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Renal 3 > Pathology > Flashcards

Pathology Flashcards

1
Q

What are the 3 types of nephropathy in persons with hyperuricemic disorders?

A
  1. Acute uric acid nephropathy
  2. Chronic urate nephropathy (gouty nephropathy)
  3. Nephrolithiasis
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2
Q

What kind of crystal precipitate and where in acute uric acid nephropathy?

A

Uric acid crystals in renal tubules (collecting ducts)

*These can be seen on biopsy as bifiringent crystals that glow

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3
Q

WHat can the precipitation of uric acid crystals in acute uric acid nephropathy lead to?

A

Obstruction of nephrons and the development of acute renal failure

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4
Q

What patietns are more likely to get acute uric acid nephropathy?

A

People with leukemia or lymphoma undergoing chemo

-Chemo increases death of tumor cells and uric acid is produced as released nucleic acids are broken down

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5
Q

What kind of crystals are deposited in chronic urate nephropathy and where?

A

Monosodium urate crystals in distal tubules, collecting ducts and intersitium

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6
Q

What are chronic urate nephropathy crysals like?

A

They are variably birefringent (long and straight) needle-like crystals in the tubular lumens or interstitium (need to polarize them to see them)

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7
Q

What is a tophus and when do you see this?

A
  • Foreign-body giant cells, other mononuclear cells and a fibrotic reaction (contain foreign elements to wall them off)
  • Chronic urate nephropathy
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8
Q

What does tubular obstruction by urates cause?

A

Cortical atrophy and scarring

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9
Q

What % of individuals with gout have uric acid stones?

A

22%

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10
Q

What % of individuals with secondary hyperuricemia have uric acid stones?

A

42%

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11
Q

What disorders are associated with hypercalcemia?

A
  • Hyperparathyroidism
  • Multiple myeloma
  • Vitamin D intoxication
  • Metastatic cancer
  • Excess calcium intake (milk-alkali syndrome) -Induce formation of calcium stones and deposition in the kidney
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12
Q

In hypercalcemia and nephrocalcinossi what is the earliest damage?

A
  1. Tubular epithelial cells: Mitochondrial distortion and other signs of cell injury (reverisible then irreversible)
  2. Calcium deposits: Mitochondria, cytoplasm, and basement membrane (purple, amorhpous)
  3. Calcified cellular debris: Obstruct tubular lumens (get actual stone formation), Obstructive atrophy of nephrons, secondary interstitial fibrosis, and inflammation (due to blockage)
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13
Q

What is the earliest functional defect in hypercalcemia and nephrocalcinosis?

A

Inability to concentrate the urine (this can be seen with many things though)

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14
Q

What are other tubular defects seen in hypercalcemia and nephrocalcinosis?

A

Tubular acidosis and salt-losing nephritis

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15
Q

What can further damage lead to in hypercalcemia and nephrocalcinosis?

A

Slowly progressive renal insufficiency (secondary to neprocalcinosis) if not taken care of

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16
Q

What do you see in acute phoshpate nephropathy?

A

Extensive accumulations of calcium phosphate crystals in tubules

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17
Q

What can cause acute phosphate nephropathy?

A

High doses of oral phosphate solutions in preparation for colonoscopy…patients aren’t hypercalcemic!!!
-This can crystalize without increase Ca levels, especially if there is poor renal function

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18
Q

What does acute phosphate nephropathy do?

A

Presents as renal insufficiency several weeks after exposure (renal function only partially recovers)

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19
Q

What is another name for light chain cast nephropathy?

A

Myeloma kidney

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20
Q

What is seen in light chain cast nephropathy?

A

Overt renal insufficiency

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21
Q

Who do you see light chain cast nephropathy in?

A

Half of those with multiple myeloma and related lymphoplasmacytic disorders

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22
Q

What are 4 contributing factors to renal damage in light- chain nepropathy?

A
  1. Bence Jones (light-chain) proteinuria and cast nephropathy
  2. Amyloidosis, of AL type formed from free light chains
  3. Light-chain deposition disease
  4. Hypercalcemia and hyperuricenia
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23
Q

Why do Bence Jones (light-chain) proteins contribute to renal damage in light chain nepropathy?

