This document discusses endogenous pigmentation of the oral mucosa. It begins by classifying pigmentation as focal, diffuse, or associated with systemic diseases. Common causes of pigmentation include melanin, hemoglobin, carotene, and hemosiderin. Specific conditions addressed include freckles, oral melanotic macules, oral melanoacanthoma, melanocytic nevi, and malignant melanoma. Diffuse pigmentation can be due to physiologic pigmentation, drugs, smoking, or post-inflammatory changes. Systemic diseases like Addison's disease and Peutz-Jeghers syndrome can also cause oral pigmentation. Histopathology and differential diagnoses are provided for many of the conditions.
Central Giant Cell Granuloma :
WHO has defined it as an intraosseous lesion consisting of cellular and fibrous tissue that contains multiple foci of hemorrhage, aggregation of multinucleated giant cells and occasionally trabaculae of woven bone
Etiology JAFFE (1953): considered this lesion to be a local reparative reaction of bone, possibly to intramedullary hemorrhage or trauma, hence the term reparative giant cell granuloma was accepted.
Charles A Waldron & W G Shafer (1966) suggested trauma be an important etiological factor in the initiation of the CGCG of the jaws
Thoma K H (1986) suggested that the lesion may be due to capillary injury caused by defective wall due to some type of trauma
J V Soames and J C Southam (1997) suggested that it could be a reaction to some form of hemodynamic disturbance in bone marrow, perhaps associated with trauma and hemorrhage REGEZI AND SCIUBBA(1999) :
Suggested that
Response to previous traumatic or inflammatory episodes.
This lesion is charecterised by proliferation of fibroblasts and multinucleated giant cells, in a densely packed stromaThe CGCG is a benign process that occurs almost exclusively within the jaw bones
CLINICAL PRESENTATION
Found predominantly in children and young adult
It has a female predilection (2:1)
Most commonly affected site is the anterior portion of the jaws, with an increased frequency of occurrence in the mandible
Majority of the CGCG of jaws are painless, expansion of bone is detected on routine examination
Few cases may be associated with pain, paresthesia or perforation of a cortical bone plate, occasionally resulting in the ulceration of the mucosal surface by the underlying lesion
Radiographic featuresCentral giant cell lesions present as radiolucent defects. Which may be unilocular or multilocular.
The defect is usually well delineated
The lesion may vary from a 5×5mm incidental radiographic findings to a destructive lesion greater than 10cm in size.
radiographic findings
A small unilocular lesion may be confused with periapical granuloma or cysts.
multilocular giant cell lesions cannot be radiographically distinguished from ameloblastomas or other multilocular lesions. Based on clinical and radiological features CGCG may be divided into two categories
- Non-aggressive lesion
- Aggressive lesion
The non aggressive lesion makes up most cases and exhibit few or no symptoms, they demonstrate slow growth and do not show cortical perforation or root resorption of teeth involved in the lesion. The aggressive lesions are characterized by pain, rapid growth, cortical perforation and root resorption and show marked tendency to recur when compared with non aggressive typeSoft spongy, brownish to reddish friable tissue of various size.
A specimen is usually coated with fresh or coagulated blood. Giant cell lesions of the jaws show a variety of features. Common to all is the presence of few to many multinucleated
Ghost cells are translucent balloon shaped , elliptical epithelial cells are recognized as swollen, pale, eosinophilic cells.
They are seen either singly or in sheets with a clear conservation of basic cellular outline, generally with apparent clear areas or with some remnants indicative of the site previously occupied by the nucleus.
The transformation of epithelial cells into more resistant terminally differentiated apoptotic cells i.e., ghost cells are responsible for the banal behavior of neoplasms and they also help in relieving the stress of the forming neoplasm.
The most accepted nature of ghost cells is aberrant keratinization that is altered form of keratin as it doesn’t stain with normal cytokeratin antibodies.
Tonofilaments have been observed universally in the ghost cells of all the odontogenic or non-odontogenic tumors but these solely don’t satisfy their nature which is also found to be positive for enamel proteins in odontogenic tumors.
Although, studies prove an intricate functional relationship exists between Wnt and Notch signalling during development of neoplasms and in assigning cells to particular fates.
