Quiz 2 Flashcards
(163 cards)
1
Q
The upper pole of each kidney is near the level of which vertebra?
A
12th thoracic
2
Q
The kidneys process how much blood per minute?
Per day?
A
1 Liter (20% of total cardiac output)
1500L
3
Q
What functions do the kidneys perform?
A
- Excrete metabolic waste
- Regulate electrolytes
- Buffer acid-base in blood
- Activate vitamin D
- Secrete renin
- Secrete erythropoietin
4
Q
Structural and functional unit of the kidney:
consists of:
A
Nephron
- glomerular capsule
- proximal convoluted tubule
- loop of Henle
- distal convoluted tubule
- collecting duct
5
Q
Capillary tuft surrounded by Bowman’s capsule:
Blood supply in and out:
A
Glomerulus
Blood IN via Afferent arteriole
Blood OUT via Efferent arteriole
6
Q
What is the GFR?
A
Glomerulur filtration rate
blood filtration rate, utilizing pressure gradient btw afferent and efferent arterioles to drive filtration
7
Q
Risk of CAKUT:
A
CAKUT - congenital abn of kidneys and urinary tract
1/3 of anomalies noted on prenatal US
predisposed adult HTN & CVD
40% of childhood end-stage renal failure
8
Q
Failure of kidney(s) to develop to normal size/weight:
A
Renal hypoplasia
unilateral MC than bilateral
smaller kidney prone to infx & scarring
9
Q
Kidneys fused at the upper or lower pole:
A
Horseshoe kidney
lower pole MC
often asx
infx may occur d/t urinary stasis
10
Q
Abnormal location of one/both kidney(s):
A
Ectopic kidney
MC locations - lower abdomen, pelvis
11
Q
Cystic lesions of the kidneys are (common/rare) and most are (asx/severe).
A
common
asx - found incidentally on imaging or post-mortem
12
Q
T/F: Simple cysts predispose an individual to developing chronic renal failure and/or neoplasia.
A
False
mb multiple, but never as numerous as polycystic kidney dz
13
Q
Autosomal recessive form of PKD:
ARPKD
A
childhood PKD
autosomal dominant - adult (ADPKD)
14
Q
Histopathology of childhood PKD:
A
multiple large cysts
lined by flattened cuboidal epithelium
fibrotic intervening parenchyma
islands of bluish cartilage
15
Q
T/F: The adult form of PKD is more commonly associated with concurrent liver cysts than is childhood PKD.
A
True
cysts not usu present at birth, develop slowly over time
assoc w/oxalate crystals in urine and cysts
16
Q
Presumed mechanism for adult PKD:
A
Abnormal collagen and elastin that results in diminished integrity
17
Q
Familial recurrence rate of ADPKD:
A
50%
18
Q
Patients on ________ commonly form kidney cysts, and are at increased risk for _________________.
A
dialysis
renal cell carcinoma
19
Q
Most forms of glomerular injury are found to be __________ mediated. Histo findings include:
A
immunologically
WBC infiltration
inflammatory cell infiltration
20
Q
Proliferation of mesangial, endothelial and epithelial cells is (common/uncommon) in glomerular dz.
A
Common
21
Q
In glomerular dz, thickening of the ___________ is a common and important finding.
A
basement membrane
usu d/t deposition of immune complexes on epithelial side of the membrane
22
Q
Immune complexes are often the result of specific antibodies to the glomerular basement membrane aka:
A
anti-GBM antibodies
23
Q
Glomerular dz’s presenting as nephrotic syndrome:
A
Lipoid nephrosis
Membranous glomerulopathy
Focal-segmental glomerulosclerosis
Nodular and diffuse glomerulosclerosis
24
Q
Characteristic findings of nephrotic syndrome (4):
A
Proteinuria (>3 gm per 24 hrs.)
