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Diseases of Immunity ppt patho exam 2

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What are the three causes of hypersensitivity diseases?
1.) autoimmunity 2.) rxn against microbes (maybe prolonged exposure to something 3.) rxn against enviromental antigens (all of us are exposed to these but only some people react to them, they are usually harmless antigens ex. Pollin)
mechanisms of immunologically mediated disorders
Type I hypersensitivity is mediated by ____ directed against specific antigens (allergens)
immunoglobulin E (IgE)
Primary mediators of type I hypersensitivity include ___, ___, ___ and ____.
histamine, adenosine, heparin and proteases
Secondary mediators of type I hypersensitivity include ____, ___, ____ and ____.
leukotrienes (which are 10x more potent than histamine), prostaglandin D2, platelet-activating factor, and cytokines
Anaphylaxis, allergies, and bronchial asthma are all prototype disorders of type ___ hypersensitivity
I
In type I hypersensitivity, both primary and secondary mediators cause ___, ____ and ____.
vascular permeability, smooth muscle contraction, and prolonged inflammation
Hypersensitivity can cause ___ and ___ reactions
local (ex. Bee sting) and systemic (ex. Anaphylactic response)
Type on hypersensitivity
Mast cells in hypersensitivity
Type II hypersensitivity is mediated by _____.
antibodies (our own body reacting to our body)
With Type II hypersensitivity, antibodies are directed against target antigens on the surface of cells or orther tissue components. This leads to _____.
inflammation
What are the three kinds of Type II hypersensitivity?
1.) complement-dependent reactions 2.) antibody-dependent cell-mediated cytotoxicity 3.) antibody-mediated cellular dysfunciton
Type 2 hypersensitivity
List the five reactions of complement-dependent Type II reactions.
1.) transfusion rxns 2.) erythroblastosis fetalis 3.)autoimmune hemolytic anemia, agranulocytosis or thrombocytopenia 4.) drug rxns 5.) pemphigus vulgaris
Type III Hypersensitivity is ______-mediated
immune complex (antigen-antibody)
What are the three mechanisms of Type III hypersensitivity?
1.) antigen-antibody complexes 2.) activates complement in tissues at site of trapping of complexes 3.) accumulation of polymorphonuclear leukocytes
With type III hypersensitivity, mediated injury can be ____ or ____.
systemic; localized
What are the three phases of type III hypersensitivity?
1.) complex formed btw antigen and antibody 2.) complex deposits in tissue 3.) this triggers recruitment of PMNs (inflammatory rxn)
Type IV hypersensitivity is _____ mediated
cell (also known as delayed)
Typer IV hypersensitivity is mediated by ____ or ____ cells
T; CD4
Type IV hypersensitivity causes the recruitment of _____
macrophages (CD8 cells)
Type IV hypersensitivity can cause _____.
cytotoxicity
TB (and other mycobacteria), fungi, protozoa, parasites, sarcoidosis, contact skin sensitivity and transplant rxns can all cause type ___ hypersensitivity.
IV
What are the two types of Type IV hypersensitivity?
1.) delayed-type hypersensitivity 2.) direct cell cytotoxicity
Delayed-type hypersensitivity is mediated by ___ cells
CD4
Direct cell cytotoxicity is mediated by ___ cells
CD8
In delayed-type hypersensitivity, CD4 T cells are activated and then differentiate into _____.
Th 1 (T-helper) cells
Delayed-type hypersensitivity activates ____ and ____
macrophages and TNF (which add more to the inflammation process ex. PPD test, contact dermatitis)
If delayed-type hypersensitivity is not resolved it can cause _____.
chornic inflammation--> multinucleated giant cells
______ is when perivascular CD4 T-cells infiltrate is replaced by macrophages over a 2-3 week time period and turn into epithelioid cells (large, flat, eosinophilic -> multinucleated giant cells)
granulomatous inflammation (ex. Poison ivy)
Epitheliod cells are surrounded by _____.
