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1

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

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

2

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

Uric acid crystals in renal tubules (collecting ducts)
*These can be seen on biopsy as bifiringent crystals that glow

3

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

Obstruction of nephrons and the development of acute renal failure

4

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

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

5

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

Monosodium urate crystals in distal tubules, collecting ducts and intersitium

6

What are chronic urate nephropathy crysals like?

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

7

What is a tophus and when do you see this?

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

8

What does tubular obstruction by urates cause?

Cortical atrophy and scarring

9

What % of individuals with gout have uric acid stones?

22%

10

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

42%

11

What disorders are associated with hypercalcemia?

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

12

In hypercalcemia and nephrocalcinossi what is the earliest damage?

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)

13

What is the earliest functional defect in hypercalcemia and nephrocalcinosis?

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

14

What are other tubular defects seen in hypercalcemia and nephrocalcinosis?

Tubular acidosis and salt-losing nephritis

15

What can further damage lead to in hypercalcemia and nephrocalcinosis?

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

16

What do you see in acute phoshpate nephropathy?

Extensive accumulations of calcium phosphate crystals in tubules

17

What can cause acute phosphate nephropathy?

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

18

What does acute phosphate nephropathy do?

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

19

What is another name for light chain cast nephropathy?

Myeloma kidney

20

What is seen in light chain cast nephropathy?

Overt renal insufficiency

21

Who do you see light chain cast nephropathy in?

Half of those with multiple myeloma and related lymphoplasmacytic disorders

22

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

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

23

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

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

24

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

Serum or urine** electrophoresis

25

What is light-chain deposition disease

-Deposition of light chains (usually kappa) in GBMs and mesangium (glomerupathy)
-Tubular BM (tubulointerstitial nephritis)

26

Describe Bence-Jones Tubular Casts

-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

27

What does obstruction increase the susceptibility to?

Infection and stone formation

28

What can unrelieved obstruction lead to?

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

29

How can unrelieved obstructions be death with?

Surgery (stents, lithotripsy, antibiotics) or medically treatable

30

What is hydronephrosis?

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

31

In complete obstruction does glomerular filtration continue?

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

32

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

Impaired concentrating ability (GFR falls later)

33

What 3 things are seen with sudden and complete obstruction?

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)

34

What 2 things are seen with subtotal or intermittent obstruction?

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

35

What is the morphology of the kidneys in hydronephrosis?

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

36

What are early features seen in the kidney during hydronephrosis?

-Simple dilation of the pelvis and calyces
-Significant intersitial inflammation

37

What is seen in chronic cases of hydronephrosis?

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

38

What happens to the kidneys in advanced cases of hydronephrosis?

-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)

39

Are men or women more commonly affected by urolithiasis?

Men

40

What is he peak age of onset for urolithiasis?

20-30 years

41

Is there a familial and hereditary predisposition to stone formation?

Yes

42

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

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

43

What is primary hyperoxaluria?

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

44

What are the 4 main types of calculi?

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

45

What is the most important determinant of stone formation?

Increased urinary concentration of the stones' constituents...this exceeds their solubility (supersaturation)

46

What else can favor supersaturation in some metabolically normal patients?

Low urine volume

47

What are calcium stones make of?

Calcium oxalate or calcium oxalate mixed with calcium phosphate

48

Are calcium stones radiopaque?

Yes

49

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

5%

50

What conditions are associated with hypercalcemia and hypercalciuria?

-Hyperparathyroidism
-Diffuse bone disease
-Sarcoidosis

51

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

55%

52

WHat things can cause hypercalciuria without hypercalcemia?

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

53

What are triple stones also called?

Struvite stones

54

What are triple stones made of?

Magnesium ammonium phosphate

55

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

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

56

What are triple stones caused by?

Bacteria: Proteus and some staphlyococci

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

57

What 2 conditions are uric acid stones common in?

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

58

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

Neither hyperuricemia nor increased urinary excretion of uric acid

59

Are uric acid stones radiopaque?

No, they are radiolucent

60

What are cystine stones from?

Cystinuria:
-Inherited genetic disorder of the transport of an AA
-Excess cystine in the urine (cystinuria) and the formation of cystine stones

61

Where are casts found?

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

62

What can casts do?

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)

63

What are casts?

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

64

Where do casts originate from?

The DCT or collecting ducts

65

When do casts form?

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

66

What does the cylindrical shape of the cast reflect?

The tubule in which they were formed

67

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

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

68

What are hyaline casts made of?

