what is erythrocyte sedimentation rate test? is it specific or sensitive?
it is an inflammation test. not specific. any inflammation with increase ESR but won't tell you what is, sensitive test
how can you evaluate the cell-mediated immune system qualitatiely?
qualitative assessment involves delayed hypersensitivity skin testing. Most normal adults will react to candida albincans, trichophyton, tetanus toxoid, munps, streptokinase-streptodornase within 48 hours. If you don't reaction, something wrong with your cell-mediated immunity
how can you evaluate cell mediated immune system quantitatively?
quantitative assessment-determine how many B/T cells and E rosette technique
what is the E rosette technique?
quantitative test to evaluate cell mediated immunity. it is used to identify cell surface receptors. signal cells that have a substance that will bind a T cell are mixed with cells. those substances that match the T cells with bind anf form a rosette around the T cell
how do you evaluate the humoral system?
immunoelectrophoresis of serum-quantitation of IgG, IgA, IgM
what's more common acquired immune deficiency or primary immune deficiency?
acquired. primary you are born with. acquired is liek transplant/AIDS etc.
what is the most common primary immune disorder?
B cell deficiency
what happens when you have hyper IgM?
viscosity of blood increases
with hyper IgM, what are the levels of serum IgG, and IgA
which cells is malfunctioning with hyper IgM
B cells-t cells are fine
in hyper IgM, B cells cannot do what?
cannot switch from making IgM to IgG and IgA. since IgM ismade first it defaults to that antibody and it can't switch
what is SCID?
severe combined immunodeiciency. complete absence of both T and B cell immunity
it is postulated that failure of multipotential lymphoid stem cells to differentiate into early pre-B and pre-T stem cells in the bone marrow will create what diseasE?
how is X-linked SCID different than SCID?
X linked affects males, and mainly T cells are affected. Lymphocytes present are mainly B cells and T cells are missing. BUT since B cells need T cells to activate them they are not useful. Defect in T cells but B cells not being activated because no T cell help so SCID because both are deficient.
what causes nezelof syndrome
it's genetic but it's an underdevelopment of the thymus
do the antibodies work in nezelof syndrome?
yes-underdeveloped thymus so B cells are unaffected=normal antibodies
Chronic mucocutaneous candidiasis results from T cells specifically failing to recognize what antigen?
T or F- T cells in chronic mucocutaneous candidiasis T celsl do not function normal and do not recognize candida
false-T cells work normal but don't recognize candida
what organs are targed in DiGeorge's syndrom?
thymus and parathyroid gland
T or F-in DiGeorge's syndrome, T cells are sufficient in circulation
false- T cells are deficient because thymus is th eproblem in this disorder so T cells arent' maturing
which disease is confused with AIDS?
T or F-B cells are usually impaired in DiGeorges
false-unimpaired-T cells affected
which antibody deficiency is mose common?
if you have no IgA, GI infections increase or decrease?
should patients with IgA deficiency be given gamma globulin?
no-they may recognize injected IgA as foreign=hypersensitive reaction
X linked lymphoproliferative disease/Duncan's disease has inadequate immuen reaction to what?
Bruton's X-linked agammaglobulinemia is a disease that causes? in what gender?
X linked and in boys. lack of B cell development that results in lack of Ig formation. Bruton=Boy=B cells
what protects bruton patients until 6 months of age?
passive antibodies from mom's breast milk. at 6 months IgG is lowest
boys with bruton's usually get infected with which two organisms?
strep pneumoniae, haemophilus influenzae
what is an important clue to diagnosis of brutons?
you get the sameinfection over and over. failure of infections to respond completely or promptly to approrpiate antibiotic therapy
to be diagnosed with brutons, you need absense or marked reduction of how many of the Ig classes?
all 5 are reduced
in bruton's, will you have plasma cells in the gut?
no-B cells don't mature into plasma cells inthis disease.
in bruton's, do you see an increased or decreased or normal amount of T cells?
normal to increased T cell levels because they are compensating for the B cells
T orF- brutons, T cell immunity is in tact
T or F-there are B cells in the blood with brutons
false-no B cells at all
what is common variable immunodeficiency?
low antibodies in the blood. chromosome 6 gene might be responsible
what is the acronyme you use for wiskott aldrich syndrome and what does it stand for?
XWASTE= x linked, Wiskott-Aldrich, Syndrome, thrombocytopenia and eczema.
what is wrong in wiskott aldrichsyndrome?
progressive deterioration of the thymus leads to impaired cell-mediated immunity
what 3 things are wrong in hereditary ataxia-Telangiectasia?
1-T cells 2-IgG 3-DNA repair
what are symptoms of hereditary ataxia telangiectasia?
ataxia=no control over movement. choreoathetosis=dance movement, telangiectases=dilated blood vessels
what is the complement system?
blood proteins that interact with B and T cells
in complement, which fragment is usually bigger a or b
a bigger. b is smaller
is complement humoral immunity or cellular immunity
complement circulates in the active or inactive form?
how is classical pathway initiated?
