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polycythemia
excessive RBC’s
2 forms of polycythemia
relative: from dehydration, easily fixed
absolute: primary or secondary
erythropoietin
hormone stimulating bone marrow to produce RBC’s
difference between primary and secondary polycythemia
polycythemia → absolute → primary or secondary
primary = non-malignant (cancerous or harmful) from overabundance of bone marrow stem cells
secondary = hypoxia from higher altitudes, COPD, smokers
low oxygen levels = compensates by overproducing erythropoietin
physiological manifestations of polycythemia
increased RBC level
increased hemoglobin
increased BV and viscosity in hematocrit
other
hypertension from the increased BV
splenomegaly
depleted iron
splenomegaly
enlargement of the spleen
manifestation of polycythemia
leukocyte types
granulocytes
neutrophils
eosinophils
basophils
agranulocytes
lymphocytes
monocytes
WBC function is affected with too few/many cells (______ changes), or if cells are functionally defective (______ changes)
[quantitative - too few/many cells] [qualitative - functionally defective cells]
leukocytosis
increase in WBC count
normal response to infection, surgery, pregnancy, hormones
can be caused by blood disorders, malignancies
leukocytopenia / leukopenia
decrease in WBC count
never a normal response
what is leukopenia caused by?
result of radiation, chemotherapy, autoimmune disease
reasons why granulocyte counts increase vs decrease
increase - due to infection types
decrease - production falls behind need
most common granulocyte type that fluctuates in its count
neutrophils - most numerous granulocyte
neutrophilia
early response to infection (shift to the left)
neutropenia
severe prolonged infections where body’s production cannot keep up with demand
starvation, HIV, autoimmune disorders, chemo
agranulocytosis (granulocytopenia)
extremely low granulocyte count caused by chemo, aplastic anemia
lymphocytosis
increase in lymph cells from viral infections
lymphocytopenia
decrease in lymph cell count - immune deficiencies, drugs
example of lymphocytosis
infectious mononucleosis (IM)
(lymphocytosis - increase in lymph cell count)
infectious mononucleosis (IM)
virus name
transmission method
cell type and count affected
age most frequently affected
epstein-barr virus (EBV) infects B lymphocytes
kissing disease - transmission through saliva
lymphocytosis - increased lymphocyte number
commonly affects 15-19 yr olds
specific antibody tested for when determining diagnosis of IM (infectious mononucleosis)
heterophile antibodies - AB that bind to antibodies other than the ones originally triggering them
pathophysiology & symptoms of IM (infectious mononucleosis)
epstein-barr virus invades upper respiratory tract (oro/nasopharynx, salivary epithelium) → moves to lymphoid tissues, infects B lymphocytes
symptoms = fever, sore throat, cervical lymph node enlargement → sometimes leads to splenomegaly
leukemia
cancer of the bone marrow stem cells (blood + blood forming organs)
genetic mutations cause abnormal immature cells to be rapidly overproducted - the immature cells do not function as mature cells, spilling into bloodstream and causing patient’s clinical manifestations as they do not function maturely (condition of pancytopenia)
pancytopenia
condition in leukemia from the reduced number of normal mature blood cells in peripheral blood - low counts cause leukemia’s physical manifestations
uncontrolled proliferation of the malignant leukocytes cause “crowding” in bone marrow, causing production of other cell types to cease
risk factors for leukemia
hereditary abnormalities (ex/ down syndrome)
cigarette smoke
ionizing radiation
infections like HIV, HCV
chemotherapies
describe leukemic cells
immature, poorly differentiated
rapid proliferation, abnormal function
interfere w/ normal blood cell maturation
infiltrate bodily organs and circulate bloodstream
leukemia vs lymphoma
leukemia - cancer of blood forming cells
lymphoma - cancer of the lymph nodes, spreads through lymphatic system
naming structure of leukemia
cell line affected/proliferating
lymphocytic - lymphoid stem cell → abnormal B and T cells
myelogenous - myeloid stem cell → abnormal RBC, granulocytes, monocytes, platelets
disease progression
acute - can develop rapidly
chronic - can develop slowly, more mature cells
4 classes of leukemia
ALL - acute lymphoblastic leukemia
AML - acute myeloid leukemia
CLL - chronic lymphocytic leukemia
CML - chronic myeloid leukemia
defining characteristics and clinical manifestations of acute leukemias
rapid growths of immature blood cells - abrupt onset and short survival time. difficult to detect early
clinical manifestaitons
anemia-induced fatigue
anorexia & weight loss
thrombocytopenia-induced bleeding
leukocytopenia (decreased # of WBC) - infections and fever
types
ALL: acute lymphocytic
AML: acute myelogenous
evaluation and treatment of acute leukemias
evaluation = blood tests and bone marrow biopsies: high immature WBC count
treatment = induction chemotherapy, blood transfusions, antimicrobial agents
cause of death for those with acute leukemias
metastatic infiltration of tissues causing infection, hemorrhage
ALL: acute lymphocytic leukemia
cell type affected
unique characteristic
B cell lymphocytes
most common type in children
AML: acute myelogenous leukemia
cell type affected
unique characteristic
cells EXCEPT lymphocytes (NEUTROPHILS, PLATELETS, ERYTHROCYTES)
occurs more in older adults
defining characteristics of chronic leukemias, clinical manifestations and types
slow growth of more mature cells, abnormal functioning, longer survival, gradual onset — majority of adult cases
clinical manifestations
fatigue
weight loss
splenomegaly
types
CLL: chronic lymphocytic leukemia
CML: chronic myelogenous leukemia
evaluation and treatment of chronic leukemias
evaluation = blood tests, bone marrow biopsies
treatments = combined chemotherapy, bone marrow transplant, biologic response modifiers (to increase immune response)
CLL: chronic lymphocytic leukemia
cell type affected
manifestations resulting from affected cell type
unique characteristic
B cell refusing apoptosis commands, accumulates while inactive. no AB production either!
increased infections due to no ABs being produced
can be slow onset, which is often asymptomatic
CML: chronic myelogenous leukemia
cell type affected
3 phases
unique characteristic (HINT: CHROMOSOME)
marrow granulocytes, RBC precursors, megakaryocytes
phases:
chronic: asymptomatic
accelerated: primary symptoms, immature cells, infections, fever
terminal blast phase: more blast cells, severe symptoms, poor prognosis
unique: philadelphia chromosome - an abnormal shortened chromosome that is apparent in 95% of CML cases
CML survival rates
90% live 5 yrs or longer
CLL survival rate
high variation survival rate: indolent forms = many years, aggressive forms = rapid onsets