EXAM 2: Immune disorders Flashcards
exaggerated
against environmental antigens
misdirected against host’s own cells
autoimmunity
directed against beneficial foreign tissues
isoimmunity (like to transplants)
hypersensitivity
- a pathologic immune response
- an exaggerated AND inappropriate immune response
Autoimmunity
-breakdown of that “code of recognition” and begins to recognize self as foreign
what causes the development of autoimmunity
- genetics
- exposure to antigens (ie: drugs/infections)
why do genetics and exposure to antigens cause autoimmunity
-thought to alter membranes (and the expression of self DNA) and induce this autoimmunity
what are the two types of hypersensitivity
- autoimmunity
- isoimmunity
isoimmunity
bodies IS reacts against tissues of usually other members of same species
type 1 hypersensitivity
IgE mediated allergic reactions
allergy/anaphylaxis
type 2 hypersensitivity
tissue-specific reaction
blood transfusion reaction
type 3 hypersensitivity
immune-complex mediated reactions
-AG-AB complexes from and deposit in tissues
type 4 hypersensitivity
cell-mediated reactions
-involve t-cells, macrophages
anaphylaxis
a rapid, immediate hypersensitivity reaction upon RE-EXPOSURE to antigen
allergy chain first time
allergen-> in contact with B cell-> produces IgE antibody specific to allergen-> IgE goes to receptors on mast cell-> mast cell for next time it comes in contact with allergen
allergy chain second time
IgE recognizes allergen-> induce mast cell degranulation-> release of histamine andleukotrienes-> S/S of allergy
which exposure causes mast cell degranulation
second exposure
localized clinical mani of allergies/anaphylaxis
- local inflammation
systemic clinical mani of allergies/anaphylaxis (5)
- bronchial constriction,
- skin is itchy and red
- increased secretions of mucous mems
- abdominal cramps, V/D
- increased vascular permeability and vasodilation
which systemic manis of allergies are life threatening
- bronchial constriction
2. vascular permeability and vasodilation
systemic lupus erythematosus
chronic, autoimmune, multisystem inflammatory disease
where is lupus common
-females
20-40 years of age
genetic predisposition
what type of hypersensitivity reaction is lupus
mostly type III
AG-AB complexes form and deposit in vessel walls
first lupus chain
B cell produces IgG immunoglobulin-> attacks cells of the vessel wall it views as foreign->antibody complexes deposit in vessel walls
second lupus chain component
T helpers-> help further stimulate B cell production of IgG
third component of lupus chain
macrophages recruited to further attach cells of vessel walls-> further destruction
fourth component of lupus chain
igG also attacks RBC’s because it sees them as foreign as well (leads to anemia)
fifth component of lupus chain
T suppressor cells are not effective in slowing down process (should have regulated/slowed destruction but didn’t)
clinical mani of lupus
- arthritis of peripheral jts
- vasculitis/photosensitivity
- renal disease
- anemia
- CV disease- pericarditis
why does renal diseases happen with lupus
-damage of vascular wall over time as well as lysed RBC’s not getting through
rheumatoid arthritis
Autoimmune, inflammatory jt disease characterized by destruction of the synovial membrane
RA patho chain
normal antibodies(IgM, IgG) are transformed into rheumatoid factor-> RF attacks cells of synovial mem->vasodialation/increased permeability->WBC enter synovial fluid->further attack synovial mem->fibrin, collagen and scar tissue is deposited in synovial jt fluid
early RA clinical mani
- synovitis (inflammation of synovial membrane)
2. systemic manifestations of inflammation (minor, low grade fever, fatigue)
what type hypersensitivity is RA
both type III and type IV
-normal antibodies become “autoantibodies (RF) (IgM, IgG) and attack “antigens” on cell mems
which jts are effected first with RA
usually peripheral jts (wrists and fingers)
later clinical mani of RA
Start to get tenderness, stiffness of jts (destruction has started)
- pain, deformity, loss of function of the jts
- rheumatoid nodules
- Ulnar drift (hand drifts toward ulnar, pinkie side)
immune dificiencies
-impaired function of the immune response
congenital (primary) immune deficiencies
Genetic (immune cells are improperly developed)
acquired (secondary) immune dificiencies
associated with conditions (PG, infancy, elderly, chronic illness, malnutrition)
iatrogenic deficiencies
(an acquired immune D)
- iatrogenic (from medical treatment_
- Trauma (burns)
- stress
HIV1
a retrovirus viral disease- carries it genetic coding in its RNA
how does HIV 1 infect
- infects and depletes a portion of the IS (cells with CD-4 receptors) (t-helpers)
- then starts to attack macrophages and cytotoxic t cells
step one HIV infection
- HIV-surface glycoprotein (gp120) attaches to CD-4 receptor and enters cell
step two HIV infection
chemokine (a co-receptor) aids in the binding of gp120
step three HIV infection
Viral RNA converted into DNA (with help from 3 enzymes, reverse transcriptase, integrase, and protease)
step four HIV infection
the DNA is inserted and integrated into the T helper cell DNA and takes over the cell
what are the three way HIV spreads to other cells
- Remain latent (no spread)
- New HIV particles but out
- Lysis of cell with release of particles
lab values in HIV
- overall # of t helper cells (n800-1000)
- Ratio of T helpers to T suppressors (n2/1)
- Viral load (the lower the better)- amount of “active” virus in the blood stream
what are the four possible conditions with HIV
- serologically negative
- serologically positive
- early stages of HIV disease
- AIDS
serologically negative
but they can have virus without an AB produced or detected YET
serologically positive
-asymptomatic
-detectable AB, but no real symptoms
(this stage is the goal)
early stages of HIV disease
symptoms but not AIDS
AIDS
- serious clinical symptoms and or malignancies
- often t helper less than 200
what is the HIV time line
- enter body
- no AB production
- AB production
- Early stages and AIDS of HIV disease
clinical mani of serologically negative
ASYMPTOMATIC
- high risk groups
- ability to unknowingly transmit the virus
clinical mani of serologically positive
ASYMPTOMATIC
-some experience a seroconversion illness resembling mono or flu
clinical mani of early stages HIV disease
- chronic lymphadenopathy
- night sweats
- recurrent fevers
- flu-like, fatigue
- anorexia, wt. loss, diarrhea
clinical mani of AIDS
- opportunistic infections
- malignancies
