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35 Cards in this Set
- Front
- Back
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Hypersensitivity
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a. Undesirable reaction produced by the normal immune system when the adaptive immune response to an antigen occurs in an exaggerated form. (because it is adaptive, the individual has to have been exposed to it previously)
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Type 1 example
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Ex. Injection of antigen in one pig, two weeks later, same injection again causing anaphylactic shock in few minutes. **Note: if we had transferred immune cells to the naïve pig, it would not have died**
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Type1 mechanism
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1. Primary antibody: IgE
2. Primary cellular component: mast cell and basophil 3. Amplifiers/modifiers: neutrophils, eosinophils, macrophages, lymphocytes Initial intro to antigen causes antibody response: IgE synthesized. Antibody binds to the FceRI receptor on the mast cell. Allergen (antigen) binds to the IgE on the mast cell causing cell to degranulate and release pharmacological mediators that cause smooth muscle contraction, vasodilation, and edema. |
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CT mast cell
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i. When high dose of antigen is injected intravaneously, mast cell activates and releases toxin granular proteins, histamines, leading to anaphylaxis.
ii. When antigen is injected subcutaneously, can see local reaction with limited histamine release. See activation of mast cells in the skin. |
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mucosal mast cell
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i. Inhalation of low dose leads to Allergic rhinitis (upper airway) caused by increased mucus production and nasal imitation. Can cause asthma (lower airway) because of contraction of bronchial smooth muscle and increased mucus secretion
ii. Ingestion of high doses causes contraction of intestinal smooth muscle inducing vomiting. Outflow of fluid into gut causes diarrhea. Antigen diffuses into blood vessels and is widely disseminated causing hives or anaphylaxis |
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primary mediators
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a. Released in immediate phase measured in Fev
b. These are preformed mediators: histamine, serotonin, proteases, chemotactic factors |
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secondary mediators
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a. Released in late phase measured in Fev.
b. Newly synthesized and takes about 10 hours, see a wider and higher inflammatory response: leukotrienes, prostaglandins, bradykinin, cytokines. |
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Uticaria and angioedema
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type 1
caused by viral infection, drug, food, latex- affects superficial or deeper layers of the skin, causes priuritic wheals with surrounding edema |
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allergic rhinitis
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type 1
affects upper respiratory tract causing sneezing, congestion, runny nose, and often accompanied by itchy or sore throat (laryngitis) and red itchy, watery eyes ( conjunctivitis) |
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food allergy
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type 1
swelling of the tongue and throat, vomiting, abdominal crumps, diarrhea, loss of consciousness, and even death |
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allergic asthma
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type 1
affects lower respiratory tract causing bronchial constriction, mucus production, inflammation of the airways |
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anaphylaxis
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systemic (more than 1 organ involved), causes systemic vasodilation, vasopermeability, hypotension, abdominal effects, throat swelling, and asphyxiation
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type 1 treatment
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1. identifyin allergen using IgE, th2, th1 and T reg cells
2. use different drugs - leukotriene block late phasse not early phase |
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corticosteroids
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When cortisol binds glucocorticoid receptor, complex acts in 3 ways:
i. DNA independent action: signals through MAP phosphatase and induces changes in cell ii. DNA dependent regulation: complex migrates to nucleus, binds DNA, induces transcription of certain genes while down regulating transc of other genes iii. Protein interference mechanism: complex binds F kappa B. Induced transcription of different immunoregulatory molecules |
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Omalizumab
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antibody binds specific portion of IgE that binds to the FcE receptor
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Type 2 example
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i. Example: Blood transfusion. Giving wrong blood to a blood recipient can cause RBC agglutination and lysis of recipient system, kidney failure, shock.
