GU Flashcards
Fetal lobulation
he fetal kidneys are subdivided into lobes that are separated with grooves. Sometimes this lobulation persists into adult life.
Fetal Lobulation VS Scarring:
Lobulation = Renal surface indentations overlie the space between the pyramids
Scarring = Renal surface indentations overlie the medullary pyraminds
Dromedary Hump
Focal bulge on the left kidney, which forms as the result of adaptation to the adjacent spleen.
Renal Agenesis
overview
- Congenital absence of one or both kidneys. If it’s unilateral this can be asymptomatic. If it’s bilateral think about the “Potter Sequence.” When it’s unilateral (it’s usually sporadic), for the purpose of multiple choice think about associated GYN anomalies in women (70% of women with unilateral renal agenesis have associated genital anomalies - unicornuate uterus). With regard to men, 20% with renal agenesis have absence of the ipsilateral epididymis and vas deferens or have an ipsilateral seminal vesicle cyst.
Renal Agenesis
associations
Ipsilateral seminal vesicle cysts, absent ipsilateral ureter, absent ipsilateral hemitrigone and absent ipsilateral vas deferens.
Potter Sequence:
Insult (maybe ACE inhibitors) = kidneys don’t form, if kidneys don’t form you can’t make piss, if you can’t make piss you can’t develop lungs (pulmonary hypoplasia).
Mayer-Rokitansky-Kuster-Hauser:
Mullerian duct anomalies including absence or atresia of the uterus. Associated with unilateral renal agenesis.
Lying Down Adrenal or “Pancake Adrenal” Sign
describes the elongated appearance of the adrenal not normally molded by the adjacent kidney. It can be used to differentiate surgically absent vs congenitally absent.
Corticomedullary Phase (CMP)
angio nephrographic - i f you
wanna sound like a pretentious prick
25- 40 Seconds
Contrast in the vascular system and the extracellular interstitial space
Cortex is enhanced the medulla is not (hence the name).
Utility:
• Characterizing renal tumor enhancement (relative to the cortex
—• clear cell similar to cortex,
— papillary less than cortex)
- Evaluation of renal arteries and veins
- Optimal phase to detect tumor invasion of the renal veins (important for staging / treatment planning)
Phase can be delayed (last longer) if the kidnevs are shit (failure, renal artery stenosis), obstructed, or in the setting of cardiac failure.
Corticomedullary Phase (CMP)
angio nephrographic - i f you
wanna sound like a pretentious prick
25- 40 Seconds
Contrast in the vascular system and the extracellular interstitial space
Cortex is enhanced the medulla is not (hence the name).
Utility:
• Characterizing renal tumor enhancement (relative to the cortex
—• clear cell similar to cortex,
— papillary less than cortex)
- Evaluation of renal arteries and veins
- Optimal phase to detect tumor invasion of the renal veins (important for staging / treatment planning)
Phase can be delayed (last longer) if the kidnevs are shit (failure, renal artery stenosis), obstructed, or in the setting of cardiac failure.
Nephrographic phase (NP)
70-180 Seconds
Contrast makes its way through the loops of Henle and the collecting tubules (“gets filtered”! Fairly unifonn enhancement of the cortex and medulla
Utility:
• Detect renal tumors
• Especially useful for small / central tumors
Excretory phase (EP)
180 Seconds - 8 Mins
Contrast is excreted into the urinary tract /collecting system
Progressive decrease in the nephrogram (depending on the timing of the exam)
Utility:
• Evaluated morphology of the papilla (necrosis etc…)
• Evaluate for urothelial cell / TCC lesions
Renal Cell Carcinoma
Overview
The most common primary renal malignancy. RCC till proven otherwise: (a) Enhances with contrast (> 15 HU), (b) calcifications in a fatty mass. Risk factors include tobacco use, syndromes like VHL, chronic dialysis (> 3years), family history. These dudes make hypervascular mets. They are ALWAYS lytic when they met to the bones.
Renal Cell Carcinoma
timing
Nephrogram phase
(80 seconds) =
Most sensitive for
detection o f RCC
Renal Cell Carcinoma
pseudoenhancement
A less than 10 HU increase in attenuation is considered within the technical limits of the study and is not considered to represent enhancement. More rare once a cyst is larger than 1.5 cm.
Renal Cell Carcino
can it have fat
Oh yeah, for sure -especially clear cell. This leads to the potential sneaky situation of a fat containing lesion in the liver (which can be a RCC met). Now to make this work they’d have to tell you the patient had RCC - or show you one. A helpful hint is that RCCs with macroscopic fat nearly always have some calcification/ossification - if they don’t it’s probably an AML.
Renal Cell Carcinoma
clear cell
Most common subtype in the general population. This is also the one associated with VHL. It is typically more aggressive than papillary, and will enhance equal to the cortex on corticomedullary phase. The most classic look is a cystic mass with enhancing components.
Renal Cell Carcinoma
papillary
This is the second most common type. It is usually less aggressive than clear cell (more rare subtypes can be very aggressive). They are less vascular and will not enhance equal to the cortex on corticomedullary phase. They also are in the classic T2 dark differential (along with lipid poor AML and hemorrhagic cyst). Risk of primary renal malignancy in the transplanted kidney is six times that of the regular Joe. A point of testable trivia is that these cancers are usually papillary subtypes.
Renal Cell Carcinoma
medullary
Associated with Sickle Cell Trait. It’s highly aggressive, and usually large and already metastasized at the time of diagnosis. Patient’s are usually younger.
Renal Cell Carcinoma
chromophobe
All you need to know is that it’s associated with Birt Hogg Dube.
Conventional RCC Staging:
Stage 1: Limited to Kidney and < 7 cm Stage 2: Limited to Kidney but > 7 cm Stage 3: Still inside Gerota’s Fascia A: Renal Vein Invaded B: IVC below diaphragm C: IVC above diaphragm Stage 4: Beyond Gerota’s Fasica Ipsilateral Adrenal
Syndrome/Association
clear cell
Most common
VHL
Syndrome/Association
papillary
Hereditary appillary renal carcinoma
Transplant kindey
Syndrome/Association
chomophobe
birt hogg dube
Syndrome/Association
medullary
sickle cell trai
Does AD Polycystic Kidney Disease increase your risk for RCC
Well No, but sorta. The genetic syndrome does NOT intrinsically increase your risk. However, dialysis does. Who gets dialysis?? People with ADPKD. It would be such a crap way to ask a question -but could happen. If you are asked, I’m recommending you say no to the increased risk, - unless the question writer specifies that the patient is on dialysis.
Renal Lymphoma
overview
This can literally look like anything. Having said that the most common appearance is bilaterally, enlarged kidneys, with small, low attenuation cortically based solid nodules or masses (“infiltrative soft tissue in the renal hilum ”), and associated lymph nodes. A solitary mass is seen in about 1/4 o f the cases.
Renal Lymphoma
triiva
Out of all the renal masses - lymphoma is the most likely to preserve the normal reniform shape.
Renal Lymphoma
trivia 2
Lymphoma is the most common metastatic tumor to invade / infiltrate the kidneys
Renal Leukemia
The kidney is the most common visceral organ involved. Typically the kidneys are smooth and enlarged. Hypodense lesions are cortically based only, with little if any involvement o f the medulla.
Angiomyolipoma (AML)
thingks to know about them
(1) They are associated with Tuberous Sclerosis — Tuberous Sclerosis can be called Bourneville Disease (for the purpose o f fucking with you)
(2) They can bleed if they get big enough (> 4cm). It’s controversial if they grow or bleed more in pregnancy (if they ask you, I guess you should say yes - because that’s the old knowledge but some modem papers are saying not for sure).
(3) They should never have calcifications (that’s probably a RCC).
(4) They can be lipid poor (about 5% are), and those are T2 dark.
Angiomyolipoma (AML)
gamesmanship
Traditional Spectral Fat Sat or In and Out o f Phase (India Ink) can be used to suggest an AML. Just remember, rarely RCCs can have fat:
renal lesion with fat and calcs
RCC
renal lesion with fat and no calcs
AML
Oncocytoma
overview
This is the second most common benign
tumor (after AML). It looks a lot like a RCC, but has a
central scar 33% of the time (and 100% of the time on
multiple choice). There will be no malignant features (such
as vessel infiltration). They cannot be distinguished from
RCC on imaging and must be treated as RCC till proven
otherwise.
Oncocytoma
imaging
If they want to ask about an Oncocytoma they can show it 3 ways: (1) Solid Mass with central scar - CT or MRI, (2) “Spoke wheel” vascular pattern on US, (3) Hotter than the surrounding renal cortex - on PET CT.
Oncocytoma
gamesmanship
So if you are shown an enhancing renal mass with a central
scar, how do you decide if it’s a RCC or an oncocytoma? The
way to figure it out is simple - just read the mind of the person
who wrote the question. If it’s a practical type then all
enhancing renal masses are RCC till proven otherwise. If it’s
the academic type then central scar = oncocytoma. You may
also think… which of these two people is more likely to
volunteer to write board questions?
Oncocytoma
the pet trick
RCC is typically COLDER
than surrounding renal
parenchyma on PET,
Oncocytoma is typically
HOTTER than surrounding
renal parenchyma on PET,
Oncocytoma trivia
A syndrome associated with bilateral oncocytomas is Birt hogg dube
(they also get chromophobe RCC).
Multilocular Cystic Nephroma
overview
“Non-communicating, fluid-filled locules, surrounded by
thick fibrous capsule.” By definition these things arecharacterized by the absence of a solid component or
necrosis.
Multilocular Cystic Nephroma
buzzword
“protrudes into the renal pelvis.”
The question is likely the bimodal occurrence
(4 year old boys, and 40 year old women).
Multilocular Cystic Nephroma
funny
I like to think of this as the Michael Jackson lesion - it loves young boys and middle aged women.
