Cancer begins in cells, the building blocks that make up tissues. Tissues make up the kidneys and the other organs of the body.
Normal cells grow and divide to form new cells as the body needs them. When normal cells grow old or get damaged, they die, and new cells take their place.
Sometimes, this process goes wrong. New cells form when the body doesn’t need them, and old or damaged cells don’t die as they should. The buildup of extra cells often forms a mass of tissue called a growth or tumor.
Tumors in the kidney can be benign (not cancer) or malignant (cancer). Benign tumors are not as harmful as malignant tumors:
Benign tumors (such as cysts):
-- are usually not a threat to life
-- can be treated or removed and usually don’t grow back
-- don’t invade the tissues around them
-- don’t spread to other parts of the body
Malignant growths:
-- may be a threat to life
-- usually can be removed but can grow back
-- can invade and damage nearby tissues and organs
-- can spread to other parts of the body
Kidney cancer cells can spread by breaking away from the kidney tumor. They can travel through lymph vessels to nearby lymph nodes. They can also spread through blood vessels to the lungs, bones, or liver. After spreading, kidney cancer cells may attach to other tissues and grow to form new tumors that may damage those tissues.
National Cancer Institute:
Cancer begins in cells, the building blocks that make up tissues. Tissues make up the kidneys and the other organs of the body.
Normal cells grow and divide to form new cells as the body needs them. When normal cells grow old or get damaged, they die, and new cells take their place.
Sometimes, this process goes wrong. New cells form when the body doesn’t need them, and old or damaged cells don’t die as they should. The buildup of extra cells often forms a mass of tissue called a growth or tumor.
Tumors in the kidney can be benign (not cancer) or malignant (cancer). Benign tumors are not as harmful as malignant tumors:
Benign tumors (such as cysts):
-- are usually not a threat to life
-- can be treated or removed and usually don’t grow back
-- don’t invade the tissues around them
-- don’t spread to other parts of the body
Malignant growths:
-- may be a threat to life
-- usually can be removed but can grow back
-- can invade and damage nearby tissues and organs
-- can spread to other parts of the body
Kidney cancer cells can spread by breaking away from the kidney tumor. They can travel through lymph vessels to nearby lymph nodes. They can also spread through blood vessels to the lungs, bones, or liver. After spreading, kidney cancer cells may attach to other tissues and grow to form new tumors that may damage those tissues.
National Cancer Institute:
Presentation about the the second most common type of ovarian tumors which have a very unique property of being similar to the testicular germ cell tumors.
MBBS 2nd Year Pathology - Neoplasia : IntroductionNida Us Sahr
Chapter 7 (Neoplasia) from Robbins and Cotran Pathologic Basis of Disease (9th Edition) for MBBS 2nd Year.
After going through this presentation, it will be easy to understand Neoplasia from Robbins.
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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
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 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
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.
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.
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.
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.
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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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
3. Malformations
• Hypospadias
– the more common of the two conditions, the
abnormal opening of the urethra is on the ventral
aspect of the penis anywhere along the shaft
• Epispadias
– the abnormal urethral orifice is on the dorsal
aspect of the penis.
6. Inflammatory Lesions
• Balanitis and balanoposthitis
– refer to local inflammation of the glans penis and
of the overlying prepuce, respectively.
– Candida albicans, anaerobic bacteria, Gardnerella,
and pyogenic bacteria.
– poor local hygiene in uncircumcised males, with
accumulations of desquamated epithelial cells,
sweat, and debris, termed smegma, acting as a
local irritant.
7. • Phimosis
– condition in which the prepuce cannot be
retracted easily over the glans penis.
– most cases are acquired from scarring of the
prepuce secondary to previous episodes of
balanoposthitis.
8. Neoplasms
• Squamous cell carcinoma in situ of the penis
– Bowendisease
– older uncircumcised males
– grossly as a solitary plaque on the shaft of the
penis.
– Histologic examination reveals morphologically
malignant cells throughout the epidermis with no
invasion of the underlying stroma
9. Carcinoma in situ (Bowen disease) of the penis. The epithelium
above the intact basement membrane shows delayed
maturation and disorganization (left). Higher magnification
(right) shows several mitotic figures, some above the basal
layer, a dyskeratotic cell, and nuclear pleomorphism.