Mucoprotein (Tamm-Horsfall protein) secreted by tubule cells

69

Where are hyaline casts formed?

The collecting duct

70

What produces a RBC cast?

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

71

What are WBC casts most typical for?

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

72

Where are cellular casts from?

Within the nepron

73

How might a waxy cast be ultimately formed?

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

74

Where do granular and waxy casts arise from?

Renal tubular cell casts

75

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

A special form of transitional epithelium (urothelium)

76

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

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

77

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

Yes

78

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

Wisps of smooth muscle that form a discontinuous muscularis mucosae

79

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

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

80

What % of autopsies contain congential anomalies in the ureters?

2%-3%

81

What does ureteropelvic junction (UPJ) obstruction result in?

Hydroneprosis

82

Who does UPJ obstruction present in?

Infants or children, more common in boys

83

What % of cases is UPJ obstruction bilateral?

20%

84

What is commonly seen in UPJ obstruction?

Other congential anomalies

85

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

UPJ obstruction

86

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

UPJ obstruction or vesicouretral reflux

87

In adults, who is UPJ obstruction more common in?

Women and unilateral

88

What is inflammation of the ureters?

Ureteritis

89

If ureteritis associated with infection?

No

90

Does ureteritis have significant clinical consequence?

No

91

What is the morphology of ureteritis?

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

In ureterits, what might the mucosa contain?

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

93

Are primary tumors of the ureter common?

No, they are rare

94

Where do small benign tumors of the ureter originate?

Mesenchyme

95

What are fibroepithelial polyps?

-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

What do primary malignant tumors of the ureter resemble?

Those arising the the renal pelvic, calyces, and bladder

97

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

Urothelial carcinomas

98

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

During the 6th and 7th decades of life

99

What can primary malignant tumors of the ureter cause?

Obstruction of the ureteral lumen

100

Can tehre be multipl primary malignant tumors of the ureter?

Yes

101

What is a diverticula?

A pouchlike-evagination of the bladder wall

102

What are the 2 ways diverticula of the bladder arise?

1. As congential defects
2. As acquired lesions

103

What causes congenital bladder diverticula?

-Focal failure of development of the normal musculature
-Urinary tract obstruction during fetal development

104

Are most diverticula of the bladder acquired or congenital?

Most are acquired

105

What causes acquired bladder diverticula?

Persistent urethral obstruction
-Prostatic enlargement: Hyperplasia or neoplasia
-Holding bladder to long, too often

106

What is the morphology of bladder diverticula?

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

107

Why are bladder diverticula clinically significant?

1. They constitute sites of urinary stasis
2. They predispose to infection and the formation of bladder calculi

108

What causes bladder extrophy?

Developmental failure in the anterior wall of the abdomen and bladder

109

What happens in bladder extrophy?

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

110

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

1. It might undergo colonic glandular metaplasia
2. It is subject to infections that often spread to upper levels of the urinary system

111

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

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

112

What coliforms are common etiologic agents of cystitis?

1. E. Coli
2. Proteus
3. Klebsiella
4. Enterobacter

113

Who is more likely to develop cystitis?

Women (again, they have shorter urethras)

114

What is tuberculous cystitis?

The sequelae to renal tuberculosis

115

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

1. Candida albicans
2. Cryptococcal agents

116

What can cause cystitis if you have been traveling?

Schistosomiasis (Schistosoma haematobium)

117

What are predisposing factors to cystitis?

-Bladder calculi
-Urinary obstruction
-DM
-Intrumentation: Procedures can cause inflammation and irritation
-Immune deficiency

118

What is a treatment that can cause cystitis?

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

119

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

Hyperemia of the mucosa with possible exudate

120

What kind of infilatrate is seen in acute cystitis?

Acute inflammatory infiltrate with neutrophils
-This will be boggy, edematous, red, hot/bothered, maybe even exudate

121

What kind of infilatrate is seen in chronic cystitis?

Chronic inflammatory infiltrate with leukocytes/lymphocytes

122

What happens in follicular cystitis?

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

123

What is eosinophilic cystitis caused by and manifested by?

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

124

What is interstitial cystitis (chronic pelvic pain syndrome)

Persistent, painful form of chronic cystitis (lymphocyte infiltration)

125

Who do you see interstitial cystitis more commonly in?

Women

126

What are symptoms of interstisial cystitis?

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

127

Is there evidence of bacterial infection in interstitial cystitis?

No

128

What are some cystoscopic findings in intersitial cystitis?

-Fissures (breaks in the mucosa)
-Punctate hemorrhages (glomerulations)

129

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

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

130

What is malacoplakia?

