Exam 4/lecture 4 Flashcards

(89 cards)

1
Q

Adult male reproductive tract is connected directly to what?

A

connected directly to the renal system and empties into the urethra below the bladder

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2
Q

What are the four parts of the male reproductive system?

A

testes; ductal system; glands and; glans penis

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3
Q
  • Glans penis is organ of what?
  • What do the gland consist of?
  • What is the utethra lined by?
A
  • Glans penis is organ of copulation & urination
  • Consists of columns of erectile tissue with urethra in center of glans penis
  • Urethra lined by pseudostratified columnar epithelium
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4
Q

Glans Penis

Most common congenital malformations are what (2)?

A

hypospadias and epispadias

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5
Q

Hypospadias:
* More or less common? What is it?
* Results in what?
* Incidence rate?
* treated how?

A
  • Hypospadias, more common, abnormal opening of urethra along ventral surface of penis
  • Results in irregular urine stream, urinary tract obstruction, increased risk for urinary tract infections, potential for infertility
  • Occurs 1:200 male births
  • Treated with reconstructive surgery
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6
Q

Epispadias:
* What is it?
* What is the incidence?
* Associated with what?
* Treatment?

A
  • Epispadias: urethral orifice on dorsal surface of penis which may promote urinary tract obstruction, urinary incontinence, infection, infertility
  • 1:30,000 births
  • Can be associated with bladder extrophy (protrusion of bladder through abdominal wall
  • Surgically more difficult to correct than hypospadias, but does respond to surgery
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7
Q
  • Aphallia:
  • Diphallia:
  • Micophallus:
  • Lateral penile curvature:
  • Penscrotal transposition:
  • Webbed penis:
  • How is it treated?
A
  • Aphallia: penile agenesis, congenital absence of penis
  • Diphallia: penile duplication
  • Micophallus: micropenis, normally formed, but abnormally short penis
  • Lateral penile curvature: one sided hypertrophy of fibrous tissue leading to penile torsion (twisting)
  • Penscrotal transposition: reversed penile & scrotal positions
  • Webbed penis: web or fold of scrotal skin obscures penoscrotal angle
  • Like hypo- & epispadias, most deformities can be corrected surgically
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8
Q

What a circumcision?

A

oldest recognized surgery
* Surgical removal of foreskin of penis (to reduce risk of infection and/or inflammation)

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9
Q

What is balanitis? What is the balanoposthitis?

A
  • Balanitis: inflammation of glans penis
  • Balanoposthitis: Balanitis involving foreskin + glans penis
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10
Q

Poor hygiene in uncircumcised males increases risk for what?

A

increases risk for accumulation of infectious agents, sweat, desquamated epithelial cells, debris (smegma) causing irritation

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11
Q
  • How can phimosis happen? What is it?
  • What happens with the foreskin at birth? one year old?
  • Treatment?
A
  • Phimosis can arise congenitally or secondary to balanoposthitis
  • Uncircumcised men frequently have persistent inflammation of foreskin that may eventually cause it to contract and painfully compress the glans as phimosis (foreskin cannot be fully retracted)
  • At birth: foreskin is adherent to glans penis
  • At 1 yr: 50% males have non- retractile foreskin
  • Treated surgically if needed
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12
Q

Sexually Transmitted Diseases (STD):
* Evident where?
* Can infect who?
* Asending infection results in what?
* Infections can lead to what?
* Examples?

A
  • Typically, evident on external genitalia
  • Can infect all male components
  • STDs affect males & females
  • Ascending infection results acute prostatitis, epididymitis and, occasionally, orchitis
  • Infections can lead to tissue/organ damage associated with infertility and/or renal dysfunction
  • Examples: syphilis, gonorrhea, chlamydia, herpes, HPV
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13
Q

Syphilis:
* Caused by what?
* How many cases in each year?
* What is the host for T. pallidum?
* Transmission through what?
* Once introduced, the organism spreads via what?
* What is the test for it?
* txt?

A
  • Caused by spirochete Treponema pallidum: Gram negative bacterium
  • 6000 new cases in US each yr, on the rise
  • Humans are only host for T. pallidum
  • Transmission is sexual through skin/mucous membranes or congenital via placenta
  • Once introduced, organism spreads via lymphatics
  • Serologic tests for syphilis involve testing for the presence of anti-treponemal antibodies in blood
  • Can be successfully treated with antibiotics, but this will not reverse permanent tissue damage
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14
Q

Syphilis: Primary syphilis
* How many days after infection? appears where?
* Primary syphilis is characterized by what?
* Chancre begins as a what and goes to what?
* Resolves when?
* Histology looks like what?