A

They are directly toxic to epithelial cells and combine with the urinary glycoprotein (Tamm-Horsfall protein) under acidic conditions forming large, histologically distinct tubular casts that obstruct the tubular lumens and induce a characteristic imflammatory reaction around the casts –> Light-chain cast nephropathy

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24
Q

What can be done to see Bence Jones (light-chain) proteinuria and cast nephropathy?

A

Serum or urine** electrophoresis

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25
Q

What is light-chain deposition disease

A
  • Deposition of light chains (usually kappa) in GBMs and mesangium (glomerupathy)
  • Tubular BM (tubulointerstitial nephritis)
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26
Q

Describe Bence-Jones Tubular Casts

A
  • Pink to blue amorphous masses: Concentrically laminated, Fill and distend the tubular lumens
  • No nuclei
  • Surrounded by multinucleate giant cells
  • Nonspecific inflammatory response and fibrosis: Adjacent interstitial tissue
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27
Q

What does obstruction increase the susceptibility to?

A

Infection and stone formation

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28
Q

What can unrelieved obstruction lead to?

A

Permanent renal atrophy… hydronephrosis (kidney swells) or obstructive uropathy (NEED TO DEAL WITH THIS)

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29
Q

How can unrelieved obstructions be death with?

A

Surgery (stents, lithotripsy, antibiotics) or medically treatable

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30
Q

What is hydronephrosis?

A

Dilation of the renal pelvis and calyces associated with progressive atrophy of the kidney due to obstruction to the outflow of urine

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31
Q

In complete obstruction does glomerular filtration continue?

A

Yes, filtrate subsequently diffuses back into the renal interstitium and perirenal spaces ultimately returning to the lympthatic and venous systems… the affected calyces and pelvis become dilated

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32
Q

What are the initial functional alterations in the tubule in hydronephrosis?

A

Impaired concentrating ability (GFR falls later)

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33
Q

What 3 things are seen with sudden and complete obstruction?

A
  1. Glomerular filtration is reduced
  2. Mild dilation of the pelvis and calyces
  3. Atrophy of the renal parenchyma (not frequent–> tissue will still function…it won’t die off)
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34
Q

What 2 things are seen with subtotal or intermittent obstruction?

A
  1. Glomerular filtration is not suppressed (no total blockage…stuff is still getting out)
  2. Progressive dilation ensues
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35
Q

What is the morphology of the kidneys in hydronephrosis?

A

They are slightly to massively enlarged (dilated) and this depends on the degree and duration of the obstruction (how long and where it is)

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36
Q

What are early features seen in the kidney during hydronephrosis?

A
  • Simple dilation of the pelvis and calyces

- Significant intersitial inflammation

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37
Q

What is seen in chronic cases of hydronephrosis?

A
  1. Cortical tubular atrophy
  2. Marked diffuse interstitial fibrosis (due to irritation and inflammation)
  3. Progressive blunting of the apices of the pyramids
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38
Q

What happens to the kidneys in advanced cases of hydronephrosis?

A
  • The kidney becomes a thin-walled cystic structure with a diameter of up to 15-20cm
  • There is parenchymal atrophy, total obliteration of the pyramids, and thinning of the cortex (it reduces to nothing)
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39
Q

Are men or women more commonly affected by urolithiasis?

A

Men

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40
Q

What is he peak age of onset for urolithiasis?

A

20-30 years

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41
Q

Is there a familial and hereditary predisposition to stone formation?

A

Yes

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42
Q

What are examples of hereditary disease that can lead to excessive production and excretion of stone-forming substances?

A

Inborn errors of metabolism: Gout, cystinuria, and primary hyperoxaluria

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43
Q

What is primary hyperoxaluria?

A

The liver makes calcium oxalate so there is lots of stone production (this requires a liver and kidney transplant

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44
Q

What are the 4 main types of calculi?

A
  1. Calcium stones (70%)
  2. Triple stones or struvite stones (15%)
  3. Uric acid stones (5%-10%)
  4. Cystine stones (1%-2%)
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45
Q

What is the most important determinant of stone formation?

