This document discusses various premalignant lesions of the skin. It begins by describing the normal architecture of the skin, including the different layers of the epidermis. It then discusses several specific premalignant lesions in more detail, including actinic keratosis, oral leukoplakia, Bowen's disease, erythroplasia of Queyrat, and Bowenoid papulosis. It also briefly mentions arsenical keratosis, Marjolin's ulcer, Paget's disease, extramammary Paget's disease, and xeroderma pigmentosum. For each condition, it provides information on clinical presentation, histopathology, causative factors, and risk of progression to
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.
NEOPLASMS AND PROLIFERATIONS OF FOLLICULAR LINEAGE
NEOPLASMS AND PROLIFERATIONS WITH SEBACEOUS DIFFERENTIATION
NEOPLASMS AND PROLIFERATIONS WITH APOCRINE DIFFERENTIATION
NEOPLASMS AND PROLIFERATIONS WITH ECCRINE DIFFERENTIATION
various cutaneous lymphomas though having low incidence but need to be diagnosed accurately. they can be mimiced by many non neoplastic conditions of skin. so discussing both T and B cell lymphomas
subcorneal
intraepidermal
subepidermal
pemphigus
nikolski's sign
pemphigus foliaceous
pemphigus vulgaris
pseudonikolski's sign
revision notes for dermatology based on lecture notes and high yield topic
based on previous year question
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.
NEOPLASMS AND PROLIFERATIONS OF FOLLICULAR LINEAGE
NEOPLASMS AND PROLIFERATIONS WITH SEBACEOUS DIFFERENTIATION
NEOPLASMS AND PROLIFERATIONS WITH APOCRINE DIFFERENTIATION
NEOPLASMS AND PROLIFERATIONS WITH ECCRINE DIFFERENTIATION
various cutaneous lymphomas though having low incidence but need to be diagnosed accurately. they can be mimiced by many non neoplastic conditions of skin. so discussing both T and B cell lymphomas
subcorneal
intraepidermal
subepidermal
pemphigus
nikolski's sign
pemphigus foliaceous
pemphigus vulgaris
pseudonikolski's sign
revision notes for dermatology based on lecture notes and high yield topic
based on previous year question
Basal Cell Carcinoma (BCC)
BCC is the most common cancer in humans.
Caused by UVR; PTCH gene mutation in most cases.
Clinically different types: nodular, ulcerating, pigmented, sclerosing , and superficial.
BCC is locally invasive, aggressive, and destructive but slow growing, and there is very limited (literally no) tendency to metastasize.
Skin Lesions: There are five clinical types:
1- Nodular
2- Ulcerating
3- Sclerosing (Cicatricial),
4- Superficial,
5- Pigmented.
1. Cutaneous T-cell pseudolymphomas
A) Primarily with stripe-like infiltration (the majority of cases)
Lymphomatoid drug eruption (most cases);
Lymphomatoid contact dermatitis;
Actinic reticuloid;
Nodular scabies (individual cases);
Idiopathic forms;
Clonal cutaneous T-cell pseudolymphomas.
B) Primarily with nodular infiltration (a small percentage
of the cases)
Drug-induced – mainly by anti-convulsive drugs
Persistent nodules after insect bites;
Nodular scabies (the majority of cases).
2. Cutaneous B-cell pseudolymphomas (with nodular infiltration)
Cutaneous lymphocytoma from Borrelia burgdorferi;
Cutaneous lymphocytoma after antigens injection;
Cutaneous lymphocytoma resulting from tattoo;
Cutaneous lymphocytoma after Herpes zoster;
Idiopathic forms;
Clonal cutaneous B-cell pseudolymphomas
A comprehensive review of Cutaneous Lymphomas - both B-Cell and T-Cell with latest treatment strategies. Target audience are oncologists, dermatologists, oncology physicians, dermatology and oncology fellows
Invasive Squamous Cell Carcinoma (SCC)
SCC of the skin is a malignant tumor of keratinocytes, arising in the epidermis.
SCC usually arises in epidermal precancerous lesions and, depending on etiology and level of differentiation, varies in its aggressiveness.
The lesion is a plaque or a nodule with varying degrees of keratinization in the nodule and/or on the surface.
Thumb rule:
Undifferentiated SCC: is soft and has no hyperkeratosis;
Differentiated SCC: is hard on palpation and has hyperkeratosis.
Exposure:
Sunlight. Phototherapy, PUVA (oral psoralen + UVA). Excessive photochemotherapy can lead to promotion of SCC, particularly in patients with skin phototypes I and II or in patients with history of previous exposure to ionizing radiation or methotrexate treatment for psoriasis.
