- The document describes three medical cases involving thyroid specimens.
- Case 1 involves a left hemithyroidectomy specimen showing hypercellular nodules and pleomorphism. The final diagnosis is dyshormonogenetic goitre.
- Case 2 involves a mastectomy specimen showing a papillary carcinoma with solid and papillary areas. The diagnosis is a solid variant of invasive papillary carcinoma.
- Case 3 involves a total thyroidectomy specimen showing cribriform morphology and lymphovascular emboli. The diagnosis is papillary thyroid carcinoma, cribriform morular variant.
Slideshow is from the University of Michigan Medical
School's M1 Embryology sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M1Embryology
A CME organised by
Deccan Association of Pathologists
in association with
Bharati Vidyapeeth Deemed University Medical College & Hospital, Sangli
MULTIDISCIPLINARY APPROACH TOWARDS BREAST LESIONS
Slideshow is from the University of Michigan Medical
School's M1 Embryology sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M1Embryology
A CME organised by
Deccan Association of Pathologists
in association with
Bharati Vidyapeeth Deemed University Medical College & Hospital, Sangli
MULTIDISCIPLINARY APPROACH TOWARDS BREAST LESIONS
KCIAPM SLIDE SEMINAR 2016: RV METROPOLIS. CASE FILESkciapm
interactive slide seminar on 24th APRIL 2016, at Lecture Hall, School of Nursing, Bowring and Lady Curzon Hospital, Shivajinagar, Bangalore.The cases are drawn from the files of RV Metropolis, Bangalore. The case details are provided in the file.
Lesions/ Tumors/ Cysts doesn't follow the text books. Hence, every enthusiastic Pathologist should be updated with the current trends in the subject. Here is an attempt made from the most common text books of Oral pathology.
The data on thyroid tumors in the fourth edition of the World Health Organization (WHO) classification of endocrine tumors published in 2017 contain significant revisions.
These revisions of the 2004 WHO classification were based on new knowledge about pathology, clinical behavior, and most importantly the genetics of the thyroid tumors.
Endometrial Ca classification and histopathological features , CAP protocol for reporting , grading and staging tumors
Reference - Robbins , Rosai & Ackerman , Sternberg ,Fletcher ,WHO classification of tumors of female reproductive system, CAP
Similar to Kciapm slide seminar 2014 presentation (20)
interactive slide seminar on 16th APRIL 2017 at Lecture Hall, School of Nursing, Bowring and Lady Curzon Hospital, Shivajinagar, Bangalore.
The cases are drawn from the files of RV Metropolis, Bangalore.
- 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
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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
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.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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
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
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
12. DYSHORMONOGENETIC GOITRE
DYSHORMONOGENETIC GOITRE
• Rare, inherited usually autosomal recessive disorder
• C i bl k i T3 /T4 th
Causing block in T3 /T4 pathway
• Defects involve
TSH unresponsiveness
TSH unresponsiveness
Defective iodine transport
Abnormal thyroid peroxidase
y
p
Formation of abnormal iodoprotein and defective
deiodination of monoiodotyrosine and diiodotyrosine
– Abnormal th roglob lin s ntheses and e cretion
Abnormal thyroglobulin syntheses and excretion
–
–
–
–
• Rarely associated with deafness (Pendred’s syndrome)
13. DYSHORMONOGENETIC GOITRE
DYSHORMONOGENETIC GOITRE
MICROSCOPIC
• Hypercellularity resulting from TSH stimulation of the gland
• Cellular nodules of trabeculae, cords, with solid or microfollicular pattern
of epithelial cells with pale colloid.
of epithelial cells with pale colloid
• May have papillary foci, marked cellular pleomorphism .
• Presence of pleomorphism at the edge of the hyperplastic nodules and
not in the entire gland.
not in the entire gland
• Mitosis, bizarre hyperchromatic nuclei are seen.
• True invasion is rare.