Their relationship along with other signalling pathways complex interaction during tumorigenesis also needs intensive evaluation and this would help revealing the missing link between odontogenic and non-odontogenic tumors exhibiting these similar looking mysterious ghost cells.
ODONTOGENIC MYXOMA :
Benign mesenchymal lesion that mimics microscopically the dental pulp or follicular connective tissue
Derived from odontogenic ectomesenchymeClinical feature:
Age : 10- 50 yrs with mean age of 30 yrs
No gender predilection
Both mandible and maxilla are equally effectedClinical feature:
Age : 10- 50 yrs with mean age of 30 yrs
No gender predilection
Both mandible and maxilla are equally effectedClinical feature:
Age : 10- 50 yrs with mean age of 30 yrs
No gender predilection
Both mandible and maxilla are equally effected
Radiographic feature :
Radiolucent and it appear as a well circumscribed or diffuse lesion
Often multilocular with honey comb pattern
Cortical plate expansion, root displacement or resorption may be seen Histopathology :
Tumor consist of acellular myxomatous connective tissue.
Benign fibroblast and myofibroblast with some amount of collagen are found in matrix
Bony island representing residual tubeculae
Capillaries are scattered through out the lesion
The presentation explain white lesions in oral cavity and the classification the demonstrate the etiology, histopathology, diagnosis and treatment for each one.
Odontogenic keratocyst (OKC) is the cyst arising from the cell rests of dental lamina. It can occur anywhere in the jaw, but commonly seen in the posterior part of the mandible. Radiographically, most OKCs are unilocular when presented at the periapex and can be mistaken for radicular or lateral periodontal cyst.
Fibro-osseous lesions of the jaws
Fibrous dysplasia
Cemento-osseous dysplasia
Focal cemento-osseous dysplasia
Periapical cemento-osseous dysplasia
Florid cemento-osseous dysplasia
Ossifying fibroma
Juvenile aggressive ossifying fibroma
Cherubism
Fibro-osseous lesions (FOL) are characterized by replacement of normal bone architecture by collagen fibers and fibroblasts containing calcified tissue.
They include a wide variety of lesions of developmental, dysplastic and neoplastic origins with clinical and radiographic presentation and behavior.
Because of the histological similarities between diverse diseases, proper diagnosis requires correlation of history, clinical and radiographic findings.Fibrous Dysplasia
2. Reactive (dysplastic lesions arising in the tooth-bearing area (presumably of periodontal origin).
a. Periapical cemento-osseous dysplasia
b. Focal cemento-osseous dysplasia
c. Florid cemento-osseous dysplasia
3. Fibro-osseous neoplasms (widely designated as cementifying fibroma, ossifying fibroma or cemento-ossifying fibroma.Bone dysplasias
a. Fibrous dyspla i. Monostotic ii. Polyostotic
iii. Polyostotic with endocrinopathy (McCune-Albright)
iv Osteofibrous dysplasia
b. Osteitis deformans c. Pagetoid heritable bone dysplasias of childhood
d. Segmental odontomaxillary dysplasia
2. Cemento-osseous dysplasias
a. Focal cemento-osseous dysplasia b. Florid cemento-osseous dysplasia
3.Inflammatory/reactive processes
a. Focal sclerosing osteomyelitis b. Diffuse sclerosing osteomyelitis
c. Proliferative periostitis
4. Metabolic Disease: hyperparathyroidism
5. Neoplastic lesions (Ossifying fibromas)
a. Ossifying fibroma b. Hyperparathyroidism jaw lesion syndrome
c. Juvenile ossifying fibroma i. Trabecular type ii. Psammomatoid type
d. Gigantiform cementomas
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Oral mucosa reflects the health of the whole human body at a first glance.If any disorder is present in the system it will first appear in oral cavity. Here is an overview of certain pigmented lesions.
Central Giant Cell Granuloma :
WHO has defined it as an intraosseous lesion consisting of cellular and fibrous tissue that contains multiple foci of hemorrhage, aggregation of multinucleated giant cells and occasionally trabaculae of woven bone
Etiology JAFFE (1953): considered this lesion to be a local reparative reaction of bone, possibly to intramedullary hemorrhage or trauma, hence the term reparative giant cell granuloma was accepted.
