This document provides an overview of pathology related to the female genital tract, including the vulva, vagina, cervix, and endometrium. It discusses infections, pre-malignant and malignant neoplasms of these structures. Some key points include that HPV is associated with most cervical cancers, endometrial carcinoma is most common in post-menopausal women due to unopposed estrogen, and endometrial hyperplasia is a risk factor for the development of endometrial cancer if not treated.
Testicular tumors are rare.
1 – 2 % of all malignant tumors.
Most common malignancy in men in the 15 to 35 year age group.
Benign lesions represent a greater percentage of cases in children than in adults.
Most curable solid neoplasm
Testicular tumors are rare.
1 – 2 % of all malignant tumors.
Most common malignancy in men in the 15 to 35 year age group.
Benign lesions represent a greater percentage of cases in children than in adults.
Most curable solid neoplasm
Benign ovarian masses include functional cysts and tumors; most are asymptomatic.Most functional cysts and benign tumors are asymptomatic. Sometimes they cause menstrual abnormalities. Hemorrhagic corpus luteum cysts may cause pain or signs of peritonitis, particularly when they rupture. Occasionally, severe abdominal pain results from adnexal torsion of a cyst or mass, usually > 4 cm. Treatment varies depending on the patient's reproductive status.
Ca ovary staging(AJCC 8th Edition& FIGO 2014) and classificationDr.Bhavin Vadodariya
Pathological classification of ovary in details.
Principles of Staging in Ca Ovary.
Staging according to AJCC 8th edition & Figo 2014.
Summary of changes in 8th Edition AJCC
Benign ovarian masses include functional cysts and tumors; most are asymptomatic.Most functional cysts and benign tumors are asymptomatic. Sometimes they cause menstrual abnormalities. Hemorrhagic corpus luteum cysts may cause pain or signs of peritonitis, particularly when they rupture. Occasionally, severe abdominal pain results from adnexal torsion of a cyst or mass, usually > 4 cm. Treatment varies depending on the patient's reproductive status.
Ca ovary staging(AJCC 8th Edition& FIGO 2014) and classificationDr.Bhavin Vadodariya
Pathological classification of ovary in details.
Principles of Staging in Ca Ovary.
Staging according to AJCC 8th edition & Figo 2014.
Summary of changes in 8th Edition AJCC
Here is a presentation made by MBChB level 3 students for the lecture series on GIT Pathology. Hope it helps you. Few typos but better will come.It includes Hirshsprung's disease, Diveticulosis, Colitis, Colorectal Carcinoma among others
This is a lecture by John W. Martel from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
Fisiopatologia do Câncer de Ovários - Apresentação de artigo - New insights i...Caroline Reis Gonçalves
Apresentação do artigo New insights in the pathophysiology of ovarian cancer and implications for screening and prevention. Farr R. Nezhat, MD, Radu Apostol, DO, Camran Nezhat, MD, Tanja Pejovic, MD, PhD
American Journal of Obstetrics and Gynecology Setembro 2015
Presentation at Chittaranjan Seva Sadan, Kolkata where Dr Dasgupta was invited as faculty in the CME organized by Medical Education and research Committee, Bengal Obstetrics and Gynaecological Society
This ppt is intended for teaching cervical pathology to medical graduates. It covers anatomy, basic inflammatory conditions, dysplasia and malignancy and its pathogenesis and diagnosis
A brief discussion over CA Cervix. All newest updates in management protocol and revised by reknowned gynecologistts. Very much helpful for both under and post graduate students/Doctors.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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
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
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.
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.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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
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.
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
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.
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
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.
4. HSV Type II
-cervix, vagina, vulva
Papules-vescicle-ulcers
Cx and vagina-- Leukorrhea
Latent Infection
Recurrence
To neonates
Diagnosis-serology,microscopy
11. Vulvar Leukoplakia
Leukoplakia: A descriptive clinical term;
refers to a white plaque or patch on a mucosal
surface
Causes of vulvar leukoplakia:
1.Vitiligo (loss of pigment)
2.Inflammatory dermatosis: p.e. psoriasis
3.Squamous intraepithelial neoplasms of the vulva
(VIN) and invasive carcinoma
4.Paget’s disease
31. Cervicitis
“Erosions” and development of the transformation zone
(T zone). Nabothian cysts.
