Actinic keratoses: Erythematous scaly lesions on sun-damaged skin & considered “precancerous” lesions that have the potential to progress into invasive SCC.
Bowen’s disease: SCC in situ It has the potential to progress to invasive SCC.
Leukoplakia: Leukoplakia refers to a white patch or plaque on the oral mucosa that cannot be wiped off and cannot be characterized clinically or pathologically as any other disease.
DARIER’S DISEASE, Keratosis folliculiris, rare genetic disorder that is manifested predominantly by skin changes, due to ATP2A2 mutation, The histology is characteristic, known as focal acantholytic dyskeratosis associated with varying degrees of papillomatosis
Actinic keratoses: Erythematous scaly lesions on sun-damaged skin & considered “precancerous” lesions that have the potential to progress into invasive SCC.
Bowen’s disease: SCC in situ It has the potential to progress to invasive SCC.
Leukoplakia: Leukoplakia refers to a white patch or plaque on the oral mucosa that cannot be wiped off and cannot be characterized clinically or pathologically as any other disease.
DARIER’S DISEASE, Keratosis folliculiris, rare genetic disorder that is manifested predominantly by skin changes, due to ATP2A2 mutation, The histology is characteristic, known as focal acantholytic dyskeratosis associated with varying degrees of papillomatosis
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Melanotic Neuroectodermal tumor of infancy.
This occurs in infants before the age of 12 months
Oral pathology
Melanotic Neuroectodermal tumor of infancy youtube video
Visit the link below for this
https://youtu.be/jaACexlb1-M
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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
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.
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
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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
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.
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
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.
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
2. COMMON ACQUIRED MELANOCYTIC NEVI
▪ A benign cluster of melanocytic naevus cells
arising as a result of
proliferation of melanocytes at the dermal–epidermal junction.
3. COMMON ACQUIRED MELANOCYTIC NEVI
▪ the melanocytes proliferate for some time
but then cease proliferation and differentiate
and come to resemble cells of neural or fibroblast lineage.
4. COMMON ACQUIRED MELANOCYTIC NEVI
CLASSIFICATION
1. Junctional
2. Compound
3. Dermal
4. Naevi of unusual sites (palms/soles/nail unit)
5. Spitz naevi
6. Blue naevi
7. Halo naevus 8. Meyerson naevus 9. Naevus en cockade
8. Atypical naevi
10. Natural history
▪ develop through childhood
▪ continue to erupt in adult life
▪ After 45 yrs of age, naevi involute
(so elderly usually have very few.)
* new naevi developing in later life should be viewed with suspicion
17. COMMON ACQUIRED MELANOCYTIC NEVI
▪ Relation to melanoma:
▪ Significant proportion of melanoma patients report the prior presence of a longstanding melanocytic naevus
▪ Histolog.: 1/3 of melanomas have naevus remnants
▪ Increased number of melanocytic naevi correlates with increased melanoma risk
18. COMMON ACQUIRED MELANOCYTIC NEVI
▪ Compound and dermal nevi typically show zonation with depth (maturation) in the dermis.
▪ Type A cells: Large epithelioid melanocytes in the superficial dermis
▪ Type B cells: melanocytes tend to have less cytoplasm with descent into the reticular dermis
▪ Type C cells: become fusiform at the base of a lesion
19. ▪ Type A cells: Large epithelioid melanocytes in the superficial
dermis
20. ▪ Type B cells: melanocytes tend to have less cytoplasm with descent
into the reticular dermis
21. ▪ Type C cells: become fusiform at the base of a lesion
22. COMMON ACQUIRED MELANOCYTIC NEVI
▪ The full range of cytologic appearances from type A to type C melanocytes is seen only in a minority of
nevi.
23. COMMON ACQUIRED MELANOCYTIC NEVI
differential diagnosis
1. Seborrhoeic keratosis
– In older adults
– ‘stuck on’ appearance
– Bulk above the normal skin contour
– More grey brown
– Surface: dull/ pitted/ tendency to crumble
24.
25. 2. Early malignant melanoma
▪ * very rapid growth / tenderness
: not features of malignant
change
26. COMMON ACQUIRED MELANOCYTIC NEVI
differential diagnosis
3. Dermatofibroma
▪ Very firm consistency
▪ ‘dimpling’ on lateral compression
▪ Central white patch on dermoscopy
▪ If the skin over the dermatofibroma is squeezed a dimple forms which indicates tethering of the
skin to the underlying fibrous tissue (dimple sign).
