Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by dry, itchy skin lesions. It is associated with elevated IgE levels and a family history of atopic diseases. The causes involve genetic susceptibility and environmental triggers that disrupt the skin barrier and promote a TH2-mediated immune response. Treatment focuses on identifying and avoiding triggers while improving the skin barrier with emollients and controlling inflammation with topical corticosteroids and calcineurin inhibitors. New targeted therapies that block cytokines and immune cells involved in AD pathogenesis are under investigation.
hanifin and rajka criteria, entymology, definition of AD, atopy, etiopathogenesis of AD, genetics in AD, filaggrin, epidermal barrier dysfunction, atopic march, hygiene hypothesis, infantile phase of AD, childhood phase of AD, adult phase of AD, pityriasis alba, denne morgan folds, dirty neck appearence, nipple dermatitis, hanifin and rajka criteria, UK refinement of hanifin and rajka criteria, millenium criteria of AD, japanese dermatological association criteria, management of AD, wet wrap therapy,
hanifin and rajka criteria, entymology, definition of AD, atopy, etiopathogenesis of AD, genetics in AD, filaggrin, epidermal barrier dysfunction, atopic march, hygiene hypothesis, infantile phase of AD, childhood phase of AD, adult phase of AD, pityriasis alba, denne morgan folds, dirty neck appearence, nipple dermatitis, hanifin and rajka criteria, UK refinement of hanifin and rajka criteria, millenium criteria of AD, japanese dermatological association criteria, management of AD, wet wrap therapy,
this ppt is about how to approach to a patient with non syndromic congenital ichthyosis..slide 32 is overall summary to approach to a patient with ichthyosis and last two slides are just about acquired ichthyosis..
by dr zuhaib alam mehsud,dermatology unit Hmc PESHAWAR
Erythroderma is defined as the scaling erythematous dermatitis involving 90% or more of the cutaneous surface.
Also known as exfoliative dermatitis
Idiopathic exfoliative dermatitis – also known as the “red man syndrome”, is characterized by marked palmoplantar keratoderma, dermatopathic lymphadenopathy,increased IgE.
Increased skin perfusion leads to
Temperature dysregulation >
Resulting in skin loss and hypothermia >
High output state >
Cardiac failure
BMR raises to compensate for heat loss
Increased dehydration due to transpiration (similar to burns)
All lead to negative nitrogen balance and characterized by edema, hypoalbuminemia, loss of muscle mass.
A discussion on various photodermatoses including sun burns, porphyria, actinic chelitis, hydroa vacciniforme and chronic actinic dermatitis. Sun tan and skin color types. Affect of Sunlight on the skin. Useful for medical residents, dermatologists and nurse. Useful in exam preparation.
this ppt is about how to approach to a patient with non syndromic congenital ichthyosis..slide 32 is overall summary to approach to a patient with ichthyosis and last two slides are just about acquired ichthyosis..
by dr zuhaib alam mehsud,dermatology unit Hmc PESHAWAR
Erythroderma is defined as the scaling erythematous dermatitis involving 90% or more of the cutaneous surface.
Also known as exfoliative dermatitis
Idiopathic exfoliative dermatitis – also known as the “red man syndrome”, is characterized by marked palmoplantar keratoderma, dermatopathic lymphadenopathy,increased IgE.
Increased skin perfusion leads to
Temperature dysregulation >
Resulting in skin loss and hypothermia >
High output state >
Cardiac failure
BMR raises to compensate for heat loss
Increased dehydration due to transpiration (similar to burns)
All lead to negative nitrogen balance and characterized by edema, hypoalbuminemia, loss of muscle mass.
A discussion on various photodermatoses including sun burns, porphyria, actinic chelitis, hydroa vacciniforme and chronic actinic dermatitis. Sun tan and skin color types. Affect of Sunlight on the skin. Useful for medical residents, dermatologists and nurse. Useful in exam preparation.
Atopic dermatitis (AD), also known as atopic eczema, is a long-term type of inflammation of the skin (dermatitis). It results in itchy, red, swollen, and cracked skin. Clear fluid may come from the affected areas, which often thickens over time. While the condition may occur at any age
Immunology Pathway of During Autoimmune Disease: A Review Articlekomalicarol
Dermatitis herpetiformis or also known as
duhring disease is a rare autoimmune vesicobulosa disease, specific and recurrent chronic in nature and has a relationship with celiac
disease and gluten-sensitive enteropathy. The diagnosis of dermatitis herpetiformis is based on a combination of physical examination, routine histopathological examination, immunofluorescence
examination, and serological testing. The typical histopathological appearance of dermatitis herpetiformis when examined using
a light microscope is a subepidermal cleft with neutrophils and
several eosinophils in the papillary dermis. immunofluorescence
examination is an examination that is also important for definitive
diagnosis.