Charles A Waldron & W G Shafer (1966) suggested trauma be an important etiological factor in the initiation of the CGCG of the jaws
Thoma K H (1986) suggested that the lesion may be due to capillary injury caused by defective wall due to some type of trauma
J V Soames and J C Southam (1997) suggested that it could be a reaction to some form of hemodynamic disturbance in bone marrow, perhaps associated with trauma and hemorrhage REGEZI AND SCIUBBA(1999) :
Suggested that
Response to previous traumatic or inflammatory episodes.
This lesion is charecterised by proliferation of fibroblasts and multinucleated giant cells, in a densely packed stromaThe CGCG is a benign process that occurs almost exclusively within the jaw bones
CLINICAL PRESENTATION
Found predominantly in children and young adult
It has a female predilection (2:1)
Most commonly affected site is the anterior portion of the jaws, with an increased frequency of occurrence in the mandible
Majority of the CGCG of jaws are painless, expansion of bone is detected on routine examination
Few cases may be associated with pain, paresthesia or perforation of a cortical bone plate, occasionally resulting in the ulceration of the mucosal surface by the underlying lesion
Radiographic featuresCentral giant cell lesions present as radiolucent defects. Which may be unilocular or multilocular.
The defect is usually well delineated
The lesion may vary from a 5×5mm incidental radiographic findings to a destructive lesion greater than 10cm in size.
radiographic findings
A small unilocular lesion may be confused with periapical granuloma or cysts.
multilocular giant cell lesions cannot be radiographically distinguished from ameloblastomas or other multilocular lesions. Based on clinical and radiological features CGCG may be divided into two categories
- Non-aggressive lesion
- Aggressive lesion
The non aggressive lesion makes up most cases and exhibit few or no symptoms, they demonstrate slow growth and do not show cortical perforation or root resorption of teeth involved in the lesion. The aggressive lesions are characterized by pain, rapid growth, cortical perforation and root resorption and show marked tendency to recur when compared with non aggressive typeSoft spongy, brownish to reddish friable tissue of various size.
A specimen is usually coated with fresh or coagulated blood. Giant cell lesions of the jaws show a variety of features. Common to all is the presence of few to many multinucleated
Ghost cells are translucent balloon shaped , elliptical epithelial cells are recognized as swollen, pale, eosinophilic cells.
They are seen either singly or in sheets with a clear conservation of basic cellular outline, generally with apparent clear areas or with some remnants indicative of the site previously occupied by the nucleus.
The transformation of epithelial cells into more resistant terminally differentiated apoptotic cells i.e., ghost cells are responsible for the banal behavior of neoplasms and they also help in relieving the stress of the forming neoplasm.
The most accepted nature of ghost cells is aberrant keratinization that is altered form of keratin as it doesn’t stain with normal cytokeratin antibodies.
Tonofilaments have been observed universally in the ghost cells of all the odontogenic or non-odontogenic tumors but these solely don’t satisfy their nature which is also found to be positive for enamel proteins in odontogenic tumors.
Although, studies prove an intricate functional relationship exists between Wnt and Notch signalling during development of neoplasms and in assigning cells to particular fates.
Their relationship along with other signalling pathways complex interaction during tumorigenesis also needs intensive evaluation and this would help revealing the missing link between odontogenic and non-odontogenic tumors exhibiting these similar looking mysterious ghost cells.
ODONTOGENIC MYXOMA :
Benign mesenchymal lesion that mimics microscopically the dental pulp or follicular connective tissue
Derived from odontogenic ectomesenchymeClinical feature:
Age : 10- 50 yrs with mean age of 30 yrs
No gender predilection
Both mandible and maxilla are equally effectedClinical feature:
Age : 10- 50 yrs with mean age of 30 yrs
No gender predilection
Both mandible and maxilla are equally effectedClinical feature:
Age : 10- 50 yrs with mean age of 30 yrs
No gender predilection
Both mandible and maxilla are equally effected
Radiographic feature :
Radiolucent and it appear as a well circumscribed or diffuse lesion
Often multilocular with honey comb pattern
Cortical plate expansion, root displacement or resorption may be seen Histopathology :
Tumor consist of acellular myxomatous connective tissue.
Benign fibroblast and myofibroblast with some amount of collagen are found in matrix
Bony island representing residual tubeculae
Capillaries are scattered through out the lesion
The presentation explain white lesions in oral cavity and the classification the demonstrate the etiology, histopathology, diagnosis and treatment for each one.
