Please find the power point (ppt.) on everything that you need to know about Malignant melanoma in very simple language by Sunil kumar Daha from very reliable references. Especially focused on surgical interventions. Thank you
Melanoma
Cutaneous Melanoma
also known as malignant melanoma, is a type of cancer that develops from the pigment-containing cells known as melanocytes.
Classification Of Melanoma
I : De novo melanoma
A. Melanoma in situ (MIS)
B. Lentigo maligna melanoma (LMM)
C. Superficial spreading melanoma (SSM)
D. Nodular melanoma (NM)
E. Acral-lentiginous melanoma (ALM)
F. Melanoma of the mucous membranes
G. Desmoplastic melanoma
II Melanoma arising from precursors
Melanoma arising in dysplastic nevomelanocytic nevi
B. Melanoma arising in congenital nevomelanocytic nevi
C. Melanoma arising in common NMN
Etiology And Pathogenesis
The etiology and pathogenesis of cutaneous melanoma are unknown.
Epidemiologic studies demonstrate a role for genetic predisposition and sun exposure in melanoma development.
The major genes involved in melanoma development reside on chromosome 9p21.
Etiology
UVR, mostly of the UVB spectrum (290–320 nm) that induces mutations in suppressor genes. The propensity for multiple BCC may be inherited. Associated with mutations in the PTCH gene in many cases.
Predisposing Factors
Genetic markers (CDKN2a mutation)
Skin type I/II
Family history of dysplastic nevi or melanoma
Personal history of melanoma
Ultraviolet irradiation, particularly sunburns during childhood and intermittent burning exposures
Number (>50) and size (>5 mm) of melanocytic nevi
Congenital nevi
Number of dysplastic nevi (>5)
Dysplastic melanocytic nevus syndrome
Immune suppression (debatable)
Number (>50) and size (>5 mm) of melanocytic nevi
Congenital nevi
Number of dysplastic nevi (>5)
Dysplastic melanocytic nevus syndrome
Immune suppression (debatable)
Six Signs of Malignant Melanoma (ABCDE Rule):
A- Asymmetry in shape—one-half unlike the other half.
B- Border is irregular—edges irregularly scalloped, notched, sharply defined.
C- Color is not uniform; mottled—haphazard display of colors; all shades of brown, black, gray, red, and white.
D- Diameter is usually large.
E- Elevation is almost always present and is irregular—surface distortion is assessed by side-lighting. others use E for Enlargement— a history of an increase in the size of lesion is one of the most important signs of malignant melanoma.
Lentigo Maligna Melanoma (LMM)
Please find the power point (ppt.) on everything that you need to know about Malignant melanoma in very simple language by Sunil kumar Daha from very reliable references. Especially focused on surgical interventions. Thank you
Melanoma
Cutaneous Melanoma
also known as malignant melanoma, is a type of cancer that develops from the pigment-containing cells known as melanocytes.
Classification Of Melanoma
I : De novo melanoma
A. Melanoma in situ (MIS)
B. Lentigo maligna melanoma (LMM)
C. Superficial spreading melanoma (SSM)
D. Nodular melanoma (NM)
E. Acral-lentiginous melanoma (ALM)
F. Melanoma of the mucous membranes
G. Desmoplastic melanoma
II Melanoma arising from precursors
Melanoma arising in dysplastic nevomelanocytic nevi
B. Melanoma arising in congenital nevomelanocytic nevi
C. Melanoma arising in common NMN
Etiology And Pathogenesis
The etiology and pathogenesis of cutaneous melanoma are unknown.
Epidemiologic studies demonstrate a role for genetic predisposition and sun exposure in melanoma development.
The major genes involved in melanoma development reside on chromosome 9p21.
Etiology
UVR, mostly of the UVB spectrum (290–320 nm) that induces mutations in suppressor genes. The propensity for multiple BCC may be inherited. Associated with mutations in the PTCH gene in many cases.
Predisposing Factors
Genetic markers (CDKN2a mutation)
Skin type I/II
Family history of dysplastic nevi or melanoma
Personal history of melanoma
Ultraviolet irradiation, particularly sunburns during childhood and intermittent burning exposures
Number (>50) and size (>5 mm) of melanocytic nevi
Congenital nevi
Number of dysplastic nevi (>5)
Dysplastic melanocytic nevus syndrome
Immune suppression (debatable)
Number (>50) and size (>5 mm) of melanocytic nevi
Congenital nevi
Number of dysplastic nevi (>5)
Dysplastic melanocytic nevus syndrome
Immune suppression (debatable)
Six Signs of Malignant Melanoma (ABCDE Rule):
A- Asymmetry in shape—one-half unlike the other half.