31. COMMON ACQUIRED MELANOCYTIC NEVI
Management:
Avoid partial removal
Residual deep dermal naevus cells may proliferate after excision
Pathologic picture similar to early melanoma
‘Pseudomelanoma’
‘Traumatically activated nevus’
32. COMMON ACQUIRED MELANOCYTIC NEVI
Balloon cell naevus
▪ Subtype of compound melanocytic naevus
▪ Cells with a high volume of foamy cytoplasm (‘balloon’)
▪ Not premalignant
36. Naevi of nail matrix
▪ Uniformly pigmented brown longitudnal bands (melanonychia striata)
▪ Regular & distinct margins
▪ D/D: early subungal melanoma
37. COMMON ACQUIRED MELANOCYTIC NEVI
▪ Subungual melanoma often starts as melanonychia.
Over weeks to months, the pigment band:
▪ Becomes wider, especially at its proximal end (cuticle)
▪ Becomes more irregular in pigmentation(light brown, dark brown)
▪ Extends to involve the adjacent nail fold (Hutchinson sign)
▪ May develop a nodule, ulcer or bleed
▪ May cause nail dystrophy
41. COMMON ACQUIRED MELANOCYTIC NEVI
▪ Whenever dermatoscopy is not accessible, criteria to help perform the biopsy are:
– A single nail affected.
– Brown or Black band > 3 mm.
– periungueal pigment effusion – Hutchinson's Sign.
43. Melanocytic nevi of genital and flexural skin
▪ Nevi in “special sites”, including genitalia, sometimes have atypical
histologic changes, making distinction from melanoma difficult.
44. Melanocytic nevi of genital and flexural skin
▪ premenopausal women (ages 14 to 40 years) : vulvar lesions.
▪ larger in size than non-genital nevi,
▪ fairly regular borders
▪ Complex mahogany color (an admixture of tan, brown and red).
45. Melanocytic nevi of genital and flexural skin
Pathology
▪ characterized by an overall symmetry
▪ well circumscribed
▪ absence of lateral extension of intraepidermal melanocytic components beyond the dermal nevus
elements
* Architectural and cytologic features similar to atypical melanocytic nevi.
56. SPITZ NAEVUS
▪ Children ( 50% cases < 14 yrs age )
▪ Rapid growth over 3-6 months, then static for years
▪ Face (esp. cheeks)
▪ Bleeds easy
57. SPITZ NAEVUS
▪ Spitzoid lesions are composed of varying proportions of spindled and epithelioid cells that display a
characteristic cytomorphology that is the common thread between the classic Spitz nevus and all its
variants.
58. SPITZ NAEVUS
▪ cells are large, contain abundant eosinophilic cytoplasm
▪ have nuclei with smooth nuclear membranes, delicate chromatin and prominent central nucleoli.
▪ Within a given lesion, spitzoid cells are generally uniform in size and appearance.
70. SPITZ NAEVUS
Agminate spitz naevi
varying numbers
of raised nevi
in a localized or segmental distribution,
arising in otherwise clinically normal skin
71. SPITZ NAEVUS
Atypical
lesions demonstrating one or more features that deviate from conventional Spitz nevi:
▪ large size (e.g. >1 cm in diameter) / ulceration / asymmetry
▪ deep involvement of the dermis or subcutis;
▪ Dermal mitoses (>2–3 mitoses/mm2)
▪ Significant pagetoid spread;
▪ prominent confluence and high density of melanocytes in the dermis
▪ lack of maturation.
76. SPITZ NAEVUS
Treatment
▪ Histological evaluation of the entire lesion is recommended.
▪ Local excision with narrow margin of 1-2 mm for confirming diagnosis
▪ Recurrence rate after complete excision : 7-16%
77. SPITZ NAEVUS
Treatment
▪ In presence of atypical features
▪ Margin of excision same as for melanoma
Tumors<2mm : 1 cm margin
Tumors > 2mm : 2cms or more margins
80. BLUE NAEVUS
▪ Comprises of aberrant collections of
pigment-producing benign melanocytes,
in the dermis rather than at the dermoepidermal junction
(as in common acquired naevi).
84. BLUE NAEVUS
Variants
1. Cellular blue naevus
2. Epitheloid blue naevus
3. Pigmented epitheloid melanocytoma
4. Malignant blue naevi
85. BLUE NAEVUS
Cellular blue nevi
▪ blue to blue–gray or black nodules or plaques,
▪ generally 1 to 3 cm in diameter but sometimes larger .
▪ The most common sites are the buttocks, sacrococcygeal area.