**Remember this is the “older” nomenclature. It is not the preferred nomenclature dude.
Nerds mined my joke. Now these are “Adult MLCNs” and “Pediatric MLCNs.”
Multilocular Cystic Nephroma
funny
I like to think of this as the Michael Jackson lesion - it loves young boys and middle aged women.
**Remember this is the “older” nomenclature. It is not the preferred nomenclature dude.
Nerds mined my joke. Now these are “Adult MLCNs” and “Pediatric MLCNs.”
Retroperitoneum
ant post anatomy
It is bordered anterior by the anterior pararenal space (black arrows) and posterior by the transversalis fascia (white arrows).
Retroperitoneum
inferior anatomy
Below the level o f the kidneys, there is a blending of the fascial planes which allows for potential spread of
disease between the retroperitoneum and the pelvis. Illustrated with the light grey part (with the black arrows) demonstrating the inferior extension / communication of the retroperitoneum.
retroperitoneum anatomy trivia
The RP contains the lower esophagus, most of the duodenum, the ascending and descending colon, the kidneys, ureters, adrenals, pancreas (minus the tail), aorta, IVC, and the upper 2/3 o f the rectum.
The classic tricks for multiple choice are:
• The pancreatic tail is NOT being part of the RP.
• Lower 1/3 o f the rectum is NOT being part of the RP.
Retroperitoneum Pathology
~75% of the primary retroperitoneal neoplasms are malignant. Any tumor in this location is guilty until proven otherwise. Having said that, there is an enormous amount o f path
that can occur in this location — I’m gonna try and focus on what I think is probably the highest
yield. The chart on the following page does not include adrenal tumors - I’ll cover those in the
endocrine chapter (and peds). RP Fibrosis is mentioned briefly- it is discussed in detail later in
the chapter. Neurogenic tumors will be covered in the neuro chapter.
Retroperitoneum
Lipomatosis
Seen in big fat people - with the classic
history o f “ incomplete bladder emptying”
You can also see this in homeless people, who go to soup kitchens… that
specialize in ice cream soup.
Overgrowth o f benign fat in the pelvis classically perirectal and perivesicular
spaces.
The bladder is displaced anterior and superior - and is “pear shaped” or inverted tear drop shaped.
Retroperitoneum
Liposarcoma
Usually seen in the thigh o f an old person - but is also the most common primary malignant RP in adults.
These things are notorious assholes with a high rate (around 2/3) o f local recurrence — hence the endless surveillance studies you end up reading post treatment.
Don’t call it a comeback (I’ve been here for years - rocking my peers puttin’ suckers in fear). Also - Don’t call it a lipoma - no matter how simple and homogenous it looks.
The deeper a fat containing lesion is - the more likely it is to be a bad actor. Fat-containing retroperitoneal lesions should be thought o f like a male resident on the mammography service- guilty o f all crimes until proven innocent.
Anything that makes them look more complex - calcifications, solid components, not fat sating out - all that makes them even more likely to be bad (not just more likely to be a cancer, but more likely to metastasize).
If you see something you think is a giant fucking AML — but you aren’t totally sure it is coming from the kidney AND it has calcifications - you should think Liposarcoma.
Retroperitoneum
Rhabdomyosarcoma
Most common soft tissue sarcoma in children.
You see a soft tissue mass (in a kid) - you should always be thinking about this.
About h a lf o f them will be in the neck, and about 1/4 o f them in the pelvis around the bladder or testicles.
No surprise - it is gonna look like a
tumor. Heterogenous, enhancing, possibly destroying nearby bone.
Retroperitoneum
Extramedullary hematopoiesisq
Abnormal deposits o f hematopoietic tissue outside the bone marrow.
The look is super nonspecific - just a bunch o f soft tissue masses in the paravertebral region.
History is the only fair way to test this — they have to tell you (or somehow show you) that the patient has a history o f hemoglobinopathy, myelofibrosis, leukemia -
etc…
Retroperitoneum
lymphoma
The Most Common RP malignancy.
Tons o f Big Nodes or a Confluent Soft Tissue Mass. Classically people talk about NHL vs HL.
- NHL nodes are more likely to be larger, noncontinuous, and involve the mesentery.
- HL nodes are more likely to involve the paraaortic region early, and be more continuous
PET/CT is excellent for Lymphoma (in particular it is very useful for disease vs
treated residual scarring — with disease being FDG avid).
Retroperitoneum
Hemorrhage
Most Common Cause = Over-Anticoagulation (high PT/INR)
2nd Most Common Cause = Rupture / Leaking Aorta
3rd Most Common Cause = Bleeding RCC or AML
Retroperitoneum
“Mantle Like Soft Tissue Mass Around the Aorta , IVC, and/or Ureters”
ddx
Lymphoma
Rf fibrosis
erheim chester
“Mantle Like Soft Tissue Mass Around the Aorta , IVC, and/or Ureters”
lymphoma
can displace the aorta forward, and be sen above the renal arteries. tends to push things rather than tether and obstruct
“Mantle Like Soft Tissue Mass Around the Aorta , IVC, and/or Ureters”
rp fibrosis
like lymphom rpf can be hot on pet. it does no usually displace the aorta anterio, is uncommon above the renal arteries and tends to tether and obstruct
“Mantle Like Soft Tissue Mass Around the Aorta , IVC, and/or Ureters”
erheim chester
huge zebra. gamesmanship would be to show you plain films of legs with bilateral symmetric sclerosis of the metaphysis (sparing the epiphysis)
Bosniak Cyst Classification:
Class 1: Simple - less than 15 HU with no enhancement
‘Class 2: Hyperdense (< 3 cm). Thin calcifications, Thin septations
‘Class 2F: Hyperdense (> 3 cm). Minimally thickened calcifications (5% chance cancer)
‘Class 3: Thick Septations, Mural Nodule (50% chance cancer)
‘Class 4: Any enhancement (>15 HU)
Hyperdense renal cysts
Basically, if the mass is greater than 70 HU and homogenous, it’s benign (hemorrhagic or proteinaceous cyst) 99.9% of the time.
ADPKD
Kidneys get
progressively larger and lose function (you get dialysis by the 5th decade). Hyperdense
contents & calcified wall are frequently seen due to prior hemorrhage. What you need to
know is: (1) it’s Autosomal Dominant “ADult”, (2) They get cysts in the liver 70% o f the
time, (3) they get seminal vesicle cysts (some sources say 60%), and (4) they get Berry
Aneurysms. As mentioned before, they don’t have an intrinsic risk o f cancer, but do get
cancer once they are on dialysis.
ARPKD
h e s e guys
get HTN and renal failure. The liver involvement is different than the adult form. Instead of
cysts they have abnormal bile ducts and fibrosis. This congenital hepatic fibrosis is
ALWAYS present in ARPKD. The ratio o f liver and kidney disease is inversely related. The
worse the liver is the better the kidneys do. The better the liver is, the worse the kidneys do.
On ultrasound the kidneys are smoothly enlarged and diffusely echogenic, with a loss of
corticomedullary differentiation.
Lithium Nephropathy
Occurs in patients who take lithium long term. Can lead to
diabetes insipidus and renal insufficiency. The kidneys are normal to small in volume
with multiple (innumerable) tiny cysts, usually 2-5 mm in diameters. These “microcysts”
are distinguishable from larger cysts associated with acquired cystic disease o f uremia.
They are probably going to show this on MRI with the history o f bipolar disorder.
Uremic Cystic Kidney Disease
About 40% o f patients with end stage renal
disease develop cysts. This rises with duration o f dialysis and is seen in about 90% in
patients after 5 year of dialysis. The thing to know is: Increased risk of malignancy with
dialysis (3-6x).
Uremic Cystic Kidney Disease
trivia
The cysts will regress after renal transplant.
Von Hippel Lindau
Autosomal dominant multisystem
disorder. 50-75% have renal cysts. 25-50% develop RCC (clear cell).
* Pancreas: Cysts, Serous Microcystic Adenomas, Neuroendocrine (islet cell) tumor
* Adrenal: Pheochromocytoma (often multiple)
* CNS: Hemangioblastoma of the cerebellum, brain stem, and spinal cord
ADPKD vs VHL vs Acquired kidney cysts
ADPKD Cysts in Liver Kidneys are BIG
VHL Cysts in Pancreas
Acquired (Uremic) Kidneys are small
Tuberous Sclerosis
kidneys
Autosomal dominant multi-system
disorder. You have hamartomas everywhere (brain, lung, heart,
skin, kidneys). The renal findings are multiple bilateral
angiomyolipomas. They also have renal cysts, and occasionally
RCC (same rate as general population, but in younger patient
population).
Tuberous Sclerosis
other organs
- Lung - LAM - thin walled cysts and chylothorax
- Cardiac - Rhabdomyosarcoma (typically involve cardiac septum)
- Brain - Giant Cell Astrocytoma, Cortical and subcortical tubers, subependymal nodules
- Renal - AMLs, RCC (in younger patients)
T2 dark renal cyst ddx
Lipid poor aml
hemorrhagic cyst
papillary subtype RCC
Renal MR
Lipid Poor AML
• A small percentage of AMLs are lipid poor in the general population.
• For the purpose of multiple choice - If you see a lipid poor AML (especially if you see a bunch of them)
you need to think about Tuberous Sclerosis - about 30% of their AMLs are lipid poor.
Renal MR
Hemorrhagic cyst
These will likely be T1 bright
Renal MR
Papillary subtype RCC
Dark on T2
- Remember that clear cells (the most common sub-type) are T2 HYPER Intense.
- Both Clear Cell and Papillary will enhance, - but the clear cell enhances more avidly (equal to cortex on cortico-medullary phase).
Multicystic Dysplastic Kidney:
overview
this is the situation where you have multiple tiny cysts forming in utcro from some type of insult.
Multicystic Dysplastic Kidney:
what you should know
- “No functioning renal tissue, ” - shown with MAG 3 exam.
