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91 Cards in this Set

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Type I hypersensitivity:
triggers

non-immunological
-tissue injury (heat cold)
-microbial cell products (formyl peptides)
-C'activation, or direct action of anaphylatoxins such as C5a
-some bee and snake venoms (mellitin)
-specific chemical (compund 48/80, Ca2+ inophores)
Type I hypersensitivity:
triggers

immunological
crosslinking of receptors by multi-valent antigen.
Type I hypersensitivity: triggers

Both immunological and non-immunological
cAMP/PKA
cAMP/PKA tubulin phosphorylation and movement of granules to membrane; swelling of granules.
Type I hypersensitivity:
triggers
Both immunological and non-immunological
PTK to Phospholipase
-PTK to Phospholipase gamma (PLC gamma) to IP3 to Calmodulin to PKC to myosin phosporylation for microfilaments and granule attachment to membrane.
Type I hypersensitivity:
triggers
Both immunological and non-immunological
Phospholipase A
formation of fusogen from lyso-PC for granules o fuse and production of prostoglandins (PGs) and leukotrienes (LTs)
Type I hypersensitivity:

what is it?
"unusual" (atopic from GK, atopos=uncommon) and not health related promoting(anaphylactic and opposed to prolactic) immunological response to exogenous agent (pollen, food, insect sting), mediated by mast cells basophils
allergens
often proteins 10-70KDa, usually polar, high sulfhydryl content, either polymeric, or associated with larger particles to form polyvalent, effective antigen.
IgE
produced from plasma cells, like others Ig's,circulates in very small amounts in the blood (genetic predisposition?)
- when exposed to an allergen that they are allergic to plasma B cells produce IgE.
- increased exposure causes increase levels of IgE in the blood.
etiology of
type 1: hypersensetivity
genetic mechanisms

IgE production is under T-cell control.
-high levels of IgE and low levels of supressor T-cells.
-MHC genes linked HLA
pathogenesis of
Type 1: hypersensitivity
mediators
-histamine
-neutrophils
-eosinophils
-lymphocytes
-macrophages
-epithelial cells
-edothelial cells
-particulary basophils
pathogenesis of
Type 1: hypersensitivity
principal effector cell
mast cells are the principal effector cell.

found in loose connective tissue.
-covered w/ IgE recptors
- they are filled with vesicles or granules with potent vasoactive
proinflamitory chemical mediators called histamine. That produce inflamation when released.
pathogenesis of
Type 1: hypersensitivity
-IgE recptor on mast cell binds to Fc portion of an IgE antibody.
-IgE antibody-binding site display ont the mast cell surface recptor were they can bind to antigen.
-crosslinking of IgE and the antigen causes an increase in intracellular Ca2+
-resulting in an immediate mast cell degranulation of proinflammatory mediators
pathogenesis of
Type 1: hypersensitivity
principal effector cell chemicals being released and
mediators
histamine
heparin
proteolytic enzyme
chemotatic factors
mediators:
superoxide
prostaglandin
thromboxanes
leukotrienes
bradykinin
interleukins
Type 1: hypersensitivity
manifestations
-smooth muscle contraction or dilation.
-vascular system dilates leading to hypotension;brochioles, GI, GU, endothelium contracts, resulting in gastric, nasal, and lacimal secration.
exact response is a function of
-route of contact
-frequency of contact
-degree of sensitivity
factors influencing sensitivity
genetic factors-
people with HLA type DW2 tend to be sensitive to ragweed.
both parents atopic have 75%chance.
one parent atropic 50%
non atropic 35%
identical twins often have identical patterns of allergy.
other factors:
emotional factors
pre-existing inflamation
Cutaneous anaphylaxis
-local reaction to local exposure
-Urticaria (hives)
-Wheal (12-18hr)
-flare (15-20min)
-erythema (redness)
-Pruritis (itching)
systemic anaphylaxisension
-allergen gte into circulation by injection of ingestion
systemic anaphylaxis
generalized dilation
shock
hypotension
dizziness
faintness
headache
smooth muscle spasm
swelling of throught and larnyx
systemic anaphylaxis