Odontogenic keratocyst (OKC) is the cyst arising from the cell rests of dental lamina. It can occur anywhere in the jaw, but commonly seen in the posterior part of the mandible. Radiographically, most OKCs are unilocular when presented at the periapex and can be mistaken for radicular or lateral periodontal cyst.
Fibro-osseous lesions of the jaws
Fibrous dysplasia
Cemento-osseous dysplasia
Focal cemento-osseous dysplasia
Periapical cemento-osseous dysplasia
Florid cemento-osseous dysplasia
Ossifying fibroma
Juvenile aggressive ossifying fibroma
Cherubism
Fibro-osseous lesions (FOL) are characterized by replacement of normal bone architecture by collagen fibers and fibroblasts containing calcified tissue.
They include a wide variety of lesions of developmental, dysplastic and neoplastic origins with clinical and radiographic presentation and behavior.
Because of the histological similarities between diverse diseases, proper diagnosis requires correlation of history, clinical and radiographic findings.Fibrous Dysplasia
2. Reactive (dysplastic lesions arising in the tooth-bearing area (presumably of periodontal origin).
a. Periapical cemento-osseous dysplasia
b. Focal cemento-osseous dysplasia
c. Florid cemento-osseous dysplasia
3. Fibro-osseous neoplasms (widely designated as cementifying fibroma, ossifying fibroma or cemento-ossifying fibroma.Bone dysplasias
a. Fibrous dyspla i. Monostotic ii. Polyostotic
iii. Polyostotic with endocrinopathy (McCune-Albright)
iv Osteofibrous dysplasia
b. Osteitis deformans c. Pagetoid heritable bone dysplasias of childhood
d. Segmental odontomaxillary dysplasia
2. Cemento-osseous dysplasias
a. Focal cemento-osseous dysplasia b. Florid cemento-osseous dysplasia
3.Inflammatory/reactive processes
a. Focal sclerosing osteomyelitis b. Diffuse sclerosing osteomyelitis
c. Proliferative periostitis
4. Metabolic Disease: hyperparathyroidism
5. Neoplastic lesions (Ossifying fibromas)
a. Ossifying fibroma b. Hyperparathyroidism jaw lesion syndrome
c. Juvenile ossifying fibroma i. Trabecular type ii. Psammomatoid type
d. Gigantiform cementomas
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Oral mucosa reflects the health of the whole human body at a first glance.If any disorder is present in the system it will first appear in oral cavity. Here is an overview of certain pigmented lesions.
Pathological evaluation of melanocytic lesionsHisashi Uhara
In this lecture, the following basic steps by which I routinely scan specimens in our hospital will be presented with examples.
1. Evaluate the specimen preparation.
1) Is the incision for the specimen made perpendicular to the skin surface?
2) Is the slice of tissue from volar skin made perpendicular to the furrows of skin?
2. Estimate the specimen size and location.
1) Estimate the size of the lesion from the magnification of the objective lens.
2) Estimate the specimen location.
3. Precaution before evaluation
1) Observe the specimens without clinical information as much as possible.
2) Obtain as much information as possible at low magnification.
4. The steps for observation
1) At low magnification: Check the symmetric properties and circumscription of the lesion based on the following points.
a. Distance from the densest area of the lesion to both ends.
b. Variation of the thickness of epidermis from the center to both ends.
c. Distribution of melanin in the coronoid layer, epidermis, and dermis.
d. Distribution of nests and distance between each nest.
e. Density of solitary distributed melanocytes.
f. Existence of inflammatory infiltration in the dermis and its distribution.
g. Continuity of the spread of nests and tumor cells in both ends.
h. Is the bottom of the lesion smooth or not?
2) At high magnification: Check the details of tumor cells.
a. Tumor cells in the epidermis: Existence of necrosis, atypia (large nucleolus), or mitosis.
b. Other findings in the epidermis: Distribution of melanin in the cornified layer, the existence of tumor cells in the upper epidermis, the polymorphism of tumor cells, the relationship between tumor cells and keratinocytes.
c. In the dermis: An overlapping, crowded, or sheet-like gathering of tumor cells, maturation of tumor cells, mitotic figures, or melanin of tumor cells at the bottom of the lesion.
d. In the adnexal area: The existence of tumor cells in adnexal walls.