A
  • 9-90 days after infection primary lesion appears at site of infection (penis, scrotum)
  • Primary syphilis is characterized by ‘hard’ chancre lesion (this is not canker)
  • Chancre lesions are full of spirochetes, highly infectious
  • Chancre begins as a painless, small firm papule that progresses to well-defined indurated (hardened, raised) margins; ulcer with clean (clear) central pit
  • Resolves by itself over 4-6 weeks to leave a scar
  • Histology of ‘hard’ chancre ulcer consists of lymphocytic and plasmacytic inflammatory infiltrate, vascular endoarteritis (inflammation of endothelium, endothelial activation & proliferation)
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15
Q

Syphilis: Secondary syphilis
* happens when?
* In secondary syphilis, spirochete does what?
* Characterized by what?
* Lesions can be what?

A
  • About 2 months after primary syphilis resolves, secondary syphilis can appear
  • In secondary syphilis, spirochete spreads and proliferates systemically
  • Characterized by lymphadenopathy & multiple mucocutaneous lesions (erythematous rash) typically appear on hands & feet
  • Lesions can be maculopapular, scaly or pustular
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16
Q

Syphilis: Secondary syphilis
* Secondary syphilis lesion where?
* Histology of secondary syphilis lesion contains of what?
* Secondary syphilis lesions can what?
* Less common 2o syphilis manifestations include?

A
  • Secondary syphilis lesion in moist skin areas (anogenital, inner thighs, axillae) can appear as condyloma lata (wart-like).
  • Histology of secondary syphilis lesion contains proliferative endoarteritis & lympho-
    plasmacytic inflammatory cells and spirochetes (highly infectious)
  • Secondary syphilis lesions can resolve on their own followed by latent phase
  • Less common 2o syphilis manifestations include: hepatitis, renal disease, irititis, GI conditions
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17
Q

Syphilis: Tertiary syphilis
* Tertiary syphilis lesions gradually develop in how much people?
* Occurs how many years after initial infection?
* Complications include what?
* Tertiary syphilis is characterized by appearance of what?

A
  • Tertiary syphilis lesions gradually develop in about 15-30% of untreated patients
  • Typically occurs 5-20 years after initial infection
  • Complications include cardiovascular syphilis (80%; infection & inflammation of heart), neurosyphilis (10%; infection of brain or spinal cord)
  • Tertiary syphilis is characterized by appearance of gummas
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18
Q

Syphilis: Tertiary syphilis
* Gummas occur in what?
* Gummas are what?
* Histologically gummas present as what/
* Spirochetes present how?

A
  • Gummas occur in bone, skin, mucous membranes of upper respiratory tract, mouth
  • Gummas are irregular, firm mass of necrotic tissue surrounded by CT (granuloma)
  • Histologically gummas present as central zone of coagulative necrosis, surrounded by lymphocytes, macrophages, plasma cells, occasional peripheral zone of fibrosis
  • Spirochetes present locally and systemically
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19
Q

Gonorrhea:
* Caused by what?
* How many cases?
* What is the natural reservoir?
* presents as?

A
  • Caused by gram-negative bacterium, Neisseria gonorrhoeae
  • Approximately 650,000 cases annually US
  • Humans are only natural reservoir for N. gonorrhoeae
  • Gonorrhea presents as dysuria, urinary frequency and a mucopurulent urethral exudate within 2-7 days of infection, congested urethra (block it)
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20
Q

Gonorrhea:
* Bacteria can be found in what?
* Ascending infection results in what?
* Disseminated infection are what?
* Similar clinical manifestations in females, untreated can lead to what?
* Can have vertical transmission to who?

A
  • Bacteria can be found in discharge, treated with antibiotics
  • Ascending infection results acute prostatitis, epididymitis, orchitis
  • Disseminated infection is rare
  • Similar clinical manifestations in females, untreated can lead to obstruction of fallopian tube due to chronic, asymptomatic infection
  • Can have vertical transmission to infant during passage in birth canal
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21
Q

Chlamydia trachomatis:
* Most or least common?
* Intracellular bacteria taken up how? and differentiates into what?
* Reticulate bodies proliferate to what/

A
  • Most common bacterial STD in US, treated with antibiotics
  • Intracellular bacteria taken up by host cells in its elementary form which then differentiates into metabolically active form – reticulate body
  • Reticulate bodies proliferate to generate elementary bodies
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22
Q
  • Chlamydia trachomatis has similar clinical manifestation of what?
  • List the symptoms?
A

Similar clinical manifestations of chlamydia & gonorrhea include:
* Mucopurulent discharge with neutrophils
* Urethritis, epididymitis, prostatitis, pharyngitis, conjunctivitis
* Differences between clinical manifestations of chlamydia & gonorrhea:
* Bacteria may not be visible in discharge
* Chlamydia may be asymptomatic

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23
Q

Herpes Simplex Virus (HSV):
* Which one dont cause cancer? Which ones do?
* What are cold sores and genital herpes? What are they associated with?
* Genital herpes require what?
* HSV-2 causes what?
* Primary infection associated with?