IMMUNOHISTOCHEMISTRY
• Thyroglobulin positive
• Calcitonin negative
Ref :Vittal S, Chandrasekaran M, Bijai Kumar K, et al.Dyshormonogenetic
Goitre. JR Coll Surg Edinb;1993;38:205‐207
25. DIAGNOSIS
Solid variant of invasive papillary carcinoma
S lid
i t fi
i
ill
i
• Multiple nodules, each representing a duct filled
with neoplastic proliferation. Cells are ovoid to
with neoplastic proliferation Cells are ovoid to
spindle exhibiting solid pattern with fibrovascular
network.
network
• Other features observed were microcystic spaces
and foamy macrophages.
and foamy macrophages.
• Well defined pushing borders
• ER positive PR focally positive P63 negative
ER positive, PR focally positive, P63 negative.
26. SOLID VARIANT OF INVASIVE
PAPILLARY CARCINOMA
• A di ti t li i l tit
A distinct clinical entity .
• Controversial whether they could be considered
low–grade tumours
low grade tumours
• Originate from large or dilated ducts
• Pi
Primary affect older women occasionally seen in
ff
ld
i
ll
i
women below 50 years of age
• 90% il t l d i i th
90% unilateral and arise in the central area of the
t l
f th
breast
• Present with a bloody nipple discharge
Present with a bloody nipple discharge
• Nodular configuration and well circumscribed
27. SOLID VARIANT OF INVASIVE
PAPILLARY CARCINOMA
• Mi
Microscopically these tumours show multiple nodules,
i ll th
t
h
lti l
d l
each representing a duct filled with neoplastic
p
proliferation. Cells are ovoid to spindle exhibiting solid
p
g
pattern with fibrovascular network.
• Other features observed may be organoid pattern,
microcystic spaces and foamy macrophages
i
ti
df
h
• Well defined pushing borders
• Positive for ER and PR
Positive for ER and PR
• Negative for CK5/6.
• Other markers useful in diagnosis include Calponin
Other markers useful in diagnosis include Calponin,
P63, Skeletal muscle myosin heavy chain
28. References
References
• Tavassoli FA, Devilee P. World Health Organization
Classification of Tumours, Tumours of the Breast
and Female Genital Organs.2nd edition,Lyon
France: IARC Press.
• Gallager HS.Pathological types of breast cancer:
their prognosis.Cancer.1984;53:623‐629.
their prognosis Cancer 1984;53:623‐629
• Pettinato G, Manivel CJ, Panico L etal.Invasive
micropapillary carcinoma of the breast;Am J Clin
i
ill
i
f h b
Cli
Pathol.2004:121(6) 857‐866.
38. DIAGNOSIS OFFERED
DIAGNOSIS OFFERED
DIAGNOSIS OFFERED
DIAGNOSIS OFFERED
Papillary cell carcinoma
Tall cell variant
ll ll
Diffuse sclerosing variant
Papillary variant of medullary
carcinoma
Papillary thyroid carcinoma‐
Cribriform morular (with foci of
C ib if
l ( ith f i f
tall cell variant )
Why it is ruled
Why it is ruled out
Nuclear features of PTC present.
However, doesn't satisfy criteria of 'tall
d
'
f
f ' ll
cells'
Lymphocytic infiltrate usually seen along
with other features with prominent
sclerosing areas.
Papillae are lined by multiple layers of
p
y
p
y
neoplastic cells with small and irregular
nuclei containing condensed chromatin.
Lack typical nuclear features of papillary
Lack typical nuclear features of papillary
carcinoma
39. DIAGNOSIS
Papillary Thyroid carcinoma (PTC) Cribriform morular
Papillary Thyroid carcinoma (PTC) Cribriform‐morular
variant.
• Complex branching papillae lined by cuboidal cells
Complex branching papillae, lined by cuboidal cells.
Nuclei are hyperchromatic, optically clear, with
longitudinal grooves .There is a blending of several
longitudinal grooves There is a blending of several
histological patterns .