Lesions :
Indurated papule, plaque, or nodule ; adherent thick keratotic scale or hyperkeratosis ; when eroded or ulcerated, the lesion may have a crust in the center and a firm, hyperkeratotic, elevated margin
Clark levels
level I, intra-epidermal;
level II, invades papillary dermis;
level III fills papillary dermis;
level IV, invades reticular dermis;
level V, invades subcutaneous fat.
Basal Cell Carcinoma (BCC)
BCC is the most common cancer in humans.
Caused by UVR; PTCH gene mutation in most cases.
Clinically different types: nodular, ulcerating, pigmented, sclerosing , and superficial.
BCC is locally invasive, aggressive, and destructive but slow growing, and there is very limited (literally no) tendency to metastasize.
Skin Lesions: There are five clinical types:
1- Nodular
2- Ulcerating
3- Sclerosing (Cicatricial),
4- Superficial,
5- Pigmented.
1. Cutaneous T-cell pseudolymphomas
A) Primarily with stripe-like infiltration (the majority of cases)
Lymphomatoid drug eruption (most cases);
Lymphomatoid contact dermatitis;
Actinic reticuloid;
Nodular scabies (individual cases);
Idiopathic forms;
Clonal cutaneous T-cell pseudolymphomas.
B) Primarily with nodular infiltration (a small percentage
of the cases)
Drug-induced – mainly by anti-convulsive drugs
Persistent nodules after insect bites;
Nodular scabies (the majority of cases).
2. Cutaneous B-cell pseudolymphomas (with nodular infiltration)
Cutaneous lymphocytoma from Borrelia burgdorferi;
Cutaneous lymphocytoma after antigens injection;
Cutaneous lymphocytoma resulting from tattoo;
Cutaneous lymphocytoma after Herpes zoster;
Idiopathic forms;
Clonal cutaneous B-cell pseudolymphomas
A comprehensive review of Cutaneous Lymphomas - both B-Cell and T-Cell with latest treatment strategies. Target audience are oncologists, dermatologists, oncology physicians, dermatology and oncology fellows
Invasive Squamous Cell Carcinoma (SCC)
SCC of the skin is a malignant tumor of keratinocytes, arising in the epidermis.
SCC usually arises in epidermal precancerous lesions and, depending on etiology and level of differentiation, varies in its aggressiveness.
The lesion is a plaque or a nodule with varying degrees of keratinization in the nodule and/or on the surface.
Thumb rule:
Undifferentiated SCC: is soft and has no hyperkeratosis;
Differentiated SCC: is hard on palpation and has hyperkeratosis.
Exposure:
Sunlight. Phototherapy, PUVA (oral psoralen + UVA). Excessive photochemotherapy can lead to promotion of SCC, particularly in patients with skin phototypes I and II or in patients with history of previous exposure to ionizing radiation or methotrexate treatment for psoriasis.
Lesions :
Indurated papule, plaque, or nodule ; adherent thick keratotic scale or hyperkeratosis ; when eroded or ulcerated, the lesion may have a crust in the center and a firm, hyperkeratotic, elevated margin
Clark levels
level I, intra-epidermal;
level II, invades papillary dermis;
level III fills papillary dermis;
level IV, invades reticular dermis;
level V, invades subcutaneous fat.
Premalignantlesions and conditions by Dr. Amit T. Suryawanshi, Oral Surgeon,...All Good Things
Hi. This is Dr. Amit T. Suryawanshi. Oral & Maxillofacial surgeon from Pune, India. I am here on slideshare.com to share some of my own presentations presented at various levels in the field of OMFS. Hope this would somehow be helpful to you making your presentations. All the best.
A brief explanation of a very common skin condition called warts. The presentation explains the types, morphology, pathogenesis and treatment of viral warts. Information taken from renowned dermatology books to assist students to prepare for USMLE, MRCP and post graduate MCPS and FCPS exams. Very beneficial for medical students, dermatologists, nurses and doctors.
A detailed presentation on the clinical features, predisposing factors and treatment of skin cancers especially Squamous Cell Carcinoma. Pre - malignant conditions like Actinic keratosis, Bowen disease, Porokeratosis are also discussed. Also the presentation provides a detail of the various differential diagnoses of the skin cancers. Useful for medical students, post graduate trainees and nursing staff. Role of sunlight is also discussed.
Introduction:
RNA interference (RNAi) or Post-Transcriptional Gene Silencing (PTGS) is an important biological process for modulating eukaryotic gene expression.
It is highly conserved process of posttranscriptional gene silencing by which double stranded RNA (dsRNA) causes sequence-specific degradation of mRNA sequences.
dsRNA-induced gene silencing (RNAi) is reported in a wide range of eukaryotes ranging from worms, insects, mammals and plants.
This process mediates resistance to both endogenous parasitic and exogenous pathogenic nucleic acids, and regulates the expression of protein-coding genes.
