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8/14/2019 Renal Pathology-Week 2
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LG 2.3 Renal Embryology
Embryology
Week 2
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LG 2.3 Renal Embryology
Around the third week the intermediate
mesoderm forms alongitudinal elevation
Urogenital Ridge
Part of the urogenitalridge turns into thenephrogenic rod
This leads to the Urinarysystem
Nephrogenic roddevelops into 3sequential nephricstructures:
Pronephros: a non-functional structure
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LG 2.3 Renal Embryology
Pronephros Starts with the development of kidneys in the
4th week
It is the cranialmost nephric structure, is atransitory structure that regresses completelyby the fifth week, and is non-functional inhumans
Mesonephros In 4th week mesonephros tubules and
mesonephric duct derive form nephrogeniccord
The mesonephros tubules forms nephrons thatempty into this collecting duct (mesophrenicduct)this connects the nephrons to the
urogenital sinus The future urinary bladder
The tubules regress by 6th week Therefore functional for a short time
The mesonephric duct (wolfian) persists No wolffian duct In females
2ndmonththe mesonephros is an ovoid
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LG 2.3 Renal Embryology
Metanephros it replaces the mesonephros as the
functional excretory organ and
develops into the adult kidney It develops from an outgrowth from
the caudal mesonephric duct calledthe Ureteric Bud and from theMetanephric Mesoderm (metanephricblastema)within the most caudalnephrogenic cord
At about week 5 begins third andfinal urinary organ, or permanentkidney
It will be functional in the fetus by week 10
initiated by the growth of the uretericbud off of the most caudal
mesonephric duct grows into the mesonephric mesoderm and
induces development of the kidney frommesoderm which condenses around it
Two separate components Collecting System: arise from the Ureteric
Bud, an outgrowth from the mesonephric
duct.
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LG 2.3 Renal Embryology
The ureteric bud grows out, contacts and eventuallypenetrates the metanephric mesoderm
Upon contact, the UB expands and branches out The branching will form the renal pelvis, the major and minor
calyces and collecting tubules
Lengthening of the proximal end of each ureteric bud forms theUreter.
Collecting tubule has MetanephricTissue Cap which itinduces to form nephrons
This tissue forms renal vesicles which differentiate into excretorytubules
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LG 2.3 Renal Embryology
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LG 2.3 Renal Embryology
At the proximal end,
capillaries willgrow into theGlomeruli andenter into eachBowmans Capsule,completing the
Nephron The kidneys develop
from two sources: Ureteric Bud-
gives rise to thecollecting system
MetanephricMesoderm-provides theexcretory units(nephrons) which
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LG 2.3 Renal Embryology
Fetal nephrons are formed until birth
At birth, the kidneys have alobulated appearance thatdisappear during infancy
Urine production begins by the 10thweek
The kidneys ascend cranially toachieve their final position inthe lower lumbar area (T-12-L3)
Between the 6th and 9th week
The ascent is caused more bydifferential growth; the kidneysstay in position
Abnormal ascent
Sometimes a kidney fails toascend to the lumbar area,creating a Pelvic Kidney
the inferior poles may fusetogether during the initialascent, creating a HorseshoeKidney
When this type of kidneystarts to ascend, it is
Pelvic
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LG 2.3 Renal Embryology
During normalascent, there is a
90 degree rotation In horseshoe
kidney, there isno rotation the
hilum continues toface ventrally ureters take an
abnormal courseacross the bridge of
renal tissue whichcan lead to partialurinary tractobstruction,
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LG 2.3 Renal Embryology
Bladder
Functioning of the fetal kidneys
begins in the 12th
week. Amniotic fluid is swallowed by
the fetus, absorbed from the gutinto the bloodstream, filtered bythe nephrons,
The urinary bladder is derivedfrom the superior anterior region
of the cloaca (most caudal end ofthe hindgut) called theUrogenital Sinus
the mesonephric (wolffian) ductenters into the urogenital sinusduring kidney development and
the allantois also joins theurogenital sinus
The Allantois is part of thedeveloping umbilical cord whichcollects the waste
The Urorectal Septum in the5th week:
separates the cloaca into
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LG 2.3 Renal Embryology
Three parts of theurinogenital sinus Urinary Bladder: The
upper and largest partthat is continuous with
the allantois Pelvic Portion: a narrow
canal which in the maleforms the prostatic andmembranous parts ofthe urethra
Phallic Portion: The lastpart, forms the penileurethra in the male
urogenital sinus portionsdevelopment differsreatl between the two
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LG 2.3 Renal Embryology
Anomalies of the
Urorectal fistula: The hindgut empties
directly into theurethra below theurinary bladder in the
male Cause: Incomplete
separation of theurogenital sinus andanorectal area by theurorectal septum
Rectovaginal fistula: due to the same
incomplete separationin a female that resultsin hindgut emptyingdirectly into the vagina
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LG 2.3 Renal Embryology
Urachal Fistula: maycause urine to drainfrom the umbilicus.