C1 complex binds to antibodies bound to antigen on bacteria
how is alternative pathway intiated?
C3 cleaves and C3b binds
how is mannose pathway intiated?
MASP binds mannose on microbe
all 3 pathways lead to what?
C3 to C3b
what are the effects of complement?
-increased vascular permeability to allow neutrophils through to site of infection -produce inflammatory mediators (chemokines attract neutrophils) -cellmembranelysis of antibody coated targets -opsonization-recognizes cell as foreign
what is the sequence in classical pathway for components (c1-c9)
which component of classical is largest in plasma?
excessive activation (currently being consumed) body not making protein, complexing of IgG or IgM antibodies
if you have a infection with neisseria you most likely have a problem with?
if you lose early components of complement in classical what could happen?
no C3b-no ability to remove immune complexes-high levels circulating in blood-tissue damage espeically to renal glomeruli *inability to remove bacteria that REQUIRE opsonization liek strep and staph *inability to lyse bacteria
what is properdin (P factor) deficiency?
properdin acts to stabalize the alternative pathway C3 convertase, deficiency leads to bacterial ifnections like meningococcemia
Hereditary angioedema HAE is deficiency in what?
Familial Mediterranean Fever is found on what chromosome and defect in what? what does it cause?
chromo 16, defect in protease in peritoneal and synovial fluid, recurrent episodes of fever nd inflammation in joints
what are interferons?
cytokines that interfere with viral replication
define-an approach to infection control used to prevent occupational exposure to blood-borne pathogens
define-blood and blood products conaminated sharps pathologic wasts and microbiologic wastes
(OSHA) infectious waste
what are vaccine-preventable diseases?
hepatitis B, influenza, measles, mumps, rubella and varicella
what are some screening tests?
TB skin test (mantoux) quantiFERON blood test for TB, rubella, hepattis B surface antigen
what should not be used if you are exposed to HCV? why?
interferon with or without ribavirin. it's not used to prevent HCV, it's used to treat HCV.
what do you do if you are exposed to HIV?
-determine antibody status of patient or specimen source -tech should be tested -high risk exposure prophylaxis includes a combo of antiretroviral agents. will give 3 drugs
what are nonanalytical factors related to testing accuracy?
-patient ID, specimen labeling, maintenance, appropriate testing methods, accurate results
define-procedures used to detect errors caused by test system failure, adverse environmental conditions, and differences between technologists
what is sensitivity
proportion of patients with a specific disease or condition who give a positive result
what is specificity
the proportion of patients without the specific condition or disease who give a negative test result
what is flocculation?
when antigen and antibody are close to each other but don't bind. they are loosely connected, a loose precipitate results
which antibody does not directly agglutinate RBCs?
what can be used to enhance agglutination with IgG?
this stage of agglutination is reversible, represents the physical attachment of antibody molecules to antigen.
sensitization is reversible. how can you reverse, or break apart, antigen/antibody complexes?
RBCs, latex and bacteria have a net ___ surface charged called ___
negative, zeta potential
which two ions have a shielding effect (decrease amount of binding of antigen/antibody), partially neutralizing the opposite charges on antigen and antibody hindering their association?
sodium and chloride
how do you fix the problem caused by Na and Cl?
put cells into low ionic strength saline (LISS) and antibody uptake is enhanced. We are decreasing the ionic strength of reaction medium
which antibody is more efficient at agglutination?
zone of antibody excess
zone of equivalence
zone of antigen excess
what is prozone phenomenon?How do you fix it?
agglutinating complexes less because there are lots of antibodies compared to antigen and results in a negative reaction. fix-serially diluting the serum to decrease antibody concentration
for temperature-IgM antibodies are __reacting. IgG antibodies are ___reaction
you have 2 antibodies in the same space and they compete with each other to binding antigen and they won't bind. it's mutual blocking. what's this called?
define-establishment of cross-links between sensitized particles (antigen) and antibodies resulting in visible aggregation
the formation of ___ ___ depends upon the ability of a cell with attached antibody on its surface to come close enough to another cell to permit the antibodies to bridge the gap and combine with an antigen receptor
what are the two stages of antigen/antibody interaction/agglutination?
1-sensitization 2-lattice formation
what methods can you use to enhance agglutination
-centrifugation, physically forcing cells together -treatment with proteolytic enzymes, removes negatively charged surface sialic acid residues and will not repel each other
IgA is associated with which disease?
IgG associated with?
IgM associated with which disease?
when do you see rouleaux?
-it is seen in conditions causing elevated proteins or globulins in the blood like multiple myeloma
rouleaux is associated with which kind agglutination?
pseudoagglutination (false appearance of clumping)
T or F- you cannot reverse rouleaux
false- you can reverse
how do you reverse rouleaux?
define-the migration of charged solutes or particles in an electrical field
T or F- serum electrophoresis results in the separation of proteins into 4 fractions