Клиническая аллергология для обучающихся на английском языке (Clinical Allergology for Learners in English)
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Тематика:
Иммунология и иммунопатология
Издательство:
НИЦ ИНФРА-М
Автор:
Макеева Ксения Сергеевна
Год издания: 2024
Кол-во страниц: 82
Дополнительно
Вид издания:
Учебное пособие
Уровень образования:
Профессиональное образование
ISBN-онлайн: 978-5-16-112683-7
Артикул: 835702.01.99
В учебном пособии по дисциплине «Клиническая иммуноло гия и аллергология» в краткой и доступной форме представлены современные сведения о механизмах этиопатогенеза, специфических методах диагностики и лечения аллергических заболеваний. Для контроля и обобщения материала после каждого раздела приведены тестовые задания, предложены ситуационные задачи для формирования клинического мышления.
Предназначено для студентов пятого курса учреждений высшего образования, обучающихся на английском языке по специальности 1-79 01 01 «Лечебное дело».
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МИНИСТЕРСТВО ЗДРАВООХРАНЕНИЯ РЕСПУБЛИКИ БЕЛАРУСЬ УЧРЕЖДЕНИЕ ОБРАЗОВАНИЯ «ГОМЕЛЬСКИЙ ГОСУДАРСТВЕННЫЙ МЕДИЦИНСКИЙ УНИВЕРСИТЕТ» КАФЕДРА КЛИНИЧЕСКОЙ ЛАБОРАТОРНОЙ ДИАГНОСТИКИ, АЛЛЕРГОЛОГИИ И ИММУНОЛОГИИ К.С. МАКЕЕВА КЛИНИЧЕСКАЯ АЛЛЕРГОЛОГИЯ ДЛЯ ОБУЧАЮЩИХСЯ НА АНГЛИЙСКОМ ЯЗЫКЕ CLINICAL ALLERGOLOGY FOR LEARNERS IN ENGLISH УЧЕБНОЕ ПОСОБИЕ Москва ИНФРА-М 2024
УДК 616(075.8) ББК 53/57я73 М15 Р е ц е н з е н т ы: Кафедра клинической лабораторной диагностики и иммунологии Гродненского государственного медицинского университета; Романива О.А., кандидат медицинских наук, врач аллерголог-иммунолог отделения аллергологии и иммунопатологии Республиканского научнопрактического центра радиационной медицины и экологии человека Макеева К.С. М15 Клиническая аллергология для обучающихся на английском языке (Clinical Allergology for Learners in English) : учебное пособие / К.С. Макеева. — Москва : ИНФРА-М, 2024. — 84 с. ISBN 978-5-16-112683-7 (online) В учебном пособии по дисциплине «Клиническая иммунология и аллергология» в краткой и доступной форме представлены современные сведения о механизмах этиопатогенеза, специфических методах диагностики и лечения аллергических заболеваний. Для контроля и обобщения материала после каждого раздела приведены тестовые задания, предложены ситуационные задачи для формирования клинического мышления. Предназначено для студентов пятого курса учреждений высшего образования, обучающихся на английском языке по специальности «Лечебное дело». УДК 616(075.8) ББК 53/57я73 ISBN 978-5-16-112683-7 (online) © Учреждение образования «Гомельский государственный медицинский университет», 2024 ФЗ № 436-ФЗ Издание не подлежит маркировке в соответствии с п. 1 ч. 2 ст. 1
TABLE OF CONTENTS Introduction ............................................................................................4 Chapter 1. Immunology of allergy ........................................................5 1.1. Factors contributing to allergies ...................................................5 1.2. Allergens. Characteristic and classification ..................................7 1.3. Mechanisms and classification of hypersensitivity reactions ........8 1.4. Review questions to chapter 1 ...................................................18 Chapter 2. Diagnosis of allergy ..........................................................22 2.1. Medical history ...........................................................................22 2.2. Physical examination ..................................................................24 2.3. Allergological examination methods ...........................................28 2.4. Review questions to chapter 2 ...................................................42 Chapter 3. The general principles of treating allergic diseases ......46 3.1. Non-medication therapy .............................................................46 3.2. Medication therapy .....................................................................49 3.3. Allergen-specific immunotherapy ...............................................52 3.4. Review questions to chapter 3 ...................................................54 Chapter 4. Allergopathology ...............................................................58 4.1. Drug allergy ................................................................................58 4.2. Anaphylaxis ................................................................................64 4.3. Emergency treatment for anaphylaxis ........................................67 4.4. Review questions to chapter 4 ...................................................69 Chapter 5. Clinical cases .....................................................................73 Answers to test tasks and clinical cases...........................................77 References ............................................................................................79 Appendix A. Allergic anamnesis card ................................................81