A

Increased urinary concentration of the stones’ constituents…this exceeds their solubility (supersaturation)

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46
Q

What else can favor supersaturation in some metabolically normal patients?

A

Low urine volume

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47
Q

What are calcium stones make of?

A

Calcium oxalate or calcium oxalate mixed with calcium phosphate

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48
Q

Are calcium stones radiopaque?

A

Yes

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49
Q

What % of patients with calcium stones have hypercalcemia and hypercalciuria?

A

5%

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50
Q

What conditions are associated with hypercalcemia and hypercalciuria?

A
  • Hyperparathyroidism
  • Diffuse bone disease
  • Sarcoidosis
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51
Q

What % of patients with calcium stones have hypercalciuria without hypercalcemia?

A

55%

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52
Q

WHat things can cause hypercalciuria without hypercalcemia?

A
  • Hyperabsorption of calcium from intestine (absorptive hypercalciuria)
  • Intrinsic impairment in renal tubular reabsorption of calcium (renal hypercalciuria)
  • Idiopathic fasting hypercalciuria with normal parathyroid function
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53
Q

What are triple stones also called?

A

Struvite stones

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54
Q

What are triple stones made of?

A

Magnesium ammonium phosphate

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55
Q

What are the largest triple stones called and where are they found?

A

Staghorn calculi and they occupy the large portions of the renal pelvis

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56
Q

What are triple stones caused by?

A

Bacteria: Proteus and some staphlyococci

-They convert urea to ammonia and the resultant alkaline urine causes the precipitation

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57
Q

What 2 conditions are uric acid stones common in?

A

Hyperuricemia (gout) and diseases with rapid cell turnover (leukemias)

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58
Q

What will more than 50% of patients with uric acid stones have?

A

Neither hyperuricemia nor increased urinary excretion of uric acid

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59
Q

Are uric acid stones radiopaque?

A

No, they are radiolucent

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60
Q

What are cystine stones from?

A

Cystinuria:

  • Inherited genetic disorder of the transport of an AA
  • Excess cystine in the urine (cystinuria) and the formation of cystine stones
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61
Q

Where are casts found?

A

In the urinary sediment (need to look at them under a microscope)

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62
Q

What can casts do?

A

Localize disease to a specific location in the GU tract (the can’t diagnose anything themselves, but can be combined with other clinical clues for diagnosis)

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63
Q

What are casts?

A

Coagulum of Tamm-Horsfall mucoprotein and the trapped contents with the tubular lumen

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64
Q

Where do casts originate from?

A

The DCT or collecting ducts

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65
Q

When do casts form?

A

In periods of urinary concentration or stasis or when the urine pH is very low

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66
Q

What does the cylindrical shape of the cast reflect?

A

The tubule in which they were formed

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67
Q

What are some prominent cellular elements that determine the type of cast?

A

Hyaline, erythrocyte, leukocyte, epithelial, granular, waxy, fatty, broad

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68
Q

What are hyaline casts made of?

A

Mucoprotein (Tamm-Horsfall protein) secreted by tubule cells

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69
Q

Where are hyaline casts formed?

A

The collecting duct

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70
Q

What produces a RBC cast?

A

Glomerular inflammation with leakage of RBCs (usually extravasation of RBC in glomerular area)
*RBC casts are formed in the distal convoluted tubule

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71
Q

What are WBC casts most typical for?

A

Acute pyelonephritis*

-Can also be seen in glomerulonephritis or with inflammation of the kidney

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72
Q

Where are cellular casts from?

A

Within the nepron

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73
Q

How might a waxy cast be ultimately formed?

A

Before being flushed into the bladder urine, cells may degenerate to become a coarsely granular cast, later a finely granular cast, and ultimately, a waxy cast

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74
Q

Where do granular and waxy casts arise from?

A

Renal tubular cell casts

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75
Q

What lines the renal pelvis, ureters, bladder, and urethra?

A

A special form of transitional epithelium (urothelium)

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76
Q

Describe the surface layer of the renal pelvis, ureters, bladder, and urethra?

A

Large, flattened “umbrella cells” with abundant cytoplasm that horizontally covers several underlying cells

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77
Q

Do the renal pelvis, ureters, bladder, and urethra have a well developed BM?