Urachal Cyst: If only alocal area of the
allantois persistsbetween the ligaments,this will result in aresulting in a epithelial-lined dilated cyst.
Urachal Sinus: Occurs
when the lumen of theupper part persistsonly.
All 3 are due to a failureof the Allantois(Urachus) and its lumen
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LG 2.3 Renal Embryology
Bladder
The mesonephric ductsare absorbed into the wallof the urinary bladder atthe same time that theureters come to separatelyopen directly into the
bladder as developmentproceeds
Caudally, the mesonephricducts move closer togetherto enter the prostaticportion of the urethra
where they form theejaculatory ducts andseminal vesiclesin themale
Mesonephric ducts in
femal
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LG 2.3 Renal Embryology
Urethra
At the end of the third month, cells inthe urethral epithelium differentiateinto the
prostate gland
seminal vesicles
ductus deferens
urogenital sinus gives rise to the
penile urethra.
In females: the distal portion of the
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Congenital Anomalies
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LG 2.4 Congenital Anomalies
Potter Syndrome
The Potter (Oligohydramnios)
Syndrome syndrome of abnormalities that are
caused by markedly reducedintrauterine urine production
>>less amniotic fluid which cushionsfetus
With less fluid, the fetus is
compressed by the uterus, causingspecific abnormalities
Physical Appearance infraorbital folds, low-set ears,
a small receding chin, aflattened nose, redundant skinfolds of the hands, club feet(varus deformity)
Pulmonary hypoplasiaincomplete development oflungs
caused by compression of thechest by the uterus
Infraorbit
al
Pulmonary
hypoplasia
Bilateral renal
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LG 2.4 Congenital Anomalies
Other anomalies
Unilateral Agenesis: relativelycommon usually they are unaware of its
presence as long as the singlekidney functions normally.
Compensatory hyperthrophy Renal Hypoplasia: the
kidneys do not develop tonormal size.
Horseshoe Kidney: fusion ofthe kidney at the midline.
Usually causes no problemunless there is an associateddefect that favors obstructionto renal flow
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LG 2.4 Congenital Anomalies
Renal Cystic
Characterized by the presenceof multiple cysts of varyingsize in the kidney and theabsence of a normalpelvocaliceal system
Results from abnormal
differentiation of the renalstructures during theembryonic period Occurs unilateral
No association with malignancy
Most common cause of anabdominal mass in newborns
The bilateral form causesoligohydramnios and resultantPotter Sequence withpulmonary hypoplasia
Clinically
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LG 2.4 Congenital Anomalies
Adult Polycistic Kidney
Characterized by multipleserous or purulent-filledcysts of both kidneys thatdestroys the interveningparenchyma
An autosomal dominant
disorder The cysts are derived from
obstructed tubules
Renal failure usually in the 30sor 40s
Cyst appear to arise from anypart of the nephron Pressure from cysts may lead to
ischemic atrophy Can lead to hemorrhage, HTN
and infection
Elevated BUN
HTN in 75% of the patients
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LG 2.4 Congenital Anomalies
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LG 2.4 Congenital Anomalies
Childhood Polycistic KidneyDi Autosomal recessive disease
enlarged bilateral kidneys Resembles sponges
In utero, there isoligohydramnios (Pottersequence)
Results in pulmonary
hypoplasia Associated with:
Congenital hepatic fibrosis.