10. • Invasive squamous cell carcinoma of the
penis
– appears as a gray, crusted, papular lesion, most
commonly on the glans penis or prepuce.
– Infiltration of the underlying connective tissue
produces an indurated, ulcerated lesion with
irregular margins.
– Histologically, it is a typical keratinizing squamous
cell carcinoma.
11. Carcinoma of the penis. The glans penis is
deformed by an ulcerated, infiltrative mass
12. • Verrucous carcinoma
– variant of squamous cell carcinoma characterized
by a papillary architecture, virtually no cytologic
atypia, and rounded, pushing deep margins.
– Locally invasive but do not metastasize.
14. Cryptorchidism
• Cryptorchidism
– represents a failure of testicular descent into the
scrotum.
– The diagnosis of cryptorchidism is only established
with certainty after the age of 1 year, particularly in
premature infants, because testicular descent into the
scrotum is not always complete at birth.
– Majority of cases, the cause of the cryptorchidism is
unknown.
– bilateral cryptorchidism causes sterility
– failure of descent is associated with a 3- to 5-fold
increased risk of testicular cancer.
15. Inflammatory Lesions
• Epididymitis and orchitis
– begin as a primary urinary tract infection that then
spreads to the testis through the vas deferens or
the lymphatics of the spermatic cord.
– The involved testis typically is swollen and tender.
– Histologic examination reveals a predominantly
neutrophilic inflammatory infiltrate.
16. Vascular Disturbances
• Torsion
– twisting of the spermatic cord,
– results in obstruction of testicular venous drainage
while leaving the thick-walled and more resilient
arteries patent, so that intense vascular
engorgement and venous infarction follow unless
the torsion is relieved.
– Neonatal torsion- in utero orshortly after birth.
– Adult torsion- in adolescence and manifests with
sudden onset of testicular pain.
17. Testicular Neoplasms
• Testicular neoplasms occur in roughly 6 per
100,000 males.
• Males In the 15- to 34-year-old age group, when
these neoplasms peak in incidence, they are the
most common tumors of men
• In postpubertal males, 95% of testicular tumors
arise from germ cells, and all are malignant.
• The cause of testicular neoplasms remains
unknown.
18. – more common in whites than in blacks
– Cryptorchidism is associated with a three- to five-fold
increase in the risk of cancer in the
undescended testis, as well as an increased risk of
cancer in the contralateral descended testis.
– Family history is important, because brothers of
males with germ cell tumors have an 8- to 10-fold
increased risk over that of the population at large,
presumably owing to inherited risk factors.
– Most testicular tumors in postpubertal males arise
from the in situ lesion intratubular germ cell
neoplasia.
19.
20. Morphology
• Pure- composed of a single histologic type
• Mixed- seen in 40% of cases
1. Seminoma
– are soft, well-demarcated, gray-white tumors that
bulge from the cut surface of the affected testis
22. – Microscopically, seminomas are composed of
large, uniform cells with distinct cell borders,
clear, glycogen-rich cytoplasm, and round nuclei
with conspicuous nucleoli
– The cells often are arrayed in small lobules with
intervening fibrous septa. A lymphocytic infiltrate
usually is present and may, on occasion,
overshadow the neoplastic cells.
23. Seminoma of the testis.
Microscopic examination reveals large cells with distinct
cell borders, pale nuclei, prominent nucleoli, and a
sparse lymphocytic infiltrate.
24. Morphology
2. Embryonal Carcinoma
– are ill-defined, invasive masses containing foci of
hemorrhage and necrosis.
– The tumor cells are large an primitivelooking,
with basophilic cytoplasm, indistinct cell borders,
and large nuclei with prominent nucleoli.
– The neoplastic cells may be arrayed in
undifferentiated, solid sheets or may contain
primitive glandular structures and irregular
papillae
26. Embryonal carcinoma.
Note the sheets of undifferentiated cells and primitive
gland-like structures. The nuclei are large and
hyperchromatic.
27. Morphology
3. Yolk sac tumors
– Are the most common primary testicular neoplasm in children
younger than 3 years of age; in this age group it has a very good
prognosis.
