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hypersensitivity
altered immunologic response to an antigen that results in disease or damage to the host
type 1 hypersensitivity
against environmental antigens
IgE binds to Fc receptors on surface of mast cells where histamine is released
type 1 hypersensitivity manifestations
GI allergy
vomiting, diarrhea, abdominal pain
skin
hives
mucosa allergens
conjunctivitis, rhinitis, asthma
lung allergens
asthma, bronchospasm, edema, thick secretions
type 2 hypersensitivity
specific cell/tissue is the target of an immune response
symptoms depend on tissue/organ involved
type 2 hypersensitivity mechanisms that can affect cells
cell is destroyed by antibodies and complement
cell destruction through phagocytosis
tissues damaged by products of neutrophils
antibody-dependent cell-mediated cytotoxicity
target cell malfunction
type 3 hypersensitivity
immune-complex mediated
antigen-antibody complexes are formed in the circulation and are later deposited in vessel walls or extravascular tissues
not organ specific
type 3 hypersensitivity manifestations
serum sickness
caused by formation of immune complexes in blood and deposition in target tissues
arthus reaction
vasculitis caused by repeated local exposure
type 4 hypersensitivity
cell-mediated which does not involve antibodies
cytotoxic t lymphocytes or lymphokine-producing TH1 and TH17 cells
direct killing of phagocytic cells
examples of type 4 hypersensitivities
graft rejection
tb skin test
allergic rxns from poison ivy or metals
allergy
deleterious effects of hypersensitivity to environmental antigens
autoimmunity
disturbance in the immunologic tolerance of self-antigens
alloimmunity
immune rxn to tissues of another individual
immune deficiency
rxn insufficient to protect the host
allergens
environmental antigens that cause atypical immunologic responses
pollens, molds, fungi, foods, animals, cigarette smoke, house dust
anaphylaxis
most rapid and severe immediate hypersensitivity rxn
systemic or cutaneous
desensitization
may reduce the severity of the allergic rxn but could also cause anaphylaxis
autoimmunity
genetic, environmental, and random factors
systemic lupus erythematosus
chronic multisystem inflammatory disease
autoantibodies against
nucleic acids
histones
ribonucleoproteins
other nuclear materials
what are the symptoms of systemic lupus erythematosus the result of
type 2 or 3 hypersensitivity rxns
systemic lupus erythematosus clinical manifestations
vasculitis and rash
arthralgias/arthritis
renal disease
hematologic changes
cardiovascular disease
transfusion rxns
occurs when person with one blood type receives another
Type O
universal donor
type AB
universal recipient
transplant rejection
MHCs are major target
classified according to time
hyperacute
immediate and rare
preexisting antibody to the antigens of the graft
acute
days to months
cell-mediated immune response
chronic
months or years
weak cell-mediated rxn against minor HLA antigens
primary immune deficiencies
usually from a single gene defect
not inherited
severe combined immunodeficiency
few detectable lymphocytes
underdeveloped thymus
absent or reduced IgM and IgA levels
bare lymphocyte deficiency
adequate b and t-cells but they don’t work
inability to produce MHC class 1 and 2
wiskott-aldrich syndrome
depressed IgM production w/ bleeding
digeorge syndrome
lack of thymus and parathyroid gland
Ca2+ deficiency
predominantly antibody deficiencies
defective b-cell development
complement deficiencies
C3 deficiency
most severe due to central role in complement cascade
results in recurrent life-threatening infections
mannose-binding lectin deficiency
defect of lectin pathway
results in risk of infection
treatment for primary immune deficiencies
iv immune globulin
stem cell transplantation
transfusion of erythrocytes
bone marrow transplants
mesenchymal stem cell injection
most people with malignancies will die from the infection or the tumor
the infection due to deficiency of immune response
immunosuppressive treatments
corticosteroids
chemotherapeutic agents
irradiation
antirejection drugs
acquired immunodeficiency syndrome (AIDS)
most advanced stage of infection of infection by HIV
depleted body’s TH cells
creates generalized immune deficiency
HIV epidemiology
blood-borne pathogen
most common in heterosexual activity and women
HIV structure
retrovirus
genetic info is RNA (reverse transcriptase)
HIV life cycle
attachment to target cell
viral capsid released into target cell cytoplasm
viral rna inserted into target cell’s genetic material
formation/release of new virions
HIV clinical manifestations
serologically negative → no detectable antibody
serologically positive but asymptomatic → positive for antibody against HIV proteins
early stages
resembles the flu
disappears after 1-6 weeks
AIDS
atypical or opportunistic infections and cancers
debilitating chronic disease
diagnosis and treatment of AIDS/HIV
decreased CD4+ t cell numbers
antiretroviral therapy
pediatric AIDS
transmitted during pregnancy, at delivery, breast-feeding
treatment must begin at time of diagnosis