asthma
congestion of the brochi w/ mucous, and constriction of bronchioles
-nonallergic
resulting in change in temp
physical activity, stress or respiratory.
systemic anaphylaxis
eyes
conjuctivities, lacrimation, ishing, allergens, same as repiratory
systemic anaphylaxis
ears
serous ottitis
systemic anaphylaxis
GI tract
cramps nausea, vomiting, diarrhea
not true allergies:
lactose intolerance
gluten sensitive enteropathy
cystic fibrosis
galactosemia
Treatmetnt
Drug therapy
-avoidance
-modify mediator release or formation (corticosteroids, chromolyn)
-modify action of mediators with receptor antagonist (antihistamines)
-modify target cell activity independent of specific mediator (smooth muscle relaxants)(albuterol and theophylline) and vasoconstrictors (pseudofed)
treatment
immunomodulation
hyposensitization
production of blocking IgG or IgA, then removal of
Ag-Ab complex
treatment
immunomodulation
tolerance
decrease of IgE production, serum IgE complexed with down regulated B cells.
Type II hypersensitivity
defined
known as tissue-specific, cytotoxic, or cytolytic hypersensitivity, is characterized by antibodies that attack the antigens on the surface of specific tissue.
- occurs after binding of antiboy to tissue specific antigen.
Type II hypersensitivity
effector cell
macrophages
platelets
killer cells
neutrophiles
esinophiles
Type II hypersensitivity
principal antibodies
IgG and IgM
Type II hypersensitivity
examples
ABO transfusion reaction
hemolytic disease of newborn
myasthenia gravis
thyroiditis
hyperacute graft rejection
autoimmune hemolytic anemia
Type II hypersensitivity
isoimmunity
hemolytic disease of newborn
ABO transfusion reaction
hyperacute graft rejection
- condition in which the immune system reacts against antigens on tissues from other member from other members of the same species.
Type II hypersensitivity
pathogenesis
-response is exposure to antigen on the surface of foreign cell.
-The Fab portion of IgG and IgM antibodies binds to antigens on the target foreign cellto form an antigen-antibody complex.
-antigen-antiboy binding with Fc bridging leads to cytotoxic and cytolysis.
Type II hypersensitivity
complement-mediate lysis
-occurs though activation of complements
-by activating complement C3b via splitting of C4 and C2 by C1.
The activated complement component C3b is bound target cell by the Fc region of IgG or IgM.
-
Type II hypersensitivity
complement-mediate lysis
Cb3
-increases opsonization
-increases the capacity of the system to allow lysis by other effector cells or by complement itself.
Type II hypersensitivity
complement-mediate lysis
lysis of foreign cells
complement via C5-C9 attack complex dissolving the plasma membrane of the cell.
Type II hypersensitivity
transfusion reaction
-occurs when a person receives blood from someone with a different blood group type.
-type A:
type A antigen and anti-B antibodies.
-if incorrectly receives type B blood
-type B antigens and anti-A antibodies.
--the anti-B will attach to the surface of type B blood cells and the anti-A will attach to the surface of the type A blood cells.
---kill many blood cells
Type II hypersensitivity
signs and symptoms
fever, chills, flushing, tachycardia, hypotension, low back pain, pleurtic chest pain, nausea,vomiting, restlessness, anxiety, oliguria, and headache

