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91 Cards in this Set
- Front
- Back
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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) |
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Type I hypersensitivity:
triggers immunological |
crosslinking of receptors by multi-valent antigen.
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Type I hypersensitivity: triggers
Both immunological and non-immunological cAMP/PKA |
cAMP/PKA tubulin phosphorylation and movement of granules to membrane; swelling of granules.
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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.
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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)
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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
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allergens
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often proteins 10-70KDa, usually polar, high sulfhydryl content, either polymeric, or associated with larger particles to form polyvalent, effective antigen.
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IgE
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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. |
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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 |
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pathogenesis of
Type 1: hypersensitivity mediators |
-histamine
-neutrophils -eosinophils -lymphocytes -macrophages -epithelial cells -edothelial cells -particulary basophils |
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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. |
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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 |
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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 |
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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 |
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factors influencing sensitivity
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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 |
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Cutaneous anaphylaxis
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-local reaction to local exposure
-Urticaria (hives) -Wheal (12-18hr) -flare (15-20min) -erythema (redness) -Pruritis (itching) |
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systemic anaphylaxisension
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-allergen gte into circulation by injection of ingestion
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systemic anaphylaxis
generalized dilation |
shock
hypotension dizziness faintness headache smooth muscle spasm swelling of throught and larnyx |
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systemic anaphylaxis
asthma |
congestion of the brochi w/ mucous, and constriction of bronchioles
-nonallergic resulting in change in temp physical activity, stress or respiratory. |
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systemic anaphylaxis
eyes |
conjuctivities, lacrimation, ishing, allergens, same as repiratory
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systemic anaphylaxis
ears |
serous ottitis
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systemic anaphylaxis
GI tract |
cramps nausea, vomiting, diarrhea
not true allergies: lactose intolerance gluten sensitive enteropathy cystic fibrosis galactosemia |
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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) |
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treatment
immunomodulation hyposensitization |
production of blocking IgG or IgA, then removal of
Ag-Ab complex |
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treatment
immunomodulation tolerance |
decrease of IgE production, serum IgE complexed with down regulated B cells.
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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. |
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Type II hypersensitivity
effector cell |
macrophages
platelets killer cells neutrophiles esinophiles |
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Type II hypersensitivity
principal antibodies |
IgG and IgM
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Type II hypersensitivity
examples |
ABO transfusion reaction
hemolytic disease of newborn myasthenia gravis thyroiditis hyperacute graft rejection autoimmune hemolytic anemia |
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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. |
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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. |
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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. - |
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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. |
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Type II hypersensitivity
complement-mediate lysis lysis of foreign cells |
complement via C5-C9 attack complex dissolving the plasma membrane of the cell.
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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 |
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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 |
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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) |
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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. |
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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. |
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Type III hypersensitivity
etiology |
results from failure of immune and phagocytic systems to get ride of antigenantibody immune complexes and is not tissue specific.
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Type III hypersensitivity
etiology arthus reaction |
characterized by antigen-antibody complex deposition into tissue, with consequent activation of complement and subsequent inflammatory reaction.
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Type III hypersensitivity
principal antibodies |
IgM and IgG
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Type III hypersensitivity
principal effectors |
neutrophiles and mast cells
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Type III hypersensitivity
principal mediator |
complements
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Type III hypersensitivity
examples |
SLE, immune complex glomerulonephritis, serum sickness, and drug induced vaculitis
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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. |
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Type III hypersensitivity
pathogenesis activation of complement cascade |
causes release of C3a and C5a and membrane attack complex.
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activation of complement cascade
C3a |
stimulates histamine from mast cells
increasing vascular permeability and vasodilation. -bronchial constriction -increase vascular permeability (endothelial cells)results edema |
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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. |
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Result of activation of complement
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neutrophiles, macrophages, mast cell attck area.
-cell lysis destruction of tissue via release of cytokines and inflammatory response. -causes tissue distruction, scarring. |
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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. |
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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 |
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Delayed type hyperseneitivity (DTH)
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-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). |
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DTH
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characterized by tissue damage resulting from delayed cellular reaction to an antigen.
