Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CPR II Exam 3 > Chapter 21: Male GU Pathology > Flashcards

Chapter 21: Male GU Pathology Flashcards

1
Q

How are bladder cancers staged?

A
  • staged based on the basis of INVASION of the DETRUSOR muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the difference between Ureteropelvic Junction Obstructions between males and females?

What is UPJ the most common cause of?

A

Male: usually early in life and BILATERAL
- seen with other congenital abnormalities
Female: usually in adulthood and UNILATERAL
- abnormal smooth muscle bundles at UPJ

most common cause of HYDRONEPHROSIS in infants and kids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Tumors of the Ureter

How frequent are they, what is a Fibroepithelial Polyp, and what is the most common primary malignant tumor?

A
  • primary tumors are RARE

Fibroepithelial Polyp: small mass projecting into lumen; vascularized and covered in urothelium

  • UROTHELIAL CARCINOMA is most common primary malignant tumor (50-60 yo) –> can lead to hydronephrosis via lumen obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is Sclerosing Retroperitoneal Fibrosis?

What Ab is it associated with and what two organs does it also affect?

A
  • fibrotic proliferative inflammatory process encasing retroperitoneal structures and causes HYDRONEPHROSIS
  • associated with IgG4 disease and can involve EXOCRINE glands, like pancreas and salivary glands

Tx: corticosteroids, stents/surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the difference between these Urinary Bladder congenital anomalies:

  1. Vesicoureteral Reflux (VUR)
  2. Urinary Bladder Diverticula
  3. Exstrophy of the Bladder
  4. Patent Urachus (Total vs Cyst)
A
  1. MOST COMMON and serious anomaly
    • renal scarring/infection –> PYELONEPHRITIS
  2. pouchlike bladder wall invaginations
    • predisposes to VUR; inc. infection and calculi risk
  3. developmental failure of anterior abdominal wall
    • bladder communicates directly with overlying skin
    • inc. risk of ADENOCARCINOMA/infections
  4. Total Patent: fistulous urinary tract; Urachal Cyst: only center part is patent (rarely becomes adenocarcinoma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 4 most common causes of bacterial Cystitis infections?

What is the difference between Acute and Chronic Cystitis (Eosinophilic/Follicular)

What is the clinical Triad of Cystitis? (F/P/D)

A

E. coli = MOST COMMON CAUSE
- Proteus, Klebsiella, Enterobacter

Acute: hyperemia of mucosa/neutrophil infiltrate
- pts. w/adenovirus –> hemorrhagic cystitis

Chronic: mononuclear cells and thick walls

  • E: eosinophils in submucosa
  • F: lymphoid follicles in bladder mucosa

Triad: frequency (15-20 min), lower abdominal pain (over bladder), dysuria (pain and burning)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is Interstitial Cystitis?

A
  • chronic cystitis, usually seen in FEMALE pts.
  • cystitis triad in ABSENCE of infection beginning with punctate hemorrhage and developing into HUNNER ULCERS
  • transmural fibrosis (bladder contraction) and inc. mucosal mast cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is Malakoplakia?

What are Michaelis-Gutmann bodies?

A
  • chronic bacterial infection (E. coli/Proteus) cystitis due to acquired defect of PHAGOCYTE function in IMMUNOCOMPROMISED PTS
  • yellow, mucosal plaques with foamy macrophages that stain PAS (+)
  • Michaelis-Gutmann bodies: macrophages loaded with undigested bacterial products (LARGE CELLS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is Polypoid Cystitis?

What is it commonly misdiagnosed as?

A
  • inflammatory lesion from irritation of bladder mucosa due to INDWELLING CATHETERS
  • see marked submucosal edema = broad bulbous polypoid projections
  • can be MISDIAGNOSED with papillary urothelial carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the difference between these metaplastic lesions of the bladder:

  1. Cystitis Grandularis/Cystitis Cystica
  2. Squamous Metaplasia
  3. Nephrogenic Adenoma
A
  1. seen in normal bladder/chronic cystitis
    • Grad: grow down into lamina propria and become cuboidal or columnar epi (instead of transitional)
    • Cystica: flattened cells lining fluid-filled cysts
  2. injury response; squamous epi replaces transitional
  3. shed tubular cells implant and proliferate at injuries
    • cuboidal epi that assumes papillary growth pattern
    • CAN extend into detrusor M., but is still benign
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the two Urothelial Tumor precursor lesions and how do Urothelial Tumors typically present?

