Dr. C. Handique presented on drug hypersensitivity reactions. The presentation discussed the different types of hypersensitivity reactions including type I-IV reactions. Type I reactions are IgE mediated and can cause anaphylaxis. Type II reactions involve cytotoxic antibodies. Type III reactions involve immune complex formation. Type IV reactions are mediated by T-cells and macrophages. Common triggers of drug hypersensitivity included antibiotics and NSAIDs. Diagnosis is based on clinical symptoms and discontinuing the offending drug is the primary treatment approach.
Allergies are becoming increasingly common in Australia for a range of reasons. These slides were developed for a course created to help the community better understand and more effectively manage allergies.
The fixed dose combination of trimethoprim and sulfamethoxazole is called cotrimoxazole.
Adverse Drug Reaction, Spectrum, Resistance and Use of Cotrimoxazole.
Diabetes mellitus is a clinical syndrome characterized by an increase in plasma blood glucose (hyperglycemia).
Diabetes has many causes but is most commonly due to type 1 or type 2 diabetes
about drugs that are causing hypersensitivity reaction in human body systems. it include aspirin,sulfonamide,pencillin,their symptoms,dianosis,prevention etac included
Drug allergy is the non-immune-mediated reaction that is often caused by the intolerance of drug . To explain about the allergic reaction and to help people avoid a major hard you can easily take the help of the Drug allergy PPT templates online. More info: http://bit.ly/1fiS4nQ
Allergies are becoming increasingly common in Australia for a range of reasons. These slides were developed for a course created to help the community better understand and more effectively manage allergies.
The fixed dose combination of trimethoprim and sulfamethoxazole is called cotrimoxazole.
Adverse Drug Reaction, Spectrum, Resistance and Use of Cotrimoxazole.
Diabetes mellitus is a clinical syndrome characterized by an increase in plasma blood glucose (hyperglycemia).
Diabetes has many causes but is most commonly due to type 1 or type 2 diabetes
about drugs that are causing hypersensitivity reaction in human body systems. it include aspirin,sulfonamide,pencillin,their symptoms,dianosis,prevention etac included
Drug allergy is the non-immune-mediated reaction that is often caused by the intolerance of drug . To explain about the allergic reaction and to help people avoid a major hard you can easily take the help of the Drug allergy PPT templates online. More info: http://bit.ly/1fiS4nQ
Self-Medication is dangerous. Self-Medication may lead to Misdiagnosis of an illness, Drug interactions, Insufficient dosage, Habituation, Allergic reactions, etc. Patients should should not Self-Medicate and consult a doctor to avoid these hazards. Asking doctor a medical query has never been so easy! Lybrate has a pool of doctors available online to offer you credible medical advice. To avail an easy access to doctors across the country, anytime, anywhere download Lybrate apps and get going.
Drug allergy is the term for a group of symptoms caused by an allergic reaction. An allergic reaction occurs when your immune system mistakes the drug for a harmful substance and mounts an inflammatory response that actually harms rather than protects you. Any medication — over-the-counter, prescription or herbal — is capable of inducing a drug allergy. However, a drug allergy is more likely with certain medications
Hypersensitivity reactions for Medical StudentsNCRIMS, Meerut
Hypersensitivity (animated) for MBBS Students
Hypersensitivity refers to undesirable (damaging, discomfort-producing and sometimes fatal) reactions produced by the normal immune system.
Hypersensitivity reactions require a pre-sensitized state of the host.
Four types of hypersensitivity
Type I – anaphylactic
Type II – cytotoxic
Type III – immune complex mediated
Type IV – contact, tuberculin and granulomatous
Anaphylaxis is defined as a life-threatening allergic reaction set in action by a wide range of antigens and involving multiple organ systems.
The true incidence is difficult to estimate, but in 1973 the Boston Collaborative Drug Surveillance Program reported six anaphylactic reactions and 0.87 deaths from anaphylaxis per 10,000 patients.
Reactions to insect stings alone are responsible for at least 50 deaths in the United States each year.
These figures reveal the importance of continued research into the biology of anaphylaxis along with developing new (and improving existing) therapies.