- Contralateral renal tract abnormalities occur like 50% of the time. Typically you think of reflux (VUR) and UPJ Obstructions
THIS vs THAT: MCDK vs Bad Hydro
In hydronephrosis, the cystic spaces are seen to communicate.
In difficult cases renal scintigraphy can be useful. MCDK will show no excretory function.
THIS vs THAT: Peripelvic Cyst vs Parapelvic Cyst
Para (beside): Originates from parenchyma, may compress the collecting
system. These look a lot like the cortical cysts that you see all the time, but
instead of bulging out - they bulge in.
Peri (around): Originates from renal sinus, mimics hydro. If you didn’t
have a pyelogram (delayed) phase - might be tricky to tell apart.
Striated Nephrogram DDx
- Acute ureteral obstruction
- Acute pyelonephritis
- Medullary sponge kidney
- Acute renal vein thrombosis
- Radiation nephritis
- Acutely following renal contusion
- Hypotension (bilateral)
- Infantile polycystic kidney (bilateral)
Pyelonephritis
This is a clinical diagnosis.
However you do end up diagnosing it. It’s
associated with stones. The most common organism
is E. Coli. In acute bacterial nephritis, alternating
bands of hypo and hyperattenuation (striated
nephrogram) are seen. These wedge shaped areas
are related to decreased perfusion. Perinephric
stranding is also commonly seen.
Renal abscess
Pyelo may be complicated by abscess, which can
present on CT as round or geographic low attenuation collections that
do not enhance centrally, but do have an enhancing rim. Bigger than
3cm and these guys might visit the IR section for drainage.
Chronic Pyelonephritis
Sort of a controversial entity. It is not clear whether the
condition is an active chronic infection, arises from multiple recurrent infections, or represents
stable changes from a remote single infection. The imaging findings are characterized by renal
scarring, atrophy and cortical thinning, with hypertrophy o f residual normal tissue. Basically,
you have a small deformed kidney, with a bunch of wedge defects, and some hypertrophied
areas.
Emphysematous Pyelonephritis
This is a life
threatening necrotizing infection characterized by gas formation
within or surrounding the kidney. What you need to know:
(1) it’s really bad, (2) diabetics almost exclusively get it,
(3) echogenic foci with dirty shadowing on ultrasound. If there is air
in the peri-nephric space , that is associated with a miserable shit
outcome.
Next Step:
• Urgent Antibiotics followed by Nephrectomy
Emphysematous Pyelitis
This is less bad relative to emphysematous pyelonephritis.
The gas is localized to the collecting system. It’s more common in women, diabetics, and people
with urinary obstruction. Radiographic finding is gas outlining the ureters and dilated calices.
Pyonephrosis
An infected or obstructed collecting system (which
is frequently enlarged). Can be from a variety o f causes; stones, tumor,
sloughed papilla secondary to pyelonephritis. Can totally jack your
renal function if left untreated. Fluid-Fluid level in the collecting
system can be seen on US. CT has trouble telling the difference
between hydro and pyonephrosis.
Next Step:
• Urgent Decompression (Nephrostomy)
Xanthogranulomatous
Pyelonephritis (XGP)
chronic
destructive granulomatous process that is
basically always seen with a staghom stone
acting as a nidus for recurrent infection. You
can have an associated psoas abscess with
minimal perirenal infection. It’s an Aunt
Minnie, with a very characteristic “Bear Paw”
appearance on CT. The kidney is not
functional, and sometimes nephrectomy is
done to treat it.
Papillary Necrosis
This is ischemic necrosis of the renal papillae, most
commonly involving the medullary pyramids.
Diabetes is the most common cause.
Other important causes include: pyelonephritis
(especially in kids), sickle cell, TB, analgesic use, and
cirrhosis.
Filling defects might be seen in the calyx.
The appearance o f a necrotic cavity in the
papillae with linear streaks o f contrast
inside the calyx has been called a “lobster
d aw sign. ”
Papillary necrosis
trivia
50% of sickle cell patients develop
papillary necrosis
Renal TB
overview
The most common extra-pulmonary site of infection is
the urinary tract. TB in the kidneys is similar to TB in the
lungs with prolonged latency (years after exposure) and
“reactivation.” You could be shown imaging findings that
occur along a spectrum of severity. For the purpose of
multiple choice strategy the more severe disease would lend
itself better to imaging, and the less severe findings would
be more likely to be asked as trivia questions.
Renal TB
imaging
Calyceal blunting (“moth eaten calices”) is the earliest finding. Remember the normal calyx should have a “gentle cup shape” — not all pointy and shit.
Distortion o f the calyx / papillary necrosis will result in
deep cups, and “w” shaped central necrosis patterns.
This is nonspecific - ischemia, diabetes, lots of things can do this
- but it is the “earliest described sign” which makes it testable.
Renal calcifications, which are very common with TB, can be
punctate, curvilinear, or replace the entire kidney. This
extensive calcification is a classic (and very testable) look for
TB - called the “Putty Kidney” - or an autonephrectomized end
stage TB kidney.
Another nonspecific finding - that can help you zero in on the
choice of TB is the presence of multiple calcified mesenteric
lymph nodes — arrows in my cartoon. Calcified adrenal glands
could also be seen.
Renal TB
imaging progression
Normal
calyx distortion/papillary necrosis
progressed necrosis leading to cavity formation. this is the most characteristic sign of renal TB
Focal stenosis of an infundibulum can result in the absence of opacification fo the calyx (phantom calyx)
Infundibulu mstenosis can also be diffuse and result in caliectasis. scarring at the renal pelvis can cause an uplifed appearance and the classic kerr kink at the renal pelvix
ureteral stenosis can cause generalized hydronephrosis
HIV Nephropathy-
overview
This is the most common cause o f renal impairment in AIDS
(CD4 < 200) patients. Although the kidneys can be normal in size, they are classically
enlarged, and bright (echogenic). Some sources will go as far as saying that normal
echotexture excludes the disease (this entity is essentially always is bright). Loss of the renal
sinus fat appearance has also been described (it’s edema in the fat, rather than loss o f the
actual fat).
HIV Nephropathy-
just think
BIG and BRIGHT kidney in HIV positive patient who is clinically in nephrotic
syndrome (massive proteinura).
HIV Nephropathy-
gamesmanship
To show you the kidney is big (longer than 12 cm) they will have
to put calibers on the kidney. Calibers on anything should be a clue that the size
being displayed is relevant.
HIV Nephropathy-
final diagnosis
via biopsy o f the big bright kidney.
Disseminated PCP
renal
n HIV patients can result in punctate (primarily cortical)
calcifications.
CIN
• Allergic reactions are a NOT considered a risk factor for CIN.
• “Risk Factors” for CIN include pre-existing renal insufficiency, diabetes mellitus (even more so with pre-existing renal insufficiency), cardiovascular disease with CHF, dehydration, and myeloma.
• Hydration via IV with 0.9% normal saline 6-12 hours before and continuing 4-12
hours after contrast administration supposedly decreases the incidence o f CIN in patients with chronic renal insufficiency (true mechanism is diluting Cr levels). Oral hydration has been shown to not work as well.
Kidney stones
types
There are several different stone types. The most likely testable trivia for each is:
- Calcium Oxalate - By far the most common type (75%)
- Struvite Stone - More common in women and associated with UTI
- Uric A c id - “Unseen” on x-ray.
- Cystine - Rare and associated with congenital disorders of metabolism
- Indinavir - Stones in HIV patients which are the ONLY stones NOT seen on CT.
Kidney stones
size matters
- Stones measuring 5 mm or smaller have a high likelihood of spontaneously passing.
- Stones measuring 1 cm or larger have a high likelihood of NOT passing spontaneously.
Kidney stones
composition (uric acis vs not uric acid)
Uric acid stones very rarely will require any kind of invasive intervention (lithotripsy,
etc…). The reason is they are very pH dependent. Big Fat People and/or diabetics tend to
have more acidic urine (from all that Mountain Dew) which leads to an increase in uric
acid stones. They can be treated with medical therapy (potassium citrate or sodium
bicarbonate) to increase the pH and melt the stones. You can’t melt a calcium stone by
messing with the pH.
Kidney stones
diagnosis of uric acid stones
Since identification of a uric acid stone is going to change management that makes it a target for trivia on multiple choice. There are 2 things that I would know:
(1) Uric Acid Stones tend to have lower attenuation (< 500 HU).
(2) Uric Acid Stones will have little if any change in H.U. with dual energy CT. The reason is they are composed of “light elements.” The larger atoms (Calcium, Phosphorous, Magnesium, and Sulfur) tend to have a larger change - which is the basis of dual energy CT (80 kv, and 140 kv) identification of stone composition.
Kidney stones
trivia
Trivia: Non Uric Acid Stones will have higher HU at 80 kVp relative to 140 kVp.
Trivia: Uric Acid Stones will be very similar at 80 kVp relative to 140 kVp. *If they do show a small change it will be the opposite - with a slightly higher HU at 140 kVp.
Trivia: Calcium stones are going to show the biggest HU change between high and low energies. In general, low/high energy ratios are going to be around 1.1 for uric acid, 1.25 for cystine, and > 1.25 for calcium.`
Cortical Nephrocalcinosis
This is typically the sequela of cortical necrosis, which can be seen after an acute drop in blood pressure (shock, postpartum, bum patients, etc...).
It starts out as a hypodense nonenhancing
rim that later
develops thin calcifications.
Mimic is disseminated PCP.
Also remember TB can have a
variable calcification pattern as
discussed earlier in the chapter.
Medullary Nephrocalcinosis
Hyperechoic renal papilla / pyramids which may or may not
shadow.
Causes:
• Hyperparathyroidism - Most people will say this is the most common.
• Medullary Sponge Kidney - Some people will say this is the most common.
• Lasix - Common cause in children.
• Renal Tubular Acidosis (distal subtype - type 1)
Trivia: RTA and Hyper PTH - tend to cause a more dense calcification that medullary sponge.