A
  1. Non-Invasive Papillary Tumors (MOST COMMON)
    • from papillary urothelial hyperplasia
  2. Carcinoma In Situ (high grade epithelial lesions)
    • cytogenically malignant but without BM invasion
  • present with PAINLESS HEMATURIA alongside inc. frequency, urgency, and dysuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Urothelial Carcinoma Risk Factors

What is the most common cause, what organism causes disease in pts from Egypt or Sudan, and what long-term exposure is linked to inc. risk of development?

A
  • CIGARETTE SMOKE = MOST IMPORTANT RISK factor
    • 50-80% of all bladder cancers are cigarette-related
  • pts from Egypt/Sudan at inc. risk of bladder cancer due to Schistosoma haematobium (endemic organism)
  • pts. with long-term exposure to ANALGESICS are also at inc. risk of Urothelial Carcinoma development
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What two Loss-of-Function and two Gain-of-Function mutations are common in pts. with Urothelial Carcinoma?

A

Loss-of-Function

  1. TP53/RB - Chr 17p deletion (almost all invasive tum)
  2. loss of Chr 9 - CDKN2A loss (non-invasives)

Gain-of-Function

  1. FGFR3 - non-invasive, low-grade papillary carcin.
    • Receptor Tyrosine Kinase
  2. HRAS - non-invasive, low-grade tumors
    • usually mutually exclusive with FGFR3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Urothelial Tumor Morphology

What is the difference between Papillomas, Inverted Papillomas, and Papillary Urothelial Neoplasms of Low Malignant Potential (PUNLMP)?

A
  1. Papilloma: MOST COMMON PATTERN
    • found in young pts (rare), EXOPHYTIC growth
    • PEDUNCULATED
  2. Inverted Papilloma: inter-anastomosing cords extending into the lamina propria
  3. PUNLMP: slightly larger than papillomas with THICKER urothelium
    • rarely progresses to high-grade

majority of papillary tumors are LOW-GRADE; usually red/elevated appearing on POSTERIOR/LATERAL areas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Urothelial Tumor Morphology

What is Carcinoma In Situ (Flat Urothelial Carcinoma)?

What is the most important factor in determining the outlook for patients with this cancer?

A
  • cytologically malignant cells with FLAT UROTHELIUM that appears as mucosal reddening with NO MASS projecting into lumen
    • if untreated –> 50-75% will invade
  • lack of cohesiveness leads to SHEDDING of malignant cells into the urine
  • MOST IMPORTANT factor is Staging at Initial Diagnosis (biopsy “understaging” is a problem)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Squamous Cell Carcinoma of the Bladder

Where is it most commonly found and why?

How are most bladder cancers treated?

A
  • inc. incidence in countries with endemic SCHISTOSOMIASIS (Middle East) –> very unusual in the United States
  • mixed urothelial and squamous carcinomas are more common than purely squamous cell bladder cancer
  • Bladder cancer responds well to chemotherapy but is not curable with current agents; currently surgery is the only curative measure available
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Mesenchymal Tumors of the Bladder

What are the most common benign tumor and what form of sarcoma is more common in children vs adults?

A

Benign: uncommon in the bladder, but usually leiomyomas if present
- isolated, intramural, encapsulated, spherical masses

Sarcomas: uncommon in the bladder; large masses that grow into vesicle lumen (soft, gray-white appear.)

  • Kids (MC): embryonal rhabdomyosarcoma
  • grape-like masses = sarcoma botryoides
  • Adults: leiomyosarcoma (MALIGNANT)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Bladder Obstructions

What is the difference in obstruction between Males and Females?

A

Male: prostate enlargement due to nodular hyperplasia

Female: cystocele of the bladder

obstructions are LESS COMMON in females than males

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Urethritis (Urethral Inflammation)

What is the difference between Gonococcal and Non-Gonococcal Urethritis?

How does this condition typically present?

A

Gonococcal: Neisseria gonorrhea (Gram - diplococcus)
- PURULENT discharge

Nongonococcal: Chlamydia trachomatis (Gram - ovoid nonmotile)

  • SEROUS discharge or no discharge at all
  • A-C serotypes = BLINDNESS
  • D-K serotypes = GU tract (urethritis, PID, ectopic pregnancy)

present with pain, itching, urinary frequency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is a Urethral Caruncle and what is the difference between Proximal and Distal Primary Carcinoma of the Urethra?