anaphylaxis, shock, and death
Type II hypersensitivity
second mechanism for antigen-antibody binding
-direct distruction by Fc-bearing effector cells such as macrophages
-macrophages can link to exposed Fc antibody region (bridging occurs)
Type II hypersensitivity
second mechanism for antigen-antibody binding
effector cells
bridging occurs the foreign cell is phagocytized and destroyed by lysosomes within effector cells.
- mediated w/ or w/out complement involvement.
Erythroblastosis fealis
(blue baby syndrome)
Rh(-) mom is sensitized to her Rh(+) fetus group antigen b/c exposure to her fetal pregnancy.
The IgG (+) antibodies cross the placental barrier and attack the fetus's red blood cells.
RhoGAM (anti-Rh antibodies)28wks and at delivary for prevention sensitization.
RhoGAM is not effective if the mother already has a positive anti-body titer for fetal Rh antigen.
Type III hypersensitivity
etiology
results from failure of immune and phagocytic systems to get ride of antigenantibody immune complexes and is not tissue specific.
Type III hypersensitivity
etiology
arthus reaction
characterized by antigen-antibody complex deposition into tissue, with consequent activation of complement and subsequent inflammatory reaction.
Type III hypersensitivity
principal antibodies
IgM and IgG
Type III hypersensitivity
principal effectors
neutrophiles and mast cells
Type III hypersensitivity
principal mediator
complements
Type III hypersensitivity
examples
SLE, immune complex glomerulonephritis, serum sickness, and drug induced vaculitis
Type III hypersensitivity
pathogenesis
ineractions b/w circulating soluble antigen and souble antibody or b/w an insouble antigen and soluble antibody.
-crosslinking of antigen anf antidoy occurs and immune complexes are formed.
---immune complexes are formed and are NOT removed and thus cause tissue damage.
-When only the antibody is soluble, the antibody reacts w/ fixed antigen in the tissue.
- antiboy w/in the complex links w/ the complement system by its Fc receptors.
Type III hypersensitivity
pathogenesis
activation of complement cascade
causes release of C3a and C5a and membrane attack complex.
activation of complement cascade
C3a
stimulates histamine from mast cells
increasing vascular permeability and vasodilation.
-bronchial constriction
-increase vascular permeability (endothelial cells)results edema
Activation of complement cascade
C5a
-release of proinflammatory mediators (action same as C3a).
-chemotatic agent for neutrophils.
-it causes respiratory burst w/in neutrophils
--increased oxygen consumption, glucose uptake and procagulant activity.
Result of activation of complement
neutrophiles, macrophages, mast cell attck area.
-cell lysis destruction of tissue via release of cytokines and inflammatory response.
-causes tissue distruction, scarring.
Type III hypersensitivity
immune complex glomerulonephritis
etiology
caused by persistent low-grade infection.
-It involves the interaction of soluble exogenous antigen w/soluble antibody.
-immune complex is deposited in glomerular capillary wall and mesangium.
Type III
glomerulonephritis
clinical manifestations and treatment
causes damage to the glomerular basement membrane with resultant proteinuria, hematuria, hypertension, oliguria, and red cell casts in urine.
-corticocosteriods
Delayed type hyperseneitivity (DTH)
-very common mechanism of contact sensitivity
1.Distinction of irritant(nonspecific) from and allergic (antigenic) mechanism
B. reaction take hours to day to develop
C. Requires sensitization and elicitation.
D. Often seen as skin reaction to drugs or chemicals and can lead to contact sensitivity-reactions to cosmetic or laundry detergent enzymes common.
E. Tuberculin reaction to PPD is a classical test which is antigen-specific.
F.Symptoms can sometimes be confused with an Arthus (immune complex reaction).
DTH
characterized by tissue damage resulting from delayed cellular reaction to an antigen.
DTH
principal mediators
lymphocytes
-producing T cell (Td) that mediates the reaction by releasing lymphokins (cytokines) and/or antigen-sensitized cytotoxic T cells (Tc) that can directly kill cells.
DTH
pricipal effectrs
lymphocytes
macrophages w/ mast cells involved in the early phases.