Infectious and non-infectious cervicitis
Vaginal flora, Chlamydia trachomatis, Ureaplasma
urealyticum, Trichomonas vaginalis, Candida
species, Neisseria gonorrhoeae, Herpes simplex II,
and HPV.
32. acute nonspecific: postpartum, Staphylococci/Streptococci
Nonspecific (chronic) cervicitis
Gross: reddening, swelling, and granularity around
margins of external cervical os.
Microscopy: Hyperplasia and reactive atypia of
epithelium, no dysplasia, glycogen depletion .
Mononuclear cell infiltrate, nabothian cysts. Viral
inclusions (HSV). Plasma cells in C. trachomatis.
37. Endocervical polyp
Inflammatory polypoid masses, cm.
Smooth surface composed of columnar
mucus-secreting cells (endocervical
epithelium) with underlying cystically
dilated glands filled with mucus. Stromal
edema inflammatory mononuclear cells.
Squamous metaplasia and ulceration.
38.
39.
40.
41. Cervical Intraepithelial Neoplasia (CIN)
and Carcinoma
Cervical cancer was the most frequent form of
cancer around the world.
Impact of Papanicolaou screening: Decrease
incidence of invasive tumors and increase
incidence in the detection of precursors
(dysplasias/CINs) lesions.
42. Cervical Intraepithelial Neoplasia (CIN)
and Carcinoma
Peak incidence
1. CIN : 30 Y
2. Invasive carcinoma: 45 y
Risk factors
1. Early age at first intercourse
2. Multiple sexual partners
3. A male partner with multiple previous
sexual partners
43. Cervical Intraepithelial Neoplasia
(CIN) and Carcinoma
Higher incidence in lower socioeconomic
groups
Genital infections
Exposure to oral contraceptives
Rarity among virgins
Multiple pregnancies
44. Cervical Intraepithelial Neoplasia
(CIN) and Carcinoma
T zone
High grade dysplasia/HPV 16 and 18
Viral isolation and typing do not predict the
course.
Follow up: cytology, colposcopy (acetic acid
test), biopsy*.
45.
46. HPV: 85-90% of lesions
Serotypes:
1. High risk: 16, 18, 31, and 33.
2. Low risk (associated with condylomas):
6, 11, 42, and 44.
Integration of viral genes into host
genome>>transcription>>translation of
specific proteins that inactivate p53 and
retinoblastoma tumor suppressor genes.
Cervical Intraepithelial Neoplasia (CIN)
and Carcinoma
47. Cervical Intraepithelial Neoplasia (CIN)
and Carcinoma
Viral infection does not mean that a women
will develop cancer.
10-15% HPV: negative
Other carcinogens, genetic factors, host
immunity, cigarette smoking.
48. Cervical Intraepithelial Neoplasia (CIN)
and Carcinoma
Importance of early detection, adequate follow up
and management.
Histologic grading of precursor lesions:
1. CIN I: Mild dysplasia
2. CIN II: Moderate dysplasia
3. CIN III : Severe dysplasia/carcinoma in situ
49.
50.
51.
52. Cervical Intraepithelial Neoplasia (CIN)
and Carcinoma
Cytologic grading of precursor lesions
1) LOW GRADE SQUAMOUS
INTRAEPITHELIAL LESIONS
[CIN I and Condylomas (koilocytosis)]
2) HIGH GRADE SQUAMOUS
INTRAEPITHELIAL LESIONS
[CIN II, CIN III/CIS]
53. Cervical Intraepithelial Neoplasia (CIN)
and Carcinoma
Natural History
Different studies = different populations = different
results
CIN I: 50 to 60% regress, persists 30%, and progress
to CIN III 20%. 1 to 5% become invasive.
CIN III: 33% regress, progression varies from 6 to
74%.
56. Invasive Carcinoma of the Cervix
ROUTES OF INVASION
Direct spread-adjacent stroma, vagina,
pelvic wall.
Local and distant spread to lymph nodes
Distant metastasis to lungs , liver ,bone
marrow etc
57.
58.
59.
60. Invasive Carcinoma of the Cervix
Squamous cell carcinoma
Well to poorly differentiated
Adenocarcinomas
Adenosquamous carcinomas
Staging
61.