– In adults, yolk sac tumors most often are seen admixed with
embryonal carcinoma.
– 90% of patients have elevated AFP
– On gross inspection, these tumors often are large and may be
well demarcated.
– Histologic examination discloses low cuboidal to columnar
epithelial cells forming microcysts, lacelike (reticular) patterns,
sheets, glands, and papillae.
– Schiller-Duvall bodies- distinctive structure resembling
premitive glomeruli
28. Yolk sac tumor
Yolk sac tumor demonstrating areas of loosely textured,
microcystic tissue and papillary structures resembling a
developing glomerulus (Schiller-Duval bodies).
29. Morphology
4. Choriocarcinomas
– are tumors in which the pluripotential neoplastic germ
cells differentiate along trophoblastic lines.
– 100% of patients have elevated HCG
– Grossly, the primary tumors often are small, nonpalpable
lesions, even those with extensive systemic metastases.
– Microscopic examination reveals that choriocarcinomas
are composed of sheets of small cuboidal cells irregularly
intermingled with or capped by large, eosinophilic
syncytial cells containing multiple dark, pleomorphic
nuclei.
– cytotrophoblastic and syncytiotrophoblastic
30. Choriocarcinoma.
Both cytotrophoblastic cells with central nuclei (arrowhead,
upper right) and syncytiotrophoblastic cells with multiple
dark nuclei embedded in eosinophilic cytoplasm (arrow,
middle) are present. Hemorrhage and necrosis are
prominent.
31. Morphology
5. Teratomas
– are tumors in which the neoplastic germ cells
differentiate along somatic cell lines. These
tumors form firm masses that on cut surface often
contain cysts and recognizable areas of cartilage.
– They may occur at any age frominfancy to adult
life.
– Pure forms of teratoma are fairly common in
infants and children, being second in frequency
only to yolk sac tumors.
32. – Teratomas are composed of a heterogeneous,
helterskelter collection of differentiated cells or
organoid structures, such as neural tissue, muscle
bundles, islands of cartilage, clusters of squamous
epithelium, structures reminiscent of thyroid
gland, bronchial epithelium, and bits of intestinal
wall or brain substance, all embedded in a fibrous
or myxoid stroma.
– In prepubertal males, teratomas are typically
benign, whereas teratomas in postpubertal males
are malignant, being capable of metastasis
regardless of whether they are composed of
mature or immature elements.
33. Teratoma.
Testicular teratomas contain mature cells from endodermal, mesodermal, and
ectodermal lines. A–D, Four different fields from the same tumor specimen contain
neural (ectodermal) (A), glandular (endodermal) (B), cartilaginous (mesodermal) (C),
and squamous epithelial (D) elements.
35. • The prostate can be divided into several
biologically distinct regions, the most important
of which are the peripheral and transition zones.
• The types of proliferative lesions are different in
each region.
• Most hyperplastic lesions arise in the inner
transition zone, while most carcinomas (70% to
80%) arise in the peripheral zones.
• The normal prostate contains glands with two cell
layers, a flat basal cell layer and an overlying
columnar secretory cell layer.
36. Prostatitis
Categories:
• acute bacterial prostatitis (2% to 5% of cases)
– caused by the same organisms associated with other acute
urinary tract infections
– is associated with fever, chills, and dysuria; it may be
complicated by sepsis. On rectal examination, the prostate
is exquisitely tender and boggy.
• chronic bacterial prostatitis (2% to 5% of cases)
– also caused by common uropathogen
– is associated with recurrent urinary tract infections
bracketed by asymptomatic periods. Presenting
manifestations may include with low back pain, dysuria, and
perineal and suprapubic discomfort.
37. • chronic nonbacterial prostatitis, or chronic pelvic
pain syndrome (90% to 95% of cases),
- in which no uropathogen is identified despite the
presence of local symptoms
• asymptomatic inflammatory prostatitis (incidence
unknown)
- associated with incidental identification of leukocytes in
prostatic secretions without uropathogens.
38. Benign Prostatic Hyperplasia
(Nodular Hyperplasia)
• BPH is characterized by proliferation of both stromal
and epithelial elements, with resultant enlargement of
the gland and in some cases, urinary obstruction.