A
  • HSV 1 & 2 don’t cause cancer, HSV8 associated with HIV/Kaposi sarcoma, EBV HSV4 with nasopharyneal carcinoma
  • HSV-1 (cold sores) & HSV-2 (genital herpes) associated with oral & anogenital lesions, cannot be cured – just managed
  • Genital herpes requires direct contact for transmission: sexual or maternal:fetal
  • HSV-2 causes painful, erythemtous vesicles (clear fluid) on mucosa/genital skin
  • Primary infection associated with mild symptoms of locally painful vesicular lesion, dysuria, urethral discharge, local lymph node enlargement & tenderness, fever, muscle ache, headache
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24
Q

HSV:
* Primary phase typically lasts how long?
* HSV is shed when?
* When is it life threatening?

A
  • Primary phase typically lasts several weeks, recurrence is common
  • HSV is shed when 1o or recurrent lesions are present
  • Life-threatening disease in neonates and immunosuppressed pt
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25
Herpes Simplex Virus: Histo?
* Histologically, HSV vesicles contain necrotic cells, fused multinucleate giant cells with intracellular inclusions (Cowdry type A) * **Cowdry type A inclusions:** droplet masses of acidophilic material surrounded by clear halos within nuclei, with disruption of host chromatin (seen in HSV, Varicella- zoster virus, and Cytomegalovirus infection)
26
Human Papilloma Virus (HPV): * How many types * transmitted how? * HPV causes what? * Genital warts have what? What else can they be called? * High risk HPVs cause what?
* 100 genetically distinct types of HPV * HPV can be transmitted sexually and to fetus during birth * HPV causes a number of squamous proliferative disorders in genital – both benign and pre-cancerous * Genital warts have low malignant potential and are associated with l**ow-risk HPVs, HPV-6 and HPV-11**. * Genital warts AKA **condyloma acuminatum** – Can range from sessile(flat) to larg epapillary lesions * H**igh-risk HPVs (types 16 and 18)** have been implicated in the genesis of several cancers, cervical, penile, oropharyngeal and anogenital SCC.
27
# Squamous cell carcinoma of penis & scrotum * Venereal warts (condyloma acuminata) are caused by what? * SCC can occur where? * Arises from what? * Histo? * Related to what? * Pronosis is associated with that?
* Venereal warts (**condyloma acuminata**) are caused by **HPV types 6 and 11** * SCC can occur on any region of skin of external male genitalia (scrotum & penis) * Arises from CIN * Histologically demonstrates **keratinization**, epithelial **pearl formation** * Related to poor hygiene in uncircumcised males, HPV 16 & 18 infection * Prognosis is associated with** lymph node involvement**: 25% 5 yr survival with inguinal node involvement; 0% 5 yr survival with iliac node involvement
28
* Penile cancers comprise of how many US male cancers? * How many cases a year?
* Penile cancers comprise 0.4% of US male cancers, higher in developing countries * Scrotal squamous cell carcinoma: < 10 cases/yr in US
29
# Testes * What are testes? * Composed of waht? * Seminiferous tubules converge onto what? * Seminiferous tubules are lined by what? What do they have?
* **Testes**, paired organs in scrotal sac, production of spermatozoa & male sex hormones * Composed of convoluted **seminiferous tubules (SE)** * **Seminiferous tubules** converge onto rete testis from which 15-20 small ducts, **ductuli efferentes** carry sperm into ductus deferens - **epididymis** * Seminiferous tubules are lined by stratified epithelium with germ cells in various stages of spermatogenesis & **Sertoli cells**
30
* What are sertoli cells and leydig cells? * Testicular disorders are called what?
* **Sertoli cells** support & nourish developing spermatozoa, comprise blood-testis barrier * **Leydig cells**, in interstitial spaces (I) between seminiferous tubules, produce and secrete male sex hormones, principally testosterone * Often testicular disorders are ‘**orchid**’ in nomenclature
31
# Congenital Anomalies of the Testis * Most common congenital abnormality is what? * 1% of male population, can confer what? * Patients with cryptorchidism are also 3-5X predisposed to what? * What is the treatment?
* Most common congenital abnormality is **cryptorchidism** (failure of testis to descend into scrotum from abdomen) * 1% of male population, can confer **infertility** * Patients with cryptorchidism are also **3-5X predisposed to testicular tumors.** * Surgical correction (**orchiopexy**) restores testicular placement, reduces risk for cancer
32
* Inflammatory lesions of testis (_) typically following what? * Nonspecific orchitis begins where? * Orchitis arises from mumps infection in about 20% of adult males where affected testis is what? * Severe mumps orchitis can lead to what?