A

Yes

78
Q

What is a feature of the lamina propria in the renal pelvis, ureters, bladder, and urethra?

A

Wisps of smooth muscle that form a discontinuous muscularis mucosae

79
Q

Why is it important to differentiate muscularis mucosae from deeper muscle bundles of the detrusor muscle (muscularis propria)?

A

Bladder cancers are staged on the basis of invasion of the muscularis propria (need to know the invasion of tumors)

80
Q

What % of autopsies contain congential anomalies in the ureters?

A

2%-3%

81
Q

What does ureteropelvic junction (UPJ) obstruction result in?

A

Hydroneprosis

82
Q

Who does UPJ obstruction present in?

A

Infants or children, more common in boys

83
Q

What % of cases is UPJ obstruction bilateral?

A

20%

84
Q

What is commonly seen in UPJ obstruction?

A

Other congential anomalies

85
Q

What is the most common cause of hydronephrosis in infants and children?

A

UPJ obstruction

86
Q

What 2 congential anomalies can lead to infection, chronic infection, fibrosis, and other problems?

A

UPJ obstruction or vesicouretral reflux

87
Q

In adults, who is UPJ obstruction more common in?

A

Women and unilateral

88
Q

What is inflammation of the ureters?

A

Ureteritis

89
Q

If ureteritis associated with infection?

A

No

90
Q

Does ureteritis have significant clinical consequence?

A

No

91
Q

What is the morphology of ureteritis?

A

Accumulation or aggregation of lymphocytes (because no infection) that form germinal centers in the subepithelial region (little bumps that can be cyst-like), causing slight elevations of the mucosa and producing a fine granular mucosal surface (ureteritis folicularis)

92
Q

In ureterits, what might the mucosa contain?

A

Scattered fine cysts (1-5mm) what are lined by flattened urothelium (ureteritis cystica)

93
Q

Are primary tumors of the ureter common?

A

No, they are rare

94
Q

Where do small benign tumors of the ureter originate?

A

Mesenchyme

95
Q

What are fibroepithelial polyps?

A
  • Like a skin-tag in the lumen of the ureter
  • Tumor-like lesion
  • Grossly presents as small mass projecting into the lumen
  • Often in children
  • Loose, vascularized connective tissue mass lying beneath the mucosa
96
Q

What do primary malignant tumors of the ureter resemble?

A

Those arising the the renal pelvic, calyces, and bladder

97
Q

What are the majority of primary malignant tumors of the ureter?

A

Urothelial carcinomas

98
Q

When are primary malignant tumors of the ureter found most frequently?

A

During the 6th and 7th decades of life

99
Q

What can primary malignant tumors of the ureter cause?

A

Obstruction of the ureteral lumen

100
Q

Can tehre be multipl primary malignant tumors of the ureter?

A

Yes

101
Q

What is a diverticula?

A

A pouchlike-evagination of the bladder wall

102
Q

What are the 2 ways diverticula of the bladder arise?

A
  1. As congential defects

2. As acquired lesions

103
Q

What causes congenital bladder diverticula?

A
  • Focal failure of development of the normal musculature

- Urinary tract obstruction during fetal development

104
Q

Are most diverticula of the bladder acquired or congenital?

A

Most are acquired

105
Q

What causes acquired bladder diverticula?

A

Persistent urethral obstruction

  • Prostatic enlargement: Hyperplasia or neoplasia
  • Holding bladder to long, too often
106
Q

What is the morphology of bladder diverticula?

A
  1. Multiple
  2. Round to ovoid, saclike pouch
  3. Varies from less than 1cm to 5-10cm in diameter
107
Q

Why are bladder diverticula clinically significant?

A
  1. They constitute sites of urinary stasis

2. They predispose to infection and the formation of bladder calculi

108
Q

What causes bladder extrophy?

A

Developmental failure in the anterior wall of the abdomen and bladder

109
Q

What happens in bladder extrophy?

A

They bladder either communicates directly through a large defect with the surface of the body or it lies as an opened sac

110
Q

What can happen to the exposed bladder mucosa in bladder extrophy?

A
  1. It might undergo colonic glandular metaplasia

2. It is subject to infections that often spread to upper levels of the urinary system

111
Q

What else is the patient at risk for with bladder extrophy?

