Confusasaurus.
CBC Differential
Neutrophils (45 - 75%) - functionally ingest and destroy invading bacteria. neutrophils will increase after injury or during inflammation and will last about 10 hrs.
Bands (0 - 4%) - these are baby neutrophils. immature little guys that are produced during/as a result of an inflammation process. the inflammatory process is happening right now.
Shift to the left - increase of (immature) bands
bands (immature) -----------> neutrophils (mature)
Shift to the right - increase of (mature) neutrophils
Eosinohpils (1 - 7%) - increase in allergic, parasitic, or inflammatory insults. they are found in the airway and the skin as well as in the blood (think allergic attack).
Basophils (0 - 2%) - same as mast cells, but called basophils in the blood. found in the GI and respiratory tracts as well as the skin. releases heparin and histamine when allergic or stressful attack occurs.
Monocytes (2 - 10%) - monocytes in the blood, macrophages in the tissue, they show up to phagocytose cells to be disposed of and foreign material.
Lymphocytes (16 - 46%) - B and T cells that provide cellular immunity and form immmunoglobins for humoral immunity. these will rise on viral attacks.
Leukopenia
Neutropenia - most relevant when the absolute neutrophil count (calculated by multiplying the percent neutrophil count by the Leukocyte count) is < 0.5E9/L. Separate severe neutropenia into acquired and congenital types:
MC acquired neutropenia - caused by MC drug therapy, viral and septic infections. tx with discontinuation of offending drug, myelowed growth factor with unctonrolled infection.
LC acquired neutropenia - less common causes are immune neutropenia, large granular lymphocyte leukemia (LGL). tx c PBS, lymphocyte immunophenotyping by flow cytrometery, TCR gene rearrangement studies, antineutrophil Ab testing
congenital neutropenia - Kostmann syndrome (congenital agranulocytosis), cyclic neutropenia. Tx hee and genetics consultation for severe neutropenia. for benign chronic neutropenia usually occurring in African or Yemenite Jewish ancestry can be handled by the family doc. Benign chronic is 0.5E9/L to 1.5E9/L neutropenia. the clinical course is asymptomatic.
Lymphopenia - yup... weak showing, lymphocytes (Ts & Bs). MC caused by recent immunosuppression drugs, corticosteroids, antilyphocyte MAbs. Acquired cases include viral infections including AIDS and even severe URIs, sepsis, lupus, RA, sarcoidosis, chronic RF, excessive alcoholism, old age, thymoma, TB. If congenital lymphopenia is suspected, ya know, like Bruton X-linked aggamaglobulinemia (low Bs), SCID (low Bs and Ts), or DiGeorge (low Ts), then get an immunology consult.
Polycythemia (Vera)
you know what this means, right? poly (many) cyte (cell) emia (in the blood). we have an excess of leukocytes, erythrocytes, and thrombocytes. PV is caused by a clonal myeloproliferative dz or secondarily by erythropoietin driven nonclonal causes. We, thus, need to differentiate between the two with this algorithm. (spoiler alert: we have to do JAK2 mutation screenings).
Thrombocytosis - thrombocyte = platelet, cytosis = greater number than normal
Primary - myeloid malignancy. ddx with /\ Hgb, MCV, WBC
Secondary - IDA, surgical asplenia, infection, chronic inflammation, hemolysis, tissue damage, nonmyeloid malignancy (reactive thrombocytosis). ddx with microcytic anemia.
why is it important to differentiate? primary can cause thrombohemorrhagic complications, but reactive will not.
general tx: firstly determine the duration of the dz. if chronic s surgical asplenia, then it's likely PT.......
this ddx gets a little involved at this point. I'm going to leave this to another post.
Leukocytosis - lots of leukocytes
first thing's first, scroll up to the top and make sure you got the CBC differential down pat.
if we have a boat load of immature precursors or blasts then we are looking at acute leukemia
this jump can be reactive (secondary) or neoplastic
neutrophilia granulocytosis - reactive flavors are leukemoid reactions. neoplastic flavors are myeloid malignancies. leukomoid reactions are caused by infection, inflammation, malignancy, or drugs. PBS showing blasts points to acute leukemia, keukoerythroblasts points to myelofibrosis c myeloid metaplasia, and left-shifts points to CML or another myeloproliferative dz (MPD). if you're dying to know if a neutrophilia is reactive and you don't have the hx to back it up (which you should be dying to know this... dying hard to know this), then we should bust out the peripheral blood FISH for bcr/abl to detect CML. We may want to get a hematologist involved at this point, as well.
eosinophilia granulocytosis - again, we have primary and secondary. let's scratch secondary off the list first by checking for parasitic (stool test), drug, comorbid, allergic, vasculitides, lymphoma, and metastatic conditions with a good hx. those can cause secondary eosinohpilia. if those are negative, then we need to fish for a primary cause. get a bone marrow biopsy to distinguis between clonal eosinophilia and hypereosinophilic syndrome. to detect HES grab a FISH for FIP1L1-PDGFRA mutation.
basophilia granulocytosis - peripheral blood basophilia means chronic basophilic leukemia. get a hematologist on board now.
Monocytosis
chronic absolute monocytosis means MPD like chronic myelomonocytic leukemia. hematologist time.
Lymphocytosis
we need to know the morphology of the excess lymphocytes, so reach for a peripheral blood smear to start c. we again want to distinguish between a reactive lymophocytosis and an LGL leukemia. reactive is caused by T-cell mediated viral immune response. LGL leukemia should be tested for by a TCR gene study from peripheral blood.
Leukemias get confusing to me. I'll be back here, methinks.