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type 2 mechanism
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1. Inducing inflammation at the site of deposition: neutrophils and macrophages come to site of deposition. Neutrophils regulate tissue injury
2. Opsonizing cells for phagocytosis: antibody binds cell surface and opsonize cell preparing it for phagocytosis Interfering with normal cellular function such as hormone receptor signaling: TSH epithelial cells make thyroid hormone. TSH epi cell has the TH receptor. When too much thyroid is being generated, it can sense and reduce secretion BUT when antibody binds, it interferes the receptor so there is constant TH release. |
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transfusion reaction
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type 2
a. IgM causes phagocyte-mediated destruction or component mediated lysis of erythrocytes for class ABO incompatibility reactions b. Treatment: stop transfusion, provide supportive care |
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autoimmune hemolytic anemia
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a. Spontaneous
b. Patient produces antibody to their own erythrocyte c. May be caused because of certain reactions to drugs (penicillin binds RBC surface and converts from hapten to antigen) d. Result of accelerated clearance of the antibody sensitized erythrocytes by spleen macrophages Treatment: corticosteroids, spleenectomy |
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Hasimoto thyroiditis
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a. Autoreacting antibodies to a number of thyroid proteins interfere with iodine uptake
b. Decreased production of thyroid hormone Treatment: TH replacement |
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Goodpasture syndrome
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type 2
a. IgG reacts with glomerular basement membrane surfaces. b. Complement ligation and kidney tissue destruction, glomerulonephritis c. Treatment: oral immunosuppressive drugs (cclophosphamide and corticosteroids) |
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rheses incompatibility
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Haemolitic disease of new borns a. Arises when Rh + sensitized Rh- mother carries second Rh+child.
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Type 3 immune complex reaction example
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i. Ex. Horse serum injected multiple times into rabbit. Observed edema formation and slower absorbance for serum with each injection
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type 3 mechanism
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iii. Mechanism A
1. Antigen injection, IgG-antigen complex formation, activation of mast cells to induce degranulation, local inflammation and increased fluid and protein release, phagocytosis and blood vessel occlusion iv. Mechanism B: Immune complex mediated tissue injury : vasculitis |
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arthus reaction
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type 3
a. Caused by immyune complexes (IgA-ag) and C3B b. Localized cutaneous inflammatory reaction occurs that progresses to a hemorrhagic necrotic leasion Treatment: immunosuppression |
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rheumatoid arthritis
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type 3
a. Chronic, inflammatory autoimmune disorder causing immune system to attach joints leading to loss of motility due to pain and joint destruction b. Treatment: corticosteroids, methotrexate, TNF inhibitor- etanercept, B cell depletion, rituximab |
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systemic lupus erythematoous
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a. Autoantibodies against nuclear components (DNA, Histones, etc)
b. Deposit in basement membrane of glomeruli and lungs where it induces complement fixation c. Kidney or lung failure d. Combined type 1 and type 3 tissue injury e. Treatment: immunosuppression |
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serum sickness
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type 3
Caused by administered antiserum or antibody derived from animals b. Can be caused by certain drugs like penicillin c. Antibody produced to these proteins from immune complexes with them d. Rashes, joint pain, fever, lymph node swelling, splenomegaly, hypotension, shock e. Treatment: removal of complexes, corticosteroids, antihistamines |
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farmer's lung
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type 3
a. Hypersensitivity pneumonitis b. Symptoms similar to asthma attacks, pneumonia, or flue Treatment: allergen avoidance |
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Type 4 - delayed type hypesensitivity example
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i. Ex. Sublethal dose of M. tuberculosis then put lethal dose two weeks later, erythema and induration two days later. Sublethal dose and then serum transfer in naïve pig, death. Sublethal dose and immune cell transfer to naïve pig, get erythema and induration
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Type 4 mechanism
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1. Contact sensitizing agent penetrates skin and binds to self-proteins which are taken up by a host cell
2. Host cell presents the peptide with the contact sensitizing agent to the Th1 cells which secrete IFN gamma and other cytokines Components activate macrophages and secrete mediators of inflammation |
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Delayed type hypersensitivity
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type 4
Ex. Tuberculin reaction: M. tuberculosis antigens are injected intradermally in a person’s forearm. Response evolves over a 24 to 48 hour period if a person has TB, has been exposed to it in the past, has been vaccinated against tuberculosis |
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contact hypersensitivity
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type 4
a. Small molecules: haptens which penetrate epidermis and attach to larger carrier-normal body proteins b. Classic contact dermatitis- poison ivy, metals-nickel, cobalt, chromium, chromates, and latex |
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gluten sensitive enteropathy
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type 4
a. Hypersensitivity to gluten derived protein gliadin b. Cause:villi damage, inflammation c. Symptoms: diarrhea, malnutrition d. Diagnosis: IgA, anti tissue translutminase e. Treatment: gluten free diet |
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dental prosthesis allergy
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type 4
tongue erythema, edema, and gingival microvesicles, with local burning warmth, and pruritus, several hours after the placement of acrylic dental prosthesis |