What are small ncRNAs?
micro RNA (miRNA)
short interfering RNA (siRNA)
Properties of small non-coding RNA:
Involved in silencing mRNA transcripts.
Called “small” because they are usually only about 21-24 nucleotides long.
Synthesized by first cutting up longer precursor sequences (like the 61nt one that Lee discovered).
Silence an mRNA by base pairing with some sequence on the mRNA.
Discovery of siRNA?
The first small RNA:
In 1993 Rosalind Lee (Victor Ambros lab) was studying a non- coding gene in C. elegans, lin-4, that was involved in silencing of another gene, lin-14, at the appropriate time in the
development of the worm C. elegans.
Two small transcripts of lin-4 (22nt and 61nt) were found to be complementary to a sequence in the 3' UTR of lin-14.
Because lin-4 encoded no protein, she deduced that it must be these transcripts that are causing the silencing by RNA-RNA interactions.
Types of RNAi ( non coding RNA)
MiRNA
Length (23-25 nt)
Trans acting
Binds with target MRNA in mismatch
Translation inhibition
Si RNA
Length 21 nt.
Cis acting
Bind with target Mrna in perfect complementary sequence
Piwi-RNA
Length ; 25 to 36 nt.
Expressed in Germ Cells
Regulates trnasposomes activity
MECHANISM OF RNAI:
First the double-stranded RNA teams up with a protein complex named Dicer, which cuts the long RNA into short pieces.
Then another protein complex called RISC (RNA-induced silencing complex) discards one of the two RNA strands.
The RISC-docked, single-stranded RNA then pairs with the homologous mRNA and destroys it.
THE RISC COMPLEX:
RISC is large(>500kD) RNA multi- protein Binding complex which triggers MRNA degradation in response to MRNA
Unwinding of double stranded Si RNA by ATP independent Helicase
Active component of RISC is Ago proteins( ENDONUCLEASE) which cleave target MRNA.
DICER: endonuclease (RNase Family III)
Argonaute: Central Component of the RNA-Induced Silencing Complex (RISC)
One strand of the dsRNA produced by Dicer is retained in the RISC complex in association with Argonaute
ARGONAUTE PROTEIN :
1.PAZ(PIWI/Argonaute/ Zwille)- Recognition of target MRNA
2.PIWI (p-element induced wimpy Testis)- breaks Phosphodiester bond of mRNA.)RNAse H activity.
MiRNA:
The Double-stranded RNAs are naturally produced in eukaryotic cells during development, and they have a key role in regulating gene expression .
Richard's aventures in two entangled wonderlandsRichard Gill
Since the loophole-free Bell experiments of 2020 and the Nobel prizes in physics of 2022, critics of Bell's work have retreated to the fortress of super-determinism. Now, super-determinism is a derogatory word - it just means "determinism". Palmer, Hance and Hossenfelder argue that quantum mechanics and determinism are not incompatible, using a sophisticated mathematical construction based on a subtle thinning of allowed states and measurements in quantum mechanics, such that what is left appears to make Bell's argument fail, without altering the empirical predictions of quantum mechanics. I think however that it is a smoke screen, and the slogan "lost in math" comes to my mind. I will discuss some other recent disproofs of Bell's theorem using the language of causality based on causal graphs. Causal thinking is also central to law and justice. I will mention surprising connections to my work on serial killer nurse cases, in particular the Dutch case of Lucia de Berk and the current UK case of Lucy Letby.
Earliest Galaxies in the JADES Origins Field: Luminosity Function and Cosmic ...Sérgio Sacani
We characterize the earliest galaxy population in the JADES Origins Field (JOF), the deepest
imaging field observed with JWST. We make use of the ancillary Hubble optical images (5 filters
spanning 0.4−0.9µm) and novel JWST images with 14 filters spanning 0.8−5µm, including 7 mediumband filters, and reaching total exposure times of up to 46 hours per filter. We combine all our data
at > 2.3µm to construct an ultradeep image, reaching as deep as ≈ 31.4 AB mag in the stack and
30.3-31.0 AB mag (5σ, r = 0.1” circular aperture) in individual filters. We measure photometric
redshifts and use robust selection criteria to identify a sample of eight galaxy candidates at redshifts
z = 11.5 − 15. These objects show compact half-light radii of R1/2 ∼ 50 − 200pc, stellar masses of
M⋆ ∼ 107−108M⊙, and star-formation rates of SFR ∼ 0.1−1 M⊙ yr−1
. Our search finds no candidates
at 15 < z < 20, placing upper limits at these redshifts. We develop a forward modeling approach to
infer the properties of the evolving luminosity function without binning in redshift or luminosity that
marginalizes over the photometric redshift uncertainty of our candidate galaxies and incorporates the
impact of non-detections. We find a z = 12 luminosity function in good agreement with prior results,
and that the luminosity function normalization and UV luminosity density decline by a factor of ∼ 2.5
from z = 12 to z = 14. We discuss the possible implications of our results in the context of theoretical
models for evolution of the dark matter halo mass function.
