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Pathology > Chapter 20, Part Of Others > Flashcards

Chapter 20, Part Of Others Flashcards

1
Q

Urothelium

A

Special form of transitional epithelium

-5-6 layers of cells with oval nuclei, often with linear nuclear grooves, and a surface layer consisting of large, flattened umbrella cells with abundant cytoplasm

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2
Q

Morphology lamina propria of bladder

A

Wisps of smooth muscle that form discontinuous muscularis mucosae

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3
Q

Muscularis proporia

A

Deeper well defined larger muscle bundles of detruser muscles
Bladder cancers are staged on the basis of invasion of detruser muscle

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4
Q

What are the 3 points of narrowing of the ureter

A

Uteropelvic junction

Where the ureter enters the bladder

Where ureter crosses the iliac vessels

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5
Q

How does the ureter enter the bladder

A

Obliquity of the intramural segment of the urethral orifice permits the enclosing bladder msuculature to act like a sphincteric valve, blocking the upward reflux of urine even in the presence of marked distention of the urinary bladder

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6
Q

Defects in the and of the ureter entering the bladder may predispose to what

A

VUR->pyelonephritis

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7
Q

Double birdie ureters

A

Come off double renal pelvis or bifid pelvis

Most are unilateral and no clinical significance

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8
Q

Ureteropelvic junction obstruction

A

Most common cause of hydronephrosis in infants and kids

Early cases are more likely to be bilateral and happen in males
-often associated with other congenital abnormalities (espicially agenesis of the other kidney)

In adults, more common in girls and unilateral
-due to abnormal smooth muscle bundles at the UPK

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9
Q

Diverticula

A

Saccular outpouchings of the urethral wall

Most are asymptomatic, but urinary stasis can sometimes lead to recurrent infections

Can be associated with: dilation (hydroureter), elongation, and tortuosite of the ureters

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10
Q

Urethritis

A

Inflammation

Actually not associated with infections, little clinical significance

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11
Q

Primary tumor of the ureter are __

A

Rare

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12
Q

Small benign tumors of the ureter are generally of ___ origin in ureter

A

Mesenchymal

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13
Q

Fibroepithelial polyp ureter

A

Tumor like lesion that presents as a small mass projecting into the lumen

Often in kids

May also occur in the bladder, renal pelvises and urethra

Polyp is composed of loose, vascularized CT overlaid by urothelium

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14
Q

Primary malignant tumor of ureter: most common?

A

Urothelial carcinoma

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15
Q

Screening for cancer with urinary cytology is diagnostic for ureter?

A

No

Renal pelvic carcinoma, bladder malignancy, urethral carcinoma==all urothelial tissue

Field effect, field cancerization—the urine with carcinogens baths all this tissue

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16
Q

When do people get primary malignant tumors of ureter

A

50-60

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17
Q

What do primary malignant tumors of the ureters cause cause

A

Hydronephrosis

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18
Q

Describe primary malignant tumor of ureter

A

Sometimes multifocal and commonly occur with similar neoplasms in the bladder or renal pelvic

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19
Q

Sclerosing retroperitoneal fibrosis in ureter

A

Obstructive lesion, fibrotic proliferative inflammatory process encasing the retroperitoneal structures (SAD PUCKERS) and causing hydronephrosis

Most idiopathic/primary (ormond disease)

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20
Q

Who gets sclerosing retroperitoneal fibrosis

A

Middle late age men associated with IgG4 related diseases sometimes

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21
Q

Sclerosing retroperitoneal fibrosis involves other tissues as well, particularly what

A

Exocrine organs such as the pancreas and salivary glands

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22
Q

What can cause sclerosing retroperitoneal fibrosis

A

Drugs-ergot derivatives, beta adrenergic blockers

Adjacent inflammatory process—vasculitis, diverticulitis, IBD

Malignant disease—lymphomas, urinary tract carcinomas

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23
Q

LM sclerosing retroperitoneal fibrosis

A

Fibrous tissue containing prominent infiltrate of lymphocytes, often with germinal centers, plasma cells (IgG4 positive) and eosinophils

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24
Q

Treat sclerosing retroperitoneal fibrosis

A

Corticosteroids, but will need stents or surgery (ureterolysis: extrication of the ureters form the surrounding fibrous tissue)

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25
Q

Urinary bladder

A

Ok

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26
Q

Vesicourectal reflux

A

Most common and serious congenital anomaly of bladder

Contributes to renal infections and scarring ->pyelonephritis

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27
Q

Urinary bladder diverticula

A

Pouchlike evaginations of the bladder wall

Congenital or acquired (prostatic enlargement)

Often due to increase intravesical pressure

Urinary stasis predisposes patients to infection and formation of bladder calculi

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28
Q

What does bladder diverticula predispose to

A

VUR

Advanced carcinoma as a result of the thin or absent muscle wall of diverticula

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29
Q

Exstrophy of bladder

A

Developmental failure of the anterior abdominal wall

Bladder communicates directly with overlying skin or is exposed sac

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30
Q

Issue with exstrophy of bladder

A

Exposure of bladder mucosa may undergo colonic glandular metaplasia and is subject to infections

Increased risk of adenocarcinoma and infections that spread to upper levels of the urinary system

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31
Q

Treat exstrophy of bladder

A

Surgical correction=long term survival

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32
Q

Patent urachus

A

Totally patent: fistulas urinary tract

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33
Q

Rachael cyst

A

Only the center is patent and is lined by urothelium or metaplastic glandular epithelium

Rarely do the cysts turn into cancer

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34
Q

Cystitis (acute or chronic)

A

Infections in the urinary bladder have retrograde spread of bugs into the kidneys and collecting systems

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35
Q

What causes cystitis infections

A

E. coli

Proteus, klebsiella, enterobacter

Chlamydia, mycoplasma,

Tuberculous cystitis
-almost always a sequel to renal tuberculosis

Candida/cryptococci

Schistosoma (Egypt)

Chlamydia, mycoplasma, adenovirus

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36
Q

Predisposition to cystitis

A

Bladder calculi

Urinary obstruction

Diabetes mellitus

Instrumentation

Immune defiency

Irradiation of the bladder

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37
Q

Morphology acute cystitis

A

Hypermedia of the mucosa and neutrophilic infiltrate (sometimes with exudate)
-patients receiving cytotoxic anti tumor drugs or infected with adenovirus can develop hemorrhagic cystitis

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38
Q

Chronic cystitis morphology

A

From chronic bacterial infection associated with mononuclear cells

Follicular cystitis: presence of lymphoid follicles within the bladder mucosa and underlying wall, not always related to infection

Eosinophilic cystitis: infiltration of eosinophils into the submucosa; not always related to infection

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39
Q

Clinical cystitis

A

Frequency (every 15-20 min)

Lower abdominal pain, localized over the bladder region/suprapubic region

Dysuria (pain burning)

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40
Q

Interstitial cystitis (chronic pelvic pain syndrom)

A

Chronic cystitis, usually female

Pain and dysuria in absence of infection

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41
Q

Early and late phase interstitial cystitis

A

Early-punctuate hemorrhages

Late/classic/ulcerative phase-chronic mucosal ulcer (hunger ulcers) with inflammation and transmural fibrosis leading to a contracted bladder

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42
Q

Morphology interstitial cystitis

A

Increased mucosal mast cells

Biopsy to rule out carcinoma in situ!!