5. After provisionally giving a pathological diagnosis, check discrepancies between the pathological diagnosis and clinical findings. Return to the pathological evaluation if necessary.
power point presentation on the various pigmented lesions in the oral mucosa with their clinical features and oral manifestations and differential diagnosis
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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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
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
These 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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
6. The normal color represents the combined effect of a
number of factors:
• The concentration and state of dilation of capillaries in the
underlying connective tissue,
• The thickness of the epithelium,
• The degree of keratinization,
• And the amount of melanin pigment in the epithelium.
9. LYSIS OF RBC
SUB MUCOSAL COLLECTION
OF
HEMOGLOBIN/HEMOSIDERIN
RED, BLUE OR BROWN
COLOUR
HEMOGLOBIN
HAEMOGLOBIN &
IRON ASSOCIATED
PIGMENTATION
a. Ecchymosis
b. Purpura /
Petechiae
c. Hemochromatosis
23. FRECKLE
Asymptomatic, small (1-3 mm), well circumscribed, tan or brown
color macule.
Sun exposed facial and perioral skin
Light skinned, red or light blond haired individuals
ETIOLOGY
Developmental in origin
Polymorphism in MCIR gene.
Ch 4q32-q34.
( Increase melanin production without concomitant increase in
no of melanocytes)
25. ORAL/LABIAL MELANOTIC MACULE
Benign pigmented lesion that has no dermal counterpart.
Most common oral lesion - melanocytic origin
Etiology – trauma?
Females - lower lip – gingiva.
<1 cm, well circumscribed, oval or irregular in outline and
uniformly pigmented.
( Increase melanin production without concomitant increase in
no of melanocytes)
A macular lesion that, histologically, exhibits increased no of
melanocytes – melanocytic hyperplasia.
29. ORAL MELANOACANTHOMA
Benign lesion unique to mucosal tissues
ETIOLOGY
Rapid Onset, Acute Trauma, Chronic Irritation
CLINICAL FEATURES
Rapidly enlarging, ill defined, darkly pigmented macular or
plaque like lesion, and most develop in black females.
Cutaneous melanoacanthoma represents a pigmented variant of
seborrheic keratosis.
(Proliferation of benign, dendritic melanocytes throughout the
full thickness of an acanthotic and spongiotic epithelial layer)
32. ACQUIRED MELANOCYTIC NEVUS
(NEVOCELLULAR NEVUS, MOLE)
Localized benign proliferation of cells from neural crest called nevus cells.
Intraoral lesions occur but not common.
CLINICAL FEATURES
Develop in skin during child hood
Sharply demarcated brown or black macule <6mm, adult – nevus cell
proliferate – slightly elevated soft papule with smooth surface.(Compound
nevus) more time – nevus loses pigmentation, surface papillomatous,
hairs seen growing from centre. (Intra dermal nevus) <6mm
Many acquired melanocytic nevi will involute and disappear.
33. INTRAORAL NEVI
Evolution and appearance similar to skin nevi
Mature lesion does not show papillary change
2/3 rd lesions found in female
Average age of diagnosis 35 yrs
CLINICAL FEATURES
Oral melanocytic nevi - small <1 cm, solitary, brown or blue, well
circumscribed nodule or macule
Hard palate, buccal mucosa, labial mucosa, gingiva.
Oral nevi common in black..
34. Pathogenesis
Nevus cells – neural crest or immature melanocytes.
Nevic melanocytes – round, ovoid or sprindle shaped.
Migrate into and within submucosal tissues.
Etiology
Genetic, sun exposure
Association with inherited diseases
Familial atypical multiple mole and melanoma syndrome
Carney complex
Turners syndrome and noonans syndrome
90% of dermal melanocytes – mutations in BRAF, HRAS, NRAS oncogenes
35. HISTOPATHOLOGY
Benign encapsulated proliferation of small ovoid cells (nevus
cells) cells have small uniform nuclei, moderate eosinophilic
cytoplasm with indistinct cell boundries.
Nevus cells lack dentritic process that melanocytes possess.
36. Relationship of nevus cells to epithelium and
connective tissue.