Medullary sponge kidney
A congenital cause of medullary nephrocalcinosis (usually
asymmetric). The underlying mechanism is a cystic
dilation of the collecting tubules of the kidney - so the
testable association with Ehlers-Danlos makes sense. The
association with Carolis also sorta makes sense. The
association with Beckwith-Wiedemann doesn’t really make
sense (and therefore is the most likely to be tested).
Think about medullary sponge kidney with unilateral less
dense medullary’ nephrocalcinosis.
Page Kidney
This is a subcapsular hematoma which
causes renal compression and complex fuckery with the renin-angiotensin system. The result is hypertension.
The capsule is the real issue here. That
capsule is tough and won’t expand so the hematoma puts the squeeze on the “meat” of the kidney. You could never get a “pagepancreas” because the pancreas has no capsule. This is the same reason why resistive indices are worthless in a pancreas Subcapsular Hematoma + HTN = Page(no capsule) but sometimes useful in a kidney (which has a capsule).
Subcapsular Hematoma + HTN
Page
Page kidney classic clinical history
htn post biopsy lithotripsy or trauma
Delayed Nephrogram
One kidney enhances and the other doesn’t (or does to a lesser
degree). Basically this is happening from pressure on the kidney, either extrinsic from a
Page kidney situation, or intrinsic from an obstructing stone.
Persistent Nephrogram
This is seen with hypotension/shock and ATN. They can show
this two ways, the first would be on a plain film of the abdomen (with dense kidneys), the
second would be on CT. The tip offs are going to be that they tell you the time (3 hours
etc…) and it’s gonna be bilateral.
Renal Infarct
overview
So wedge shaped hypodensities in the kidney can be seen with lots o f stuff (infarct, tumor,
infection, etc…)- Renal infarcts are most easily identified on post contrast imaging in the
cortical phase. If the entire renal artery is out, well then it won’t enhance (duh).
Renal Infarct
cortical rim sign
which is absent
immediately after the insult, but is seen 8 hours
to days later. You have a dual blood supply,
which allows the cortex to stay perfused.
Renal Infarct
flip flop enhancement
can be seen
where a region o f hypodensity / poor
enhancement on early phases becomes
relatively hyperdense on delayed imaging.
Renal Vein Thrombosis
Numerous causes; including dehydration, indwelling umbilical venous catheters (most
common in neonates), and nephrotic syndrome (most common in adults). This can mimic a
renal stone; presenting with flank pain, an enlarged kidney, and a delayed nephrogram.
On Doppler they are going to show you Reversed arterial diastolic flow and absent venous
flow.
T r a n s p l a n t
kidney overview
Renal transplant is the best treatment for end stage renal disease, and the quality of life is
significantly better than that of a long term dialysis patient (which fucking sucks !!!). The
transplanted kidney is most commonly placed in the extraperitoneal iliac fossa so that the
allograft can be anastomosed with the iliac vasculature and urinary bladder.
The way they do this surgery depends on where the kidney comes from (living vs cadaveric). The
main thing to know is that a kidney “harvested” from a hobo found floating in the river will have
not only the kidney and renal artery removed but also a segment of the aorta - that can be used for
end-to-side anastomosis to the recipient external iliac artery. In a living donation they aren’t gonna
carve on the aorta (cuz you need your aorta to live). In both cases, end to side anastomosis is
preferred for the vein and artery - typically to the external iliac vein and artery (although you can
see the internal iliac used in some situations).
transplant normal kidney flow
The superficial location of the transplant in the iliac fossa makes ultrasound the
modality of choice for evaluation. A transplant kidney is just like a native kidney. It should
have low resistance (it’s always “on”). The upstroke should be brisk, and the flow in diastole
forward (remember it’s always “on”).
Understanding renal RIs
There are two major points to know first when thinking about RIs. The first is the kidney has
a capsule, and that capsule is unforgiving (it believes in nothing Lebowski). The second is a
sick kidney is a swollen kidney.
Peak Systolic - End Diastolic “lowest diastolic”
Now lets look at this formula: ™ =
Peak Systolic
If the meat (parenchyma) of the kidney
is sick and swollen, but can’t expand
because it is wrapped in a tight
unforgiving capsule you can imagine
the blood vessels going through that
kidney are going to get the squeeze.
You can also probably imagine that the
passive diastolic flow would be more
impaired (compared to the active
systolic flow) by this squeeze.
If the meat of the kidney becomes
“sick” from whatever the cause might
be (rejection, infection, inflammation,
etc…) it swells increasing resistance.
RI’s should stay below 0.7. The higher the RI the sicker the kidney. This is why RIs are useful,
and this is why an upward trend in RI is worrisome. It is important to remember, RIs are not
specific since elevation occurs with basically every pathology. For the purpose of multiple
choice, you should never use elevated RIs to exclude answers (unless the answer is normal).
Elevation in RIs does tell you something is wrong, especially if there is an upward trend.
Urologic complication in transplant kidney
Obstruction
The ureter must also be surgically implanted (ureteral neocystostomy to the bladder
dome). Just like in a native kidney the ureter can get obstructed. Don’t be fooled by the ultimate asshole trick o f
showing you mild hydro on a transplant (especially one with normal labs) and trying to get you to call obstruction.
Transplanted kidneys pretty much all have some mild hydro - this is related to denervation o f the transplant, and
floppy tone to the ureter. If there is a true obstruction it is usually at the site o f ureteral implantation to the bladder.
The common causes are post operative edema, scarring, or technical errors leading to kinking. Stones, clots, etc.. are
less common. Having said that - transplants are more likely to have stones compared to the general population - it is
just that other stuff (edema, scar, kink , e tc … is more common).
Urologic complication in transplant kidney
hematoma
Common immediately post op. Usually resolves spontaneously. Large hematoma can produce
hydro. Acute hematoma will be echogenic, and this will progressively become less echogenic (with older
hematomas more anechoic and septated).
Urologic complication in transplant kidney
urinoma
This is usually found in the first 2 weeks post op. Urine leak or urinoma will appear as an
anechoic fluid collection with no septations, that is rapidly increasing in size. Most leaks (urine extravasation)
are going to be at the ureterovesical anastomosis. MAG 3 nuclear medicine scan can be used to demonstrate
this (or the cheaper ultrasound).
Urologic complication in transplant kidney
lymphocele
Lymphoceles typically occur 1-2 months after transplant. They are caused by leakage of
lymph from surgical disruption o f lymphatics or leaking lymphatics in the setting o f inflammation. The fluid
collection is usually medial to the transplant (between the graft and the bladder). They are actually the most
common fluid collection to cause transplant hydronephrosis.
ipsilateral lower edema from femoral vein compression
Hematoma post op renal transplant
overview
Immediate Post Op — Till about 1 week
Think Complex Collection
Heterogenous, Septa, Etc…
CT: Appearance will depend on how acute it is. Acute = more dense.
MRI: T1 Bright (usually)
urinoma post op renal transplant
overview
Around Day 10
Think Simple Collection between the bladder and the kidney
CT: If you do a delayed phase you can see leakage o f contrast
Nukes: Tracers like MAG3 and DTPAwill accumulate outside the expected location o f the bladder.
Fluid Cr > Serum Cr
Fluid K+ > Serum K+
These things happen from ischemia to the ureter or obstruction (usually)
abscess post op renal transplant
overview
Weeks to Months
Think Complex Hyperemic Collection
CT: Peripheral Enhancement
US: Hyperemia (increased flow at the periphery)
Fever and Elevated WBC would be obvious clues - although I expect the assholes would deliberately withhold that information
lymphocele post op renal transplant overview
2 weeks - 6 Months
Think Simple Collection (may have tiny septa).
CT: If you do a delayed phase you will NOT see leakage of contrast
Nukes: Tracers like MAG3 and DTPA will NOT accumulate outside the expected location o f the bladder.
Fluid Cr ~ Serum Cr
Fluid K+ ~ Serum K.+
They will Not usually drain these things (they ju st come back). If they do opt to treat them its usually via sclerosing agent.
Renal transplant
rejection overview
Rejection is complicated business with a bunch of fancy sounding French words (maybe Latin)
associated with numerous overlapping biopsy related classification criteria and which subtype of
the T-Cell mediated pathway blah blah blah. None of that shit matters to Radiologists. Rejection
workup involves, labs, considering the time interval, ultrasound, maybe nukes, and in many
cases a biopsy to actually prove it.
Renal transplant
hyperacute rejection
is an immediate failure of the graft - and you rarely see this
imaged. It is basically a dead on arrival transplant.
Renal transplant
acute rejection
usually seen around week 1-3 (it is actually rare in the first 3 days).
There is overlap between the antibody mediated types (which occur early) and the T-cell
activated types (which occur later) - but again that shit is irrelevant to Radiologists. Up to 20% of
transplant patients will have some early rejection. The graft may swell and Rls will go up.
Rejection vs ATN is the common question - and MAG3 can help (see chart on the next page).
Regardless o f the Nukes Exam, most sources say “biopsy” is the standard for differentiating the
two.
Renal transplant
acute tubular necrosis
common and occurs to variable degrees on basically
every transplant. The mechanism is ischemia in the kidney after they carve it out o f the Hobo
(presuming the transplant is from the usual donor - Hobo found floating in the river). So in the
time it takes to carve it out of the Hobo and sew it into an affluent celebrity (Selena Gomez,
Tracy Morgan, etc..) there is going to be some ischemia - and therefore ATN.
Lingo: “Delayed Graft Function (DGF) ” = transplant requiring dialysis in the first week. The
amount of “cold ischemia” (how long the hobo kidney is on ice) is said to be the best predictor.
Renal transplant
cyclosporin toxicity (calcineurin inhibitor)
Immunosuppressive therapy
necessary to keep the body from rejecting the graft can ironically end up poisoning the graft.
The timing is usually later than ATN (around a month). The MAG3 exam can also look like
ATN (normal perfusion, with retained tracer) but will NOT be seen in the immediate post op
period.