If survives, may results inportal hypertension
Splenomegaly
the kidneys are markedlyenlarged and tend to fill the entireretroperitoneum and displace theabdominal contents
numerous small uniform cysts inthe cortex and medulla
Leads to renal failure after
Enlarged
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LG 2.4 Congenital Anomalies
Medullary Sponge Kidney
A congenital conditionwithout a definedinheritance pattern
Often bilateral
Symptomatic inadolescence or earlyadulthood withhematuria and/or UTIs Due to renal stones
which develops in 65% ofpatients
Eventual pyelonephritisbut without RF
Polycistic changes withdialysis
Policystic changes
with dialysis
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LG 2.4 Congenital Anomalies
Simple Renal Cysts
Cysts found in overhalf of patients over50 yoa Rarely produce
clinical symptoms Solitary or multiple
fluid-filled cysts foundin the outer cortex
Duplication of ureters Single or multiple
ureters may beduplicated on the sideof the fetal urinarybladder
May be unilateral orDuplication of
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LG 2.4 Congenital Anomalies
Congenital Hydroureter
AKA congenitalmegaureter
May be due toobstruction at theuretal orifice intothe bladder
May be unilateral orbilateral
If dilation involvesrenal pelvis Can cause
Congenital Hydroureter withResultant Hydronephrosis
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LG 2.4 Congenital Anomalies
Congenital Diverticuli
Sac-like outpouchingsof the bladder wallrelated to incompleteformation of themuscle layers May be solitary or
multiple Urine is retained
inside the diverticuliand can cause
infections With time it can lead
to urinary stones(complication)
Diverticuli may also
Acquired Bladder
Congenital DiverticuliUrinary Bladder
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LG 2.4 Congenital Anomalies
Urachal Cyst
A cyst occurring inthe remnants of theumbilicus and theurinary bladderpresenting as aextraperitonealmass in theumbilical region Caused by
incomplete
involution Presents with
abdominal pain andfever if infected,possible leading to
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LG 2.5 Pathology of Renal Tumors
Benign and Malignant
Tumors
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LG 2.5 Pathology of Renal Tumors
Renal Adenomas
A renal epithelialneoplasm
Less than 3 cm Composed ofsmall
cuboidal cells with round,regular nuclei, arranged inclosely packed tubules orpapillary configurations
Most are located in theouter cortex
Increase in frequency withage
Found in over 40% of
Renal cortical
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LG 2.5 Pathology of Renal Tumors
Medullary FibromaAKA Renomedullary Interstitial Cell Tumors
Small, pale white,well-circumscribedbenign tumors
located in themidportion of themedullary pyramid
Composed of small,
stellate to polygonalcells lying in a loosestroma
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LG 2.5 Pathology of Renal Tumors
Angiomyolipomas
Benign lesions that exhibit anadmixture of: well-differentiated adipose
tissue,
smooth muscle and
thick-walled blood vessels
Tumors are yellow andbosselated
Resemble renalcarcinoma BUT this one is always
encapsulated withoutareas of necrosis
Associated with tuberoussclerosis A disease characterized by
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LG 2.5 Pathology of Renal Tumors
Congenital Mesoblastic
A congenital benigntumor usually discoveredin the first three monthsof life because of anabdominal mass
Gross Grossly, the tumor is
usually solitary andunilateral with tan fleshyill-defined borders
Histology Monomorphic spindle-
shaped cells resemblingfibroblasts with scantinterstitial collagen withminimal compression
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LG 2.5 Pathology of Renal Tumors
Oncocytoma
Grossly resembles a renalcell carcinoma but tends tobe more uniform tan tobrown color
Made of oncocytesEpithelial cell
characterized by anexcessive amount ofmitochondria, resulting inan abundant acidophilic,granular cytoplasm.
Accounts for 5-15% of
renal neoplasms Good prognosis because it
typically acts in a benignfashion, and is notassociated with aparaneoplastic syndrome.
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LG 2.5 Pathology of Renal Tumors
Malignant Tumors
Renal Cell Carcinoma comprise 85% of allkidney tumors.
Transitional Cell Carcinoma of the renal pelvis
comprise another 10% Wilms Tumor, a pediatric tumor, comprises
5%.
