nod scleros: lots lymph, few RS w bands of collagen encircling 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 lymph RS>lymph, often older men w d
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
Created by: ehstephns on 2010-10-16

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