Hematology Flashcards
CML
BCL-ABL Tyrosine kinase fusion on chromosome 9/22
Tyrosine kinase inhibitor: imatinib
Howel-Jolly Bodies
Found in patients with asplenia or functional asplenia. Remnants of RBCs nucleus that was not removed.
Basophilic stipling
Found in patients with thalassemias or heavy metal poisoning.
Heinz bodies
Found in patients with G6PD deficiency or thalassemia.. Aggregates of Hb. Sometimes removed by macrophages which will cause “Bite Cells”
Sail Sign on CXR
Thymus can present in the right lung field in children up to three years old. This is a normal finding.
Lead Screening
Must have venous blood for confirmation. Tx if levels greater than 45ug Succimer if less than 75 Dimercaprol + EDTA if >75 or encephalopathic Xray if suspicion for lead ingestion
Acquired Sideroblastic Anemia
Microcytic hypochromic anemia with two distinct RBC populations mimics IDA but has increased ferritin and decreased TIBC.
Uremic patients have ______ bleeding time
increased, high levels of uremia cause platelet dysfunctions.
Diamond-Blackfan Anemia
Congenital erythroid aplasia
Craniofacial abnormalities, triphalangeal thumbs, increased risk of malignancy
Macrocytic, reticulopenic anemia
normal platelets and WBCs
Tx: steroids and transfusions
Beta Thal Major
95% Fetal 5% A2, survival into 50s or 60s but will required chronic transfusions and chelation therapy.
Hypocalcemia in massive transfusion
Citrate in RBC packs and other blood products chelates calcium.
Spherocytes
Spherocytosis or AIHA (Coombs+)
Tumor Lysis Syndrome
Hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia
Causes of Acquired Sideroblastic Anemia
Seen in thalassemias and pyridoxine deficiency.
ITP
Idiopathic thrombocytopenic purpura can present without the rash. Other cell lines should be normal. All those with ITP should have HIV and HepC screening.
Lead Poisoning Symptoms
GI symptoms, cognitive deficits, peripheral neuropathy, Anemia
HITT
Heparin induces a conformational change in platelets which exposes an antigen.
Serotonin release assay is the gold standard.
CLL
Fatigue in an old person
Lymphadenopathy, HSM, often asymptomatic
mild anemia/thrombocytopenia
severe lymphocytosis and smudge cells
Rouleaux Formations
MM
PAD occlusive crisis
Heparin
Spherocytosis
Increased indirect bilirubin, increased MCHC, decreased to normal MCV
Tx: Folate, transfusion, splenectomy
Timing of anticoag in DVT vs PE
DVT symptoms only do not require empiric anticoagulation
Macrocytosis in an alcoholic
Folate deficiency
Most common complication of sickle cell trait
hematuria (papillary necrosis)
ALL
Most common childhood cancer
2-5yo
Lymphadenopathy, HSM, petechiae
Dx: Bm Bx with >25% blasts
Microangiopathic hemolytic anemia
Elevated LDH, reticulocyte count, and bilirubin
Schistocytes
Commonly occurs with DIC.
CF associated bleeding pathology
Decreased fat soluble vitamin absorption (Vit K)
Vit K is used to activate factors 2, 7, 9, 10.
Prolonged PT
Dx of CLL
Flowcytometry, lymph node biopsy is generally not needed
PNH
Autoimmune hemolysis 2/2 lack of proteins (CD55/59) that prevent complement formation on RBCs
Signs of hemolysis and hypercoagulability (portal vein thrombosis), 40yo
Pancytopenia, Elevated LDH, and decreased haptoglobin
Tx: Fe, Folate, Ecluzimab (inhibits complement fixation)
Anemia of prematurity
impaired EPO production
Usually asymptomatic
Low Hb, low reticulocytes, normocytic/normochromic
Tx: Fe
Hereditary hemorrhagic telangiectasia
AKA Osler-Weber-Rendu Syndrome
Autosomal dominant
Diffuse telangiectasia, recurrent epistaxis, AVMs
AVMs in the lungs can cause shunting and increased Hg
Immune thrombocytopenic purpura
Autoantibodies to platelets shortly after a viral illness.
Platelets are normal sized or enlarged.