* Inflammatory lesions of testis (**orchitis**) typically following inflammation of epididymis * **Nonspecific orchitis begins urinary tract infection** traveling to testis so involved testis is swollen, tender & contains a neutrophilic inflammatory infiltrate. * **Orchitis arises from mumps** infection in about 20% of adult males where affected testis is edematous, congested & contains a lymphoplasmacytic inflammatory infiltrate * Severe mumps orchitis can lead to testicular atrophy, fibrosis and sterility
33
* Testicular torsion is what? * Requires what?
* **Testicular torsion:** twisting of spermatic cord results in obstruction of venous drainage leading to potential venous congestion, infarction and ischemia * Immediately painful * Requires immediate surgical intervention to maintain testicular viability
34
# Male infertility * Male reproductive years are not limited by what? * 30-50% infertility among couples is what? * Low sperm count it what? * Examination of semen reveals what?
* Male reproductive years are not limited by age following puberty; continuous spermatogenesis results in 300 million sperm/ejaculate * 30-50% infertility among couples is male infertility (**90% low sperm count/low sperm quality**) * Low **sperm** count: <15 million sperm/ejaculate * Examination of **semen** reveal **sperm disorders** based on sperm count, motility, viability, morphology:
35
* Aspermia: * Azoospermia: (what are the two types) * Oligospermia: * Asthenozoospermia: * Pyospermia/leukocytospermia: * Necrospermia: * Teratospermia:
* **Aspermia**: lack of semen * **Azoospermia**: absence of sperm in semen – Obstructive (OA) vs. Non-obstructive (NOA) * **Oligospermia**: low sperm count * **Asthenozoospermia**: poor motility * **Pyospermia/leukocytospermia**: high levels of seminal fluid leukocytes-> infectious material * **Necrospermia**: sperm are dead * **Teratospermia**: abnormal morphology
36
Chromosomal causes for male infertility: Klinefelter Syndrome * Y chromosome defines what? What does an extra X chromosome do? * Arises from what? * What are signs? * What is reduced? what is increased? * Rarely what? * What is impair? * Increase risk for what?
1
37
Steroid hormone synthesis pathway?
38
# 17-beta hydroxysteroid dehydrogenase deficiency * What is the disease? * What is delayed and present? * Presence of what? * Some, but incomplete development of what? * Historically raised as what?
* **Rare autosomal recessive** disease in XY males (1:150,000 newborns) resulting in reduced/defective testosterone production * Delays male sexual development, at birth present with **‘ambiguous genitalia’**, micropenis, hypospadias, undescended testes * Presence of Wolffian duct derivatives (epididymis, vas deferens, seminal vesicles) * Some, but incomplete development of secondary sex characteristics; infertile; gynecomastia * Historically raised as females
39
# 3-Beta-hydroxysteroid dehydrogenase deficiency * By converting pregnenolone to progesterone, DHEA to androstenedione, androstenediol to testosterone, 3B-HSD is important for what? * Downstream products of progesterone also include what?
* By converting pregnenolone to progesterone, DHEA to androstenedione, androstenediol to testosterone, **3B-HSD** is important for production of androgens, estrogens * Downstream products of progesterone also include **corticosterone/aldosterone & cortisol**
40
# 3-Beta-hydroxysteroid dehydrogenase deficiency * What is the type of disease? * Enzyme involved in production of what? * Deficiencies in 3B-HSD impact what? * Males are what? * Most serious conditions are what?
* Inherited **autosomal recessive** disorder affecting gonads and adrenal gland; rare disorder (<100 patients reported) * Enzyme involved in production of **androgens, estrogens, cortisol & aldosterone** * **Deficiencies in 3B-HSD impact reproductive, renal & metabolic function** * **Males**: incompletely masculinized at birth, hypospadias, unpalpable testes; gynecomastia in pubertal males * Most serious conditions are male or female newborns with adrenal glucocorticoid & mineralocorticoid insufficiency resulting in circulatory collapse, low serum sodium (**salt- wasting disease/fatal**), high serum K+
41
# Neoplasms of the Testis * Occur as what? * Sex-cord stromal tumors are what? * Germ cell tumors are what? * Present in who? * Are what? * How many cases a year?
* Occur as **germ cell tumors** (from spermatogonia) or **sex-cord stromal tumors** (from Sertoli or Leydig cells) * **Sex-cord stromal tumors**: rare, generally benign * Germ cell tumors: malignant, account for 95% of post-pubertal testicular cancers, AKA **testicular cancers** * Most present in young men (**15-34 yr, range from 1.5->65 yrs**) * Are unilateral, **not initially painful** * 8000 new cases/yr US with only 400 deaths
42
