Polycythemia

 This is increase above the normal range of RBCs in the

circulacion. Concern that the Hb level may be abnormally
high should be triggered at a level of 170 g/L (17g/dL) in
men and 150 g/L (1g g/dL) in woman.
 Polycythemia found incidentally at routine blood count.
Relative erythrocytosis, due to plasma volume loss (e.g
severe dehidration, burns) does not represent a true increase
in total RBC mass. Absolute erythtrocytosis is a true in
increase in total RBC mass.
 Causes polycythemia vera ( a clonal myeloproliferative
disorder) erythtropoietin-producing neoplasms ( e.g renal
cancer, cerebellar hemangioma). Chronic hypoxemia (e.g
high altitude, pulmonary disease), carboxyhemoglobin excess
(e.g smokers), high affinity hemoglobin variants . cushing’s
syndrome. Androgen excess. Polycytemia vera is
distinguished from secondary polycythemia by the presence
of spenomegaly, leukocitosis, trombocytosis and elevated
vitamin B12 levels and by decreased erythropoietin levels.
 Complication hyperviscosity (with diminished o2 delivery)
with risk of ischemic organ injury and thrombosis (venous or
arterial) are most common.
 Treatment plebotomy recommended for hct ≥ 55%,
regardless of cause to low normal range.
LYMPHADENOPATY
 Exposure to antigen through a break in the skin or mucosa
results in antigen being taken up by an antigen – presenting
cell and carried via lymphatic channels to the nearest lymph
node. Lymph channels course troughout the body except for
the brain and the bones. Lymph enters to the through the
afferent vessel and leavels through an effernt vessel. As
antigen-presenting cells past through lymph nodes, they
present antigen-naive lymphocytes from the blood. They are
retained in the node via special homing receptors. B cells
populate the the lymphoid follicles in the cortex ; T celss
populate the paracortical regions.
 When a b cell encounters an antigen to which its surface
immunoglobulin can bind, it stays in the follicle for a few
days and froms a germinal center where the immunoglobulin
gene is mutated in an effoert to make an antibody with higher
affinity for the antigen. The b cell then migrates to the
medullary region, differentiates into plasma cell, and secretes
imunoglobulin into the efferent lymph.
 The efferent lymph laden with antibodies and T cells spesific
for the inciting antigen passed through several nodes on its
way tho the thoracic duct, which drains lymph from most of
the body. From the thoracic duct, lymph enters the
bloodstream at the left subcavian vein. Lymph from the head
and neck and the right arm drain into the raight subclavin
vein. From the bloodstream, the antibodyvand T cells localize
to the site of infection.
Approach to the Patient
 History Age, occupation, animal exposures, sexual
orientation, substance abuse history, medication history, and
concomitant symptoms influence diagnostic workup.
Adenopathy is more commonly malignant in origin in those
over age 40. Farmers have an increased incidence of
brucellosis and lymphoma. Male homosexuals may have
AIDS-associated adenopathy. Alcohol and tobacco abuse
increase risk of malignancy. Phenytoin may induce
adenopathy. The concomitant presence of cervical adenopathy
with sore throat or with fever, night sweats, and weight loss
suggests particular diagnoses (mononucleosis in the former
instance, Hodgkin's disease in the latter).
Physical Examination
 Location of adenopathy, size, node texture, and the presence
of tendemess are important in differential diagnosis.
Generalized adenopathy (three or more anatomic regions)
implies systemic infection or lymphoma. Subclavian or
scalene adenOpathy is always abnormal and should be
biopsied. Nodes > 4 cm should be biopsied immediately.
Rock hard nodes fixed to surrounding soft tissue are usually a
sign of metastatic carcinoma. Tender nodes are most often
benign.
Laboratory Tests
 Usually lab tests are not required in the setting of localized
adenopathy. lf generalized adenopathy is noted, an exeisional
node biopsy should be performed for diagnosis, rather than a
panoply of laboratory test.
Treatment

 Pts over age 40, those with scalene or supraclavicular

adenopathy, those with lymph nodes > 4 cm in diameter, and
those with hard nontender nodes should undergo immediate
excisional biopsy. ln younger patients with smaller nodes that
are rubbery in consistency or tender, a period of observation
for 7-14 days is reasonable. Empirical antibiotics are not
indicated. If the nodes shrink no further evaluation is
necessary. If they enlarge, excisional biopsy is indicated.
SPLENOMEGALY
 Just as the lymph nodes are specialized to light pathogens in
the tissues, the spleen is the lymphoid organ specialized to
fight bloodborne pathogens. lt has no afferent lymphatics. The
spleen has specialized areas like the lymph nodes for making
antibodies (follicles) and amplifying antigen-specific T cells
(peiarteriolar lymphatic sheath, or PALS).