This pdf is about the Schizophrenia.
For more details visit on YouTube; @SELF-EXPLANATORY;
https://www.youtube.com/channel/UCAiarMZDNhe1A3Rnpr_WkzA/videos
Thanks...!
Nutraceutical market, scope and growth: Herbal drug technologyLokesh Patil
As consumer awareness of health and wellness rises, the nutraceutical market—which includes goods like functional meals, drinks, and dietary supplements that provide health advantages beyond basic nutrition—is growing significantly. As healthcare expenses rise, the population ages, and people want natural and preventative health solutions more and more, this industry is increasing quickly. Further driving market expansion are product formulation innovations and the use of cutting-edge technology for customized nutrition. With its worldwide reach, the nutraceutical industry is expected to keep growing and provide significant chances for research and investment in a number of categories, including vitamins, minerals, probiotics, and herbal supplements.
Observation of Io’s Resurfacing via Plume Deposition Using Ground-based Adapt...Sérgio Sacani
Since volcanic activity was first discovered on Io from Voyager images in 1979, changes
on Io’s surface have been monitored from both spacecraft and ground-based telescopes.
Here, we present the highest spatial resolution images of Io ever obtained from a groundbased telescope. These images, acquired by the SHARK-VIS instrument on the Large
Binocular Telescope, show evidence of a major resurfacing event on Io’s trailing hemisphere. When compared to the most recent spacecraft images, the SHARK-VIS images
show that a plume deposit from a powerful eruption at Pillan Patera has covered part
of the long-lived Pele plume deposit. Although this type of resurfacing event may be common on Io, few have been detected due to the rarity of spacecraft visits and the previously low spatial resolution available from Earth-based telescopes. The SHARK-VIS instrument ushers in a new era of high resolution imaging of Io’s surface using adaptive
optics at visible wavelengths.
Multi-source connectivity as the driver of solar wind variability in the heli...Sérgio Sacani
The ambient solar wind that flls the heliosphere originates from multiple
sources in the solar corona and is highly structured. It is often described
as high-speed, relatively homogeneous, plasma streams from coronal
holes and slow-speed, highly variable, streams whose source regions are
under debate. A key goal of ESA/NASA’s Solar Orbiter mission is to identify
solar wind sources and understand what drives the complexity seen in the
heliosphere. By combining magnetic feld modelling and spectroscopic
techniques with high-resolution observations and measurements, we show
that the solar wind variability detected in situ by Solar Orbiter in March
2022 is driven by spatio-temporal changes in the magnetic connectivity to
multiple sources in the solar atmosphere. The magnetic feld footpoints
connected to the spacecraft moved from the boundaries of a coronal hole
to one active region (12961) and then across to another region (12957). This
is refected in the in situ measurements, which show the transition from fast
to highly Alfvénic then to slow solar wind that is disrupted by the arrival of
a coronal mass ejection. Our results describe solar wind variability at 0.5 au
but are applicable to near-Earth observatories.
A brief information about the SCOP protein database used in bioinformatics.
The Structural Classification of Proteins (SCOP) database is a comprehensive and authoritative resource for the structural and evolutionary relationships of proteins. It provides a detailed and curated classification of protein structures, grouping them into families, superfamilies, and folds based on their structural and sequence similarities.
Cancer cell metabolism: special Reference to Lactate PathwayAADYARAJPANDEY1
Normal Cell Metabolism:
Cellular respiration describes the series of steps that cells use to break down sugar and other chemicals to get the energy we need to function.
Energy is stored in the bonds of glucose and when glucose is broken down, much of that energy is released.
Cell utilize energy in the form of ATP.
The first step of respiration is called glycolysis. In a series of steps, glycolysis breaks glucose into two smaller molecules - a chemical called pyruvate. A small amount of ATP is formed during this process.
Most healthy cells continue the breakdown in a second process, called the Kreb's cycle. The Kreb's cycle allows cells to “burn” the pyruvates made in glycolysis to get more ATP.
The last step in the breakdown of glucose is called oxidative phosphorylation (Ox-Phos).
It takes place in specialized cell structures called mitochondria. This process produces a large amount of ATP. Importantly, cells need oxygen to complete oxidative phosphorylation.
If a cell completes only glycolysis, only 2 molecules of ATP are made per glucose. However, if the cell completes the entire respiration process (glycolysis - Kreb's - oxidative phosphorylation), about 36 molecules of ATP are created, giving it much more energy to use.