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LG 2.5 Pathology of Renal Tumors
Renal Cell Carcinomas
It is more common in males than in females Ages 50-70
Higher incidence in cigarette smokers
Gross Appear as nodules or masses
They arise from either the upper or lower poles of the kidneys
Originates in the renal tubules
Histology composed of cuboidal cells reminiscent of renal tubules that have
either clear or granular cytoplasm, filled with glycogen and lipids(adenocarcinoma)
Metabolic Paraneoplastic findings, such as hypercalcemia andpolycythemia may present but it is rare
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LG 2.5 Pathology of Renal Tumors
Transitional Cell Carcinoma
Papillary neoplasmsof the renal pelvisthat resemble
carcinomas of theurinary bladder
Most tumors presentwith hematuria or
urinary obstructionearly in the course
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LG 2.5 Pathology of Renal Tumors
Wilms Tumor The most common of all the solidabdominal tumors in infants andchildren
Tumordevelops from remnants of theimmature kidney (nephrogenic elements)
Presents with a large solitary or multi-nodularpalpable abdominal mass thatreplaces the kidney
In 5-7%, the tumor arises in thecontext ofthree different
congenital syndromes Children complain of abdominal
pain, intestinal obstruction,hematuria, hypertension, andfever
Patients < 2 yoa have a better prognosis
than older children due to increasedanaplasia of the tumor
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LG 2.5 Pathology of Renal Tumors
Wilms Tumor Congenital Syndromes
WAGR Syndrome
WilmsTumor,
Aniridia (absence of an iris),
Genitourinary Anomalies, and Mental
Retardation. Due to a deletion of the shortarm of chromosome 11
Denys-Drashsyndrome (DDS): Wilms Tumor,and Glomerulopathy. Due to mutations of WT1
Beckwith-Weidmann Syndrome (BWS)
Wilms Tumor, Gigantism withVisceromegaly, and Macroglossia. Due todeletion of WT2. (both WT1 and WT2 areconsidered tumor suppressor genes)
Fetal Tissues Metanephric Blastema (immature
kidneys): consisting of small ovoidcells growing in nests
Immature mesenchymal stroma:loose spindle cells resemblingfibroblasts with possible foci ofskeletal or smooth muscle, fat, orbone
Immature epithelial elements:small tubular structures andimmature glomeruli
Wilms Tumor withBlastema and Stroma
Primitive Glomerular and TubularStructures of Wilms Tumor
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LG 2.5 Pathology of Renal Tumors
Metastatic Tumors to the
Lymphomas arethe most commonmalignancies thatmetastasize to the
kidneys Also leukemias,
lung, colon andmalignantmelanomas
Usually small,asymptomatic, andoccasionally cause
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LG 2.5 Pathology of Renal Tumors
XanthogranulomatousP l n hriti
An uncommon formofchronicpyelonephritis,often caused by a
Proteus (gramneg.) infection
There are nodulesof yellow within the
renal parenchymawhich arenumerous lipid-laden macrophages
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Urothelial tumors, more than 90% aretransitional cell carcinomas. Squamous cellcarcinoma (7%)--exposure toSchistosoma
Urothelium consists of a 3- to 7-cellmucosal layer within the muscular bladder
Transitional cell papilloma Benign tumor
Painless hematuria People >50 yoa
Two types Exophytic Papillomas
single lesions mostly, 2-5 cm indiameter
Inverted Papillomas typically present as nodular mucosal
lesions covered by normal urotheliumfrom which cords of transitionalepithelium descend into the laminapropria
Transitional cell carcinoma in-
situ -
Inverted
Exophytic
Transitional cell
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Cancer of the urinar bladder Most common urinary tract neoplasm
2-3x more common than renal cell
cancer Tumors are often multifocal
can occur in any part of the urinary tractlined by transitional epithelium, from therenal pelvis to the urethra.
