Chapter 13-Reactive (Inflammatory) Proliferations of White Cells & Lymph Nodes Flashcards
What is leukocytosis?
Leukocytosis refers to an increase in the number of white cells in the blood . It is a common
reaction to a variety of inflammatory states.
What is the pathogenesis of Leukocytosis?
Pathogenesis.
The peripheral blood leukocyte count is influenced by several factors, including:
- • The size of the myeloid and lymphoid precursor and storage cell pools in the bone marrow, thymus, circulation, and peripheral tissues
- • The rate of release of cells from the storage pools into the circulation
- • The proportion of cells that are adherent to blood vessel walls at any time (the marginal pool)
- • The rate of extravasation of cells from the blood into tissues
What maintains the hemostasis of
leukocyte homeostasis is maintained by cytokines, growth factors, and adhesion molecules through their effects on the commitment, proliferation,
differentiation, and extravasation of leukocytes and their progenitors
In acute infection there is a rapid increase in the egress of mature granulocytes from the bone marrow pool.
What happens when the infection is prolonged?
If the infection is prolonged, the release of interleukin-1 (IL-1), tumor necrosis factor (TNF), and other inflammatory cytokines stimulates bone marrow stromal cells and T cells to produce increased amounts of hematopoietic growth factors, which enhance the proliferation and differentiation of committed granulocytic progenitors and, over several
days, cause a sustained increase in neutrophil production.
TABLE 13-2 – Mechanisms and Causes of Leukocytosis
INCREASED PRODUCTION IN THE MARROW
- Chronic infection or inflammation (growth factor-dependent)
- Paraneoplastic (e.g., Hodgkin lymphoma; growth factor-dependent)
- Myeloproliferative disorders (e.g., chronic myeloid leukemia; growth factorindependent)
TABLE 13-2 – Mechanisms and Causes of Leukocytosis
INCREASED RELEASE FROM MARROW STORES
- Endotoxemia
- Infection
- Hypoxia
TABLE 13-2 – Mechanisms and Causes of Leukocytosis
DECREASED MARGINATION
Exercise
Catecholamines
TABLE 13-2 – Mechanisms and Causes of Leukocytosis
DECREASED EXTRAVASATION INTO TISSUES
Glucocorticoids
Some growth factors preferentially stimulate the production of a single type of leukocyte.
For example, IL-5 mainly stimulates_________,
eosinophil production
Some growth factors preferentially stimulate the production of a single type of leukocyte.
G-CSF induces ___________
neutrophilia.
TABLE 13-3 – Causes of Leukocytosis
Neutrophilic
leukocytosis
- Acute bacterial infections, especially those caused by pyogenic organisms;
- sterileinflammation caused by, for example, tissue necrosis (myocardial infarction, burns)
TABLE 13-3 – Causes of Leukocyosis
Eosinophilic leukocytosis
(eosinophilia)
- Allergic disorders such as asthma, hay fever;
- certain skin diseases (e.g., pemphigus, dermatitis herpetiformis); parasitic infestations;
- drug reactions;
- certain malignancies (e.g., Hodgkin and some non-Hodgkin lymphomas);
- collagen vascular disorders and some vasculitides; atheroembolic disease (transient)
TABLE 13-3 – Causes of Leukocyosis
Basophilic
leukocytosis
(basophilia)
Rare, often indicative of a myeloproliferative disease (e.g., chronic myeloid leukemia)
TABLE 13-3 – Causes of Leukocyosis
Monocytosis
- Monocytosis Chronic infections (e.g., tuberculosis), bacterial endocarditis, rickettsiosis, and
- malaria; collagen vascular diseases (e.g., systemic lupus erythematosus);
- inflammatory bowel diseases (e.g., ulcerative colitis)
TABLE 13-3 – Causes of Leukocyosis
Lymphocytosis
- Accompanies monocytosis in many disorders associated with chronic immunological stimulation (e.g., tuberculosis, brucellosis);
- viral infections (e.g., hepatitis A, cytomegalovirus, Epstein-Barr virus);
- Bordetella pertussis infection
What are Döhle bodies
I.
