Pathology Flashcards
(191 cards)
1
Q
What are the 3 types of nephropathy in persons with hyperuricemic disorders?
A
- Acute uric acid nephropathy
- Chronic urate nephropathy (gouty nephropathy)
- Nephrolithiasis
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
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
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
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
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)
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
8
Q
What does tubular obstruction by urates cause?
A
Cortical atrophy and scarring
9
Q
What % of individuals with gout have uric acid stones?
A
22%
10
Q
What % of individuals with secondary hyperuricemia have uric acid stones?
A
42%
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
12
Q
In hypercalcemia and nephrocalcinossi what is the earliest damage?
A
- Tubular epithelial cells: Mitochondrial distortion and other signs of cell injury (reverisible then irreversible)
- Calcium deposits: Mitochondria, cytoplasm, and basement membrane (purple, amorhpous)
- Calcified cellular debris: Obstruct tubular lumens (get actual stone formation), Obstructive atrophy of nephrons, secondary interstitial fibrosis, and inflammation (due to blockage)
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)
14
Q
What are other tubular defects seen in hypercalcemia and nephrocalcinosis?
A
Tubular acidosis and salt-losing nephritis
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
16
Q
What do you see in acute phoshpate nephropathy?
A
Extensive accumulations of calcium phosphate crystals in tubules
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
18
Q
What does acute phosphate nephropathy do?
A
Presents as renal insufficiency several weeks after exposure (renal function only partially recovers)
19
Q
What is another name for light chain cast nephropathy?
A
Myeloma kidney
20
Q
What is seen in light chain cast nephropathy?
A
Overt renal insufficiency
21
Q
Who do you see light chain cast nephropathy in?
A
Half of those with multiple myeloma and related lymphoplasmacytic disorders
22
Q
What are 4 contributing factors to renal damage in light- chain nepropathy?
A
- Bence Jones (light-chain) proteinuria and cast nephropathy
- Amyloidosis, of AL type formed from free light chains
- Light-chain deposition disease
- Hypercalcemia and hyperuricenia
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
24
Q
What can be done to see Bence Jones (light-chain) proteinuria and cast nephropathy?
A
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