A

Increased risk of adenocarcinoma arising in the bladder remnant (Not the bladder itself)
-Because the mucosa is exposed, it can undergo metaplasia

112
Q

What coliforms are common etiologic agents of cystitis?

A
  1. E. Coli
  2. Proteus
  3. Klebsiella
  4. Enterobacter
113
Q

Who is more likely to develop cystitis?

A

Women (again, they have shorter urethras)

114
Q

What is tuberculous cystitis?

A

The sequelae to renal tuberculosis

115
Q

In patients who are immunosuppressed or those receiving long-term antibiotics, what types of this cause cystitis?

A
  1. Candida albicans

2. Cryptococcal agents

116
Q

What can cause cystitis if you have been traveling?

A

Schistosomiasis (Schistosoma haematobium)

117
Q

What are predisposing factors to cystitis?

A
  • Bladder calculi
  • Urinary obstruction
  • DM
  • Intrumentation: Procedures can cause inflammation and irritation
  • Immune deficiency
118
Q

What is a treatment that can cause cystitis?

A

Radiation: Can cause inflammation and fibrosis if you get irradiation of the bladder region

119
Q

What is the gross appearance in nonspecific acute or chronic inflammation of the bladder?

A

Hyperemia of the mucosa with possible exudate

120
Q

What kind of infilatrate is seen in acute cystitis?

A

Acute inflammatory infiltrate with neutrophils

-This will be boggy, edematous, red, hot/bothered, maybe even exudate

121
Q

What kind of infilatrate is seen in chronic cystitis?

A

Chronic inflammatory infiltrate with leukocytes/lymphocytes

122
Q

What happens in follicular cystitis?

A

Aggregation of lymphocytes into lymphoid follicles in the bladder mucosa and underlying wall
-Looks like lymphoid tissue with collections of ink dots everywehere

123
Q

What is eosinophilic cystitis caused by and manifested by?

A

It is caused by parasites (maybe schistosomiasis) and is manifested by infiltration with submucosal eosinophils

124
Q

What is interstitial cystitis (chronic pelvic pain syndrome)

A

Persistent, painful form of chronic cystitis (lymphocyte infiltration)

125
Q

Who do you see interstitial cystitis more commonly in?

A

Women

126
Q

What are symptoms of interstisial cystitis?

A

Intermittent, severe suprapubic pain, urinary frequency, urgency, hematuria, dysuria…. feels like a UTI but no infection (pain, urinary issues, pelvic dysfunction)

127
Q

Is there evidence of bacterial infection in interstitial cystitis?

A

No

128
Q

What are some cystoscopic findings in intersitial cystitis?

A
  • Fissures (breaks in the mucosa)

- Punctate hemorrhages (glomerulations)

129
Q

What can be seen in the late phase of interstitial cystitis?

A

Chronic mucosal ulcers (Hunner ulcers) which are seen in the late (classic, ulcerative) phase of cystitis

130
Q

What is malacoplakia?

A
  1. Peculiar pattern of vesical inflammatory reaction
  2. Soft, yellow, slightly raised mucosal plaques, 3-4cm in diameter
  3. Infiltration with large, foamy macrophages, mixed with occasional multinucleated giant cells and interspersed lymphocytes (like ink dots)
131
Q

What are Michaelis-Gutmann bodies?

A

Laminated mineralized concentrations within macrophages seen in Malacoplakia (they are random dark dots that are too big to be a lymphocyte)

132
Q

What is malacoplakia related to?

A

Chronic bacterial infection:

  • E. COLI***
  • Proteus (occassionally)
  • Increased frequency in immunosuppressed transplant recipients
133
Q

What is associated with malacoplakia in terms of macrophages?

A

Defects in phagocytic or degradative function of macrophages… the phagosomes become overloaded with undigested bacterial products
-These patients might always be sick since their macrophages are dysfunctional

134
Q

What is polypoid cystitis?

A

An inflammatory condition/irritation to the bladder mucosa

135
Q

What is the most common culprit of polypoid cystitis?