INTRODUCTION This course material aid covers current issues in clinical allergology. Allergic diseases are a serious problem of public health affecting a large part of the population. The incidence of allergic diseases continuously increases every year, both among adults and children. Allergopathology is encountered not only in the practice of allergologists and immunologists, but also in the practice of doctors of other specialties. These diseases require comprehensive understanding of the underlying immunological mechanisms for their effective diagnosis and treatment. This course material aid is intended for students who are studying medicine at a medical university. The current manuals and textbooks on immunology and allergology are too voluminous and complex, which causes certain difficulties for students; the main task of this course material aid is to present the basics of clinical allergology in an accessible and brief form. The material is divided into 5 parts. The first part provides general information about allergic diseases, risk factors, allergens, and immunological mechanisms. The second part deals with current issues in the diagnosis of allergic diseases. Part 3 contains treatment guidelines for allergic diseases. Part 4 provides information on the most topical issues of private allergology – drug allergy and anaphylaxis, as well as emergency treatment for anaphylaxis. At the end of chapters 1–4 is a number of test tasks which students will need to answer in order to check knowledge of the subject. The fifth chapter contains situational exercises to develop the students’ clinical thinking.
CHAPTER 1 IMMUNOLOGY OF ALLERGY Von Pirquet, who recognized that in both protective immunity and hypersensitivity reactions antigens had induced changes in reactivity, introduced the term “allergy” in 1906. Allergy is now used to describe a hypersensitivity reaction initiated by immunologic mechanism [7]. Allergies are a number of conditions caused by hypersensitivity of the immune system to something in the environment that usually causes little or no problem in most people. Allergic diseases are common, and their prevalence is increasing to epidemic proportions. In both industrialized and industrializing countries, they affect between 10–50% of the world’s population, having a noticeable impact on patients’ quality of life and incurring significant costs. Allergic diseases can occur at almost any age, some allergies are most likely to develop for the first time in particular age groups. The prevalence of childhood allergic diseases, such as allergic asthma, allergic rhinitis, and atopic dermatitis, has increased exponentially [10, 15, 16]. Atopic march, sometime called allergic march, refers to the natural history or typical progression of allergic diseases that often begins early in life. As the child grows, so also their atopy, for example – eczema, is most likely to occur between birth and 3 months of age. Food allergy is most common in second year of life, nasal allergy manifests itself between ages of 3 and 7 years. Asthma onset most likely to occur when a youngster is between 7 to 14 years [19]. 1.1. Factors contributing to allergies Among them are: – Genetics. Hereditary predisposition to allergies is reflected in the term “atopy,” introduced to refer to “allergic constitution” – a genetically mediated predisposition to allergic reactions. Familial predisposition to allergies is associated with polygenic inheritance. Different genes provide: the ability of the immune system to develop a primary immune response with the production of IgE to a particular allergen; the ability of the immune system
to “build up” a high level of specific IgE; high functional activity of T-helper type II in the production of IL-4 and IL-5; high reactivity of the bronchi and skin [8, 10, 16]. – Allergens exposure. The likelihood of developing allergies could potentially be decreased through exposure to microbes in the early stages of childhood. A plausible reason for the higher occurrence of asthma and other atopic diseases in industrialized nations is the relatively lower rate of infections or exposure to microbial products in these countries. A variety of epidemiologic data demonstrate that being exposed to environmental microbes during early childhood, particularly those found on farms and not in cities, is linked to a lower occurrence of allergic disease. The hygiene hypothesis was formulated based on this evidence, proposing that exposure to environmental and commensal microbes and infections during early-life and even perinatal stages encourages a regulated immune system maturation, possibly leading to the early development of regulatory T cells. Consequently, individuals who experience early-life exposure to environmental and commensal microbes and infections are less inclined to develop Th2 responses to noninfectious environmental antigens, and therefore, less prone to developing allergic diseases later in life. Infections caused by respiratory viruses and bacteria can contribute to the