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56 Cards in this Set
- Front
- Back
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what Ig antibody(s) is produced in Type 1 hypersensitivity? Type 2? Type 3?
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1: IgE
2: IgM and IgG 3: IgM or IgG |
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what type of cells mediate type four hypersensitivity?
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T cell mediated so CD4 (delayed hypersensitivity) and CD8 CTLs (T-cell mediated cytolysis)
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what type of cells response to type 1 hypersensitivity? type 2? type 3? type 4?
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1: mast cells and their mediators
2: leukocytes (macrophages and neutrophils) 3: leukocytes 4: macrophages and cytokine mediated inflammation |
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describe the molecular process of type 1 hypersensitivity.
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1. activation of Th2 cells by antigen
2. induced B cell class switching to IgE 3. production of IgE and binding of secreted IgE to Mast cell FceR 4. Activation, degranulation, and tissue damage by Mast cells upon secondary exposure to antigen |
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which interleukin is responsible for Th2 differentiation in type 1 hypersensitivity?
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IL-4
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where are mast cells typically found?
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tissues near blood vessels and nerves and beneath epithelia
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what leads to the release of granules in type 1 hypersensitivity?
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crosslinking/antigen binding of FCeRI/ IgE
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T/F
Mast cells have preformed exocytotic vesicles waiting to release their cargo outside the cell. |
True
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What is responsible for the "wheal and flare"? why?
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histamine, because it causes vasodilation and vascular leakage
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what is initially released from mast cells in type 1 hypersensitivity? what effect does it have?
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histamine- cause smooth muscle contraction
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what is synthesized after initial activation and vesicle release in type 1 hypersensitivity?
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TNF-alpha, IL-4, IL-3, IL-5, GM-CSF, and Leukotrienes C4, D4, and E4.
5 cytokines and 3 lipid mediators |
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how late is late phase in type 1 hypersensitivity? is the magnitude less or more than immediate?
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6-8 hours; more
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what cell mediator is limited in type 1 hypersensitivity? why?
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eosinophils because they are extremely powerful and can do more harm to the body than the pathogen
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when do eosinophils express the FCeRI?
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after activation
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what is functionally similar to mast cells, but in a different location? where are they located?
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basophils- recruited to, but do not a resident of the mucosal tissue
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for eosinophils, what is synthesized after initial activation and vesicle release?
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IL-3, IL-5, GM-CSF, and Leukotrienes C4, D4, and E4
3 cytokines and 3 lipid mediators |
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which muscles will contraction with histamine? what is the exception?
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most smooth muscle; exception: blood vessels
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what are the classic type 1 reactions?
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allergic asthma, allergic rhinitis/hay fever, food allergies, insect sting allergies
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what is unique to type 1 symptoms?
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they are episodic or seasonal
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16 YO male was taken to the ER immediately after eating at a seafood bar with a friend. Complains of an itchy sensation and some stomach pain. On examination, the pt has rashes on his tongue. What does the pt have? what toxic mediator is at fault?
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Food allergy; histamine
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T/F
watery rhinorrhea is bacterial. |
false: it is viral or allergic
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what is the major concern with insect sting allergies?
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injection of allergen into the blood stream causing system anaphylaxis
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what are the three common causes of systemic anaphylaxis? Give an example of each
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IV drug administration (penicillin), Insect sting (bee sting), rapid absorption of food allergen (peanut)
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22 YOF is rushed via into the ER after hyperventilating and then passing out at the dinner table during dinner one night. On examination, the pt had a swollen tongue and their BP was 90/60. What is the diagnosis? who is the main culprit? how do we treat it?
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diagnosis: systemic anaphylaxis
culprit: Histamine--> mast cell activation and granule release treatment: emergent: epi injection within 20 minutes delayed: IV fluids, anti-histamines, corticosteroids |
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what does the release of histamine lead to?
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1. vasodilation
2. capillary permeability 3.sensory neuron activation 4. mucous gland secretions |
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for eosinophils, what is synthesized after initial activation and vesicle release?
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IL-3, IL-5, GM-CSF, and Leukotrienes C4, D4, and E4
3 cytokines and 3 lipid mediators |
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which muscles will contraction with histamine? what is the exception?
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most smooth muscle; exception: blood vessels
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what are the classic type 1 reactions?
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allergic asthma, allergic rhinitis/hay fever, food allergies, insect sting allergies
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what is unique to type 1 symptoms?
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they are episodic or seasonal
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16 YO male was taken to the ER immediately after eating at a seafood bar with a friend. Complains of an itchy sensation and some stomach pain. On examination, the pt has rashes on his tongue. What does the pt have? what toxic mediator is at fault?
