Melanin is the pigment produced by melanocytes in the skin that determines skin color. It protects the skin from UV damage. Vitiligo is a condition where melanocytes die or stop functioning, causing white patches of skin where no melanin is produced. It can affect any part of the body and is associated with autoimmune diseases. Treatments include cosmetic camouflage, phototherapy (PUVA), topical corticosteroids, and skin grafting. Prognosis varies and vitiligo may continue in cycles of pigment loss and stability.
Rosacea is a chronic (long-term) disease
that affects the skin and sometimes the eyes. The disorder is characterized by
redness, pimples, and, in advanced stages, thickened skin. Rosacea usually
affects the face. Skin on other parts of the upper body is only rarely
involved.
Melasma| Melasma and its Treatment| Facial Pigmentation| Post-Pregnancy Pigm...Dr. Rajat Sachdeva
Melasma, Pigmentation on facial skin, most commonly occur on the face of female and in Dark Skin Races.
Treatment for melasma, Sun protection, avoid waxing, Tretinoin, Hydroquinone, Corticosteroid, Azeloic Acid, Glycolic Acid, Chemical Peels, Microdermabrasion, Laser Intensed Pulse Light,
Skin warts are benign tumours caused by infection of keratinocytes with HPV, visible as well‐defined hyperkeratotic protrusions. We will explore the detailed types, presentation, and treatment modalities of most common warts.
This is a seminar conducted by 4th year medical student under supervision of a lecturer. Sorry for not attaching the references.
Information were from few textbooks, google and also from previous dermatology posting group's seminar.
Rosacea is a chronic (long-term) disease
that affects the skin and sometimes the eyes. The disorder is characterized by
redness, pimples, and, in advanced stages, thickened skin. Rosacea usually
affects the face. Skin on other parts of the upper body is only rarely
involved.
Melasma| Melasma and its Treatment| Facial Pigmentation| Post-Pregnancy Pigm...Dr. Rajat Sachdeva
Melasma, Pigmentation on facial skin, most commonly occur on the face of female and in Dark Skin Races.
Treatment for melasma, Sun protection, avoid waxing, Tretinoin, Hydroquinone, Corticosteroid, Azeloic Acid, Glycolic Acid, Chemical Peels, Microdermabrasion, Laser Intensed Pulse Light,
Skin warts are benign tumours caused by infection of keratinocytes with HPV, visible as well‐defined hyperkeratotic protrusions. We will explore the detailed types, presentation, and treatment modalities of most common warts.
This is a seminar conducted by 4th year medical student under supervision of a lecturer. Sorry for not attaching the references.
Information were from few textbooks, google and also from previous dermatology posting group's seminar.
Vitiligo is an acquired pigmentary disorder of the skin and mucous membranes characterized by circumscribed depigmented macules and patches that result from a progressive loss of functional melanocytes that are selectively destroyed.
Aquí os dejo una presentación que realicé y entregué a mi profesor de Informática con el objetivo de que la evaluara.
El tema ha sido el que desarrollo en este blog, por lo que os brindo la oportunidad de que la valoréis vosotros mismos.
Vitiligo in Croatia: a case report Vedrana Bulat, Mirna Šitum Department of...VR Foundation
INTRODUCTION
Vitiligo is an acquired chronic disease characterized by depigmented macular patches due to loss of epidermal melanocytes. It affects 1,6% of the general population in Croatia.
Female patients are more affected (53,95%) than male patients, with no difference in the severity of vitiligo. Most of our patients were in generally good health, showing no association of vitiligo with thyroid dysfunction, diabetes mellitus, pernicious anemia nor gonadal failure. Localized form of vitiligo most frequently affects 21 to 28-year-old patients, while generalized form prevails in the age group from 29 to 36 years. Patients older than 77 years of age are very rarely affected. The most common localized type was focal (93,28%), and the most common generalized type was vitiligo vulgaris (53,7%). Most of our patients were admitted in September, probably due to increased contrast between involved and uninvolved skin. Most patients attribute the onset of their disease to specific life events (physical injury, emotional distress, illness or pregnancy).
AIMS
The aim of this case report was to present our patient suffering from vitiligo vulgaris, and to evaluate clinical presentation, diagnostic and therapeutic difficulties in this condition.
