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Leukopenia

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Leukopenia
Decrease in WBC
1)Neutropenia/Agranulocytosis
2)Lymphopenia
Neutropenia/Agranulocytosis
Reduction in the number of granulocytes in the blood
-WBC count reduced to from 1000cells/μL - 200cells/μL

Agranulocytosis: very severe cases
What are granulocytes
1)Neutrophils
-50-60% of circulating WBC
-fast responders
-professional bacteria phagocytoser

2)Eosinophils
-professional antigen presenters(limited phagocytosing ability)
-Bind IgE
-kill parasites and tumors

3)Basophils(less than 2% of WBC)
-IgE, IgG, complement and histamine
-trigger inflammation to fight infection
2 mechanisms that cause neutropenia
1)Inadequate or ineffective granulopoiesis
a)marrow failure
-aplastic anemia
-leukemia
b)Chemotherapy
-cause marrow aplasia

2)Accelerated removal or destruction of neutrophils
a)immune mediated injury
-drugs
-idiopathic
b)overwhelming infection
-uses them all
c)enlarged spleen
-lead to sequestration and accelerated removal
Benign changes in different WBC
-neutrophils
1)Neutrophilic leukocytosis(neutrophilia)
2)Neutropenia
neutrophilic leukocytosis
neutrophil count > 7000cells/mm

Etiology
1)infection(acute appendicitis)
2)sterile inflammation with necrosis(acute MI)
3)Drugs(corticosteroids)

Pathogenesis
1)increased bone marrow neutrophil production
**results in "left shift": increased # of immature neutrophils
2)decreased activation of neutrophil adhesion molecules
-fewer neutrophils adhere to endothelial cells
Neutropenia
absolute neutrophil count <1500 cells/mm

Etiology
1)aplastic anemia
2)immune destruction
**SLE
3)Septic shock

Pathogenesis
1)decreased production
2)increased destruction
*by complement, macrophages
3)activation of neutrophil adhesion molecules
a)increase # of neutrophils adhering to endothelium
Leukomoid reaction
-etiology
-pathogensis
-who
Looks like leukemia but is not

-Can involve any of the 3 cell lines but often involves leukocytes counts >50,000cells/mm

Etiology
-caused by serious infection
ex:
a)Perforated appendicitis(neutrophils)
b)Whooping cough(lymphocytes)
c)Cutaneous larva migrans(eosinophils)
d)ottitis media(neutrophils)
**particularly in kids
e)TB
f)Sepsis

Pathogenesis
1)exaggerated response to infection

Who: Kids most likely to get exaggerated response
Note on leukomoid, pertussis and pediatricians
Pertussis can cause a leukomoid reaction and pediatricians get very nervous because you get 60,000 lymphocytosis

So it looks like:
acute lymphoblastic luekemia

Except you get no:
1)anemia
2)Thrombocytopenia
Lymphocytosis
-what are lymphocytes
-etiology
-pathogenesis
-pertussis mechanism?
Lymphocytes
1)T-cell: cell mediated immunity
2)B-cell: Ag, humoral immunity
3)NK cell: innate kills tumors and viruses

Lymphocytosis: absolute lymphocyte count >4000 cells/mm

Etiology
1)Viral: Mono, CMV
2)Bacterial: Pertussis
3)Drugs: phenytoin
4)Graves Disease

Pathogenesis
1)increased production
2)decreased entry into lymph nodes
*ex: in pertussis lymphocytosis-promoting factor decreases lymphocyte entry into lymph nodes and so it increases blood amt=lymphocytosis
Atypical lymphocyte
-appearance
-etiology
What happens when lymphocyte responds to antigen and becomes really big

Etiology:

Diseases:
1)Mono
2)CMV
3)toxoplasmosis
4)viral hepittitis
Drug
1)Phenytoin
-also produces macrocytic anemia

Appearance
-stain blue with prominent nuclei and lots of cytoplasm. They are very large
Infectious Mononucleosis
-pathogenesis
-clinical
-labs
-Epstein-Barr Virus

Pathogenesis
1)Replication in epithelial cells in oropharynx
2)Infections spreads to B cells in lymph nodes
a)attaches to CD21 on B cell
b)causes B-cell proliferation and increased synthesis of IgM antibodies
c)virus remain dormant in B cells and can recurre


Clinical:
1)severe fatigue
2)exudative tonsillitis
3)always have hepatitis
**but no jaundice
4)hepatosplenomegaly
5)generalized painful lymphadenopathy
6)Rash with ampicillin tx

Labs
1)Transaminases very high(due to liver damage)
2)Atypical lymphocytes
3)positive heterophil antibody test(monospot)
detects IgM ab against horse, sheep or bovine RBC
4)Antiviral capsid antigen(VCA) antibodies
*develop early
*persist for life
5)Anti-early antigen(AE) antibodies
6)Anti-Epstein Barr nuclear antigen(EBNA) antibodies

**once you have mono you always have it and it can recur
Monocytosis
-monocytes
-etiology
Monocyte:
-form: macrophages and dendritic cells
-the kings of chronic infections

Etiology: chronic infections
1)Rheumatoid arthritis
2)Cron's disease
3)SLE
4)Malignacy
Eosinophilia
-etiology
-pathogenesis
-What type of worms don't give it to you
Eosinophil count > 700cells/mm

Etiology
1)Type I hypersensitivity reaction
-asthma
-hay fever
-drug allergies
2)Invasive helminthic infection
3)Polyarteritis nodosa
4)SLE
5)Addison disease(cortisol deficiency)

Pathogenesis:
1)release of eosinophil chemotactic factor from mast cells
**type I hypersensitivity
2)No sequestering of eosinophils in lymph nodes
ex: hypocortisolism(cushing)

**But not pinworm or adult ascariasis!!!!!
Eosinopenia
-etiology
1)hypercoritisolism(cushing)
2)Corticosterioids
-sequester eosinophils in lymph nodes