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USMLE2 Medicine 10


bone marrow filled with plasma cells, serum with functionless Ig's multiple myeloma
most common initial sx of multiple myeloma bone pain in back and ribs (pathologic fractures), radiculopathy from nerve root compression, hyperCa
multiple myeloma is xxchromic and xxcytic anemia normochromic, normocytic
Protein electrophoresis with markedly elevated monoclonal immunoglobulin spike multiple myeloma
xray with punched out lytic lesions overproduction of osteoclast activating factor from plasma cells, multiple myeloma
elevated B2 microglobulin multiple myeloma
Bence Jones protein multiple myeloma, found via acidification of Bence Jones protein
dx multiple myeloma BM bx with >10% plasma cells
Tx of multiple myeloma in younger pts thalidomide and prednisone --> autologous BMT (stem cells from self)
Tx of multiple myeloma in older pts melphalan, prednisone, and thalidomide. PMT
tx of hyperCa loop diuretics (furosemide) and then bisphosphonate (pamidronate)
MGUS asx overproduction of Ig by plasma cells
who gets MGUS >50
Tx of MGUS not necessary
Reed Sternberg cells Hodgkin lymphoma
who gets Hodgkin lymphoma? bimodal - 20's and 60's
pt with enlarged, painless, rubbery nonerythematous, nontender cervical/supravclavicular/axillary LN's Hodgkin lymphoma
B sx's night sweats, 10% wt loss, fever
Hodgkin/non-Hodgkin lymphoma Stage I one lymphatic grp or one extra-lymphatic site
Hodgkin/non-Hodgkin lymphoma Stage II two lymphatic grps or extra-lymphatic site on same side of diaphragm
Hodgkin/non-Hodgkin lymphoma Stage III lymphatic grps on both sides of diaphragm OR any extra-lymphatic organ contig to primary nodal site
Hodgkin/non-Hodgkin lymphoma Stage IV widespread disease with diffuse extralymphatic sites such as BM or liver
dx of Hodgkin/non-Hodgkin lymphoma excisional LN bx
adverse prognostic factors in Hodgkin lymphoma LEBA (LAD, ESR, B sx, Age): Large mediastinal LAD, >40yo, B sx's, inc ESR
Tx for Hodgkin/non-Hodgkin lymphoma Stages I and II: radiation, B sx's or stage III and IV: for Hodg, ABVD (adriamycin [doxorubicin], bleomycin, vinblastine, dacarbazine); for non-Hodgkin CHOP (cyclophosphamide, Hydroxy-adriamycin, oncovin (vincristine), prednisone)
which Hodgkin lymphoma with best prognosis? which has worst prognosis? lymphocyte predominant is best; lymphocyte depleted is worst
which lymphoma associated more with extralymphatic spread? non-Hodgkin lymphoma
What infections predispose to development of non-Hodgkin lymphoma? HIV, Hep C, EBV, HTLV-1 and H.pylori
HIV and EBV most often associated with.... Burkitt lymphoma
enlarged painless rubbery nonrythematous nontender LN's, PLUS extra lymphatic / blood involvement non-Hodgkin lymphoma
relapse of non-Hodgkin lymphoma tx with what? autologous BMT
which non-Hodgkin lymphoma pt should get rituximab? those with lots of CD20 cells (rituximab is anti-CD20, inc survival when added to CHOP)
Idiopathic Thrombocytopenic Purpura (ITP) Ab to plt --> eaten by macrophage --> removal by spleen --> dec plt count
ITP associated with what? CHCL (chuckle): Lymphoma, CLL, HIV, and connective tissue diseases
bone marrow in ITP filled with what? megakaryocytes (prob is plt destruction, not production because plenty of megakaryocytes)
Tx for ITP 1) prednisone, 2) 10K to 20K plt - splenectomy, 3) <10K plt IVIG or Rhogam in (Rh+ pts since binds to Rh antigen on RBCs, only pts WITH spleens), 4) rituximab as last resort
plt type bleeding epistaxis, petechiae, bruising, menstrual abnl
inheritance of vWD autosomal dominant
what is the problem in vWD? decreased ability of plt to adhere to endothelial lining of blood vessels (plt aggregation still nl)
plt count and appearance in vWD both are normal
test to dx vWD ristocetin platelet aggregation (tests plt ability to bind to an artificial endothelial surface -ristocetin)
PT/PTT in vWD PT nl, PTT elevated (decrease in factor 8)
Tx for vWD 1. DDAVP (release vWF), 2. Factor 8 (contains vWF).
What med shouldn't person with vWD NOT use? ASA
Diseases with prolonged PT extrinsic pathway (on R). Factor 7 deficiency/inhibitor, Vit K def, Liver dz, warfarin.
diseases with prolonged PTT intrinsic pathway (on L). vWF/Factor 8 9 11 12 def, heparin, APL Ab
Diseases with prolonge PT and PTT Def/inhib: prothrombin, fibrinogen, factor 5, factor 10. DIC. Supratherapeutic heparin or warfarin.
Hemophilia A def of factor 8
Hemophilia B def of factor 9
hemophilia inheritance pattern X-linked recessive --> males only because females who are homozygous have intrauterine death
which is more common hemophilia - A or B? A (factor 8)
factor-type bleeding (as opposed to plt type bleeding) deeper: hemarthroses, hematoma, GI bleed, urinary bleed, bruising, CNS bleeding
PT/PTT profile of hemophilia prolonged PTT (intrinsic) and nl PT (extrinsic)
mixing study. what does it mean if PTT normalizes? what does it mean if PTT doesn't normalize? hemophilia - 50:50 mix of pt blood with normal blood brings PTT to nl. if does not normalize, then think of inhibitors of Factors 8 or 9
tx for mild hemophilia Hemophilia A: DDAVP, also use before surgery, or replacement of Factor 8. Hemophilia B: FFP, cryotherapy.
What factors affected with Vit K def? 2 7 9 10
In vit K def, what is affected? PT PTT both. PT first and more severe.
Tx of Vit K def severe - infusion of FFP. Also give Vit K at the same time (takes a while to kick in)
what clotting factors not made in liver? Factor 8 and vWF
which coag factor depleted first in liver disease Factor 7
most common site of bleeding in liver disease GI tract
how to tx severe bleeding in liver disease FFP acutely. long term - tx liver disease.
DIC pathologic activation of coagulation with consumption of plt and clotting factors. small blood clots form inside vessels --> consume coagulation proteins and platelets --> normal coagulation is disrupted and abnormal bleeding occurs
microangiopathic hemolysis ass with DIC
d-dimers associated with.... What are they? ass with DIC. a fibrin degradation product, present after a blood clot is degraded by fibrinolysis
fibrinogen levels in pt with DIC, d-dimers fibrinogen low because it's being consumed. d-dimer high because it's a fibrin degradation prod released after blood clot is degraded, which is happening a lot in DIC
Tx DIC FFP and plt transfusions, correct underlying disorder
if supratherapeutic INR >9, <20, how to tx hold warfarin and give 5 to 10 oral VitK. resume warf at lower dose once INR is therapeutic
if supratherapeutic INR >20, how to tx hold warfarin and give 10 IV VitK, FFP. resume warf at lower dose once INR is therapeutic
Created by: christinapham



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