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Food allergy; histamine
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T/F
watery rhinorrhea is bacterial. |
false: it is viral or allergic
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what is the major concern with insect sting allergies?
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injection of allergen into the blood stream causing system anaphylaxis
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what are the three common causes of systemic anaphylaxis? Give an example of each
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IV drug administration (penicillin), Insect sting (bee sting), rapid absorption of food allergen (peanut)
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22 YOF is rushed via into the ER after hyperventilating and then passing out at the dinner table during dinner one night. On examination, the pt had a swollen tongue and their BP was 90/60. What is the diagnosis? who is the main culprit? how do we treat it?
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diagnosis: systemic anaphylaxis
culprit: Histamine--> mast cell activation and granule release treatment: emergent: epi injection within 20 minutes delayed: IV fluids, anti-histamines, corticosteroids |
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what does the release of histamine lead to?
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1. vasodilation
2. capillary permeability 3.sensory neuron activation 4. mucous gland secretions |
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which type of hypersensitivity has fixed antibodies? what is the most common example of this type of hypersensitivity?
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type 2- penicillin
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what are the classic type 2 hypersensitivity reactions? who are the main culprits?
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drug induced anemia or thrombocytopenia due to: penicillin, quinidine, methldopa.
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what distinguishes type 1 and type 2 based on response?
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type 1: immediate and only on secondary exposure to the antigen
type 2: delayed and can respond on first exposure |
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what are some examples of type 2 autoimmune reactions?
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autoimmune hemolytic anemia, Goodpasture's syndrome, Grave's disease, and myasthenia gravis
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what is type 3 hypersenitivity mediated by? what organ does this type never involve?
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immune complex; lung
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T/F
Type 3 involves a fixed antigen. |
FALSE: only type 2 has a fixed antigen, all the rest are soluble
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how does type 3 hypersensitivity activate inflammation? what is the basis of the reaction?
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by forming incomplete complex sediments in vessels or tubules. They get deposited there and cannot be cleared.
basis: you need 2 IgG per immune complex to fix complement and clear the antigen. |
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when does type 3 hypersensitivity usually occur?
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early in the response due to the lack of antibody and large amount of antigen.
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what type 3 reaction is comparable to another form of hypersensitivity? what is the other hypersensitivity and how do they differ?
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arthus reaction is comparable to Type 1; type 1 is immediate, and type 3 takes 1-2 hours
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what are the common depositions in type 3? what do they cause?
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kidney tubules, vessel walls and joints.
causes: nephritis, vasculitis, and arthritis |
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44 YOM comes into your office complaining of joint pain and problems on urination starting two days ago. Pt had just had a liver transplant a little over a week ago. Creatine kinase comes back evelated and positive for blood in the urine. what type of hypersensitivity is this? how do you know? what is the diagnosis? explain
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type 3. This is understood because the patient came in complaining of joint pain and kidney problems (arthritis and nephritis), two key indicators for type 3.
Diagnosis: serum sickness-- symptoms started 7-10 days after his transplant. Probably was on anti-lymphocyte globulin. |
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what are the three common examples of drug reactions causing serum sickness? what are they used for? what is the hypersensitivity?
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streptokinase (thrombolysis), anti-lymphocyte globulin (transplants), and penicillin (antibiotic). Type 3
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what is the difference between arthus reaction and serum sickness?
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arthus: subcutaneous injection of an antigen. Pt is an immune individual (this is their second exposure). v similar to type 1.
serum sickness: intravenous injection of high doses of antigen. pt is a non-immune individual (primary exposure). similar to type 2 except not fixed. |
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what is the key thing to remember for type 4 hypersensitivity? what is it mediated by?
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antigen dose; mediated by T cells
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what type of cells activates the T cells?
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antigen presenting cells
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T/F
type 4 hypersensitivity requires a TON of more antigen to elicit a response? |
true: 100-1000 times more
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what are the two categories of type 4 hypersensitivity?
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delayed type and contact
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what is the most common example of delayed type hyerpsensitivity? how long does it take? what T cells and cell mediators are involved?
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skin response (ie TB skin test)
24-72 hours Th1 (primarily) and sometimes Th2 cell mediators: IFN-gamma, TNF-alpha, and (IL-4 w/ Th2 involvement). |
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what T cell responds in contact dermatitis? what are the most common examples?
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CTL; poison ivy and metal allergies
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what are some examples of autoimmune T cell responses?
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type 1 diabetes, RA, MS, IBD, autoimmune myocarditis, Gillain-Barre syndrome
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Pencillin can cause hypersensitivity, which one(s)? what disease or disorder does that lead to?
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type 1: systemic anaphylaxis
type 2: anemia type 3: serum sickness |