A

UC: painful, small, red inflammatory lesion of external urethral meatus in older females

  • bleed easily due to ulceration
  • excision is curative

Proximal urethra: urothelial carcinomas
Distal urethra: squamous cell carcinomas
adenocarcinoma uncommon, but in women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Penile Congenital Anomalies

What is the difference between:

  1. Hypospadias
  2. Epispadias
  3. Phimosis
A
  1. urethral opening on VENTRAL aspect of penis
    • more common than epispadias
  2. urethral opening on DORSAL aspect of penis
    • *if near base of penis = ejaculation can be hindered**
    • *usually leads to urine obstruction**
  3. foreskin is too tight and cannot be retracted properly (usually secondary to inflammation that causes scarring of preputial ring)
    • predisposes to infection and carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is Balanoposthitis?

A
  • infection of the glans and prepuce by non-specific organisms (NOT STDs)
  • typically seen due to poor local hygiene in uncircumcised males
  • leads to smegma accumulation that can become scarred, causing phimosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Benign Penile Tumors

What is the difference between Condyloma Acuminata and Peyronie Disease?

A

CA: sexually transmitted wart associated with HPV 6 > 11 (sessile, pedunculated, red papillary excrescences)

  • Acanthosis: hyperkeratosis/thickening of epidermis
  • Koilocytosis: cytoplasmic vacuolization of squamous cells (HPV characteristic)

PD: proliferation of fibroblasts that cause fibrous bands around the penile corpus cavernosum
- causes PENILE CURVATURE and pain during sex

24
Q

Carcinoma In Situ of the Penis

What is it associated with?

What is the difference between Bowen Disease and Bowenoid Papulosis?

A
  • malignant tumor associated with HPV 16

BD: solitary thickened, gray plaque over shaft or red shiny lesions on glans/prepuce in pts > 35 yo
- BM intact, but 10% become infiltrating SCC

BP: multiple, pigmented papular lesions on external genitalia in younger, sexually active adults

  • multiple, reddish-brown papular lesions
  • rarely evolve to invasive carcinoma
25
Q

Squamous Cell Carcinoma of the Penis

What is it associated with, what is its morphology (Flat vs Papillary vs Verrucous), and how does it present clinically?

A
  • associated with poor genital hygiene and HPV 16/18 in pts 40-70 yo (inc. risk in regions that do not CIRCUMCISE due to smegma accumulation under foreskin)
    • SMOKING inc. risk of development too

Flat: on glans/prepuce; progresses to ulcerated papule
Papillary: graying/fissuring; cauliflower-like fungation
Verrucous: exophytic, well-differentiated; local invasion

C: slow-growing and locally invasive and is NOT painful until it ulcerates or becomes infected

  • usually metastases to inguinal/iliac LNs
  • distant metastases uncommon unless ADVANCED
26
Q

What is Cryptorchidism and how does it present clinically?

When do the testis typically descend in boys?

A
  • most common congenital abnormality of the TESTES; due to failure of testis descent = tubular atrophy/sterility (75% unilateral)
  • dec. germ cell development; seminiferous tubules will become hyaline CT cords; fibrosis that spares Leydig cells

C: completely asymptomatic (comes to attention with empty scrotal sac); pts at inc. risk for developing testicular cancer and being damaged by trauma
- most testis descend before the age of 1 yo

27
Q

Testis and Epididymis Inflammation

Which ones is more prone to inflammation and what are the typical causes of inflammation in each area?

A
  • epididymis inflammation is MORE COMMON than testis inflammation

Epididymis: gonorrhea and TB
Testis: syphilis (epididymis typically spared)

28
Q

What is Nonspecific Epididymitis and Orchitis, and what do they look like morphologically?

What are the common causes in children, pts < 35 yo, and pts > 35 yo?

A
  • primary UTI reaching the epididymis via vas deferens of spermatic cord lymphatics

M: congestion, edema neutrophilia, MO/lymphocytes infiltrates

children: congenital or gram (-) rods
< 35 yo (sexually active): Chlamydia, Gonorrhea
> 35 yo men: common UTI agents (E. coli/Pseudo)

29
Q

What is Granulomatous Orchitis?

A
  • painless/mod. painful testicular mass of sudden onset occurring in MIDDLE AGE
  • granulomas develop due to autoimmune rxn and are restricted to spermatic tubules
30
Q

How do Mumps, TB, and Syphilis present in pts with Testis inflammation?