Renal transplant
chronic rejection
gradual progress process which occurs months to years after
transplant. The kidney may enlarge, and you can lose corticomedullary differentiation. The Rls
will elevate (> 0.7), which is nonspecific.
Acute rejection
US RI
mechanism
timing
mag3-flow
mag3 uptake
mag3 making piss
US RI elevated
mechanism antibody cell mediated
timing first week
mag3-flow crap
mag3 uptake crap/delayd
mag3 making piss crap slow progressive excretion
ATN
US RI
mechanism
timing
mag3-flow
mag3 uptake
mag3 making piss
US RI elevated
mechanism ischemia during harvesting
timing first week
mag3-flow normal to mild delay
mag3 uptake pretty much normal
mag3 making piss crap slow progressive excretion
Cyclosporin toxicity
US RI
mechanism
timing
mag3-flow
mag3 uptake
mag3 making piss
US RI elevated
mechanism nephrotoxin reaction to immunosuppressive
timing month
mag3-flow normal to mild delay
mag3 uptake pretty much normal
mag3 making piss crap slow progressive excretion
Chronic rejection
US RI elevated
mechanism cellular immune t cell mediated
timing months
mag3-flow crap
mag3 uptake crap/delayed
mag3 making piss crap slow progressive excretion
Renal transplant renal artery thrombosis
Almost always seen within the first month (usually minutes to
hours post opt, resulting from technical factors - kinking or torsion of the vessel. Unless the patient
is undergoing rejection, or has renal artery stenosis (which has progressed to full on thrombosis) it is
pretty fucking rare to see this outside the early post-operative period. As a point of trivia - this is
different than hepatic artery transplant thrombosis — which is described as a later complication ( >
than 1 month post op) — so don’t get it twisted and let the bastards trick you.
Renal transplant
Renal Artery Stenosis
Typically seen within the first year after transplant (usually weeks
to months). Easily the most common vascular complication o f transplant. This usually occurs at
the anastomosis (especially end-to-end types). CMV is a risk factor. The clinical / scenario buzzword
is going to be “refractory hypertension.”
Renal transplant
renal artery stenosis criteria
- PSV > 200-300 cm/s. (some people say 340-400 cm/s)
- PSV ratio > 1.8-2.5x (Stenotic Part vs Non Stenotic Part)
- Tardus Parvus: Measured at the Main Renal Artery Hilum (NOT at the arcuatcs)
- Anastomotic Jetting
Renal transplant
renal vein thrombosis
Typically seen within the first week. Typically the kidney is
swollen. Instead of showing you the Doppler of the renal vein (which would show no flow), they will
most likely show you the artery, which classically has reversed diastolic flow.
Renal transplant
avf
These occur secondary to biopsy. They occur about 20% of
the time post biopsy, but are usually small and asymptomatic. They will likely show it with tissue
vibration artifact (perivascular, mosaic color assignment due to tissue vibration), with high arterial
velocity, and pulsatile flow in the vein.
Renal transplant
pseudoaneurysm
These also occur secondary to biopsy, but are less common. They can also
occur in the setting of graft infection, or anastomotic dehiscence. They will most likely show you the
classic “yin-yang” color picture. Alternatively, they could show Doppler with biphasic flow at the
neck of the pseudoaneurysm.
Renal transplant
renal allograft compartment syndrome
overview
Seen immediately - usually < 2 hours post transplantation
This is usually an operative complication where the kidney was too big for the pelvic extraperitoneal space they decided to jam it and when they stitch the fascia back up it puts the squeeze
on the kidney. You can imagine if there was a fluid collection nearby that would
make it worse
Doppler: Absent or almost totally absent cortical flow in the kidney (color or
power Doppler)
Transplant Size matters - a large transplanted kidney is the main risk factor associated with RACS.
Renal transplant
Renal vein thrombosis overview
Usually the first 5 days (peak at 48 hours)
Depending on who you ask - like 30% o f kids have graft failure because o f this…
The incidence is less that RAS - but the morbidity associated with it is still high.
Doppler: Flow in the vein is gone. Reversed diastolic arterial flow.
Grey Scale: Swollen /enlarged kidney.
Renal transplant
Renal artery stenosis overview
3 months to 2 years depending on who you ask
Depending on who you ask - this is the most common vascular complication in a transplant.
Classic History is “hypertension refractory to treatment”
The lesion is usually at the level o f the surgical anastomosis.
Doppler: PSV > 250 cm/s or 1.8-2.5x increase from the “normal” vessel.
There is a trend towards using 340-400 cm/s for a more specific call. Which number will the test writer want you to use? Simply read his or her mind to find out and answer accordingly.
Rx: Most places will try and angioplasty the stenosis first. Having said that, if it is right over the anastomosis - you will hear people say surgery might be safer / better (higher risk of ripping the thing in half when you stretch it)
Renal transplant
renal artery thrombosis overview
Usually very early (mins to hours) as a post op complication (clamp injury etc…)
It is rare to see this late (in the absence o f progressive stenosis or raging rejection)
Doppler: Flow is gone
Grey Scale: Might see wedge shaped hypoechoic infarcts
Renal transplant
occuring at anytime after trauma or procedure
av fistula
pseudoaneurysm
traumatic hematoma
Renal transplant
av fistula overview
Feeding artery with a high velocity low resistance waveform
Vein with a turbulent arterial appearance.
Tissue Vibration Artifact
Usually - no clinically significant hemodynamic consequence and no intervention needed
Renal transplant
pseudoaneurysm overview
To-and-Fro pattern of blood flow within the neck
Yin-yang sign o f swirling blood within the sac
Often need an intervention - especially i f large (historically > 2 cm) or increasing in size
Renal transplant
Traumatic hematoma
This can occur after biopsy or from blunt trauma.
Transplant kidneys don’t have ribs and are fairly superficial - so they can get banged up in minor trauma.
Complex Collection
Heterogenous, Septa, Etc…
Transplant kidney Renal cancer
risk of new cancer
The prolonged immunosuppression therapy that renal transplant patients are on places them
at significantly (lOOx) increased risk o f developing some type o f cancer. In particular, they
get more nonmelanomatous skin cancer, lymphoma, and colon cancer. In fact - annual skin
exams are a recommendation for all renal transplant patients — that is kinda random …. and
possibly testable.
Transplant kidney
RCC
Increased risk, with most o f the cancers (90%) actually occurring in the native
kidney. Etiology is not totally understood; maybe it’s the immunosuppression or the fact that
many transplant patients were on dialysis (a known risk factor) that leads to the cancer risk.
In reality it doesn’t matter, and is probably both.
Risk o f primary renal malignancy in the transplanted kidney is six times that o f the regular
Joe. A point o f testable trivia is that these cancers are usually papillary subtypes.
Transplant kidney
Post Transplant Lymphoproliferative Disorder (PTLD)
This is an
uncommon complication of organ transplant, associated with B-Cell proliferation. EBV is a
risk factor and that is one o f the main reasons they screen for it - and will put people on
Rituximab (if they mention that drug - they could be hinting that patient was EBV positive).
It is most common in the first year post transplant, and often involves multiple organs. The
most typical look is a mass lesion encasing / replacing the hilum - although the appearance is
notoriously variable. The treatment is to back off the immunosuppression.
Renal Transplant + BK Virus = Urothelial Malignancy
WTF is “BK Vints ” ? It is some random virus that pretty much everyone gets and doesn’t even
notice. Nephrologists love to write papers on this critter. Supposedly… (yes I read their stupid
papers) it is usually the donor kidney that has it and then it reactivates something crazy once the
patient is immunosuppressed. Sometimes it even mimics rejection.
Just know BK = Urothelial Cancer.
Transplant kidney
cyclophosphamide
As a point of trivia, significant exposure to cyclophosphamide
(less common now with the development of cyclosporin A) is associated with increased risk
of urothelial cancer.
Renal trauma gamesmanship
A good “Next Step” type question in the setting o f renal trauma
(or pelvic fracture) would be to prompt you to get delayed imaging - this is helpful
to demonstrate a urine leak.
Fractured kidney
A laceration, which extends
the full depth of the renal parenchyma. By definition the
laceration must connect two cortical surfaces - so think
about it going all the way through.
Shattered kidney
This is a more severe form of
a fractured kidney. A kidney with 3 or more fragments -
this is the most severe form o f renal fracture.
Renal Wedge Shaped Perfusion
Abnormality
thinsk segmental artery injury
renal diffuse nonperfusion
think devascularized kidney
Renal persistant nephrogram
thingk renal vein injury/thrombosis
renal trauma trivia
A transplant kidney is at increased risk o f injury in most trauma because of its superficial
location (and loss o f the normal rib protection).
ureteral stones
Stones tend to lodge in 3 spots: UPJ, UVJ, pelvic brim.
Ureteral Wall Calcifications
Wall calcifications should make you think about two things: (1) TB, (2) Schistosomiasis (worms).
Ureteritis cystica
Numerous tiny subepithelial fluid-filled cysts within the wall of
the ureter. The condition is the result o f chronic inflammation (from stones and/or chronic
infection). Typically this is seen in diabetics with recurrent UTI. There may be an increased
risk of cancer.
Ureteral pseudodiverticulosis
This is similar to ureteritis cystica in that both
conditions are the result o f chronic inflammation (stones, infection). Instead of being cystic
filling defects, these guys are multiple small outpouchings. They are bilateral 75% of the
time, and favor the upper and middle third. There is an association with malignancy.
malokoplakia
overview
( “The Accursed”) - Former Lord o f the Dark Elves of Svartalfheim and rare chronic granulomatous condition, this pathology can create soft tissue nodularity /plaques in the bladder and ureters (bladder more often). It is seen in the setting of chronic UTIs (highly associated with E.Coli). often in female immunocompromised patients. There is also a more remote association with the Casket o f Ancient Winters. Since malakoplakia most frequently manifests as a mucosal mass involving the ureter or bladder, the most common renal finding is obstruction secondary to a lesion in the lower tract. Step
1 buzzword = Michaelis-Gutmann Bodies.