IN CANCER CELL:
Unlike healthy cells that "burn" the entire molecule of sugar to capture a large amount of energy as ATP, cancer cells are wasteful.
Cancer cells only partially break down sugar molecules. They overuse the first step of respiration, glycolysis. They frequently do not complete the second step, oxidative phosphorylation.
This results in only 2 molecules of ATP per each glucose molecule instead of the 36 or so ATPs healthy cells gain. As a result, cancer cells need to use a lot more sugar molecules to get enough energy to survive.
Unlike healthy cells that "burn" the entire molecule of sugar to capture a large amount of energy as ATP, cancer cells are wasteful.
Cancer cells only partially break down sugar molecules. They overuse the first step of respiration, glycolysis. They frequently do not complete the second step, oxidative phosphorylation.
This results in only 2 molecules of ATP per each glucose molecule instead of the 36 or so ATPs healthy cells gain. As a result, cancer cells need to use a lot more sugar molecules to get enough energy to survive.
introduction to WARBERG PHENOMENA:
WARBURG EFFECT Usually, cancer cells are highly glycolytic (glucose addiction) and take up more glucose than do normal cells from outside.
Otto Heinrich Warburg (; 8 October 1883 – 1 August 1970) In 1931 was awarded the Nobel Prize in Physiology for his "discovery of the nature and mode of action of the respiratory enzyme.
WARNBURG EFFECT : cancer cells under aerobic (well-oxygenated) conditions to metabolize glucose to lactate (aerobic glycolysis) is known as the Warburg effect. Warburg made the observation that tumor slices consume glucose and secrete lactate at a higher rate than normal tissues.
4. Layers of epidermis
Stratum basale
(germinativum)
Stratum spinosum
Stratum granulosum
Stratum lucidum (may not
be present)
Stratum corneum
5.
6. Stratum basale
(germinativum)
Single layer of cells on basal
lamina
Stem cells which give rise to
keratinocytes
Contain melanin transferred
from melanocytes
May see mitotic figures
Desmosomes and
hemidesmomes
7. Stratum spinosum
Several cells thick
Have cytoplasmic processes
(spines)
Desmosomes
8. Stratum granulosum
1 to 3 layers of fusiform shaped
basophilic cells
Keratohyalin granules
contain cystine-rich and
histidine-rich proteins that
associate with keratin
filaments
10. Stratum corneum
Superifical keratinized layer
Cells
Almost filled with keratin
Flattened, non nucleate
Coated with extra-cellular
lipids that form water barrier
of skin
Layer that varies most in thickness
11. Actinic keratosis
Seen as multiple lesions in sun-exposed
areas
Excessive exposure to sunlight over many
years and inadequate protection against it
are the essential predisposing factors
Seen most commonly on the face and the
dorsa of the hands and in the bald portions
of the scalp in men
12. lesions measure less than 1 cm in
diameter
erythematous, are often covered by
adherent scales
May pigmented and show peripheral
spreading
Occasionally, lesions show marked
hyperkeratosis and then have the clinical
aspect of cutaneous horns.
13. Analogous lesion on the vermilion border of the lower
lip as solar cheilitis and may show areas of erosion and
hyperkeratosis
Both can develop into squamous cell carcinoma
Incidence of this transformation varies but It has been
estimated that in 20% of patients have SCC in one or
more of the lesions .
SCC arising either in actinic keratoses or de novo in
sun-damaged skin do not metastasize
14.
15.
16. Actinic keratosis. Tall columns of parakeratotic keratin alternate
with bands of orthokeratotic keratin with moderate atypia of the
underlying keratinocytes
18. Actinic keratoses are keratinocytic dysplasias or
squamous cell carcinomas in situ
Types- I) Hypertrophic,
II) Atrophic,
III) Bowenoid,
IV) Acantholytic,
V) Pigmented
19. Hypertrophic type of actinic
keratosis
Hyperkeratosis is pronounced and is usually intermingled
with areas of parakeratosis
Mild or moderate papillomatosis may be present
The epidermis is thickened in most areas and shows
irregular downward proliferation that is limited to the
uppermost dermis and does not represent frank invasion
Stratum malpighii show a loss of polarity and a disorderly
arrangement
Lichenoid actinic keratosis –a well known variant
20. Actinic keratosis, Hypertrophic type. The lesion shows hyperkeratosis and
papillomatosis with prominent cytologic atypia. There is a moderate
lymphocytic infiltrate in the underlying papillary dermis.