CASE REPORT
A 23-year-old Caucasian female patient was admitted to our Hospital in September 2010, due to prominent, generalized depigmented patches.
The disease begun acutely, “over night” (in patients` own words), and progressed in the following order: dorsal aspects of hands, upper extremities, trunk, face and lower extremities. Within a few weeks 60% of her body was affected.
On admission to our Hospital her height was 175 centimeters and weight was 60 kilograms, body mass index was normal (19,6).
The affected area had no associated scaling. There was a lack of cutaneous induration or sclerosis. Skin lesions were asymptomatic and lack clinical sings of inflammation. During dermatological examination leukotrichia of the occipital area was found. There was no mucosal involvement. She was without any subjective difficulties (e.g. pain, fever, weight loss).
There was family history of this disorder (her 12-year-old brother has acrofacial vitiligo). The disease appeared almost simultaneously with his sister`s condition. She attributed the onset of her disease to emotional stress, while her parents died in a car accident six months before she has noticed first signs of vitiligo.
She had also noticed new depigmented lesions in sites of physical injury (Koebner phenomena).
History of chronic sun exposure was negative. She was non-smoker.
Illumination with Wood`s lamp showed no fluorescence of the affected depigmented skin.CL has been diagnosed based on the clinical picture and pathohistological appearance.
- Disclaimer-
This PPT is loaded as student material "as is", from the VRF Vitiligo Master Class Barcelona November 2011; VRF does not endorse or otherwise approve it.
DLQI SCORE IN VITILIGO PATIENTS IN RE-MEDIKA HOSPITAL Cross-sectional study -...VR Foundation
Vitiligo is a common acquired, idiopathic and often familiar depigmentation disorder that affects both sexes equally worldwide.
Although not painful or life-threatening, this disfiguring disorder can have a devastating effect on a patient’s psychosocial wellbeing and social life
Skin Pigmentation disorders and its management .pptxJagruti Marathe
Some of the most common are pigmented birthmarks, macular stains, hemangiomas, port wine stains, while disorders include albinism, melasma, vitiligo and pigmentation loss due to skin damage. Birthmarks and other skin pigmentation (coloration) disorders affect many people.
Skin pigmentation disorders are conditions that affect the color of the skin. Some common types of skin pigmentation disorders include:
Pigmented birthmarks
Macular stains
Hemangiomas
Port wine stains
Albinism
Melasma
Vitiligo
Skin pigment loss due to sun damage
Other factors that can affect skin pigmentation include: Pregnancy, Addison's disease, Sun exposure.
Some treatments for skin pigmentation disorders include:
Over-the-counter or prescription creams
Topical pimecrolimus or tacrolimus
Light therapy
Melanocytes in the basal epidermis control skin pigmentation through synthesis of melanin, a complex process thought to be primarily regulated by alpha-melanocyte stimulating hormone (αMSH)
Light therapy exposes your skin to a type of ultraviolet (UV) light that can restore your natural skin color. If a large area of your body needs treatment, your dermatologist may prescribe a type of light therapy called phototherapy. During phototherapy, you expose your skin to UV light for a specific amount of time.
It is a disease with no cure that's why i am going for a research on this disease and get back with some new perspective of patients, I think these perspectives are helpful for the better treatment of this disease.
Skin pigmentation:
Pigmentation means coloring. Skin pigmentation disorders affect the color of your skin. Your skin gets its color from a pigment called melanin. Special cells in the skin make melanin. When these cells become damaged or unhealthy, it affects melanin production. Some pigmentation disorders affect just patches of skin. Others affect your entire body.
For more information, you can book an appointment at
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Many aspects of our daily life can have a huge impact on our skin health. What we eat and how stressful our life is affects how healthy our skin is, as does ultraviolet (UV) light exposure from the sun. Good daily habits that can benefit the skin include drinking lots of water; eating fruits, vegetables, healthy carbohydrates and proteins; and making sure that we control or reduce our stress. Staying hydrated gives the skin the moisture it needs so it doesn't become dry and flaky. A healthy diet provides the nutrients that skin needs to stay strong and stretchy, and to regenerate itself. Reducing stress, either through lifestyle changes or relaxation techniques, can reduce the sensitivity of your skin. It's also important to remember to wear sunscreen or protective clothing to protect your skin from harmful UV rays.