Higher incidence in Egypt, Sudan andother A. Countries due to the
Schistosomiasis, which increasesfrequency of squamous cell carcinoma
Higher incidence in the US amongurban white people and lowerincidence among blacks
Risk Factors cigarette smoking
Azo dyes and chemicals used in the rubberindustry, and textile printing
They are conjugated in the liver andmetabolites excreted in the urine(arylamines), which is acidic and leads tothe production of reactive arylnitrenium ions carginogenic to bladder mucosal cells
Infection with Schistosoma haematobium
(parasite)in Egypt primarily Cyclophosphamide
MucinousAdenocarcinoma of the
Sarcoma botryoides of the
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Bladder Cancer The exophytic type arises most
frequently from the lateral walls of
the bladder Histologically, they are classified into
three grades of increasing severityand invasiveness
Grades Grade 1 (Low Grade): Papillary
projections lined by neoplastic
transitional cells with minimalpleomorphism, mitotic activity,resting on long papillae
Grade 2 (Intermediate Grade): Similarhistologic features, but more severenuclear and cytoplasmic changes.
Grade 3 (High Grade): Significantnuclear pleomorphism, frequent mitoses
with fusion of the papillae. Invasion is more common with this grade.
Metastasis extension of the tumor into the muscle
layers of the bladder and into theadjacent pelvic organs
Initially found in the pelvic and periaortic
Transitional CellCancer of the BladderExophytic Tumor inthe Bladder Neck
Transitional CellCarcinoma-BladderPapillary, Solid, andNecrotic
Grade 1Resting on long
Grade 2
Transitional cell
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Prostate Gland It is about the size of a chestnut, and
secretes an alkaline fluid and
constitutes 13-33% of semen Contains 30-50 individual compound
tubuloalveolar glands, each gland having its own duct that
delivers the secretory product to theprostatic urethra
Lined by a simple to pseudostratifiedcolumnar epithelium
Lumen of these glands frequently houseround to oval prostatic concretions(corpora amylacea), composed ofcalcified glycoproteins and whosenumbers increase with age
Prostatitis inflammation of the prostate gland that
can occur as either an acute or chronicform
Usually caused by E.coli or others such as,chlamydia, trichomonas or mycoplasma.Histoplasma capsulatum can causegranulomatous prostatis
Acute Commonly caused by E.coli
PMNs are seen
Intense discomfort on urination and is
Acute bacterial prostatitiswith PMNs
Acute Prostatitis-Neutrophils within aLarge Gland and Surrounding Stroma
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Chronic Prostatitis May be preceded
by an episode ofacute prostatitis
lymphocytes,plasma cells, andmacrophages areseen
Suprapubic,
perineal, and lowback pain andexperience dysuriaand nocturia. The
Chronic Prostatitis-Mononuclear Cellswithin the Stroma
Chronic
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Benign Prostatic Reactive, benign hyperplastic lesion that
may obstruct the flow of urine, relatedto male hormonal changes thatoccurs with aging
Occurs in the periurethral portion of theprostate
a part of the prostate located at the neck ofthe urinary bladder
The enlargement impedes urination
Central located hyperplastic nodulescompresses and expands the peripheraltissue
Higher among U.S. blacks than whitesand the disease peaks at about 70 years
75% of men over 80 years of age havesome degree of BPH
Testosterone may play a crucial role sinceprostate develops in puberty only in thepresence testosterone
Proliferated glands may dilate cystically,and accumulate prostatic secretions
This may predispose the affected individualto infection
BPH causes distortion and elongation
Bladder MucosalTrabeculations due toObstructive Uropathy
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BPH Contd.
ComplicationsThe increased pressure
of urine in the bladdermay cause reflux ofurine into the ureters
Dilation of the ureter(hydroureter)
Dilation of the renalcollecting system(hydronephrosis)
May lead to end-stagerenal disease
Treated surgically witha TransurethralResection of theProstate (TURP)
Renal calculus due toobstruction Hydronephrosis
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Prostate Carcinoma The most common diagnosed cancer in
men
3rd most common cause of cancer relateddeaths in males
75% are 60-80 years of age
The highest frequencies for prostate cancerare seen in the U.S. and the Scandinaviancountries
The lowest are seen in Mexico,Japan and
Greece American blacks exhibit a rate twice as
high as that of American whites
Intake of yellow and green vegetablesappears to have a protective effect and adiet high in fat contributes to anincreased incidence
It is believed that testosterone stimulates
the growth of prostatic carcinoma Castration of carcinoma patients is
thought to retard the tumor growth
Testosterone receptors have beendemonstrated on prostatic cancer cells
No evidence that prostate carcinomaoriginates from hyperplastic nodules (BPH)
Prostate intrae ithelial Neo lasia (PIN)
PI
i f h
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Carcinoma of thePr t t
Presence of PIN in prostatecancer Many patients with PIN have been shown
on subsequent follow-up biopsies monthslater to have invasive cancer
Peripheral location for both lesions
The cytological similarity of high-gradePIN to invasive carcinoma and the close
proximity of both lesions in the samebiopsy when present
98% of prostate cancers areAdenocarcinomas
Pathology Grossly they are multicentric (or
sometimes a single nodule) lesions
located in the peripheral zones ofthe prostate. (posterior lobes)
irregular, yellow-white, firm andbosselated subcapsular nodules.