21. Atrophic type of actinic keratosis
Hyperkeratosis usually is slight
Epidermis is thinned and devoid of rete ridges
Atypicality of the cells is found predominantly in the
basal cell layer
Atypical basal layer may proliferate into the dermis as
buds and duct-like structures
22. Bowenoid type of actinic
keratosis
Histologically indistinguishable from Bowen's disease
Also be referred to as squamous cell carcinoma in situ
As in Bowen's disease, there is within the epidermis
considerable disorder in the arrangement of the
nuclei, as well as clumping of nuclei and dyskeratosis
23. Actinic keratosis, Bowenoid type (squamous cell carcinoma in situ). Low
magnification. Beneath a thick layer of parakeratotic keratin the epidermis
shows cytologic atypia.
24. Actinic keratosis, Bowenoid type (squamous cell carcinoma in situ).
Medium magnification. Marked cellular and nuclear pleomorphism are
present together with frequent and atypical mitoses
25. Actinic keratosis, Bowenoid type (squamous cell carcinoma in situ). High
magnification. Large atypical mitoses are prominent in this Bowenoid
actinic keratosis
26. Acantholytic type of actinic
keratosis
Immediately above the atypical cells composing the basal
cell layer there are clefts or lacunae
Result of anaplastic changes in the lowermost epidermis,
resulting in dyskeratosis and loss of the intercellular bridges
Above the acantholytic clefts, the epidermis shows varying
degrees of atypicality but generally less atypicality than
basal layer
When atypia is full-thickness or high-grade, the term
acantholytic squamous cell carcinoma in situ may be
applied.
27. Actinic keratosis, acantholytic type. Low magnification. The epidermis is
markedly hyperkeratotic. In the dermis, there is a dense lichenoid
inflammatory infiltrate. The keratosis shows focal acantholytic change
28. Actinic keratosis, acantholytic type. Medium magnification. In the dermis,
there is a dense lichenoid inflammatory infiltrate. The keratosis shows
focal acantholytic change
29. Actinic keratosis, acantholytic type. High magnification. Keratinocytes in
the basal layer are crowded, with an ↑ N:C ratio, and tend to become
separated from one another and to adopt a rounded configuration
30. Pigmented type of actinic
keratosis
Excessive amounts of melanin are present, especially
in the basal cell layer
Almost all the melanin is retained within the cell
bodies and dendrites of the melanocytes, indicating
some block in melanin transfer
Numerous melanophages are seen in most cases in the
superficial dermis
31. In all five types of actinic keratosis, the upper dermis
usually shows a fairly dense, chronic inflammatory
infiltrate composed predominantly of lymphoid cells
but often also containing plasma cells
Solar cheilitis, more frequently than actinic keratosis
of the skin, shows an inflammatory infiltrate in which
plasma cells predominate
32. ORAL LEUKOPLAKIA
Leukoplakia carries no histologic connotation and is used
only as a clinical description
Defined as a white patch or plaque that will not rub off and
that cannot be characterized clinically or histologically as any
specific disease (e.g., lichen planus, lupus erythematosus,
candidiasis, white sponge nevus)
Chemical irritation through tobacco or mechanical irritation
through dental stumps or ill-fitting dentures plays a role.
Any leukoplakia that is growing or altering its appearance
requires a repeat biopsy
33. Clinically, lesions of leukoplakia on the oral mucosa
consist of one or several white patches that may not be
raised and that appear ill defined
If slightly elevated, they appear sharply demarcated, with
an irregular outline
Frequently show C. albicans as a secondary invader, a
finding that may give rise to an incorrect diagnosis of
candidiasis
Induced by papillomaviruses, especially by HPV-11 and
HPV-16
34. 80% of the lesions found to be benign
Remaining 20% of the cases, 17% show varying degrees
of dysplasia or in situ carcinoma, and 3% show
infiltrating SCC
Leukoplakias on the buccal mucosa were found to be
benign in 96% of the cases; whereas on the floor of the
mouth, only 32% of the leukoplakias were benign, 31%
showed a carcinoma in situ, and 37% an invasive
carcinoma
35.
36. Oral leukoplakia. In this example, the squamous epithelium is
hyperkeratotic and acanthotic but shows no evidence of dysplasia.
37. BOWEN'S DISEASE
Solitary lesion
May occur on exposed or on unexposed skin
Exposed skin by exposure to the sun and on unexposed skin
by the ingestion of arsenic
Can form in lesions of epidermodysplasia verruciformis
caused by HPV-5
Slowly enlarging erythematous patch of sharp but irregular
outline, showing little or no infiltration.
