Hematology/Oncology?Psych102 Flashcards
normocytic anemias are due to
decreased production (ACD) or increased destruction (hemolytic) of normal rbcs, or an increase in plasma volume or acute blood loss
Normocytic anemiia with an increased reticulocyte count is due to
acute blood loss
normocytic anemia with normal or decreased reticulocyte count
ACD or hemolytic anemia
high iron foods
meat, beans, raisins, spinach
AE of iron supplementation and how to avoid
can stain teeth–dilute liquid and use straw
heartburn, constipation, black tarry stool
TO avoid take with only a little food, best absorbed with acid/vit c; take with stool softener
small abnormally shaped rbs and decreased Hgb
microcytic anemia
IDA, thalassemias
large rbcs; due to defective DNA synthesis resulting in ineffective hematopoeisis
Macrocytic anemia
(large cells (megaloblasts) become trapped in marrow, decreased in life span and in #-megaloblastic anemia)
Pernicious anemia, folate deficiency anemia, alcohol-related anemia
quickly acquired anemia can be fatal in adults in Hgb is under
8
foods high in folate
leafy green vegetables, bran, dry beans, nuts
most common cause of megaloblastic anemia
folate deficiency
folate needed by women of childbearing age to avoid
neural tube defects, spina bifida
this anemia results in myelin degeneration causing neurological signs: paresthesias, gait disturbances, weakness, confusion
vitamin B12 deficiency anemia
infection and bleeding precautions will be needed with this anemia
aplastic anemia
enzyme made by kidneys in response to decreased oxygen carrying capacity that simulates myeloid stem cells in marrow
erythropoeitin (EPO)
Jaundice is seen in these anemias
hemolytic, sickle-cell anemia
abnormal increase in rbcs, wbcs, and plts
polycythemia
two types of polycythemia
Vera- caused by chromosomal mutation
Secondary- caused by hypoxia causing release of too much EPO
major danger of polycythemia
increased blood viscosity increases risk of clot
after treatment for polycythemia pts tend to develop
acute leukemia
dangerous plt levels
<10 risk for spontaneous bleeding
Disease where antibodies destroy platelets faster than they can be replaces
Immune Thrombocytopenic Purpura
ITP triggers
viral illness, SLE, pregnancy
often self-limiting in children
can be acute or chronic
Disease in which platelets clump abnormally and clog capillaries, causing tissue ischemia
Thrombotic Thrombocytopenic Purpura
often first sign of HIT is
breathing problem
sensitivity to heparin that forms in up to 25% of pts; antibodies formed to heparin-plt complex increasing risk of DVT or PE
Heparin-induced Thrombocytopenia
how to monitor for HIT
watch for decreased plt count to less than 50% of baseline 4-14 days after beginning therapy
In a pt with HIT, this anticoagulant is used instead of heparin
Agatroban
Classic hemophilia (80%) is this type, and is related to this CF
Hemophilia A; Factor VIII
Often is first sign of hemophilia
hemiarthrosis-joint bleeding
most common bleeding disorder; less severe than hemophilia, equally common in men and women
VonWillebrand’s Disease
also involves Factor VIII
Hemophilia B aka and involves what CF
Christmas disease
Factor IX
Vitamin K is needed
by liver to synthesize clotting factors
common sign of Vitamin K deficiency
bleeding mucous membranes
population at most risk for vitamin K deficiency
newborns-don’t have intestinal bacteria to make vitamin K
Granulocytes
Neutrophils, Eosinophils, and Basophils
agranulocytes
Lymphocytes and monocytes
stab/band cells
immature neutrophils
when body senses an infection band count will increase
involved in allergic reaction and parasite infection
Eosinophils
Philadelphia chromosome mutation results in
CML
Mutation in myeloid stem cell increases production of blast cells
CML
% of neutrophils and lymphocytes in diff
neutrophils: 60-70%
lymphocytes: 20-40%
Oral treatment for CML that inhibits cell division in only cells with the Phildelphia chromosome mutation
Gleevec
CML prognosis directly related to ability to
maintain a remission
acute exacerbation of CML
blast crisis
excess development of granulocytes, expanding marrow into the long bones, and inducing hematopoesis in liver and spleen causing them to enlarge occurs in
CML
major complication of chemotherapy treatment in any leukemia
Tumor Lysis Syndrome (increased uric acid, K, phos, and decreased Ca)
BMT for CML?
only in young, is a chronic disease
Leukemia of too many baby wbcs (granulocytes)
CML
Leukemia of too many non-functional adult lymphocytes
CLL
Leukemias are classified according to
which type of leukocyte is involved
malignant clone of (usually B) lymphocyte produces a non-functional adult appearing cell
CLL
In CLL, these become infiltrated with dysfunctional lymphocytes and enlarge
Lymph nodes, spleen and liver
CLL prognosis related to
extent of organ infiltration and patient wishes (no cure)
Typical presenting symptom on Hodgkin’s Lymphoma
Painless enlargement of lymph nodes
Reed-Sternberg cells are the malignant cell and diagnostic criterion for
Hodgkin’s Lymphoma
Lymphomas have increased incidence with exposure to
chronic immunosuppressive drugs and agent orange; EBV?
Abnormal, giant, multinucleated cells that replace other cells in the lymph nodes
Reed-Sternberg cells in Hodgkin’s
Hodgkin’s Lymphoma ususally presents in
20-40 years of age, more men
which leukemias present older?
Both 60+
CLL
Non-Hodgkin
Group of cancers originating from malignant lymphoid tissue with extensive infiltration of nodes and cells in many stages of development
Non-Hodgkin Lymphoma
Lymphoma diagnosed by
lymph node and/or BM biopsy
Suspect CLL instead of CML if these three s/s
splenomegaly, hepatomegaly, and presents at an older age
CBC results of pt with leukemia
WBC count 15-500
increased plts
unique symptom of pernicious anemia
tingling and numbness in extremeties