# Neoplasms of the Testis * Usual therapy is what? * Good prognosis for all types except what? * Risks for testicular cancer include what? * Underlying cause is unknown, but germ cell tumors contain what?
* Usual therapy is **orchiectomy** & chemotherapy * Good prognosis for all types except **choriocarcinomas** * Risks for testicular cancer include **cryptorchidism, familial history** * Underlying cause is unknown, but germ cell tumors contain an **isochromosome of chr 12**p (extra copies of 12p)
43
# Germ Cell Tumors of the Testis * Germ cell tumors arise in boys/men in what? * Classified as what? * Seminomas and non-seminomas?
* Germ cell tumors arise in boys/men in **spermatogonium cells** * Classified as seminomas or non-seminomas germ cell tumors: * **Seminomas**: pure seminoma & spermatocytic seminoma * **Non-seminomas**: embryonal carcinoma, yolk sac tumor, choriocarcinoma, teratoma
44
Germ Cell Tumors of the Testis: * Gross appearance? * Present or absence of serum what? * Related and unique what?
45
# Proliferation & differentiation of embryonic cells Fertilized egg (_) grow and differentiate into what?
Fertilized egg (**oocyte + sperm – originally from diploid stem cell**) grow and differentiate into fetus, placenta, embryonic membranes.
46
Testicular germ cell tumor subtypes represent developmental elements of what?
47
Pure Seminomas: * Typical patient age is what? * Appear grossly as what? * Rare areas of what? * 10-30% patients with seminomas may have what? * Most are cured by?
* Typical patient age **40-50 yrs** * Appear grossly as **firm, well-demarcated gray-white** tumors on testicular surface * Rare areas of coagulative necrosis * 10-30% patients with seminomas may have **mild serum elevations of hCG** * Most are cured by radical **orchiectomy**
48
Pure Seminomas: * Often confined to what? * Even in patients with widely metastatic seminoma, cure rates are what? * Overall good or bad prognosis?
* Often **confined to testis for long periods**, but can metastasize via iliac & para- aortic lymph nodes * Even in patients with widely metastatic seminoma, cure rates are very high with conventional chemotherapy, since most pure seminomas are especially s**ensitive to radiation therapy or chemotherapy** * Overall good prognosis
49
Pure Seminomas: * Tumor cells correspond to what? * Tumor cells are what? * Occasional what? * Usually infiltrated by what?
* Tumor cells correspond to **gondal cell lineage** differentiation (i.e. spermatogonial stem cells) * Homogenous tumor cells (red arrow) * Tumor cells are **large, uniform**, distinct cell borders, glycogen rich clear cytoplasm, round nucleus with prominent nucleoli * **Occasional syncytiotrophoblasts** (black arrow) * Usually infiltrated by small lymphocytes (few to many lymphocytes)
50
Spermatocytic Seminomas: * Pts are what? * Appear grossly as what? * Areas of what may be present? * Most are cured by what? * Often confined to what? * Generally do not what?
* Pts are **>65 yrs** * Appear grossly as **firm, yellowish cystic** tumors on testicular surface * Areas of coagulative necrosis & hemorrhage may be present * **Do not produce hCG** (different to pure) * Most are cured by radical orchiectomy * Often **confined to testis for long periods**, but can metastasize via iliac & para- aortic lymph nodes * Generally **do not metastasize**, cure rates are very high with conventional chemotherapy, since most seminomas are especially **sensitive to radiation therapy or chemotherapy** * Overall good prognosis
51
Spermatocytic Seminomas: * Tumor cells correspond to what? * Tumors consist of what? * Tumors lack what?
* Tumor cells correspond to **gondal cell lineage** differentiation (i.e. spermatogonial stem cells) * Tumors consist of **varying sizes of polygonal tumor cells** arranged in nodules or sheets * Tumors **lack lymphocytic infiltration and syncytiotrophoblasts** present in pure (true) seminomas
52
# Nonseminomatous Germ Cell Tumors * Nonseminomatous germ cell tumors are what? (compared to seminomas) * Metastasize?
* Nonseminomatous germ cell tumors are more differentiated & aggressive than seminomas * **Metastasize earlier** than seminomas, commonly spread to lungs & liver, spread by lymphatic and hematologic routes
53
Nonseminomatous germ cell tumors recapitulate different embryonic and postembryonic structures:
– **Embryonal carcinoma** corresponds to undifferentiated, pluripotent stem **cells of fetus** – **Yolk sac tumor** corresponds to **primitive blood-forming organs** – Choriocarcinoma corresponds to **placental** trophoblast – **Teratoma** corresponds to tumors with **somatic tissues from all three embryonic layers**: skin/nervous (ectoderm); muscle/bone/blood (mesoderm); GI (endoderm) corresponds to fetal gonadal/spermatogonium cells
54
