allergy – Chemistry – Flashcards
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| what is dr. feldman's definition of an allergy? |
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| your body perceives a substance as harmful/noxious stimuli, and “mistakenly” reacts to it (thus, tries to get rid of it) |
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| what are the 3 components to the allergy reaction? |
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| allergy cell (mast cells, eosinophils), IgE, and trigger |
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| what is anaphylaxis? what is anaphylactoid? |
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| severe, whole body reaction to an allergen involving 2 or more organ systems (ex. skin/mucosa involvement, respiratory difficulties, low BP, GI symptoms). anaphyalactoid resembles anaphylaxis, but dosen't require an immunological mechanism |
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| what are the major cells involved in allergy reactions? |
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| mast cells and eosinophils (degranulate preformed granules/membrane breaks down to give prostaglandins+leukotrienes) |
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| what are common allergy triggers? |
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| pollen, dust mites, mold, pet dander, strong odors, smoke, chemical fumes |
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| what role does IgE play in *atopic allergic rxns? |
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| IgE has common/hypervariable regions and is *very specific for allergenic triggers |
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| how do inhaled allergens affect B cells in a primary exposure? |
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| the stimulate IgE production by B lymphocytes and in the development of asthma exacerbation, the B lymphocytes differentiate into plasma cells (epsilon switch), that produces+releases IgE antibodies into circulation |
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| once IgE are released into circulation by plasma cells, what do they do in a primary exposure? |
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| released IgE circulate, binding to high-affinity IgE receptors (Fc epsilon RI) on the surface of mast cells (in tissue) or basophils (peripheral-blood) |
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| what happens when the individual is re-exposed to an allergen they have previousl produced IgE for? |
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| the allergen binds to IgE on B cells, which induces the release of inflammatory mediators -> leading to bronchoconstriction (via allergic inflammation, stimulation of eosinophils and lymphocytes) |
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| how many kinds of T cells are there? which one drives pts to become atopic? what activates them? what do they do? do they inhibit anything? |
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| TH1,2,7,9. TH2 drives pts to become atopic, and are activated by IFN-gamma. activated TH2 cells secrete interleukins that help mature and differentiate cells contributing to an allergic rxn, (mast cells, B cells, eosinophils). TH2 secrete IL-2,10 which inhibits TH1 |
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| when APCs such as macrophages/dendritic/kupffer cells engulf/process/present allergic antigen what happens next? |
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| TH2 CD4 cells which then secrete IL-4,5, stimulating differentiation of B cells into plasma cells that make an IgE for that particular allergen/antigen which then circulate and interact with mast cells |
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| how do IgE bind to mast cells? |
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| IgE have Fc epsilon RI binding sites and mast cells ahve Fc epsilon RI receptors (high affinity, low is Fc epsilon RII) |
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| what happens immediately when IgE binds to mast cells via Fc epsilon RI? |
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| immediately: granule contents; *histamine, TNF-alpha, proteases, heparin are released. this causes sneezing, nasal congestion, itchy/runny nose, watery eyes. |
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| what happens over minutes when IgE binds to mast cells via Fc epsilon RI? |
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| in minutes: lipid mediators prostaglandin and leukotrienes are released, causing wheezing and bronchoconstriction |
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| what happens over hours when IgE binds to mast cells via Fc epsilon RI? |
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| over hours: cytokine production, (IL-4 and IL-13) lead to mucus production and eosinophil recruitment |
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| what characterizes the *biphasic allergic response, early vs late? |
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| early: immediate/histamine driven late: can last longer, may be stronger, perpetuates the allergy cycle, and involves inflammatory cells |
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| how do we know that the allergy rxn is biphasic? |
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| tissue bx has confirmed presence of histamine and inflammatory cells at various points of an allergic rxn |
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| what is the forced expiratory volume (FEV)? what is seen when this test is performed? |
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| this assesses normal lung function vs allergen-induced asthma. the pt is monitored over exposure time to an allergen; early response consists of immediate decrease in lung function (due to mast cells, macrophages, and platelets) followed by quick improvement, while late response sees more sustained decrease in lung function due to eosinophils/neutrophils |
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| what is seen with FEV's in terms of repeated exposure to allergens? |
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| hyper-reactivity which can lead to a decline in lung function, mediated by monocytes, lymphocytes and eosinophils |
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| what is the most common allergic disease? what are systemic symptoms? |
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| allergic rhinitis, which is a systemic disease inclucing lethargy, fatigue and arthralgia/myalgia |
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| **hat are some common conditions comorbid with allergic rhinitis? |
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| asthma, sinustitis, otitis media, nasal polyps, URI, malocclusion, sleep apnea |
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| what are the three most common bacteria involved with sinusitis? |