Leukoplakia =
premalignant
malakoplakia =
not premalignant
malakoplakia most easily tested piece of trivia
Not premalignant and usually gets better with antibiotics
Leukoplakia overview
This is essentially squamous metaplasia secondary to chronic irritation
(stones or infections). The bladder is more commonly involved than the ureter. Imaging
findings are unlikely to be shown, but would be mural filling defects.
Leukoplakia most easily tested trivia
is considered premalignant and the
cancer is squamous cell.
Leukoplakia
trivia
associated with squamous cell carcinoma NOT transitional cell
Retroperitoneal Fibrosis
overview
This condition is characterized by proliferation o f aberrant fibro-inflammatory tissue, which
typically surrounds the aorta, IVC, iliac vessels, and frequently traps and obstructs the
ureters. It is idiopathic 75% o f the time. Other causes include prior radiation, medications
(methyldopa, ergotamine, methysergide), inflammatory causes (pancreatitis, pyelonephritis,
inflammatory aneurysm), and malignancy (desmoplastic reaction, lymphoma).
Retroperitoneal Fibrosis
trivia
- Mostly (75 %) idiopathic AKA“Ormond Disease”
• Associated with IgG4 disorders (autoimmune pancreatitis, Riedel’s thyroiditis, inflammatory pseudotumor)
• Classically shown with medial deviation o f ureters
• It’s more common in men - Malignancy associated RP fibrosis occurs about 10% o f the time (some people advocate
using PET to find a primary) - The Fibrosis will be Gallium avid, and PET hot in its early stages and cold in its late stages (mirroring its inflammatory stages). Metabolically active RP fibrosis will show increased FDG and Gallium uptake, regardless o f a benign or malignant underlying cause
Subepithelial Renal Pelvis Hematoma:
overview
This tends to occur in patients on long-term anticoagulation or a history o f hemophilia. You are going to have a thickened upper tract wall - which is a classic mimic for TCC.
Subepithelial Renal Pelvis Hematoma:
gamesmanship
would expect pre and post contrast images so that you can make the classic findings o f hyperdense clot on the pre-contrast that does NOT enhance. Although a non-contrast alone (showing blood in the urinary pelvis) with the history of hemophilia should also be enough to seal the deal.
LAteral deviation of the ureters
Retroperitoneal Adenopathy
Aortic Aneurysm
Psoas Hypertrophy (proximal ureter)
medial deviation of the ureters
Retroperitoneal Fibrosis
Retrocaval Ureter (right side)
Pelvic Lipomatosis Psoas Hypertrophy (distal ureter)
Transitional Cell Carcinoma (Urothelial Carcinoma)
high yield trivia
a way to remember this is where ever the urine sits static the longest is more likely to have the cancer.
So: Bladder > Renal Pelvis > Ureter. If you are getting cancers in the
ureter than you probably also have them in the bladder
• Ureter is the least common location for TCC of the urinary tract
• TCC of the renal pelvis is 2x -3x times more common than ureter
• TCC of the bladder is lOOx times more common than ureter
• In the ureter 75% of the TCCs are in the bottom 1/3
• If you have upper tract TCC there is a 40% chance of developing a bladder TCC
• If you have bladder TCC there is a 4% chance of developing a Renal Pelvis or Ureteral TCC
• Ureteral TCC is bilateral 5%
Transitional Cell Carcinoma (Urothelial Carcinoma)
risk factors
- Smoking
- Azo Dye
- Cyclophosphamide
- Aristolochic acid (Balkan Nephropathy - see below)
- Horseshoe Kidney
- Stones
- Ureteral Pseudodiverticulosis
- Hereditary Non-Polyposis Colon Cancer (type 2)
Balkan Nephropathy
This is some zebra degenerative nephropathy endemic to
the Balkan States. The only reason I mention it is that it has a super high rate of renal pelvis and upper ureter TCCs. It’s thought to be secondary to eating aristolochic acid (AA) in seeds of the Aristolochia clematitis plant (herb).
Squamous Cell
ureter
This is much less common than TCC (in the US anyway). The major predisposing factor is schistosomiasis (they both start with an “S”).
Hematogenous Metastasis
ureter
Mets to the ureters are rare but can occur (GI, Prostate, Renal, Breast). They typically infiltrate the periureteral soft tissues and demonstrate transmural
involvement.
Fibroepithelial Polyp
ureter
This is a benign entity presents as a filling defect in the renal pelvis or proximal ureter - which mimics a TCC (blood clot or radiolucent stone). The diagnosis is typically made post nephrectomy - since the assumption is nearly always TCC.
Fibroepithelial polyp
gamesmanship
For the purpose of multiple choice (and real life), renal pelvis filling defects should always be assumed to be either clot, calcium (stone), or cancer. The only way I can think that a polyp question could be ask would be something like “which features would make a polyp more likely?” It has to be a trivia question, they couldn’t (in good conscious) expect you to pick polyp over TCC with imaging alone — even if the findings and demographics were perfect - that would be teaching a terrible clinical message.
This vs that polyp vs tcc
polyp
younger 30-40
smooth/oblong
mobile
This vs that polyp vs tcc
tcc
older 60-70
irregular
fixed
Bladder development anomalies
prune belly (eagle barrett syndrome)
This is a malformation triad which occurs in males. Classically
shown on a babygram with a kid shaped like a pear (big wide
belly).
Bladder development anomalies
prune belly triad
• Deficiency of abdominal musculature
• Hydroureteronephrosis
• Cryptorchidism
(bladder distention interferes with descent o f testes)
Bladder development anomalies
urachus
This is also discussed in the Peds chapter. I will briefly mention that the primary concern is the development of a midline adenocarcinoma. Most of the time the presence of a midline mass makes
it obvious although calcification within any urachal soft tissue should
make you think cancer.
bladder diverticula
These are more common in boys, and can be seen in a few situations. Most bladder diverticula can also be acquired secondary to chronic outlet obstruction (big prostate). There are a few syndromes (Ehlers Danlos is the big testable one) that you see them in as well.
bladder ears
“Transitory extraperitoneal herniation of the bladder” if you want to sound
smart. This is not a diverticulum. Instead, it’s transient lateral protrusion of the bladder into the
inguinal canal. It’s very common to see, and likely doesn’t mean crap. However, some sources
say an inguinal hernia may be present 20% of the time. Smooth walls, and usually wide necks can
help distinguish them from diverticula.
bladder ears
“Transitory extraperitoneal herniation of the bladder” if you want to sound
smart. This is not a diverticulum. Instead, it’s transient lateral protrusion of the bladder into the
inguinal canal. It’s very common to see, and likely doesn’t mean crap. However, some sources
say an inguinal hernia may be present 20% of the time. Smooth walls, and usually wide necks can
help distinguish them from diverticula.
Bladder Cancer
gamesmanship
GROSS hematuria confers a 4x greater risk than microscopic hematuria. If the question header specifically indicates “GROSS” hematuria - think bladder cancer first.
Bladder Cancer
next step
Along these lines if the history is GROSS hematuria, and the patient is 50 or older
they should get a CT Hematuria Protocol / Urography (pre and post, with delays), and also cystoscopy.
Bladder Cancer
what does marcelus walls bladder cancer look like
Short answer = soft tissue in the bladder. If you are looking at a well distended bladder (which is pretty much required to say shit about the bladder) focal wall thickening or nodules should be considered cancer till proven otherwise.
Bladder Cancer
what about diffuse circumferential bladder wall thickening
This isn’t usually cancer, especially in
the world of multiple choice. This is probably more of an inflammation or infection situation - or chronic
partial outlet obstruction (if the prostate is enormous). I’d only call a cancer in this situation if there was
really asymmetric nodular thickening superimposed on circumferential thickening.
Bladder Cancer
what about enhancement
You will hear people refer to bladder cancers as hypovascular tumors - but
they can and often do enhance, especially on early arterial phases. Any focal enhancement should trigger
you to think cancer - unless you’ve got good reasons to think otherwise. Having said all that - most
people will say the delayed phase is the most important for identifying bladder cancers - and that is the
choice I would recommend if you are forced to choose (white background of contrast - makes soft tissue
masses easier to see).
Bladder Cancer
types of cancer/mimics
rhabdomyosarcoma
This is the most common bladder cancer in humans less than 10 years of age. They arc often infiltrative, and it’s hard to tell where they originate. “Paratesticular Mass” is often a
buzzword. They can met to the lungs, bones, and nodes. The Botryoid variant produces a polypoid
mass, which looks like a bunch of grapes.
Bladder Cancer
types of cancer/mimics
tcc
As stated above, the bladder is the most
common site, and this is by far the most common subtype. All the risk factors, arc the same as above.
If anyone asks “superficial papillary” is the most common TCC bladder subtype.
Bladder Cancer
types of cancer/mimics
scc
When I say Squamous Cell Bladder, you say Schistosomiasis. This is
convenient because they both start with an “S.” The classic picture is a heavily calcified bladder and
distal ureters (usually shown on plain film, but could also be on CT). Another common association
with squamous cell cancer of the bladder in the presence of a longstanding Suprapubic catheter. This
also starts with an “S.”
Bladder Cancer
types of cancer/mimics
adenocacinoma
This is a common trick question. When I say Adenocarcinoma of
the Bladder, you say Urachus. 90% of urachal cancers are located midline at the bladder dome.
Bladder Exstrophy is also associated with an increased risk of adenocarcinoma.