Non-seminoma Germ Cell Tumors: Embryonal Carcinoma * Peak age is what? * Typically presents as what? * Tumor borders as waht? * Negative for what? * Cured by what? * Can metastazise via what? * Respond to ?
* Peak age of incidence is **20-30 years** of age * Typically presents as a **hemorrhagic mass with necrosis** * Tumor borders are ill-defined * **Negative for serum tumor markers** * Most are cured by radical **orchiectomy** * Can metastasize via iliac & para-aortic lymph nodes * **Respond well to surgery & chemotherapy** so overall good prognosis
55
# Non-seminoma Germ Cell Tumors: Embryonal Carcinoma * Tumor cells correspond to what? * Tumor cells are what? * Cells can form what?
* Tumor cells correspond to **fetal stem cells** (i.e. totipotent stem cells) * Tumor cells are **large and undifferentiated** with basophilic cytoplasm, **indistinct cell borders**, large prominent nucleoli * Cells can **form irregular epithelial-like structures (red arrow)**
56
# Nonseminomatous Germ Cell Tumors: Yolk Sac Tumors Yolk sac tumors are most common germ * cell tumor in pts? * Grossly? * What is present? * What is produced? * Preoperative measurement of serum tumor marker levels is important for what? * Patients respond well to what?
* Yolk sac tumors are most common germ cell tumor in pts **< 3 yrs of age** * Grossly, yolk sac tumors have smooth, glistening appearance contains cystic **structures** * **Some hemorrhaging present** * **Frequently produce α-fetoprotein (AFP)** **that is elevated in serum** * Preoperative measurement of serum tumor marker levels is important for managing patients postoperatively * Patients **respond well to surgery & chemotherapy** * Very good prognosis
57
# Nonseminomatous Germ Cell Tumors: Yolk Sac Tumors * Tumor cells correspond to what? * Composed of what? * Characterized by presence of what?
* Tumor cells correspond to **blood stem cells** (i.e. bone marrow cells) Composed of **low cuboidal to columnar epithelial cells** forming cysts, lacelike patterns, sheets or papillae * Characterized by presence of **Schiller-Duvall bodies** (rosette in center of photo) that resemble glomerular
58
# Nonseminomatous Germ Cell Tumors: Choriocarcinoma * Presents in who? * Tumors are what? * All choriocarcinomas produce what? * Highly what? * Usually what?
* Presents in adolescents or young adults (**20-30 yrs age**) * Tumors are small in size, but are **hemorrhagic and necrotic** * All choriocarcinomas produce **high levels of serum hCG** * Highly **malignant, prone to metastasize, poor prognosis** * Usually fatal
59
# Nonseminomatous Germ Cell Tumors: Choriocarcinoma * Tumor cells correspond to what? * Similar to placenta, but what? * Composed of what?
* Tumor cells correspond to **placental tissue** * Similar to placenta, but no villous structures are not formed * Composed of **cytotrophoblastic and syncytiotrophoblastic cells** (arrow)
60
# Nonseminomatous Germ Cell Tumors: Teratomas * What are the types? * Occur when? * Negative for what? * represent neoplastic growth of what? * Patients respond well to what?
* Benign (**mature**) & malignant (**immature**) teratomas * Occur at **any age**, most cases of malignant teratomas occur in adults * **Negative for serum biomarkers** * Represent neoplastic growth of germ cells along all three germ layers * Patients respond well to surgery & chemotherapy * Very good prognosis
61
Teratomas Benign vs malignant?
62
Nonseminomatous Germ Cell Tumors: Teratomas * Teratomas represent differentiation of what? * What is the histo appearance?
* Teratomas represent differentiation of neoplastic germ cells along all three germ layers * Heterogeneous histologic appearance
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# Vas deferens * Common inflammatory/infections conditions of vas deferens related what? * Cystic fibrosis contributes to what? * Conditions of vas deferens typically confer what? * What is a vasectomy?
* Common inflammatory/infections conditions of vas deferens related to **blockage** * Cystic fibrosis contributes to congenital absence of vas deferens bz mucus clogs vas deferens during development so they deteriorate prior to birth * Conditions of vas deferens typically confer infertility * Vasectomy: ligation of vas deferens
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* Adult prostate weighs how much? * What does it encircle? * Composed of what? * What is prominent in prostatic hyperplasia? * Epithelial cells produce what? * Glandular products drain into what? * Surrounding connective tissue consists of what?
* Adult male prostate weighs approximately 20 grams * Encircles neck of bladder and urethra * Composed of gland & stroma * **Basal epithelial cells** are prominent in **prostatic hyperplasia** * Epithelial cells produce 30-50% seminal fluid & prostate specific antigen * Glandular products drain into urethra * Surrounding connective tissue consists of smooth muscle (controls urine flow/ejaculation) and fibrous tissue