development of asthma and can worsen pre-existing asthma. Up to 80% of asthma attacks in children are believed to occur following respiratory viral infections. Although it may appear inconsistent with the hygiene hypothesis, the infections linked to asthma are caused by human pathogens that can potentially harm pulmonary mucosal barriers. The evidence that supports the hygiene hypothesis concentrates on exposure to various environmental bacteria that may not necessarily cause tissue damage. Some epidemiologic studies indicate that a failure to colonize the respiratory or gastrointestinal tract early in life by particular commensal microbes can increase the risk for respiratory viral infections that induce asthma [8, 10]. – Environmental pollution. Urbanization. Normally, the bronchial epithelium produces mediators that reduce the bronchoconstrictor effect. Under the influence of pollutants (NO2, SO2), the airway epithelium is damaged and neuropeptides are released, which triggers the neurogenic component of inflammation. Pollutants also contribute to the activation of arachidonic acid metabolism and suppression of antioxidant defenses. Pollutants activate bronchial epithelial cells with formation and secretion of pro-inflammatory cytokines
(IL-8, tumor-necrotizing factor). Exhaust particles also activate airway epithelial cells with release of pro-inflammatory cytokines. Tobacco smoke is not only a respiratory irritant. It weakens the protective functions of the mucous membranes of the respiratory tract, contributes to easier penetration of allergens, and contributes to the development of bronchial hyperresponsiveness. Tobacco smoke has cross-allergenic properties with plant pollen [10, 13, 16]. To this, one can add the following factors: – The peculiarities of infant nutrition, in particular early transfer to artificial feeding. – Eating disorders in adults (irregular intake of food, violation of the ratio between the amount of food products, abuse of one type of food) [13 15, 16, 17]. 1.2. Allergens. Characteristic and classification An allergen is a type of harmless antigen that causes an abnormally elevated immune response in the sensitized body and to which most healthy people are tolerant. Properties of the allergens: – Relatively small molecular mass. – Capacity of sorption and aggregation in small particles thus diffusing mucous secrets and integumentary tissues without evident defects of the latter. – High solubility and easy elution in liquid media of organism. – In vivo chemical stability (allergens do not metabolize easily at least). – Among proteins the most frequent allergens are enzymes, proteases. Non-protein allergens are distinguished by their capacity to join protein compounds of own organism (haptens) [15, 16, 17]. Allergens are able to produce a small effect. For instance, significant pathogenic total dosing of ambrosia allergen is 1 mcg per year. The broadest definition of an allergen is that it is any molecule that binds IgE antibodies. – A major allergen is an allergen that is recognized by IgE antibodies of >50% of patients allergic to the allergen source. – A minor allergen is recognized by <50% of the allergic population [7, 17].
All allergens fall into two large groups: – endoallergens formed within the body (they can be cells damaged by infection, chemical, physical or other influences); – exoallergens – substances that affect a person from the outside. In turn, exoallergens are divided into two large groups: infectious and noninfectious nature [15, 17]. Infectious allergens include antigens of bacterial, viral, fungal, proto zoan and helminth antigens. Allergic reactions mainly occur upon contact with opportunistic and non-pathogenic microorganisms, less often with pathogens [17]. Non-infectious allergens include pollen, food, household, epidermal, insect, medicinal and industrial allergens. Allergens are divided by the way they enter the body – inhalation (aeroallergens), ingestion, injection, skin contact. Allergens are classified according to their origin: – Animal products (Fel d 1 (allergy to cats), fur and dander, cockroach calyx, wool, dust mite excretion). – Foods (celery and celeriac, corn or maize, eggs (typically albumen, the white), fruit, pumpkin, eggplant, legumes, beans, peas, peanuts, soybeans, milk, seafood, sesame, soy, tree nuts, pecans, almonds, wheat). – Insect stings (bee sting venom, wasp sting venom, mosquito stings). – Mold spores. – Metals (nickel, chromium). – Plant pollens (grass – ryegrass, Timothy grass; weeds – ragweed, plantago, nettle, Artemisia vulgaris, Chenopodium album; sorrel, trees – birch, alder, hazel, hornbeam, Aesculus, willow, poplar, Platanus, Tilia, Olea, Ashe juniper, Alstonia scholaris). – Drugs (penicillin, sulfonamides). – Other (latex, wood) [15, 17, 19]. 1.3. Mechanisms and classification of hypersensitivity reactions Adaptive immunity serves the important function of host defense against microbial infections, but immune responses are also capable of causing tissue injury and disease.
