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DT4-Exam 1 > Male GU Path (Sigdel +Norton) - Melissa*** > Flashcards

Male GU Path (Sigdel +Norton) - Melissa*** Flashcards

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1
Q

Define Hypospadias.
With what other congenital anomaly may it also be associated?
What causes it?

A

Urethra opens on VENTRAL (HYPO= below) side of penis

  • Asstd. w undescended testes
  • **Failure of urethral folds to close
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2
Q

Define Epispadias.
With what TWO congenital anomalies may it also be associated?
What causes it?
How frequent?

A

Urethra opens on DORSAL (EPI= upon)

  • Asstd. w undescended testes + bladder Exstrophy
  • **Abnormal positioning of genital tubercle

-Much less common than hypospadias, needs corrected because it leads to recurrent infection.

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3
Q

What is a…

  • Micropenis
  • Diphallus
  • Bifid Scrotum
A
  • VERY LITTLE WEENIE
  • TWO WEENIES
  • TWO BALL SACS
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4
Q

What is Phimosis?

What causes it and what are TWO possible complications that might ensue?

A

Congenital or Inflammatory Process–>
Orifice or prepuce too small to retract–>
Infection or Carcinoma

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5
Q

Balanoposthitis

A

Nonspecific, NON-STI infection or glans and prepuce

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6
Q

Herpes of the Penile Variety:

  • Name the 2 viruses and describe their genome + capsid
  • What kind of infections can it cause (2)
  • High yield dx test?
  • Treatment?
A

HSV2*** or HSV1 (linear dsDNA; icosahedral)

  • TORCH infection
  • Superficial PAINFUL ulcer
  • DX: with Tzanck smear (“Tzanck God I don’t have Herpes!)
  • TX: Valacyclovir within first 48
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7
Q

Syphilis:

  • Causative organism
  • Describe PRIMARY infection
  • How is it diagnosed?
  • How is it treated?
A

Treponema Pallidum (spirochete)
NONPAINFUL CHANCRE; red shallow ulcer on testes –> epididymis
-DX: dark field microscopy FTA-ABS PCR
-TX: PEN-G

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8
Q 
Pemphigus Vulgaris of the Penis: 
Describe the blister 
Describe the autoimmune process
Describe the IF stain pattern 
Nikolsky + or - ?
A

Vulgaris:

  • Suprabasal acantholytic blisters
  • IgG against desmosomes
  • IF stain = net-like
  • Nikolsky (+)

pemphigu(S) (s)uperficial blisters
pemphigoi(D) (d)eeper blisters

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9
Q

Bullous Pemphigoid of the Penis:
Describe the autoimmune process
Describe the IF stain
Nikolsky + or - ?

A

Bullous Pemphigoid:

  • IgG against hemidesmosomes
  • IF stain = Linear
  • Nikolsky (-)
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10
Q

Lichen Planus of the Penis:
What causes the disease?
What do the lesions look like?

A
  • Typically autoimmune; otherwise unknown etiology

- Self limited flat-topped pink-purple macules

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11
Q

Fournier’s Gangrine
Where in the penis is the infection?
What might you see in he lesion (2)?
How dangerous is the infection?

A

SubQ infection –>
Gas production + necrosis–>
May spread; 40% fatal

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12
Q 
Peyroine’s Disease: 
What happens in this disease? 
What does the lesion CAUSE? 
Is it painful? 
What medical problem may be associated with this disease?
A
  • Fibrous thickening of penile CT
  • Causes Penis curves TOWARDS lesion
  • PAINFUL
  • Asstd w chronic urethritis
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13
Q

Condyloma Acuminatum:
Causative infection
What do the lesions look like?
What are 3 components of the histology?

A

HPV6, 11

  • Sessile or Pedunculate lesions
  • BENIGN but RECUR

-Histo: Acanthosis (epidermal thickening), hyperkeratosis, KOILOCYTOSIS (look for perinuclear clearing)

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14
Q

Giant Condyloma:
Who gets this?
What do the lesions look like?
Are they dangerous?

A

Population: Elderly

  • Multiple large cauliflower-like lesions
  • Can be verrucous carcinoma
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15
Q

Erythroplasia de Queryat:
Describe the lesion (specific location):
Does it cause visceral malignancy?

A

Erythroplakia on glans penis –> ~ squamous cell ca.

