clin path Flashcards
myeloid stem cells
give rise to RBCs, platelets, leukocytes
lymphoid stem cell
gives rise to lymphocytes
basophil morphology
segemented nucleus
granular
basophilic (blue/purple)
rare
relative differential count
do not make interpretations from relative percentages
absolute differential count
/ul
use this for making interpretations
corrected WBC (cWBC)
know this formula
use when nRBC is above reference interval (1-5)
impedence WBC count
WBC impedence count (WIC) must be corrected for nRBCs
use when nRBC is above reference interval (1-5)
optical WBC count
WBC optical count (WOC)
does NOT need to be corrected for nRBC
covert relative WBC to absolute
(WBC relative %) x (total WBC count) = absolute WBC count
how long does proliferation/maturation take in the bone marrow?
5 days
how long are neutrophils in the blood?
10-12hrs
how long are neutrophils in the tissues?
< 2 days
marginal vs circulating WBCs
WBCs that stick to/roll over the walls of vessels
not measured in blood draws
dogs and cats vs cattle and horses neutrophil storage
dogs and cats have more neut storage in marrow
neutrophil regenerative left shift
neutrophilia
increased bands (more immature)
overall more segmented neuts than bands
degenerative neutrophil left shift
more bands than segmented neutrophils
neutropenia
segmented neutrophils are being used up somewhere
overwhelming inflammation
neutrophil deep left shift
can see metamyelocytes or myelocytes (band neutrophil precursors)
toxic neutrophils
early release of neutrophils before maturation is finished
order of toxicity of WBC
- diffuse cytoplasmic basophilia (due to greater amt of RNA)
- Dhole bodies: blue/grey amorphous cytoplasmic inclusions
- toxic vacuolization
- toxic granulation (dust like purple to dark pink)
- donut shaped nucleus
- giant neutrophil (rare)
3 main causes of neutrophilia
- stress (cortisol mediated)
- excitment/physiologic (epinephrine mediated)
- inflammation
stress neutrophilia
MILD neutrophilia
increased cortisol levels (stress, exogenous glucocorticoids, neoplasia)
* storage pool of neutrophils released
* downregulate adhesion molecules and marginal neuts become circulating
no bands, no left shift, no toxicity
also decreased lymphocytes, increased glucose
increased ALP (only in dogs)
excitement/physiologic neutrophilia
mild neutrophilia
* neuts moved from marginal to circulating
* splenic contraction
no left shift
increased lymphs, RBCs, platelets, glucose
fairly transitory, fight/flight response
inflammatory neutrophilia
maturation and storage stores released from bone marrow
recruit marginal pool into area of inflammation
myeloid hyperplasia
left shift, toxic neutrophils
lymphocytosis (if chronic), hyperglobulinemia, hypoalbuminemia
leukemoid response
neutrophil numbers > 50,000/ul (highly increased)
subtype of chronic inflammation
causes:
* IMHA: tissue hypoxia, necrosis
* 5 P’s: Pus, peritonitis, pyothorax, pyelonephritis, pneumonia, paraneoplastic
* hepatozoonosis infection
leukemia-like
paraneoplastic
inflammation from cancer producing inflammatory cytokines
rare
inflammation without neutrophilia
normal neut numbers with left shift, toxicity
inflammatory neutropenia
more neuts are used than can be produced
caused by:
* severe infection/sepsis
* overwhelming acute inflammation (ruminants, horses not as serious)
Left shift, toxic neuts
bands > neuts
decreased production neutropenia
**myelosuppressive agents **
* Viruses: FeLV, parvovirus
* Bacteria: Ehrlichia
* Drugs: Chemotherapy
* Toxins: Plants
* Idiopathic: Autoantibodies
myelophthisis (Myelitis, Leukemia, Myelofibrosis)
no left shift, no toxicity
decreased production of marrow cells
sequestration neutropenia
seen with endotoxemia from gr - bacteria
endotoxin causes acute inflammatory response
he mostly skipped this
primary lymphoid tissue
bone marrow (B cells), thymus (T cells)
Lymphocyte kinetics/migration
- leave capillary and move into tissue
- move into lymphatic vessel
- move into lymph node
- returned to blood via lymphatic duct
size of lymphocytes
same size or smaller than neutrophils
5 main causes of lymphocytosis
- physiologic (excitment, epinephrine)
- chronic inflammation (antigenic stim)
- young animals
- hypoadrenocorticism (Addisons)
- Lymphoid neoplasia
physiologic/excitment lymphocytosis
neutrophilia (no left shift, marginal neuts moved into circ)
erythrocytosis and thrombocytosis (splenic contraction)
hyperglycemia
transitory
chronic inflammitory lymphocytosis
lymphoid hyperplasia
neutrophilia (left shift w/toxic changes)
+/- monocytosis (inflammation)
anemia of chronic dz
hypoglobulinemia
lymphocytosis due to young age
pseudolymphocytosis
young animals have more lymphocytes
maybe decreased MCV, PCV (young animal)
maybe increased phosphorus, calcium, ALP, GGT (young animal)
hypoadrenocorticism
Addison’s dz
persistant lymphocytosis: opposite of stress
normal neutrophil count
+/- eosinophilia
+/- mild non regen anemia
+/- hypoglycemia, hypoproteinemia, hypercalcemia, hyponatremia, hyperkalemia
lymphoma
neoplastic lymphocytosis
Originates from lymph node
Lymphadenopathy (enlarged lymph nodes)
+/-Lymphopenia: presense of atypical lymphocytes
+/- Blasts in circulation
Numerous types (Sm, Lg, B, T)
neoplastic proliferation of a clone of lymphocytes (intermediate to larger) arising outside bone marrow (lymph node, spleen, thymus, intestine)
Acute lymphoblastic leukemia
originates in Bone marrow
Blasts >20%
+/- Pan-bicytopenia
+/- Myelopathies
Spleen-hepatomegaly
Poor prognosis
neoplastic proliferation of immature large lymphoid cells arising within bone marrow
chronic lymphocytic leukemia
originiates in bone marrow
Small lymphocytes
lymphocytosis >12K dogs, >20K cats
Tend to liver longer
neoplastic proliferation of a clone of small lymphocytes arising within bone marrow
reactive vs neoplastic lymphocytosis rule of thumb
neoplastic > 20,000/ul, clonal on PARR, much more severe
reactive: dogs and cats <20,000 /ul not clonal on PARR
lymphopenia
stress
acute inflammation
depletion
* lymphoid effusion, lymphangiectasia (loss of lymph)
lymphoid hypoplasia (immunosuppression, radiation, virus, congenital)
NOT from bone marrow injury (lymphocytes already in seconday lymphoid tissue)
combined B and T cell deficiency