Disorders caused by immune responses are called hypersensitivity diseases. This term arose from the clinical definition of immunity as “sensitivity,” which is based on the observation that an individual who has been exposed to an antigen exhibits a detectable reaction or is “sensitive” to subsequent encounters with that antigen. Hypersensitivity is exaggerated immune responses of detriment to the host. They are classified according to the system devised by Gell and Coombs. Hypersensitivity diseases are commonly classified according to the type of immune response and the effector mechanism responsible for cell and tissue injury (Figure 1): – type I immediate hypersensitivity; – type II antibody-mediated hypersensitivity; – type III immune complex-mediated hypersensitivity; – type IV cell-mediated hypersensitivity [1, 10, 16]. Regardless of the immune mechanisms involved, hypersensitivity reactions can be divided into two phases: a sensitization phase and a detrimental effector phase. Depending on the length of time between the beginning of contact of the sensitized organism with the antigen and the occurrence of clinical manifestations, allergic reactions are divided: – immediate type – develops within 15–20 min or sooner); – late (postponed) allergic reactions – develop within 4–6 hrs; – delayed allergic reactions – develop within 48–72 hrs [10, 12, 11]. Hypersensitivity type I Immediate hypersensitivity is an IgE antibody – and mast cell-mediated reaction to certain antigens that causes rapid vascular leakage and mucosal secretions, often followed by inflammation (Figure 2). Disorders in which IgE-mediated immediate hypersensitivity is prominent are also called allergy, or atopy, and individuals with a propensity to develop these reactions are said to be atopic. Immediate hypersensitivity may affect various tissues and may be of varying severity in different individuals. Sensitization phase The sensitization phase of type I immediate hypersensitivity reactions occurs when antigen exposure induces IgE production with IgE binding to FcεR on mast cells and basophils.
Figure 1 ‒ Types of hypersensitivity reactions [1] Note. In the four major types of hypersensitivity reactions, different immune effector mechanisms cause tissue injury and disease. CTLs – cytotoxic T-lymphocytes; Ig – immunoglobulin.
Antibodies IgE, rather than other isotypes, are produced depending on the CD4+ T-cell-derived cytokines present in the B-cell microenvironment during its activation. T-cell clones, specific for defined allergens and isolated from atopic individuals, are predominantly a Th2 phenotype associated with production of the cytokines IL-4 and IL-10, rather than IL-2 and IFNγ. The presence of IL-4/IL-10 during T-dependent B-cell activation induces isotype switching to IgE. Antibodies IgE bind to high affinity Fcε receptors present on mast cells and basophils, “awaiting” re-exposure to the initiating antigen. Effector phase Tissue damage is caused by inflammatory mediators (histamine, prostaglandins, leukotrienes, and platelet activating factor) released from mast cells and basophils following antigen binding to cell bound IgE. These substances induce increased vascular permeability, vasodilatation, and smooth muscle contraction, either locally or systemically, depending on the site of antigen exposure. Latephase The immediate wheal and flare reaction is followed 2 to 4 hrs later by a late phase reaction consisting of the accumulation of inflammatory leukocytes, including neutrophils, eosinophils, basophils, and Th2 cells. Figure 2 ‒ The sequence of events in immediate hypersensitivity [1]