(most intraoral melanocytic nevi are classified
microscopically as intramucosal nevi)
JUNCTIONAL NEVUS
COMPOUND NEVUS
INTRADERMAL/INTRAMUCOSAL NEVUS
49. • Least common, most deadly of all primary skin cancers.
RISK FACTORS
• Multiple episode of acute sun exposures,
immunosuppression, multiple cutaneous nevi, family history
of melanoma.
• Mutations in tumour suppressor genes- cdkna2/p16ink4a ,cdk4
• Mutation in BRAF, HRAS, and NRAS proto oncogenes (similar
to melanocytic nevi)
50. CLINICAL FEATURES
Common in white who live in sunbelt region of world.
Mortality rates high in blacks and hispanics.
Increased incidence in patients, especially males over 45.
On facial skin malar region affected (sun exposure)
53. • Radial growth phase
• Vertical growth phase
Nodular melanoma –radial growth phase is very short or nonexistent and
vertical growth phase predominates
58. PHYSIOLOGIC PIGMENTATION
Most common
Dark complexioned indivudals, including blacks, asians, south
americans.
Microscopically-increased amount of melanin pigment within
the basal layer.
Differential diagnosis - idiopathic, drug induced, smoking
induced melanosis.
62. Smoker’s melanosis
• Patchy brown macular pigmentations are sometimes present
in the buccal mucosa among heavy cigarette smokers.
• These macules are 0.5 to 1.0 cm spots that are multiple and
bilateral. Microscopically they are forms of basilar melanosis
without melanocyte proliferation.
• The mechanism for this association is unknown.
64. • The pathogenesis is believed to be related to a component in
tobacco smoke that stimulates melanocytes.
• Smoking up to nine cigarettes per day has been sufficient to
produce gingival melanin deposition
69. • These basilar melanosis of the skin may also involve the lips,
indeed, perioral and periorbital diffuse brown macular
pigmentation
• Their genesis is probably related to hormonal changes that
affect melanosome stimulation
• Following delivery and upon cessation of birth control
administration, the Cutaneous lesions slowly in volute.
70. MELANOSIS ASSOCIATED WITH SYSTEMIC OR GENETIC DISEASE
HYPOADRENOCORTICISM (ADDISONS DISEASE)
CUSHINGS SYNDROME
HYPERTHYROIDISM
PRIMARY BILIARY CIRRHOSIS
VITAMIN B 12 DEFICIENCY
PEUTZ JEGHERS SYNDROME
CAFÉ AU LAIT PIGMENTATION
HIV/AIDS ASSOCIATED MELANOSIS
73. • Generalized bronzing of skin and diffuse but patchy melanosis
of oral mucosa.
• Increased melanin in basal layer with melanin incontinence.
• Hyperpigmentation, hyponatremia, hyperkalemia.
74. Café au lait pigmentation
Bronze and tan diffuse and multifocal macular pigmentations
appear on the skin in neurofibromatosis, an autosomal
dominantly inherited disease characterized by multiple skin
nodules or even pendulous tumors.
These pale brown macules may be several centimeters wide.
They can occur anywhere, including the face and neck, and
occasionally, oral mucosa pigmentations arise. Owing to their
pale brown color, they are referred to as café au lait spots.
75. • Café-au-lait macules may be associated with albright’s syndrome
(polyostotic fibrous dysplasia, endocrine dysfunction, precocious puberty,
café-au-lait macules), noonan syndrome, watson syndrome, bloom
syndrome, ring chromosome syndromes, and others. The café-au-lait
macules of albright’s syndrome tend to be large and unilateral and have
irregular borders.
• Microscopically, café-au-lait macules are not particularly remarkable. They
generally show excess amounts of melanin in basal keratinocytes and
subjacent macrophages. Melanocytes are normal in appearance and may
be slightly increased in number.
76. • Albright syndrome – The borders of pigmented macules are
irregularly outlined.
• Neurofibromatosis – Borders smooth.
83. REFERENCE:
Greenberg, Glick, Ship. Burket`s Oral Medicine.
Neville, Allen, Bouquot. Oral And Maxillofacial
Pathology.
Jean M. Bruch. Clinical Oral Medicine And Pathology.
Lewis R. Eversole. Clinical Outline Of Oral Pathology..
Silverman, Eversole. Essentials Of Oral medicine.
