This document discusses skin pigmentation and disorders of pigmentation. It begins by explaining the basis of skin pigmentation including melanosomes, melanin synthesis and transport. It then discusses different types of chromophores and pigments that determine skin color. The document further describes melanocyte development, migration and function. It provides details on melanin types, melanosome biogenesis and transfer. Finally it discusses various disorders of hypopigmentation and hyperpigmentation.
Definition, development, function & Site-specific of Melanocyte Definition, formation & function of Melanosomes, Definition & function of Melanin
Melanogenesis
Definition, development, function & Site-specific of Melanocyte Definition, formation & function of Melanosomes, Definition & function of Melanin
Melanogenesis
This is a powerpoint presentation on the epidermal keratinization and its associated disorders, presented by Dr. Jerriton, Dermatology resident of SVMCH, Pondicherry.
Merkel cells (MCs) constitute a very unique population of postmitotic cells scattered along the dermoepidermal
junction. These cells that have synaptic contacts with somatosensory afferents are regarded
to have a pivotal role in sensory discernment. Several concerns exist till date as to their origin,
multiplication, and relevance in skin biology.
This is a powerpoint presentation on the epidermal keratinization and its associated disorders, presented by Dr. Jerriton, Dermatology resident of SVMCH, Pondicherry.
Merkel cells (MCs) constitute a very unique population of postmitotic cells scattered along the dermoepidermal
junction. These cells that have synaptic contacts with somatosensory afferents are regarded
to have a pivotal role in sensory discernment. Several concerns exist till date as to their origin,
multiplication, and relevance in skin biology.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Biology of melanocyte - Professor Torello Lotti, MD - University G.Marconi,...VR Foundation
Although almost everyone has the same amount of melanocytes, the amount and size of the melanosomes and melanin particles produced can differ immensely in humans, resulting in the different races of the world. Dendritic prolongations take contact with nearby keratinocytes, and serve as melanosomes carriers.
dendritic cells are part of innate immune system, antigen presenting cells in skin, activation of t cells and inducing and maintaining immune tolerance, 4 types- langerhans cells, dermal dendritic cells, merkel cells, melanocytes
power point presentation on the various pigmented lesions in the oral mucosa with their clinical features and oral manifestations and differential diagnosis
Skin cancers or cutaneous malignancies including Basal cell carcinoma, Squamous cell carcinoma and Melanoma and with a brief introduction of skin as an organ itself.
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
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
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.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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!
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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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
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
- 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
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.
2. BASIS OF SKIN PIGMENTATION
MELANOSOMES-types ,synthesis & maturation
SYNTHESIS OF MELANIN
TRANSPORT OF MELANIN
DISORDERS OF HYPOMELANOSIS
DISORDERS OF HYPERMELANOSIS
3. DIFFERENT COLOR OF SKIN IS
DUE TO :
1. Presence of CHROMATOPHORES
(pigment containing cells )
2. Presence & Distribution of
Pigments(coloured particles)
3. Hormonal and Neural control
REASON FOR VARIABLE SHADES OF
COLORATION
1. CAMOUFLAGE ( protective
resemblance),mimesis / crypsis
2. Aggressive Resemblance
Best example is CHAMELEON
4.
5.
6.
7. Determined by : melanin
haemoglobin
carotenoids
At the level of Epidermis : Melanin , the major determinant and
carotenoids
At the level of Dermis - by oxygenated haemoglobin (red) in
capillaries - by reduced haemoglobin (blue) in venules
Constitutive skin colour : genetically predetermined
Facultative skin colour : induced by sun exposure(UV),
hormones & other regulatory factors
8. derive from pluripotent neural crest cells
that differentiate into numerous cell
lineages including neurons, glia,smooth
muscle, craniofacial bone, cartilage, and
melanocytes.
Progenitor melanoblasts migrate
dorsolaterally between the mesodermal
and ectodermal layers
reach the hair follicles and the skin as
well as inner ear cochlea, choroid, ciliary
body, and iris.
Melanoblast migration and
differentiation influenced by signaling
molecules Wnt, (ET)-3, bone
morphogenetic proteins (BMPs), steel
factor (SF) , and hepatocyte growth
factor .
9. Melanoblasts migrate
dorsolaterally and then ventrally
around the trunk to the ventral
midline & differentiation into
melanocytes.