62.
63.
64. Invasive Carcinoma of the Cervix
CIS: Asymptomatic, Leukorrhea
Carcinoma: Vaginal bleeding, leukorrhea,
painful coitus, and dysurea
DX: Colposcopy: acetic acid test, Bx
Mortality: Related to local extension*:
ureter obstruction or invasion of bladder or
rectum.
65. Invasive Carcinoma of the Cervix
Importance of early diagnosis
Time….?
5-year survival rate:
1. Stage 0 (CIS): 100%
2. Stage I: 85% to 90%
3. Stage II: 70 to 75%
4. Stage III: 35%
5. Stage IV: 10%
66. Invasive Carcinoma of the Cervix
Stage 0: Carcinoma in situ
Stage I: Tumor confined to the cervix
Stage II: Tumor extends beyond the cervix but not
onto the pelvic side wall
Stage III: Tumor extends to the pelvic side wall or
to the lower one third of vagina, or causes
hydronephrosis, or a nonfunctioning kidney
Stage IV: Tumor extends beyond true pelvis, or
biopsy-proved involvement of bladder or rectal
mucosa.
67. Invasive Carcinoma of the Cervix
Management
LEEP
Conization
Hysterectomy
Pelvic exenteration
Radiotherapy
72. Body of the Uterus
Endometritis
Adenomyosis
Endometriosis
Dysfunctional uterine bleeding
Endometrial hyperplasia
Endometrial polyps
Leiomyomas and leiomyosarcomas
Endometrial carcinomas
73. Endometritis
Clinical settings:
1. Chronic gonorrheal pelvic disease
2. Tuberculosis
3. Retained Product of conception
4. IUD
5. Spontaneously
Histology: Irregular disposition and
proliferation of endometrial glands, plasma cells
and lymphocytes in the stroma
74. Adenomyosis
Growth of the basal layer of endometrium
(glands and stroma) down into the
myometrium between the muscle bundles
Thick myometrium: reactive hypertrophy
Nonfunctional: no bleeding*
Menorrhagia, dysmenorrhea, and
premenstrual pain
75.
76. Endometriosis
Infertility, dysmenorrhea, pelvic pain.
Foci of endometrial tissue in pelvis
(ovaries, pouch of Douglas, uterine
ligaments, tubes, rectovaginal septum).
Sometimes in umbilicus, LNs, lungs, skin,
heart, bone.
Theories of genesis: Regurgitation,
metaplastic, and lymphovascular
77. Endometriosis
Functional endometrium: cyclic bleeding
Complications:Fibrosis,adhesions: pain, sterility
Gross: red-blue to yellow-brown nodules,
chocolate cysts in ovaries
Microscopy: Endometrial glands, stroma, and
hemosiderin deposition
78. Endometriosis
Theories of genesis:
1. Regurgitation: menstrual backflow
through fallopian tubes and subsequent
implantation
2. Metaplastic: metaplasia of coelomic
epithelium
3. Lymphovascular dissemination
83. Dysfunctional Uterine Bleeding
abnormal bleeding with no organic lesion
Etiology of uterine bleeding varies with age
:prepuberty
, adolescence,
reproductive age,
perimenopause, and postmenopause.
84. Dysfunctional Uterine Bleeding
Three functional groups (E/P)
1. Anovulatory cycles-metabolic
disorders, ovarian lesions,sys
diseases,unexplainable
2. Inadequate luteal phase-inadequate
corpus leuteum
3. Contraceptive induced bleeding
85. Anovulatory Cycles
Common at both ends of reproductive life
Hypothalamic-pituitary axis, thyroid, or adrenal
dysfunction
Functioning ovarian producing lesion,
malnutrition, obesity, stress, debilitating disease
Persistence of proliferative “growth” until
endometrium collapse, spiral arteries rupture, and
bleeding occurs.