A

Mumps: systemic viral infection, usually in kids

  • testicular involvement is rare
  • orchitis 1 wk after inflamed PAROTID GLANDS

TB: caseating granulomas

Syphilis: two different morphologies

  1. nodular gummas
  2. obliterative endarteritis with perivascular cuffs
31
Q

What is Testicular Torsion?

A
  • twisting of the spermatic cord cutting off venous drainage, leading to vascular engorgement with potential for infarct (hemorrhage)
    • arterial supply remains INTACT
  • testis will become enlarged, soft, necrotic, and hemorrhagic –> testicular infarct
  • surgery in < 6 hrs can preserve viability
32
Q

Spermatic Cord and Paratesticular Tumors

What is the difference between these tumors:

  1. Lipoma
  2. Adenomatoid Tumor
  3. Rhabdomyosarcoma
  4. Liposarcoma
A
  1. lesions of PROXIMAL spermatic cord
    • can look like retroperitoneal fat in inguinal canal
  2. MOST COMMON benign paratesticular neoplasm
    • well circumscribed, small mesothelial nodules
    • near upper epidydimal pole
  3. most common paratesticular tumor of CHILDREN
  4. most common paratesticular tumor of ADULTS
33
Q

Testicular Germ Cells Tumors

What are they, what is Testicular Dysgenesis Syndrome (3 characterizations), and what are two genetics factors for development?

A
  • malignant testicular tumors seen in Caucasian men 15-34 yo (sex cord stromal tumors = BENIGN)

TDS = due to environmental risk factors

  • cryptorchidism, hypospadias, poor sperm quality
  • due to pesticides and nonsteroidal estrogens

Genetics: KIT and BAK (receptor tyrosine kinase)

34
Q

Testicular Germ Cell Tumors

What are the two classifications and how does the tumor develop?

A
  1. Seminomatous Tumors
    • look like primordial germ cells or early gonadocytes
    • Ex: spermatocytic seminoma
  2. Nonseminomatous Tumors
    • undifferentiated cells that look like embryonic stem cells and cells that have already differentiated
    • Ex: yolk sac tumors, choriocarcinomas, teratomas

P: mostly develop from Intratubular Germ Cell Neoplasia (ITGCN) = precursor lesion

  • remains dormant until puberty
  • has totipotent transcript factors: OCT3/4, NANOG
  • duplication of short arm of chromosome 12
35
Q

Seminoma

What is it, what genetics does it have, and what does it look like?

A
  • most common type of Germ Cell Tumor occurring in 20-30 yos but NEVER in infants
  • expresses isochromosome 12p, OCT3/4, and NANOG

M: lobulated, gray-white masses devoid of necrosis/hemorrhage

  • tunica albuginea remains intact
  • irregular stoma lobules w/clear or watery cytoplasm
  • may have syncytiotrophoblasts and inc. HCG lvls
36
Q

Spermatocytic Seminoma

What is it, what is it NOT associated with, and what does it look like?

A
  • rare, slow-growing testicular GCT in pts. > 65 yr that DOES NOT metastasize (EXCELLENT PROGNOSIS)
  • NOT associated with ITGCN

M: soft, gray cut surface with mucoid cysts

  • medium sized cells with round nucleus
  • EOSINOPHILIC cytoplasm
  • no lymphocytes, granulomas, syncytiotrophoblasts
37
Q

Embryonal Carcinoma

What is it, what does it look like, and what 4 genetic markers is it positive for? (O/P/C/C)

Which genetic marker is it NOT positive for?

A
  • more aggressive than seminomas and is found in 20-30 yo pts.

M: poorly demarcated, small, gray-white mass with HEMORRHAGE and necrosis

  • extends THROUGH Tunica Albuginea
  • undifferentiated lesions show sheets of cells

(+): OCT3/4, PLAP, CD30, Cytokeratin
(-): cKIT

38
Q

Yolk Sac Tumor

What is it, what does it look like (SDB), and what two markers are highly characteristic of it?

A
  • most common testicular tumor in children < 3 yo with a VERY GOOD prognosis

M: infiltrative, homogenous, yellow-white mucinous tumor with SCHILLER-DUVAL BODIES (primitive glomeruli)

  • has eosinophilic hyaline globules with AFP and a1-antitrypsin (VERY CHARACTERISTIC of tumor)
39
Q

Choriocarcinoma

What is it, what two cell types does it contain, and what molecule is typically elevated in this tumor?

