CT and Heme
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| four types of SLE | 1) spontaneous, 2) discoid (skin lesions w/o other involvement), 3) Rx induced, 4) ANA -
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| characteristics of ANA - SLE | Ro (SS-A) +, has arthritis, Raynauds, subacute cutaneous Lupus, risk of neonatal Lupus
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| 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
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| 3 MC sympt in Lupus | malar rash (1/3), joint pain (90%), fatigue (common)
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| 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
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| describe LE (lupus erythemosus) prep | ANAs bind nuclei damaged cells creating LE bodies
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| name some of the other connective tissue dzs that can be ANA + | RA, scleroderma, Sjorgens, polymyositis and dermatomyositis
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| 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
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| 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,
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| tx SLE | NSAIDs, local or systemic steroids +/- hydroxychloroquine
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| 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
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| 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)
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| 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
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| what's the MC presenting sympt of scleroderma | Reynauds
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| what dz is commonly found w Scleroderma | Sjorgens (20%)
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| key Abs for scleroderma | CREST or limited=anti-centromere; diffuse=anti-Scl70 (or topoisomerase?)
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| CREST stands for | Calcinosis digits, raynauds, esophageal, sclerodactyly, telangiectasia (digits, nails)
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| 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
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| what need to monitor in scleroderma | esophageal motility w Ba swallow and PFTs (MC cause of death is pulmon)
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| describe sympt unique to diffuse scleroderma | ILD, peripheral edema, polyarteritis and carpal tunnel, fatigue, mscle involvement, + visceral involvement of lungs, heart, GI, kidney
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| describe pathophys of Sjorgen | lymphocytes invade lacrimal and salivary glands
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| describe 2 types of Sjorgens | primary w/o another connective tissue dz, 2ry w RA, sclero, SLE, polymyositis
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| what Ab + in Sjorgens | in 50% Ro (SS-A) and La (SS-B) are + [not specific]; note: SS-A at risk for neonatal SLE
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| tx Sjorgens drops | pilocarpine and eye
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| what Ab + in mixed connective tissue dz; describe the dz | anti-UI-RNP; overlap of dzs but don't nec occur simultaneously
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| pts who present w RA | usu women 20-40
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| 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
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| key findings accompany RA | C1, C2 cervical instability, pl eff common, pericarditis, episcleritis, rheum nodules
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| kids w uveitis, inflamm arthritis, RF -…what dz? | RA (often RF isn't + and in pauciarticular)
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| 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
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| MC cause of arthritis | osteoarthritis
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| key findings of OA on radiography | joint space narrowing, osteophytes, sclerosis of subchondral bone, subchondral cysts; Bouchards=PIP and Heberdens DIP
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| name of genetic syndrome assoc w gout | Lesch Nyhan defic in hypoxanthine guanidine phosphoryibosyltrxse
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| joint aspirate of gout v pseudogout v RA | all will have WBC>5,000, gout has needle shaped - birefringent, pseudogout has wkly + rod/rhomboid
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| 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
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| tx acute gout | NSAIDs (indomethacin) and colchicine [not ASA makes worse, not acetaminophin bc doesn't have anti-inflamm prop]
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| SE of colchicine | GI (80%): N/V, abd cramps, severe diarrhea
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| 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
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| 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]
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| what type of crystals form in pseudo gout | calcium pyrophosphate
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| 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)
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| how is pseudogout treated | esstly same as gout
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| clinical findings common to polymyositis and dermatomyositis | symmetrical prox mscle wknss (trbl getting up from chair, climbing steps), myalgia (1/3), dysphagia (1/3)
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| what skin findings seen in dermatomyositis | heliotrope rash, V sign, shawl sign, Gotton's papules=papular, eryth scaly lesions over knuckles
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| once dermatomyositis is dx what do you need to look for | other malignancy
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| 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
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| how is mscl bx different bw polymyositis and dermatomyositis | polymyositis (and inclusion body)=endomysial inflamm and fibrosis; dermatomyositis=perivascular and perimysial
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| 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
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| who does polymyalgia rheumatica occur in, what else to look for? | more elderly women, 10% have temporal arteritis
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| what are the muscles most often affects in polymyalgia rheumatica? | neck, shoulder, pelvic girdle [also for myositis]
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| what is clinical dx for fibromylagia | 11 of 18 points >3mos
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| 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
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| name the seronegative spondylarthropathies | ankylosing spondylitis, reactive arthritis/Reiters, psoriatic arthritis
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| what are clinical findings of ankylosing spondylitis | key is low back pain (bilateral sacroilitis) w limited motion, can have constitutional +/- uveitis
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| 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
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| classic Reiters characteristics | arthritis, uveitis, urethritis after enteric or GU infxn +/- genital and oral ulcers like Behcets
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| name the large artery vasculitis | Takayasu and temporal
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| name the med vessel arteritis (5) | PAN, Kawasaki, Wegeners, Churg Strauss, microscopic polyangitis
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| name the small arteritis (3) | HSP, hypersensitivity vasculitis, Behcets
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| 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
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| 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
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| 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
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| 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)
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| 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
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| common present of Behcets | young male 20s w painful oral and genital ulcers +/- uveitis, arthritis, eryth nodosum (but no prior infxn unlike Reiters)
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| dx, tx Behcets | need bx, steroids
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| 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
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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, acute chest, splenomegaly as child that infarcts and becomes asplenic and not palpable 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
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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
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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, 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
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| 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
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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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|
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