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43
Q

Malakoplakia

A

Chronic bacterial cystitis (e coli or proteus)

Acquired defect of phagocyte function

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44
Q

Who gets malakoplakia

A

Immunocompromised

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45
Q

Morphology malakoplakia

A

3-4 cm soft, yellow, mucosal plaques with foamy macrophages

Macrophages with abundant granular PAS positive cytoplasm

Michaelis-Guzman bodies: macrophages with intra-lysosomal laminated calcified concretions

Macrophages become overloaded with undirected bacterial products and become giant

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46
Q

Polypoid cystitis

A

Inflammatory lesion from irritation of bladder mucosa

Most commonly due to indwelling catheters, but can be due to any injurious agent

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47
Q

Morphology polypoid cystitis

A

Marked submucosal edema—>broad bulbous polypoid projections

Confused with papillary urothelial carcinoma both clinically and histologically

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48
Q

Cystitis glandularis and cystitis cystica

A

Metaplastic lesions seen in normal bladders or chronic cystitis

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49
Q

Morphology cystitis glandularis and cystitis cystica

A

Nests of transitional epithelium (brunn nests) grow downward into lamina proporia

Nests transform into cuboidal or columnar epithelium (glandularis )

These conditions occur together often and is called cystitis cystica et glandularis

Flattened cells lining fluid filled cysts

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50
Q

Squamous metaplasia

A

Response to injury

Urothelium replaced by non keratinize game squamous epithelium

Should be distinguished from glycosylated squamous epithelium that is normally found in women at the trigone

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51
Q

Nephrogenic adenoma (benign)

A

She’d tubular cells implant and proliferate at sites of injured urothelium

Urothelium turns into cuboidal epithelium that assumes a papillary growth pattern

Possible extends into superficial detruser muscle and mimics a malignant process (still benign)

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52
Q

Bladder neoplasm

A

95% of bladder cancer are of epithelial origin

Called urothelial or transitional tumors

Remaining cancers are mesenchymal

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53
Q

Urothelial tumors

A

90% of all bladder tumors
-may arise anywhere there is urothelium (renal pelvis to distal urethra)

Small benign lesions to aggressive cancers

Often multifocal at presentation

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54
Q

What are the two distinct precursor lesions or urothelial tumors

A

Noninvasive papillary tumors (most)

Flat noninvasive urothelial carcinoma

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55
Q

Non invasive papillary tumors

A

Most common precursor lesion to urothelial tumors

Originates from papillary urothelial hyperplasia

Lesions range in atypia that reflects biological behavior

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56
Q

Carcinoma in situ

A

Term used to describe high grade epithelial lesions that have the cytology features of malignant cells but are confined to the epithelium but show no evidence of basement membrane invasion

High grade lesions

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57
Q

Invasive bladder cancer

A

The high grade invasive component destroys the precursor lesion

Typically appears as a large, ulcerated mass

Invasion into the LP worsens prognosis, but invasion into the muscularis propria is major factor for survival

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58
Q

Risk factors for urothelial carcinoma

A 
Male
50-80
CIGARETTE (50-80%)
-cigars, pipes, and smokeless tobacco less
Industrial exposure to aryl amines 
-15-40 years after exposure

Schistosoma haematobium
-Egypt Sudan

Long term use of analgesics

Heavy exposure to cyclophosphamide (immunosuppressive)
-also induces hemorrhagic sytitis

Irradiation of other pelvic malignancy
-bladder cancers occur many years after

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59
Q

Genetic alterations of urothelial carcinoma leading to constitutive activation of growth factors receptor signaling cascades

A

FGFR3 (receptor tyrosine kinase)

TP53 and RB

HRAS

Loss of 9p

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60
Q

FGFR3 urothelial carcinoma

A

Gain of function mutation; oncogene

Non invasive, low grade papillary carcinomas

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61
Q

TP53 and RB

A

Loss of function mutation ; tumor suppressor

Almost always seen in high grade and muscle invasive tumors

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62
Q

HRAS uretheliocarcinoma

A

Gain of function mutation; oncogene

Low grade non invasive tumors

HRAS and FGFR3 are generally mutually exclusive in bladder cancer bc RAS signal transducers act downstream of receptor tyrosinase kinases

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63
Q

Loss of chromosome 9p urothelium carcinoma

A

Specifically loss of CDKN2A (p16/INK4 and ARF) tumor suppressor gene

Often the only abnormality seen in superficial non invasive papillary tumors and occasionally in non invasive flat tumors

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64
Q

Mostmorphology urothelial tumors

A

Most arise from the lateral and posterior walls at bladder base

Papillary lesions are red and elevated

Multiple, discrete tumors are often present

Overall majority of papillary tumors are low grade
-encompass a range from benign papilloma to highly aggressive anaplastic cancer

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65
Q

Papillomas

A

Rare bladder cancer found in young

Exophytic papilloma grow out

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66
Q

Histology papillomas

A

Arise singly as a delicate urothelium cover over finger like papillae with a loose fibromuscular core histologically identical to normal urothelium

Superficially attached to the mucosa by stalk (pedunculated)

Extremely low incidence of progression or recurrence—benign

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67
Q

Inverted papilloma (benign)

A

Inter anastomoses cords of bland urothelium extending into the LP

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68
Q

Papillary urothelial neoplasms of low malignant potential (PUNLMP)

A

Share many histologically features with papilloma , except:

  • slightly larger than papillomas
  • thicker urothelium

Rarely progress to higher grade—doesn’t mean they don’t

Looks bad but the pathologist doesn’t think it looks like a malignancy

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69
Q

Low grade papillary urothelial carcinomas

A

Orderly cytology and architecture

Minimal atypia

Rarely invade

Rarely fatal

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70
Q

High grade papillary urothelial cancer

A

Discohesive cells with anaplastic features

  • architectural disarray, loss of polarity
  • large, hyperchromatic nuclei
  • atypical mitosis figures
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71
Q

High grade papillary urothelial cancer has high risk of what

A

Invasion into the muscular layer, higher risk of progression and significant metastatic potential

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72
Q

Metastases or urothelial tumors of the bladder

A

Adjacent structure invasion

Fistulas communications with vagina or rectum

40% to regional LNs

Hematogenous spread to liver, lungs, bone

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73
Q

Carcinoma in situ (flat urothelial carcinoma)

A

Cytogically malignant cells within a flat urothelium

Can range from full thickness atypia to scattered malignant cells in an otherwise normal urothelium (pagetoid spread)

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74
Q

Morphology carcinoma in situ

A

Lack of cohesiveness leads to shedding of malignant cells into urine
-when extensive , only a few CIS cells may be left clinging to a largely denuded BM

Appears as an area of mucosal reddening, granularity, or thickening, but no mass projecting into the lumen-flat

No evident intraluminal mass

Multifocal

Flat urothelial lesions are always carcinoma in situ

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75
Q

If untreated what percent of CIS will invade

A

50-75%

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76
Q

Invasive urothelial cancer is associated with what

A

Papillary urothelial cancer, high grade or adjacent CIS

Invasion of muscularis mucosae (detruser) is prognostically important

Biopsy understating is a problem-staging at the initial diagnosis is the most important factor in determining the outlook for the patient
-extend of spread=staging

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77
Q

Squamous cell carcinoma of the bladder

A

Increased incidence in countries with endemic schistosomiasis-middle east
-only place; very unusual in the US

Associated with chronic bladder irritation and infection

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78
Q

Mixed urothelial carcinoma with areas of squamous carcinoma of the bladder

A

Invasive, fungating and/or infiltrating and ulcerations tumors

More common that purely squamous cell bladder cancers

Can be well differentiated or anaplastic

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79
Q

Adenocarcinoma of the bladder

A

Rare

Histologically identical to adenocarcinomas seen in GI tract

Some arise from Rachael remnants or in the setting of intestinal metaplasia

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80
Q

Small cell carcinoma of the bladder

A

Indistinguishable from small cells arcinoma of the lungs

Often associated with urothelial, squamous adenocarcinoma

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81
Q

Bladder cancer presntation

A

Painless hematuria

Frequency, urgency, dysuria

Pyelonephritis or hydronephrosis may follow if the urethral orifice is involved

Tend to recur after excision at a higher grade in different sites

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82
Q

Prognosis bladder cancer

A

Papillomas or low grade papillary urothelial cancer have 98% 10 year survival rate

Less than 10% progress to a higher grade lesion, but if they do 25% of those patients expire

Patients with primary carcinoma in site are less likely to progress to muscle invasive cancer as compared to carcinoma in situ associated with infiltrating urothelial carcinoma

Urothelial carcinoma has a 30% chance of being fatal if it invades the LP but otherwise squamous cell carcinoma and adenoacarcinoma are associated with worst prognosis

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83
Q

Treat bladder cancer: small, localized low grade papillary tumors

A

Diagnostic transurethral resection; follow with cystoscope and urine cytology

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84
Q

Treat bladder cancer : patients at high risk for recurrence==intra vesical instillation of an attenuated strain of mycobacterium Boris BCG

A

Bacterial elicit a local inflammatory reactions hat destroys the tumor

Radical cystectomy reserved for really advanced cancers

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85
Q

Treat bladder cancer: advanced

A

Radical cystectomy

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86
Q

How cure bladder cancer

A

Respond well to chemo, but need surgery to cure

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87
Q

Mesenchymal tumors of the bladder

A

Benign tumors

Rare but most common are leiomyomas

They grow as isolated, intramural , encapsulated, oval to spherical masses

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88
Q

Sarcomas of bladder

A

Uncommon
Produce large masses that grow into the vesicle lumen

Have soft grey white appearance

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89
Q

What sarcoma most common in kids

A

Embryonal rhabdomyosarcoma, can grow into a grape like mass (sarcoma botryoides)

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90
Q

Most common sarcoma in adults

A

Leiomyosarcoma

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91
Q

Secondary tumors

A

From direct extension from primary lesion in nearby structure (cervic, uterus, prostate, rectum)

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92
Q

Obstruction

A

Males or femelas?

