Untitled - D Ank Unlimited

drug-induced immune hemolytic anemia 237 dust, nuclear (leukocytoclasis)
is seen with nitrofurantoin, in which the autoimmunity
involves cell-mediated phenomena without evidence of
autoantibodies.
drug-induced immune hemolytic anemia
Acquired hemolytic anemia that develops as a consequence
of immunological reactions following the administration of
certain drugs. Clinically, this anemia resembles autoimmune
hemolytic anemia of idiopathic origin. A particular drug may
induce hemolysis in one patient, thrombocytopenia in another,
neutropenia in yet another, and occasionally combinations
of these in a single patient. The drug-induced antibodies that
produce these immune cytopenias are cell-specific. Drugs
that cause hemolysis by complement-mediated lysis include
quinine, quinidine, rifampicin, chlorpropamide, hydrochlorothiazide,
nomifensine phenacetin, salicylazosulfapyridine, the
sodium salt of p-aminosalicylic acid, and stibophen. Drugdependent
immune hemolytic anemia in which the mechanism
is extravascular hemolysis may occur with prolonged
high dose penicillin therapy or other penicillin derivatives as
well as cephalosporins and tetracycline.
drug-induced lupus (DIL)
Drugs that alone can induce a limited form of systemic
lupus erythematosus (SLE) include the aromatic amines
or hydrazines, the two most common being procainamide
and hydralazine. Other drugs that can induce DIL include
isoniazid, methyldopa, quinidine, and chlorpromazine. This
drug-induced disease remits on discontinuation of the drug.
The autoimmune response is very restricted.
DTaP vaccine
Acellular preparation used for protective immunization and
composed of diphtheria and tetanus toxoids and acellular
pertussis proteins. It is used to induce protective immunity in
children against diphtheria, tetanus, and pertussis. Children
should receive DTaP vaccine at the ages of 2, 4, 6, and 15
months, with a booster at 4 to 6 years of age. The tetanus
and diphtheria toxoids should be repeated at 14 to 16 years
of age. The vaccine is contraindicated in individuals who
have shown prior allergic reactions to DTaP or in subjects
with acute or developing neurologic disease. DTaP vaccine is
effective in preventing most cases of the diseases it addresses.
DTH
Delayed-type hypersensitivity. Refer to type IV
hypersensitivity.
DTH T cell
CD4 + T lymphocyte sensitized against a delayed-type
hypersensitivity antigen.
dual tropic HIV
HIV strains capable of infecting macrophages, primary T
cells, and cultured immortalized T cell lines.
Duffy blood group
Human erythrocyte epitopes encoded by Fya and Fyb
genes located on chromosome 1. Because these epitopes are
receptors for Plasmodium vivax, African-Americans who
often express the Fy(a-b-) phenotype are not susceptible
to the type of malaria induced by this species. A mother
immunized through exposure to fetal red cells bearing the
Duffy antigens that she does not possess may synthesize
antibodies that cross the placenta and induce hemolytic
disease of the newborn.
Duncan’s syndrome
Marked lymphoproliferation and agammaglobulinemia
associated with Epstein–Barr virus infection. The rapidly
proliferating B lymphocytes produce neoplasms that may
rupture the spleen. This defect in the immune response with
susceptibility to infection is inherited as an X-linked recessive
disorder. Affected individuals are not able to successfully
resist infection by the Epstein–Barr virus.
Durham, Herbert (1866–1945)
An English graduate student working in Max von Grüber’s
laboratory in Vienna in 1896. He studied agglutination of bacteria
by the blood and published several papers on the subject.
dust, nuclear (leukocytoclasis)
Extensive basophilic granular material representing karyolytic
nuclear debris that accompanies areas of inflammation
and necrosis, as in leukocytoclastic vasculitis.
N
29
N
44
66
86
100
NH 2
Fya /Fyb 18
120
132
152
Cytoplasm
Herbert Durham.
180
162
181
201
230
210
Exterior
237 280
257 260
294
314
Membrane
COOH
Schematic representation of the proposed topography of the Duffy
glycoprotein within the red cell membrane. Numbers represent amino
acid residues with the transcription-initiating methionine residue as 1.
An extracellular N-terminal domain of 65 amino acids containing two
N-glycosylation sites (N) and the site of the Fya/Fyb polymorphism is
follwed by nonmembrane-spanning domains, or alternatively, seven-
membrane-spanning domains in common with other chemokine receptors.
D