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HemeReview 2013

Clinical Medicine

IDA (causes) -chronic blood loss --> GI tract most common -Chronic NSAID/ASA use -Pregnancy -menstrual blood loss -low iron intake (women, children)
IDA (ssx) -pallor, fatigue, DOE, tachycardia -*pica* -esophageal webs (plummer-vinson syndrome)
IDA (dx) -hypochromic, microcytic anemia -elevated TIBC -low Fe, ferritin, and transferritin
IDA (tx) -tx underlying cause -iron supplementation with ferrous sulfate x 6-12 months
Lead Poisoning (ssx) -difficulty concentrating, fatigue, muscle weakness, paralytic ileus
Lead Poisoning (dx) -mild microcytic anemia -basophilic stippling of RBC -elevated lead lvl
Lead Poisoning (tx) -remove lead source -chelating agents if symptomatic or severe toxicity
Thalassemia -inherited disorder of alpha or beta globulin synthesis -typically family hx -genetic counseling in sever forms
Thalassemia (dx) -microcytic anemai that does not respond to iron therapy -normal iron and ferritin levels -confirm w/ hbg electrophoresis
alpha thal (dx) -peripheral smear: target cells -Hgb H on electrophoresis
alpha thal (tx) -Avoid iron -avoid oxidative drugs -folic acid supplements
beta thal major -Cooley anemia -onset 4-6 months of age, seveer anemia, growth retardation, osteopenia, deformities, hepatosplenomegaly
beta thal minor -moderate anemia
beta thal (dx) -peripheral smear: basophilic stippling, target cells -microcytic
beta thal major (tx) -transfusion with deferoxamine to prevent hemosiderosis
beta thal minor (tx) -avoid iron -monitor
B12 deficiency -vegans, pancreatic insufficiency, gastric bypass surgery, crohn's
B12 deficiency (exam) -glossitis, pale icterus -neuro: stocking-glove paresthesias, loss of tast and vibratory sensation, ataxia
B12 deficiency (Dx) -macrocytic anemia, poikilocytosis, anisocytosis -low retic count and serum B12 -high LDH and bilirubin
B12 deficiency (tx) -high dose oral B12, nasal spray or IM
B12 deficiency (neuro ssx) -will resolve if tx is initiated within 6 months of onset -if not corrected damage is irreversible
pernicious anemia -autoimmune destruction of gastric parietal cells causing lack of intrinsic factor -most common cause of B12 deficiency
pernicious anemia (dx) -macrocytic anemia -low serum B12 -shilling test positive
pernicious anemai (tx) -lifelong IM B12 supplement
folic acid deficiency -poor intake, EtOH abuse, pregnancy, bactrim, suflasalazine
folic acid deficiency (dx) -macrocytic -hypersegmented PMNCs -folate level <150 ng/mL
folic acid deficiency (tx) -folic acid 1 mg/day by mouth
hemolytic anemias (cuases) -TTP, ITP, DIC -medication/transfusion reactions -sickle cell -G6PD deficiency -ifxns (malaria, parvo b19)
hemolytic anemias (exam) -splenomegaly
hemolytic anemias (dx) -elevated retic; falling hct -elevated indirect bilirubin -elevated LDH
sickle cell anemia -autosomal recessive hemolytic anemia; african americans
sickle cell anemia (aggravators) -sickling of RBCs increased by hypoxemia, high altitudes
sickle cell anemia (prognosis) -life expectancy = 40-50 yrs
sickle cell anemia (ssx) -painful crises, cholelithiasis, poor wound healing, priaprism, splenomegaly, AVN of femoral head
sickle cell anemia (dx) -Hgb electrophoresis shows Hgb S in RBCs -sickled cells, target cells, howell-jolly bodies
sickle cell anemia (tx: symptomatic) -analgesics, fluids, O2
sickle cell anemia (tx: crises) -possible transfusion
sickle cell anemia (tx: asx) -pneumococcal vaccine/folate supplements -genetic counseling
G6PD deficiency -X linked recessive; mediterranean populations and african american males
G6PD deficiency (path) -leads to episodic hemolysis or chonic hemolysis if severe
G6PD deficiency (risks) -oxidative drugs; infxn -fava beans
G6PD deficiency (dx) -bite cells, heinz bodies -G6PD low after hemolytic episode