A
  • highly MALIGNANT tumor presenting as small palpable tumor WITHOUT testicular enlargement
  • contains Cytotrophoblasts (grow in cords/masses with single uniform nucleus) and Syncytiotrophoblasts (large, multinucleated cells w/eosinophilic vacuolated cytoplasm)
  • HIGH serum lvls of hCG are present
40
Q

Testicular Teratoma

What is it, what is the difference in presentation between pre-pubertal and post-pubertal pts, and what does it look like?

What clinical implications does this disease have?

A
  • can occur at any age and are usually mixed with other germ cell tumors; all 3 germ layers are present
    • pure forms are common in infants/kids (BENIGN)
    • pure forms are RARE in adults (MALIGNANT)

M: large with heterogenous appearance; all 3 germ layers are present and embedded in fibrous (Myxoid) stroma

  • do NOT elaborate biomarkers
  • cure for malignant versions depends on ability to resect

C: painless enlargement of testis; tumor spillage is possible during surgery
- hematogenous spread to LUNGS, liver, brain, bone

41
Q

What is a Pure Choriocarcinoma and how does it present?

What is the difference between Stage 1, Stage II, and Stage 3 Testicular Tumors?

A
  • most aggressive form of NSGCT that presents with NO testicular ENLARGEMENT
  • rapid hematogenous spread to lungs and liver (involved in virtually EVERY case)

Stage 1: confined to testis, epididymis, sperm cord
Stage 2: retroperitoneal LNs (BELOW diaphragm)
- persistent hCG/AFP conc. following orchiectomy
Stage 3: metz outside RP LNs or ABOVE diaphragm

42
Q

What does Lactate Dehydrogenase tell clinicians about testicular tumors?

A
  • biomarker elevation correlates with MASS of the tumor cells
  • allows assessment of the TUMOR BURDEN
43
Q

Leydig Cell Tumors

What are they and what do they produce, and what do they look like (ERC)?

A

benign tumors in 20-60 yos that produce androgens, estrogens, and corticosteroids

  • present with testicular swelling or changes do to hormonal elaboration (GYNECOMASTIA)

M: circumscribed homogenous golden brown tumors with eosinophilic Reinke Crystalloids (rod-shaped)
- lipid droplets and lipofuscin pigment

44
Q

What are Sertoli Cell Tumors and Gonadoblastomas?

A

SCT: hormonally silent and present as a testicular mass (firm and small)

  • homogenous gray-white to yellow
  • tall, columnar cells in trabeculae

G: rare and comprised of mixture of germ cells and gonadal stromal elements

45
Q

Testicular Lymphoma

A
  • most common testicular tumor in pts OLDER THAN 60
  • usually diffuse, large B cell non-Hodgkin lymphoma that disseminates widely
  • high incidence of CNS involvement
46
Q

Lesions of the Tunica Vaginalis (Exterior Testis)

What is the difference between:

  1. Hydrocele
  2. Hematocele
  3. Chylocele
  4. Spermatocele
  5. Varicocele
A
  1. serous fluid accumulation in tunica vaginalis
    • scrotal sac enlargement
  2. blood accumulation 2nd to trauma, torsion, bleeding
  3. lymphatic fluid accumulation
    • leads to ELEPHANTIASIS
  4. cystic accumulation of semen in dilated efferent ducts
  5. dilated vein of spermatic cord
47
Q

Where on the prostate do most carcinomas and hyperplasia occur?

What is normal prostate growth controlled by and where is this control made?

A

Carcinomas: typically on PERIPHERAL prostate

Hyperplasia: typically on TRANSITIONAL prostate
- much more common than tumors

  • growth controlled by DHT that is made by the LEYDIG cells via type 2 %a-reductase
48
Q

What is the difference between Acute Bacterial Prostatitis and Chronic Bacterial Prostatitis?

A

ABP: caused by common UTI pathogens

  • dysuria, fever, chills, perianal pain
  • do NOT biopsy –> can lead to SEPSIS

CBP: due to frequent bouts of UTI

  • dysuria, pelvic discomfort, lower back pain
  • Dx: leukocytosis in prostatic secretions w/positive bacterial cultures

antibiotics penetrate the prostate poorly = safe haven for bacterial seeding

49
Q

What are Nonbacterial Chronic Prostatitis and Granulomatous Prostatitis?