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93
Q

Prostate enlargement

A

Obstruction of bladder in men due to nodular hyperplasia

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94
Q

Cystocele of bladder

A

Most common obstrucion in females

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95
Q

Morphology of obstruction

A

The bladder wall continues to thicken
With time, the wall can be so thick that crypt and eventually diverticula will form

The bladder can become very enlarged and thinned in some cases where the bladder can reach to the brim of the pelvis or to the umbilicus

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96
Q

Urethra

A

Ok

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97
Q

Urethritis

A

Gonococcal or nongonoccal

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98
Q

Conococcal urethritis

A

Early manifestations of neisseria gonorrhea infection (gram - diplodocus)

Often have a more pursuant discharge

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99
Q

No gonococcal urethritis

A

Most commonly caused by chlamydia trachmoatis (gram - , ovoid, and nonmotile)
-more serous discharge

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100
Q

A-C serotypes of nongonococcal urethritis

A

Leading cause of blindness in the world

Cause trachoma

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101
Q

D-K serotypes of nongonococcal

A

The GU tract one; cause urethritis, pelvic inflammatory disease, ectopic pregnancy, neonatal pneumonia, and neonatal conjunctivitis

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102
Q

L1, 2, 3, nongonoccocal

A

Lymphogranuloma venereum (painless lesion

Chancre is painful

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103
Q

What else can cause nongonoccal urethritis

A

Mycoplasma

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104
Q

What is urethritis associated with in women and men

A

Cystitis women

Prostatitis men

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105
Q

Clinical urethritis

A

Local pain, itching, urinary frequency

May warn of more serious problems that are further up the tract

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106
Q

Urethral carbuncle

A

Painful, small, red inflammatory lesion of the external urethral meatus in (older) females

Granulation tissue with friable mucosa covering
Bleed easily due to ulceration

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107
Q

Treat urethral caruncle

A

Excision is curative

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108
Q

Primary carcinoma of the urethra: proximal urethra

A

Show urothelial differentiation and are just like ones in the bladder

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109
Q

Primary carcinoma: distal urethra

A

More commonly squamous cell carcinoma

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110
Q

___ carcinomas are uncommon in the urethra, but occur in women when they appear

A

Adeno

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111
Q

Hypospadias

A

Urethral opening on the ventral aspect of the penis

More common than epispadias

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112
Q

Epispadias

A

Urethral opening not he dorsal surface of the penis

Less common

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113
Q

What are hypospadias and epispadias associated with

A

Abnormalities of normal descent of the testes and comorbid with other malformations of the urinary tract

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114
Q

Problem with hypospadias and epispadias

A

Abnormal openings are often constricted and lead to obstruction of urine

If the openings are located near the base of the penis, ejaculation/insemination may be hindered

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115
Q

Phimosis

A

Prepuce orifice is too small to permit normal retraction

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116
Q

Why get phimosis

A

Developmental causes are less common than secondary to inflammation that cause scarring of the preputial ring

Predisposition to secondary infections and even carcinoma

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117
Q

Balanoposthitis

A

Infection of the glans and prepuce by non specific organisms (not STD)

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118
Q

What organisms cause balanoposthitis

A

Candida albicans

Anaerobic bacteria

Gardnerella

Pyogenic bacteria

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119
Q

How does balanoposthitis

A

Poor local hygiene in uncircumscribed males->smegma accumulation->inflammatory scarring->phimosis

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120
Q

Condyloma acumunita (penile tumor)

A

Benign sexually transmitted wart

HPV 6>11
-gardasil==HPV 6,11,16, and 18

Single of multiple sessile or pedunculated, red papillary excrescences

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121
Q

Condyloma recurrence

A

Recurs after excision, but rarely transforms to malignancy

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122
Q

Where is a condyloma acuminata

A

At coronal sulcus or inner prepuce

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123
Q

Acanthosis with condyloma acuminata

A

Superficial hyperkeratosis and thickening of the underlying epidermis

-branching, villous, papillary CT stroma is covered by orderly, hyperplastic stratified squamous epithelium

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124
Q

Koliocytosis condyloma acuminata

A

Cytoplasmic vacuolization of the squamous cells; characteristic of HPV

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125
Q

Peyronie disease

A

Benign proliferation of fibroblasts

Results in fibrous bands involving the penile corpus cavernous

Causes penile curvature and pain during intercourse

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126
Q

Malignant tumors now

A

Ok

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127
Q

Carcinoma in situ

A

Malignant tumors
Strongly associated with HPV 16
-gardasil 6, 11, 16, 18

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128
Q

What are the two types of carcinoma in situ

A

Bowen and bowenoid

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129
Q

Bowen disease who gets it

A

Male of female >35

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130
Q

Morphology Bowen

A

Solitary thickened, gray white plaques over penile shaft or red shiny lesions on the glans and prepuce

Epidermis I’d hyperproliferative, lots of mitosis, some atypia, dysplasia, no orderly maturation

Hyperchromatic nuclei

Intact BM, but 10% can turn into invasive squamous carcinoma
-Bowen disease will transform into infiltrating squamous cell carcinoma in 10% of patients over a span of many years

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131
Q

Bowenoid papulosis who gets

A

Younger, sexually alive adult patients

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132
Q

Morphology bowenoid papulosis

A

Multiple, pigmented popular lesions on external genitalia

Multiple (instead of solitary) reddish brown popular lesions

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133
Q

Clinical bowenoid

A

Frequently spontaneously regress

Rarely evolve to invasive carcinoma

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134
Q

Clinical Bowen

A

Will transform into infiltrating squamous cell carcinoma in 10% of patients over a span of many years

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135
Q

Histology of Bowen and bowenoid papulosis are __-

A

Indistinguishable

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136
Q

How differentiate Bowen from bowenoid

A

Age and number of lesions

Bowen->35 , solitary lesion-invade in 10% over many years

Bowenoid-younger, multiple-rarely evolves to invasive carcinoma

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137
Q

Squamous cell carcinoma of the penis is associated with what

A

Poor genital hygiene+high risk HPV infection (gardasil 6, 11, 16, 18)

40-70

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138
Q

Where is squamous cell carcinoma of the penis common

A

<1% of male cancer, but can account for a lot more in Asia, Africa, and South America

Regions that don’t circumcise:higher prevelance due to smegma accumulation under foreskin

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139
Q

Circumcision is ___ for squamous cell carcinoma fo the penis

A

Protective —-rare in Muslims and jews

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140
Q

Which HPV most commonly causes squamous cell carcinoma of the penis

A

6, 11, 16, 18

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141
Q

What lifestyle factor is a huge risk for squamous cell carcinoma of the penis

A

Smoking

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142
Q

Morphology squamous cell carcinoma of the penis: flat pattern

A

Epithelial thickening on the glans or inner surface of the prepuce

Progresses to an ulcerated papule

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143
Q

Morphology squamous cell carcinoma of the penis :papillary

A

Epithelial thickening with graying and fissuring of the mucosal surface

Stimulated condyloma acuminata and may produce a cauliflower like fungating mass

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144
Q

Morphology squamous cell arcinoma of the penis :verrucous carcinoma

A

Uncommon
Exophytic, well differentiated variant of squamous cell carcinoma

Locally invasive; rarely metastasizes

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145
Q

Squamous cell carcinoma of the penis is __ growing and ___ invasive

A

Slow

Locally

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146
Q

Presntation of squamous cell carcinoma of the penis

A

For a year of more before brought to medical attention

Not painful until they secondarily ulcerate and become infected

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147
Q

Where does squamous cell carcinoma of the penis metasticize to

A

Regional (inguinal and iliac nodes), distant is uncommon until far advances

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148
Q

Prognosis squamous cell carcinoma of the penis

A

50% of men contain cancer in their enlarged inguinal nodes-

5 year survival based on stage
66% if confined
27% with lymph node involvement

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149
Q

What is the most commmon congenital anomaly of the testes

A

Cryptorchisdism

150
Q

Cryptorchidism : what is it and what is problem

A

Failure of testis descent =tubular atrophy and sterility
75% unilateral
1% of 1 year old boys
Usually isolated anomaly