During embryogenesis, melanin
producing melanocytes are found
diffusely throughout the dermis.
By the end of gestation, active
dermal melanocytes disappear,
except in three anatomic locations
1. the head and neck,
2. the dorsal aspects of the
distal extremities
3. the presacral area
that coincide with the most common
sites for dermal melanocytosis and
dermal melanocytomas (blue nevi)
10. Melanocytes in skin synthesize &
store melanin in cytosolic
organelles called melanosomes
A constant need for synthesis &
transfer of melanosomes from
melanocytes to keratinocytes to
maintain cutaneous pigmentation.
Melanocyte density/square mm
ranges from 550 to 1500, with the
highest concentration within face &
genitalia
Association of a melanocyte with
approximately 30–40 surrounding
keratinocytes to which it transfers
melanosomes
11. Follicular melanin unit undergoes cyclic
modifications along with the hair cycle
located in the proximal hair bulb during anagen
proliferate, migrate, and undergo maturation
during early to mid anagen.
Melanogenesis and melanin transfer to
keratinocytes occurs throughout anagen.
Melanocyteneventually apoptose during late
catagen
in hair, melanocyte transfer melanin to
differentiated keratinocytes that ultimately form
the hair shaft.
determine hair color by the amount of melanin
transferred, as well as by the ratio of eumelanin
(black–brown) to pheomelanin (red–yellow)
12.
13. C . Ocular Melanocytes
- Unlike cutaneous melanocytes, ocular melanocytes are in contact
only with each other & don’t transfer melanosomes.
-Albinos may have visual abnormalities due to absence of melanin
D . Otic Melanocytes
- reside in cochlea & are important for hearing loss of otic melanocytes
may leads to deafness as in Waardenburg syndrome TYPE II
14. Depends upon :>
1) Melanogenic activity within the melanocyte
2) The proportion of mature melanosomes
3) Size of melanosomes
4) Type of melanin (eumelanin, or pheomelanin)
5) Melanosomes transfer & distribution within the
keratinocyte
15.
16. Definition: membrane-bound unique organelle
within the cytoplasm of melanocytes in which
in which melanin pigments are synthesized,
deposited and transported.
And depending on the type of melanin
(eumelanin or pheomelanin) synthesized,
melanosomes can be divided into:
Eumelanosome and Pheomelanosome
17.
18.
19.
20.
21.
22.
23.
24. 1) Transcription of proteins required for melanin
synthesis
2) Melanosome biogenesis
3) Sorting of melanogenic proteins into
melanosomes to initiate melanin synthesis
within the melanosome
4) Transport of the mature melanosomes to the
tips of melanocyte dendrites migrates via
microtubules
5) Transfer of melanosomes to keratinocyte
25.
26. 1 .EXOCYTOSIS
- fusion of the melanosomal membrane with the melanocyte plasma membrane
- melanosome is released to the intercellular space
- phagocytosis by surrounding keratinocytes occur
2 .CYTOPHAGOCYTOSIS: projection of dendrites into keratinocyte cytoplasm
then keratinocytes cytophagocytose the tip of a melanocyte dendrite.
3. Fusion of melanocyte & keratinocyte plasma membrane create a space
through which melanosomes are transferred
4.Shedding of melanosome-filled vesicles followed by phagocytosis of the
vesicles by keratinocyte
27.
28.
29. A . Specific genes
B . Hormones: 1.MSH 2. ACTH 3. Estrogens
C . Biochemical factors: IL-1 2, IL-6 , TNF-alpha , basic
fibroblast growth factor (bFGF) 5- Endothelin-1, 3
D. External factors:
1- UV light (amount and wave-length)
2- melanocyte stimulating chemicals like
photosensitizers
30.
31.
32.
33.
34.
35. MITF, a basic-helix-loop-helix and leucine zipper transcription factor,
the master gene for melanocyte survival
A key factor regulating the transcription of the major melanogenic
proteins, tyrosinase, TRP-1, TRP-2 , PKC-β
In melanocytes, it is the MITF-M isoform that stimulates transcription of
tyrosinase and PKC-b.
MITF binds to conserved consensus elements in gene promoters, specifically
the M- (AGTCATGTGCT) and E- (CATGTG) boxes.
MITF comprises a family of nine isoforms: (1) MITFM, (2) -A, (3) -B,
(4) –H , (5) -C, (6) -D, (7) -E, (8) -J, and (9) -Mc.