B- Border is irregular—edges irregularly scalloped, notched, sharply defined.
C- Color is not uniform; mottled—haphazard display of colors; all shades of brown, black, gray, red, and white.
D- Diameter is usually large.
E- Elevation is almost always present and is irregular—surface distortion is assessed by side-lighting. others use E for Enlargement— a history of an increase in the size of lesion is one of the most important signs of malignant melanoma.
Lentigo Maligna Melanoma (LMM)
Subspecialty of dermatology and pathology focused on performing and interpreting tests on human tissue samples to provide scientific data and consultative opinions to referring clinicians
Melanoma, the most serious type of skin cancer.
This presentation presents the skin cancer, basal cell carcinoma, Squamous cell carcinoma, and its symptoms, treatment, case
Subspecialty of dermatology and pathology focused on performing and interpreting tests on human tissue samples to provide scientific data and consultative opinions to referring clinicians
Melanoma, the most serious type of skin cancer.
This presentation presents the skin cancer, basal cell carcinoma, Squamous cell carcinoma, and its symptoms, treatment, case
Dr Patrick Treacy on Diagnosis and Treatment of Malignant Melanoma Dr. Patrick J. Treacy
A 23-year-old Siberian female patient presented with a changing lesion on her abdomen. The patient stated the lesion was present for about two years and it started
off from within a freckle, which started to grow larger and somewhat darken in appearance. It had the clinical appearance of a melanoma and the dermoscopy three-point checklist (designed to allow non-experts not to miss detection of melanomas) was used to determine whether this had a high likelihood of malignancy. It included:
Asymmetry: asymmetry of colour and structure in one or
two perpendicular axes
Atypical network: pigment network with irregular holes
and thick lines
Blue-white structures: there was some evidence of blue-
white veil and regression structures
Dr Patrick Treacy shares some of his most challenging cases.
This month he talks about treating Cutaneous Malignant Melanoma. Melanoma, also known as malignant melanoma, is a type of cancer that develops from the pigment-containing cells known as melanocytes. They typically occur in the skin but may rarely occur in the mouth, intestines, or eye. In women they most commonly occur on the legs, while in men they are most common on the back. Sometimes they develop from a mole with concerning changes including an increase in size, irregular edges, change in color, itchiness, or skin breakdown
A presentation created by Dr. Henry N. Ho, Medical Director, Head and Neck Program, Florida Hospital Cancer Institute, discussing everything you need to know about head and neck melanoma.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- 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
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
3. Arise from melanocytes in basal layer in the epidermis
The worst prognosis and morbidity in all skin cancers
Incidence is increasing by every year (3-7% per year)
accounts for only 4% of all skin cancers, but responsible
for more than 77% of skin cancer deaths
Early detection and treatment important, because it
reduces the mortality and increases survival
Prognosis ( 5 years) Local disease > % 90
Regional disease 60 %
Distant metastasis 5%
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3074354/
3
4. Mostly arise from skin ( 95 % )
But also found in the eyes, ears, GI tract, and mucous
membranes
Unknown primary or metastasis (3 %)
4
8. Very fair skinned,
◦ particularly those with fair or red hair
Tendency to sun burn
Excessive childhood sun exposure
EX: blistering childhood sun burns
Age :
◦ the incidence steadily rises with age
◦ The highest incidence is in those over 80
The development of melanoma is multifactorial
and appears to be related to multiple risk factors
8
9. No of mole
◦ more moles you have on your body, the higher your
risk of melanoma
◦ more than 100 Atypical or dysplastic nevi
Born in a hot country
◦ Ex: Australia or Israel
Malignant melanoma in the first degree relative
◦ (3-10 %)
People who work outdoors and so are in the sun
Ex:sailors, farmers
9
13. People who have risk factors
should be follow and have
preventive efforts
13
14. A changing mole
◦ Most common warning sign
Pruritis
◦ most common early sign of melanoma is pruritis
Bleeding and ulceration are late signs showing
advanced disease
14
15. A- Asymmetry:
One half of the lesion does not match the other half.
B- Border irregularity:
The edges are ragged, notched, or blurred.
C- Color varieation:
Pigmentation is not uniform and may display shades of tan,
brown, or black; white, reddish, or blue discoloration is of
particular concern.
D- Diameter:
A diameter greater than 6 mm is characteristic, although some
melanomas may have smaller diameters; any growth in a nevus
warrants an evaluation.
E- Evolving:
Changes in the lesion over time
15
16. All suspected lesions are removed for
histopathologic examination
16
17. Excision
◦ (Golden standard)
*İncision biopsy
*Punch biopsy
Partial thickness or shaving biopsies are contraindicated
*All dermis layers should be removed
Balch CM, Houghton AN, Sober AJ, Soong S.