Skin is a dynamic organ that requires care and attention. At every stage in the life cycle there are challenges posed, both environmental and genetic, to our skin. This presentation gives an overview of the needs of childhood and adult skin at different stages. Skin care routines, including moisturizers, sunscreens and cosmetic products and techniques covered.
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K5 Lipogel is a lightly perfumed, hydroquinone-free formulation, having an effective whitening action on the brown skin spots due to excessive sun exposure, age, oral contraceptives, use of photosensitizing products, freckles and pigmentation around scars caused by acne or surgical intervention. K5 Lipogel does not undergo microbiological contamination because it is made of 99% of lipidic ingredients that do not offer a proper culture media for microbial growth. Epicutaneous patch tests (15 minutes and 24
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These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
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Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
3. • Melanocytes are special cells in our skin
that specialize in making a molecule
called melanin.
• What is Melanin?
• Melanin is something called a pigment,
which is the molecule that gives our skin
colour a darker shade.
MELANOCYTES AND MELANIN
4. What does melanin actually do?
Melanin protects our skin from the damaging
Ultraviolet (UV) rays from the sun.
Going sun tanning induces your body to
produce more melanin, which is why people
who return from tanning look darker.
More melanin in the skin is the reason why
people who are darker usually do not get
sunburned.
7. In our skin, we all have around the same number
of melanocytes, which are the cells that produce
melanin.
However, the melanocytes in each of our bodies
produce different amounts of melanin.
The more melanin you have in your skin, the
darker your skin color will be.
9. • It is a skin condition that can manifest after
birth at any point in someone’s life.
• It leads to death or loss of function of the
melanocytes in the body, which leads to the
inability to produce any more melanin in the
skin.
• Vitiligo is very visible on someone with a very
dark complexion due to the prevalence of white
splotches of skin.
10. • Chronic skin disease
• Other name = Leukoderma
• White spots occur when the skin no longer
forms melanin (pigment that determines the
color of your skin, hair, and eyes)
• The white patches of irregular shapes begin to
appear on your skin
11. • Any part of the body may be affected.
• Common sites are exposed areas (face,
neck, eyes, nostrils, nipples, navel,
genitalia), body folds (armpits, groin),
sites of injury (cuts, scrapes, burns)
and around pigmented moles (halo
naevi)
12. SYMPTOMS & SIGNS
• White patches of skin
• Whitening or graying of the hair on your scalp,
eyelashes, eyebrows or beard (leukotichia – seen in
segmental)
• Loss of color in the tissues that line the inside of your
mouth
• Loss or change in color of the inner layer of your eye
13. • The degree of pigment loss can vary within
each vitiligo patch which means that there
may be different shades of brown in a
vitiligo patch.
• This is called ‘trichrome’.
• A border of darker skin may circle an area
of light skin.
14.
15.
16.
17.
18.
19.
20.
21. ASSOCIATIONS
• Premature graying of hairs in relatives.
• Koebner phenomenon.
• Emotional or Physical stress.
• Drugs → Chloroquine and Clofazimine.
24. PSYCHOLOGICAL IMPACT
• Feelings of stress, embarrassment and self
consciousness.
• Perception of discrimination.
• Low self esteem.
• Disturbed sexual relationships.
25. ETIOLOGICAL THEORIES
• Familial Theory
• Auto-immune Theory
• Autocytotoxic Theory
• Neural Theory
• Self destruction Theory
26. FAMILIAL THEORY
• Epidemilogically, 25 - 33% have family
members with disease.
• Close biologic relatives → 4 - 5 folds
increased risk.
• HLA studies have variable results.
• No specific genetic pattern.
27. AUTO-IMMUNE
THEORY
• Antibodies against melanocyte surface
antigens, correlate with the extent of
depigmentation.
• Antityrosinase ab., Antimelanin ab. and
melanin-sensitized lymphocytes.
• Leukocyte migration inhibition factor
levels and circulating immune complex
levels markedly elevated.
28.
29. AUTOCYTOTOXIC
THEORY
• Increased melanocyte activity, leads to its own
demise.
• Inhibition of Thioredoxin reductase, by
Calcium.
• Higher Ca levels cause ↑↑ superoxide radicle
formation.
• Levels of Catalase, markedly decreased.
30. NEURAL THEORY
• Based on the following observations:
• Patients with nerve injury and vitiligo in
denervated areas .