• Cribriform areas with back to back crowding with
Cribriform areas with back to back crowding, with
arches of cells in the absence of intervening
fibrovascular stroma
fibrovascular stroma
• Solid areas consisting of morules of squamoid cells that
do not show any keratinization or intercellular bridges.
41. REFERENCES
• Harach HR, Williams GT, Williams ED. Familial
adenomatous polyposis associated with thyroid
adenomatous polyposis associated with thyroid
carcinoma: a distinct type of follicular cell
neoplasm. Histopathology.1994;6: 549 561.
neoplasm Histopathology 1994;6: 549‐561
• Cameselle‐TeijeiroJ Chan JK Cribriform‐morular
Cameselle‐TeijeiroJ, Chan JK. Cribriform‐morular
vriant of papillary carcinoma; a distinctive variant
p
presenting the sporadic counterpart of familial
g
p
p
ff
adenomatous polyposis associated thyroid
carcinoma? Mod Pathol.1999;4: 400‐411.
45. Bronchoscopy - mass occluding right middle lobe bronchus
Bronchial wash – AFB – negative
Cytology – negative for atypical cells
46. CT scan –
soft tissue density mass measuring 5.4 x 5.7 x 5.8 cms in the right
middle lobe of lung in the perihilar region.
Enlarged pretracheal and subcarinal group of lymph nodes
largest measuring 2.1 x 1.3 cms.
Features suggestive of BRONCHOGENIC CARCINOMA with
metastasis to pretracheal and subcarinal lymphnodes.
47. Biopsy –
Gross - grey white tissue fragment measuring 0.2x0.2x0.1 cms.
Microscopy – small sized bland appearing tumor cells with
round to oval nucleus arranged in sheets and separated by
hyalinized stroma.
y
I
Impression – F t
i
Features favoring a benign neoplasm of salivary
f
i
b i
l
f li
gland type; possibility of myoepithelioma is suggested.
48.
49.
50. PER‐
PER‐OPERATIVE
Right posterolateral thoracotomy, bilobectomy and lymph
node clearance
Per operative findings – hard mass measuring about 6 x 4 cms
in right middle lobe. Mutiple subcarinal and paratracheal
lymphnodes.
51. HISTOPATHOLOGY
Gross – right middle and lower lobes of lung. Tumor with pushing
margins in the middle lobe with occlusion of bronchus. Tumor
g
6 x 5 x 4 cms. Yellow white appearance.
dissection , largest node 2.5 x 1.0 x 0.5 cms.
Lymph node
52.
53.
54.
55.
56. Microscopy Tumor composed of squmaous cells, intermediate cells and
mucin secreting cells.
All lymph nodes exhibit reactive changes
changes.
61. DIFFERENTIALS
•
•
•
•
•
•
•
•
•
•
Large cell undifferntiated carcinoma
L
ll diff
ti t d
i
Large cell neuroendocrine carcinoma
Mucoepidermoid carcinoma
Squamous cell carcinoma
Lymphoepithelioma like carcinoma
Adenoid cystic carcinoma
Neuroendocrine tumor
Adenosquamous carcinoma
Ad
i
Adenoid cystic variant of diffuse malignant mesotheliomabiphasic type with ? Asbestosis
p
yp
Neuroendocrine carcinoma mixed variant
63. IMMUNOHISTOCHEMISTRY
Pan CK – positive in tumor cells
S-100 – negative in tumor cells
Vimentin – negative in tumor cells
GFAP ( courtesy NIMHANS ) – negative in tumor cells
t
ti i t
ll
68. DISCUSSION
Rare primar tumor of lung – 0 1 – 0 2 %
primary t mor
l ng 0.1 0.2
Wide age range – mean age 40 years
Slow growing tumor
Main bronchus- submucosal glands of the
bronchus
• Classified under salivary gland neoplasms of
the lung
• Lobectomy, local resection or endoscopic
removal – excellent prognosis
• Diff
Differential di
ti l diagnosis iis adenosquamous and
i
d
d
adenocarcinoma of lung
•
•
•
•
69. REFERENCES
• Respiratory Medicine Case Reports 9
(2013) 18-20
• Arch Pathol Lab Med – Vol 131,
,
September 2007
• The new World Health Organization
classification of lung tumourE. Brambilla 1 , W.D.