Cutaneous Melanoma. St Louis QMP 1998 17
19. most common subtype of melanoma, occurring in
approximately 70% of patients
most common on the trunk in men and on the legs in
women
most commonly seen in individuals aged 30-50 years
Manifest as a flat or slightly elevated brown lesion with
variegate pigmentation (ie, black, blue, pink, or white
discoloration)
generally greater than 6 mm in diameter
Irregular asymmetric borders are characteristic
19
21. Nodular melanoma is the second most common subtype
of melanoma, occurs in 15-30% of patients
Sseen most commonly on the legs and trunk
Rapid growth occurs over weeks to months
Lack of an identifiable in situ (or radial growth) phase
Rresponsible for most thick melanomas
Mmanifests as a dark brown-to-black papule or dome-
shaped nodule, which may ulcerate and bleed with
minor trauma
Tends to lack the typical ABCDE melanoma warning
signs
21
23. accounts for 4-15% of cutaneous melanoma cases
typically located on the head, neck, and arms (sun-
damaged skin) of fair-skinned older individuals (average
age 65 y)
grows slowly over 5-20 years
Only 5% to 8% of lentigo maligna are estimated to
evolve to invasive melanoma.
Lentigo maligna appears as a tan to brown macule or
patch with variation in pigment or areas of regression
that appear hypopigmented clinically.
Lentigo maligna melanoma is characterized by nodular
development within the precursor lesion.
23
25. Acral lentiginous melanoma is the least common
subtype, representing only 2% to 8% of
melanoma in Caucasians,
It typically occurs on the palms or soles or
beneath the nail plate (subungual variant).
Irregular pigmentation, large size (>3 cm
diameter), and plantar location are characteristic
features of acral lentiginous melanoma.
25
26. Subungual melanoma may be confused with a
benign junctional nevus, pyogenic granuloma, or
subungual hematoma.
Rapid onset of diftuse nail discoloration or a
longitudinal pigmented band within the nail
plate warrants biopsy of the nail matrix, from
which these melanomas arise.
The additional presence of pigmentation in the
proximal or lateral nail folds (Hutchinson's sign)
is diagnostic of subungual melanoma
26
29. Spread of melanoma with the depth of invasion
from its origin in the epidermis. There are five
levels of invasion
classification
of the Melanoma by Clark
29
30. Level I — the atypical melanocytes are confined
to the epidermis (in situ melanoma);
Level II — the atypical melanocytes have extended into
the papillary dermis but have not reached
the reticular dermis;
Level III — the atypical melanocytes have penetrated to
the interface between the papillary dermis and
the reticular dermis but do not extend into the
reticular dermis;
Level IV — the atypical melanocytes have extended
into the reticular dermis;
Level V — the atypical melanocytes have reached into the
subcutaneous fat.
30
31. According to the thickness of the lesion
as measured by an ocular micrometer
from the top of the granular zone of
the epidermis to the base of the neoplasm
clasification by Breslow
31
32. Level 1: less than 0.76 mm thick
Level 2: between 0.76– 1.50 mm
Level 3: between 1.50 - 4.00 mm
Level 4: exceed 4.00 mm in thickness
32
36. Stage I : No metastasis (Local Disease)
Stage II : Nodal metastasis (Regional Disease)
Stage III : Distant Metastasis (Systemic Diasese )
36
37. T Staging: Primary tumor thickness
T1 : </= 1 mm a) no ulceration, mitosis < 1mm2
b) ulceration exist, mitoz > 1mm2
T2 : 1-2 mm a) no ulceration
b) ulceration exist
T3 : 2,01-4 mm a) no ulceration
b) ulceration exist
T4 : >4 mm a) no ulceration
b) ulceration exist
TNM Classification
AJCC 2009
37
38. TNM Classification
AJCC 2009
N Staging : Lymph node status
N1 : 1 Lymph Node
N2 : 2-3 Lymph Node .