88. BLUE NAEVUS
Malignant blue nevi
▪ Cutaneous melnnoma arising in or having features of blue naevus.
▪ Multinodular/ plaque like
▪ Scalp (most common)
91. BLUE NAEVUS
Treatment
▪ <1 cm in diameter,
▪ clinically stable,
▪ do not have atypical features
▪ located in a typical anatomic site
do not
require removal.
92. BLUE NAEVUS
Treatment
▪ lesions that appear de novo,
▪ are multinodular or plaque-like,
▪ have undergone change
▪ Atypical cellular blue nevi and pigmented epithelioid melanocytomas should be resected completely (risk
for malignant transformation)
Histological evaluation
94. HALO NAEVUS / SUTTON’S NAEVUS
▪ A melanocytic naevus surrounded by a depigmented
halo of otherwise normal skin.
95. HALO NAEVUS
under the age of 20
a central melanocytic nevus component
well-circumscribed annulus of hypo- or
depigmented
Skin
Erythema occasionally precedes
97. HALO NAEVUS / SUTTON’S NAEVUS
▪ upper back
▪ 50% of affected individuals have two or more halo nevi
▪ usually regresses over months to years, leaving a white macule
▪ Complete repigmentation of the skin is seen in the vast majority
98. HALO NAEVUS / SUTTON’S NAEVUS
Pathogenesis
▪ an immune response against antigenically altered nevus cells associated with tumor progression
(dysplasia)
99. HALO NAEVUS / SUTTON’S NAEVUS
Pathology
▪ Variants of compound melanocytic naevi
▪ At the time of appearance of the halo they show a very striking lymphocytic infi ltrate admixed with the
intradermal naevus cells.
▪ The use of DOPA stains will reveal a loss of epidermal melanocytes in the halo area.
100. HALO NAEVUS / SUTTON’S NAEVUS
Management
▪ personal or family history of cutaneous melanoma, atypical nevi and vitiligo.
▪ Inspected for features of an atypical melanocytic nevus or melanoma
101. HALO NAEVUS / SUTTON’S NAEVUS
Management
▪ If no atypical features, the patient should be followed with periodic skin examinations.
▪ Clinically atypical halo nevi should be examined histologically.
105. MEYERSON’S NAEVUS
Pathology
▪ A banal, usually compound, naevus with associated spongiotic dermatitis in the overlying dermis.
106. MEYERSON’S NAEVUS
Treatment.
▪ 1–2 weeks of moderately potent topical steroid
▪ secondary eczematous reaction settles
▪ Then , dermoscopy to ensure that the underlying naevus is benign
110. ATYPICAL (DYSPLASTIC) MELANOCYTIC NEVUS
Clark’s nevus/ Nevus with architectural disorder / B-K mole /
The mole of FAMM (familial atypical mole and melanoma syndrome)
111. ATYPICAL (DYSPLASTIC) MELANOCYTIC NEVUS
▪ Elder
▪ A controversial clinical designation for :
– Various naevi that have morphological changes (asymmetry / irregular
borders / colour variation)
– Naevi with architectural changes and / or cytological atypia.
112. ATYPICAL (DYSPLASTIC) MELANOCYTIC NEVUS
1. Nevi with atypical clinical features
2. Nevi with abnormal histopathological features
3. Nevi with both abnormal clinical and histopathological features
4. Nevi with histopathological features that are equivocal or of unknown significance
113. ATYPICAL (DYSPLASTIC) MELANOCYTIC NEVUS
A melanocytic naevus,
– which is 5 mm or larger in diameter,
– with an irregular or diffuse edge
– variable or mottled pigmentation
* Although there are histological correlates, the diagnosis is clinical.