Increased risk testical germ cell tumors

151
Q

Morphology cryptorchordism

A

Decreased germ cell development, thickening and hyalinization of seminiferous tubule basement membrane

Fibrosis with sparing of prominent leydig cells

152
Q

Clinical cryptorchidism

A

Completely asymptomatic and comes to attention when the scrotal sac is discovered to be empty by the patient or examining physician

153
Q

Why does concomitant inguinal hernia accompany

A

When testis lie in inguinal canal, it is more prone to trauma and crushing injuries

154
Q

What are undeserved testes a risk for

A

Testicular cancer

155
Q

Treat cryptorchidism

A

Most will descend on their own by 1 but will need surgery before 2 if not

If uncorrected cryptorchidism testicle may develop

156
Q

Inflammation is more commmon in the ___ than the ___

A

Epididymis

Testis

157
Q

Epididymis first, then to tests

A

Gonorrhea

TB

158
Q

Testis then to epididymis (exception)

A

Syphilis

Epididymis is commonly spared altogether

159
Q

Nonspecific epiddiymitis and orchiitis

A

Due to UTI reaching the epididymis via vas deferens or spermatic cord lymphatics

160
Q

Childhood cause of nonspecific epididymitis and orchitis

A

Congenital or gram negative rods

161
Q

Sexually active <35 cause of nonspecific epididymitis and orchitis

A

Chlamydia trachomatis, neisseria gonorrhea

162
Q

Cause of nonspecific epiddymitis and orchitis in men>35

A

Common UTI agents (E coli, pseudomonas)

163
Q

Morphology nonspecific epididymitis and orchitis

A

Nonspecific congestion, edema and neutrophilic, macrophage and lymphocyte infiltrates

Can progress to abscess formation and complete suppurative necrosis of the entire epididymis

Sterilize due to infalmmmation testis by traveling through the epididymis leading to fibrous scarring of both

Local lymphatics channels

Leydig cells less affected, thus testosterone levels generally maintained

164
Q

Granulomatous (autoimmune) orchitis

A

Painless moderately tender testicular mass of sudden onset sometimes associated with fever in middle aged people

Can loops like tubercles,but is found diffusely throughout the testis

165
Q

Granulomatous orchitis is restricted to where

A

Spermatic tubules

166
Q

Gonorrhea

A

Retrograde expansion of infection from posterior urethra to prostate, seminal vesicles and epididymis

  • ascending infection
  • from neglected gonococcal infection
167
Q

Severe gonorrhea

A

Epiidymal abscess==destruction and scarring

168
Q

Untreated gonorrhea

A

Testis suppurative orchitis

169
Q

Mumps

A

Systemic viral infection

Commonly affects children, though testicular involvement at this age is rare

20-30% or post pubertal men who are infected present with orchitis 1 week after inflammation of parotid glands

170
Q

Tuberculosis

A

Begins in the epididymis

Secondary testis involvement

Caseating granulomas with histology identical to granulomas elsewhere in the body

171
Q

Syphilis

A

Congenital or acquired

Testes are involved first and the epididymis is commonly spared

172
Q

What are the two different morph pattterns of symphysis

A

Nodular gummas

Diffuse interstitial inflammation that produces the histologic hallmark of syphilitic infections, obliterating endarteritis associated with perivascular cuffs of lymphocytes and plasma cells

173
Q

Torsion

A

Twisting of the spermatic cord cuts off testicular venous drainage

174
Q

Neonatal torsion

A

Occurs in utero or shortly after birth, not associated with congenital anomaly

175
Q

Adult torsion

A

Adolescence, occcurs without prior injury, even during sleep

Comes from an anatomical defect (bell clapper abnormality) that leads to increased mobility of the testes

Orchiopexy performed bilaterally to prevent similar fate in contralateral testis

176
Q

Problem with torsion

A

Vascular engorgement with potential for hemorrhagic infarct

Arterial supply remains patent-torsion occluded the venous outflow (thinner wall, less pressure, more compressible)

177
Q

Treat torsion

A

UROLOGIC EMERGENCY, without treatment testes enlarge, soften, necrosis, and hemorrhagic
-leads to testicular infarction

Surgery<6 hours can preserve testicular viability

178
Q

Lipoma

A

Lesions that involve the proximal spermatic cord

Fat around the cord may represent retroperitoneal adipose tissue pulled into the inguinal canal with a hernia sac rather than a true neoplasm
-identified at the time of inguinal hernia repair

179
Q

Adenomatoid tumor

A

Most common benign paratesticular neoplasm

Small nodules of mesothelioma cells near the upper epidydimal pole
-not mesothelioma

Well circumscribed

180
Q

LM adenomatoid tumor

A

Minimal invasion into adjacent testis

181
Q

If an adenomatoid tumor is identified as benign intraoperatively the surgeon should do what

A

Can spare the patient and orchid to my and locally excise the tumor

182
Q

Rhabdomyosarcoma

A

Most common paratesticular tumor in kids

183
Q

Liposarcoma

A

Most common paratesticular tumor in adults

184
Q

Testicular tumors now

A

Ok

185
Q

Germ cell tumors (95% of testicular tumors)

A

Malignant

Most common malignancy in men 15-34

186
Q

Two types of germ cell testicular tumors

A

Seminomas and nonseminomas

187
Q

White:black ration for testicular tumors

A

5:1

188
Q

Sex cord stromal tumors (5% o testicular tumors)

A

Generally benign testicular tumor

189
Q

Environmental risk factors of testicular germ cell tumors

A

Testicular dysgenesiis syndrome

Klinefelters syndroem XXY

190
Q

Testicular dysgenesis syndrome

A

Characterized by cryptorchidism , hypospadias, and poor sperm quality

Associated with pesticides and nonsteroidal estrogens

191
Q

Klinefeltes syndrome

A

50x greater risk of mediastinal germ cell tumros, even though they don’t develop testicular tumros

192
Q

Genetic risk factors for testicular germ cell tumors

A

KIT, BAK (receptor tyrosinase kinase)

193
Q

Nonseminomatous tumors

A

Composed of cells that look like primordial germ cells or early gonadocytes

194
Q

Nonseminomatous tumors

A

Composed of undifferentiated cells that look like embryonic stem cells and cells that have differentiated along different lineages
-creates yolk sac tumors, choriocarcinomas, and teratomas

195
Q

60% of germ cell tumors are

A

Both aspects of seminomatous and nonseminomatous tumours

196
Q

Pathogenesis germ cell tumor

A

Mostly come from precursor lesionLintratubular germ cell neoplasia (ITGCN)
-except for:yolk sac tumor, teratomas, adult spermatocytic seminoma

ITGCN occurs in utero, dormant until puberty

ITGCN consists of atypical primordial germ cells with large nuclei and clear cytpplasm. Also retain totipotential transcription factors (OCT34, NANOG)

ITGCN commonly has a duplication of the short arm 12 which is always found in all invasive germ cell tumors, and most patients with the lesion will progress to that level
-reduplication of the short arm of chromosome 12 (12p) in the form of an isochromosome i(12p), a cytogenetic alteration that is invariably found in invasive germ cell tumors regardless of histological type

197
Q

Seminoma

A

Most comon type of germ cell tumor 50%

198
Q

Who gets seminoma

A

20-30 year old, almost never infants

199
Q

Seminoma has an identical tumor in the ovary called ____

A

Dysgerminoma

200
Q

Getentics seminoma

A

Expresses isochromosome 12p and OCT3/4 NANOG

25% have gain of function KIT

201
Q

Morphology seminoma

A

Large, round/polyhedral with a distinct cell membrane

Homogenous, lobulated, gray white masses, devoid of hemorrhage or necrosis
Tunica albuginea remains intact, but there can be extension to the epididymis, spermatic cord or scrotal sac occurs