86. Inadequate Luteal Phase
Corpus luteum fail to mature normally or regress
prematurely: less progesterone is produced: delay
and inadequate secretory phase
Contraceptive Induced Bleeding
Imbalance in the ratio Estrogen/Progesterone
87. Endometrial Hyperplasia
estrogen>>>>Progesterone: Polycystic
ovaries(Stein-Leventhal syndrome), cortical stromal
hyperplasia, granulosa-theca ovarian tumors
Simple Hyperplasia
Complex Hyperplasia without atypia
Complex Hyperplasia with atypia: 20/25% risk of
carcinoma
Continuum of changes based on duration and level of
estrogen excess
Causes irregular uterine bleeding
Biopsy and follow up
90. Endometrial Polyps
Uterine bleeding
Gross: Sessile(rarely pedunculated) rounded
lesions: 0.5 to 3 cm
Microscopy: Surface lined by columnar
epithelium, stroma (monoclonal stromal cells with
rearrangement of 6p21) with thick-walled vessels,
and endometrial glands some of which appear
cystically dilated.
Occur at any age, but common around menopause
94. Leiomyoma
Benign smooth muscle tumor
“Fibroids”, “Myomas”
30 to 50% of women during reproductive life.
Estrogen stimulates their growth
Involutes after menopause
Monoclonal, 40% have non-random
chromosomal abnormalities
95. Leiomyoma
Gross: Well circumscribed, firm, gray, white mass.
Whorled cut surface.
Singly or multiple. Few cm to large masses.
Intramucosal, intramural, and/or subserosal
location. Parasitic leiomyomas
Microscopy: Interlacing bundles of smooth muscle
cells. Foci of ischemic necrosis, fibrosis, cyst
degeneration, hemorrhage, and calcification are not
uncommon.
104. Endometrial Carcinoma
Most frequent cancer of the female genital tract in
USA
55 to 65 y (uncommon <40y)
Risk factors:
1. Obesity: synthesis of estrogen in fat deposits
2. Diabetes
3. Hypertension
4. Infertility: anovulatory cycles
105. Endometrial Carcinoma
Hyperestrinism : HRT, estrogen secreting
ovarian tumors, etc.
Background of endometrial hyperplasia
20%: no Hyperestrinism and no hyperplasia:
older patients, poor prognosis
106. Endometrial Carcinoma
Gross:
Diffuse thickening of uterine wall: Infiltrative
Exophytic form
Filling of the endometrial cavity with a firm
to soft partially necrotic tumor.
Myometrium invasion/ serosa/ LN
111. Endometrial Carcinoma
Grade: Degree of cytologic differentiation. GH1,
G2, and G3
Stage: Spread of the tumor
1. I: Confined to corpus
2. II: Extension to cervix
3. III: Extension outside the uterus , but still
confined to pelvis
4. IV: Extension outside the pelvis
112. Endometrial Carcinoma
Leukorrhea and irregular bleeding in a
postmenopausal patient
Enlargement of uterus and fixation to surrounding
structures
Late metastasizing neoplasm to LN and other organs
5-year survival rate:
1. Stage I: 90%
2. Stage II: 30 to 0%
3. Stage III and IV: less than 20%
128. Normal Cycle of Endometrium
Proliferative phase: Active growth of
glands, stroma and vessels influenced by
estradiol production by granular cells in the
follicles ( follicular phase).
Secretory phase: reflects the effect of the
combined production of progesterone and
estradiol by luteinized granulosa and theca
cells of the corpus luteum (luteal phase).
129. PAROVARIAN/PARATUBAL (MESONEPHRIC)
CYST
Common lesions, vary in size, often bilateral
Large cysts may become palpable, undergo
torsion with/without infarction, and cause pelvic
pain
They are benign
mesonephric cysts: lined by cuboidal cells;
usually arise in ovarian hilum
paramesonephric cysts: lined by columnar
tubal - type epithelium; adjacent to fallopian
tube
130.
131. FOLLICLE AND LUTEAL CYSTS OF OVARIES
Functional Cysts
Very common
Originate in unruptured Graffian follicles or in
follicles which have ruptured and resealed
Often multiple, they are located immediately
subjacent to the serosa
Lined by granulosa cells or by luteal cells
Usually small (1 - 1.5 cm), filled with clear fluid
Occasionally larger, up to 5cm, and may then be
palpable
Occasionally rupture, causing pain and
intraperitoneal bleeding
139. Ovarian Neoplasms
Clinical Presentation
Despite their considerable pathologic
diversity, the clinical presentation of
ovarian neoplasms is similar:
Usually asymptomatic until large enough
to cause pressure symptoms (pain, GI
complaints, urinary frequency)
30% are discovered incidentally during
routine GYN exams
140. Ovarian Neoplasms
Clinical Presentation
large masses may cause increased
abdominal girth
Occasionally, the masses undergo torsion
severe abdominal pain and acute
abdomen
Fibromas and malignant epithelial tumors
can cause ascites
mucinous tumors can cause
pseudomyxoma peritonei
tumors may cause endocrinopathies
141.