Drug induced Hypersensitivity reactions Presentation by Supriya SUCPPARUL UNIVERSITY
Injurious or pathologic, immune reactions are called Hypersensitivity Reactions
Hypersensitivity reactions may occur in two situations.
First responses to foreign antigens may be dysregulated or uncontrolled, resulting in tissue injury.
Second the immune responses may be directed against self antigens, as a result of the failure of self-tolerance (autoimmunity).
Hypersensitivity/ Allergy ppt by DR.C.P.PRINCEDR.PRINCE C P
Hypersensitivity refers to undesirable reactions produced by the normal immune system, including allergies .
These reactions may be damaging, uncomfortable, or occasionally fatal.
ALLERGEN: non-parasite antigens that can stimulate a hypersensitivity response
Occurs in two stages : sensitization phase and shocking phase
Classified into Immediate and Delayed hypersensitivity based on time required to develop the symptoms
Type I hypersensitivity is also known as immediate or anaphylactic hypersensitivity.
The reaction may involve skin(urticaria and eczema), eyes(conjunctivitis), nasopharynx (rhinorrhea, rhinitis), bronchopulmonary tissues(asthma) and gastrointestinal tract (gastroenteritis).
Hypersensitivity (Allergy) - Drug allergy, Contact dermatitis, Allergic asthmaAvinandan Jana
A condition in which the immune system reacts abnormally to a foreign substance.
Drug allergy
An abnormal reaction of the immune system to a medication.
Food allergies
An unpleasant or dangerous immune system reaction after a certain food is eaten.
Contact dermatitis
A skin rash caused by contact with a certain substance.
Latex allergy
An allergic reaction to certain proteins found in natural rubber latex.
Allergic asthma
Asthma triggered by exposure to the same substances that trigger allergy symptoms.
Seasonal allergies
An allergic response causing itchy, watery eyes, sneezing and other similar symptoms.
Animal allergy
An abnormal immune reaction to proteins in an animal's skin cells, saliva or urine.
Anaphylaxis
A severe, potentially life-threatening allergic reaction.
Allergy to mold
An abnormal allergic reaction to mould spores.
Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
3. Hypersensitivity refers to undesirable reactions produced
by the normal immune system, including allergies
and autoimmunity.
These reactions may be damaging, uncomfortable, or
occasionally fatal.
Hypersensitivity reactions require a pre-sensitized
(immune) state of the host.
6. It is an immunologically mediated reaction producing
symptoms unrelated to the pharmacodynamic profile of the
drug, generally occuring with much smaller doses and have
a different time course of onset and duration.
Drug hypersensitivity reactions account for about 1/6th of all
adverse drug reactions.
Drug hypersensitivity reactions can become manifest in a
great variety of clinical symptoms and diseases, some of
which are quite severe and even fatal.
7. The most common allergic reactions occur in the skin and
are observed in 2-3% of hospitalized patients.
Antibiotics and antiepileptics are the drugs most frequently
causing them.
The risk of sensitization and the severity of clinical
symptoms depend on the state of immune activation of the
individual, the dose and duration of treatment, sex and the
immunogenetic predisposition.
8.
9. Type Mechanism Example
I IgE mediated hypersensitivty Anaphylaxis, urticaria,
asthma
II Cytotoxic, antibody dependent Hemolytic anaemia,
thrombocytopenia,
interstitial nephritis
III Immune complex damage Serum sickness, arthus
reaction, PSGN, SLE
IV Delayed or cellular
hypersensitivity
Contact dermatitis
transplant rejections
11. The IgE system is geared to react to small amounts of
antigens.
Very small amounts of a drug are apparently sufficient to
interact and stimulate these receptor-bound IgE molecules.
The drug causes formation of tissue sensitizing IgE
antibodies that are fixed to mast cells or leucocytes.
The subsequent exposure to drug, degranulates mast cells or
activates leucocytes with release of chemical mediators of
allergy.
12. IgE-mediated reactions to drugs are usually thought to
depend on the prior development of an immune response to a
hapten/carrier complex.
This sensitization phase is asymptomatic and may have
occurred during an earlier drug treatment.
These reactions include anaphylaxis, atopy and asthma.
13.
14. Clinical features
IgE-mediated reactions can cause mild to severe, even lethal,
diseases.