Fibrous stroma produces irregular lobules with lymphocytic infiltrate

Clear or watery cytoplasm

Large central nucleus with 1-2 prominent nucleoli

Along with the other testicular germ cell tumors genetic factors, also express placental alkaline phosphatase (PLAP)

Some seminomas contain syncytiotrophoblasts and the patient willl have higher level of HCG but not as high as choriocarcinoma

Ill defined granulomas

202
Q

Spermatic seminoma

A

Rare and slow growing testicular germ cell tumor

In patients over 65

203
Q

Prognosis spermatic seminoma

A

Excellent

Indolent, doesn’t metasticize

204
Q

Morphology spermatic seminoma

A 
Soft, gray cut surface with mucosa cysts
Mixture of cell types
-medium sized cells with round nucleus and eosinophilia cytoplasm (most numerous) that may also have chromatin in the meiosis phase (spireme chromatin)
-secondary spermatocytes
-scattered giant cells

Lack lymphocytes, granulomas, syncytiotrophoblasts, extra-testicular sites of origin, and admixture with other germ cell tumors

NO ASSOCIATION WITH ITGCN

205
Q

Embryonal carcinoma

A

In 20-30 year olds and more aggressive than seminomas

206
Q

Morphology embryonal carcinoma

A

Poorly demarcated, small gray white mass with hemorrhage and/or necrosisi

Commonly extend through tunica albuginea into epididymis or cord

Grow in alveolar or tubular patterns, sometimes with papillary convolutions, but the undifferentiated lesions display sheets of cells

Cells are anaplastic, large with an epithelial appearance and indistinct border

Giant cells and mitotic figures

207
Q

Genetics embryonal carcinoam

A

+ for OCT3/4, PLAP, CD30, cytokeratin

  • for cKIT
208
Q

Yolk sac tumor (endodermal sinus tumor

A

Most common testicular tumor in children <3

209
Q

Prognosis yolk sac tumor

A

Good

210
Q

Morphology yolk sac tumor

A

Infiltrating, homogenous, yellow white mucinous tumor

Cuboidal or flat neoplasticcells in a lacelike network

Schiller-duval bodies (primitive glomeruli) are found in 50%
-resemble endodermal sinuses
-consist of a mesodermal core with a central capillary and a visceral and parietal layer of cells
Eosinophilic hyaline globules with AFP a1-antitrypsin
-presence is AFP in the tumor cells is highly characteristic

211
Q

Choriocarcinoma

A

Highly malignant neoplasm (<1% of all germ cell tumors)

Small palpable nodule, without testicular enlargement

212
Q

What two types of cells are in choriocarcinoma

A

Cytotrophoblasts

Syncytiotrophoblasts

213
Q

Cytotrophoblasts

A

Polygonal, distinct border+clear cytoplasm

Grow in cords or masses and have a single, fairly uniform nucleus

214
Q

Syncytiotrophoblasts

A

Large, multinucleated cells

Abundant eosinophilic vacuolated cytoplasm with hCG-shoriocarcinomas pump out hCG
-hCG reaches very high levels in the serum

215
Q

Teratomas

A

Occur at any age

Pure forms common in infants and kids (benign)

Pure forms of teratomas rare in adults (malignant)

216
Q

In children, differentiated mature teratomas are __ and post pubertal teratomas are ___

A

Benign

Malignant

217
Q

Teratomas are mixed with other germ cell tumors __% of the time

A

45

218
Q

Teratoma: differentiation also endodermal, mesodermal and ectodermal lines

A

All three germ layers!

219
Q

Teratoma morphology

A

Large, heterogenous appearance, hemorrhage and necrosis suggest admixture with embryonal andchoriocarcinoma

Haphazard differentiated mesoderm, ectoderm and endoderm neural , muscle cartilage, squamous , epithelial, thyroid gland, bronchial epithelial intestinal wall-all three layers
-all embedded in a fibrous or myxoid stroma

Mature or immature tissue

Do not have biomarkers

220
Q

Teratoma with malignant transformation

A

Non germ cell malignancy developing within a teratoma

Non germ cell spreads outside the testis, it does not respond to chemo

Cure is dependent on ability to respect

Non germ cell malignancies retain isochromosome 12p, proving a colonial relationship to the preceding teratoma

221
Q

Clinical features of testicular germ cell tumors

A

Painless enlargement of testis

Tumor spillage is possible during biopsy, so assume it is malignant and start with a radical orchiectomy

Retroperitoneal, paraaortic lymph nodes first involved as testicular tumors have a common lymphatic spread

Hematogenous spread to lungs (most common), liver, brain, bones

222
Q

Seminoma clinical features

A

Remain localized to testis for long time

Radiosensitive

70% stage 1

95% with stage 1 or 3

Lymph nodes typically involved

Hematogenous spread later in disease

Best prognosis with 95% stage 1

223
Q

Nonseminomatous germ cell tumor

A

More aggressive

Radioresistant

Metastasize early

Hematogenous spread more frequently

60% of patients present with advanced disease

90% acheived remission with chemo, except for pure choriocarcinoma has a worse prognossi

Histologically subtype does not influence prognosis significantly, thus all are considered as a group

224
Q

Pure choriocarcinoma

A

Most aggressive NSGCT

No testicular enlargement

Rapid hematogenous spread

Lungs and liver are involved early in virtually every case

225
Q

Testicular tumor stages

A

Stage I-confined to testis, epididymis, or spermatic cord

Stage II-distant spread confined to retroperitoneal nodes below the diaphragm
-persistent elevation of hCG or AFP concentrations following orchiectomy, even if the lymph appear normal, indicates stage II

Stage III-metastases outside the retroperitoneal nodes or above the diaphragm

226
Q

Biomarkers yolk sac tumor

A

AFP

227
Q

Biomarkers choriocarcinoma

A

HCG in 15%

228
Q

NSGT biomarkers

A

AFP or hCG elevated at time of diagnosis (80%)

229
Q

Seminomas biomarkers

A

HCG in 15%

230
Q

Lactate dehydrogenase biomarker

A

Elevation correlates with the mass of the tumor cell

Allows assessment of the tumor burden

231
Q

Serum biomarkers

A

Elevate testicular mass

Stage testicular germ cell tumors

Assess tumor burden

Monitor response to therapy
-with serial measurements, it is often possible to predict recurrence before the patient becomes symptomatic or develop any other lingual signs of relapse

232
Q

Tumors of sex cord gonadal stroma

A

Leydig tumros

Sertoli cell tumors

Germ cell tumors -95%

233
Q

Leydig cell tumors

A

2%

Most benign

10% invade/metasticize

234
Q

Who gets leydig cell tumors

A

20-60 yo

235
Q

What do leydig cell tumors produce

A

Androgens, estrogens, and/corticosteroids

236
Q

Presetnation leydig tumors

A

Testicular swelling or changes resulting from hormone elaboration (gynecomastia), these are typically first seen in kids

237
Q

Leydig cell tumor morphology

A

Grossly circumscribed nodules with a homogenous, golden brown cut surface

25% have eosinophilic reinke crystalloids (rod sharp)

Polygonal cells with abundant granular, eosinophilic cytoplasm and indistinct cell borders

Lipid droplets, vacuoles, lipofuscin pigment

238
Q

Sertoli cell tumor

A

Hormonal silent and present as a testicular mass

Firm and small

10% malignant

Homogenous gray white to yellow masses of variable size lesions: tall, Coleman cells in trabecular

May form cords or tubules

239
Q

Gonadoblastoma

A

Rare neoplasm comprised of a mixture of germ cells and gonadal stromal elements

Arise in gonads with testicular tubules

Germ cell component can become malignant giving rise to seminoma

240
Q

Testicular lymphoma

A

Most common form of testicular tumor in patients older than 60

5% of all testicular neoplasms

Usually diffuse, large B cell non Hodgkin lymphomas

Disseminate widely

High incidence of CNS involvement

241
Q

Othe testicular lymphomas

A

Burkitt

EBV+ extranodal NK/T cell lymphoma

242
Q

Tunica vaginalis=

A

mesothelioma lined surface exterior to the testis

243
Q

Hydrocele

A

Accumulation of serous fluid within the mesothelioma lined tunica vaginalis
-leads to enlargement of the scrotal sac that contains a clear fluid

Lined by mesothelioma cells

244
Q

Hepatocellular

A

Accumulation of blood secondary to trauma, torsion, or generalized bleeding diathesis

