Study Guide Flashcards
Neutrophilia
Bacterial infxns, acute inflammation, necrosis, MI
Toxic granulation
Dark coarse granules found in granulocytes (esp neutrophils) dt impaired cytoplasmic maturation because trying to generate large numbers.
Seen in peripheral blood of pts w inflammatory conditions (esp sepsis)
Lymphocyte predominance
Acute viral infxn (EBV, CMV, viral hepatitis) and chronic inflammation (TB, etc)
Eosinophilia
Allergy (drugs, food, inhalants), parasitic infxn
What is bandemia and what does it suggest?
Excess band/immature WBCs released by BM into blood.
Infection, sepsis, inflammation
Mesenteric adenitis
Inflammation of mesenteric LNs in abdomen. Bacterium–Yesira entercolitica. If in RLQ can be confused w appendicitis.
Has pharyngitis, HA, NO vomiting, NO rebound tenderness
Cells in paracortical areas of LNs
T cells
Cells in secondary lymphoid follicle
Mostly B cells
Cells in medullary cords of LNs
Macrophages and plasma cells
Enlarged LN dt follicular hyperplasia is assoc w
Activated humoral response–RA, toxoplasmosis, early stages of HIV infxn.
Activate B cell rich germinal centers
Enlarged LN dt paracortical lymphoid hyperplasia is assoc w..
Distention and prominence of lymphatic sinusoids/nodes draining cancers–carcinoma of breast
Cells involved: endothelial cells and histiocytes
2 types of genetic derangements that cause WBC neoplasms…
Chromosome translocation
Oncogenes
How does the presentation of Hodgkin’s lymphoma differ from Non-Hodgkin’s re tenderness and location?
All Hodgkin’s: non tender.
2/3 non-Hodgkin’s: non tender. 1/3 extra nodal sites (skin, stomach, brain, etc)
Majority of lymphoid neoplasms…
B-cell origin (80-85%)
How does Hodgkin’s lymphoma spread?
Orderly, LN to LN
Which lymphoma has reed Sternberg cells?
Hodgkin’s
Non-Hodgkin’s has mutated B cells or T cells
Hodgkin’s vs non-Hodgkin’s
HL: 15-24 yrs, >60yrs. 1% of cancers/15% lymphomas. Begins in neck lymph nodes.
NHL: >60yrs. 4% of cancers/85% of lymphomas. Can begin anywhere. Less orderly, more aggressive, caught in advanced stages
Characteristics of ALL
Predominant precursor B cell tumors and manifests in childhood
T cell ALL: less common, present in adolescent males, thymic involvement.
ALL chromosomal abnormality
Hyperploidy (>50 chromosomes), Philadelphia chromosome t(9,22)
Most common leukemia of adults in western world?
CLL
*only leukemia not assoc w radiation or drug exposure
In which disease are smudge cells seen?
CLL
Morphology of CLL
BM involvement. SLL tumor cells usu infiltrate the splenic white and red pulp and hepatic portal tracts. Chromosomal trans locations are rare. Distinct immunophenotype.
Clinical presentation of CLL
Average 60yrs, M:F 2:1, survival 4-6 yrs. lymphadenopathy and hepatosplenomegaly.
GI infiltrates–> diarrhea, malabsorption, ulcers, megaloblasric anemia.
Disrupted immune fxn (hypogammaglobulinemia, antibodies to RBCs or platelets)
Fatigue, wt loss, anorexia, DOE, abdominal fullness, LA
Most common form of non-Hodgkin’s lymphoma
Follicular lymphoma