142.
143. Surface Coelomic Ovarian
Neoplasm
SEROUS TUMORS
MUCINOUS TUMORS
ENDOMETRIOID TUMORS - Most are
malignant; adenocarcinoma of
endometrium present in 15-30% of
cases
BRENNER TUMORS- Most are benign
144. Surface Coelomic Ovarian
Neoplasm
Most surface tumors present with
nonspecifically low abdominal pain
and/or abdominal mass
Malignant tumors grow through
capsule and widely seed the
peritoneal cavity with tumor
nodules and ascites; also distant
metastases
145. Surface Epithelial Tumors
They are derived from coelomic
epithelium.
They can be strictly epithelial, e.g.
serous, mucinous or endometroid.
They can also have a distinct stromal
component, cystadenofibroma or
Brenner tumor.
They are traditionally divided into
benign, low malignant potential or
malignant.
146. Serous Tumors
60% Benign, 15% borderline (LMP),
and 25% malignant.
Size ranges from 5-40cm.
Unilocular or multilocular containing
clear serous fluid.
Benign forms show smooth glistening
surface.
The surface of the malignant forms
appears multinodular.
147. Serous Tumors of the
Ovary
Single most common group of ovarian
tumors
benign and borderline: ages 20 - 50
years
malignant: ages 40 - 60+ years
Usually at least partially if not entirely
cystic:
“cystadenomas;
cystadenocarcinomas”
148. Serous Tumors of the Ovary
Behavior depends on degree of
differentiation and distribution
May occur on the ovarian surface,
occasionally arises from peritoneal
surface
155. Serous Tumor
of Low Malignant Potential
Papillary Tufting No evidence of
stromal invasion
156.
157. Borderline Vs. Malignant
Serous Tumors
Both may penetrate (or arise from) the ovarian
surface, shedding cells which implant on
peritoneal surfaces and produce ascites
Only malignant serous tumors invade the ovarian
stroma and metastasize to lymph nodes or other
sites
If confined to ovary, survival at 5 years:
Borderline - 100% ;
Malignant - 70%
161. Mucinous tumors
Benign tumors usually occur between 3rd.
And 5th. Decade of life
Most common tumor seen during pregnancy
most often associated with acute abdomen due
to torsion
162. Mucinous Tumors of Ovary
10% BENIGN - only 5% bilateral
10% BORDERLINE
10% MALIGNANT - only 20% BILATERAL
Note that Mucinous tumors are much less likely to
be bilateral and to be malignant than serous
tumors!
Often larger and more likely multiloculated than
Serous tumors; lack psammoma bodies
have endocervix-like or intestine-like lining cells
164. Mucinous Tumors of the Ovary
5% of cases are complicated by
pseudomyxoma peritonei:
peritoneal cavity becomes filled with
gelatinous mucinous fluid (similar to cyst
contents), which mats together the
abdominal viscera.
Rx is surgical, and repeated operations
are sometimes required
168. Mucinous tumor of low malignant
potential
10-15% of all mucinous tumors
6-8% of intestinal subtype are bilateral, Vs.
40% of endocervical type
100% long term survival in patients with
stage I mucinous tumor of LMP ( no
malignant potential)
169. Mucinous tumor of low malignant
potential
10-15% of all mucinous tumors
6-8% of intestinal subtype are bilateral, Vs.
40% of endocervical type
100% long term survival in patients with
stage I mucinous tumor of LMP ( no
malignant potential)
175. Endometroid tumors
Benign, unilateral masses, occurring in
older patient>57 Y/O
Endometroid tumor of low malignant
potential, rare, defining criteria are not
well established
Endometroid carcinoma, second most
common of ovarian epithelial
malignancy
176.