Within the patch are generally areas of scaling and crusting
38. An intraepidermal squamous cell carcinoma referred
to also as squamous cell carcinoma in situ
Epidermis shows acanthosis with elongation and
thickening of the rete ridges,
Cells lie in complete disorder, resulting in a windblown
appearance
Horny layer usually is thickened and consists largely of
parakeratotic cells with atypical, hyperchromatic
nuclei
39. Atypical individual cell keratinization
Dyskeratotic cells are large and round and have a
homogeneous, strongly eosinophilic cytoplasm and a
hyperchromatic nucleus
Border between the epidermis and dermis everywhere
appears sharp, and the basement membrane remains
intact
Occasionally vacuolization of the cells, especially in the
upper portion of the epidermis seen
So long as Bowen's disease remains in its intraepidermal
stage, metastases do not occur
40.
41.
42. Bowen's disease. The epidermis is irregularly thickened. The
normal maturation pattern is effaced
44. ERYTHROPLASIA OF QUEYRAT
Carcinoma in situ located on the glans penis
Clinically and histologically, it is identical to
Bowen's disease
Seen almost exclusively in uncircumcised
men
Asymptomatic, sharply demarcated, bright
red, shiny, very slightly infiltrated plaque on
the glans penis, or less often, in the coronal
sulcus or on the inner surface of the prepuce
45. Role of HPV in causation
Progression into an invasive squamous cell carcinoma
has been observed in up to 30% of the patients , with
metastases in about 20%
Has a greater tendency toward invasion and metastasis
than Bowen's disease of the skin
46.
47. BOWENOID PAPULOSIS
Occurs in young adults
Most commonly located on the penile shaft,usually
multicentric
Papules coalesce to form plaques that resemble
condyloma acuminata
An indolent clinical course
Varying degrees of hyperkeratosis, parakeratosis,
irregular acanthosis, and papillomatosis
Viral(HPV),immunologic,hormonal, or chemical causes.
50. ARSENICAL KERATOSIS
Careless handling of industrial wastes
Arsenical keratoses of the palms and soles,
consisting of verrucous papules without
surrounding inflammation
Cutaneous carcinomas following arsenic
ingestion are usually multiple, and about three-
fourths of them are located on the trunk
Erythematous, scaling, occasionally crusted
patches that slowly increase in size
51. Avg latency between the beginning of
arsenic intake and the onset of carcinoma
about 18 yrs
Visceral carcinoma -most common
locations bronchi and the genitourinary
system
Commonly hyperkeratosis and acanthosis
without evidence of nuclear atypicality
but deeper sections show atypicality may
become apparent
Cutaneous carcinoma that follows arsenic
ingestion can be either squamous cell
carcinoma or basal cell carcinoma
52.
53. Marjolin's ulcer
An aggressive ulcerating squamous cell carcinoma
presenting in an area of previously traumatized
chronically inflamed, or scarred skin
Commonly present in the context of chronic
wounds including burn injuries , venous ulcers, ulcers
from osteomyelitis and post radiotherapy scars.
Slow growth, painlessness (as the ulcer is usually not
associated with nerve tissue), and absence of lymphatic
spread due to local destruction of lymphatic channels
54. Histologically the tumour is a well-diffrentiated squamous
cell carcinoma. This carcinoma is aggressive in nature,
spreads locally and is associated with a poor prognosis
40% occur on the lower limb and the malignant change is
usually painless.
This malignant change of the wound happens a long time
after initial trauma, usually 10–25 years later.
Its edge is everted and not always raised.
57. PAGET'S DISEASE
Paget's disease of the breast occurs almost exclusively in
women
In the male breast after treatment of a carcinoma of the
prostate with estrogen
Begins either on the nipple or the areola of the breast and
extends slowly to the surrounding skin
Always unilateral and consists of a sharply defined, slightly
infiltrated area of erythema showing scaling, oozing, and
crusting.
There may or may not be ulceration or retraction of the
nipple
58. Nearly always associated with carcinoma of the breast
Paget cell - They are large, rounded cells that are devoid of
intercellular bridges and contain a large nucleus and ample
cytoplasm. The cytoplasm of these cells stains much lighter
than that of the adjacent squamous cells
The dermis shows a moderately severe chronic
inflammatory reaction. Although Paget cells do not invade
the dermis from the epidermis, may be seen extending from
the epidermis into the epithelium of hair follicles
59.
60. Paget's disease. The epidermis is permeated with
numerous Paget cells lying singly and in groups. There is
no invasion of the dermis by Paget cells.
61. Paget's disease. High magnification. Paget cells are scattered
through the epidermis. They are large rounded cells devoid of
intercellular bridges, with ample pale-staining cytoplasm
62. EXTRAMAMMARY PAGET'S
DISEASE
Most commonly affects the vulva , less commonly the
male genital area, or the perianal area,and rarely the
axillae, the region of the ceruminal glands or that of
Moll's glands
Clinical picture shows a slowly enlarging reddish patch
with oozing and crusting. The patch resembles an
eczematous lesion, but has a sharp, irregular border
In contrast to the mammary type, itching is common.