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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. |
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DTH
pricipal effectrs |
lymphocytes
macrophages w/ mast cells involved in the early phases. |
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DTH
examples |
cutaneous basophil hypersensitivity (jones-mote)
contact hypersens. tuberculin granulomatous |
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hapten
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lipid soluble antigen
-must penetrate the epidermis. -linked w/ normal body protein in the epidermis called a carrier. |
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hapten conjugate
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hapten combines w/ carrier is a complete antigen
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langerhans cells
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complete antigen is processed by epidermal macrophages
-located in the suprabasal epidermis. -they move to lymph node |
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CD4+
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then the antigen-sensitized CD4+ T cells release lymphokines, which initiate an inflammatory reponse and attract other effect cells.
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Primary lymphokines (cytokins)
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IL-2, IL-3, interferon, TNF, and macrophages-stimulating factor.
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lymphokine cascade
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prsentation of antigen to T-cells by langerhans cell
-vasoactive and cytoactive substances.(inflammation) |
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Decrease lymphokine cascade
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degradation of the antigen and production of prostiglandin E, which inhibits IL-1 and IL2 production
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Rheumatoid arthritis
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-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 |
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Scleroderma
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-"hard skin" (over-production of collagen)
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CREST syndrome
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calcinosis, Raynauds, esophageal dysfunction, sclerodactyly, teleangiectasia
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Sytematic autoimmune diseases
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fever, weakness, arthritis, skin rash, pleurisy, and kidney disfunction, multiple tissue autoantibodies (DNA, RBCs, platelets, clotting factos, etc)
DX: antinuclear antibodies |
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Multiple scerosis
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neurodegenerative disorder often mediated by anti-myelin antibodies; may activated T cells that are cytotoxic to nerves, leads to muscle weakness, paralysis, numbness, blindness
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Myashenia gravis
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antibodies bind to ACH receptors on the muslce membrane surfaces, primarly the motor end plate.
-causes extrame muscle weaknesss associated w/ myasthenia gravis |
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Hashimoto's thyroiditis
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lymphocyte thyroiditis
-enlarged thyroid glands. -decrease hormone stimulating release of TSH from pituitary, indicating gypoactive thyroid gland pg985 |
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SLS (systemic lupus erythematosus)
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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 |
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HLA antigen disease
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ankylosing spondylitis
rheumatoid arthritis graves Type 1 diabetic Systemic lupus erythematosus narcolepsy |
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Non-steroidal anti-inflammatory (NSAIDs)
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aspirin, ibuprofen COX-2 inhibitors
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Steroidal anti-inflammatory
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Cortison, prednisone
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anti-rheumatic
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hydroxychloroquine
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Immunosuppressants
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cyslosporines A, FK-506, rapamycin, MABs
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Antineoplastic
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MTX, azothioprine, cyclophosphamide
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pooled and specific Ig
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Anti-TNF, anti-IL-1, rituximab
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Replacemnt TX
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insulin, platelets, T3/T4 TXP
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Primary immunodeficiency
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-immune system failure to protect host against disease causing agents
-inherited |
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Adaotive immunodeficiency
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Lymphoid (B or T cells)
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Innate immunodeficiency
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myleoid (phagocytic deficeincy)
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secondary deficiencies
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conditions that impair immune function as a result of other processes, such as poor nutrition, stress, or drugs.
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Consequences of primary deficiency
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-usually leathal in first few years of life
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cellular immunity defect
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reduction in cell-mediated cytotoxicity and delayed hypersensitivity, increased susceptibility to viral, protozoan and fugal inflections.
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humoral immune deffects
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increased inflection by bacteria and diminished response to immunizations
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treatment of primary immune deficiencies
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replace missing protein, cell type/lineage, defective gene
-administer Ig -IFNgamma CGD -stem cell transplant -gene therapy- adenosine deaminase (vivo treatment of stem cells) |
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Antibodies bind surface of RBCs and hemolytic anemia ensues
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autoimmune
drug-induced (penicillic, procainamide) |
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autoimmune hemolytic anemia
diagnosed |
coob's test that uses anti-HuIgM or anti-HuIgG to look for agglutination of RBCs
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Auto-antibodies against WBCs may cause agranulocytosis
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Abs bind platelets and thrombocytopenia (ITP) occurs
-Abs bind neutrophils and neutropenia ensues |