177. Endometroid adenocarcinoma
Occur in 5th. and 6th. Decade
About 15-25% are associated with similar
lesion in the endometrium
Can arise from endometriotic cyst, usually in
younger women
Synchronous or metachronous endometroid
adenocarcinoma of cervix has been reported
Primary extraovarian site has been reported
178. Clear cell tumor
Benign, rare
Low malignant potential, rare
Malignant
can arise from areas of endometriosis, have
been seen in association with endometroid
adenocarcinoma, both in ovary and
endometrium. They can also be associated
with hypercalcemia
179. Clear cell carcinoma
These tumors have the highest association
with pelvic endometriosis and Para
endocrine hypercalcemia.
180.
181. Brenner Tumor
Over 95% are diagnosed between the ages of
30-70.
Are usually unilateral and benign.
182.
183. Fibroma
Any age
Unilateral
Solid grey
Most hormonally inactive
Can produce hydrothorax and ascites
(Meigs Syndrome)
Rarely malignant
186. Thecoma
Any age
Unilateral
Yellow
Can elaborate estrogen resulting in excess
endogenous estrogen
Can also elaborate androgen resulting in
hirsutism
187.
188.
189. Sertoli Leydig Cell Tumor
All ages
Unilateral, usually small
Gray to yellow brown
Composed of tubuli or cords and plump
pink leydig cells
Most are androgenic
Small percentage are malignant
190. Leydig Cell Tumor
These tumors are usually
yellow in color, high
lipid content.
Uniform cell population,
presence of crystals
of Reinke are
diagnostic.
191.
192. Granulosa cell tumor
Any age, two different type, adult form and
juvenile form
Unilateral
Most elaborate large amount of estrogen
5-25% are malignant, adult form only
Composed of mixture of cuboidal Granulosa
cells in cords, sheets, or strands with
spindled or plump lipid laden theca cells
198. Dysgerminoma
Peak incidence: 2nd
and 3rd
decade.
80-90% unilateral
Gross: Solid small or large gray mass
Micro: Sheets and cords of large cleared
cells separated by scant fibrous strands.
Stroma contains lymphocytes.
Prognosis: malignant, but only 1/3
aggressive and spread; all radiosensitive
with 80% cure
201. Teratoma of the Ovary
BENIGN (MATURE) CYSTIC TERATOMA
Histologically mature
IMMATURE MALIGNANT TERATOMA
Average age 18 years
Most are predominantly solid
Foci of immaturity, usually of neuroepithelial type
Aggressive, metastasize widely
SPECIALIZED TERATOMAS
Struma ovarii: mature thyroid tissue; may cause
hyperthyroidism
Carcinoid: may cause carcinoid syndrome
202. Mature (benign) Cystic Teratoma
(“DERMOID CYST”)
Unilocular cyst, bilateral in 10% of cases
Lined by epidermis with all adnexal structures
bone, cartilage, thyroid, and other organoid
formations including tooth anlage, bronchi, gut,
brain, eye, etc. often present
Rarely exceed 10 cm diameter
Young women (late teens, 20’s); present most often
as asymptomatic ovarian masses on PE or X-ray
10-15% undergo torsion, present as acute abdomen
Karyotype of benign cystic teratoma always 46,XX
Malignant transformation in 1%, squamous cell ca.
208. Endodermal Sinus Tumor
Yolk Sac Tumor
Predominantly in young patients
Large partially cystic ovarian mass
Aggressive behavior, survival rate for
stage I tumors are 70-90% and 30-
50% for higher stage tumors.
209. Endodermal Sinus tumor
Serum AFP (alfa fetoprotein) is elevated in
almost all patients.
commonly show Shiller Duval Bodies.
210.
211. Metastases to Ovary
Older women
Usually bilateral
Tumors can be up to 20 cm
Common primary sites include breast,
lung, gastrointestinal tract
215. Gestational Trophoblastic Disease
Hydatidiform mole, complete and partial
Invasive mole
Choriocarcinoma
Persistent trophoblastic Disease”
All elaborate human chorionic gonadotropin
HCG, which can be detected in the blood
and the urine.
216. Hydatidiform Mole
Is a voluminous mass of swollen , sometimes
cystically dilated, chorionic villi,
appearing grossly as grape like structures.
The swollen villi are covered by varying
amount of banal to highly atypical
chorionic epithelium.
217.
218.