G6PD deficiency (tx) -most cases are self-limited -avoid oxidative meds (ASA, dapsone, sulfonamides, nitrofurantoin)
ACD (anemia of chronic dz) -associated w/ kidney, liver, endocrine dz, or malignancy -renal dz leads to decreased EPO
ACD (dx) -mild normochromic, normocytic anemia -normal cell morphology
ACD (tx) -treat underlying dz and anemia will resolve -give EPO
aplastic anemia (ssx) -weakness, bleeding, bacterial and fungal infections, purpura, petichiae, hepatosplenomagaly
aplastic anemia (causes) -most common: T cell mediated autoimmune suppression -radiation, chemotherapy, medications, SLE
aplastic anemia (dx) -pancytopenia w/ normocytic anemia -hypocellular marrow
aplastic anemia (tx: mild) -supportive; EPO/transfusions
aplastic anemai (tx: severe) -bone marrow transplant
polycythemia vera (primary) -JAK 2 mutation -splenomegaly, normal O2 sat, increased red cell mass
polycythemia vera (secondary) -chronic hypoxia, smoking, renal tumors -splenomegaly absent
polycythemia vera (who?) -males>females -age>60
polycythemia vera (complications) -bleeding (PUD/epistaxis), thrombosis, progression to leukemia
polycythemia vera (ssx) -tinnitus, HA, dizziness, blurred vision, plethora -pruritis after bathing
polycythemia vera (dx) -elevated Hct -leukocytosis, increased large/bizarre platelets -hypercellular bone marrow
polycythemia vera (tx) -phlebotomy -hydroxyurea -low dose ASA
thrombocytopenia -decrease in the number of platelets -most common cause of abnormal bleeding -associated w/ SLE and CLL
thrombocytopenia (ssx) -gingival bleeding, epistaxis, menorrhagia, petichiae
thrombocytopenia (causal drugs) -heparin, sulfonamides, thiazides, cimetidine
ITP -autoimmune, IgG mediated
acute ITP (ssx) -petechia, purpura, hemorrhagic bullae on skin
acute ITP (tx) -most are self-limiting -steroids -splenectomy if severe
acute ITP (who?) -children, following a viral infection
chronic ITP (who?) -women>men; ages 20-50 yrs
chronic ITP (ssx) -petechiae on skin and mucous membranes -associated w/ autoimmine conditions (SLE)
chronic ITP (tx) -high dose steroids; IVIG; SCT -splenectomy -avoid ASA -platelet transfusion for severe bleeding
TTP (who?) -women>men; age 20-50; previously healthy
TTP -associated w/ HIV, pregnancy, estrogen, quinine, ticlopidine -rare but can be fatal
TTP (ssx) -severe thrombocytopenia, anemia (schistocytes), elevated LDH, thrombosis -pallor, petechiae, purpura, pancreatitis, fever -neurologic signs that come and go
TTP (tx) -emergent plasmapheresis (NO PLATELETS) -prednisone -antiplatelet agents
DIC -SAS -occurs pts w/ sever systemic illnesses; sepsis, cancer, transfution reactions, trauma -high mortality (30-80%)
DIC (ssx) -shock, hemorrhage from skin and mucous membranes, digital ischemia, gangrene
DIC (labs) -coagulopathy: elevated D-dimer, prolonged PT
DIC (tx) -urgently treat underlying cause -component blood transfusions -cyroprecipitate -+/- heparin
vW dz -most common congenital coagulopathy -deficiency of facter VIII antigen and defective vWF
vW dz (gentics) -autosomal dominant bleeding disorder
vW dz (ssx) -bleeding of nasal passages, vagina, GI tract
vW dz (labs) -prolonged bleeding time -decreased vWF
vW dz (tx) -desmopressin acetate -factor VIII concentrates -avoid ASA and exogenous estrogen -pregnancy may exacerbate symptoms
hemophilia A -most common hemophilia; factor VIII deficiancy -most severe bleeding disorder: 2nd most common congenital coagulopathy
hemophilia (genetics) -x-linked recessive
hemophilia A (ssx) -range from severe hemarthrosis, intracranial bleeding to milder prolonged post op bleeding
hemophilia A (labs) -prolonged PTT -low factor VIII:C levels -normal vWF
hemophilia A (tx) -heat treated factor VIII concentrates -mild dz can be treated w/ desopressin -avoid ASA
hemophilia B -factor IX deficiency or Christmas dz -x-linked recessive; males