The initial tumor is limited to the glands,bounded by the basement membrane(PIN)
Later may give rise to locally invasive
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Carcinoma of the Prostate Histologic findings
Most feature small to medium-sized glands that lackorganization and infiltrate thesurrounding fibromuscular stroma
The well-differentiated neoplasticglands are lined by a single layerof cuboidal epithelium
Loss of differentiation is seen with
increased variability of glandsize and shape, papillary andsolid cords of tumor cells withlittle gland formation, or
solid sheets of neoplastic cellswith no gland formation
Cytologic Features Usually there is marked
pleomorphism andovercrowding of cells withhyperchromatic nuclei
one or two prominentnucleoli, in a slightly eosinophilicor vacuolated cytoplasm
cribriform arrangement of theglands in the mid-grade lesions toa more solid appearances in the
P.D. Carcinoma
with no Glands,Cellular Cords andAbundant Stroma
Solid P. D.Adenocarcinoma
of the Prostatewith no Gland
Prostate Carcinomawith ProminentNucleoli and
With Small Backto Back Glands
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Gleason Grading System
Gleason grading system Five histologic patterns of
tumor gland formation andinfiltration
the Gleason score is the sumof the grades, numbered 1-5for
(1) the most prominentpattern and a (2)secondscoring for the minoritypattern
1 being the best or welldifferentiated
5 being the poorestdifferentiated
Best differentiated tumors willhave a total Gleason score of 2(1+1).
Most poorly-differentiatedcancers will have a totalGleason score of 10 (5+5)
When combined with the
Pattern 2 withUniform Round
Pattern 3 withCrowded Glands andProminent Nucleoli
Gleason Pattern 4with Cords and of
Back to Back
Pattern 5 with SolidSheet of
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Clinical Features Asymptomatic and is found incidentally
after a digital exam, PSA, or biopsy forBPH
When clinical features are present , thetumor has often expanded beyond thecapsule or into the urethra, obstructing it,
causing urinary frequency, urgency, andincontinence (symptoms of BPH)
Bone pain and pathologic fractures areseen in metastatic disease
Screening If the serum PSA is elevated, the diagnosis
is confirmed by needle biopsies of theprostate
Both malignant and normal prostaticcells express a specific antigen calledProstate Specific Antigen
Tumor cells release this antigen intothe circulation
osteoblastic metastases will cause of theserum alkaline phos-phatase levels
Originates in the peripheral parts of theprostate
Therefore no compression of the urethra orurinary problems until late in the course ofthe disease.
Prostatic cells normally produce ProstaticAcid Phosphatase (PAP)
the tumor cells, which are not organizedinto normal glands, release PAP into the
immunoperoxidase
Treatment and Prognosis
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Treatment and Prognosis Early tumors that are limited to the prostate are
the only forms of cancer amenable to successful
tx Tumor extension into the surrounding organs
usually are associated with pain, due toperineural invasion
Early prostate cancer is best treated surgically,(Radical Prostatectomy) but extensive tumors(T3) are usually treated with radiation therapy
Staging of Prostate Cancer The staging is based on the TMN system and
there are 4 subtypes of T for primary tumor T1: A clinically inapparent tumor not palpable or visible
by imaging. T2: The tumor is confined to the prostate. T3: The tumor extends through the prostate capsule. T4: The tumor is fixed or invades adjacent structures.