Hematology/Oncology Flashcards
Thalassemia
Eti: Hereditary disorders characterized by reduction in the synthesis of globulin chains.
Minor: no significant clinical impact (insignificant microcytic anemia)
Alpha major: no hemoglobin produced: stillborn fetus.
Beta major: stunted growth, bony deformities, HSM, jaundice, cirrhosis, thrombophilia.
Alpha: predominantly asian descent
Beta: mediterranean descent
Folic acid deficiency (vit B9)
Eti: most common cause adequate dietary intake (ETOH and anorectic patients
S/sx: similar to B12 def, but none of the neurologic def.
B12 deficiency
Eti: Obtained by diet. Pernicious anemia: auto-antibodies
S/sx: Glossitis, GI disturbances (anorexia and diarrhea)…..
Prevention: nutrition if deficient
Treatment: parenteral b12 if severe
Macrocytic anemias
Most macrocytic anemias are megaloblastic.
Megaloblastic: enlarged RBC precursor with non-condensed chromatin.
Megaloblastic type: usually B12 or folate deficieny
Nonmegaloblastic: No DNA synthesis impairment. Disorders with increased membrane surface area, accelerated erythropoiesis, ETOH, COPD
Aplastic anemia
Bone marrow failure characterized by peripheral pancytopenia and marrow hypoplasia.
Usually normocytic anemia.
Anemia due to liver disease
Macrocytic, but no megaloblastic
Think about clotting issues, increased bleeding (GI bleeds).
Look for ascites, pancytopenia, caput medusae, (thinking about portal hypertension).
Diag: Macrocytic RBCs, with target cells
Anemia due to kidney disease
Patho: kidneys make majority of EPO, liver makes a little
S/s: fatigue, dyspnea, syncope, confusion, weakness
Diag: macrocytic
Tx: exogenous EPO
Anemia of chronic disease
Patho: anemia of inflammation (IBD, RA, CA are examples).
Generally normocytic
Tx: treat the disease
Sickle cell anemia
Patho: Abnormal hemoglobin causes sickling
S/sx: chronic hemolytic anemia: jaundice, gallstones, splenomegaly, vasoocculsion
Hemolytic crisis: Spleen sequesters sickle cells
Aplastic crisis: bone marrow compensation is reduced by infection or folate def.
Labs: low crit, reticulocytosis, howell-jolly bodies
Tx: folic acid, hydroxyurea (makes rbc’s more flexible)
Paroxysmal nocturnal hemoglobinuria
hematopoietic stem cell disorder: RBC membrane sensitivity to complement, leading to lysis
S/sx: First morning urine is reddish brown
Triad: hemolysis, pancytopenia, thrombosis
Sickle cell trait
Sickling happens at low O2 concentrations
Hereditary spherocytosis
decrease surface-to-volume ratio and a spherical RBC shape. Get trapped in spleen.
S/sx: Jaundice, cholecystitis, splenomegaly
G6PD deficiency
Patho: Hemolytic anemia from RBCs not able to deal with oxidative stresses. Hemoglobin denatures and forms heinz bodies.
S/sx: Hemollysis at time of infection or exposure to certain drugs. Jaundice, pale skin, back/belly pain.
Lab: Smear shows: bite cells, blister cells, heinz bodies
Autoimmune hemolytic anemia
Eti: acuired IgG autoantibody binds to RBCs.
Examples: SLE (10% of these patients), CLL, lymphoma
Hemochromatosis
Dysregulation of iron absorption: in the liver, pancreas, heart, adrenals, testes, pituitary and kidneys
S/sx: most asymp,
Advanced D: hepatomegaly, splenomegaly, increased pigmentation, spider angiomas
Acute Lymphoid Lekuemia (ALL)
Most common acute leukemia in children
Epi: 5-6yo or around 50
S/sx: hepatosplenomegaly, LAD, bone pain, anemia, thrombocytopenia, petechiae
Labs: CBC, manuel diff, …
Acute Myeloid Leukemia (AML)
Epi: median age presentation: 60
Patho: neoplasm derived from hematopoieti precursors that ifive rise to granulocytes, monocytes, erythrocytes, platelets.
S/sx: Malaise, fatigue, dyspnea, wt. loss, gingival hyperplasia…
Labs: abnormal CBC: high or low WBC, AUER RODs,
Chronic lymphocytic leukemia (CLL)
Neoplasm of more mature B cells.
Expansion of a neoplastic clone results in an increased # of small long-lived lymphocutes that are immunocompetent. Results in immunosuprresion
Epi: Most common leukemia in US, 2x men compared to women
Labs: lymphocytosis >5000/ mL, 75-98 % of circulating cells are lymphocytes, SMUDGE cells
Tx: no cure
Chronic Myeloid Luekemia (CML)
Eti: over production of myeloid cells, but are not as effective as regular myeloid cells
Epi: median age presentation is 50.
S/sx: fatigue, night sweats, low grade fever, abdominal fullness,
Pathophys: Philadelphia 22 chromosome
Labs: Elevated WBC count:
Tx: Imatinib (targeted therapy)
Polycythemia vera
An acquired myeloproliferative disorder causing overproduction of 3 hematopoietic cell lines, but most elevated are the RBCs
S/sx: HA, dizziness, tinnitus, blurred vision, fatigue, generalized pruritus
Phys exam: engorged retinal veins, spleen is palpable in 75% of cases.
Dx: HCT >54% men, >51% in women
Complications: Thrombosis, increased viscosity of blood and abnormal platelet function.
Hodgkin’s disease
Eti: Malignant cell is a B lymphocyte
Epi: bimodal, 20-30yo and >50yo
Cell type: Reed-Sternberg cells
S/sx: painless lymphadenopathy, constitutional symptoms (fever, wt. loss, night sweats, generalized pruritis)
Distribution: contiguous lymph node spread.
Non-hodgkin’s lymphoma
Heterogenous group of cancers of lymphocytes usually presenting as enlarged lymph nodes.
S/sx: Painless lymphadenopathy, consititional sxs (fever, night sweats, wt loss).
Dx: lymph node biopsy
Distribution: noncontiguous lymph node spread
Multiple myeloma
Eti: malignancy of plasma cells. Replacement of bone marrow, bone destruction, and paraprotein formation.
Abnormal proteins can cause kidney problems.
Epi: mean age 65 years.
Patho: Paraprotein: abnormal immunoglobulin that is produced by abnormal proliferation of plasma cells.
S/sx: Bone pain (often spine, hips, ribs, proximal long bones). Infection, Kidney failure.
Labs: Anemia, hypercalcemia, proteinuria, elevated ESR, BENCE JONES PROTEINS.
Burkitt’s Lymphoma
Very fast growing non-hodgkins lymphoma
Epi: more men, mean age 30
S/sx: 65% present with abdominal mass. Lymphadenopathy. FEVER, NIGHT SWEATS,