Prognosis generally is better than that of mammary
Paget's disease
63. XERODERMA
PIGMENTOSUM
An autosomal recessive disorder
Neucleotide excision repair enzymes are mutated
Lesions occur chiefly in areas of the skin habitually exposed
to sunlight
Three stages – I) Diffuse erythema is associated with scaling
II) Atrophy of the skin, mottled pigmentation,
and telangiectases
III) Various types of malignant tumors of the
skin appear, often causing death
64. Hyperkeratosis, thinning of the
stratum malpighii with atrophy
of some of the rete ridges
Squamous cell carcinoma, basal
cell epithelioma, and, rarely,
fibrosarcoma and malignant
melanoma
65.
66. Spitz Nevus
Benign juvenile melanoma & spindle and epithelioid cell
nevus.
Solitary and is seen most commonly on the lower extremities
and face
Dome-shaped, hairless, small pink nodule
Microscopically, most Spitz nevi are of the compound type,
with a prominent intraepidermal component
Composed of spindle cells, epithelioid cells, or an admixture
of both.
67. The spindle cell variant is characterized by cigar-shaped cells
with large nuclei and prominent nucleoli
Epithelioid type have similar nuclei and a large, polygonal
cytoplasm with distinct borders
Multinucleated giant melanocyte containing up to 10–20
nuclei can be seen
Mitoses are found in approximately half of the cases
Pigmentation may occur(Reed Nevus)
Variants – desmoplastic, pagetoid, plexiform, angiomatoid
68.
69. Spitz nevus of spindle cell type. This example is predominantly
junctional in location.
70. A and B, Spitz nevus of epithelioid type. The tumor cells feature
large size, polygonal shape, occasional multinucleation, and a
strongly eosinophilic cytoplasm.
A and B, Spitz nevus of epithelioid type. The tumor cells feature
large size, polygonal shape, occasional multinucleation, and a
strongly eosinophilic cytoplasm
71. Reed nevus. The tumor is heavily pigmented, in contrast to the
usual type of Spitz nevus.
72. Spitz nevus of the spindle cell type associated with
pseudoepitheliomatous hyperplasia.
73. MELTUMPS
Melanocytic tumor of uncertain malignant potential
Heterogeneous group of melanocytic tumors that exhibit
some features indicative of possible malignancy, such as
nuclear atypia, macronucleoli, mitotic activity, necrosis, or
ulceration, but in number or degree insufficient to justify a
malignant diagnosis
Quite bulky neoplasms of the order of several millimeters
in diameter and thickness, composed of pigmented often
spindle-shaped cells
↑cellularity, atypical mitosis or focal necrosis may be seen
74. Giant Congenital Nevus
Variant of congenital nevus characterized by its extensive
size, its surface area being by definition 144 cm2 or larger
Also been defined as a nevus that measures more than
20 cm in diameter in an adult, or that occupies 20% or
more of the body surface area
Distribute along a dermatome and often has a ‘bathing
trunk’ or ‘garment’ configuration
Also referred to as giant pigmented nevus and giant hairy
nevus
May involve a whole extremity, the entire scalp, and most
of the trunk and even extend into the placenta
75. Commonly show BRAF mutation
Sometimes associated with meningeal or cerebral
melanosis (neurocutaneous melanosis or melanocytosis’)
May give rise to malignant melanoma of the skin or central
nervous system and to related malignant neuroectodermal
tumors with a variety of patterns, including malignant
peripheral nerve sheath tumor, (‘cutaneous malignant
melanotic neurocristic tumor’) rhabdomyosarcoma,
liposarcoma, and round cell or spindle cell undifferentiated
forms
80. Dysplastic Nevus
Occurs as a genetically determined syndrome in families
prone to develop malignant melanoma (dysplastic nevus
syndrome)
Appear in adolescence and continue to develop in adult life
Clinically atypical, with a relatively large size (>5 mm),
irregular outline, and variegated
Compound nevi exhibiting marked lentiginous
proliferation of melanocytes at the dermoepidermal
junction, with or without theques
81. Dermis shows eosinophilic and lamellar fibroplasia,
focal perivascular lymphocytic infiltrate, and vascular
dialation.
Collectively referred to as architectural atypia, are
usually matched by a mild to moderate degree of
cytologic atypia, manifested by nuclear
hyperchromasia, prominent nucleoli, and dusty
melanin pigment
82. A and B, Clinical appearance of dysplastic nevi in patient with the
dysplastic nevus syndrome. These nevi are large, have an irregular
outline, and feature a variegated appearance
83. A and B, Dysplastic nevus. There is dermal fibrosis, inflammation,
and a proliferation of melanocytes at the dermoepidermal junction,
with bridging of rete ridges.