DTH
examples
cutaneous basophil hypersensitivity (jones-mote)
contact hypersens.
tuberculin
granulomatous
hapten
lipid soluble antigen
-must penetrate the epidermis.
-linked w/ normal body protein in the epidermis called a carrier.
hapten conjugate
hapten combines w/ carrier is a complete antigen
langerhans cells
complete antigen is processed by epidermal macrophages
-located in the suprabasal epidermis.
-they move to lymph node
CD4+
then the antigen-sensitized CD4+ T cells release lymphokines, which initiate an inflammatory reponse and attract other effect cells.
Primary lymphokines (cytokins)
IL-2, IL-3, interferon, TNF, and macrophages-stimulating factor.
lymphokine cascade
prsentation of antigen to T-cells by langerhans cell
-vasoactive and cytoactive substances.(inflammation)
Decrease lymphokine cascade
degradation of the antigen and production of prostiglandin E, which inhibits IL-1 and IL2 production
Rheumatoid arthritis
-arthritis and the presence of rheumatoid factor(RF)
-RF typically IgM antibodies to human IgG Fc region determinants
-immune compleses (IgM-IgG) activate complement and deposit in joints and leads to chronic inflammation, swellling, pain, stiffness
Scleroderma
-"hard skin" (over-production of collagen)
CREST syndrome
calcinosis, Raynauds, esophageal dysfunction, sclerodactyly, teleangiectasia
Sytematic autoimmune diseases
fever, weakness, arthritis, skin rash, pleurisy, and kidney disfunction, multiple tissue autoantibodies (DNA, RBCs, platelets, clotting factos, etc)
DX: antinuclear antibodies
Multiple scerosis
neurodegenerative disorder often mediated by anti-myelin antibodies; may activated T cells that are cytotoxic to nerves, leads to muscle weakness, paralysis, numbness, blindness
Myashenia gravis
antibodies bind to ACH receptors on the muslce membrane surfaces, primarly the motor end plate.
-causes extrame muscle weaknesss associated w/ myasthenia gravis
Hashimoto's thyroiditis
lymphocyte thyroiditis
-enlarged thyroid glands.
-decrease hormone stimulating release of TSH from pituitary, indicating gypoactive thyroid gland
pg985
SLS (systemic lupus erythematosus)
affect all systems
-joint, tendons, and bones pain, arthralgias and synovitis.
-scales or plaques develop
-latticelike venular skni changes (livedo reticularis)
-alopecia
-pericarditis
-myocarditis
-congestive heart failure
-pleuritis
-glomernephritis
-proteinuria
-hematuria
-necrosis
-ptosis
-diplopia
-ataxia
-seizures
-psychosis
HLA antigen disease
ankylosing spondylitis
rheumatoid arthritis
graves
Type 1 diabetic
Systemic lupus erythematosus
narcolepsy
Non-steroidal anti-inflammatory (NSAIDs)
aspirin, ibuprofen COX-2 inhibitors
Steroidal anti-inflammatory
Cortison, prednisone
anti-rheumatic
hydroxychloroquine
Immunosuppressants
cyslosporines A, FK-506, rapamycin, MABs
Antineoplastic
MTX, azothioprine, cyclophosphamide
pooled and specific Ig
Anti-TNF, anti-IL-1, rituximab
Replacemnt TX
insulin, platelets, T3/T4 TXP
Primary immunodeficiency
-immune system failure to protect host against disease causing agents
-inherited
Adaotive immunodeficiency
Lymphoid (B or T cells)
Innate immunodeficiency
myleoid (phagocytic deficeincy)
secondary deficiencies
conditions that impair immune function as a result of other processes, such as poor nutrition, stress, or drugs.
Consequences of primary deficiency
-usually leathal in first few years of life
cellular immunity defect
reduction in cell-mediated cytotoxicity and delayed hypersensitivity, increased susceptibility to viral, protozoan and fugal inflections.
humoral immune deffects
increased inflection by bacteria and diminished response to immunizations
treatment of primary immune deficiencies
replace missing protein, cell type/lineage, defective gene
-administer Ig
-IFNgamma CGD
-stem cell transplant
-gene therapy- adenosine deaminase (vivo treatment of stem cells)
Antibodies bind surface of RBCs and hemolytic anemia ensues
autoimmune
drug-induced (penicillic, procainamide)
autoimmune hemolytic anemia
diagnosed
coob's test that uses anti-HuIgM or anti-HuIgG to look for agglutination of RBCs
Auto-antibodies against WBCs may cause agranulocytosis
Abs bind platelets and thrombocytopenia (ITP) occurs
-Abs bind neutrophils and neutropenia ensues