lymphocytes
What mediates Type I hypersensitivity
IgE antigens (e.g. mast cells--> histamine)
anaphylaxis, angioedema and atopic allergy are examples of
Type 1 (immediate)
How fast do Type I hypersensitivities occur
1 hour
Type I hypersensitivity is also known as ______
Immediate
Type II hypersensitivity is also known as ______
Cytotoxic Antibody Reaction
Type II hypersensitivity is mediated by_____ and _____ antigens
IgG (more important) IgM
reactions to transfusion, Rh incompatibility and Hashimoto's thyroditis are examples of
Type II (cytotoxic antibody reaction)
Type III hypersensitivity is also known as _______
immune complex reaction
How fast does Type III hypersensitivity occur
1-3 weeks after exposure
SLE, erythema nodsum and RA are examples of ______
Type III (immune complex reaction)
Type III hypersensitivity should be associated with_____
antigen-antibody complex deposits in tissue
Type IV hypersensitivity is also known as ____
delayed type
Type IV hypersensitivity should be associated with_____
cellular response
Type IV hypersensitivity is mediated by _______
T-lymphcytes to specific antigens
PPD and contact dermatitis are examples of this hypersensitivity
Type IV (delayed type)
How fast does Type IV hypersensitivity occur
2-7 days post-exposure
Which type of hypersensitivity involves MHC
Type IV (delayed type)
MHC (stands for?)
major histocompatibility complex)
What is the role of MHC?
Once a pathogen is engulfed and broken down into peptides the MHC is activated and results in antigen presentation so the T-cell can recognize infected cells
________reactions to _________is the cause of certain human disease
immune; self-antigens (presence of antigens alone is not pathologic)
__________reactions cause systemic disease
cell-mediated
APC's (Stands for?)
antigen presenting cell
describe the general process of tissue injury due to autoimmune disease
The individual has self-reactive lymphocytes which binds to their own cells activating APC's thus causing an increase of lymphocytes into tissue which leads to tissue injury
of systemic lupus erythematous (SLE)
failure to maintain self-tolerance
Lupus affects ________in the _____or______decade of life
females; 2nd/3rd
what are the 11 criteria for classification of SLE
malar rash, discoid rash, photsensitivty, oral ulcers, arthritis, serosis, renal disorder, neurologic disorder (seizures or psychosis), hematologic disorder, immunologic disorder or antinuclear antibody
is characterized by the destruction of articular carlage and bone
RA
A 16-year-old black female presents to her primary care physician with symptoms of fatigue, musculoskeletal pain, and a facial rash. On examination she is noted to be thin with malar skin changes. No other abnormality is found
SLE
A 52-year-old woman presents with a 2-month history of bilateral hand and wrist pain, and swelling in her fingers. She has also recently noted similar pain in the balls of her feet. She finds it hard to get going in the morning and feels stiff for hours after waking up. She also complains of increasing fatigue and is unable to turn on and off faucets or use a keyboard at work without a significant amount of pain in her hands.She also presents with leg ulcers that have been chronic and has ulnar deviation of the hands bilaterally. She denies any infections before or since her symptoms started
RA
pathologic changes that begin in ligmentous attachments to bone; frequently involves SI joints
Seronegative spondyloarthropathies
A 45-year-old woman presents with fatigue and a history of positive anti-nuclear antibodies. She has had recurrent sensation of sand/gravel in eyes and dry mouth every day for more than 3 months.