hemophilia B (tx) -factor IX concentrates -FFP (fresh frozen plasma)
Vit K deficiency -most common acquired coagulopathy
Vit K deficiency (causes) -chronic liver dz (most common), dietary, meds
Vit K deficiency (ssx) -post surgical pts; soft tissue bleeding
Vit K deficiency (labs) -PT/PTT are prolonged -elevated LFTs -decreased Factors VII, IX, X, II (SNOT)
Vit K deficiency (tx) -oral or IV vit K -treat acute bleeds with FFP
thrombotic disorders -pts: >40, family history, recurrent thrombosis
aquired thrombotic disorders -malignancy, estrogen use, immobilization, nephrotic syndrome, ulcerativ colitis, crohn's, heparin
congenital thrombotic disorders -antithrombin III deficiency, factor V leiden, protein C&S deficiencies, lupus anticoagulant
thrombotic disorders (tx) -anticoagulation w/ LMWH or coumadin -predinsone for lupus anticoagulant
hodgkin's dz (who?) -men>women; ages 15-45
hodgkin's dz -enlargement of lymphoid tissue, liver/spleen -associated w/ EBV
hodgkin's dz (ssx) -painless LAD, fever, night sweats, pruritis, fatigue -pain w/ EtOH
hodgkin's dz (dx) -ann arbor creteria -staging -staging tests: CT neck, chest, abdomen, pelvis, BM bx -*reed-sternberg cells*
hodgkin's dz (tx) -combinations chemotherapy or radiation depending of stage at diagnosis -majority of pts are cured
non-hodgkin's lymphoma -malignancy of lymphocytes (MC B lymphocytes) -age 20-40; more common with HIV/immune compromise
non-hodgkin's lymphoma (ssx) -painless persistent LAD -abdominal fullness in Burkitt's lymphoma -spread to bone, bone marrow, GI, skin
non-hodgkin's lymphoma (labs) -biopsy enlarged nodes -stage w/ CXR, CT abdomen and pelvis -BM bx
non-hodgkin's lymphoma (tx) -radiation for single node -rituximab +/- chemotherapy -high grade: sct -spontaneous remission may occur
multiple myeloma -malignancy of the plasma cells -more common in AA
multiple myeloma (ssx) -osteolytic lesions, LAD, recurrent infections
multiple myeloma (labs) -hypercalcemia -*rouleaux formation* of RBCs -monoclonal spike on electrophoresis (M spike on SPEP) -bence-jones proteins in urine
multiple myeloma (tx) -dexamethason, doxorubicin, lenalidomide -bisphosphonates for osteoporosis
acute leukemia (ssx) -epistaxis, gingival bleeding, gram-negatic bacterial infxns -anemai, DIC, elevated uric acid
acute leukemia (dx) -pancytopenia w/ circulating blasts -elevated WBCs -confirm w/ BM bx
acute leukemia (tx) -induction chemotherapy followed by consolidation therapy -allopurinol/diuretcs to prevent uric acid stones -sct
ALL -most common childhood leukemia
ALL (ssx) -rapid onset of fever, fatigue, joint pain, bone pain (sternum, femor), frank bleeding
ALL (cxr) -mediastinal mass
ALL (labs) -leukocytosis w/ lymphocytosis -philadelphia chromosome (poor prognosis)
ALL (tx) - >50% cure rate for children undergoing chemotheraphy
AML (who?) -adults: median onset of age 60 -MC acute leukemia
AML (ssx) -gradual onset of fatigue, decreased appetite, weight loss, and dyspnea
AML (dx) -*auer rods*
AML (tx) -high remission rate in pts < 60
CLL (who?) -MC of all leukemias -men>women -median age of onset 65 years
CLL -malignancy of B lymphocytes, median survival 6 years
CLL (ssx) -recurrent infections, LAD, Richter's syndrome
CLL (staging) -Rai system
CLL (dx) -lymphocytosis -peripheral smear: *smudge cells*
CLL (tx) -palliative w/ advanced dz
CML -myeloproliferative disorder seeen in middle aged adults
CML (ssx) -gradual onset of weight loss, low grade fever, fatigue, sweating, splenomegaly, early satiety
CML (triphasic) -progression from chronic to accelerated to acute phase (blast crisis/decreased survival
CML (dx) -leukocytosis -*philadelphia chromosome* -bcr-abl gene identification -hypercellular bone marrow
CML (tx) -imantinib mesylate(Gleevec), dasatinib, nilotinib -allogenic sct only curativ therapy (reserved for progressive disease)
Created by: duanea00