MITF-M expression is highly specific for melanocytic cells.
37. AD disorder of melanocyte development a/w Kit/SNCA gene
mutation
Common characteristics include a congenital white forelock,
scattered normal pigmented and hypopigmented macules and a
triangular shaped depigmented patch on the forehead..
In some cases, piebaldism occurs together with severe
developmental problems, as in Waardenburg
syndrome and Hirschsprung's disease.
A kind of neurocristopathy, involving defects of various neural
crest cell lineages that include melanocytes, but also involving
many other tissues derived from the neural crest
39. AD neurocutaneous syndrome
with skin lesions, mental
retardation and epilepsy
Skin lesions are ash-leaf
macules, angiofibromas and
shagreen patches
Ash-leaf macules - present at
birth in > 90% cases, so
important in early diagnosis
Oval or ash-leaf shaped,
hypopigmented macules, look
prominent in Wood’s lamp Long
axis is axial on limbs and
transverse on trunk
40. HERMANSKYPUDLAK
SYNDROME
autosomal recessive disorder
Albinism and eye problems:
(photophobia), strabismus
(crossed eyes), and nystagmus
(involuntary eye movements)
Bleeding disorders: due to
platelet dysfunction.
Cellular storage disorders: The
syndrome causes a wax-like
substance (ceroid) to
accumulate in the body tissues
and cause damage, especially
in the lungs and kidneys
CHEDIAKHIGASHI
SYNDROME
A rare autosomal recessive disorder
that arises from a mutation of a
lysosomal trafficking regulator
protein,[ which leads to a decrease
in phagocytosis.
results in
recurrent pyogenic infection
s, albinism and
peripheral neuropathy
41.
42. May be epidermal or dermal
Epidermal hyperpigmentation due to - Increased
melanin with normal number of melanocytes -
Increased number of melanocytes
Dermal hyperpigmentation due to - Melanin from
epidermis transferred to dermis - Melanin formed
in dermal melanocytes - Melanin pigments
appears blue-gray due to Tyndall effect
46. Also known as Futcher’s or Voight’s
lines
are borders of abrupt transition
between more deeply pigmented
skin and that of lighter pigmentation
do not correspond to Blaschko’s lines
or dermatomal lines but to voigt’
lines
Considered by some to be a variant
of normal pigmentation
47. Can be divided into five five categories:
Group A - lines along the outer upper arms with variable extension
across the chest
Group B - lines along the posteromedial aspect of the lower limb
Group C - Paired median or paramedian lines on the chest, with
midline abdominal extension
Group D - medial, over the spine
Group E - bilaterally symmetrical, obliquely oriented, hypopigmented
macules on the chest
48. Benign proliferations of cells at the dermo-epidermal
junction
May be congenital or acquired
Acquired nevi are more common
Appear in infancy or childhood, slowly grow and mature
and then regress in older life
Important for cosmetic reasons and as precursors for
melanoma (esp. in white)
49. Round or oval, uniformly coloured and sharply bordered lesions
Appear after birth
Increase in frequency during childhood & adolescence and plateaus during middle age
Most of them start as junctional nevi which are flat and histologically confined to
dermalepidermal junction
Gradually mature to compound nevi which have nests and columns of nevus cells in
dermis along with the junctional component. These are raised, rounded, brown or black
Intradermal nevi : Compound nevi mature to intradermal nevi with nevus cells only in
dermis having neuron like appearance. These are dome shaped, nonpigmented and may
have one or more coarse hair
50.
51.
52. Acquired, pigmented, hairy
plaque common on trunk,
more common in males
Appears in first or second
decade
Common sites: shoulder,
chest, back
May become verrucous with
hair growth and then remains
stable
53. Circumscribed, brown
macules with irregular
margins, 2-5 cm in size
Isolated CALM may occur
in 10-20% of normal
population
No increase in the number
of melanocytes
Five or more CALM of
size >0.5 cm in
prepubertal age group
and >1.5 cm in an adult
are strongly suggestive of
neurofibromatosis
54. A common macular brown
coloured lesion seen on face in
males and females
Common in pregnancy: Mask of
pregnancy (clears in few months)
Forehead, nose, cheeks affected.
The three clinical patterns are:
centrofacial, malar, mandibular
Exacerbation on sun exposure
Histologically may be epidermal,
dermal or mixed