245
Q

Chylocele

A

Accumulation of lymphatic fluid secondary to lymphatic obstruction
-elephantiasis

246
Q

Spermatocele

A

Local cystic accumulation of semen in dilated efferent ducts or ducts of the rete testis

247
Q

Cariococele

A

Dilated vein in the spermatic cord

May be asymptomatic

Can contribute to infertility

Correct with surgery

248
Q

Describe the prostate

A 
Weight 20 grams and is divided into 4 zones
Peripheral
Central
Transitional
Peri-urethral
249
Q

Which sone of the prostate do carcinomas most commonly aris

A

Peripheral

250
Q

Which zone of the prostate does hyperplasia occur

A

Transitional

251
Q

Tubular glands separated by ___ ___ devoid of a distinct capsule

A

Fibromuscular stroma

252
Q

Glands are lined by two layers of epithelial cells

A

Basal layer of low cuboidal epithelium

Layer of columnar secretory cells

253
Q

Normal growth of the prostate is controlled by what

A

Dihydrotestosterone DHT

254
Q

DHT

A

Made by leydig cells and an enzyme called 2 5a reductase (T->DHT)

255
Q

Castration

A

Widespread apoptosis _>prostatic atrophy

256
Q

DHT stimulates _ cells

A

Stromal

257
Q

Acute bacterial prostatis

A

Caused by similar pathogens as those that cause UTI-e coli, other gram negative rods, enterococci and staphylococci

Spread by intra-prostatic reflux of urine from the posterior urethra or from the urinary bladder

Sometimes spread via the lymph/blood from distant locations (lymphohematogenously)

258
Q

Symptoms acute bacterial prostatis

A

Dysuria, fever, chills, perianal pain; prostate is tender and soft

259
Q

Acute bacterial prostatis morphology

A

Minute, dissemination’s abscesses or large coalescent focal areas of necrosis or diffuse edema, congestiona and boggy suppurations of the entire gland

260
Q

Biopsy acute bacterial prostatis

A

Contraindicated may lead to sepsis

261
Q

Chronic bacterial prostatis

A

Frequent bouts of UTI lead to frequent prostatic infection

262
Q

Symptoms chronic bacterial prostatis

A

Dysuria, pelvic discomfort and lower back pain
-can also be asymptomatic

Often no antecedent acute attack, and the disease appears insidiously and without obvious provocation

Infiltrates of plasma cells, lymphocytes, and macrophages

263
Q

Antibiotics and chronic bacterial prostatis

A

Most antibiotics penetrate the prostate poorly—> bacteria find safe haven in the parenchyma and constantly seed the urinary tract
-history of recurrent UTI

264
Q

Diagnose chronic bacterial prostatis

A

Based on leukocytosis int he expressed prostatic secretions with positive bacterial cultures

265
Q

Nonbacterial prostatis

A

Most common prostatis

266
Q

Symptoms nonbacterial chronic prostatis

A

Signs and symptoms just like that of chronic bacterial prostatis—dysuria, pelvic discomfort and lower back pain

Expressed prostatic secretions do show more than 10 leukocytes per high powered field but cultures are uniformly negative (likely to be an atypical bug (mycoplasma/chlamydia)

No history of recurrent UTI

267
Q

Granulomatous prostatis

A

Specific-etiologic infectious agent identified

Non specific -etiologic infections agent cannot be identified

268
Q

Diagnose granulomatous prostatis

A

Histologically which may be necrotizing or non necrotizing

-may mimic prostatic carcinoma clinically, grossly and histologically

269
Q

The most common caus ein the US for granulomatous prostatis

A

Installation of BCG into the bladder for treatment of superficial bladder cancer
-this is of no clinical significance and doesn’t need treatment

270
Q

Final granulomatous

A

Only in immunocompromised

271
Q

Benign prostatic hyperplasia =nodular hyperplasia

A

Most common prostatic disorder defined as enlargement of prostate due to hyperplasia of prostatic stromal and epithelial cells

Often leads to urinary obstrucion -> bilateral hydronephrosis?

272
Q

Characterization BHP

A

Large, fairly discrete nodules int he peri retinal region of the prostate

Stromal proliferation!!!

273
Q

Incidence of BHP

A

20% of men by age 40 and 90% by 8-

No correlation between histology and clinical symptoms

274
Q

Pathogenesis BHP

A

Increased # of epithelial cells and stromal components in the peri urethral area of the prostate
-no clear evidence of increased epithelial cell proliferation

Believed that hyperplasia stems from impaired cell death-still not a premalignant lesion

  • assimilation os senescent cells in the prostate
  • androgens increase cellular proliferation and inhibit cell death

T->DHT via 2 5a reductase

  • type 2 5a-reductase found almost exclusively in prostate and stromal cells
  • type 1 5a reductase converts T->DHT in the liter and skin; DNT from here may have endocrine effects

DHT activated FGF and TGF-b
-FGF mitogen for fibroblasts and other mesenchymal cells
TGF-b -inhibitor of epithelial proliferatgen

DHT induced growth factors act by increasing the proliferation of stromal cells and decreasing the death of epithelial cells

  • with age, testosterone decreases, estrogen increases, and DHT status same
  • estrogens increase sensitivity for DHT receptors in prostate
  • testosterone really doesn’t play any role
  • DHT (from leydig cells) has an increased selectivity on epithelial nuclear androgen receptors that induce glandular and stromal proliferation
275
Q

Morphology BHP

A

Enlargement begins in the transitional zone and early nodules are made of stromal cells

After a there are epithelial cell nodules that arise
-causes compressiona nd obstruction or urethra->bilateral hydronephrosis?

276
Q

BHP median lobe hypertrophy

A

Nodular enlargement that projects up into the floor of the urethra as a hemispheric mass directly beneath the mucosa

277
Q

Gross morph BHP

A

Mostly glandular; yellow-pink, soft, and exude a milky white prostatic fluid

Mostly fibromuscular: large firm pale grey, do not exude fluid and are less clearly demarcated

278
Q

Histology BHP

A 
Glandular hyperplasia (with a double layer of epithelial cells: inner secretory columnar and outer low cuboidal)
-occasionally, foci of reactive squamous metaplasia mimicking urothelial carcinoma are seen adjacent to prostatic infarcts in prostatis with prominent BPH
279
Q

Diagnose BHP

A

Can’t be made with needle biopsy

Biopsies are too small to appreciate the modularity of the process and do not SJSU ally sample the transitional zone

280
Q

Who gets BPH

A

Men 50s 90% have at 80

Black>white

281
Q

Prestnation BHP

A

Nocturnal, urgency, hesitancy, difficulty in starting and stopping stream, overflow dribbling, dysuria, and have an increased risk of bacterial infections of the bladder and kidney
Can’t completely void bladder->reservoir of residual urine==commmon source of infection

282
Q

Digital rectal exam BPH

A

Palpate a firm rubbery mass

283
Q

Complete obstruction from BPH causes what

A

Urinary retention predisposing for bladder hypertrophy, systitis, and hydroureter/hydronephrosis
-sudden acute urinary retention needs catheterization as treatment

284
Q

BPH premalignante

A

No

285
Q

Treat BPH if mild

A

Decreasefluid intake, espicially before bed; decrease alcohol and caffeine intake

286
Q

Treat more progressed BPH

A

Alpha blockers block smooth muscle tone int he prostate, 5 a-reductase (converts testosterone into HT) inhibitor or surgery (TURP_

287
Q

TURP

A

Transurethral resection fo the prostate

Gold standard

First line if recurrent urinary retention

288
Q

Adenocarcinoma of the prostate

A

Most common cancer in men (16% lifetime risk)

Tied with colorectal cancer for cancer related death

Uncommon in Asian

Common in blacks

289
Q

Genetic risk for adenocarcinoma of prostate

A

Epigenetic alteration is hypermethylation (down regulation) of glutathione s transferase (GSTP1) gene on chronometer 11

290
Q

GSTP1

A

Important part of the pathway that prevents damage from a wide range of carcinogens

291
Q

First degree relative with adenocarcinoma of prostate

A

2x risk

292
Q

Two first degree relatives with adenocarcinoma of prostate

A

5x risk

293
Q

Mutation in BRCA2 adenocarcinoma of prostate

A

20x risk

294
Q

HOXB1 mutation and adenocarcinoma

A

Greater risk

295
Q

Rearrangement of ETS family transcription factor (ERG or ETV1) next to the androgen regulated TMPRSS2 promoter