- Not asstd. with visceral cancer

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16
Q 
Bowen’s Disease
Who gets this? 
Describe the lesion 
Are they associated with visceral malignancy? 
Describe the histo:
A
  • Population: Elderly
  • Leukoplakia (single bright red plaque w moist surface) ~squamous cell ca.
  • 30% Asstd. with visceral malignancy
  • Histo: Dysplastic cells in epi layer
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17
Q

Bowenoid Papulosis
Who gets this?
Describe the lesions and disease progression
Describe the histo
With what infection is this lesion associated?

A

Population: Sexually active patients UNDER 40 yoa

  • Multiple reddish papules NO PROGRESSION to squamous cell ca.
  • Histo: identical to Bowen’s disease
  • Exceptionally strong assn. with HPV 16
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18
Q

Squamous Cell Ca. of Penis
Population?
What can be done to prevent the disease?
Describe the lesion and disease progression?
How common is it?
With what infections is it associated?
Briefly describe the histo.

A

Population: Elderly; protect with circumcision and good hygiene

  • Slow growing and starts as plaque/ precursor lesion
  • # 1 malignancy of penis
  • HPV 16/ ~18
  • Histo: intercellular bridging; keratin pearls
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19
Q 
Cryptorchid Testis: 
How common is it? 
Where is it?
What are the risks assc?
Histo: 2 changes + result of untreated testis.
A

Population: 1% of 1yom, usually unilateral idiopathic

  • Testes stuck in inguinal canal or abdomen
  • Sterility if bilateral; ^ risk cancer by age 2

histo: ^^ hyaline and leydig cells, atrophy if not repaired
(balls not meant to live in abdomen, they will die here.)

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20
Q

Testicular Atrophy
What are some potential causes?
What are two histo changes?
What is the result?

A

Age/ Atherosclerosis/inflammation/ cryptorchidism etc –>

Histo: scarring; BM thickening
Result: STOP spermatogenesis

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21
Q 
Mumps Orchitis:
Who gets this? 
What is the causative virus (describe genome and capsid) 
What are the histo changes? 
Final sequelae?
A

Population: Adolescents/ Adults (NOT CHILDREN)

Paramyxovirus: linear (-)ssRNA; helical nucleocapsid

Histo: mononuclear infiltrate +/- neutros and abscesses

Result: atrophy/ infertility

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22
Q

Gonorrhea:

Who gets this? 
What is the causative organism? 
Where is the infection? 
Is the libido effected? 
List some complications (4) 
How is it treated?
A

Population: YA
Gram (-) Diplococcus
-Infection spreads from epididymis –> testes
-spares Leydig cells and thus libido

Complications: abscesses = risk sterility
also: Reiters/ PID/ Fitz Hugh Curtis

Tx: Third gen. Ceph or Pen G

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23
Q

Syphilis:
Where is the infection?
Why do you see histologically? (3)

A

Treponema Pallidum, spirochete
Infection spreads from testes –> epididymis

Histo: GUMMAS (chronic granulomas); Obliterative endarteritis; perivascular cuffing

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24
Q

Chronic Orchitis: most common cause?