Bladder Cancer
types of cancer/mimics
leiomyoma (bladder fibroid)
Benign tumor (not cancer - even though this section is bladder cancer) its often indicentally discovered (most common at the trigone)
most common benign bladder tumor
looks like a fibroid (smooth, solid, homogenous)
clinical buzzword urinary hesitance or dribbling
TCC bladder cancer overview
high yield
By far the Most Common Type (like 90%)
Smoking is the classic risk factor, but other poisons including arsenic, aniline, benzidine - etc or as they call it in Flint Michigan “Tap Water” - have a documented relationship
Bladder Diverticulum - 2-10% increased risk (related to stasis). In this setting early perivesical fat invasion is classic (because a diverticulum has limited muscle in the wall to slow the invasion)
Favors the base (inferior posterior)
Sub-divided into Papillary vs Non Papillary.
Papillary ones look like shrubs “frond like ” and tend to be low grade.
Non-Papillary tends to be more aggressive.
SCC bladder cancer
high yield
Second Most Common Type (like ~ 8%)
Classic Associations:
• Recurrent urinary tract infections and stone disease
• Schistosoma Hematobium (asshole jungle worm)
• Longstanding Suprapubic Catheter
This is convenient because they both start with an “S.”
The classic picture is a heavily calcified bladder and distal ureters (usually shown on plain film, but could also be on CT).
Tumor favors the trigone and lateral walls
The ones NOT associated with Schistosomiasis tend to be more aggressive.
adenocarcinoma bladder cancer
high yield
Third Most Common Type (like 2%)
Classic Associations:
• Urachal Remnant
• Bladder Exstrophy 90% of urachal cancers arc located midline at the bladder dome.
The classic picture is a large midline mass associated with a urachal remnant with scattered calcifications.
70% of cases have calcification (if you see calcifications in a urachal remnant it should make you think about an early cancer).
Rhabdomyosarcoma bladder cancer
high yield
Most common bladder tumor in Peds.
They are often infiltrative, and it’s hard to tell where they originate.
Paratesticular Mass” is often a buzzword.
They can met to the lungs, bones, and nodes.
The classic look is Grape-like polypoid masses — this is the sarcoma botryoides variant
Diversion Surgery
overview
After radical cystectomy for bladder cancer there are several urinary diversion procedures that
can be done. People generally group these into incontinent and continent procedures. There
are a ton o f these (over 50 have been described). I just want to touch on the big points, and
focus on complications (the most testable subject matter). The general idea is that a piece of
bowel is made into either a conduit or reservoir, and then the ureters are attached to it.
Diversion Surgery
early complications
- Alteration in bowel function: Adynamic ileus is the most common early complication, occurring in almost 25% o f cases. In about 3% o f cases you can get SBO, usually from adhesions near the enteroenteric anastomosis.
- Urinary Leakage: This occurs in about 5% o f cases, and usually at the ureteral reservoir anastomosis. A urinoma can develop when the leaked urine is not collected by urinary drains.
- Fistula: This is uncommon and seen more in patients who have had pelvic radiation.
Diversion Surgery
late complications (>30 days)
- Urinary infection: This can be early or late.
- Stones: Remember to look on the non-contrast study.
- Parastomal Herniation: This occurs about 15% of the time with ileal conduits. Obesity is a contributing factor. Most don’t matter, but 10% will need a surgical fix.
- Urinary’ stricture: The left side is higher risk than the right, secondary to the angulation (it’s brought through or under the mesentery).
- Tumor Recurrence: The more advanced the original disease, the higher the risk for recurrence. The incidence is between 3-15%, and can present as a soft tissue mass at the ureter, bladder, or pelvic lymph node.
Psoas Hitch
overview
The “psoas hitch” procedure results in an Aunt Minnie appearance o f the bladder, making it uniquely testable.
This procedure is done in the situation where you have had an injury or pathology (stricture, cancer, etc…) involving a long segment o f the distal ureter. Normally you would just cut that
shit out and re-implant into the bladder. But what if the left over portion o f the ureter is too short? The solution is to stretch the ipsilateral portion of the bladder towards the short ureter
and sew it (“hitch it”) to the psoas muscle. That way you can get away with a short ureter, because you stretched the bladder to bridge the gap.
Psoas Hitch
why its done
Used for people with long segment distal ureter injury / disease
Psoas Hitch
aunt minnie
CT I VP or Plain Film IVP (with contrast filling the bladder).
The “hitched” side has an upward projection towards the psoasmuscle.
Emphysematous Cystitis
Gas forming organism in the wall o f the bladder. More than half the time it’s a diabetic patient. It’s usually from E. Coli. It’s gonna be very obvious on plain film and CT. Ultrasound would be sneaky, and you’d see dirty shadowing.
Bladder
TB
The upper GU tract is more commonly effected, with secondary involvement o f the bladder. Can eventually lead to a thick contracted bladder. Calcifications might be present.
Bladder
Schistosomiasis
Common in the third world. Eggs are deposited in the bladder wall which leads to chronic inflammation. Things to know: the entire bladder will calcify (often shown on plain film or CT), and you get squamous cell cancer.
Bladder
Fistula
This occurs basically in 3 conditions; (1) diverticulitis, (2) Crohns, (3) Cancer. This is more common in men, although women are at significantly increased risk after hysterectomy (the uterus protects the bladder).
Bladder
Neurogenic Bladder
This comes in two flavors: (a) small contracted bladder, (b) atonic large bladder. The buzzword / classic sign is “pine cone” bladder, because of its appearance. It can lead to urine stasis, and that stasis can predispose to bladder CA, stones, and infection.
Acquired bladder diverticula
these can be acquired mainly via outlet obstruction (just think big prostate). They are most common at the UVJ. They can
lead to stasis, and that stasis can predispose to bladder CA, stones, and infection.
Bladder stones
These guys show up in two scenarios: (1) they are bom as kidney stones and drop into the bladder (2) they develop in the bladder secondary to stasis (outlet obstruction, or neurogenic bladder). They can cause chronic irritation and are a known risk factor for both TCC and SCC.
Pear shaped bladder
This is more o f a sign than a pathology
Think two things (1) pelvic lipomatosis, and (2) hematoma.
Bladder fistual most common etiology
- Colovesicial Fistula = Diverticular Disease
- Ileovesical Fistula = Crohns
- Rectovesical Fistula = Neoplasm or Trauma
Bladder Trauma-
overview
In the setting of bladder trauma - Cystography (scanning the bladder after filling it with contrast
“retrograde” via foley) is the gold standard — this can be done under fluoro or CT. I’ve head people say
this is “100%” sensitive for bladder rupture. It’s pretty obvious — if it looks intact … its intact. If it
looks like a deflated balloon — its ruptured. Having said that — here is a testable piece of trivia, you
must distend the bladder — that means 300-400 mL of diluted water soluble (not barium!) contrast.
Inadequate bladder distention = loss of sensitivity.
What they want you to know is; extra versus intra peritoneal rapture. CT Cystography (contrast
distending bladder) is the best test — make sure the bladder is distended (300-400 mL).
Bladder Trauma-
extraperitoneal
This one is more common (80-90%). Almost always associated with pelvic fracture. This can be managed medically.
• If there is a pelvic fracture, then the chance of a bladder rupture is 10%.
• If there is a bladder rapture, there is almost always a pelvic fracture
• Molar Tooth Sign: Contrast surrounding the bladder, in the prevesicle space of Retzius. This indicates extraperitoneal bladder rapture.
Bladder Trauma-
intraperitoneal
This one is less common. A direct blow to a full bladder, basically pops the balloon and blows the top off (bladder dome is the weakest part). The dude will have contrast outlining bowel loops
and in the paracolic gutters. This requires surgery.
Bladder Trauma-
pseudo azotemia
If the bladder is ruptured the creatinine in urine can be absorbed via the peritoneal lining. This will massively elevate the creatinine making it seem like the patient is in acute renal failure. The kidneys are normal.
Male urethra anatomy
• The length is highly variable with most texts using the following graded scale: (itty bitty -> teeny tiny -> tiny -> small -> medium -> large -> extra large -> Lionhart sized).
• Anatomists divide the thing into two main parts - anterior and posterior. The anterior part is made up of the penile urethra + the bulbar urethra. The posterior part is made up of the membranous and prostatic urethra.
• The most anterior portion of the urethra is termed the fossa navicularis which has a Latin / French sound to it, so it is probably testable.
• The “Verumontanum” (another fancy sounding term) is an ovoid mound that lies in the posterior wall of the prostatic urethra. An additional testable piece of trivia is that in the center of this thing is the prostatic utricle (which is an embryologic “mullerian” remnant).
• The anterior part fills with a retrograde study (RUG). The posterior part fills with an antegrade study (voiding urethrography). “Dynamic Urethrography” is the term used when these studies are
combined. You can fill the whole thing with a RUG - but that requires pressure to overcome the normal spasms of this cruel and unusual procedure.
• There are two methods for identifying the bulbar-membranous junction (which is important for delineating pathology - anterior vs posterior). The first is to find the “cone” shaped appearance of
the proximal bulbar urethra. The cone will taper into the membranous portion. The second (used if you can’t opacify the urethra) is to draw a line connecting the inferior margins of the obturator
foramina.
Urethra trauma
Trauma + Blood in the meatus =
“Next Step” RUG.
Urethra trauma
anterior injury
Classic = Crashed your bicycle (or tricycle), i.e. = Straddle Injury. Unicycle
wreck is less often associated with urethral injury (because of the lack o f cross bar) but is often associated with various juggling, fire eating, and sword swallowing injury patterns - as well as mania, and histrionic personality disorder.
urethra trauma
posterior injury
Classic = Crashed your Ferrari.