A

Happens in 50% of white prostatic cancer patients

Makes the cancer more invasive, although it does not give a worse prognosis

296
Q

Genomic deletions and amplification are more common in prostate cancer than point mutations involving oncogenes

A

In contrast to breast and colon cancers

Amplification of 8q24 (MYC oncogene)

Deletions involving PTEN tumor suppressor locus

Late stages include a loss of TP53

Deletions involving RB

Amplifications of the androgen receptor gene locus

297
Q

Long trinucleotide expansion of CAGs in x linked androgen receptor gene causes a rare neurodegenerative disorder called ___ disease characterized by muscle cramping and fatigue

A

Kennedy

298
Q

In Kennedy there is an __ relationship between the length of the expansion to androgen sensitivity

A

Inverse

Short expansion more sensitivity

299
Q

Short expansion in ___, intermediate expansion in___ and long expansion in ____. Parallels the incidence and mortality of restate cancer in these groups

A

Black

Caucasian

Asian

300
Q

Length of the repeat is __ related to rate at which prostate cancer develops in mice

A

Inverse

301
Q

Possible precursor lesion

A

Begins with prostatic intraepithelial neoplasia (PIN)

Begins in the peripheral zone

PIN is not CIS

302
Q

Environmental factors

A

Red meat, lycopenes(tomato), soy, VD

Set at early age and multipl partners, STD

Mechanical manipulation(vasectomy)

Diets high in fat which may inhibit VA absorption

Urban dwelling have increased risk of contraction and death due to potential exposure

Cadmium is a metal associated with carcinoma of prostate

North south gradient : Northern European more (VD sunlight thing)

SMOKING NOT LINKED

303
Q

Clinical pancreatic adenocarcinoma

A

Obstruction of the urinary tract presenting like BPH

-most prostatic cancer arise peripherally away from the urethra and therefore urinary symptoms cure late

304
Q

Rectal exam adenocarcinoma prostate

A

Firm, discrete nodules on rectal exam

  • DRE and transreectal ultrasonography=low sensitivity and low specificity
  • transrectal needle biopsy is needed to confirm the diagnosis
305
Q

Metastatic disease adenocarcinoma of prostate

A

Finding of osteoblasts metastases by skeletal surveys or the much more sensitive radionuclide bone scanning is virtually diagnostic of prostate cancer in men: bony metastases are typically osteoblastic and this feature in men points strongly to prostatic origin

306
Q

Paraneoplastic syndrome with adenocarcinoma prostate

A

DVT, DIC, nonbacterial thrombotic endocarditis

307
Q

PSA and PAP levels are elevated in both adenocarcinoma and BPH

A

Elevated blood levels of PSA occur in associated with localized as well as advanced cancer

PAS and PAP are used as screens
-PSA lacks sensitivity and specificity
PSA is organ specific, not cancer specific

308
Q

PCA3

A

Noncoding RNA overexpressed in 95% of prostate cancers

Currently used as an additional biomarker in patients suspected to have prostate cancer bc of elevated PSA but who had a negative prostate biopsy

309
Q

Screen for prostate cancer

A

Begin at 50, blacks 40

310
Q

Prognosis prostate cancer

A

Doubling time is slow (204 years) meaning it may remain asymptomatic for a long time, with an excellent 10 year survival rate

311
Q

Treatment prostate cancer

A

90% 15 year survival

Surgery

Radiotherapy

Therapeutic effect of castration or treatment with anti-DHT->induced disease regression

  • most tumors will eventually become resistant to androgen blockade
  • loss of PTEN gene causes the tumor to no longer need androgens
312
Q

Precursor to malignancy

A

Prostatic intraepithelial neoplasia

313
Q

Morphology prostate cancer

A

Arises in the peripheral zone of the gland in 70% of cases, classically in a posterior location

May be difficult to see on gross, but palpable on rectal exam as it is typically found in the posterior region

Neoplastic tissue is gritty and firm

314
Q

Local extension of prostate cancer

A

Commonly involves the pero prostatic tissue, seminal vesicles, and the base of the urinary bladder

Metastases spread via lymph to the obturator nodes and eventually to the para aortic nodes

Metastases spread via the blood mainly to the axial bones but also the the viscera in some cases

315
Q

Describe the lesion of prostatic adenocarcinoma

A

Glands are typically smaller, more crowded and ess branched than the benign ones

Lined by a single layer of cuboidal or low columnar epithelium

The outer basal cell layer is absent

Benign prostate-contains basal cells

Malignant prostate-absent basal cells

Cytoplasm ranges from pale clear to amphilic

Large nuclei with one or more large nucleoli

Mitotic figures NO

316
Q

Histology pancreatic adenocarcinoma

A

Prominent nucleoli, blue mucin, and perineural invasion
——-specific for prostate cancer

The tumor looks just like PIN, but the PIN are surrounded by a patchy layer of basal cells and an intact BM

317
Q

Biomarkers prostatic adenocarcinoma

A

Alpha methylacyl-coenzyme a race made (AMACR)==upregulated in prostate cancer

318
Q

Grading staging prostatic adenocarcinoma

A

Grading based on Gleason grading system which is determined by cellular architecture

Staging is determined based on invasion and metastasis

319
Q

Gleason 1

A

Well differentiated , orderly packed, round, well circumscribed

320
Q

Gleason 5

A

No glandular differentiation with tumor cells infiltrating the stroma in the form of cords, sheets, and nests

321
Q

Multiple samples are taken where the dominant pattern (primary grade0 is added to the second most frequent artery (secondary grade) to get the Gleason score

A

If there is only one pattern, then primary grade==secondary grade and the score is doubles

If there are 3 patterns, the most common and highest scores are added together

322
Q

Scores 206

A

Excellent prognosis

2 minimum gealson score and most well differentiated

323
Q

3+4=7

A

Moderately differentiated tumors

324
Q

3+4=7

A

Moderately to poorly differentiated tumros

325
Q

8-10

A

Poorly differentiated tumros

10 Hughes and least differentiated

326
Q

2-4

A

Small tumors found incidentally in TURP when looking for BPH

327
Q

6-7

A

Majority of the treatable tumors found

328
Q

8-10

A

Less likely to be cured

329
Q

There staging

A

TNM designation

330
Q

T1

A

Found incidentally either on TURP or needle biopsy
T1a do not progress when followed for 10 or more years
T1b are more ominous and have 20% mortality if left untreated

331
Q

T2

A

Organ confined cancer

332
Q

T2a and T3b

A

Tumors show extra prostatic extension, with and without seminal invasion

333
Q

T4

A

Direct invasion of contiguous organs

334
Q

Any spread of tumor to the lymph nodes regardless of extend is eventually associated with a fatal outcome

A

NO and N1==reflects presence or absence

335
Q

Colloid carcinoma of prostate

A

Prostate cancer that reveal abundant mucinous secretions

Associated with thrombotic complications

336
Q

Small cell cancer

A

Most aggressive variant of prostate cancer

Also know as neuroendocrine carcinoma
Almost all cases are rapidly fatal

337
Q

Most common tumor secondarily involve the prostate

A

Urothelial cancer

Large invasive urothelial cancers can directly invade from the bladder into the prostate or

Carcinoma in site of the bladder can extend into the prostatic urethra and down into the prostatic ducts and acini

338
Q

Morphology and clinical features of chronic complications of diabetes

A

Important morphological changes are related to the many late systemic complciations of diabetes

339
Q

Morphology capillary basement membrane thickening diabetes

A

Widespread thickening of the GBM occurs in virtually all diabetic nephropathy

340
Q

Diabetic nephropathy

A

Renal failure is second to MI in death

  1. Glomerular lesions
  2. Renal vascular lesions, principally arteriosclerosis
  3. Pyelonephritis, including necrotizing papillomas
341
Q

Pure capillary BM thickening can only be detected with __

A

EM

342
Q

When do diabetics get thickening of BM

A

As early as 2 years after diagnosis and 5 years 30% increase

Thickening is progressive with mesangial widening. Simultaneously there is thickening of the tubular basement membranes