• Clinical evidence of segmental dermatomal
vitiligo.
• Increased sweating and vasoconstriction in
vitiliginous areas.
31. NEURAL THEORY…
[CONT.]
• Depigmentation in animal models with severed
nerve fibres.
• Degenerative and regenerative autonomic
nerves in depigmented patches.
• Increased urinary excretion of VMA and HVA
in active vitiligo.
32. • It suggests that melanocytes are
destroyed by flaws in the protective
mechanism that removes the chemical
toxins that is generated in
melanogenesis.
SELF DESTRUCTION THEORY
33.
34.
35. MEDICAL SCREENINGS:
A family history of vitiligo
Look to see if there is a rash,
sunburn, or other skin trauma
that has occurred within 2 or
3 months after pigmentation
was discovered
Premature graying of the hair
(before age 35)
Stress or physical illness
Also they may ask for an eye
examination (inflammation of
your eye) and/or blood test
(autoimmune disease)
36. HISTOPATHOLOGY
• Uniform absence of Melanocytes.
• Periphery of depigmented patch show : signs of
cellular death.
• Dilatation of rough endoplasmic reticulum in
melanocytes.
• Inflammatory changes in dermis.
37. EVALUATION
• Total body Wood’s light examination.
• TSH levels [Thyroid disease].
• CBC [Pernicious anemia].
• Evaluation about Diabetes Mellitus.
• Ophthalmological examination.
38. TREATMENT
1. Cosmetic
2. PUVA
a. Topical
b. Systemic
3. Corticosteroids
4. Surgical Treatment
5. Monobenzyl ether of Hydroquinone
39. COSMETIC TREATMENT
• Patches on exposed parts can be concealed by:
Make up brands : Cover Mark, Derma blend, Derma color
etc.
Topical dyes : Clinique bronze gel, Vitadye, Dyoderm etc.
Tanning creams : Chromelin, self tanning milk etc.
Advantages:
Cost, ease of application, lack of side effects.
Disadvantages:
Vigorous physical activities and in extensive disease.
40. P U V A
• Historically, Egyptians in 13th century
The herb “Ammi majus linnaeus”
Ammoidin
8-MOP, 5-MOP and 8-isoamylene OP
• 1904, Montgomery, Light therapy in vitiligo
• 1948, Al-Moftey, First use of light therapy in
combination with psoralens.
41. MECHANISM OF ACTION [PUVA]
• Immunologically mediated action.
• Stimulation of tyrosinase activity.
• Inhibition of DNA and protein synthesis.
• Depletion of EGF expression.
• Depletion of vitiligo - associated melanocyte
antigens.
42. MELANOCYTE
REPIGMENTATION
• Activation of inactive cells [spared in vitiligo
process] in the middle and lower part of follicle
and in outer sheath.
• These inactive cells contain structural and
melanosomal proteins, but do not contain
enzymes, required for melanogenesis.
43. MELANOCYTE REPIGM. [CONT.]
• Migration of melanocyte from lower hair follicle to
epidermis, depends on :
a) Cytokine release, like FGF, IL-1,
b) Inflammatory mediators such as : TGF-α,
leukotriene C4, D4, and endothelin-1.
44. TOPICAL PSORALENS
• Patients with less than 20% of total body
surface.
• Initially 0.05% or 0.1% strength.
• Artificial UVA source for 30 seconds initially
and increasing exposure to up to10 minutes 2 - 3
times per week.
• At 10 minutes, higher strength (0.1% to 0.15%)
prescribed.
45. TOPICAL PSORALENS (CONT.)
• Shielding uninvolved skin and eyes.
• Wash off the topical solution immediately
after treatment.
• Sun blocks, Avoiding direct and filtered
sunlight for the rest of the day.
• Side effects →→ Blistering, Burning and
Perilesional hyperpigmentation.
46. • Most effective treatment available
• PUVA therapy is to repigment the
white patches
• time-consuming, and care must be
taken to avoid side effects
• Psoralen is a drug that contains
chemicals that react with ultraviolet
light to cause darkening of the
skin.
• Psoralen is injected orally or is
applied to the skin
• Then skin is carefully timed
exposure to sunlight or to
ultraviolet A (UVA) light that
comes from a special lamp.
