Busy. Please wait.

show password
Forgot Password?

Don't have an account?  Sign up 

Username is available taken
show password


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
We do not share your email address with others. It is only used to allow you to reset your password. For details read our Privacy Policy and Terms of Service.

Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.

Remove ads
Don't know
remaining cards
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
restart all cards

Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

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