343
Q

Diffuse mesangial sclerosis chronic diabetes

A

Lesion consists of diffuse increase in mesangial matrix. There can be mild proliferation of mesangial cells early in the disease process but cell proliferation is not a prominent part of injury. The mesangial increase in typically associated with the overall B< thickening. The matrix depositions are PAs positive. As the disease progresses, the expansion of mesangial areas can extend to nodular configurations. The progressive expansion of the mesangium has been shown to correlate well with measures of deteriorating renal function such as increasing proteinuria

344
Q

Nodular glomerulosclerosis

A

This is also known as intercapillary glomerulosclerosis or Kimmelstiel-Wilson dis­ease . The glomerular lesions take the form of ovoid or spherical, often laminated, nodules of matrix situated in the periphery of the glomerulus. The nodules are PAS-positive. They lie within the mesangial core of the glomerular lobules and can be surrounded by patent peripheral capillary loops ( Fig. 24-39 ) or loops that are markedly dilated. The nodules often show features of mesangiolysis with fraying of the mesangial/capillary lumen interface and disruption of sites at which the capillaries are anchored into the mesangial stalks. The latter may produce capillary microaneurysms as the untethered capillaries distend outward due to force imparted by intracapillary blood pressure and flow. Usually, not all the lobules in individual glomeruli are involved by nodular lesions, but even uninvolved lobules and glomeruli show striking diffuse mesangial sclerosis. As the disease advances, the individual nodules enlarge and may eventually compress and engulf capillaries, obliterating the glomerular tuft. These nodular lesions are frequently accompanied by prominent accumulations of hyaline material in capillary loops (“ fibrin caps ”) or adherent to Bowman capsules (“ capsular drops ”). Both afferent and efferent glomerular hilar arterioles show hyalinosis. As a consequence of the glomerular and arteriolar lesions, the kidney suffers from ischemia, develops tubular atrophy and interstitial fibrosis, and usually undergoes overall contraction in size ( Fig. 24-40 ). Approximately 15% to 30% of individuals with long-term diabetes develop nodular glomerulosclerosis, and in most instances it is associated with renal failure

345
Q

Renal atherosclerosis and arteriosclerosis

A

constitute part of the macrovascular disease in diabetics. The kidney is one of the most frequently and severely affected organs; however, the changes in the arteries and arterioles are similar to those found in other tissues. Hyaline arteriolosclerosis affects not only the afferent but also the efferent arteriole. Such efferent arteriolosclerosis is rarely, if ever, encountered in individuals who do not have diabetes

346
Q

Pyelonephritis

A

Pyelonephritis is an acute or chronic inflammation of the kidneys that usually begins in the interstitial tissue and then spreads to affect the tubules. Both the acute and chronic forms of this disease are more common in diabetics than in the general population, and, once affected, diabetics tend to have more severe involvement. One special pattern of acute pyelonephritis, necrotizing papillitis (or papillary necrosis), is much more prevalent in diabetics than in nondiabetics

347
Q

What are long term complications of diabetes

A

Retinopathy cataracts glaucoma

Microangiopathy, cerebral vascular infarcts, hemorrhage

HTN
Atherosclerosis
MI

Nephrosclerosis-glomerulosclerosis, arteriosclerosis, pyelonephritis

Islet cell loss-insulitis (type I) amyloid type II

Peripheral vascular atherosclerosis-gangrene and infections

Peripheral neuropathy
-autonomic neuropathy

348
Q

What kills people with iabetes

A

Long term effects ,more than cute metabolic complications

Usually these happen 15-20 years after onset

349
Q

Most common mortality of diabetics

A

Microvascular complications such as MI, renal vascular insuffiency, and cerebrovascular accidents

350
Q

Diabetic nephropathy is a leading cause of end stage renal disease in the US

A

30-40% get(more type I)

Genes-higher in native americans, Hispanics, and blacks than whites

Early sign is albumin in urine, microalbuminuria

351
Q

Microalbumina and diabetes is also sign of what

A

Increased CVD morbidity should do a macrovascular test

352
Q

Without intervention microabulminiar turns to what

A

Macroalbuminuria usually with HTN

To end stage renal disease

20% type 2 75% type I by 20 years

353
Q

Wilma tumor

A

Most common primary renal tumor of childhood and 4th most common pediatric malignancy in US

354
Q

When do people get wilms

A

2-5

355
Q

5-10% of wilms tumors involve both kidney and present about 10 months earlier, most likely due to what

A

Germline mutation

-first hit

356
Q

Only 10% of non syndromes wilms tumors have ___ mutations suggesting that.a majority of these tumros are caused by other gene mutation

A

WT1

357
Q

Nephrogenic rests

A

Putative precursor lesions of wilms tumors and are seen in the renal parenchyma adjacent to approximately 25-40% of unilateral tumros, nearly 100% of bilateral tumors

Share genetic alterations with the adjacent wilms tumors-preneoplastic

Important to document the presence of nephrogenic rests in the resected specimen bc these patients are at an increased risk of developing wilms tumor in the contralateral kidney and require frequent and regular surveillance for many years

358
Q

WAGR

A

Wilms tumors
Aniridia
Genital anomalies
Metal retardation

359
Q

Why get WAGR

A

Germline encoded deletions of 11p13 and the associated genes WT1 and PAX6-first hit

WT1 deletions is more at risk for wilms
-normal WT1->no increased risk of wilms

PAX6 mutation is more at risk for aniridia

  • if only PAX6 is deleted->sporadic aniridia without wilms
  • provides instructions for making a protein that is involved int he early development of the eyes, brain spinal cord and pancreas
360
Q

Deny crash syndrome

A

Wilms 90%, gonadal dysgenesis (male psedohermpahroditism), and earl yonset nephropathy leading to renal failure

  • characteristic glomerular lesion-diffuse mesangial sclerosis
  • wilms tumor arising demonstrates bi allelic inactivation of WT1
361
Q

Deny crash WT! Mutation

A

Dominant negative missense mutation in the zinc finger of the WT1 protein that affects DNA binding
-duffieicnt only in causing genitourinary abnormalities, not tumors

362
Q

WT! Encodes a DNA binding TF that is expresssed within several tissues including the kidneys an dgonads

A

Critical for the normal development of the kidneys and gonads during embryogenesis

Individuals with mutation WT1 have increased risk of developing germ cell tumors called gonadoblastoma

363
Q

Beckwith wiedemann syndrome

A

Organometallic, wilms(5%), macroglossia, hemihypertrophy, omphalocele, and abnormal large cellsin the Adriano cortex (adrenal cytomegaly)

364
Q

Genes beckwith wiedemann

A

Chromosomal region involved 11p15.5 WT2

Normally expressed from one of the parent alleles with imprinting not he other copy

BWS has served as the model for a non classical mechanism of tumorigenesis-imprinting

Genetic basis of BWS is considerably more heterogenous in that no single gene is involved in all cases

365
Q

IGF2 beckwith

A

Located in this region too and is typically only expressed by the paternal allele—maternal allele is imprinted

In some wilms tumors, there is less of imprinting-expression of both alleles

Or there is deletion of the maternal copy->uniparental disomy

Has greatest effect of tumorigenesis of all the WT@

366
Q

CDKN1C beckwith

A

P57 mutation but have a lower risk of developing wilms

Have increased risk of hepatoblastoma, pancreatoblastoma, adrenocortical tumors, and rhabdomyosarcoma

367
Q

Beta catenin beckwith

A

Some have beta catenin gain of function

368
Q

Wilms tumor morphology

A

Large, solitary well circumscribed

10% bilateral or multi centric

Soft homogenous tan grey

Can have necrosis, cysts formation or hemorrhages

5% anaplasia=TP53 mutation

Can have heterozygous elements

369
Q

Triphasic combination wilms

A

Blastemal-blue Small cells in sheets with few distinct features

Stromal-usually fibrotic or. Myxoid in nature

Epithelial-abortive tubules or glomeruli

370
Q

Clinical features wilms

A

Present with large abdominal mass that may extend across midline or into pelvis

Hematuria, pain, bowel obstruction, HTN

Some present with pulmonary metastasis

Most can be cured

Anaplasia associated with worse prognosis (need to sample tumor well)
Loss of genetic material 11q and 16q, or gain of 1q worse prognosis

Increased risk of seconda primary tumors of bone, soft tissue sarcomas, leukemia, lymphoma, and breast cancer to the germline mutation or therapy

Pathology (36 decks)

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