Toxic granules, which are coarser and darker
than the normal neutrophilic granules, represent abnormal azurophilic (primary) granules.
Döhle bodies are patches of dilated endoplasmic reticulum that appear as sky-blue cytoplasmic
“puddles
Where can you find Döhle
bodies, and cytoplasmic vacuoles ?
In sepsis or severe inflammatory disorders (such as Kawasaki disease), leukocytosis is often
accompanied by morphologic changes in the neutrophils, such as toxic granulations, Döhle
bodies, and cytoplasmic vacuoles ( Fig. 13-2 )
FIGURE 13-2 Reactive changes in neutrophils.
Neutrophils containing coarse purple cytoplasmic granules (toxic granulations) and blue cytoplasmic patches of dilated endoplasmic reticulum (Döhle bodies, arrow) are observed in this peripheral blood smear prepared from a patient with bacterial sepsis
In most instances it is not difficult to distinguish reactive and neoplastic leukocytoses, but
uncertainties may arise in two settings.
- Acute viral infections, particularly in children, can cause the appearance of large numbers of activated lym phocytes that resemble neoplastic lymphoid cells.
- At other times, particularly in severe infections, many immature granulocytes appear in the blood, simulating a myeloid leukemia (leukemoid reaction) .
Special laboratory studies (discussed later) are helpful in distinguishing reactive and neoplastic leukocytoses.
What is a leukemoid reaction?
At other times, particularly in severe infections, many immature granulocytes appear in the blood, simulating a myeloid leukemia (leukemoid reaction) .
Following their initial development from precursors in the bone marrow (B cells) and the thymus (T cells), lymphocytes circulate through the blood and, under the influence of specific cytokines
and chemokines, home to lymph nodes, spleen, tonsils, adenoids, and Peyer’s patches, which
constitute the peripheral lymphoid tissues.
What is the most widely distributed and easily
accessible lymphoid tissue?
Lymph nodes, the most widely distributed and easily
accessible lymphoid tissue, are frequently examined for diagnostic purposes.
They are discrete encapsulated structures that contain well-organized B-cell and T-cell zones, which are richly
invested with phagocytes and antigen-presenting cells ( Fig. 6-6 , Chapter 6 ).
What happens when there is activation of resident immune cells?
The activation of resident immune cells leads to morphologic changes in lymph nodes
- Within several days of antigenic stimulation, the primary follicles enlarge and are transformed into pale-staining germinal centers, highly dynamic structures in which B cells acquire the capacity to make high-affinity antibodies against specific antigens.
- Paracortical T-cell zones may also undergo hyperplasia.
The degree and pattern of the morphologic changes are dependent on
the inciting stimulus and the intensity of the response. Trivial injuries and infections induce
subtle changes, while more significant infections inevitably produce nodal enlargement and sometimes leave residual scarring.
For this reason, lymph nodes in adults are almost never “normal” or “resting,” and it is often necessary to distinguish morphologic changes secondary to
past experience from those related to present disease.
Infections and inflammatory stimuli often
elicit regional or systemic immune reactions within lymph nodes.
Some that produce distinctive
morphologic patterns are described in other chapters. Most, however, cause stereotypical
patterns of lymph node reaction designated acute and chronic nonspecific lymphadenitis.
What are Acute Nonspecific Lymphadenitis?
Acute lymphadenitis in the cervical region is most often due to microbial drainage from
infections of the teeth or tonsils, while in the axillary or inguinal regions it is most often caused
by infections in the extremities .
Acute lymphadenitis also occurs in mesenteric lymph nodes draining acute appendicitis.
Unfortunately, other self-limited infections may also cause acute mesenteric adenitis and induce symptoms mimicking acute appendicitis, a differential diagnosis
that plagues the surgeon.
Systemic viral infections (particularly in children) and bacteremia
often produce acute generalized lymphadenopathy.