sjogren's syndrome
the pathogenesis of sjogrens syndrome
B-cell hyperactivity
genetic factors of sjogren's syndrome
HLA association
what are the two groups of systemic sclerosis (SS)
diffuse and limited scleroderma
widespread skin involvement and rapid progression of early visceral involvment
diffuse SS
skin involvment is confined to fingers/face, visceral involvement occurs late, presents with CREST
limited scleroderma SS
Calcinosis, Raynaud phenomenon, Esophageal dysmotility, Sclerodactyly, and telangiectasia
CREST syndrome
calcinosis
calcium deposits in the skin
raynaud's phenomenon
spasm of blood vessels in response to cold/stress
esophageal dysfunction
acid reflux and decrease in motility of esophagus
sclerodactyly
thickening and tightening of the skin on the fingers and hands
telangiectasias
diallation of capillaries causing red marks on surface of skin
what is the next step in the immune response after mast cells and macrophages are recruited
release of fibroblast growth and chemotactic factors or endothelial cell injury
Heliotrope rash associated with_______
dermatomyositis
characterized by decreased antibodies, T/B-cells, phagocytes or complements
primary immunodeficiency
Ex of decreased T-cells
Thymic aplasia, DiGeorge's syndrome
Ex of decreased antibodies
X-linked hypgammaglobulinemia
characterized by old age, chronic malnutrition, widespread malignancy, metabolic (DM, liver failure...), drugs, splenectomy or HIV
Secondary immunodeficiency
RNA retrovirus
HIV
which type of HIV is more prevalent in our geographic location?Africa?
HIV 1; HIV2
Name some high risk groups of HIV
risky sex, IV drug users, homosexual, transfusion pts, and hyperphiliacs
what cells are affected mainly by HIV infection
CD4 cells
how is HIV transmitted
body fluids, mother to fetus
HIV is a ______ retrovirus
RNA
HIV-2 is prevelent in
Africa
HIV-1 is prevelent
US
HIV is transmitted via
Bodily Fluids, vertical transmissions
HIV High Risk groups include
IV drug users, homosexuals, transfusions, hemopheliacs
HIV affects ______ cells
CD-4
With HIV you can test for a ________
Viral Load
In HIV _____ binds to ______
gp120/CD-4
In HIV after binding to CD-4 gp41 ________
penetrates the membrane
HIV _____ off of cell
buds
HIV clinical latency is considered a CD-4 of greater than _______
200
Three phases of HIV
Early acute, clinical latency, crisis phase
AIDS defining diseases include (6)
toxoplasmosis, candidiasis, salmonella, kaposi's sarcoma, non-hodgkin's lymphoma, TB
Amyloidosis
most common amyloid
AL (amyloid light chain)
plasma cells and immunoglobin light chain)
AA (amyloid-associated)
non-immunoglobulin synthesized in the liver
cerebral lesion of alzheimer disease
Nonspecific complaints of amyloidosis
weakness, fatigue, initial weight loss, renal involvement (proteinuria-nephrotic syndrome), hepatomegaly, splenomegaly, cardiac abnormalities (arrhythmias
Dx of Amyloidosis
biopsy, and congo red staining
Catagorized as "systemic amyloidosis" (5)
Immunocyte dyscrasias (primary), reactive systemic (secondary), hemodialysis, hereditary (familial mediterranean fever or familial amyloidotic neuropathies), systemic senile
catagorized as "localized amyloidosis" (3)
Senile cerebral, endocrine (medullary carcinoma of thyroid, islet of langerhans), isolated atrial amyloidosis
disease associated with immunocyte dyscrasias with amyloidosis
multiple myeloma and other monoclonal B-cell proliferations
disease associated with reactive systemic amyloidosis
chronic inflammatory conditions
disease assoc w/ hemodialysis associated amyloidosis
chronic renal failure
disease assoc w/ senile cerebral amyloidosis
alzheimer disease
disease assoc. w/ islet of langerhans
type 2 diabetes
Immunocyte dyscarasias fibril protein
AL
Reactive systemic amyloidosis fibril protein
AA
Hemodialysis associated major fibril protein
Senile Cerebral Fibril protein
Familial mediteranean fever fibril protein
AA
Insoluble Fibrils
stimulus------soluble precursor
AL Protein
Carcinogen-----monoclonal B lymphocyte proliferation----plasma cells-----immunoglobulin light chains (limited proteolysis)
AA Protein
chronic inflammation ----macrophage activation----interleukins 1 and 6----- liver cells----SAA protein (limited proteolysis)