• It is present in a significant number of men by the age
of 40, and its frequency rises progressively with age,
reaching 90% by the eighth decade of life.
• Dihydrotestosterone (DHT), the ultimate mediator of
prostatic growth, is synthesized in the prostate from
circulating testosterone by the action of the enzyme
5α-reductase, type 2.
39. Morphology
– BPH virtually always occurs in the inner, transitional zone
of the prostate.
– weighing between 60 and 100 g
– The nodules may appear solid or contain cystic spaces, the
latter corresponding to dilated glandular elements.
– The urethra is usually compressed by the hyperplastic
nodules, often to a narrow slit.
– Microscopically the hyperplastic nodules are composed of
variable proportions of proliferating glandular elements
and fibromuscular stroma. The hyperplastic glands are
lined by tall, columnar epithelial cells and a peripheral
layer of flattened basal cells
41. Nodular hyperplasia of the prostate.
Low-power photomicrograph demonstrates a well-demarcated nodule
at the right of the field with a portion of urethra seen to the left.
42. Carcinoma of the Prostate
• Adenocarcinoma of the prostate occurs mainly
in men older than 50 years of age.
• It is the most common form of cancer in men,
accounting for 25% of cancer in men in the
United States in 2009.
43. Morphology
• Carcinoma of the Prostate
– Most carcinomas detected clinically are not visible grossly. More
advanced lesions appear as firm, gray-white lesions with ill-defined
margins that infiltrate the adjacent gland.
– On histologic examination, most lesions are moderately
differentiated adenocarcinomas that produce well-defined
glands.
– The glands typically are smaller than benign glands and are lined
by a single uniform layer of cuboidal or low columnar epithelium,
lacking the basal cell layer seen in benign glands.
– In further contrast with benign glands, malignant glands are
crowded together and characteristically lack branching and
papillary infolding. The cytoplasm of the tumor cells ranges from
pale-clear (as in benign glands) to a distinctive amphophilic (dark
purple) appearance. Nuclei are enlarged and often contain one or
more prominent nucleoli
44.
45. Adenocarcinoma of the prostate demonstrating small
glands crowded in between larger benign glands
46. Adenocarcinoma
Higher magnification shows several small malignant
glands with enlarged nuclei, prominent nucleoli, and
dark cytoplasm, as compared with the larger, benign
gland
47. Adenocarcinoma of the prostate.
Carcinomatous tissue is seen on the posterior aspect (lower left). Note the
solid whiter tissue of cancer, in contrast with the spongy appearance of the
benign peripheral zone on the contralateral side.
49. Ureter
• Ureteropelvic junction (UPJ) obstruction
– usually manifests in infancy or childhood, much more commonly in
boys. It is the most frequent cause of hydronephrosis in infants and
children.
• Primary malignant tumors
– follow patterns similar to those arising in the renal pelvis, calyces, and
bladder, and a majority are urothelial carcinomas
• Retroperitoneal fibrosis
– is an uncommon cause of ureteral narrowing or obstruction
characterized by a fibrous proliferative inflammatory process encasing
the retroperitoneal structures and causing hydronephrosis.
– middle to old age.
50. Urinary Bladder
(Non-neoplastic Conditions)
• A bladder or vesical diverticulum
– consists of a pouchlike evagination of the bladder
wall. Diverticula may be congenital but more
commonly are acquired lesions that arise as a
consequence of persistent urethral obstruction
– lead to urinary stasis and predispose to infection.
51. Urinary Bladder
(Non-neoplastic Conditions)
Cystitis
• Interstitial cystitis
– (i.e., chronic pelvic pain syndrome) is a persistent,
painful form of chronic cystitis occurring most
frequently in women. It is characterized by
intermittent, often severe suprapubic pain, urinary
frequency, urgency, hematuria and dysuria without
evidence of bacterial infection
– cystoscopic findings of fissures and punctate
hemorrhages (glomerulations) in the bladder mucosa.
52. Urinary Bladder
(Non-neoplastic Conditions)
• Malakoplakia
– most commonly occurs in the bladder and results
from defects in phagocytic or degradative function
of macrophages, such that phagosomes become
overloaded with undigested bacterial products.