Travis 2 , T.V. Colby 3 , B. Corrin 4 and Y. Shimosato 5ERJ
December 1, 2001 vol. 18 no. 6 1059 1068
December 1 2001 vol 18 no 6 1059‐1068
71. CLINICAL PRESENTATION
Male 25 years old
Male,
Mass per abdomen since 4 months
Bilateral undescended testes
Radiological finding – mass in right lumbar region measuring 20
x 20 cms. Extension upto liver superiorly pelvis inferiorly and
cms
superiorly,
crossing midline laterally.
73. HISTOPATHOLOGY
Gross – specimen altogether weighed 2140 grams and
measured 21 x 17 x 7 cms. Specimen consisted of a large, solid
pale brown tumor mass, spermatic cord, omentum and a
smaller tumor mass. Mid segment of spermatic cord showed a
g
p
nodular area measuring 2 cms.
74.
75.
76.
77. Microscopy –
Features of classical seminoma in both nodular masses
masses.
Adjacent testicular parenchyma from the smaller testicuar
mass exhibit features of intratubular germ cell neoplasia.
Nodular area in spermatic cord exhibits endometrial glands ,
endometrial stroma and smooth muscle.
Omentum exhibiting features of reactive mesothelial
hyperplasia.
h perplasia
83. DIFFERENTIALS
•
•
•
•
•
•
•
Leydig
L di cell h
ll hyperplasia with atrophic t b l and germ cell
l i
ith t
hi tubules
d
ll
tumor- seminoma
Persistent mullerian duct syndrome with seminoma and leydig
y
y g
cell hyperplasia
Persistent mullerian duct syndrome with cryptorchidism and
ITGCN and seminoma
Gonadal dysgenesis
True hermaphrodite
p
Anaplastic seminoma
Spermatocytic seminoma
84. Impression –
Classical seminoma – bilateral testes
Intratubular germ cell neoplasia – right testis
P i t t Mullerian duct syndrome
Persistent M ll i
d t
d
85. DISCUSSION
•
•
•
•
•
•
Rare form of male pseudohermaphroditisim ( 46 XY)
R
f
f
l
d h
h diti i
Persistence of mullerian duct structures due to lack of antimullerian hormone
X linked or autosomal recessive
Phenotypically male
Unilateral or bilateral cryptorchidism
15% risk of germ cell neoplasms and ITGCN
92. Microscopy
• Tumor cells are polygonal to oval
• Arranged in distinctive organoid pattern
• Separated by fibrocollagenous stroma and
Sepa ated
b oco age ous st o a a d
surrounded by blood vessels
99. • Primary / metastatic
• No clinical evidence of primary
sweating, palpitations,
• No history of sweating palpitations hypertension
100. • Primary paragangliomas of craniospinal axis arise in
cauda equina
• Encapsulated intradural masses attached to filum
terminale or less commonly the spinal roots
• Functionally silent
• Erosion into the neighbouring bone
• Osseous metastases
• Good number of cases of primary paragangliomas of
the i l
th spinal canal have been published
lh
b
bli h d
101. Immunohistochemistry
• Chief cells - chromogranin, synaptophysin, neuron
specific enolase, serotonin, neurofilament and neural
ifi
l
i
fil
d
l
cell adhesion molecule
• S-100 protein negative
102. REFERENCES
1. Rosai J. Surgical pathology. 9th ed. 19(2): 2586 to 2587
2. Lmejjati M, Parker F, Lacroix C et al. “Paraganglioma of sacral spine”.
Neurosciences 2011;16(3):270-272.