A

Indwelling catheters are the most common culprits (ICU, nursing home), but any injurious agent may give rise to this lesion

136
Q

What is seen in the urothelium of polypoid cystitis?

A

Broad bulbous polypoid projections secondary to submucosal edema (due to the edema/inflammation)

137
Q

What can polypoid cysitis be confused with?

A

Papillary urothelial carinoma (clinically and histologically)

138
Q

What is cystitis cystica and cystitis glandularis?

A

Common lesions of the urinary bladder that are nests of urothelium (Brunn nests) that grow downward into the lamina propria (these can also be confused with urothelial CA)

139
Q

What do central epithelial cells transform into in cystitis glandularis?

A

Cuboidal or columnar epithelium lining

GLANDS ..it can become more glandular like goblet cells)

140
Q

What do central epithelial cells transform into in cystitis cystica?

A

Cystic spaces filled with clear fluid lined by flatten urothelium (Dilations

141
Q

Do cystitis cystica and cystitis glandularis often coexist?

A

Yes… this is reffered to as cystitis et glandularis

142
Q

Is cystitis et glandularis and incidental finding in normal bladders?

A

Yes, there’s nothing to do about it

143
Q

If you see cystic spaces in the bladder do you instantly think cancer?

A

NOPE… could be cystitic cystica or other things

144
Q

What does nephrogenic ademona result from?

A

Shed renal tubular cells that implant in sites of injured urothelium

145
Q

What does neprogenic ademona resemble histologicall?

A

Renal tubules

146
Q

What can happen to the overlying urothelium in nephrogenic adenoma?

A

It might be focally replaced by cuboidal epithelium and assume a papillary growth pattern

147
Q

How big are nephrogenic adenomas?

A

Typically less than a cm, but lesions may be sizeable and may resemble cancewr clinically
(You have to biopsy it because is may be small and can look like CA)

148
Q

What % of cancers are bladder cancer?

A

7%

149
Q

What % of cancer mortality in the US is due to bladder cancer?

A

3%

150
Q

What % of bladder tumors are of epithelial origin?

A

95%

151
Q

Bladder tumors of epithelial origin are composed of what and also called what?

A
  • Composed of urothelial (transitional cell) type

- Interchangeable called urothelial or transitional tumors

152
Q

What other types of tumors may occur?

A

Squamous and glandular carcinomas as well as mesenchymal

153
Q

What % of bladder tumors are urothelial tumors?

A

90%

154
Q

What are 2 distinct precursor lesions to invasive urothelial carincoma?

A
  1. Non-invasive papillary tumors

2. Flat non-invasive urothelial carcinoma

155
Q

What is the most common precursor lesion?

A

Non-invasive papillary tumors

156
Q

Where do non-invasive papillary tumors originate from

A

Papillary urothelial hyperplasia (these are graded on biological behavior

157
Q

What is another name for flat non-invasive urothelial carcinoma?

A

Carcinoma in situ (CIS)

158
Q

Describe carcinoma in situ

A
  1. Epithelial lesions for cytologic changes of malignancy
  2. Confined to the epithelium, without BM invasion
  3. High grade
159
Q

What are 3 features seen in patient with invasive bladder cancer?

A
  1. The tumor has already invaded the bladder wall
  2. No precursor lesions may be detected (the precursor lesion has been destroyed by the high-grade invasive component…large, ulcerated mass)
  3. Invasion into the lamina propria worsens the prognosis: Major decrease in survival is associated with invasion of the muscularis propria (detrusor muscle)
160
Q

WHat is the mortality rate with invasion of the muscularis propria?

A

30% 5 year mortality rate

161
Q

What are gross patterns of urothelial tumors?

A

Purepapillary to nodular or flat

162
Q

Describe papillary lesions

A

Red, elevated excrescences, exophytic papillomas, true papillary structure has a fibrovascular core

163
Q

Are the majority of papillary tumors low grade?

A

YES

164
Q

Where do most papillary tumors arise from?

A

Lateral or posterior walls at bladder base

165
Q

What patients get papillar lesions?

A

Younger patients

166
Q

What are papillary urothelial neoplasma of low malignant potential (PUNLMPs)?

A

They are similar to papilloma, but have thicker urothelium and diffuse nuclear enlargement

167
Q

Are PUNMLPs associated with invasion?