Course director, Anthony J. Mancini, MD, FAAP, FAAD, prepared atopic dermatitis infographics for this CME activity titled "Improving the Care of Young Patients With Atopic Dermatitis: Recognizing the Differences Between Children, Adolescents, and Adults." For the full presentation, monograph, complete CME information, and to apply for credit, please visit us at http://bit.ly/320x7ZG. CME credit will be available until July 9, 2020.
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).
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
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
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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.
2. Reference
DERMATOLOGY Text Book. 3rd Edition 2012. Eds: Jean L Bolognia, Joseph L Jorizzo, Julie V Schaffer. ElSevier Publishing
Atopic Dermatitis
3. DEFINITION OF ATOPY
The term “atopy” is tightly linked to the presence of allergen-specific IgE antibodies in the serum, as documented by positive fluorescence enzyme immunoassays (previously radioallergosorbent [RAST] tests) or skin prick tests.
Atopic Dermatitis
4. SPECTRUM OF AD
Spectrum of AD
An IgE associated or allergic form of dermatitis corresponds to AD in the strict sense (formerly known as extrinsic AD
The remaining 20–30% of patients with the clinical phenotype of AD who have no evidence of IgE-sensitization are categorized as having a non-IgE-associated or non-allergic form of dermatitis (formerly known as intrinsic AD).
Atopic Dermatitis
6. PATHOGENESIS of Atopic Dermatitis
AD
Genetic
Environ- mental
Immunologic Mechanisms
Epidermal Barrier Dysfunction
Atopic Dermatitis
7. GENETICS
The entities in the atopic triad cluster together in families.
AD is a complex genetic disease, and both gene– gene and gene–environment interactions have pathogenic roles.
Existence of genes specific to ADermtitis
Genes encoding proteins with immunologic functions
Genes encoding epidermal proteins
Atopic Dermatitis
8. Filaggrin
Mutations in the filaggrin gene (FLG), which encodes a protein that aggregates keratin filaments during terminal differentiation of the epidermis.
The presence of the filaggrin variants is correlated with early-onset, relatively severe, “extrinsic” (specific IgE-associated) AD that tends to persist into adulthood.
Affected individuals have an increased risk of eczema herpeticum and peanut allergies as well as a propensity to later develop asthma
Atopic Dermatitis
9. Epidermal Barrier Dysfunction
The consequence of epidermal barrier dysfunction and an altered stratum corneum leading to increased transepidermal water loss
Cork et al. Journal of Investigative Dermatology
(2009) 129:
1892–1908
Atopic Dermatitis
10. IMMUNOLOGIC MECHANISMS
Main component/player
Disturbed Item
Degradation of corneodesmosomes, deficiency of Filaggrin
Impairment Of The Epidermal Barrier
Increased epidermal protease activity, dyscohesion
Mechanisms Of Inflammation In The Absence Of IgE-mediated Sensitization
high levels of thymic stromal lymphopoietin (TSLP) by keratinocytes leads to Th2 polarization
Epicutaneous Sensitization
Langerhans cells (LCs) and inflammatory dendritic epidermal cells:
present allergens to Th1/Th2 cells
Role Of Dendritic Cells (Dcs)
TH 2 predoninates in acute,
Th1 in chronic
T-cell Responses, Cytokines And Chemokines
decreased levels of antimicrobial peptides, S. aureus adherence to skin
Role Of Microbial Colonization
circulating IgE antibodies
Role Of Autoimmunity
Atopic Dermatitis
11. PRURITUS & IL-31
Classic antihistamines are ineffective in AD
neuropeptides, proteases, kinins, and cytokines such as interleukin (IL)-31 are known to induce itch.
IL-31 is strongly pruritogenic and exerts its biologic activity through a heterodimeric receptor composed of the IL-31 receptor A and oncostatin M receptor β protein, both of which are overexpressed in lesional skin of AD.
Atopic Dermatitis
12. CLINICAL FEATURES
Disease Course
In childhood AD (age 2 to 12 years)
Adult/adolescent AD (age >12 years)
Infantile AD
(age <2 years)
Senile AD (age >60 years)
Atopic Dermatitis
13. Clinical diagnosis of AD
Atopic stigmata
1.Xerosis
2.Keratosis Pilaris
3.Ichthyosis Vulgaris
4.Dennie Morgan lines
5.Periorbital darkening
6.White dermoographism
Pruritus
eczematous skin lesions in typical age-specific distribution patterns,
a chronic or chronically relapsing course,
Early age at onset,
A personal and/or family history of atopy.