Symptoms may start with palmar, plantar, genital, and axillar
itch, and facial and thoracal redness
They often herald a severe, anaphylactic reaction, developing
rapidly within minutes.
Anaphylactic shock occurs often within 10 to 15 minutes, and
asphyxia due to laryngeal edema often occurs between 15 and
60 minutes.
15.
16. It rely on the formation of complement-fixing IgG
antibodies.
The mediator of type II reactions is IgG/ IgM, complement
or membrane attack complex.
It results when drug binds to RBC and is recognized by IgG
antibody.
The antigen antibody reaction then triggers the lysis of RBC
either by activating the complement system or by the action
of cytotoxic T cells or by phagocytosis by macrophages.
17. It is rare and best documented for high-dose penicillin and
cephalosporin.
Quinine-induced immune thrombocytopenia
It is caused by a remarkable class of IgG and/or IgM
immunoglobulins.
They react with selected epitopes on platelet membrane
glycoproteins, only when the drug is present in its soluble form.
Hemolytic anemia attributed to penicillin and its derivatives,
cephalosporins, levodopa, methyldopa, quinidine and some
antiinflammatory drugs is also a type II reaction to these drugs
18.
19. Soluble antigen antibody forms soluble complexes which
are deposited on vascular endothelium and activate
complement
This occurs within 1-2 weeks of drug administration
It is characterized by allergic inflammatory reactions in
tissues, glomerular nephritis and serum sickness.
Formation of immune complexes is a common event in the
frame of a normal immune response and does not normally
cause symptoms.
20. Immune complexes may be formed during drug treatment :
either if the drug forms a hapten-carrier complex and thus
gives rise to an immune reaction,
or if the drug is a (partly) foreign protein, which elicits an
immune reaction itself (e.g. a chimeric antibody).
21.
22. Clinical features
The clinical symptoms of a type III reaction may be
hypersensitivity, small vessel vasculitis and/or serum
sickness
Serum sickness was first described with the use of
heterologous or foreign serum for passive immunizations
Hypersensitivity vasculitis reportedly has an incidence of 10–
30 cases per million people per year.
Most reports concern cefaclor, followed by trimethoprim-
sulfamethoxazole, cephalexin, amoxicillin, NSAIDs and
diuretics.
23.
24.
25. These reactions are mediated by T cells and monocytes/
macrophages rather than by antibodies.
The activation of sensitized T cells results in the release of
cytokines which activate macrophages, granulocytes and
natural killer cells
The term delayed is used to differentiate a secondary cellular
response, which appears 48-72 hours after antigen exposure,
from an immediate hypersensitivity response.
Often mentioned disorders are contact dermatitis, chronic
transplant rejections and hypersensitivity pneumonitis
26.
27. They are a pathogenetically poorly defined problem
Most of these reactions resemble the clinical features of
milder forms of immediate, IgE-mediated reactions, but
some reactions cause anaphylaxis and can be lethal.
Detection of specific immune mechanism is negative.
NSAID induced pseudoallergic reactions seem to arise less
rapidly often >15 minutes after intake than true IgE-
mediated allergies
They may require higher drug doses than true IgE-mediated
reactions
28. Neither IgE nor Tcell reactions are evident.
The reactions are recurrent, but provocation tests often
remain negative.
The most common form of such reactions is related to
NSAIDs.
29.
30. Drug reactions commonly manifest
with dermatologic symptoms
The most common dermatologic
manifestation of drug reaction are
morbilliform rashes.
Urticaria is typically a
manifestation of a truly allergic,
Type I reaction, but it may appear
with Type III or pseudoallergic
reactions as well.
31. Severe nonallergic, hypersensitivity cutaneous reactions
include erythema multiforme, Stevens-Johnson syndrome,
and toxic epidermal necrolysis.
Eczematous rashes are most commonly associated with
topical medications and usually represent contact dermatitis,
which is classified as Type IV reaction to a drug exposure.
32.
33. Anaphylaxis is a serious allergic reaction that is rapid in
onset and may cause death.
Anaphylaxis typically presents many different symptoms over
minutes or hours with an average onset of 5 to 30 minutes if
exposure is intravenous and 2 hours for foods.