47. ORAL PSORALEN / UVA
• Patients with extensive disease.
• 0.5 mg / kg, 2 hours before treatment.
• Started at 1-2 j / cm2
of light 2 - 3 times a week.
• Darker pigmented patients and children
respond better to PUVA.
48. ORAL PSORALEN / UVA
• Trunk, proximal extremities and face respond
better to PUVA.
• Distal extremities, periorificial and dermatomal
lesions do not respond better.
• Side effects →→ burns, nausea, erythema,
pruritus, xerosis, fatigue, carcinogenecity,
pigmentation, cataracts and aging.
49. ORAL PSORALEN / UVA
• Contraindicated in →
• Pregnant women, breast feeding, h/o skin cancer,
arsenic exposure, photosensitivity, radiotherapy,
and cataracts.
• Advised to →
• Visit Ophthalmologist yearly, wear goggles, avoid
direct and filtered sunlight for 24 hours after
treatment.
50. CORTICOSTEROIDS
• First used in 1959 by Japanese.
• Both systemic and oral.
• Localized depigmented patches.
• High potency steroids for 1 - 2 months.
• Slowly tapered to lower strength.
• Usual side effects.
51. TOPICAL STEROID THERAPY
• The use of steroid creams may be helpful in returning the color to
the white patches
• A mild topical corticosteroid cream for children under 10 years
old and a stronger one for adults
• Cream must be applied to the white patches on the skin for at
least 3 months before seeing any results
• Corticosteroid creams are the simplest and safest treatment for
vitiligo, but are not as effective as psoralen photo chemotherapy
• SIDE EFFECTS occur in areas where the skin is thin, such as on
the face and armpits, or in the genital region
• They can be minimized by using weaker formulations of steroid
creams in these areas.
52. SURGICAL MODALITIES
• Localized non-progressive patch in a non- acral
location.
• Epidermal grafting
• Autologous minigrafting
• Transplantation of in vitro-cultured epidermis.
• Transplantation of non-cultured melanocytes.
53. EPIDERMAL GRAFTING
• Blisters at donor and recipient sites by suction or
liquid nitrogen.
• Roof of the blister is removed from both sites and
donor epidermis is placed on denuded recipient site.
• Reinforcement with biological dressing.
• Repigmentation seen in 2 weeks to 3 months.
• Pre-treating donor site with topical PUVA, to
stimulate melanogenesis, may enhance re-
pigmentation.
• Low incidence of scarring.
54. AUTOLOGOUS MINIGRAFTING
Multiple small punch biopsy specimens.
At Inconspicuous donor site, close together.
At recipient site, separated by 4 - 5 mm.
Test area chosen and 3 - 5 minigrafts are placed to
determine the ability.
After 2 months, if the pigment has spread, grafting
of the entire region continued.
55. IN VITRO CULTURED EPIDERMIS
Blisters at both donor and recipient sites.
Epidermis from donor site is treated with trypsin.
Melanocytes isolated and grown in cell culture for
3 weeks.
Melanocytes adhere to Vaseline gauze, which is
divided, and placed over the denuded recipient
site.
56. IN VITRO CULTURED EPIDERMIS
With this procedure, repigmented site can be as
large as 10 times the donor site.
Pitfalls of this technique :
1. Variegated color, due to variable
melanocyte concentration on the gauze.
2. Spotty graft failure
57. NON CULTURED MELANOCYTES
Non cultured melanocytes obtained with
dermatome from donor site.
Melanocytes treated with trypsin, EDTA, and
placed in a saline solution.
Injected as suspension into blisters in the recipient
site created by liquid nitrogen.
Repigmentation is faster than in vitro melanocytes.
58. HYDROQUINONES
Used in extensive disease where, remaining normal
skin is depigmented.
Inhibit tyrosinase, Decrease the number of
melanized melanosome, Alter melanosomal
configuration, and Cause melanocyte organelle
disuption and lysis.
Results may take from one month to one year, to
depigment completely.
59. • Vitiligo frequently begins with a rapid loss of
pigment which may be followed by a lengthy
period when the skin color does not change.
• Later, the pigment loss may begin again.
• The loss of color may continue until, for
unknown reasons, the process stops.
• Cycles of pigment loss followed by periods of
stability may continue indefinitely.
PROGNOSIS