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acute myelogenous leukemia (AML) 15 acute poststreptococcal glomerulonephritis
Acute lymphoblastic leukemia.
children with L1 morphology cells experience complete
remission with chemotherapy. Patients may experience
a profound reduction in the concentration of the serum
immunoglobulins, possibly due to malignant expansion of
suppressor T lymphocytes.
acute myelogenous leukemia (AML)
A heterogeneous group of disorders characterized by neoplastic
transformation in a multipotential hematopoietic stem cell
or in one of restricted lineage potential. Because multipotential
hematopoietic stem cells are the precursors of granulocytes,
monocytes, erythrocytes, and megakaryocytes, one or
all of these cell types may be affected. Differentiation usually
ends at the blast stage, causing myeloblasts to accumulate
in the bone marrow. AML is diagnosed by the discovery of
30% myelogenous blasts in the bone marrow, whether or not
they are present in the peripheral blood. The total peripheral
blood leukocyte count may be normal, low, or elevated.
There may be thrombocytopenia, neutropenia, and anemia.
The presenting symptoms and signs are nonspecific and may
be secondary to anemia. Patients may experience fatigue,
weakness, and pallor. One third of AML patients are found
to have hepatosplenomegaly. One third of patients may have
bleeding secondary to thrombocytopenia. Gastrointestinal
tract or central nervous system hemorrhage may occur when
platelet counts fall below 20,000/μL. Decreased neutrophil
counts may increase secondary infections. Unfavorable
prognostic findings include: (1) an age at diagnosis above 60
years, (2) 5q- and 7q- chromosomal abnormalities, (3) a history
of myelodysplastic syndrome, (4) a history of radiation
or chemotherapy for cancer, and (5) a leukocytosis exceeding
100,000/μL. If untreated, AML leads to death in less than 2
months through hemorrhage or infection. Both chemotherapy
and bone marrow transplantation are modes of therapy.
acute-phase proteins
Plasma proteins, synthesized by the liver, that increase in
concentration during inflammation. They are active during
early phases of host defense against infection. They
include mannose-binding protein (MBP), C-reactive protein
(CRPJ), fibrinogen, selected complement components, and
interferons. These proteins interact with cell wall constituents
of microorganisms and activate complement.
acute-phase reactants
Serum proteins that increase during acute inflammation.
These proteins, which migrate in the α-1 and α-2
electrophoretic regions, include α-1 antitrypsin, α-1
glycoprotein, amyloid A&P, antithrombin III, C-reactive
protein, C1 esterase inhibitor, C3 complement, ceruloplasmin,
fibrinogen, haptoglobin, orosomucoid, plasminogen,
and transferrin. Most of the acute-phase reactant proteins
are synthesized in the liver and increase soon after infection
as part of the systemic inflammatory response syndrome
(SIRS). Inflammatory cytokines upregulate these molecules,
including interleukin-6 (IL-6) and tumor necrosis
factor (TNF). Acute-phase reactants participate in the
natural or innate response to microorganisms.
100
Acute Phase
Response
(i.e., C-Reactive
Protein)
0
Infection
Disease
0 2 4 6 8 10 12 14
Time in Days
Acute-phase response.
Recovery
acute-phase response (APR)
A nonspecific response by an individual stimulated by
interleukin-1, interleukin-6, interferons, and tumor necrosis
factor. C-reactive protein may show a striking rise within a
few hours. Infection, inflammation, tissue injury, and, very
infrequently, neoplasm may be associated with APR. The liver
produces acute-phase proteins at an accelerated rate, and the
endocrine system is affected with elevated gluconeogenesis,
impaired thyroid function, and other changes. Immunologic
and hematopoietic system changes include hypergammaglobulinemia
and leukocytosis with a shift to the left. Diminished
formation of albumin, elevated ceruloplasmin, and diminished
zinc and iron are also observed. Cellular elements may also be
produced in addition to the acute-phase proteins.
acute-phase serum
A serum sample drawn from an infectious disease patient in
the acute phase.
acute poststreptococcal glomerulonephritis
A disease of the kidney, with a good prognosis for most
patients, that follows streptococcal infection of the skin
or streptococcal pharyngitis by 10 days to 3 weeks in
children. The subject presents with hematuria, fever,
general malaise, facial swelling, and smoky urine, as well
as mild proteinuria and red blood cells in the urine. These
children often have headaches, are hypertensive, and have
elevated blood pressure. Serum C3 levels are decreased.
The erythrocyte sedimentation rate (ESR) is elevated, and
an abdominal x-ray may reveal enlarged kidneys. Renal
biopsy reveals infiltration of glomeruli by polymorphonuclear
leukocytes and monocytes and a diffuse proliferative
process. Immunofluorescence shows granular deposits of
IgG and C3 on the epithelial sides of peripheral capillary
loops. Electron microscopy shows subepithelial “humps.”
The process usually resolves spontaneously within 1
week after onset of renal signs and symptoms, the patient
becomes afebrile, and the malaise disappears. The disease
is attributable to nephritogenic streptococci of types 1, 4,
12, and 49.
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