The most common areas affected include
skin, respiratory, gastrointestinal, heart and vasculature and
central nervous system with usually two or more being
involved.
34.
35.
36. Treatment for anaphylaxis
Immediate treatment with adrenaline is imperative.
Adrenaline 0.5 mg im is given. It is to be repeated every 5-10
min in case patient doesn’t improve.
H1 antihistaminic chlorpeniramine 20 mg im/slow iv acts as
an adjuvant.
Intravenous hydrocortisone sodium succinate 200 mg should
be added in severe/recurrent cases.
It may be followed by oral prednisolone for 3 days.
37. Anaphylactoid reactions refer to clinically similar events as
anaphylaxis but are not mediated by IgE.
It is also known as pseudoanaphylaxis.
They are a type of anaphylaxis that does not involve an
allergic reaction but are due to direct mast
cell degranulation.
40. Multivalency
Generally, an antigen must be presented to the immune
system in a multivalent form to elicit a specific immune
response.
Valency refers to the number of binding sites available to
bind antibody.
Multivalency is necessary to ensure cross-linking of
receptors on the surface of cells, which then causes
transduction of the signal within the cell and the initiation of
an immune response.
41. Drugs alone are poor stimulators of immune responses due
to their simple structure and low molecular weight.
Drugs can fulfill the requirement for multivalency and elicit
an immune response in two ways:
(1) Form hapten-carrier complexes and
(2) Be converted into reactive intermediates.
42. Haptenization
A hapten would be a particular drug, which would be
immunogenic in protein-conjugated but not free form.
An example would be penicillins and other betalactams that
bind covalently to proteins.
43. Conversion into reactive intermediates
This may occur via drug metabolism in the liver or
elsewhere.
This is the case with sulfonamides, which are acetylated
and oxidated to yield the predominant N4-sulfonamidoyl
hapten.
44. Chronic diseases that require continuous or frequent courses of
therapy with the same or cross-reactive drugs
Some allergic reactions are more likely to occur with certain
infections
Aminopenicillins with EBV infection,
Sulfonamides with AIDS patients
Atopy, a genetically determined state of hypersensitivity,
manifested as asthma, hay fever, and atopic dermatitis
History of other drug allergy
45.
46. The diagnosis of drug hypersensitivity is usually based on
clinical judgment, because definitive, confirmatory drug-
specific testing is often difficult.
General criteria for drug hypersensitivity
The patient’s symptomatology is consistent with an
immunologic reaction.
The patient was administered a drug known to cause such
symptoms.
47. The temporal sequence of drug administration and
appearance of symptoms is consistent with drug reaction.
Laboratory data are supportive of an immunologic
mechanism to explain the drug reaction.
48. Lab tests for IgE mediated
reactions
Skin testing
RAST testing
Serum Tryptase
49. Lab tests done for type II cytolytic reactions
50. Lab tests for type III immune complex reactions include
ESR
CRP
ANA
AHA
Complement studies
Tissue immunofluroscence studies
51. Lab tests for type IV
hypersensitivity reaction
Patch test
Lymphocyte proliferation assay
52. The most important and effective measure is the
discontinuation of the offending medication.
Alternative medications with unrelated chemical structures
should be substituted when available.
In the majority of patients, symptoms will resolve within two
weeks if the diagnosis of drug hypersensitivity is correct
53. Additional therapy for drug hypersensitivity reactions is
supportive and symptomatic.
Systemic corticosteroids may speed recovery in severe cases.
Topical corticosteroids and oral antihistamines may improve
dermatologic symptoms.
The severe drug reactions of Stevens-Johnson syndrome and
toxic epidermal necrolysis require additional intensive
therapy.
54. Desensitization is a method to reduce or eliminate an
organism's negative reaction to a substance or stimulus.
It is the loss of responsiveness to the continuing or
increasing dose of a drug
Desensitization is a reversible process that is dependent on
the continued presence of the drug.
It is also drug-dose dependent in that a substantial dose
increase may result in breakthrough allergic symptoms.
55. The starting dose for the drug can be determined by
performing intradermal skin tests with the native drug at a
dose that does not cause a non-specific irritant reaction.
