Lecture 4 Flashcards
Hypersensitivity disorders
increased or inappropriate immune response to the presence of an antigen that results in tissue destruction due to the host immune response itself
Allergen
special class of antigens that elicits an allergic response
Rapidity of immune response categories
Immediate = occur within minutes of exposure
Late phase = persist for hours-days after allergens are removed
Delayed = occurs after sensitization to antigens, several days later
Type 1 hypersensitivity
immediate, called atopic conditions. examples include hay fever, hives, asthma, anaphylaxis
pathogenesis of type 1 hypersensitivity
some people in response to antigens have hereditary predisposition to produce IgE instead of IgG in response to common environmental agents
IgE bind to mast cells, when allergen combines with mast cells, histamine is produced
Local reactions of type 1 hypersensitivity
nose because IgE combines to mast cells to release histamine
Serious systemic reactions of type 1 hypersensitivity
anaphylaxis = widespread histamine release occurs
causes widespread vasodilation, bronchospasm, increased mucus production, edema, irticaria, rhinorrhea
Edema
accumulation of plasma in interstitial tissue
Type 2 hypersensitivity
antibody mediated
examples: cross-reaction between pathogen and body tissue, like rheumatic fever/blood transfusion reactions
Pathogenesis type 2 hypersensitivity
antibodies that attack antigens on the surface of cells
process starts by binding of antibodies to tissue specific antigens
activation of complement occurs, leading to clumping and phagocytosis of pathogens
body can misinterpret its own cells during immune response to pathogen
Type 3 hypersensitivity
immune complex mediated disease
excessive immune complexes in circulation are cleared by complement and phagocytic cells
if IC are able to deposit in tissues, complement system is activated, leads to inflammation and local tissue injury
results in vasculitis (inflammation of blood vessels), which damages tissues
skin = urticaria
joints = arthritis
kidneys = nephritis
lungs = pleuritis
Type 4 hypersensitivity
cell-mediated immunity, delayed
developed later in adulthood
includes contact dermatitis, latex sensitivity, transplant rejections
Pathogenesis Type 4 hypersensitivity
tissue damage results from delayed cellular reaction to an antigen
slow onset/offset begins 24 hr exposure and last up to 14 days
primary antibody involvement is absent
antigen is processed by macrophages and presented to helper t cells
T cells secrete cytokines, helps to recruit lymphocytes, monocytes, macrophages, neutrophils
Autoimmune disorers
failure in distinguishing self from non self
usually present in connective tissue
shared findings = HLA types, WBC counts, presence of autoantibodies
differentiation/diagnosis are often quite difficult
treatment is difficult, trying to quiet immune system while helping it function
glucocorticoids are the most helpful
Lupus Erythematosus
chronic inflammatory autoimmune disorder
Types: SLE, discoid lupus (affects only skin), drug induced (stops when drug is stopped)
no recent estimates of prevalence and incidence
Risk factors for lupus
young female
non-caucasian women
infection with epstein barr virus
Pathogenesis of lupus
exact cause is unknown
multifactorial: immunological, genetic, hormonal, environmental
generalized autoimmune disease
causes deposition of antibody antigen complexes
the body makes antibodies against anything cellular
Immune complex
bonded connection of antibody with antigen
Clinical presentation of lupus
flares
signs/symptoms usually develop at intervals, rather than all at once
many organ systems can be affected
musculoskeletal = arthralgia, arthritis
renal = renal failure, anemia
cutaneous = butterfly rash
Treatment of lupus
there is no cure
goals are to decrease autoimmune and inflammatory processes, prevent flare ups, achieve remission
pharamacological management
NSAIDs, antimalarial drugs, immunotherapy, glucocorticoids
Patient education
rest is necessary
practice energy conservation (perform activities during peaks, reduce energy for task, analyze task before completing it)
photoprotection is vital
medication adherence
stress reduction is beneficial
avoid smoking
dietary consult
exercise is vital
Prognosis of lupus
outlook of most people has become increasingly favorable due to early diagnosis and treatment
significant morbidity and mortality
illness pursues relapsing and remitting course. natural history varies
15 year survival rate
mortality is caused by CVD, infections, renal disease
Complication of Lupus
Avascular necrosis
Renal problems
Adverse drug reactions
Avascular necrosis
when blood supply to bone diminshes
tiny breaks in bone occur, leading to collapsed bone
can be due to lupus or medication
most common in the hip, increased pain with weightbearing
Renal problems
note any new or increased HTN or edema and alert MD immediately
Adverse drug reactions
occur in patients taking systemic glucocorticoids
cushing syndrome (thinning of skin, thin extremities, poor wound healing, easy bruising)