219. Complete Hydatidiform mole
All of the chorionic villi are abnormal
Chorionic epithelial cells are diploid, 46 XX or
uncommonly 46XY.
An empty egg is fertilized by two spermatozoa.
Incidence is 1-1.5/ 2000 pregnancies in US, higher
incidence in Asian countries.
More common before age of 20 and after age of
40.
220. Complete hydatidiform mole
The condition is usually discovered in 4th month
of gestation.
Ultrasound studies show a diagnostic pattern
which resembles snowflakes. Fetal heart tone is
usually absent.
The uterine cavity is filled with a delicate friable
mass of thin-walled translucent cystic structures.
Striking proliferation of cytotrophoblasts and
syncytiotrophoblasts present.
Markedly elevated serum HCG
2% progress to choriocarcinoma
221.
222. Partial hydatidiform mole
Is developed as the result of fertilization of
a normal egg by two spermatozoa.
Is always triploid (69XXY).
Villous edema is only seen in some villi.
Trophoblastic proliferation is focal.
Serum HCG level is less elevated.
Rarely progresses to choriocarcinoma.
224. GESTATIONAL TROPHOBLASTIC DISEASE:
HYDATIDIFORM MOLE, COMPLETE TYPE
Swollen, avascular
villi covered by
chorionic
epithelium
(trophoblast) of
varying atypia
Gross appearance is
that of a
voluminous mass
of grape like
structures
225. GESTATIONAL TROPHOBLASTIC DISEASE:
COMPLETE VERSUS PARTIAL HYDATIDIFORM MOLE
FEATURE COMPLETE PARTIAL
Karyotype 46, XX (rare XY) 69, XXY
Villous edema all villi some villi
Trophoblast Pro- diffuse; circum- partial
liferation ferential
Atypia often absent
serum HCG elevated less elevated
HCG in tissue ++++ +
Behavior 2% get chorio- rare chorio-
carcinoma carcinoma
226. GESTATIONAL TROPHOBLASTIC
DISEASE:
PARTIAL HYDATIDIFORM MOLE
A fetus or fetal parts may also be
present
Some villi are normal
Almost always triploid
Normal egg + two spermatozoa 69,XXY
Rarely becomes malignant
227. Invasive Hydatidiform Mole
An invasive mole retains hydropic villi, which
penetrate the uterine wall.
Can cause uterine rupture and can be life
threatening.
Hydropic villi may embolize to distant organs,
but this tumor does not have metastatic potential.
Cure is possible by hysterectomy or
chemotherapy.
228. Choriocarcinoma
Is very aggressive malignant tumor arises
either from gestational chorionic
epithelium or less frequently, from
totipotential cells within gonads or
elsewhere.
Incidence is 1/ 30,000 pregnancies in US.
More common in Asian and African
countries.
229. Choriocarcinoma
Incidence
In US 1/30,000 pregnancies
50% follow complete molar pregnancy, 25%
following abortion, remainder following normal
pregnancy
In Asia and Africa can be as high as
1/2,000 pregnancies
230. Choriocarcinoma
Most cases are discovered by the appearance of a
bloody, brownish discharge, accompanied by a
rising titer of HCG, particularly the beta subunit.
Usually appear as very hemorrhagic, necrotic
masses within the uterus.
The tumor is entirely composed of
cytotrophoblasts and syncytiotrophoblasts.
Widespread dissemination via blood, lung (50%),
vagina (30-40%), brain, liver and kidney.
231. Choriocarcinoma
Chemotherapy results in almost 100% cure or
remission in all patients except some who have
high risk metastatic trophoblastic disease.
Many of the cured patients have subsequent
normal pregnancies.
By contrast, non-gestational choriocarcinoma are
much more resistant to therapy.
Drug of choice is methotrexate.
236. PLACENTA ACCRETA
DEFINITION: Partial or complete absence of the decidua,
with adherence of the placental villi directly to the
myometrium:
placenta increta - extends part way thru myometrium
placenta percreta - extends thru entire wall of uterus
CLINICAL IMPORTANCE:
1. 60% of cases associated with placenta previa, in
which implantation is in lower uterine segment or cervix
ante partum bleeding; many cases occur in C-section scars
2. Postpartum bleeding, often life threatening, due to
failure of placental separation