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Alterations of Leukocyte,
Lymphoid, and Hemostatic
Function
Chapter 27
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Alterations of Leukocyte Function
Quantitative disorders
Increases or decreases in cell numbers
Bone marrow disorders or premature destruction
of cells
Response to infectious microorganism invasion
Qualitative disorders
Disruption of cellular function
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Quantitative Alterations of
Leukocytes
Leukocytosis
Leukocytosis is a normal protective physiologic
response to physiologic stressors
Leukopenia
Leukopenia is not normal and not beneficial
A low white count predisposes a patient to
infections
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Granulocytosis (Neutrophilia)
Neutrophilia is evident in the first stages of an
infection or inflammation
If the need for neutrophils increases beyond the
supply, immature neutrophils (banded neutrophils)
are released into the blood
This premature release is detected in the manual
WBC differential and is termed a shift-to-the-left
When the population returns to normal, it is termed
a shift-to-the-right
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Neutropenia
Reduction in circulating neutrophils
Causes:
Prolonged severe infection
Decreased production
Reduced survival
Abnormal neutrophil distribution and
sequestration
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Granulocytopenia
(Agranulocytosis)
Causes:
Interference with hematopoiesis
Immune mechanisms
Chemotherapy destruction
Ionizing radiation
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Eosinophilia
Hypersensitivity reactions trigger the
release of eosinophilic chemotactic factor of
anaphylaxis from mast cells
Increased in allergic disorders
Increased in parasitic invasions
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Eosinopenia
Decrease in circulation numbers of
eosinophils
Usually caused by migration of cells to
inflammatory sites
Other causes:
Surgery, shock, trauma, burns, or mental
distress
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Basophils
Basophils account for only 0% to 1% of the
circulating WBCs
Basophilia
Response to inflammation and hypersensitivity
reactions
Basopenia
Occurs in acute infections, hyperthyroidism,
and long-term steroid therapy
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Monocytes
Monocytosis
Poor correlation with disease
Usually occurs with neutropenia in later stages of
infections
Monocytes are needed to phagocytize organisms
and debris
Monocytopenia
Very little known about this condition
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Lymphocytes
Lymphocytosis
Acute viral infections
Epstein-Barr virus
Lymphocytopenia
Immune deficiencies, drug destruction, viral
destruction
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Infectious Mononucleosis
Acute, self-limiting infection of B
lymphocytes transmitted by saliva through
personal contact
Commonly caused by the Epstein-Barr virus
(EBV)—85%
B cells have an EBV receptor site
Others viral agents resembling IM
Cytomegalovirus (CMV), hepatitis, influenza, HIV
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Infectious Mononucleosis
Symptoms: fever, sore throat, swollen cervical
lymph nodes, increased lymphocyte count, and
atypical (activated) lymphocytes
Serious complications are infrequent (<5%)
>50% lymphocytes and at least 10% atypical
lymphocytes
Diagnostic test
Splenic rupture is the most common cause of death
Monospot qualitative test for heterophilic antibodies
Treatment: symptomatic
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Leukemias
Malignant disorder of the blood and blood-forming
organs
Excessive accumulation of leukemic cells
Acute leukemia
Presence of undifferentiated or immature cells, usually
blast cells
Chronic leukemia
Predominant cell is mature but does not function
normally
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Leukemias
Acute lymphocytic leukemia (ALL)
Acute myelogenous leukemia (AML)
Chronic myelogenous leukemia (CML)
Chronic lymphocytic leukemia (CLL)
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Leukemias
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Leukemias
Signs and symptoms of leukemias
Anemia, bleeding purpura, petechiae,
ecchymosis, thrombosis, hemorrhage, DIC,
infection, weight loss, bone pain, elevated uric
acid, and liver, spleen, and lymph node
enlargement
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Philadelphia Chromosome
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Myeloma
Proliferation of plasma cells
The tumor may be solitary or multifocal (multiple
myeloma)
The malignant plasma cells produce abnormally
large amounts of one class of immunoglobulin or
incomplete immunoglobulin
The unattached light chains of the immunoglobulins
(Bence Jones proteins) can pass through the glomerulus
and damage the renal tubular cells
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Myeloma
Multiple myeloma causes increased
osteoclastic bone destruction
Clinical manifestations
Cortical and medullary bone loss
Skeletal pain
Recurring infections due to loss of the humoral
immune response
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Lymphadenopathy
Enlarged lymph nodes that become palpable
and tender
Local lymphadenopathy
Drainage of an inflammatory lesion located near
the enlarged node
General lymphadenopathy
Occurs in the presence of malignant or
nonmalignant disease
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Lymphadenopathy
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Malignant Lymphomas
Malignant transformation of a lymphocyte