; ( )
3. Shin JY, lee SM, Hwang MY et al. “ MR findings of spinal
paraganglioma:report of 3 cases”. J Korean Med Sci. 2001;16:522 6.
cases
Sci 2001;16:522-6
4. Moran Ca, Rush W, Mena H. “primary spinal paragangliomas:a
clinicopathological and immunohistochemical study of 30 cases .
cases”
Histopathology. 1997;31(2):167-173
122. • Atypical, bizarre, symplastic or pleomorphic
leiomyomas
• Spontaneously or in patients taking progestin
compounds
• Electron microscopy demonstrates actin filaments
with associated dense bodies as well as incomplete
basal lamina (features characteristic of smooth
muscle cells)
• Low risk of recurrence
123.
124. REFERENCES
1. Rosai J. Surgical pathology. 9th ed. 19(2):1569-1636
2.
2 Fechner RE. Atypical leiomyomas and synthetic progestin therapy Am J
RE
therapy.
Clin Pathol. 1968,49:697-703
139. Criteria for primary melanoma of
bladder
• Ainsworth criteria
i
h i i
• Careful physical examination including the skin
p y
g
with Wood’s light together with detailed
y
history to exclude cutaneous melanoma
• Exclusion of visceral melanoma
• Pattern of recurrence consistent with primary
Pattern of recurrence consistent with primary
melanoma of bladder
• Histologically proved primary atypical
melanocytes
140. Treatment and prognosis
Treatment and prognosis
• R di l
Radical resection
ti
• Poor prognosis
• R f
References
•
•
•
•
•
•
•
Jalal Eddine El Ammari et al, “Primary malignant melanoma of the bladder,” Case reports in
urology,vol.2011
B. S. Stein and A. R. Kendall, Malignant melanoma of the genitourinary tract, Journal of
B S Stein and A R Kendall “Malignant melanoma of the genitourinary tract ” Journal of
Urology, vol. 132, no. 5, pp. 859–868, 1984. View at Scopus
A. M. Ainsworth, et al., “Primary malignant melanoma of the urinary bladder,” Cancer, vol.
37, no. 4, pp. 1928–1936, 1976. View at Scopus
B. Helpap, Nonepithelial neoplasms of the urinary bladder, Virchows Archiv, vol. 439, no. 4,
B Helpap “Nonepithelial neoplasms of the urinary bladder ” Virchows Archiv vol 439 no 4
pp. 497–503, 2001. View at Publisher ∙ View at Google Scholar ∙ View at Scopus
M. C. Wheelock, “Sarcoma of the urinary bladder,” The Journal of Urology, vol. 48, p. 628,
1942.
N. M. Anichkov and A. A. Nikonov, Primary malignant melanomas of the bladder, The
N M Anichkov and A A Nikonov “Primary malignant melanomas of the bladder ” The
Journal of Urology, vol. 128, no. 4, pp. 813–815, 1982.
C. T. Su and C. L. Prince, “Melanoma of the bladder,” The Journal of Urology, vol. 87, pp. 365–
367, 1962.
148. Cutaneous mastocytosis
• 80% of cases are urticaria pigmentosa
% f
i i i
• Mast cells
– 8‐15 microns in diameter
– Round or oval or fusiform in shape
Round or oval or fusiform in shape
– Granular cytoplasm
– Granules stain metachromatically with toludene
Granules stain metachromatically with toludene
blue or giemsa
– Granules are modified lysosomes containing
Granules are modified lysosomes containing
histamines and leukotrienes
157. Differential Diagnosis
Differential Diagnosis
Sertoli ll d l i t hi t ti
S t li cell nodule in atrophic testis.
Gonadoblastoma
Sex cord stromal tumor with annular tubules .
Testicular microlithiasis
Complete maturation arrest with corpora
amylacea and microlithiasis.