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| streptococcus pneumoniae (most common pathogen – in both adults and children), haemophilus influenzae, moraxella catarrhalis (only in children) |
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| what is obstructive sleep apnea? who is at risk? |
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| sleep disorder characterized by pauses in breathing during sleep, pts experience an O2 decrease during sleep and wake up when it hit 89% O2 level. individuals with neck diameters exceeding 15.5” in females and 16.5” in males have an elevated risk of sleep apnea |
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| what are questions to ask when investigating sleep apnea? |
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| when do you sleep at night? do you fall asleep within 10 minutes? do you dream? do you wake up at night? how do you feel waking up in the morning? |
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| in diagnosing/treating pts with allergic rhinitis, what are some important questions to ask concerning the nose? |
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| binary yes/no questions about location of congestion, sneezing, itching, congestion, inability to smell/taste, unilateral blockage? (unilateral blockage is usually due to polyps, not allergy) |
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| in diagnosing/treating pts with allergic rhinitis, what are some important questions to ask concerning the eyes? |
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| binary questions about itching/watery eyes (burning eyes aren’t a result of allergies) |
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| in diagnosing/treating pts with allergic rhinitis, what are some important questions to ask concerning the chest? |
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| binary questions about: tightness/wheezing/dyspnea/exertional symptoms |
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| what are hives? |
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| hives - aka ectopic dermatitis are itchy lesions that seldom last longer than 24-28 hours |
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| what are the most pruritogenic inflammatory mediators? |
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| histamine, trypsin, chymase, papain, kallikrein, substance P, VIP |
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| what are less pruritogenic inflammatory mediators? |
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| prostaglandins (however they potentiate the itch of other mediators), serotonin, endorphins, enkephalins |
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| what is the easiest/most sensitive way to ID IgE? |
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| allergy skin testing |
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| what the three modalities of treatment for allergic rhinits? |
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| allergy avoidance, pharmacotherapy and immunotherapy |
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| what does allergy avoidance consist of? |
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| finding the triggers, determining feasability of avoidance. make sure bedroom environment is allergy-free |
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| what does rx tx of allergic rhinitis consist of? |
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| antihistamines, intranasal steroids, leukotriene modifiers, de-congestants and anti-IgE therapy |
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| what are the two generations of antihistamines? do these help with congestion? |
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| 1st gen antihistamines like benadryl have significant sedative effects (anticholinergics cause: SLUD, inhibition of salivation, lacrimation, urination, defecation). 2nd gen antihistamines such as allegra have a longer duration, less side effects and are larger/more polar (don't get into brain -> less side effects). antihistamines help with sneezing/pruritis, but have minimal affects on congestion |
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| what is the first line of medical therapy for allergic rhinitis? how are they applied? are these safe to use over time? |
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| intranasal steroids, which are more effective than antihistamines in decreasing sneezing, pruritis and nasal blockage. they are applied using the L hand to spray R nostril and vica versa, keeping the spray off the septum (causes bleeding/irritation). these are safe to use (except for afrin) over time, no atrophy has been shown. |
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| what are leukotriene modifiers? |
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| singular etc, these do work for allergies, but only make sense to use if you have an atopic asthmatic pt. they are expensive |
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| what are other names for allergy immunotherapy? what is it? |
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| allergen vaccines, desensitization, hyposensitization & allergy shots. allergy immunotherapy is the process of treating immunologic IgE mediated diseases using increasing doses of allergenic extracts and the goal is to produce a tolerance towards a specific allergenic trigger |
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| what can allergy immunotherapy be used for? |
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| pts suffering from atopic disease, (bee sting, allergic asthma, allergic rhinitis), constantly needs rx/has adverse effects to rxs, and/or has a life threatening allergies. |
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| what is the mechanism of action for immunotherapy? |
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| it is thought to decrease a seasonal rise in a specific IgE, inhibit early/late reactions, cytokine modulation via T regs* (inhibit allergy problems), production of IgG-4 which doesn't bind complement and IgA which is mucosal |
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| what is allergic immunotherapy successful in treating? what does its effectiveness depend on? |
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| asthma, allergic rhinitis, stinging insect anaphylaxis. effectiveness depends on appropriate dosage and duration of immunotherapy treatment. serious reactions are uncommon |
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| what is sublingual immunotherapy? is it done in the US? |
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| sublingual immunotherapy, aka “SLIT” consists of small amounts of allergenic substances are placed under the tongue in increasing amounts. it is used to treat atopic conditions in europe, but not the US? |