13
14. Associated Features
Associated Complications
Pityriasis Alba
Pruritus
Atopic Stigmata
Infections, esp eczema herpeticum
Occular complications
14
15. Diagnostic criteria of AD
Validated scores to assess the severity of AD
1.EASI (Eczema Area Scoring Index)
2.SCORAD (SCORing Atopic Dermatitis)
3.POEM (Patient- Oriented Eczema Measure
Differential Diagnosis
Seborrheic dermatitis in infants.
Allergic Contact Dermatitis
Mycosis Fungoides
Pathology: mainly to exclude other mimics (as MF).
15
16. MANAGEMENT CONCEPTS
Avoidance of trigger factors, including irritants, relevant allergens and microbial agents.
Skin care that aims to compensate for the genetically determined impaired epidermal barrier function.
Anti-inflammatory therapy to control subclinical inflammation as well as overt flares.
In selected cases, adjunctive or complementary modalities.
16
17. Avoidance of Trigger Factors
Intermittent use of intranasal mupirocin ointment over a 1- to 3-month
S. aureus strains that colonize and superinfect patients with AD are more likely to be susceptible to first-generation cephalosporins (e.g.cephalexin)
Cleansers and emollients containing antiseptics???
use mild, non-alkaline cleansers
Atopic Dermatitis
18. Avoidance of Trigger Factors
According to Patch test/RAST IgE test
Avoid House mites
Avoid Food Allergens
A continuous basic therapy with emollients, even in periods and sites in which the AD is not active.
Atopic Dermatitis
19. Topical Anti-inflammatory Therapy
The corticosteroid with appropriate potency to quickly gain control of the flare, continuation of daily therapy until active dermatitis minimized.
In moderate to severe AD, risk of relapse can be significantly reduced by proactive maintenance with twice-weekly application of a mid-potency topical corticosteroid.
Topical calcineurin inhibitors (TCIs)
Atopic Dermatitis
20. Phototherapy: UVA1, UVA combined with UVB, and narrowband UVB
Narrowband UVB and high-dose UVA1 can both be helpful for chronic AD, and UVA1 may also be useful in the treatment of acute flares.
T cell apoptosis, reduction of dendritic cells, and modified cytokine expression, (e.g. decreased IL-5, IL-13 and IL-31 with UVA1).
UVB reduces S. aureus colonization of the skin in AD patients.
Atopic Dermatitis
21. Systemic Anti-inflammatory Therapy
Systemic corticosteroids should be avoided
Mycophenolate mofetil (1–2.5 g/day); 25–50 mg/kg/day in children
Azathioprine 2–3.5 mg/kg/day, watch for TPMT deficiency
Oral cyclosporine typically leads to rapid improvement of skin disease and associated pruritus (5 mg/kg/day, reduced to 2mg /kg/day)
Atopic Dermatitis
22. Adjunctive Pharmacologic Therapy
Alternative/Complementary Therapy
Sedating antihistamines (e.g. hydroxyzine)
Non-Sedating antihistamines in very high doses.
Leukotriene inhibitors
Antimicrobial agents
Dietary lipid supplements (e.g. evening primrose and borage oils)
Chinese herbal therapy
Hypnotherapy
22
23. Targeted Molecular Therapy (“Biologics”)
Emerging Therapies
Anti-IgE monoclonal antibody omalizumab, which inhibits the binding of IgE to its high-affinity receptor (FcεRI), is FDA-approved for the treatment of asthma in patients ≥12 years.
The anti-CD20 monoclonal antibody rituximab (administered via 2 IV infusions separated by 2 weeks), which inhibits mature B cells
mepolizumab inhibits IL-5, a crucial factor for growth and differentiation of eosinophils. Although mepolizumab can decrease the eosinophil count in patients with AD, it failed to lead to a significant clinical improvement
Goals of blocking factors such as cytokines involved in the regulation of IgE synthesis (e.g. IL-4) or chemoattractant receptor- homologous molecule expressed
on Th2 cells (CRTH2).
23
24. Primary Prevention
Educational Programs
For infants with a family history of atopy, exclusive breastfeeding during the first 4-6 months.
Administration of probiotics (e.g. lactobacilli) or prebiotics (nondigestible oligosaccharides that promote the growth of desirable bacteria) to pregnant mothers and infants led to decreased frequencies of AD at 1 to 4 years of age.
Accepting “control” rather than a “cure”
Parents are anxious about corticosteroid use, which often leads to delayed, inadequate treatment
24
25. Resumé: The APPROACH TO AD
Management should not be concentrated solely on the treatment of acute flares, but also be directed towards improving the underlying genetically determined epidermal barrier dysfunction and preventing active dermatitis (e.g. via maintenance therapy).
Such an approach could potentially block the sensitizations and ongoing inflammation that drive the atopic march forward
Atopic Dermatitis