A

Usually nonspecific

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25
TB in the testes or epididymis: What do you see? Where does the infection start?
*Caseating* granulomas -Infection spreads from epididymis--> testes (opposite of syphillis) ***NOTE: if NONCASEATING granulomas think SARCOID, that shit can happen anywhere.
26
``` Torsion of Testes: Who gets this? what causes it? What is the ultimate result? What do you see on PE? ```
-Adolescents/ Kids -Testes don’t attach to processus vaginalis -Spermatic cord twists--> STOP venous drainage--> Hemorrhagic infarction -acute pain/ swelling + ABSENT cremasteric reflex
27
Varicocele What is the most common cause? What is the classic PE finding? what might be the end result if not treated?
- Obstruction of lt. renal vein--> Dilation of spermatic vein -scrotal swelling “bag of worms” - infertility if untreated
28
Hydrocele: Describe how this happens What is the classic PE finding?
-Incomplete CLOSURE of processes vaginalis--> Communication of scrotum with peritoneal cavity = fluid -Testis transluminates on PE
29
Three stages of testicular tumors:
I: confined to testes II: Spread Retroperit; nodes below diaphragm III: Outside retroperit; nodes above diaphragm
30
Adenomatoid Tumor: Benign or malignant? Source? What are the histo changes (2)? How is it treated?
- Benign mesothelial tumor of the epididymis - Histo: cuboidal cords, vacuoles - Tx: simple excision
31
Intratubular Germ Cell Neoplasm: What kind of tumor is this? List the most important tumor marker:
- Ca in situ --> precursor to germ cell tumors | - Isochromosome 12p
32
4 Tumor markers associated with ALL GERM CELL TUMORS OF THE TESTES (including precurosor intratubular lesion)
- Isochromosome 12p - OCT3/4 - NANOG - KIT I remember: OCTNANKIT
33
What are the two main types of germ cell tumors of the testes? What are the tumors that fall within these two categories? (2 and 4, respectively)
Seminomatous: (Seminoma, Spermatocytic seminoma) | Non-Seminomatous: Embryonal Ca., Yolk sac Ca., Choriocarcinoma, Teratoma
34
Germ cell tumors: - how common? - benign of malignant? - How are they all treated?
- Most common tumors of testes - Aggressive, but Responsive to tx - RADICAL ORCHIECTOMY ONLY (biopsy= tumor spillage)
35
``` Seminoma: Population? How common? Are they aggressive? Macro + Micro Histo: Marker? ```
Young adults; 50% all germ cell tumors; slow to met MACRO: Golden lobulated tumor MICRO: Large cells w prominent nucleoli + clear cytoplasm; sparse lymphs PLAP +
36
Spermatocytic Seminoma Population? Do they typically occur with other tumors? How aggressive are they compared to seminomas? Describe the histo (cell type) *What is the most aggressive subtype called
- Older adults - Do not occur w other testicular tumors; isolated/pure - Rarely met but more aggressive than seminoma, poor prognosis - histo: 3 cell types (small, intermediate, large) *Aggressive subtype = sarcomatoid
37
``` Embryonal Ca: Population? Macro? (large or small?) micro histo (cell type + pattern) Describe the prognosis. ``` Marker?
Population: 20-30yoa MACRO: Small tumors MICRO: Tubular/ papillary/ or alveolar pattern; **large anaplastic undifferentiated cells** *Prog: WORSE than others PLAP +
38
PLAP (+) Tumors? (2) AFP (+) tumors? (1) HCG (+) tumors? (1)
PLAP: Seminoma, Embryonal Ca. AFP: Yolk sac HCG: choriocarcinoma
39
Yolk Sac Tumor: When is it pure vs. mixed and which has better prognosis? Preceded by ITGN? Describe the micro histo (pattern + special cells): Marker?
- Pure in infants/kids (better prognosis) - Mixed embryonal in adults - NOT preceded by ITGCN MICRO: - Sinus pattern (central core) - SCHILLER DUVALL BODIES (look like primitive glomeruli) AFP+
40
Choriocarcinoma: How aggressive? Which is more common: mixed or pure? Describe the micro histo; what are the two cell types? Marker?
- Highly malignant - Mets to lung + liver @ presentation - Typically mixed form MICRO: - Hemorrhage +necrosis - Synctrophoblastic cells (large w irregular nuclei) - Cytotrophoblastic cells (small w clear cytoplasm) HCG+
41
What are the two types of sex cord tumors? | How aggressive the they?
Leydig and Sertoli Tumors; typically benign
42
Leydig Tumors: Population? What does the tumor secrete? Assc sx? Describe the micro histo (cell type + body)
Population: 20-60 yoa - May present w gynecomastia - Secretes androgens MICRO: - polygonal cells - Rod shaped *Crystalloids of Renke*
43
Sertoli Tumors What do they secrete? Describe the micro histo: (2)
-Hormonally silent | MICRO: trabeculae w cordlike structures
44
Teratoma: Who gets them and what type of tissue do they come from?
Pure in kiddos; Mixed (germ) in adults MICRO: Ectoderm, Endoderm, Mesoderm (all tissue derivatives)
45
Mixed Testicular tumors: How common are they and what are some examples?
60% all testicular tumors - Teratoma + embryonal + yolk sac - Seminoma + embryonal - Teratoma + embryonal
46
What is the #1 Testicular tumor? | Who gets this tumor?
