Hemato-onco Flashcards
Very large nucleated cells (blasts) with purple-red inclusions (Auer rots) is a hallmark of
It’s most common in
Acute myeloid leukemia
65 year old patients
Hallmarks of Hodgkin lymphoma
-Reed-stenberg cells
-B sts + presents with mass
Hypersegmented neutrophils with6 or more lobules should always make you suspect
Megaloblastic anemia
Hallmarks of B12 deficiency
Neurological disfx: usually start affecting proprioception (recurrent falls) and vibration
-MVC > 110 (also in Folic acid def)
-Hypersegmented neutros (“ “)
How and why does an Acute hemolytic transfusion rx present?
Fever, chills, dyspnea, chest or back pain and hemoglobinuria within min to hours of transfusion.
Usually due to ABO incompatibility (Type ll hypersensitivity rx - mainly IgM)
Possible triggers of DIC
Sepsis
Malignancy
Trauma
Obstetric complications
Pancytopenia in the settings of sepsis most likely indicates
DIC
What’s the mec of DIC due to sepsis ?
Endotoxins activate coagulation cascade which leads to widespread fibrin deposition, shearing of RBC = schistocytes
Atypical lymphocytes are usually seen in
Infections, specially Mononucleosis
Howell-Jolly bodies are round, dark, purple-red inclusions in RBC seen in
Splenectomy, spleen disfx, sickle cell disease.
Howell-Jolly bodies are round, dark, purple-red inclusions in RBC seen in
Splenectomy, spleen disfx, sickle cell disease.
Which type of donor is most appropriate for Congenital diseases that require bone marrow transplants?
Matched unrelated donor (can have near perfect HLA matching)
Why aren’t Autologous and syngenetic donor a good option for congenital genetic disorders?
Autologous = Cells harvested from patients (eg umbilical cord) will have the same problem.
Syngenetic = cells from identical twin will have exact HLA match and not be rejected but will have same congenital mutation
Pathophysiology Chronic myeloid leukemia ?
Translocation of genes between chromosomes 9 and 22 with the resulting fusion of genes BCR-ABL
Sickle cell disease hallmarks
-hemolysis
-vasoocclusion
-Infections
*small and firm spleen
Pathophisiology of sickle cell disease
Beta globin Mut (Glu for Val) Polymerization of HbS lead to sickle shaped RBCs which cause small vessel occlusion and hemolysis
Numerous plasma cells (>10%) in BM aspirate is characteristic of
Multiple myeloma
Features of multiple myeloma
-Monoclonal ig spike
-Normo-normo anemia
-hypercalcemia and bone lesions
-Light-chain cast nephropathy/renal insuf
-Amyloidosis
Main difference between sickle cell anemia and sickle cell disease
No HbC present in SC anemia
Pathophysiology of Homozygous sickle cell anemia
Mut in both beta globin genes (change of glutamate for valine) = forms beta sickle globins = unable of producing HbA (has beta globin) but can produce HbF and HbA2 (don’t have beta globin)
Acute intermittent porphyria presents as
Recurrent abdominal pain
Neurological symptoms
Port-wine colored urine
Pathophysiology of Acute intermittent porphyria and tto
Failure to produce heme. Accumulation of perphyrin precursors in blood and urine due to enzyme deficiency (porphobilinogen deaminase.
tto is hemin infusion (downreg aminolevilinate synthase)
A mutation in beta globin gene (beta thalassemia) affects which cellular process?
Initiation of translation bc mutation occurs before methionine start codon (AUG) needed for the Kozak consensus seq to initiate protein translation
Blood smear Findings in Beta thalassemia:
-microcytosis
-increased central pallor (hypochromia)
-target cells
-anisopoikilocytosis (different shape,sizes)
-basopholic stippling