and proliferation of lymphocytes, histiocytes,
their precursors, and derivatives in lymphoid
tissues
Two major categories
Hodgkin lymphoma
Non-Hodgkin lymphomas
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Hodgkin Lymphoma
Characterized by the presence of ReedSternberg cells in the lymph nodes
Reed-Sternberg cells are necessary for diagnosis,
but they are not specific to Hodgkin lymphoma
Classical Hodgkin lymphoma
Nodular lymphocyte predominant Hodgkin
lymphoma
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Hodgkin Lymphoma
Physical findings
Symptoms
Fever, weight loss, night sweats, pruritus
Laboratory findings
Adenopathy, mediastinal mass, splenomegaly,
and abdominal mass
Thrombocytosis, leukocytosis, eosinophilia,
elevated ESR, and elevated alkaline phosphatase
Paraneoplastic syndromes
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Hodgkin Lymphoma
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Hodgkin Lymphoma
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Non-Hodgkin Lymphoma
Generic term for a diverse group of
lymphomas
The lymphomas can be differentiated based
on etiology, unique features, and response to
therapies
Non-Hodgkin lymphomas are linked to
chromosome translocations, viral and
bacterial infections, environmental agents,
immunodeficiencies, and autoimmune
disorders
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Non-Hodgkin Lymphoma
Clonal expansion of B cells, T cells, and/or
NK cells
Changes in proto-oncogenes and tumorsuppressor genes contribute to cell
immortality and thus an increase in
malignant cells
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Burkitt Lymphoma
Most common type of non-Hodgkin
lymphoma in children
Burkitt lymphoma is a very fast-growing
tumor of the jaw and facial bones
Epstein-Barr virus is found in nasopharyngeal
secretions of patients
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Burkitt Lymphoma
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Alterations in Splenic Function
Splenomegaly
Hypersplenism
Congestive splenomegaly
Infiltrative splenomegaly
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Disorders of Platelets
Thrombocytopenia
Platelet count <100,000/mm3
<50,000/mm3—hemorrhage from minor trauma
<15,000/mm3—spontaneous bleeding
<10,000/mm3—severe bleeding
Causes:
Hypersplenism, autoimmune disease, hypothermia,
and viral or bacterial infections that cause
disseminated intravascular coagulation (DIC)
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Disorders of Platelets
Immune thrombocytopenic purpura (ITP)
IgG antibody that targets platelet glycoproteins
Antibody-coated platelets are sequestered and
removed from the circulation
The acute form of ITP that often develops after a
viral infection is one of the most common
childhood bleeding disorders
Manifestations
Petechiae and purpura, progressing to major
hemorrhage
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Disorders of Platelets
Thrombotic thrombocytopenic purpura
(TTP)
A thrombotic microangiopathy
Platelets aggregate, form microthrombi, and cause
occlusion of arterioles and capillaries
Chronic relapsing TTP
Acute idiopathic TTP
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Disorders of Platelets
Essential (primary) thrombocythemia
Thrombocythemia is characterized by platelet
counts >600,000/mm3
Myeloproliferative disorder of platelet precursor
cells
Megakaryocytes in the bone marrow are produced in
excess
Microvasculature thrombosis occurs
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Alterations of Platelet Function
Qualitative alterations in platelet function
demonstrate an increased bleeding time in
the presence of a normal platelet count
Platelet function disorders result from
platelet membrane glycoprotein and von
Willebrand factor deficiencies
Manifestations
Petechiae, purpura, mucosal bleeding, gingival
bleeding, and spontaneous bruising
Disorders can be congenital or acquired
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Alterations of Coagulation
Vitamin K deficiency
Vitamin K is necessary for synthesis and
regulation of prothrombin, the prothrombin
factors (II, VII, XI, X), and proteins C and S
(anticoagulants)
Liver disease
Liver disease causes a broad range of hemostasis
disorders
Defects in coagulation, fibrinolysis, and platelet
number and function
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Disseminated Intravascular
Coagulation (DIC)
Complex, acquired disorder in which clotting
and hemorrhage simultaneously occur
DIC is the result of increased protease
activity in the blood caused by unregulated
release of thrombin with subsequent fibrin
formation and accelerated fibrinolysis
Endothelial damage is the primary initiator
of DIC
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Disseminated Intravascular
Coagulation (DIC)
The amount of activated thrombin exceeds
the body’s antithrombins and the thrombin
does not remain localized
The widespread thromboses created cause
widespread ischemia, infarction, and organ
hypoperfusion
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Disseminated Intravascular
Coagulation (DIC)
By activating the fibrinolytic system
(plasmin), the patient’s fibrin degradation
product (FDP) and D-dimer levels will
increase
Due to the patient’s clinical state, the
disorder has a high mortality rate
Treatment is to remove the stimulus
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Disseminated Intravascular
Coagulation (DIC)
Clinical signs and symptoms demonstrate
wide variability
Bleeding from venipuncture sites
Bleeding from arterial lines
Purpura, petechiae, and hematomas
Symmetric cyanosis of the fingers and toes
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