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NUR 376 Exam 1 Blueprint test questions and answers
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NUR 376 Exam 1 Blueprint test questions and answers
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NUR 376 Exam 1 Blueprint testquestions and answers
vascular permeability
vasodilation increases permeability of the vessel wall to allow WBC,
platelets, etc. to move to the site of injury.
cellular chemotaxis
during the cellular phase of inflammation, a chemical signal from
microbial agents, endothelial cells, and WBCs attracts platelets and
other WBCs to the site of injury.
Brainpower
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systemic responses
fever
pain
general malaise
lymphadenopathy
anorexia
sleepiness
lethargy
anemia
weight loss
titer
blood test that measures the amount of antibodies to a specific
pathogen in blood.
HIV labs
CD4 less than 500-immune impairment
CD4 less than 200-AIDS
Inversion of CD4 to CD8 ratio(2:1 changes to 1:2
Viral load-RNA assay <10,000 AIDS risk is low, >100,00 AIDS high
Post seroconversion-ELISA, confirmed by Western blot
E. coli portal of entry
,Usually fecal oral-route causing GI signs. FECES
Can adhere to bladder mucosa and cause UTIs, female anatomy
increase risk d/t proximity to anus.
Immunocompetence
the ability of an individual to protect oneself from a specific
infectious agent because of a strong immune system.
Immunosuppression
indicates a defective immune system putting an individual at risk
for infection
Innate immunity responses-1st defense
inflammation and fever, granulocytes and macrophages (arise from
monocytes), natural killer cells (t-lymphocytes), complement
system, dendritic cells (APCs), antimicrobial proteins-lysozymes,
interferon, cytokines (PG, TNF, IL), mucous membranes, coughing,
sneezing, other natural barriers- skin, ciliated cells
Adaptive immunity
allows the body to recognize an antigen, target the specific antigen,
limit its response to that antigen, and develop memory for the
antigen for future reference.
B-lymphocyte immunity
humoral immunity-antigen stimulates b-lymphocyte to mature to
plasma cell and secrete Ig
T-lymphocyte immunity
cell-mediated immunity-CD4 cells attack, CD8 (cytotoxic) attack
when presented an antigen by dendritic cell.
Adaptive immunity components
b-cells, t-cells, MHC I and II, CD4, CD8, plasma cells, dendritic cells
(APCs), immunoglobulins, antibodies.
acquired (adaptive) immunity
acquired through exposure to an antigen either from infection or
immunization.
passive (adaptive) immunity
, an individual is given pre-made, fully formed antibodies against an
antigen. Ex: infants breastmilk, antibodies from mother
Type 1 hypersensitivity
IgE mediated hypersensitivity
Ex: Allergies
Type II hypersensitivity
labeled cytotoxic/ cytolytic & involve IgM or IgG interacting with
foreign cells to cause their destruction (cell lysis), such as when
donor blood is rejected or Rh mother forms antibodies against Rh+
fetus
Type III hypersensitivity
labeled immune complex; antigens combine with antibodies and
deposit in tissues & blood vessels, causing inflammation & tissue
destruction. Autoimmune disease
Type IV hypersensitivity
delayed hypersensitivity t-lymphocytes, organ transplant, poison
ivy.
SLE etiology
Unknown
Genetics play a role
Environmental factors include: sunlight (UV), meds, chemicals, diet,
estrogen hormones, epstein barr virus
SLE pathophysiology
T cells show defects in signaling and effector function
Loss of Immune Tolerance
Dysregulated lymphocytes begin targeting intracellular antigens
Antigen-Antibody complexes deposit on basement membrane of
various tissues.
SLE clinical manifestations
Joint pain and swelling, skin rashes, fatigue, pericardial effusion
(swelling around the heart), pleural effusion (swelling around the
lungs)
BUTTERFLY RASH (malar rash), high ANA
HIV etiology
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