For example, if a 0.02 ml intradermal injection of a drug at
1 mg/ml concentration does not cause a local or systemic
reaction, oral desensitization may be started at the dose
injected
Parenteral desensitization should be using 1/10 or 1/100 of
the dose that was administered intradermally.
57. All forms of natural and semisynthetic penicillins can cause
allergy, but it is more commonly seen after parenteral than oral
administration.
The reported history of penicillin allergy ranges from 1% to
10%.
Anaphylaxis is rare i.e 1 to 4 per 10,000 patients but may be
fatal.
It has been estimated that up to 60% of penicillin-allergic
patients will experience another allergic event if given the drug
again
58. There are two clinical pictures of penicillin allergy, acute
and sub-acute reactions mediated by IgE and IgG antibodies
respectively.
The acute allergic reaction arises immediately or rapidly
within minutes to an hour or two and includes sudden
anaphylaxis.
Sub acute picture may occur 7 to 10 days after penicillin
treatment starts or 1–2 days after repeat therapy. In this
setting the picture is sub-acute and can include urticaria,
fever and arthralgias or arthritis.
59. Major and Minor Determinants
The betalactam ring is unstable and readily acylates lysine
residues in proteins.
The penicilloyl epitope is produced, which is called the
“major determinant”
Penicilloyl IgE responses are associated with urticarial
reactions.
Beta lactams also haptenize covalently through carboxyl
and thiol groups, which results in a variety of “minor”
determinants.
Minor determinant IgE responses are associated with
anaphylaxis
60. Penicillin skin sensitivity testing
A positive skin test indicates the presence of IgE antibodies
to penicillin and immediately excludes the use of it and
related ß-lactam antibiotics
A BPO-polylysine conjugate and penicillin G in a
concentration of 1000U/ml are available for skin testing
It is performed by prick technique-a drop of a dilute
allergenic extract is placed on the skin, which is then pricked
or punctured through the extract, usually by “tenting” up
the skin with the tip of a stylet.
61. Hypersensitivity reactions are the most important adverse
effects of cephalosporins.
Rashes are the most frequent manifestation.
Anaphylactic reactions to cephalosporins are much less
common than anaphylaxis associated with penicillin
About 10% patients allergic to penicillin show cross
reactivity with cephalosporins.
62. Skin testing
Currently there are no reliable cephalosporin allergens
available for skin testing.
A positive Coomb’s test occurs in many patients, but
hemolysis is rare
Allergic reactions to cephalosporins do not appear to
correlate with positive penicillin test reactions.
63. Co-trimoxazole is used extensively in the HIV population for
prophylaxis against Pneumocystis carinii pneumonia.
The overall prevalence of sulfa hypersensitivity in the general
population is approximately 3.3%, while in the HIV population
it is in the range of 17-20%
The incidence of adverse events to cotrimazole is greater than
50% in patients receiving the medication for treatment for
active PCP
64. Sulfa drugs are metabolized in the liver by two pathways:
--oxidative metabolism by the cytochrome p450 system
- acetylation by N-acetyltransferase.
Sulfamethoxazole is predominantly cleared by acetylation
and excreted by active tubular excretion.
The alternative pathway yields a reactive metabolite,
sulfamethoxazole hydroxylamine, which can generate an
immune response
65. Mechanism
The mechanism of hypersensitivity to cotrimoxazole is poorly
understood.
Several hypotheses have been put forward to explain the
predominance of reactions in HIV patients:
◦ slow acetylation in HIV patients
◦ polypharmacy with drugs such as INH and rifampin that
compete for metabolism in the liver
◦ reduced availability of cellular glutathione
66. Hypersensitivity diseases caused by NSAIDs are relatively
common in the population
The prevalence of these reactions in the population varies
between 0.1% and 0.3%
Immunologic reactions to NSAIDs can be subdivided into
immediate and delayed.
Immediate Reactions
Urticaria and Angioedema - acetaminophen, and aspirin
68. Nonallergic Hypersensitivity
It includes Aspirin-induced asthma which is characterized by
asthma, rhinosinusitis, nasal polyposis, and aspirin
hypersensitivity.
Asthmatic reactions induced by NSAIDs occur in 5% to 20%
of adult asthmatic patients.