– Michaelis-Gutmann bodies
• laminated mineralized concretions resulting from
deposition of calcium in enlarged lysosomes are
present within the macrophages
53. Urinary Bladder
(Non-neoplastic Conditions)
• Polypoid cystitis
– is an inflammatory condition resulting from
irritation to the bladder mucosa in which the
urothelium is thrown into broad bulbous polypoid
projections as a result of marked submucosal
edema.
54. Urinary Bladder
(Neoplasms)
• Bladder cancer accounts for approximately 7%
of cancers. The vast majority of bladder
cancers (90%) are urothelial carcinomas.
• Carcinoma of the bladder is more common in
men than in women, in industrialized than in
developing nations, and in urban than in rural
dwellers
• About 80% of patients are between the ages
of 50 and 80 years.
55. Morphology
• Noninvasive papillary urothelial neoplasms
demonstrate a range of atypia and are graded
to reflect their biologic behavior
– (1) papilloma
– (2) papillary urothelial neoplasm of low
malignant potential (PUNLMP)
– (3) low-grade papillary urothelial carcinoma
– 4)high-grade papillary urothelial carcinoma
58. Morphology
• Carcinoma in situ
– defined by the presence of cytologically malignant
cells within a flat urothelium Like high-grade papillary
urothelial carcinoma, CIS tumor cells lack
cohesiveness. This leads to the shedding of malignant
cells into the urine, where they can be detected by
cytology.
– commonly is multifocal and sometimes involves most
of the bladder surface or extends into the ureters and
urethra.
– Without treatment, 50% to 75% of CIS cases progress
to muscle-invasive cancer.
59. Carcinoma in situ (CIS) with enlarged hyperchromatic
nuclei and a mitotic figure
62. Syphilis
– Syphilis, or lues, is a chronic venereal infection
caused by the spirochete Treponema pallidum.
– T. pallidum is a fastidious organism whose only
natural host is man. The usual source of infection
is contact with a cutaneous or mucosal lesion in a
sexual partner in the early (primary or secondary)
stages of syphilis.
– The organism is transmitted from such lesions
during sexual activity through minute breaks in
the skin or mucous membranes.
63. Primary Syphilis
• The chancre of syphilis is characteristically indurated and
has been referred to as a “hard chancre,” to distinguish it
from the “soft chancre” of chancroid caused by
Haemophilus ducreyi.
• The chancre begins as a small, firm papule, which gradually
enlarges to produce a painless ulcer with well-defined,
indurated margins and a “clean,” moist base.
• Histologic examination of the ulcer reveals the usual
lymphocytic and plasmacytic inflammatory infiltrate and
proliferative vascular changes.
• Even without therapy, the primary chancre resolves over a
period of several weeks to form a subtlescar.
64. Syphilitic chancre of the scrotum.
Such lesions typically are painless despite the
presence of ulceration, and they heal
spontaneously
65. Histologic features of the chancre include
a diffuse plasma cell infiltrate beneath
squamous epithelium of skin.
66. Secondary Syphilis
• Within approximately 2 months of resolution of
the chancre, the lesions of secondary syphilis
appear.
• The manifestations of secondary syphilis are
varied but typically include a combination of
generalized lymph node enlargement and a
variety of mucocutaneous lesions.
• Skin lesions usually are symmetrically distributed
and may be maculopapular, scaly, or pustular.
Involvement of the palms of the hands and soles
of the feet is common
67. Secondary Syphilis
• Histologic examination of mucocutaneous lesions during the
secondary phase of the disease reveals the characteristic
proliferative endarteritis, accompanied by a
lymphoplasmacytic inflammatory infiltrate.
• Spirochetes are present and often abundant within these
mucocutaneous lesions; they are therefore contagious.
• Lymph node enlargement is most common in the neck and
inguinal areas.
• The mucocutaneous lesions of secondary syphilis resolve over
several weeks, at which point the disease enters its early
latent phase, which lasts approximately 1 year.
68. Tertiary Syphilis
• Tertiary syphilis develops in approximately one third of untreated
patients, usually after a latent period of 5 years or more.