• Partial maturation arrest with testicular
microlithiasis
• Parasitic cysts
• ITGCN
•
•
•
•
•
160. Statistics
• Affects 1 in 20,400 people
Affects 1 in 20,400 people
– 2/3 of cases inherited from mother
– 1/3 of cases come from a spontaneous mutation in
1/3 of cases come from a spontaneous mutation in
the egg
• No effect on life expectancy
p
y
• No racial differences
• A genetic condition where affected people have male
g
p p
chromosomes and male gonads with complete or partial
feminization of the external genitals
• An inherited X linked recessive disease with a mutation
An inherited X‐linked recessive disease with a mutation
in the Androgen Receptor (AR) gene resulting in:
– Functioning Y sex chromosome
g
– Abnormality on X sex chromosome
162. References
References
• 1991;10(2):126‐44.
• The androgen insensitivity syndrome
The androgen insensitivity syndrome
(testicular feminization): a clinicopathologic
study of 43 cases.
study of 43 cases
• Rutgers JL, Scully RE. University of California,
Los Angeles
163. •
•
•
•
•
•
•
Forty‐three patients with the androgen insensitivity syndrome (AIS), ages
Forty three patients with the androgen insensitivity syndrome (AIS) ages
14 to 83 (average 27) years, were studied.
Forty patients had complete AIS and three patients had incomplete AIS.
Microscopic examination of the testes revealed immature tubules, which
Microscopic examination of the testes revealed immature tubules which
contained rare spermatogonia in 28% of the cases.
Prominent Leydig cells and a spindle‐cell stroma resembling ovarian
stroma were found in a majority of cases
were found in a majority of cases.
The organization of the testicular parenchyma could be classified into one
of four patterns: diffuse tubulostromal, lobular tubulostromal, mixed
,
p
tubulostromal, or stromal‐predominant.
Hamartomas were present in 63% and Sertoli cell adenomas in 23% of the
cases.
g
p
p
p
Malignant tumors developed in 9% of the patients and comprised two
seminomas, one intratubular germ cell neoplasm with early stromal
invasion, and a malignant sex cord tumor
164. References
• Arch Pathol Lab Med‐ Vol 123, March 1999
• Ackerman’s Surgical Pathology, Male
Ackerman s Surgical Pathology, Male
reproductive system , Pg 1438‐ 1439
172. Differential diagnosis
Differential diagnosis
• C t lli
Crystalline nephropathy
h
th
• Crystalline nephropathy‐ post chemotherapy for leukemia /
lymphoma
y p
• Crystalluria – Urate
• Oxalosis
• Infantile nephropathic cystinosis
• Nephrocalcinosis
• T b l i t titi l nephritis associated with tubular necrosis
Tubulointerstitial
h iti
i t d ith t b l
i
• Nephrocalcinois
• Storage disease ?
Storage disease ?
• Multicystic renal dysplasia
• Nephronophthisis
p
p
191. Q1: Where do they come from?
Q1: Where do they come from?
Neural crest = sympathetic nervous system
Neuroblasts, Ganglion cells, Schwann cells
Satellite cell
Ganglion cell
Nerve roots
Neck to pelvis……
192. Differentiate from ..for
confusion/clarity
• Peripheral
i h l
neuroblastic tumors
(pNTs)
( NT )
• neoplastic cells with a
neuronal phenotype
l h
• of neuronal (neural
crest) cellular origin...