The pathogenesis seems to involve the combined effects of
chronic inflammation and a pharmacogenetic abnormality
of arachidonic acid metabolism in response to NSAIDs.
69.
70. This reaction typically occurs 7 to 10 days after exposure and
causes fever, arthralgias, and rash.
Mechanism involves drug-antibody complexes and complement
activation.
Some patients have frank arthritis, edema, or GI symptoms.
Symptoms are self-limited, lasting 1 to 2 wk.
β-lactam and sulfonamide antibiotics, iron dextran and
carbamazepine are mostly implicated.
Serum Sickness
71.
72. This disorder may develop when a drug alters the RBC
membrane, uncovering an antigen that induces autoantibody
production.
Antibodies then develop against the red blood cells. The
antibodies attach to red blood cells and cause them to break
down too early.
Drugs that can cause this type of hemolytic anemia include:
Cephalosporins, Dapsone, Levodopa, Levofloxacin,
Methyldopa, Nitrofurantoin , Quinidine
Hemolytic Anaemia
73. This reaction, can start up to 12 wk after initiation of drug
treatment and can occur after a dose increase.
Symptoms may persist or recur for several weeks after stopping
drug treatment.
Patients have prominent eosinophilia and often develop
hepatitis, exanthema, facial swelling, generalized edema, and
lymphadenopathy.
Carbamazepine, phenytoin, allopurinol and lamotrigine are
frequently implicated
DRESS
74. Hydralazine, propylthiouracil and procainamide
can cause an SLE-like syndrome.
It may be mild with arthralgias, fever, and rash or fairly
dramatic with serositis, high fevers, and malaise
The antinuclear antibody test is positive.
Penicillamine can cause SLE and other autoimmune
disorders like myasthenia gravis.
Some drugs can cause perinuclear antineutrophil
cytoplasmic autoantibodies (p-ANCA)–associated vasculitis. .
Other Autoimmune Diseases
75. Here a patient without previous pulmonary disease develops
respiratory symptoms, chest x-ray changes, deterioration of
pulmonary function, histologic changes, or several of these
findings in association with drug therapy.
Depending on the drug, it can cause interstitial fibrosis,
organizing pneumonia, asthma, noncardiogenic pulmonary
edema, pleural effusions, pulmonary eosinophilia,
pulmonary hemorrhage, or veno-occlusive disease
Pumonary Effects
78. Tubulointerstitial nephritis is the most common allergic
renal reaction
It is primary injury to renal tubules and interstitium
resulting in decreased renal function.
The acute form is most often due to allergic drug reactions
or to infections
The symptoms include fever, rash and enlarged kidneys
About 23% of patients have eosinophilia. There may be
hematuria, sterile pyuria or proteinuria
79. The drugs commonly implicated are antibiotics like
methicillin, anticonvulsants, diuretics and NSAIDS.
Corticosteroids are not useful in this setting.
Therapy consists of adequate fluid intake, which can require
several liters of extra fluid.
81. It is a form of a life-threatening skin condition, in which cell
death causes the epidermis to separate from the dermis.
The syndrome is thought to be a hypersensitivity complex that
affects the skin and the mucous membranes
This immune reaction can be triggered by drugs or infections.
Genetic factors are associated with a predisposition to SJS.
Slow acetylators, patients who are immunocompromised, and
patients with brain tumors undergoing radiotherapy with
concomitant antiepileptics are among those at most risk.
84. A life-threatening skin condition that is usually caused by a
reaction to drugs.
The disease causes the epidermis to detach the dermis, all
over the body.
Microscopically, TEN causes cell death throughout the
epidermis.
Often, the diagnosis is made clinically.
If the clinical history is consistent with Stevens–Johnson
syndrome, and the skin lesion covers greater than 30% of the
body surface area, the diagnosis of TEN is appropriate
86. To conclude..
Drug Hypersensitivity Syndrome is potentially life-
threatening with significant morbidity.
Prompt diagnosis is vital, along with identification and early
withdrawal of suspect medicines.
However many of these drug reactions are pharmacological
reactions rather than hypersensitivity reactions.
So in assessing drug reactions, a detailed clinical history and
careful documentation of reactions are most important.