• Complications:
– Cardiovascular syphilis- syphlitic aortitis and accounts 80% of
tertiary cases.
– Neurosyphilis- accounts for 10% of cases of tertiary syphilis overall
but occurs at increased frequency in those with concomitant HIV
infection
– Benign tertiary syphilis- is an uncommon form marked by the
development of gummas in various sites. Emergence of these lesions
probably is related to the development of delayed hypersensitivity.
• Gummas occur most commonly in bone, skin, and the mucous
membranes of the upper airway and mouth, but any organ may
be affected
69. Congenital Syphilis
• T. pallidum may be transmitted across the placenta from an
infected mother to the fetus at any time during pregnancy.
• The likelihood of transmission is greatest during the early
(primary and secondary) stages of disease, when spirochetes
are most numerous.
• Routine serologic testing for syphilis is mandatory in all
pregnancies. The stigmata of congenital syphilis typically do
not develop until after the fourth month of pregnancy.
• Manifestations:
– Stillbirth syphilis
– Infantile syphilis
– Late (tardive) congenital syphilis
70. • Still birth syphilis
– Among infants who are stillborn, the most
common manifestations are hepatomegaly, bone
abnormalities, pancreatic fibrosis, and
pneumonitis.
– Spirochetes are readily demonstrable in tissue
sections. In cases of congenital syphilis, the
placenta is enlarged, pale, and edematous.
71. • Infantile syphilis
– Refers to congenital syphilis in liveborn infants
that is clinically manifest at birth or within the first
few months of life.
– Affected infants present with chronic rhinitis
(snuffles) and mucocutaneous lesions similar to
those seen in secondary syphilis in adults.
72. • Late, or tardive, congenital syphilis
– Refers to cases of untreated congenital syphilis of
more than 2 years’ duration.
– Hutchinson triad:
• notched central incisors
• interstitial keratitis with blindness,
• deafness from eighth cranial nerve injury
– Other changes include a so-called saber shin
deformity caused by chronic inflammation of the
periosteum of the tibia, deformed molar teeth
(“mulberry molars”), chronic meningitis,
chorioretinitis, and gummas of the nasal bone and
cartilage with a resultant “saddlenose” deformity.
73. Serologic Tests for Syphilis
• serology remains the mainstay of diagnosis.
• Serologic tests for syphilis include nontreponemal antibody tests
and antitreponemal antibody tests.
• Nontreponemal tests measure antibody to cardiolipin, an antigen
that is present in both host tissues and the treponemal cell wall.
These antibodies are detected by the rapid plasma reagin (RPR)
and Venereal Disease Research Laboratory (VDRL) tests.
• Nontreponemal antibody tests are usually positive by 4 to 6 weeks
of infectio and are strongly positive in the secondary phase of
infection.
– However, nontreponemal antibody test results may revert to
negative during the tertiary phase or, conversely, may on
occasion be persistently positive in some patients after
successful treatment.
74. • Nontreponemal antibody test results often are
negative during the early stages of disease, even
in the presence of a primary chancre.
– direct visualization of the spirochetes by darkfield or
immunofluorescence microscopy may be the only way
to confirm the diagnosis.
• Treponemal antibody tests also become positive
within 4 to 6 weeks after an infection, but, unlike
those for nontreponemal an
• tibody tests, they usually remain positive
indefinitely, even after successful treatment.
75. Gonorrhea
• is a sexually transmitted infection of the lower
genitourinary tract caused by Neisseria gonorrhoeae.
• Humans are the only natural reservoir for N.
gonorrhoeae.
• The organism is highly fastidious, and spread of
infection requires direct contact with the mucosa of
an infected person, usually during sexual activity.
• Pregnant women can transmit gonorrhea to
newborns during passage through the birth canal.
• Diagnosis can be made by culture of the exudates as
well as by nucleic acid amplification techniques.
76. Morphology
• N. gonorrhoeae provokes an intense,
suppurative inflammatory reaction.
• In males this manifests most often as a purulent
urethral discharge, associated with an
edematous, congested urethral meatus.
• Gram-negative diplococci, many within the
cytoplasm of neutrophils, are readily identified in
Gram stains of the purulent exudate
• Ascending infection may result in the
development of acuteprostatitis, epididymitis or
orchitis.