114. ATYPICAL (DYSPLASTIC) MELANOCYTIC NEVUS
Natural history
▪ The naural history of benign acquired naevi
▪ Proliferation of melanocytes, until naevus reaches upto 5mm diameter
▪ Then proliferation at DEJ ceases
▪ The naevus cells migrate down into dermis
115. ATYPICAL (DYSPLASTIC) MELANOCYTIC NEVUS
Natural history
▪ Subsequently clinical senescence occurs
▪ Resulting in developent of compound naevus
▪ finally a cellular dermal naevus
116. ATYPICAL (DYSPLASTIC) MELANOCYTIC NEVUS
Natural history
▪ The natural history of an atypical naevi
▪ Melanocyte proliferation continues
▪ Naevus continues to grow in size (beyond the usual size)
▪ Junctional proliferative component may show
some features similar to early melanoma
117. ATYPICAL (DYSPLASTIC) MELANOCYTIC NEVUS
Natural history
▪ Results in irregularity of shape & color clinically
▪ Majority : Minority:
▪ Proliferation cease eventually continue to grow
Compound / dermal naevus May evolve into a Melanoma
119. ATYPICAL (DYSPLASTIC) MELANOCYTIC NEVUS
Data from literature
▪ 1. Irrespective of histology,
Melanoma risk is directly related to the numbers of ordinary naevi
+
Presence & number of atypical naevi
120. ATYPICAL (DYSPLASTIC) MELANOCYTIC NEVUS
Data from literature
▪ 2. very poor correlation between,
Clinically atypical melanocytic naevi
&
Histologically atypical melanocytic naevi
121. ATYPICAL (DYSPLASTIC) MELANOCYTIC NEVUS
Data from literature
▪ 3. Almost no data showing relationship between,
Histologically atypical melanocytic naevi
&
Increased Melanoma risk
132. ATYPICAL (DYSPLASTIC) MELANOCYTIC NEVUS
Pathology
▪ Architectural disorder:
▪ – Circumscription: Junctional component nested at both edges vs. single-cell in at least one edge
▪ – Symmetrical: Good overall symmetry regarding edges, size of junctional nests, and stromal response
▪ – Cohesiveness of nests: >50% of nests cohesive
▪ – Pagetoid spread: prominent, at periphery
▪ – Confluent growth: in >50% of the junctional melanocytic proliferation, either as ridging of melanocytic nests or as
contiguous single cells
▪ – Single cell proliferation: Junctional melanocytes arranged as single cells in more than 20% of the lesion
134. ▪ shouldering (S), or extension of
the junctional component
beyond the dermal nests of
melanocytes (D).
▪ Rete ridges are irregular and
distorted with bridging (B)
▪ Eosinophilic fibrosis (arrows).
▪ Scattered lymphocytic infiltrate
is often present (*)
135. Two histologic features of architectural disorder include:
1. concentric eosinophilic fibrosis (E), in which fibrosis encircles a rete peg;
2. lamellar fibroplasia (L), in which the fibrosis is confined to the tip of the rete peg with stacks of collagen fibers.
Nests of melanocytes in the DEJ
demonstrate random cytologic
atypia (arrows).
136. ATYPICAL (DYSPLASTIC) MELANOCYTIC NEVUS
▪ Cytological atypia in a dysplastic naevus is generally random and patchy, with atypical cells punctuating a
background of cells with minimal or no atypia.
▪ The presence of a monotonous population of severely atypical cells (in one region, or throughout the
lesion) is worrying for melanoma.
138. ATYPICAL (DYSPLASTIC) MELANOCYTIC NEVUS
Treatment
▪ All patients diagnosed with 1 or more atypical mole (AM) should undergo a complete cutaneous
examination.
▪ self-examination to detect changes in existing moles and to recognize clinical features of melanomas.
▪ baseline and serial color photograph
139. ATYPICAL (DYSPLASTIC) MELANOCYTIC NEVUS
Treatment
▪ the prophylactic removal of all atypical moles does not prevent the development of melanoma and is not
recommended.
▪ Regardless of the risk group, any pigmented lesion suspicious for melanoma and any persistently and
significantly changing lesion should,, be excised completely with approximately 2 mm margins for
histopathologic examination to exclude in situ melanoma.
▪ Such naevi should NEVER be punch biopsied or an incisional biopsy taken, as sampling error may cause
an early melanoma to be missed.
140. ATYPICAL (DYSPLASTIC) MELANOCYTIC NEVUS
Treatment
▪ FAMMM ( Familial Atypical Multiple Mole Melanoma Syndrome)
▪ the phenotype is a marker of risk and that risk cannot be removed by removal of the naevi.
▪ Such patients must be counselled about avoidance of sunburn for themselves and their children.
▪ They should be taught how to self examine with the aid of images
▪ a short period of follow-up
The histological appearance of an atypical spitzoid tumour, showing relative lack of symmetry.
Cytologic atypia beyond that which is typical for a Spitz nevus:
Pleomorphism
Variation in chromatin pattern
Nucleomegaly
Variation in nucleoli
Host response:
Patchy to band-like upper dermal mononuclear infiltrates
Fibroplasia
Dermal component:
Disordered architecture:
Thus, although the majority of atypical naevi behave in a benign manner, they are viewed as lesions exhibiting a more proliferative phenotype than
common acquired naevi, and are therefore both markers of risk of melanoma and precursor lesions for melanoma.