Testicular Lymphoma Population: Older Adults #1 TESTICULAR TUMOR; Diffuse Large B cell
47
How much does a normal prostate weigh? Where is it located? What controls its growth?
- 20 g - encircles bladder neck + urethra - testicular androgens
48
What are the 4 zones of the prostate? | Where do the most ca and hypertrophy occur?
Four Zones: - Peripheral *most ca. - Central - Transitional *site of hyperplasia - Anterior fibromuscular stroma
49
What separates the prostatic glands? Describe the lining of the prostatic glands? What do the glands secrete/ why? What might you see in them?
- Separated by fibromuscular stroma - Lined by 2 layers of cells: basal = cuboidal, luminal = columnar (secretory) - secretes prostatic fluid (motility of sperm) - ~Corpora Amylacea
50
Acute Bacterial Prostatitis: Describe the pathogenesis and #1 organism What are the clinical findings? What might you see on culture?
Urine reflux--> UTI bacteria #1 E. Coli--> Prostatic infection - Clinical: Systemic signs/ sx. + dysuria, TENDER BOGGY FEELING PROSTATE - Culture: WBC (+); Bacteria (+)
51
Chronic Bacterial Prostatitis: Why is it hard to dx? Describe the patient history. What might you see on culture?
Difficult to dx because typically asx. Or mild sx. - Hx recurrent UTI with same organism - Culture: WBC (+); Bacteria (+), same as acute
52
Chronic ABACTERIAL prostatitis: How common? Describe the clinical findings and culture.
#1 Prostatitis! - Clinical: presents like chronic bacterial prostatitis - Culture: WBC (+); Bacteria (-)
53
Granulomatous prostatitis: Cause and clinical progression? What is the significance of the problem?
Patient w superficial bladder cancer--> **BCG Tx instilled into bladder--> Granulomatous prostatitis ensues w voiding urine Not clinically problematic
54
BPH: who gets it?
Patients 50+yoa | Incidence ^ w age (90% by 80 yoa)
55
BPH pathogenesis (3 steps)
1. Testosterone -->DHT (#1 Prostate Androgen) * *via 5-a Reductase** (produced by stromal cells) 2. DHT binds Androgen receptors on stromal + epithelial nuclei 3. Transcription of growth factor genes
56
BPH morphology: early vs. late | How much can it grow to weigh?
Early: Transitional Zone: white-gray stromal cell nodules Late: Diffuse pink-yellow glandular nodules w epi cells that secrete prostatic fluid -can weigh 60-100g, normal is 20
57
What would you see on biopsy in BPH? | Is it diagnosed this way?
-Prominent nodules Cystically dilated glands; lined by 2 LAYERS of cells (Basal layer intact-- not seen in CANCER) *Usually do not dx this way!!
58
BPH clinical: describe the progression of illness and how it leads to sx.
- Urethral obstruction Bladder hypertrophy + Distention--> | - Urinary stasis/ Incomplete voiding--> Nocturia; dysuria/ sudden acute anuria
59
BPH Treatment (1,2,3rd line)
- Decrease fluid before bed; lower caffeine or ETOH--> - a-Blockers +/- 5a-reductase inhibitors--> - Transurethral resection of prostate (TURP)
60
Prostate Intraepithelial Neoplasia: Definition? Histo features? Location?
- precurosr to adenocarcinoma in peripheral zone | - large folding glands, BM still intact!
61
Adenocarcinoma of prostate: - Who gets it/ how common? - Who DOESNT get it?
``` #1 MALE CANCER IN USA; M50+ yoa Less common in Asians and AA’s ```
62
Adenocarcinoma of prostate: Risk factors (3)
- high fat diet - high androgens - family hx
63
Adenocarcinoma of prostate: Clinical findings
Hard nodules on DRE
64
Adenocarcinoma of prostate: Histo features (4) | -mitoses? gland layers? # of glands? nuclei? stroma?
- Small crowded glands w little stromal material between - SINGLE cells (no basal cell layer) - Hyperchromatic cells w prominent nucleoli - NO pleomorphism/ mitosis
65
Adenocarcinoma of prostate: where does it met?
- Local extension - from lymph to obturator/ periaortic nodes - from blood to *bone* -- classic rx question
66
Adenocarcinoma: Describe the Gleason Grading system
``` 1 = Well differentiated; uniform; round glands w well circumscribed nodules 5= NO GLANDULAR DIFFERENTIATION; cells form stromal cords, sheets, nests ``` *Add two patterns present OR most prominent and highest grade present 2-4: good // 5-6: Intermediate // 7: Moderate // 8-10: High grade
67
Adenocarcinoma: Describe the staging system
T1: Unapparent// T2: palpable or visible // T3: Local extension // T4: Beyond local extension N0: No regional nodes // N1: Regional nodes M0: No distant mets // M1: Distant mets present
68
Prostatic Adenocarcinoma Screening: How does DRE effect PSA? What are normal PSA levels?
``` PSA DRE doesnt effect PSA normal is less than 4 ng/nl **but 25% of men with normal levels may have cancer!!!** (high false negative rate) ```
69
Adenocarcinoma of the prostate: How do we treat it?
Survaillence of PSA levels; Radical prostectomy; Radiation; Hormone manipulation *Serial PSAs assist in assessing response to tx

DT4-Exam 1 (17 decks)

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