Decreased serum proteins
Increased serum lipid levels
Generalized edema
25
MC cause of nephrotic syndrome in children:
| Peak incidence at ____ years.
lipoid nephrosis - 90% of cases
| 2-3 y.o.
26
Lipoid nephrosis accounts for ___% of adult nephrotic syndrome.
20-30%
27
Lipoid nephrosis exhibits _______________, in that _______ is the only protein commonly in the urine.
selective proteinuria
| albumin
28
Minimal change dz (MCD) is characterized by:
effacement of the epithelial cell foot process (podocyte) and loss of the normal charge barrier
albumin selectively leaks out
proteinuria ensues
29
MC cause of adult nephrotic syndrome:
Membranous glomerulopathy (aka membranous glomerulosclerosis)
30
Etiology of most cases of membranous glomerulopathy:
unknown (idiopathic)
can develop via response to antigenic stimulation to infectious agent/toxin
31
Membranous glomerulopathy is known to follow infx, such as:
| or drug therapy, such as:
```
Hep B
Hep C
Syphilis
Malaria
Schistosomiasis
```
gold therapy
Captopril
32
Tumors have been known to lead to membranous glomerulopathy, such as:
lung cancer
colon cancer
melanoma
lymphoma
33
In membranous glomerulopathy, the (capillary loops/loops of Henle) are usually (atrophied/thickened) and prominent.
capillary loops
| thickened
34
Light microscopy findings in membranous glomerulopathy:
* diffuse thickening of basement membrane
| * spiked appearance w/silver or Jones stain
35
Membranous glomerulopathy is generally a ____________ mediated disease in which deposits of __________ and _________ collect in the basement membrane.
immunologically
IgG and/or IgM
complement (usually C3)
36
_________________ is the MC cause of nephrotic syndrome in African-Americans.
Focal segmental glomerulosclerosis (FSGS)
and accts for 15% of nephrotic syndrome cases in adults and children (1/6 of cases)
37
T/F: Immune complexes are always in FSGS, pointing to the cause of dz.
False.
Immune complexes are not always seen and focal sclerosis appears to be idiopathic.
commonly seen in AIDS pts [d/t dz or drug toxicity; drugs like NSAIDs, lithium, interferon implicated]
38
T/F: In contrast to minimal change disease, patients with focal segmental glomerulosclerosis are far more likely to present with non-selective proteinuria.
True
clinical outcome often poor
inevitable renal failure
39
The hypercellularity of post-infectious glomerulonephritis is due to increased numbers of:
* epithelial, endothelial, and mesangial cells
| * presence of neutrophils in/around the glomerular capillary loops
40
T/F: Rapidly progressive glomerulonephritis (RPGN) is a description, not a specific disease.
True
it can be seen d/t a variety of causes
only rarely seen as result streptococcal infx
41
MC cause of chronic renal failure in the US:
| Thus it's called:
DM
| Diabetic nephropathy
42
In many diabetics, renal sx are (sudden/insidious) and findings include:
insidious - over 10-20 years
proteinuria
glycosuria
progressive decrease of renal function
43
Possible renal complications due to diabetes:
arteriosclerosis
glomerulosclerosis
pyelonephritis
renal failure
44
A commonly noted histologic change seen in patients who develop diabetic nephropathy:
glomerulosclerosis - generally appears several years after onset of DM
described as: nodular, diffuse, or mixed
45
Nodular glomerulosclerosis related to diabetes is referred to as:
Kimmelstiel-Wilson disease
46
The first abN lab in diabetic nephropathy is:
microalbuminuria
may also show glucose
late findings - elev serum creatinine and BUN
47
Etiology of primary amyloidosis:
| Characterized by:
idiopathic
amyloid depositions in one or more organs
48
Histologically, amyloid appears:
| Light microscopy:
pink
eosinophilic
acellular
homogenous
highly refractive
affinity for Congo red
49
With renal involvement, amyloid is first deposited in:
mesangium and capillary walls
| eventually in glomerular & tubular BM
50
Pt undergoes a procedure, and starts to develop spontaneous periorbital ecchymosis without trauma to the face. What should be in your ddx?
Amyloidosis
51
UA of pts with amyloid dz shows:
protein
fatty casts
fat bodies
52
Characteristic amyloidosis finding w/electron microscopy:
fibrils within the amyloid deposition
| non-branching filaments, 8-12nm wide, perpendicular to BM
53
Acute nephritis is characterized by the presence of:
* hematuria with red blood casts
* oliguria
* uremia
* varying degree of HTN
* minimal (no) proteinuria
54
MC cause worldwide of glomerulonephritis:
IgA nephropathy (aka Berger's dz)
d/t marked hyper secretion of IgA in response to an antigenic stimulus)
55
T/F: Edema is most usually associated with nephritic syndrome.
False - not usually, if present it is mild.
56
Findings of nephritic syndrome:
PHAROH
* proteinuria
* hematuria
* azotemia (elev blood N)
* RBC casts (KEYNOTE)
* oliguria
* HTN (KEYNOTE)
57
IgA nephropathy is more common in pts with ________.
celiac dz
58
IgA nephropathy pts generally present with new onset hematuria within days of:
a respiratory, gastrointestinal or genitourinary infx
usu disappears in days, my recur for mos/yrs
50% renal failure @20yrs
59
Another dz state of IgA over-secretion, a hypersensitivity vasculitis involving blood vessel walls in the skin, kidneys and/or G.I. tract:
Henoch-Schonlein purpura
60
Exam findings in H-S purpura:
PE: skin lesions, jt tenderness
UA: hematuria
Skin bx: vasculitis
61
H-S purpura may occur at any age, but peak incidence is:
3-8 yrs
more severe sx/sequelae in adults
62
Mesangial deposits - if IgA could be:
| If IgG:
IgA - H-S purpura OR IgA nephropathy
| IgG - lupus nephritis
63
Primary or secondary immune-mediated renal disease characterized by inflammation of the glomeruli:
Glomerulonephritis
64
Glomerulonephritis may present with:
* isolated hematuria and/or proteinuria
* nephrotic syndrome,
* nephritic syndrome
* acute renal failure
* chronic renal failure
65
Non-proliferative glomerulonephritis is characterized by:
| Frequently present with (nephritic/nephrotic) syndrome.
low numbers of cells (lack of hypercellularity) in glomeruli.
nephrOtic
(e.g. MCD, FSGS)
66
Proliferative glomerulonephritis is characterized by:
| Often present with (nephritic/nephrotic) syndrome and can progress to end-stage renal failure in:
increased number of cells (hypercellularity) in the glomerulus.
Nephritic
weeks to years
67
MC cause of acute nephritic syndrome:
PSGN (post-streptococcal glomerulonephritis)
68
T/F: PSGN can follow strep throat or impetigo.
True
nephrogenic strain of group A beta-hemolytic strep
[compare to Rheumatic Heart Dz - pharynx strain only]
69
PSGN ssx:
```
1-2 wk latency after infx
RBCs on UA
possible casts
fever
chills
HTN usu develops
```
70
T/F: Early abx intervention appears to significantly alter the course of PSGN.
False
this suggests genetic disposition to certain strains
71
Light microscopy of the glomeruli affected by PSGN usually reveal infiltration by:
PMNs and mononuclear macrophages
| Endothelial and mesangial proliferation
72
Immunofluorescent studies of PSGN demonstrate a granular deposition of:
Electron microscopy characteristically shows:
IgG, C3 and mesangial fibrin
“lumpy” appearance w/ dx finding of sub-endothelial “clumps of humps”
73
Broad term for the type of glomerular destruction and renal dz that may be d/t several different etiologic agents:
RPGN (rapidly progressing)
must often begin dialysis and/or await renal transplantation in order to survive.
74
Initial symptoms of RPGN:
hematuria
oliguria
HTN
75
Conditions known to cause or increase the risk for RPGN:
```
vasculitis
polyarteritis
SLE
Goodpasture's syndrome
H-S purpura
IgA nephropathy
membranoproliferative GN
internal organ abcess (any)
Hx of malignant tumor
blood/lymph system d/o
hydrocarbon solvent exposure
```
76
RPGN is also called __________ GN, for the characteristic bands of ________ that form around _________________.
Crescentic
fibrin
glomerular capillaries throughout capillary tufts
77
With RPGN, immunofluorescent staining reveals:
deposition of IgM, IgG and fibrin:
* 1/3 granular
* 1/3 linear
* 1/3 non-specific
78
Goodpasture's often presents with RPGN and is characterized by _________________.
It is MC seen in___________ in their 20s and 30s.
___________ is common.
IgG deposition in a _______ pattern.
Circulating anti-basement membrane antibodies
Caucasian males
Pulmonary hemorrhage
linear
79
Goodpasture's is usu treated aggressively with:
| Cause of death is usu:
steroids, chemo, plasma exchange
| pulmonary hemorrhage
80
Form of vasculitis that commonly involves kidneys, with potential for multi-organ involvement:
Presenting sxs may be:
Wegener's granulomatosis
* mucosal surface inflammation & ulceration
* purulent otitis media
* severe sinusitis.
* hemoptysis
* pleuritis
81
Wegener's granulomatosis findings:
* lung nodules/infiltrates
* conjunctivitis
* scleritis/episcleritis
* swelling/hemorrhage/ulceration of the gums
82
The classic renal pathology in Wegener’s is ______________________ accompanied by ___________ of renal vessels.
the combination of focal & segmental glomerulonephritis
| granulomatous vasculitis
83
T/F: In Wegener's, serology is often positive for P-ANCA.
False - C-ANCA
P-ANCA is seen in polyarteritis nodosum, another vasculitis.
84
Acute tubular necrosis is characterized by _____________ and is usu classified as being either ______ or ________.
proximal tubular epithelium necrosis
toxic or ischemic
Necrotic cells fall into the tubule lumen, obliterating it and eventually resulting in acute renal failure.
85
In toxic ATN, the affected tubular cells characteristically reveal an (absence/abundance) of nuclei and a (heterogenous/homogenous) cytoplasm which stains (mildly/intensely) eosinophilic and preserves it’s normal shape.
absence
homogenous
intensely
86
T/F: full recovery of renal function is possible if the underlying ATN cause is removed.
True
Because tubular cells normally undergo continual replacement
87
Ischemic ATN causes ________ through the tubules due to differences in ________ within the kidney
skip lesions
| perfusion
88
Acute interstitial nephritis (AIN) is MC a result of:
| It may also be linked to ___________ and may result in ___________.
an allergic response to a drug
```
infectious agents (CMV, streptococcus, legionella)
acute rejection of a renal transplant
```
89
AIN may be in the ddx when acute renal dz begins after ___________ or the start of a ______________.
```
recent infx
new medication
* ibuprofen/NSAIDs
* acetaminophen
* penicillin
* cephalosporin
* cimetidine
* thiazide diuretics
* cyclosporin
```
90
AIN refers to:
presence of edema, inflammatory cell infiltration in renal parechyma, and often tubular injury
drug/infx agent acts as hapten, binds to membrane binding site, w/ 2° immune-mediated injury (type I or IV).
91
Dx findings of AIN:
Eosinophilia (serum, urine)
definitive - kidney bx
92
Chronic interstitial nephritis (CIN) is caused by disorders that ultimately lead to _________ of the _________.
Causes include:
progressive scarring
interstitium
* persisting AIN
* hematologic malignancies (lymphoma, mult myeloma)
* chronic exposure to toxin (lead)
93
T/F: CIN has no cure.
True
some pts will require dialysis
mb eventual transplanation
94
Histopathology of CIN:
* interstitium expanded by fibrosis
* distortion of tubules
* peri-glomerular fibrosis
* glomerulus unchanged
95
Dz of the proximal renal tubules in which glucose, amino acids, uric acid, phosphate & bicarbonate are passed into the urine instead of being reabsorbed:
Fanconi's syndrome
hereditary
drugs
heavy metals
96
T/F: The term renal tubular acidosis (RTA) refers to individuals with poor urinary acidification d/t poor-functioning kidneys.
False
RTA refers to poor acidification in otherwise healthy kidneys, and several types exist (1, 2, 4)
97
Compare types 1, 2, and 4 of RTA.
| Consider location, acidosis, potassium, & pathophys.
Type 1 - distal tubules
severe acidosis
hypOkalemia
no H+ secretion by intercalated cells
Type 2 - proximal tubules
mod. acidosis
hypOkalemia
too little HCO3 reabsorption
Type 4 - adrenal
mild acidosis
hypErkalemia
resistance to/low aldosterone
98
Light microscopy of Fanconi's:
atrophic and hyalinized glomeruli
| seen in end-stage kidney dz
99
Analgesic nephropathy occurs after ingestion of (small/large) amounts of analgesics over a (short/long) period of time.
```
large
long
(vs. AIN which mb 1 dose/short course)
```
leads to papillary necrosis, spares cortex
100
Two of the MC drugs responsible for analgesic nephropathy:
acetaminophen [covalent bond to papilla, 2° oxid. dmg]
| aspirin [inhibits prostaglandin synthesis]
101
Atherosclerotic changes in the renal blood vessels:
benign nephrosclerosis
occurs as a renal complication of HTN (seen on bx in diabetics w/HTN)
102
The surface of the benign nephrosclerotic kidney has a characteristic granular appearance due to:
Microscopically:
patchy ischemic atrophy w/in the kidney
focal loss of parenchyma
hyaline thickening of walls of small arteries/arterioles
103
Malignant nephrosclerosis:
* severe changes in renal architecture d/t malignant HTN
* focal small hemorrhages
* small arteries/arterioles become hyperplastic, “onion ring” appearance
104
Narrowing or blockage of a renal artery is called __________ and mb d/t
renal artery stenosis (RAS)
* atherosclerosis
* fibromuscular dysplasia of renal a.
* atheroembolic renal dz
* scar formation
105
T/F: Renal artery stenosis often causes mild HTN that responds well to treatment.
False
often causes HTN that may be severe and resistant to tx
106
How is RAS typically found?
on work up for difficult to control HTN
in some cases bruits mb heard in mid-back
among the MC causes of 2° HTN
107
Systemic dz that results in widespread thrombosis in capillaries & arterioles, and may have a significant effect on the kidneys and renal function.
Thrombotic microangiopathy
hallmark: widespread formation of hyaline thrombi in microcirculation (dense platelet accumulations surrounding fibrin)
108
The 2 MC conditions with thrombotic microangiopathy:
HUS and TTP
[or mb better HUS/TTP syndrome d/t overlap]
Hemolytic uremic syndrome
thrombotic thrombocytopenic purpura
109
What appears to be the initiating event in thrombotic microangiopathy?
```
Endothelial injury resulting in thrombus formation
triggers:
* bacterial endotoxins
* cytotoxins
* cytokines
* viruses
* drugs
* endothelial abs
* septicemia
and in many cases is unknown
```
110
Classic triad of HUS:
* acute renal failure
* microangiopathic hemolytic anemia
* thrombocytopenia
111
MC causes of acute renal failure in children:
| which involved bacteria is MC?
HUS
E coli 0157:H7
verocytotoxin releasing bacteria
112
How does HUS work?
* Endothelium shows inc. adhesion of leucocytes.
* Inc endothelin production.
* Loss of endothelial nitric acid production.
* Cytokines (eg TNF) involved in lysis of endothelial cells.
* Resultant vasoconstriction & thrombosis causing classis microangiopathy.
113
Hx finding in HUS:
* recent gastroenteritis (83%)
* fever (56%)
* bloody diarrhea (50%)
* seizures
* acute renal failure
* anuria
114
Histopathology of HUS:
* capillary lumens often occluded by debris/thrombi
* patchy or diffuse microangiopathy
* swelling of endothelium
* cortical necrosis
* thick capillary walls in glomeruli
115
HUS/TTP syndrome in adults follows/correlates with:
* viral infx
* septicemia
* typhoid, shigella, E coli
* SLE, scleroderma
* antiphospholipid ab
* malignant HTN
* chemo/immunosuppressive drugs
* pregnancy/post-partum
116
Source of most renal artery emboli?
a cardiac source (i.e. enlarged left atrium)
MC non-cardiac source - ruptured aortic atheromatous plaque (spontaneous or post-sx/angioplasty)
incidence increases with age
117
Biopsy of renal tissue affected by embolic disease often reveals
cholesterol laden emboli w/in involved arteries
cholesterol usu dissolves leaving cleft-like spaces on slides
118
T/F: Renal ischemia of any kind will show poor uptake of "vital" stain, which are taken up by metabolically active cells.
True
A gross specimen of ischemic renal tissue may appear normal but anoxic tissue to the degree of infarction will have a classic wedge-shape to the infarcted tissue
119
Kidney stones (renal calculi) are:
crystalline accumulations that precipitate out of urine they would normally be dissolved in.
120
Does dehydration contribute to stone formation?
Yes, because the resulting supersaturation by one or more substances will precipitate out of solution.
121
Kidney stones most often develop in the ________ of the kidney and are usu composed of ___________________.
pelvis
* oxalates
* phosphates
* uric acid
* carbonates
122
Approx 75% of kidney stones are:
calcium oxalate stones
123
Remaining 25% of kidney stones are:
15% - triple phosphate (struvite) stones
6% - uric acid
1% - cystine
124
T/F: Most calcium oxalate stones are assoc w/ hypercalcemia & hypercalciuria.
False! only 5%
abN renal absorption of Ca+ is found in 55%
risk factor: inc serum oxalate
many pts w/stones have NO risk factors
125
Triple phosphate stones (magnesium ammonium phosphate) are seen most commonly in association with:
UTIs by bacteria which are urea-splitting:
* proteus spp.
* staphylococcus (some)
these convert ammonia to urea => increase pH
126
Staghorn crystals are:
triple phosphate stones
some of the largest!
127
Uric acid crystals are seen in:
* normal pts (esp w/acidic urine
128
Cystine stones are caused by:
genetic defects in the renal reabsorption of amino acids, including cystine, leading to cystinuria.
Precipitate more readily out of acidic urine.
129
Benign tumors of the kidneys are generally (severe/moderate/asx) and are usually noted ______________.
asx
incidentally on autopsy
malignant tumors of the kidney cause considerable morbidity and mortality.
130
Benign renal tumors:
* Renal papillary adenoma (fronds)
* Renal fibroma or hamartoma
* Angiomyolipoma
* Oncocytoma
131
Renal adenomas are often called ______________ because they are MC found in the __________. Most are __mm or (less/more)
papillary adenomas
papilla
5mm or less
132
Epithelial tumor composed of oncocytes, large eosinophilic cells that are round to polygonal shaped cells with benign-appearing nuclei with large nucleoli:
oncocytoma
133
Characteristic histopathology of oncocytoma:
| Electron microscopy:
* large polygonal cells
* round nuclei
* uniform appearance
* numerous prominent mitochondria, "stacked"
134
Primary renal malignancies include:
* renal cell carcinoma
* transitional cell carcinoma
- papillary & non
* Wilm's tumor (nephroblastoma)
* renal sarcoma
* lymphoma
135
MC kidney malignancy:
Renal cell carcinoma (85%)
2nd - mets
2nd primary renal malignancy - TCC
136
RCCA is (asx/painful) in early stage, sx are (specific/nonspecific) and mb:
asx - until advanced stage (25% have distant mets on dx)
fever
malaise
weakness
wt loss
137
Class triad of RCCA that suggests advanced dz:
flank pain
hematuria
palpable abd mass
138
Major risk factors for RCCA:
```
TOBACCO
cadmium/asbestos exposure
FHx
obesity
HTN
unopposed estrogen therapy
radiation therapy to kidney area
```
139
RCCA tumors range from _______ cm.
2-25cm!
140
What are the 5 types of RCCA? Which is most prevalent?
```
Clear cell carcinoma (75-85%)
chromophilic carcinoma
chromophobic carcinoma
oncocytic carcinoma
collecting duct carcinoma
```
141
Histologic appearance of RCCA:
neoplastic cells
clear cytoplasm
nest of tumor cells w/intervening vessels
142
Common sites of mets for RCCA:
```
lungs
lymph nodes
bone
liver
brain
ipsilateral adrenal gland
contralateral kidney
renal vein -> vena cava
```
143
Risk factors for urothelial (transitional cell) carcinoma:
```
Cigarette smoking (lower risk w/pipes, etc)
chemical exposure
- petroleum
- paint
- pigments
* aniline dyes
- agrochemicals
```
144
MC primary renal tumor in children:
Age of dx:
Related to defects in:
Wilm's tumor
2-5 y.o.
chromosome 11
145
Pt's with Wilm's tumor have a noted propensity for:
developing other kinds of primary tumors
* genito-urinary tumors
* bone tumors
* soft tissue sarcoma
* leukemia
146
MC cause of hydronephrosis in infants/children:
ureteropelvic junction obstruction
147
Abnormal movement of urine from the bladder into the ureters and potentially to the kidneys:
vesicoureteral reflux
148
Obstructive lesions of the ureter:
* calculi - usu
149
Bilateral ureteral obstruction generally occurs as a result of __________, where unilateral obstruction is typically ________.
ascending pathology from (near) the bladder - BPH, tumor
| descending pathology from the kidney
150
MC ureteral malignancies:
Transitional cell carcinoma (TCC)
151
Failure of normal development of the anterior wall of the abdomen and bladder:
exstropy - repairable with surgery
inc risk of bladder adenocarcinoma later in life
152
Embryological canal connecting the urinary bladder with the allantoids, which is normally obliterated during development, but leads to risk of cysts when persisting:
urachus
bladder adenocarcinoma can arise in cysts
153
Inflammation or infection of the urinary bladder:
cystitis
154
Microscopically, the urothelial mucosa of the bladder in chronic cystitis show inflammatory cells in the _____________.
lamina propria - mostly lymphocytes
155
Pattern of bladder change as a result of chronic inflammation:
malakoplakia
156
Malakoplakia, microscopic findings:
foamy histiocytes
round basophilic inclusions
* Michaelis-Gutmann bodies (pathognomonic)
157
Urinary bladder dz of unknown origin characterized by dysuria, frequency, urgency, and pressure:
interstitial cystitis
158
Definitive dx of IC requires:
cystoscopy
159
The pathognomonic lesion of IC:
Hunner's ulcer
160
Non-infectious causes of IC:
cytotoxic anti tumor drugs
* methotrexate
* cyclophosphamide
radiation to the bladder
161
MC bladder cancer:
TCC
| M:F 3:1
162
Bladder cancer risk factors:
```
cigarette smoking
long term use of analgesics
radiation to the bladder
aryl amine exposure (industrial)
schistosomiasis infx
```
163
What are the 2 distinctive precursor bladder cancer lesions:
* noninvasive papillary tumors - MC
| * urothelial carcinoma in situ (CIS) - worse prognosis