N3 : > 4 metastatic nodes, or matted nodes, or in
transit metastases/satellites with
metastatic nodes
38
39. M Staging: Distant Metastases
M1 : Distant skin,subcutaneous or lymph node
Normal LDH
M2 :Pulmonary metastases Normal LDH
M3 : Visceral Organ or other distant metastases
Normal LDH
TNM Classification
AJCC 2009
39
43. Suggested surgical margins:
(according to breslow thickness)
In-situ MM 0,5-1 cm
Breslow thickness < 1mm : 1 cm
Breslow thickness 1-4 mm: 2 cm
Breslow thickness >4 mm: > 3 cm
43
44. METASTATIC MALIGNANT MELANOMA
LYMPHATIC METASTASES
HAEMOTOGENIC METASTASES
IN –TRANSIT METASTASES
LOCAL SATELITE METASTASES
44
45. Effect of Lymph Node metastases on
Survival
10 years Survival
%
Microscopic Lymph
Node metastases
48
No Lymph Node
metastases
65
Palpabl Lymph Node
metastases
12
45
46. Treatment of Lymph Nodes
Wait and see (no treatment)
Elective Lymph Node Dissection
Sentinel Lymphadenectomy
46
47. Elective Lymph Node Dissection
Removing the regional lymph nodes for
prevention in no clinical palpable lymph node
There is no consensus on survival advantage of
Elective Lymph Node Dissection (ELND)
47
50. Sentinel Lymphadenectomy
Morton introduced for Stage I Melanoma
patients in 1992
Vital blue dye intradermal injection was used for
lymphatic mapping
Lymphatic drainage of primary tumor goes
specific lymph node in regional lymph basin.
This is the first node in the basin. This is called
as sentinel lymph node
50
51. Sentinel lymph node shows the regional node
status
If sentinel lymph node negative, others lymph
nodes in the basin are also negative
If sentinel lymph node contains tumor cells, It
means disease spread to the regional nodal
basin
51
53. Sentinel Lymphadenectomy
Intradermal injection of tc99 m labeled sulfur colloid
and lymphoscintigraphy
intra-operative vital blu dye injection
Removing blue stained and hot lymph node as
sentinel nodes
Serial section of nodes, immunohistopathologic
examination by S 100, HMB 45 (melenoma spesific)
54
54. Advantages of Sentinel
Lymphadenectomy
Provides staging
Prevents of Electice Lymph node dissection
morbidity
Gives a specimen to pathologist to examine in detail
Provides psychological support
Can be done by local anesthesia
Less costly
55
57. Treatment of Distant Metastases
Soliter skin and distant lymph nodes are
removed
İsoleted pulmonary metastases can be removed
in selected cases
Brain and GI metastases are removed for
palliation
Radiotherapy may be benefical for selected
patients (mainly for pain treatment)
58
58. Avarege life expentancy is 6-9 months
There is no real treatment for Stage IV patients
Most realistic goal is palliation and preservation of
quality of life
59
60. Most common cancer in the world
Represents the most common form of cancer in
Caucasians
Continuing increase in incidence worldwide
Currently2–3 million new cases are diagnosed
worldwide every year
Most common risk factors is exposure to ultraviolet
(UV) light
BCC accounts for 75% of cases of NMSC
SCC accounts for the remaining majority of NMSC
61
62. UVB radiation
Sun light exposure
Increase in incidence in sunnier climates
lower rates in darker skin types
BCC has been more associated with
intermittent and childhood sun exposure
SCC more related to chronic UV exposure
63
63. UV light is thought to induce direct DNA
mutation
Use of tanning devices is associated with
2.5-fold increase in SCC risk and 1.5-fold
increase in BCC risk
Phototherapy, utilized in the treatment of
various skin diseases, is also associated
with increased risk of NMSC
64
64. UV effect reduced by hair, thick stratum
corneum, and melanin
More pigments protect the UVB , absorbs the
light
Exposure as child increases risk
Exposures to arsenic, organic hydrocarbon,
ionizing radiation, and cigarette smoke have
been associated with increasing risk for SCC
65
65. Genetic mutations are cofactor in the
development of NMSC
Mutation of patched gene on chromosome
9q22 associated with multiple BCC
Mutations of PTCH have been found in
70% of sporadic human BCC
66
66. Mutation of cytochrome450 (CYP),
glutathione S-transferase (GST) and p53
are associated with BCC
CYP and GST are known to detoxify
mutagens
p53 has an important function as a tumor
suppressor gene regulating the cell cycle
67
67. Actinic keratosis (AK) and Bowen’s disease
are precursor for SCC
72% of SCC have been noted to develop
within AK or actinically damaged skin
Errors in p53 signalling and mutations of
p53 have been identified in 69% to over
90% of invasive SCC
Other reported mutations for SCC include
WNT, p16INK4, NF-κB and c-Myc
68
68. Fair or red hair, blue eyes, increasing
number of melanocytic naevi
Human papillomavirus(HPV) pathogenic
for SCC
HPV prolong keratinocyte cell cycle, with
degradation of p53
69
69. Impaired immunity, especially cell-
mediated , is a well-established cause of
SCC
Chronically immunosuppressed patients
who undergone organ transplantation
Immunosuppressive drugs such as
azathioprine, cyclosporine, and prednisone
increase the risk for SCC by 50%
70
70. After 10 years of immunosuppression,
NMSC develop in 10% of patients ,after
20 years increases to 40%
Acquired impaired cell-mediated immunity,
including lymphomas, leukemias, post
radiotherapy, autoimmune diseases and
human papillomavirus(HPV)infection are
risk factor for SCC
71
71. Old scar, old burn scar
Actinic keratosis
Common above middle age and elderly
Characterized by papule or plaque with rough
surface
May develop cutaneous horn or become malignant
10-20% of lesions progress to SCC
72
72. Cutaneous Horn
Hard, yellowish brown, horny outgrowth,
often curved with circumferential ridges.
