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.
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.
What is Lymphoma?
Malignant lymphoma is a term given to tumors of the lymphoid system and specifically of lymphocytes and their precursor cells
i.e.
Cancer of the lymphatic system.
Many lymphomas are known to be due to specific genetic mutations.
What is Lymphoma?
Malignant lymphoma is a term given to tumors of the lymphoid system and specifically of lymphocytes and their precursor cells
i.e.
Cancer of the lymphatic system.
Many lymphomas are known to be due to specific genetic mutations.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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
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
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
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
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
1. Malignant Melanoma
Clinical Features, Pathology and Management
By
Dr Madhu kumar
Under guidance
Dr PV Budha MS
Dr Venkat Reddy MS
Dr Sailajarani MS
Dr Satyanaryana MS
Dr Ayyapasrinivas MS
2. What is Melanoma
• Melanoma is a very
serious form of skin
cancer.
• Melanoma is cancer of
the melanocytes.
• Melanocytes are
located in the Stratum
Basale and produce
melanin.
3. Melanocytes
• When skin is exposed to sunlight, melanocytes
produce more pigment, causing the skin to tan.
• Sometimes, clusters of melanocytes form
noncancerous (benign) growths called moles.
• Moles can be either flat or raised, round or oval, and
are smaller than a pencil eraser.
– Generally harmless, but can become cancerous
4. Incidence
• Although melanoma accounts for only about
5% of all skin cancer cases, it causes most skin
cancer-related deaths
• The incidence is rising by 3% a year
5. Causes of Melanoma
• 90% of all melanomas are linked to UV
radiation. (Sun exposure)
• 8% are due to chromosomal abnormalities
• About 2% are unknown
6. Risk Factors
• Family history of melanoma
• Dysplastic nevi (noncancerous, but unusual- looking
moles)
• Previous melanoma
• Many nevi (ordinary moles): more than 50
• Severe, blistering sunburns
• Freckling tendency
• Fair skin
• Excessive use of tanning beds
• Genetic predisposition
7. Signs and symptoms of melanoma
• Melanoma can appear suddenly as a new mole,
or it can develop slowly in or near an existing
mole.
• In men, melanomas are often found between the
shoulders and hips, or the head and neck area.
• In women, melanoma often develops on the
lower legs as well as between the shoulders and
hips.
• It may also appear under the fingernails or
toenails or on the palms or soles
8. ABCDE of melanoma
• A is for Asymmetry:
– One half of a mole or birthmark does not match the other.
• B is for Border:
– The edges are irregular, ragged, notched, or blurred.
• C is for Color:
– The color is not the same all over and may include shades
of brown or black, or sometimes with patches of pink, red,
white, or blue.
• D is for Diameter:
– The spot is larger than 6 millimeters across (about ¼ inch –
the size of a pencil eraser), although melanomas can
sometimes be smaller than this.
• E is for Evolving:
– The mole is changing in size, shape, or color.
9. Biopsy
Small and accessible lesions
– Excision with 1 cm margins in suspicious lesions
Large lesions
– Incisional or punch biopsy ?
Shave biopsy discouraged
18. Clark Classification (Level of Invasion)
• Level I: Lesions involving only the epidermis (in
situ melanoma); not an invasive lesion.
• Level II: Invasion of the papillary dermis but does
not reach the papillary-reticular dermal interface.
• Level III: Invasion fills and expands the papillary
dermis but does not penetrate the reticular
dermis.
• Level IV: Invasion into the reticular dermis but
not into the subcutaneous tissue.
• Level V: Invasion through the reticular dermis
into the subcutaneous tissue.
19. Breslow level of invasion
• Current stage system is based on depth of
invasion
• Measured using ocular micrometer
• Currently Breslows level 0f < 1mm, 1 to 4mm
and > 4 mm is used for TNM staging
20.
21.
22.
23.
24. • Metastatic workup done for stage III onwards
• Chest x ray
• CT Chest and abdomen
• PET CT
• MRI brain
26. • Early stages:
– Wide local excision
• More advanced:
– Wide local excision plus sentinel node biopsy,
– Based on the pathology
• Lympadnectomy
• observation
• interferon
• Metastatic:
– Clinical trial
– Radiation and systemic therapy
27.
28. Wide Excision
• Regardless of tumor depth or extension,
surgical excision is the management of choice
• If the deep fascia is not involved fascia is left
intact
32. Elective lymph node dissection (ELND)
• Use of prophylactic dissection (clinically negative
nodes) is controversial
• No prospective, randomized studies have
demonstrated that elective LN dissection
improves survival in patients with intermediate-
thickness melanomas
• By SLN biopsy micrometastasis is identified
removed node sent for frozen-section
examination, a complete LN dissection is
performed
33. • Dissection should be complete
• Groin dissection
– Deep (iliac) nodes must be removed along with
the superficial (inguinal) nodes
• Axillary dissection
– All levels I, II, III should be removed
• Head and Neck
– Superficial parotidectomy to remove parotid
nodes and a modified neck dissection
35. In-transit disease (local disease in
lymphatics)
• 5 to 8% of melanoma patients with a high-risk
primary melanoma (>1.5 mm)
• Hyperthermic regional perfusion
• Melphalan is the chemotherapeutic agent
used
36. • Melphalan generally is heated to an elevated
temperature [up to 41.5°C, (106.7°F)] and
perfused for 60 to 90 minutes
• Produce a high response rate (greater than
50%)
• Complications
– neutropenia, amputation, death
• Tumor necrosis factor alpha or interferon-alfa
along with melphalan regression rate 90%
41. Follow up
• Early melanomas
– Every 6 months for 2 yrs them annually
• Advanced melanomas
– Every 3-4 months for 3-4 yrs, every 6 months for 1
year, latter annually