A

NCP: MOST COMMON prostatitis that has similar presentation to Chronic Bacterial form

  • NO history of recurrent UTI
  • prostatic secretions with leukocytes but bacterial cultures are uniformly NEGATIVE

GP: either specific (known cause) or non-specific (can’t tell) and is most commonly caused by installation of BCG into the bladder for treatment of SUPERFICIAL BLADDER CANCER
- Fungal seen in IMMUNOCOMPROMISED pts

50
Q

Benign Prostatic Hyperplasia

What is it, who is it commonly seen in, and how does it develop?

A
  • most common prostatic disorder defined by hyperplasia of prostate STROMAL cells; can lead to urinary obstruction
    • see discrete nodules in PERI-URETHRAL regions
  • 20% of men get by age 40, 90% by age 80

P: inc. number of stromal components due to accumulation of senescent cells in the prostate (androgens inhibit cell death)

  • 5a-reductase: Testosterone –> DHT
  • DHT activates FGF and TGF-B
  • estrogen inc. sensitivity of DHT receptors in prostate
51
Q

Benign Prostatic Hyperplasia

What does the prostate look like grossly, what histology is present, and how does BPH present clinically?

A

G: enlargement begins in TRANSITIONAL zone; median lobe enlargement that projects into floor of the urethra
Glandular: yellow-pink, soft, milk white prostatic fluid
Fibromuscular: large, pale, firm, NO milky fluid

H: glandular hyperplasia

  • Dx CANNOT be made on needle biopsy
  • too small; does not sample transition zone

C: nocturia, urgency, hesitation, difficulty starting/stopping, overflow, inc. risk of bacterial infect.

  • inability to completely void bladder
  • firm, rubbery mass on digital rectal exam
52
Q

Adenocarcinoma of the Prostate

What is it, what genetics is it associated with (H/B/H), and what genomic changes are commonly seen in this cancer?

What genetic rearrangement is commonly seen in Caucasian pts. with prostate adenocarcinoma?

A
  • most common cancer in men
  • most epigenetics due to HYPERMETHYLATION of GSTP1 gene on chromosome 11
    • BRCA2 and HOXB13 mutations inc. risk GREATLY
  • genomic DELETIONS/AMPLIFICATIONS more common that point mutations (in contrast to breast and colon cancer)
  • 50% of white pts can have rearrangement of ETS family transcription factor genes (ERG/ETV1) next to androgen-regulated TMPRSS2 promotor
53
Q

Adenocarcinoma of the Prostate

How do CAGs trinucleotide repeats relate to disease, where does cancer develop from and through what, and what are two environmental factors that inc. risk of development (location/metal)?

A
  • CAGs in X-linked androgen receptor genes cause rare Kennedy Disease (muscle cramps/fatigue)
    • inverse relationship: shorter repeat, inc. sensitivity
    • parallels incidence/mortality of cancer in black, white, asian pt. populations
  • cancer beings in PERIPHERAL ZONE as prostatic intraepithelial neoplasia (PIN, NOT CIS)

RF: cadmium exposure and North-South Gradients (northern Europeans have inc risk of development)

54
Q

Adenocarcinoma of the Prostate

When do urinary symptoms develop, what is felt on rectal exam, where does it like to metastasize to, and what two molecules are typically elevated?

A
  • urinary symptoms develop LATE due to cancer arising PERIPHERALLY away from urethra

DRE: firm, discrete nodules felt
- requires transrectal needle biopsy to confirm Dx.

  • Osteoblastic metastases by radionucleotide bone scanning is virtually diagnostic of prostate cancer
    • can also see Paraneoplastic Syndromes
  • PSA and PAP lvls are elevated (also seen in BPH) and are typically used as screens for cancer
55
Q

Adenocarcinoma of the Prostate

What is an additional marker checked in pts. with high PSA lvls but who have a negative prostate biopsy?

What is the difference in basal cells and epithelium between benign and malignant prostate glands?

A
  • PRA3 = noncoding RNA overexpressed in 95% of prostate cancers
    • AMARC also upregulated in prostate cancer

Malignant Prostate Glands

  • have ABSENT basal cells
  • single layer of cuboidal epi with no outer basal

Benign Prostate Glands
- Basal Cells ARE present

CPR II Exam 3 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions