GU Flashcards
(160 cards)
1
Q
What separates the three components of the retroperitoneum?
A
Separated by the anterior and posterior renal fascia and lateral conal fascia
2
Q
What are the three compartments of the retropertoneum?
A
Anterior pararenal space
Perirenal space - surrounds each kidney
Posterior pararenal space
3
Q
What is in the anterior pararenal space?
A
Ascending colon
Descending colon
(2nd and 3rd) duodenum
Pancreas
4
Q
What is in the perirenal space?
A
Surrounds each kidney
Kidneys
Proximal ureter
Adrenals
Lots of fat
5
Q
What is in the posterior pararenal space?
A
Potential space, contains only fat
May become secondarily involved in inflammatory processes
Clinically important as a pathway for potential disease spread due to secondary involvement of inflammation or neoplasm.
6
Q
MC primary retroperitoneal retroperiteonal tumor?
A
Liposarcoma
7
Q
What is retroperitoneal fibrosis?
A
Rare inflammatory disorder causing increased fibrotic deposition in the retroperitoneum, often leading to ureteral obstruction.
Unlike malignant retroperiteonal adenopathy, retroperitoneal fibrosis tends not to elevate the aorta off the spine.
8
Q
What are the two components of the adrenal glands and what are they derived from?
A
The cortex is derived from mesothelium
The medulla is derived from neural crest
9
Q
What does the adrenal cortex make?
A
Synthesizes the steroid hormones aldosterone, glucocorticoids, and androgens, which are all biochemical derivatives of cholesterol.
10
Q
What are the three layers of the adrenal cortex and what do they make?
A
Zona glomerulosa (most superficial): Produces aldosterone.
Zona fasciculata: Produces glucocorticoids in response to pituitary adrenocorticotropic hormone (ACTH).
Zona reticularis (deepest; closest to the adrenal medulla): Produces androgens.
11
Q
What pathology can affect the adrenal cortex?
A
Adrenal hyperplasia
Adrenal adenoma
Adrenal cortical carcinoma
12
Q
What does the adrenal medulla make?
A
Central portion of the adrenal gland and produces the catecholamines norepinephrine and epinephrine, which are derived from tyrosine.
13
Q
What pathology can affect the adrenal medulla?
A
Pathology of the adrenal medulla includes pheochromocytoma and the neuroblastic tumors (ganglioneuroma, ganglioneuroblastoma, and neuroblastoma).
14
Q
Conditions associated with adrenal hyperfunction?
A
Cushing syndrome is excess cortisol production from non-pituitary disease, such as idiopathic adrenal hyperplasia, adrenal adenoma, or ectopic/paraneoplastic ACTH (e.g., from small cell lung cancer).
Cushing disease is excess cortisol production driven by excessive pituitary ACTH.
Conn syndrome is excess aldosterone production, most commonly from an adrenal adenoma, which causes hypertension and hypokalemia. The adenomas implicated in Conn syndrome are typically small and may be difficult to detect on CT. Localizing the side of excess hormone production with venous sampling may be a helpful diagnostic adjunct.
Adrenal cortical carcinoma is a very rare adrenal malignancy that arises from the cortex and typically causes a disordered increase in all cortical adrenal hormones and precursors.
Pheochromocytoma is a usually benign tumor of the adrenal medulla that causes an increase in catecholamines.
15
Q
What is Waterhouse–Friderichsen syndrome?
A
Post-hemorrhagic adrenal failure secondary to Neisseria Meningitidis bacteremia.
Idiopathic adrenal hemorrhage is usually unilateral and rarely causes adrenal hypofunction.
16
Q
What percentage of adrenal adenomas are lipid-rich (<10 HU)?
A
80%
17
Q
What is a collision tumor?
A
Metastasis into an adrenal gland with a pre-existing adenoma
“Adenoma” appears heterogeneous or has shown an interval increase in size, then a collision tumor should be considered in a patietn with known primary even if region attenuates <10 HU.
18
Q
Why do adrenal adenomas contain fat?
A
Intracytoplasmic lipid due to steroid production.
19
Q
What malignancies also contain intracytoplasmic lipid and would also lose signal on out-of-phase images similar to an adenoma?
A
Well-differentiated adrenocortical carcinoma (very rare).
Clear cell renal cell carcinomas metastatic to the adrenal gland.
Hepatocellular carcinoma metastatic to the adrenal gland.
Liposarcoma (typically a predominantly fatty mass that is rarely confused with adrenal adenoma).
20
Q
How do adenomas washout compared to metastases?
A
Adrenal adenomas demonstrate more rapid contrast washout than metastases do. The more rapid contrast washout of benign adenomas appears to be true even compared to adrenal metastases of hypervascular primaries.
The timing of the washout phase remains controversial, with recent evidence suggesting 15-minute washout has greater sensitivity than 10 minutes.
> 60% absolute washout is diagnostic of adenoma
21
Q
What is the adrenal washout formula?
A
%washout = (enhanced attenuation - delayed attenuation) / (enhanced attenuation - unenhanced attenuation)
> 60% absolute washout is diagnostic of adenoma
22
Q
What is adrenal relative washout?
A
If unenhanced CT is not available or not performed due to concern for radiation
exposure
% relative washout = (enhanced attenuation - delayed attenuation) / (enhanced attenuation)
> 40% relative washout is diagnostic of adenoma
23
Q
What % washout is diagnostic of adenoma on absolute and relative?
A
Absolute >60%
Relative >40%
24
Q
In patient with known primary what is a lesion that does not demonstrate benign washout kinetics?
A
Suspicious for, but not diagnostic of, metastasis.
25
What is an adrenal myelolipoma?
Benign neoplasm consisting of myeloid cells (i.e., erythrocyte precursors) and fat cells.
26
What is a Pheochromocytoma?
Pheocytoma is a neoplasm of chromaffin cells, usually arising from the adrenal medulla. Pheochromocytoma may cause hypertension and episodic headaches/ diaphoresis.
27
What is the "rule of 10s" with pheochromocytomas?
10% are extra-adrenal.
10% are bilateral.
10% are malignant.
10% are familial or syndromic.
28
What syndromes are Pheochromocytomas associated with?
Multiple endocrine neoplasia (MEN) 2A and 2B: Typically bilateral intra-adrenal pheochromocytomas.
von Hippel–Lindau.
Neurofibromatosis type 1.
Carney’s triad (gastric leiomyosarcoma, pulmonary chondroma, and extra-adrenal pheochromocytoma).
29
What is an extra-adrenal pheochromocytoma called?
Paraganglioma
30
Locations of paragangliomas (extra-adrenal pheochromocytomas)?
The most common intraabdominal location of a paraganglioma is the organ of Zuckerkandl, located at the aortic bifurcation.
A rare intra-abdominal location of a paraganglioma is the bladder, producing the distinctive clinical presentation of post-micturition syncope (syncope after urination).
Paragangliomas occur in the head and neck in characteristic locations. Paragangliomas of the head and neck are generally called glomus tumors and may be associated with the tympanic membrane (glomus tympanicum), the jugular foramen (glomus jugulare), the carotid body (called a carotid body tumor), or the vagus nerve (glomus vagale).
31
MC cancers to cause adrenal metastases?
Lung and melanoma
32
What causes adrenal calcification?
Wegener granulomatosis
TB
Hisoplasmosis
Old hemorrhage
33
What is Gerota's Fascia?
Anterior renal fascia - separates the anterior pararenal and perirenal space.
34
What is Zuckerkandl's Fascia?
Posterior renal fascia - separates the perirenal fascia and the posterior renal fascia
35
What is a renal mass protocol multiphase CT?
Unenhanced, nephrographic (100 second delay), and pyelographic (excretory phase - 15 min delay) phases.
36
Timing of the nephrographic phase?
100 second delay
37
Timing of the pyelographic/excretory phase?
15 minute delay
38
What is the most important characteristic to distinguish between a benign and malignant non-fat-containing renal mass?
Enhancement
A lesion containing intralesional fat is almost always a benign AML, even if it enhances.
39
What is considered enhancement in CT?
Quantified as the absolute increase in HU on post-contrast images, compared to pre-contrast:
<10 HU: no enhancement
10-19: equivocal enhancement
>20 HU: enhancement
40
What is considered enhancement in MRI?
Quantified as percent increase in signal intensity as measured on postcontrast images:
<15%: no enhancement
15-19%: equivocal enhancement
>20% enhancement
41
When is a lesion "too small to characterize"?
If the lesion diameter is smaller than twice the slice thickness.
Ex, 3 mm slices, a lesion less than 6 mm cannot be accurately characterized based on attenuation or enhancement.
42
What do RCCs arise from?
Renal tubular cells
43
Risk factors for development of RCC
Smoking, acquired cystic kidney disease, VHL, and tuberous sclerosis
44
What are the subtypes of RCC?
```
Clear cell - MC
Papillary
Chromophobe
Collecting duct carcinoma
Medullary carcinoma
```
45
What is the MC subtype of RCC?
Clear cell
Enhances more avidly than the less common subtypes.
Can be sporadic or associated with VHL
46
Characteristics of clear cell RCC?
Enhances more avidly than the less common subtypes.
| Can be sporadic or associated with VHL
47
What subtype of RCC is associated with VHL?
Clear Cell
48
Characteristics of Papillary RCC?
Hypovascular subtype- 80-90% 5-year survivial
Enhances only mildly due to its hypovascularity.
A renal "adenoma" is frequently seen on autopsy specimens and is a papillary carcinoma <5 mm.
49
Hypovascular subtype of RCC?
Papillary RCC
50
What is the Chromophobe subtype of RCC?
Best prognosis - 90% 5 year survival.
51
Subtype of RCC with best prognosis?
Chromophobe - 90% 5-year survival.
52
What is Medullary Carcinoma RCC?
Rare, but known to affect mostly young adult males with sickle cell trait.
Extremely aggressive neoplasm with mean survival of 15 months, not helped by chemotherapy.
53
Subtype of RCC associated with sickle cell trait?
Medullary Carcinoma RCC.
54
Staging of RCC
Robson System - characterizes fascial extension and vascular/lymph node involvement. I-III are resectable.
Stage I: tumor confined to w/in the renal capsule
Stage II: Tumor extends out of the renal capsule but remains confined with Gerota's fascia.
Stage III: Vascular and/or LN involvement
A: RV involvement or IVC involvement.
B: LN involvement
C: Venous and LN involvement
Stage IVA: Tumor growth through Gerota's Fascia
Stage IVB: Distant metastasis
55
MC benign renal neoplasm?
AML
56
Characteristics of AML in fat saturation vs in an out of phase imaging?
Will follow retroperitoneal fat on all sequences and will saturate out on fat-saturated sequences.
Intracytoplasmic lipid is not a feature of AML, so there should be no significant signal drop-out on dual-phase MRI.
57
Small hyperdense enhancing mass does not contain macroscopic fat - what to do next?
MRI - T2-weighted images to distinguish from RCC
T2 hyperintense mass suggests RCC (clear cell subtype) - surgery
T2 hypointense mass is nonspecific and can represent either RCC (papillary type) or AML with minimal fat. Although AML would enhance avidly than a papillary RCC, biopsy is warranted for definitive diagnosis.
58
What is an Oncocytoma?
Most commonly resected benign renal mass and has overlapping imaging findings with RCC.
Can suggest oncocytoma on imaging, but imaging features are not specific and cannot be reliably differentiated from RCC.
Imaging features suggestive of oncocytoma are homogeneous enhancement and a central scar.
Oncocytic cells can sometimes be found in the rare chromophobe RCC subtype- can distinguish between clear and papillary RCC.
59
What imaging findings can suggest oncocytoma?
Homogeneous enhancement and a central scar.
60
Patterns of renal involvement of lymphoma
Primary renal lymphoma is rare - no native lymphoid tissue. May become involved from hematogenously disseminated disease or spread from the retroperitoneum.
Multiple lymphomatous masses (MC pattern - 50%)
Solitary renal mass
Diffuse lymphomatous infiltration, causing nephromegaly
Direct extension of retroperitoneal disease
61
What are non-neoplastic solid renal masses?
Infection- especially focal pyelonephritis. Renal abscess may be difficult to differentiate on imaging from a cystic RCC.
Renal AVM- will avidly enhance and mimic a hypervascular renal mass. Clue: asymmetric enhancement of the renal vein on the affected side, due to early shunting of venous blood.
62
What are the renal pseudotumors?
Normal variations of renal morphology that may mimic a renal mass.
Hypertrophied column of Bertin
Persistent fetal lobation/lobulation
63
What are the columns of Bertin?
The columns (septa) of Bertin are normal structures that anchor the renal cortex to the hilum and create the separations between the renal pyramids.
64
What are persistent fetal lobation/lobulation?
In normal fetal development- the fetal kidneys are divided into discrete lobes. Occasionally, can persist in adulthood, producing an indentation of the renal cortex. This indentation can cause an adjacent focal bulge that stimulates a renal mass. Can usually be distinguished from a true mass by the presence of septa of Bertin on either side.
65
Syndromes with renal masses?
VHL
Birt-Hogg-Dube
Tuberous Sclerosis
66
What is VHL?
AD multiorgan syndrome caused by a mutation in the VHL tumor suppressor gene on chromosome 3, which leads to cysts and neoplasms in multiple organs.
Primary manifestation is in GU is bilateral or multifocal RCCs, most commonly the clear-cell subtype.
Other: multifocal pheochromocytoma and renal cysts.
CNS: hemangioblastoma of brainstem, cerebellum, or spinal cord.
Pancreatic and hepatic: malignant neuroendocrine pancreatic tumor, pancreatic serous cystadenoma (benign), and pancreatic/hepatic cysts.
67
Cause of VHL?
AD multiorgan syndrome caused by a mutation in the VHL tumor suppressor gene on chromosome 3, which leads to cysts and neoplasms in multiple organs.
68
GU manifestations of VHL?
Primary manifestation is in GU is bilateral or multifocal RCCs, most commonly the clear-cell subtype.
Other: multifocal pheochromocytoma and renal cysts.
69
CNS manifestations of VHL?
Hemangioblastoma of brainstem, cerebellum, or spinal cord.
70
Pancreatic and hepatic manifestations of VHL?
Malignant neuroendocrine pancreatic tumor, pancreatic serous cystadenoma (benign), and pancreatic/hepatic cysts.
71
What is Birt-Hogg-Dube?
AD syndrome of dermatologic lesions, cystic lung disease, and multiple renal oncocytomas and RCCs.
72
What is Tuberous Sclerosis?
AD neurocutaneous disease caused by a tumor suppressor gene mutation. Seizures, developmental delay, and (mostly) benign tumors in multiple organ systems.
MC renal manifestation is multiple bilateral AMLs. 50% of patients with TS will have at least one AML.
Renal cysts in ~25%
Relative risk of RCC is increased in patients with TS.
Heart: rhabdomyoma
Lung: smooth muscle proliferation identical to lymphangioleiomyomatosis- causing cystic replacement of lung parenchyma.
73
What causes Tuberous Sclerosis?
AD neurocutaneous disease caused by a tumor suppressor gene mutation. Seizures, developmental delay, and (mostly) benign tumors in multiple organ systems.
74
GU manifestations of Tuberous Sclerosis?
MC renal manifestation is multiple bilateral AMLs. 50% of patients with TS will have at least one AML.
Renal cysts in ~25%
Relative risk of RCC is increased in patients with TS.
75
Finding of Tuberous Sclerosis in the heart?
Rhabdomyoma
76
Findings of Tuberous Sclerosis in the lungs?
Smooth muscle proliferation identical to lymphangioleiomyomatosis- causing cystic replacement of lung parenchyma.
77
What are the two MC entities to cause a cystic renal mass?
RCC and renal abscess.
78
What is the DDx of a cystic renal mass?
Cystic RCC.
Multilocular cystic nephroma - benign cystic neoplasm with enhancing septa that occurs in a bimodal age distribution in baby boys and middle aged women.
Characteristic, but nonspecific finding is propensity to herniate into the renal pelvis, causing hydronephrosis.
In adults, can be indistinguishable from cystic RCC.
Children, can be indistinguishable from cystic Wilms tumor.
Mixed Epithelial and Stromal Tumor (MEST)- benign neoplasm composed of epithelial and mesenchymal elements, typically found in middle-aged women. May appear as either a solid or cystic mass.
79
What is a Multilocular Cystic Nephroma?
Benign cystic neoplasm with enhancing septa that occurs in a bimodal age distribution in baby boys and middle aged women.
Characteristic, but nonspecific finding is propensity to herniate into the renal pelvis, causing hydronephrosis.
In adults, can be indistinguishable from cystic RCC.
Children, can be indistinguishable from cystic Wilms tumor.
80
What is Mixed Epithelial and Stromal Tumor (MEST)?
Benign neoplasm composed of epithelial and mesenchymal elements, typically found in middle-aged women. May appear as either a solid or cystic mass.
81
What is the role of MRI in evaluation of complex cystic renal masses?
MRI has limited role. Key advantage is more accurate enhancement characterization, as MRI doesn't suffer from the CT phenomenon of pseudoenhancement due to beam hardening from adjacent densely enhancing renal parenchyma.
The increased accuracy of MRI to characterize enhancement is most useful to distinguish a Bosniak IIF from a Bosniak III lesion. Thickening of a septation or cyst wall that shows measurable enhancement defines a Bosniak III lesion.
MRI is more sensitive for detecting septations compared to CT.
Calcifications are more difficult to detect with MRI.
82
What is the difference between peripelvic and parapelvic cysts?
Both renal sinus cysts.
Parapelvic - renal cortical cyst that herniates into the renal sinus. Usually large, but solitary.
Peripelvic cysts- lymphatic in origin and usually small and multiple.
83
What is a hyperdense cyst?
Homogeneous renal cyst with an attenuation >70 HU on noncontrast imaging represents a benign hyperdense cyst, likely secondary to prior hemorrhage.
Hyperdense cyst cannot be distinguished if only post-contrast imaging is available as there is no way to distinguish a hyperdense cyst from an enhancing renal mass.
84
What are the Bosniak classifications and their risk stratification?
Category I and II - no risk of malignancy. No f/u necessary.
Category IIF- small risk of malignancy. Imaging f/u is needed.
Category III and IV: Surgical lesions, concerning for cystic RCC.
85
What is a Bosniak I Cyst?
Water-attenuation cyst, with hairline wall and no areas of enhancement.
Always benign. No f/u needed.
86
What is a Bosniak II Cyst?
Water-attenuation cyst containing a few (3 or fewer) harline septa. May contain fine septal calcifications. No enhancement.
Also includes small (<3 cm) hyperattenuating cysts w/o enhancement.
Essentially always benign. No f/u needed.
87
Bosniak classification of a water-attenuation cyst containing a few (3 or fewer) harline septa. May contain fine septal calcifications. No enhancement.
Bosniak II
88
Bosniak classification of a small (<3 cm) hyperattenuating cysts w/o enhancement?
Bosniak II
89
What is a Bosniak IIF Cyst?
Multiple septa, with minimal smooth thickening (3 mm or less). May have thick and nodular mural calcification.
Walls may slightly enhance.
Also includes large (>3 cm) hyperattenuating cysts w/o enhancement.
Usually benign. Radiographic f/u is recommended, where morphologic change or new enhancement would be concerning for malignancy.
90
Bosniak classification of a cyst with multiple septa, with minimal smooth thickening (3 mm or less). May have thick and nodular mural calcification. Walls may slightly enhance
Bosniak IIF
91
Bosniak classification of a large (>3 cm) hyperattenuating cysts w/o enhancement.
Bosniak IIF
92
What is a Bosniak III cyst?
Thickened, irregular walls or septa, with measurable enhancement.
Concern for malignancy, but may be benign (e.g. infection, multilocular cystic nephroma). Without comorbidities, treatment is surgical.
93
Bosniak classification of a cyst with thickened, irregular walls or septa, with measurable enhancement
Bosniak III
94
What is a Bosniak IV cyst?
Distinguishing feature is enhancing nodular component separate from the wall or septa.
Clearly malignant. Surgical lesion unless significant comorbidities.
95
Bosniak classification of a cyst where the distinguishing feature is enhancing nodular component separate from the wall or septa.
Bosniak IV
96
What is ADPKD associated with?
Saccular aneurysm of the COW.
Does not increase the risk of RCC
97
DDx of a unilateral enlarged kidney
Pyelonephritis, acute ureteral obstruction, renal vein thrombosis, and compensatory hypertrophy.
98
DDx for a striated nephrogram?
```
Pyelonephritis
Renal infarct
Renal vein thrombosis or vasculitis
Renal contusion (typically focal)
Acute urinary obstruction
Renal tumor (espeically lymphoma if infiltrative)
Radiation nephritis
```
99
What is Xanthogranulomatous Pyelonephritis?
Chronic renal infection due to obstructing calculi, leading to replacement of renal parenchyma with fibrofatty inflammatory tissue.
Proteus mirabilis and E. Coli
Flank pain and nonspecific constituional symptoms- fever and weight loss. Anemia and hematuria are common.
Can be diffuse (85%) or localized. Localized ("tumefactive XGP") may mimic a renal mass.
Fibrofatty replacement of the renal parenchyma, marked perinephric inflammatory stranding, and staghorn calculi.
Bear paw sign- hypoattenuating fibrofatty masses arranged in a radial pattern, reminiscent of a bear's paw.
100
Composition of calcified stones?
Calcium oxalate and phosphate, pure calcium oxalate, or pure calcium phosphate.
101
Composition of radiolucent stones?
Uric acid, xanthine, matrix, pure struvite, and indinavir (seen in HIV patients on antiretroviral therapy).
Virtually all stones are radiopaque on CT except for indinavir stones and very rare uncalcified matrix stones made of mucin.
102
Causes of Papillary Necrosis?
```
Pyelonephritis
Obstruction
Sickle Cell Disease
TB
Cirrhosis
Analgesics (NSAIDs)
Renal Vein Thrombosis
Diabetes
```
NSAIDS, sickle cell, DM, and RV thrombosis are MC.
103
What is Papillary Necrosis?
Necrosis and sloughing of the renal papillary tissue- clinically, gross hematuria and may lead to chronic renal insufficiency.
Delayed contrast CT urography - multiple small poolings of extra-calyceal contrast adjacent to the renal calyces.
Three classic uroradiologic signs:
Ball on tee sign - contrast filling a central papilla
Lobster Claw Sign- Contrast filling only the periphery of the papilla
Signet Ring Sign- Contrast surrounding the sloughed papilla.
104
What causes delayed (prolonged) nephrogram?
Unilateral- acute ureteral obstruction, renal vein thrombosis, and renal artery stenosis.
Bilateral- bilateral obstruction, contrast nephropathy, systemic hypotension, and myeloma kidney.
105
Causes of medullary nephrocalcinosis?
Hypercalcemic state (e.g. hyperparathyroidism, sarcoidosis, etc.)
Medullary sponge kidney (cystic dilation of distal collecting ducts; may be unilateral or segmental).
Distal (type 1) renal tubular acidosis (RTA)
Furosemide therapy in a child.
106
Causes of cortical nephrocalcinosis?
```
Acute cortical necrosis
Chronic glomerulonephritis
Chronic transplant rejection
Hyperoxaluria
Alport Syndrome (hereditary nephropathy and deafness).
```
107
Renal Trauma Grading Scale
Grade I- Renal contusion or subcapsular hematoma.
Grade II- Superficial laceration (<1 cm) or confined perinephric hematoma, w/o urinary extravasation.
Grade III- deeper laceration (>1 cm) w/o urinary extravasation.
Grade IV- Deep laceration that etends into the collecting system (causing urinary extravasation), or injury to the renal artery or vein with contained hemorrhage.
Grade V- Shattered kidney, or avulsion of the renal hilum.
108
What is a Page Kidney?
Subcapsular hematoma compresses the renal parenchyma and decreases its blood flow. Increased renin secretion, which can lead to HTN.
109
What is the MC benign tumor of the ureter?
Fibroepithelial Polyp - affects proximal ureter. Features a long stalk and appears as an elongated smooth tubular lesion.
110
What is Ureteritis Cystica?
Benign response to chronic urinary tract inflammation, such as chronic infection or stone disease.
Several small subepithelial cysts are found unilateral in the proximal third of the ureter and renal pelvis.
Does not have malignant potential.
111
What is ureteral leukoplakia?
AKA squamous metaplasia- rare urothelial inflammatory condition named for the characteristic white patch that is produced. Not though to be premalignant in the renal collecting system.
112
Multifocal ureteral stenosis are suggestive of?
Ureteral TB.
113
DDx of ureteral filling defect?
```
Ureteral malignancy- TCC is MC
Ureteral calculus- almost always visible on pre-contrast images.
Blood clot
Malacoplakia (multiple flat defects)
Leukoplakia
Infectious debris
Sloughed renal papilla
Benign ureteral mass (e.g., fibroepithelial polyp)
```
114
What is Malacoplakia?
Inflammatory condition associated with chronic urinary tract infection (usually E. coli) that is typically seen in middle-aged women. Not premalignant.
Multiple flat filling defects that characteristically involve the distal ureter.
115
Difference between orthotopic and ectopic ureterocele?
Orthotopic- normally inserting ureter
Ectopic- in setting of duplicated collecting system, with ectopic insertion of the upper pole ureter into the bladder, and is usually diagnosed in children.
116
What is a pseudoureterocele?
Intussusception of the distal ureter into the bladder, which may be due to tumor, radiation cystitis, or ureterovesicular junction stone.
117
What is bladder adenocarcinoma?
Rare but is associated with a urachal remnant.
MC bladder tumor is TCC.
118
MC type of bladder rupture?
Extraperitoneal - more commonly associated with pelvic fractures - direct laceration.
119
What are the sections of the male urethra?
```
Prostatic urethra (posterior)
Membranous urethra (posterior)
Bulbous urethra (anterior)
Penile urethra (anterior)
```
120
What is the Prostatic Urethra?
Posterior urethra
Courses within the prostate and is lined with transitional epithelium.
The verumontanum is a prominent ridge of smooth muscle in the posterior portion of the prostatic urethra, and is the site of the paired ejaculatory duct orifices. Site of obstruction in posterior urethral valves in children.
The prostatic utricle is a Mullerian duct derivative and is the blind-ending male homologue of the uterus and vagina, which is also located at the verumontanum.
121
What is the verumontanum?
The verumontanum is a prominent ridge of smooth muscle in the posterior portion of the prostatic urethra, and is the site of the paired ejaculatory duct orifices. Site of obstruction in posterior urethral valves in children.
The prostatic utricle is a Mullerian duct derivative and is the blind-ending male homologue of the uterus and vagina, which is also located at the verumontanum.
122
What is the site of obstruction in posterior urethral valves in children?
The verumontanum
123
What is the prostatic utricle?
The prostatic utricle is a Mullerian duct derivative and is the blind-ending male homologue of the uterus and vagina, which is also located at the verumontanum.
124
What is the membranous urethra?
Posterior urethra.
Shortest, least mobile urethral segment.
Contained within the urogenital diaphragm, which contains the external urethral sphincter and the paired Cowper's glands.
125
What is the Bulbous Urethra?
Anterior urethra
Site of drainage of the Cowper's glands
126
Site of drainage of the Cowper's glands?
Bulbous urethra
127
What is the penile urethra?
Longest urethral segment, lined by squamous epithelium.
Fossa navicularis is the dilated distal portion at the glans penis.
The glands of Littre are small mucous glands of the penile urethra. Tend to opacify more prominently when inflamed in the setting of urethritis.
128
What are the glands of Littre?
The glands of Littre are small mucous glands of the penile urethra. Tend to opacify more prominently when inflamed in the setting of urethritis.
129
MC cause of urethral strictures?
STDs- gonorrhea.
Occur MC in the bulbous urethra.
130
MC site of urethral strictures?
Bulbous urethra with both infectious and traumatic.
131
MC type of urethral injury?
Type III.
Disruption of the urogenital diaphragm and rupture of the bulbomembranous urethra.
Contrast extravasates both into the pelvis and out into the perineum.
132
Female equivalent of the prostate?
Skene glands.
133
Site of BPH?
Transitional Zone - around the urethra.
134
Where do 70% of prostate cancers arise?
Peripheral zone
135
What are the two components of the prostate that can be resolved on MRI?
Peripheral Zone and Central Gland
Central gland refers to both the central zone and transition zone - transitional zone is around the urethra.
In younger men, the central gland is composed mostly of the central zone; however, the transition zone enlarges as benign prostatic hyperplasia develops. These changes result in the central gland becoming predominantly composed of transition zone in older males.
136
DDx of prostate peripheral zone T2 hypointensity?
Prostate Cancer
Prostatitis
Hemorrhage
Involutional changes from Androgen-deprivation therapy
137
What will MRI spectroscopy of prostate cancer show?
Elevated choline and depressed citrate peaks compared to normal prostate.
138
What is the role of MRI in prostate cancer?
Distinguish between surgical and nonsurgical disease. Cancer that is contained within the gland (tumor stage T2) is generally amenable to radical prostatectomy, while cancer that has spread outside of the gland (T3 and above) is typically treated non surgically (e.g., anti androgen and radiation therapy).
139
T staging of prostate cancer?
T1: Tumor apparent by biopsy only.
T2: Tumor confined within the prostate.
T2a: <50% of one lobe;
T2b: >50% of one lobe;
T2c: Tumor involves both lobes.
T3: Tumor extends through the prostate capsule. May involve seminal vesicles.
T4: Tumor invades adjacent structures other than seminal vesicles.
140
What is the normal zonal anatomy of the uterus on T2?
Endometrial stripe: hyperintense on T2
Junctional Zone (first zone of myometrium): T2 hypointense - due to extremely compact smooth muscle, should be <12 mm - thickening can be seen in adenomyosis
Outer myometrium: relatively T2 hypointense, although less than junctional zone.
141
Normal size of the endometrial stripe?
T2 hypointense due to compact smooth muscle
Should be <12 mm - thickening can be seen in adenomyosis.
142
What is Adenomyosis?
Ectopic endometrial glands within the myometrium. In contrast to endometriosis, the ectopic endometrial tissue seen in adenomyosis is nonfunctioning.
Can present with similar symptoms to leiomyomas, with pain and bleeding.
Best seen on T2-weighted images as a thickened junctional zone (>12 mm), often with multiple small foci of T2 hyperintensity. Borderline thickening of the junctional zone (8–12 mm) may be due to adenomyosis, but is not diagnostic of the condition.
Focal adenomyosis may mimic a leiomyoma, but features indistinct margins incontrast to a leiomyoma.
143
What is the MC female gynecologic malignancy?
Endometrial carcinoma
144
Function of MRI for endometrial cancer?
Extent of myometrial invasion.
In a premenopausal patient, an intact junctional zone confirms that there is no myometrial invasion. The junctional zone cannot be distinguished in post menopausal patients, however. The depth of myometrial invasion highly correlates with the presence of lymph node metastasis
Post-contrast images demonstrate the tumor with the highest conspicuity, as endometrial cancer enhances less avidly than the surrounding myometrium.
145
Staging of endometrial cancer
Stage I: Tumor confined to the uterus. Stage IA: <50% of myometrial invasion; stage IB: >50% myometrial invasion.
Stage II: Spread to the cervical stroma, but tumor still contained within the uterus. Involvement of the endocervical glands only is stage I.
Stage III: Spread to adnexa or uterine serosa (IIIA), vagina (IIIB), pelvic lymph nodes (IIIC1), or para-aortic lymph nodes (IIIC2). Prognosis is worse with para-aortic nodes, even in the absence of pelvic adenopathy.
Stage IVA: Spread to bladder or bowel mucosa.
Stage IVB: Distant metastases or inguinal lymph node spread.
146
Normal cervical anatomy on T2
Endocervical canal: T2 hyperintense due to mucin, analogous to uterine endometrium.
Cervical mucosa: Intermediate T2 signal intensity.
Inner cervical stroma: Very hypointense on T2, analogous to the uterine junctional zone. Unlike the uterine junctional zone, however, the decreased T2 signal is due to compact fibrous tissue, not smooth muscle. The superior aspect of the inner cervical stroma is continuous with junctional zone of the uterus.
147
Staging of cervical cancer
Stage I: Confined to cervix or uterus.
IA: Microscopic lesion.
IB: Clinically visible lesion.
Stage IIA: Spread to upper 2/3 vagina, without parametrial invasion. Typically treated surgically.
Stage IIB: Parametrial invasion. Typically treated non-surgically (e.g., brachytherapy).
Stage IIIA: Spread to lower vagina.
Stage IIIB: Pelvic sidewall extension, hydronephrosis, or pelvic nodal involvement.
Stage IVA: Spread to bladder or rectum; Stage IVB: Distant metastasis.
148
What are the MC uterine anomalies?
Septate and bicornuate uterus
149
What is a Septate Uterus?
Caused by incomplete resorption of the septum of fused Müllerian ducts.
Single external fundus but a fibrous or muscular septation dividing two endometrial canals.
Infertility is more common in women with septate uterus compared to bicornuate uterus. Metroplasty (resection of the septum) can be performed hysteroscopically if the septum is fibrous, or via an open approach if the septum is muscular.
150
Infertility is more common in women with bicornuate or septate uterus?
Septate
151
What is a bicornuate uterus?
Due to incomplete fusion of the Müllerian ducts.
Partially split uterus with two separate uterine fundi. In contrast to a septate uterus, the fundus of a bicornuate uterus pinches inwards >15 mm.
If treated, metroplasty must be performed transabdominally, which is a more invasive procedure compared to hysteroscopic metroplasty.
152
MRI findings of endometriosis
Multiple hyperintense masses on T1-weighted images, which demonstrate shading (a gradient of signal intensity) on T2-weighted images. Endometriosis does not suppress on fat saturated sequences. Less commonly, endometriosis may appear hyperintense on both T1- and T2-weighted images
Tiny hemorrhagic endometrial implants may only be apparent as tiny hyperintense foci on T1-weighted images
Laparoscopy is the gold standard for evaluation of suspected endometriosis.
153
Utility of MRI for ovarian cancer
Characterize intermediate adnexal masses, rather than for staging.
Presence of a solid enhancing component, intra lesional necrosis, ascites, or peritoneal nodularity suggests a malignant lesion, although no finding is 100% specific
MRI is highly sensitive to detect peritoneal implants, which occur most commonly in the pouch of Douglas, paracolic gutters, bowel surface, greater omentum, and liver surface.
154
Types of ovarian cancer
Epithelial (90%), germ cell, sex-cord stromal, or metastatic in origin
155
Types of epithelial ovarian cancer.
90%
Serous tumors are the most common epithelial subtype, followed by mucinous, endometrioid, and clear cell
156
What is serous cysadenocarcinoma of the ovary?
MC epithelial subtype.
Frequently bilateral and typically appear as mixed solid and cystic masses. The solid portions demonstrate avid enhancement. There is often concomitant ascites.
157
What is Mucinous Cystadenocarcinoma of the ovary?
Large, most commonly unilateral, and occur in older patients compared to serous cystadenocarcinomas.
Mucinous cystadenocarcinomas typically present as a multiloculated cystic mass containing mucin-rich T1 hyperintense fluid.
158
Subtypes of ovarian cancer associated with endometriosis?
Clear cell carcinoma and less commonly endometrioid carcinoma.
159
What are the malignant germ cell ovarian tumors?
Dysgerminoma, endodermal sinus tumor, and immature teratoma.
160
What are the sex-cord stromal ovarian tumors?
```
Granulosa cell (hormonally active) and Sertoli–Leydig
(rare).
```