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What does the central zone of prostate surround? What cannot be done?
* Central zone surrounds ejaculatory duct * Bz zone farthest from rectum, this zone cannot be felt during a digital rectal exam (DRE) | Closest to uretha
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Where is the peropheral zone located ? What is usually here?
* Peripheral zone extends around gland * Closest to rectum so can be **palpated by DRE** * Majority of **prostate tumors** (approximately 75%) are found in the peripheral zone
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* Where is the transition zone of prostate located? * With age, transition zone enlarges due to what? * As transition zone enlarges, it does what?
* **Transition zone** between peripheral and central zones, surrounds the urethra * With age, transition zone enlarges due to **benign prostatic hyperplasia (BPH)**, until it becomes largest area of prostate * As transition zone enlarges, it pushes peripheral zone toward rectum so enlarged prostate can be palpated
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What is the anterior zone of prostate made up of and what does it surround?
* Anterior zone is composed of fibromuscular tissue, devoid of glandular elements * Surrounds apex of prostate
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What are some prostatic conditions?
Both benign (**prostatitis, benign prostatic hyperplasia** – BPH) or malignant prostatic **carcinoma** can enlarge prostate
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When prostate enlarges, it can constrict the urethra and produce one or more of these clinical symptoms:
* Need to urinate frequently during the day or night (**nocturia**) * **Sudden urgent need** to urinate * Difficulty initiating urinary stream * Feeling like you still need to urinate even though you recently urinated * Feeling like you need to push or strain to empty your bladder (**urinary** **hesitancy**) * Decrease in force of urine stream * Loss of small amounts of urine (**dribbling** urine) * Pain during urination (**dysuria**) * Abdominal/pelvic **pain**
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# Inflammatory Conditions of the Prostate: Prostatitis * Makes up of how much prostate conditions? * Can be what? * Infectious prostatitis is associated with what?
* Prostatitis accounts for about 8% of prostate conditions * Can be infectious or non-infectious cause * Infectious prostatitis associated with urinary tract infections
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Prostatitis can be what (4)?
* asymptomic inflammatory prostatitis (?%) * acute bacterial (2-5%) * chronic bacterial (2-5%), * chronic non-bacterial (chronic pelvic pain syndrome – 90-95%)
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Acute prostatitis: * How many cases of prostatitis? * Patients present with what? * What is the prostate? * Characterized by what?
* Acute: 2-5% of all cases of prostatitis * Patients present with fever, chills, **dysuria** * Palpated prostate is tender, swollen * Characterized by **neutrophilic** inflammatory infiltrate & stromal edema * Treated with antibiotics
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# Asymptomatic inflammatory prostatitis: * Inflammation of prostate with presence of what? * What is not present? * Usually detected when? * Limited to what?
* **Inflammation of prostate with presence of leukocytes** in semen * **Without genitourinary symptoms, no pain, no evidence of infection** * Estimate of incidence is under reported bz it’s asymptomatic * Usually detected secondarily – i.e. may occur with benign prostatic hyperplasia * Limited response to antibiotics/anti-inflammatory agents
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Chronic prostatitis: * How many cases of prostatitis? * May follow after what? * Typically associated with what? * Can present as what? * With disease progession, what happens? * What is there a varying amounts of? * Chronic prostatitis may serve as what? * Responds to what?
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Chronic Non-Bacterial Prostatitis: * Also called what? * Up to how many prostatitis cases? * What is not present? * Requires what? * Presents with what?
* (AKA: Chronic pelvic pain syndrome) * Up to 95% of all prostatitis cases * Difficult to diagnosis, no known etiology, no infectious agent present * Requires physical examination and ruling out presence of infection * Presents with **lower back pain, perineal and/or pelvic pain, dysuria, pain with ejaculation, reduced urine output, tender & enlarged prostate.** * No adequate therapies, does not respond to antibiotics