Surrounded by acanthotic collarette
Seen on exposed areas specially upper
part of face and ears
73
73. Bowen's disease
An early stage intraepidermal SCC
Common above 60 years
Common at genitalia
Typically presents as a gradually enlarging,
well-demarcated erythematous plaque with
irregular border, crusted or scaling surface
74
75. BCC
Tumour size greater than
2cm
Infiltrative, micronodular
Histological subtype
Perineural invasion
Anatomic site over central
face
SCC
Tumour size greater than 2
cm
Tumour thickness greater
than 4 mm
Moderate or poor histological
differentiation
Anatomic site over ear,
lip,Genitalia
Perineural invasion,
Lymphovascular invasion
Immunosuppressed patients
Tumours arising from chronic
scars or ulcers
76
81. Basel cell nevus
syndrome
Childhood onset
Autosomal
dominant
Multiple
Associate with
other
anomalies(skin pit
on palm,sole,bifid
fid rib)
82
82. Sun exposed area
Squamous epithelial cell ivade the dermis
with well differentiated keratinization
Poorly differentiated, keratinization and
inflammation minimal or absent
Poorly differentiated lesion may have
pseudo glandular appearance
83
84. In classical cases diagnosis can be made
clinically
Curretage biopsy
Local anaesthesia
Scrap with dermal curet
Tumor cell group soft and easily removed
85
85. Shave biopsy
Upper half of dermis sampled with
minimal deformity
Punch Biopsy
3-4 mm sufficient for diagnosis
May destroy normal dermal barrier and
allow extension into deeper structures
86
86. Excisional Biopsy
Treatment of choice for primary BCC or
pigmented lision
Impractical for large tumor when border
are not clear
Deep wedge biopsy is helpful in diagnosis
and depth
87
87. Choice of treatment dependent on
Risk stratification of the tumor, patient
preference or suitability, and availability of
local services
High-risk tumor have greater risk of
recurrence and require more aggressive
treatment
88
88. The gold standard for high-risk BCC and
SCC is Mohs micrographicsurgery (MMS)
If MMS is not available, excision with
predetermined wide margins
Radiotherapy may be considered
89
89. Under local anesthesia
Margin for resection is not well defined
Commonly 3-4 mm of normal appearing
skin
Local recurrence is greater then 90 %
90
90. Mohs micrographic surgery(MMS)
First developed by Frederic Mohs in1941
In standard surgical excision (SE) with
predetermined margins
100% of the peripheral and deep margin is
analysed to confirm the presence or absence of
any residual tumor
Once complete clearance is achieved, the wound
is repaired direct closure, local skin flap or skin
graft, secondary intention
91
92. Curettage and cautery( C and D)
Removing epidermis and dermis containing
tumour tissue
This process can be repeated immediately once or
twice
Effective treatment of low-risk NMSC
Increasing diameter, cure rates significantly
decreased
High cure rates for low risk
93
93. Cryosurgery
Delivery of liquid nitrogen to freeze and
then thaw the target tumour tissue
Local cellular destruction
High cure rates have been reported for
NMSC
94
94. Low cure rate for high-risk NMSC
Recommended for low-risk BCC
Not recommended for SCC as HCC have a
potential for metastasis
Cryosurgery will also manifest a
hypopigmented scar
95
95. Photodynamic therapy
Effective therapy for BCC or low-risk
nodular BCC of less than 2 mm thickness
Topical application of 5- aminolaevulinic
acid (ALA) or methyl aminolaevulinic(MAL)
Uptake of the drug into the tumour cells
preferentially, distruction occur
Excellent choice of treatmentfor BCC
96
96. Radiotherapy
Effective treatment modality for patients with
unable to undergo surgery
Efficacy is overall lower than with MMS
Beneficial for postoperatively tumors with
perineural invasion
When complete margin excision is not possible
Increase the risk of subsequent BCC and SCC
97