t) ll l
i i
• deletion of
chromosome 1p and
h
1
d
MYCN amplification
• pPNET ( i h l
PNET (peripheral
primitive
neuroectodermal tumor)
• neuronal phenotype but
• of unknown (presumably
f k
(
bl
non‐neuronal) origin
• unique chromosomal
i
h
l
translocation fusing
EWS/ETS
193. How do they look?
International Neuroblastoma P th l
I t
ti
lN
bl t
Pathology Classification
Cl ifi ti
(INPC ‐ Shimada system)
• Four categories are discriminated according to the degree of
differentiation
[ganglionic cells 'organoid' maturation with the development
cells, organoid maturation with the development
of a Schwann cell stroma, and co‐existence of clones of
different maturity or of distinct aggressiveness]:
Neuroblastoma (Schwannian stroma‐poor)
(undifferentiated, poorly differentiated, dfferentiating)
Ganglioneuroblastoma intermixed (Schwannian stroma‐rich)
Ganglioneuroblastoma nodular
g
(composite Schwannian stroma‐rich/and stroma‐poor)
Ganglioneuroma (Schwannian stroma‐dominant)
(maturing, mature)
(maturing mature)
195. How do they behave? stratification….
How do they behave? stratification
• Clear stratification – “favourable”/
Clear stratification favourable /
“unfavourable” clinical/biological behaviors:
• Favourable (with/without treatment)
Favourable (with/without treatment)
– involution,
– spontaneous regression
spontaneous regression,
– tumor maturation,
• Unfavorable: OR aggressive progression
Unfavorable: OR aggressive progression,
• Closely related to the molecular/genetic
properties of the tumors of individual cases not –
i
f h
f i di id l
tumor margins/necrosis/vascular invasion/
spread…
d
196. How do they behave? stratification
How do they behave? stratification
• I t
International Neuroblastoma Ri k G
ti
lN
bl t
Risk Grouping,
i
INRG: Prior to any treatment patients will be put
into a risk category
into a risk category
• Favourable/unfavourable histology
– Age
– Mitosis/karryorhhexis index (MKI)
• Low: <100/5000 cells
/
• Intermediate: 100‐200/5000 cells
• High: >200/5000 cells
– DNA l id (FISH)
DNA ploidy
– MYCN amplification status
197.
198. Why bother?...treatment
Why bother? treatment
• In European countries , the treatment of
i
h
f
neuroblastoma patients depends on
– age at diagnosis (below or over 1 year of age),
– extent of the disease (stage)
g
– a genetic parameter, i.e. the amplification of the
MYCN oncogene
• In United States and Australia, DNA Index of
the tumour cells and histopathology (INPC)
the tumour cells and histopathology (INPC)
are also included in therapy stratification
201. The Wrong Right
I screened the slide back and forth
As I peeked through the microscope
A furious looking cell stared at me
Eureka! I exclaimed with pride and glee
p
g
‘Carcinoma’ was my undoubted decree
My adamant colleague refused to agree
He made a mockery of my grey cell ability
As he dismissed my verdict with a tinge of hostility
‘Tis just a inflammatory cell, buddy
As benign as a dead flea!
My expertise doubted, my self‐esteem trampled
A severe blow to my medical arrogance
I took i up as a challenge
k it
h ll
My insult I needed to avenge
How can “I” be proven erroneous?
Both of us sought the counsel of Big Boss
Whose eyes can swoop on a cell like a hawk
I prayed my belligerent colleague be proven wrong
p y
y
g
g
p
g
And my joy knew no bounds
“It is malignancy” he assertively pronounced
202. My battered ego appeased
Out of the hospital stormed an egotist
Ecstatic at being proven a whiz
I deserved to treat myself to a drink
Three cheers for me –An adept pathologist!
On my way I glanced at the lady, frail and old
Awaiting her young son’s report with hope
I did not to notice her, of course
d d o o o ce e , o cou se
Coz I wasn’t going to be the one to give her the news
That her young son had only a few tomorrows
I sat in my car and pondered where to party that evening
But something gnawed at my heart; an intense aching
Hot Tears poured down my cheeks sans warning
Undid the façade I was sporting
The wee bit of a human hidden in me startled my being
Late into the sleepless night I had a dream
Big Boss admonished me, yet on my f
d
h d
face I saw a gleam
l
A single streak of the whitener fluid he drew
To erase my reporting and write one anew
Do early morning dreams really come true?
Reeta Subramaniam Mani