A

No

168
Q

Do PUNLMPs recur as higer grade tumors associated with invasion and progression?

A

No, this rarely happens

169
Q

What do low-grade papillary urothelial carcinomas look like?

A
  • Orderly appearance: Architecturally and cytologically
  • Cells are evenly spaced and cohesive
  • Few atypical nuclei
  • Infrequent mitotic figures
  • Mild variation in nuclear size and shape
170
Q

Can low-grade papillary urothelial carcinomas recur and invade?

A

YES…although this is rare

171
Q

What to high-grade papillary urothelial cancers look like?

A
  • Contain discohesive cells
  • Large hyperchromatic nuclei
  • Frank anaplasia
  • Frequent mitotic figures
  • Disarray and loss of polarity
172
Q

Do high-grade papillary urothelial cancers have a higher incidence of invasion into the muscular layer?

A

Yes…they have a higher risk of progression than low-grade lesions

173
Q

When invasion is present in high-grade papillary urothelial cancers, is there a significant metastatic potential?

A

Yes

174
Q

What % of bladder cancers in the US are caused by squamous cell carcinoma?

A

3-7%

175
Q

What are squamous cell carcinomas caused by?

A

Chronic bladder irritation and infection

176
Q

What are the tumors like in squamous cell carcinomas?

A

Invasive, fungating, infiltrative, ulcerative

177
Q

What are adenocarcinomas of the bladder like?

A

Histologically identical to those seen in the GI tract (these are rare though)

178
Q

What are small-cell carcinomas that arise in the bladder associated with?

A

Urothelial, squamous, or adenocarcinoma

179
Q

What are clinical features of urothelial CA?

A
  • Classically produce a painless hematuria: Dominant and sometimes only clinical manifestation
  • Frequency, urgency, and dysuria occasionally accompany the hematuria (but the 1st 3 can be due to other things)
180
Q

If you have hmeaturia, what should you do?

A

Get worried and do a cystoscopy…when you see the lesion go from there

181
Q

What does progsosis of urothelial CA depend on?

A
  • Histological grade of the papillary tumor

- Stage at diagnosis

182
Q

What are some causes of urothelial carcinoma?

A
  • Cigarette smoking*: Most important influence and Increases risk threefold to sevenfold
  • Cigars, pipes, and smokeless tobacco are associated with a smaller risk
  • Industrial exposure to arylamines—particularly 2-naphthylamine: Cancers appear 15 to 40 years after* the first exposure
  • Schistosoma haematobium infections in endemic areas (Egypt, Sudan)
  • Long-term use of analgesics is implicated, as it is in analgesic nephropathy (chronic pain patient)
  • Heavy long-term exposure to cyclophosphamide-I
  • Prior exposure of the bladder to irradiation
183
Q

What do schistosoma haematobium infections do in the bladder?

A
  • Ova are deposited in the bladder wall and incite a brisk chronic inflammatory response
  • This induces progressive mucosal squamous metaplasia and dysplasia
184
Q

What is cyclophosphamide?

A

An immunosuppressive agent that causes hemorrhagic cystitis

185
Q

What are the 3 genetic alterations seen in urothelial CA?

A
  1. Chromosome 9 monosomy
  2. Deletions of 9p and 9q
  3. Deletions of 17p, 13q, 11p, and 14q
186
Q

What can cause obstruction in the renal pelvis?

A

Calculi, tumors, uteropelvic stricture (fibrosis/inflammation)

187
Q

What can cause intrinsic obstruction in the ureter?

A

Calculi, tumors, clots, sloughed papillae inflammation (Necrotic: Analgesic nephropathy)

188
Q

What can cause extrinsic obstruction in the ureter?

A

Pregnancy, tumors (cervic or ovarian), retroperitoneal fibrosis…infection surgery, ect.

189
Q

What can cause obstruction in the bladder?

A

Calculi, tumors, functional (neurogenic)

190
Q

What can cause obstruction in the prostate?

A

Hyperplasia, carcinoma, prostatitis

191
Q

What can cause obstrction in the urethra?

A

Posterior valve stricture, tumors

Renal 3 (17 decks)

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