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Benign Prostatic Hyperplasia: * Enlarged prostate to? * BPS affects how many people? * Arises from where? * impinges what? * Cause? * Treatment? * No risk for what?
* BPH **enlarges prostate** to 60-100g (normal size 7-11g = 4 pennies) * BPH affects 70% of US men 60–69 years of age and 80% of those 70 years of age or older * Arises from **inner transitional zone** * Impinges urinary & sperm output * Cause is unknown, but is **dihydrotestosterone** (DHT)-dependent for growth * Treatment: alpha-blockers to relax muscle, **anti-androgen ** therapy and/or surgery * However, **surgery is problematic** due to anatomical investment of prostatic glandular tissue into urethra * **No risk for progression to prostatic cancer**
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histologic appearance of BPH: * BPH is characterized by? * hyperplastic glands are what? * what is there a formation of? * BPH associated with what? * Glandular lumina often contain what? * What is produced?
* BPH characterized by proliferation of epithelial & stromal elements * Hyperplastic glands are **2 cell layers thick, lined by tall, columnar secretory epithelial cells & a basal layer of flat-cuboidal basal cells** * Formation of **papillary projections in some glands** * BPH usually associated with chronic inflammatory cell infiltrate * Glandular lumina often contain proteinaceous material = **corpora amylacea** * Hyperplastic epithelial cells can produce **PSA**
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# Prostate Carcinoma How many males experience prostatic problems? How many are male cancer deaths? Present as what?
* 75% males experience prostatic problems by 70 years of age * 9% all male cancer deaths (31,620/321,670 cancer deaths) * Present as firm, gray-white lesions with ill-defined borders, infiltrate glandular elements
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What are the risk factors of prostate carcinoma?
* **Age**: Average age of diagnosis 72 years old * **Family history/hereditary** of disease in first degree relatives (father, brothers); BRCA2 mutations * **Race/ethnicity**: More common African Americans * **Environment/lifestyle:** smoking, diet high in saturated fats * **Acquired somatic mutations**: 40-50% prostate cancer acquire translocation of androgen promoter to ETS gene (**TPRSS2- ETS**) which drives PI3K/AKT signaling pathway for cellular proliferation * **NOT BPH**
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# Prostate Carcinoma: Clinical Presentation * Arise where? * Non initally associated with what? * What is elevated? * Where does it metastasize to? * Respond to what?
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Prostate Adenocarcinoma: Histological appearance
* Prostate adenocarcinomas from prostatic glandular epithelial cells * Adenocarcinomas lined **by single layer of cuboidal to columnar epithelial cells** * Glandular elements **lack branching, papillary structures (vs BPH)** * **PIN** found present in 85% prostatic adenocarcinomas, but does not cause elevated serum PSA levels on its own & cannot be detected by DRE or ultrasound (imaging)
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What is the gleason score?
* Most prostate cancers contains areas of differing tumor grade (heterogenous grade) * Gleason grading score based on glandular histological, pattern & degree of differentiation with categories from 1 to 5 * Gleason score is **sum of grades of most prominent pattern & minority pattern of tumor gland** formation and infiltration
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* Gleason grades 1 and 2 tumors are usually what? * Grade 3 are what? * Grade 4 and 5?
* Gleason grades 1 and 2 tumors are usually indolent and rarely cause death. * Grade 3 tumors are the most common grade tumor * Gleason grades 4 & 5 tumors are aggressive & associated with lymph node and bone metastases
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# ``` ``` Histopathology of Gleason Scores
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What grades are these?
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What grades are these?
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* Overall prostate carcinomas are typically scored by what? * What is the survival rate? * Treatment choices depend on what?
* Overall prostate carcinomas are typically scored by combination of **PSA levels, Gleason score & TNM score** (T2N0M0/PSA <20/Gleason 7) * Survival rates: 5-yr is 99%; 10-yr is 91%; 15-yr is 76% * Patient age, co-morbidities, PSA levels, Gleason score, metastasis, urinary symptoms, tumor size
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What are the different treatments of prostate cancer?