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

What are Michaelis-Gutmann bodies?

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

132

What is malacoplakia related to?

Chronic bacterial infection:
-E. COLI***
-Proteus (occassionally)
-Increased frequency in immunosuppressed transplant recipients

133

What is associated with malacoplakia in terms of macrophages?

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

What is polypoid cystitis?

An inflammatory condition/irritation to the bladder mucosa

135

What is the most common culprit of polypoid cystitis?

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

136

What is seen in the urothelium of polypoid cystitis?

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

137

What can polypoid cysitis be confused with?

Papillary urothelial carinoma (clinically and histologically)

138

What is cystitis cystica and cystitis glandularis?

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

What do central epithelial cells transform into in cystitis glandularis?

Cuboidal or columnar epithelium lining
GLANDS ..it can become more glandular like goblet cells)

140

What do central epithelial cells transform into in cystitis cystica?

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

141

Do cystitis cystica and cystitis glandularis often coexist?

Yes... this is reffered to as cystitis et glandularis

142

Is cystitis et glandularis and incidental finding in normal bladders?

Yes, there's nothing to do about it

143

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

NOPE... could be cystitic cystica or other things

144

What does nephrogenic ademona result from?

Shed renal tubular cells that implant in sites of injured urothelium

145

What does neprogenic ademona resemble histologicall?

Renal tubules

146

What can happen to the overlying urothelium in nephrogenic adenoma?

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

147

How big are nephrogenic adenomas?

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

What % of cancers are bladder cancer?

7%

149

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

3%

150

What % of bladder tumors are of epithelial origin?

95%

151

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

-Composed of urothelial (transitional cell) type
-Interchangeable called urothelial or transitional tumors

152

What other types of tumors may occur?

Squamous and glandular carcinomas as well as mesenchymal

153

What % of bladder tumors are urothelial tumors?

90%

154

What are 2 distinct precursor lesions to invasive urothelial carincoma?

1. Non-invasive papillary tumors
2. Flat non-invasive urothelial carcinoma

155

What is the most common precursor lesion?

Non-invasive papillary tumors

156

Where do non-invasive papillary tumors originate from

Papillary urothelial hyperplasia (these are graded on biological behavior

157

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

Carcinoma in situ (CIS)

158

Describe carcinoma in situ

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

159

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

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

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

30% 5 year mortality rate

161

What are gross patterns of urothelial tumors?

Purepapillary to nodular or flat

162

Describe papillary lesions

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

163

Are the majority of papillary tumors low grade?

YES

164

Where do most papillary tumors arise from?

Lateral or posterior walls at bladder base

165

What patients get papillar lesions?

Younger patients

166

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

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

167

Are PUNMLPs associated with invasion?

No

168

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

No, this rarely happens

169

What do low-grade papillary urothelial carcinomas look like?

-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

Can low-grade papillary urothelial carcinomas recur and invade?

YES...although this is rare

171

What to high-grade papillary urothelial cancers look like?

-Contain discohesive cells
-Large hyperchromatic nuclei
-Frank anaplasia
-Frequent mitotic figures
-Disarray and loss of polarity

172

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

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

173

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

Yes

174

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

3-7%

175

What are squamous cell carcinomas caused by?

Chronic bladder irritation and infection

176

What are the tumors like in squamous cell carcinomas?

Invasive, fungating, infiltrative, ulcerative

177

What are adenocarcinomas of the bladder like?

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

178

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

Urothelial, squamous, or adenocarcinoma

179

What are clinical features of urothelial CA?

-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

If you have hmeaturia, what should you do?

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

181

What does progsosis of urothelial CA depend on?

-Histological grade of the papillary tumor
-Stage at diagnosis

182

What are some causes of urothelial carcinoma?

-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

What do schistosoma haematobium infections do in the bladder?

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

184

What is cyclophosphamide?

An immunosuppressive agent that causes hemorrhagic cystitis

185

What are the 3 genetic alterations seen in urothelial CA?

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

186

What can cause obstruction in the renal pelvis?

Calculi, tumors, uteropelvic stricture (fibrosis/inflammation)

187

What can cause intrinsic obstruction in the ureter?

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

188

What can cause extrinsic obstruction in the ureter?

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

189

What can cause obstruction in the bladder?

Calculi, tumors, functional (neurogenic)

190

What can cause obstruction in the prostate?

Hyperplasia, carcinoma, prostatitis

191

What can cause obstrction in the urethra?

Posterior valve stricture, tumors