78. Acute epididymitis caused by gonococcal infection.
The epididymis is involved by an abscess.
Normal testis is seen on the right.
79. Nongonococcal Urethritis and
Cervicitis
• Nongonococcal urethritis (NGU) and cervicitis are the
most common forms of STD.
• C. trachomatis, Trichomonas vaginalis, U. urealyticum,
and Mycoplasma genitalium.
• Most cases are apparently caused by C. Trachomatis
– is a small gram-negative bacterium that is an
obligate intracellular pathogen. It exists in two
forms. The infectious form, the elementary body, is
capable of at least limited survival in the
extracellular environment.
80. – The elementary body is taken up by host
cells, primarily through a process of
receptor-mediated endocytosis.
– Once inside the cell, the elementary body
differentiates into a metabolically active
form, termed the reticulate body.
– Using energy sources from the host cell, the
reticulate body replicates and ultimately
forms new elementary bodies capable of
infecting additional cells.
81. Chancroid (Soft Chancre)
• Chancroid, sometimes called the “third” venereal
disease (after syphilis and gonorrhea), is an acute,
ulcerative infection caused by Haemophilus ducreyi, a
small, gram-negative coccobacillus.
• The disease is most common in tropical and subtropical
areas and is more prevalent in lower socioeconomic
groups, particularly among men who have regular
contact with prostitutes.
• A definitive diagnosis of chancroid requires the
identification of H. ducreyi on special culture media.
82. Morphology
• At 4 to 7 days after inoculation, a tender, erythematous papule
develops on the external genitalia. In male patients, the
primary lesion is usually on the penis; in female patients, most
lesions occur in the vagina or periurethral area.
• the primary lesion erodes to produce an irregular ulcer, which is
more likely to be painful in males than in females.
• The base of the ulcer is covered by shaggy, yellow-gray exudate.
The regional lymph nodes, particularly in the inguinal region,
become enlarged and tender in about 50% of cases within 1 to 2
weeks of the primary inoculation.
• On microscopic examination, the ulcer of chancroid contains a
superficial zone of neutrophilic debris and fibrin, with an
underlying zone of granulation tissue containing areas of
necrosis and thrombosed vessels.
84. Genital Herpes Simplex
• Genital herpes infection, or herpes genitalis, is a
common STD. Both herpes simplex virus 1 (HSV-1) and
HSV-2 can cause anogenital or oral infections, most
cases of anogenital herpes are caused by HSV-2.
• Recent years have seen a rise in the number of genital
infections caused by HSV-1, in part due to the
increasing practice of oral sex.
• Up to 95% of HIV-positive men who have sex with men
are seropositive for HSV-1 and/or HSV-2.
• HSV is transmitted when the virus comes into contact
with a mucosal surface or broken skin of a susceptible
host.
85. Morphology
• The initial lesions of genital HSV infection are painful,
erythematous vesicles on the mucosa or skin of the lower
genitalia and adjacent extragenital sites.
• Histologic changes include the presence of intraepithelial
vesicles accompanied by necrotic cellular debris, neutrophils,
and cells harboring characteristic intranuclear viral inclusions.
• The classic Cowdry type A inclusion appears as a light purple,
homogeneous intranuclear structure surrounded by a clear
halo.
• Infected cells commonly fuse to form multinucleate syncytia.
The inclusions readily stain with antibodies to HSV, permitting
a rapid, specific diagnosis of HSV infection in histologic
sections or smears.
87. Human Papillomavirus Infection
• HPV causes a number of squamous proliferations
in the genital tract, including precancerous
lesions that commonly undergo transformation to
carcinomas; these most commonly involve the
cervix 18), but also occur in the penis, vulva, and
oropharyngeal tonsils.
• Condylomata acuminata
– also known as venereal warts, are caused by HPV
types 6 and 11. These lesions occur on the penis as
well as on the female genitalia.
88. Morphology
• In males, condylomata acuminata usually
occur on the coronal sulcus or inner surface of
the prepuce, where they range in size from
small, sessile lesions to large, papillary
proliferations measuring several centimeters
in diameter.