Testable trivia = Often associated with a
pelvic fracture and bladder injury. 1 speculate that crashing one’s Ferrari is also associated with sudden and severe atrophy of the penis.
urethra injury type 1
stretched
posterior
urethra is intact and normal on rug
urethra injury type 2
membraouns urethra tear
posterior
above an intact ug diaphragm
extraperitoneal contrast is present
no perineum contrast (intact ug diaphrag prevents this)
associated with incontinence
urethra injury type 3
most common
membranous and bulbar urethra tear
anteior and posterior
ug diaphragm is ruptured
extraperitoneal contrast is present
perineum contrast (UG diapragm is torn) contrast in the scrotum
associated with incontinence
urethra injury type 4
bladder base injury extending into prostatic urethra
posterior
associated with incontinence
urethra injury type 5
bulbous uretha “anterior”
anterior
straddle injury
Urethral strictures
straddle injury
The most common external cause of traumatic stricture is this type of mechanism. The physiology is compression o f the urethra against the inferior edge o f the pubic symphysis. The bulbous urethra is the site of injury
(this is the most likely question).
short segment of the bulbous urethra
Urethral strictures
gonococcal urethral stricture
This tends to be a long irregular stricture (the straddle stricture was short). It occurs in the distal bulbous urethra.
long segment and irregular - bulbous urethra
Male urethra
pancreatic transplant
This has been known to cause urethral injury, if the drainage is to the
bladder (the old way of doing it). Extravasation from urethral injury is said to occur in about 5% of
cases and is secondary to pancreatic enzymes jacking the urethra.
Male urethra
condyloma acuminatum
Multiple small filling defects seen on a RUG should make you think this. Although, instrumentation including a retrograde urethrography is actually not recommended because of the possibility of retrograde seeding.
Male urethra``
urethrorectal fistula
This may occur post radiation, and is classically described with brachytherapy (occurs in 1% of patients).
Male urethra
urethral diverticulum
In a man, this is almost always the result of long term foley placement.
Male urethra
cancer
Malignant tumors of the male urethra are rare. When they do occur, 80% are squamous cell cancers (the e x c e p tio n is th a t p ro sta tic u re th ra a c tu a lly has tra n s itio n a l c e ll 90% o f th e tim e ).
Male urethra
urethral diverticulum cancer
Cancer in a urethral diverticulum is nearly ALWAYS adenocarcinoma (rather than squamous cell).
Female urethral diverticulum
overview
Urethral diverticulum is way more common in females. They are usually the result of repeated infection of the periurethral glands (classic history is “repeated urinary tract infections”).
In case books and conferences this is classically shown as a Sagittal MRI. The majority of urethral diverticula are located in the middle third of the urethra and involve the posterolateral wall
Female urethral diverticulum
buzzword
The buzzword is “saddle-bag” configuration, which supposedly is how you tell it from the urethra.
Female urethral diverticulum
stones
can also develop in these things. All this infection and irritation leads to increased risk of cancer, and the very common high yield factoid is this is most commonly adenocarcinoma (60%).
Renal Cancer (Adenocarcinoma) blitz
clear cell
Enhances equal to cortex on CM Phase
Overall Most Common in Gen Pop
Von Hippel-Lindau
Renal Cancer (Adenocarcinoma) blitz
papillar
Enhances less than cortex on CM Phase
Hereditary Papillary Renal Carcinoma
Transplant Kidney
Renal Cancer (Adenocarcinoma) blirz
chromophobic
birt hogg dube
Renal Cancer (Adenocarcinoma) blitz
medullary
sickle cell trait
U re te ra l Cancer (Transitional Cell - now called Urothelial) blitz
location
Location - think about where you get the most stasis
• Renal Pelvis - Twice as common as Ureter
• Distal Third of Ureter - Most common site
• Middle is 2nd, and Proximal is Third
U re te ra l Cancer (Transitional Cell - now called Urothelial)
blitz
relationship to bladder ca
- Bladder CA is way more common (like lOOx more).
- So if you have bladder CA you don’t need upper tract CA. Since upper tract CA is not all that common, if you smoked enough Marlboro Reds to get renal pelvis CA, you probably smoked enough to get multifocal disease including the bladder.
- Bottom Line: Bladder can be isolated , Ureteral CA usually also has bladder CA
Bladder cancer blitz
TCC
- “The usual one” - like 90%
- Favors the base (inferior posterior)
- 40% o f them are multiple
- “Frond like ” Papillary Tumors are
the Most Common Subtype - Known to be multicentric with
synchronous and metachronous
bladder and upper tract lesions —
but remember the bladder is the
most common site.
Bladder cancer SCC blitz
- Think this when you see Calcifications - Favors the Trigone and Lateral Walls - Association with Schistosomiasis - Association with Chronic Suprapubic Catheter / Urinary Status
bladder cancer adenocarcinoma blitz
- Midline Location is Classic
- Association with Urachal
Remnant - Association with Bladder
Exstrophy
Urethral cancer location
urethral diverticulum
adenocarcinoma
Urethral cancer location
bulbar./penile urethra
scc (80%)
Urethral cancer location
prostatic urethra
TCC (90%)
think about it loike a bladder ca
The Uterus - Changes During Life
neonate
Uterus is larger than you would think for a baby (maternal / placental hormones are still working). If you look close, the shape is a little weird with the cervix often largerthan the fundus.
The Uterus - Changes During Life
prepuberty
The shape of the uterus changes - becoming more tube-like, with the cervix and uterus the same size.
The Uterus - Changes During Life
puberty
he shape o f the uterus changes again, now looking more like an adult (pear-like) - with the fundus larger than the cervix. In puberty, the uterus starts to have a visibleendometrium - with phases that vary during the cycle.
The Ovaries - Changes During Life
Just like with the uterus, infants tend to have larger ovaries (volume around 1 cc), which then decrease and remain around or less than 1 cc until about age 6. The ovaries then gradually increase to normal adult size as puberty approaches and occurs.
Turner Syndrome -
The XO kids. Besides often having aortic coarctations, and horseshoe kidneys they will have a pre-puberty uterus and streaky ovaries.
Embryology female
The quick and dirty of it is that the mullerian ducts make the uterus and upper 2/3 of the vagina.
The urogenital sinus grows up to meet the mullerian ducts and makes the bottom 1/3 o f the vagina.
Wolffian ducts are the boy parts, and should regress completely in girls.
mullerian ducts make up
uterus
fallopian tubes
upper 2/3 of vagina
wolffian ducts make up
vas deferans
seminal vesicles
epididymis
urogenital sinus makes
prostate
lower / of vagina
three basic embryologic problems
failure to form (unilateral kidney and unicarnuate uterus)
failure to fuse (tuerus diedelphys or bicornuate)
failure to cleave septate uterus
Failure to form
muillerian agenesis
(Mayer-Rokitansky-Kuster-Hauser
syndrome): Has three features: (1) vaginal atresia, (2) absent or
rudimentary uterus (unicomuate or bicomuate) and (3) normal
ovaries. The key piece of trivia is that the kidneys have issues
(agenesis, ectopia) in about half the cases
cornus =
collis =
uterus
cervical
failure to form
unicornuate uterus overview
If you see a unicomuate uterus the classic teaching is to look for a rudimentary horn. The reason is the
rudimentary horns can have endometrium - and if present can cause lots of phantom female belly pain
problems (dysmenorrhea, hematometra, hematosalpinx, etc…, etc…, so on a so forth). Endometrial tissue
in a rudimentary hom (communicating or not) - increases the risk of miscarriage. An additional problem
could be a pregnancy in the rudimentary hom - in both the communicating and noncommunicating typesalthough
especially bad in the non-communicating sub-type because it nearly always results in
rudimentary hom rupture (life-threatening bleeding).
Renal agenesis contralateral to the main uterine hom (ipsilateral to the rudimentary horn) is the most
common abnonnality.
unicronuate uterus variants
llnicornuate + Communicating Cavitary Rudimentary Horn
univrouate + non communicating cavitary horn
unicornuate + noncavitary rudimentary horn
isolated unicornuate (most common)q
FAilure to fuse
uterus didelphys
This is a complete uterine duplication (two cervices, two uteri, and two upper 1/3 vagina). A vaginal septum is present 75% of the time. If the patient does not have vaginal obstruction this is usually asymptomatic.
failure to fuse bicornuate
This comes in two flavors (one cervix
“unicollis”, or two cervix “bicollis”). There
will be separation of the uterus by a deep
myometrial cleft - makes it look “heart
shaped”. Vaginal septum is seen around 25%
of the time (less than didelphys). Although
they can have an increased risk of fetal loss,
it’s much less of an issue compared to Septate.
Fertility isn’t as much of a “size thing” as it is
a blood supply thing. Remember you can have
8 babies in your belly at once and have them
live… live long enough to take part in your
reality show.
failure to fuse
t shaped
This is the DES related anomaly. It is historical trivia, and therefore extremely high yield for the “exam of the future.” DES was a synthetic estrogen given to prevent miscarriage in the 1940s. The daughters of patients who took this dmg ended up with vaginal clear cell carcinoma, and uterine anomalies - classically “T-Shaped.”
failure to cleave
septate
This one has two endometrial canals separated
by a fibrous (or muscular) septum. Fibrous vs Muscular can
be determined with MRI and this distinction changes surgical
management (different approaches). There is an increased risk
o f infertility and recurrent spontaneous abortion. The septum
has a shitty blood supply, and if there is implantation on it - it
will fail early. They can resect the septum - which improves
outcomes.
This is the most common Mullerian duct anomaly associated
with miscarriage. This is improved with resection o f the
septum.
failure to cleave
arcuate uterus
Mild smooth concavity o f the uterine
fundus (instead o f normal straight or convex) This is not really
a malformation, but more o f a normal variant. It is NOT
associated with infertility or obstetric complications.
THIS vs THAT: Bicornuate vs Septate
bicornuate
• “H e a rt S h a p e d ’’ - Fundal co n to u r is
less than 5 mm abo ve the tuba l ostia
• No s ig n ifica n t infertility issues
• Resection of the “s e p tum ” results in
poo r o u tcom e s
THIS vs THAT: Bicornuate vs Septate
septate
• Fundal co n to u r is Normal; more than
5 mm abo ve the tubal ostia
• L e g it infertility issues - impla ntation
fails on the se ptum (it’s a b lo od
s u p p ly th in g )
• Resection of the septum can help
days of the cycle
0-7 “Rag Week,” 7-14 Proliferative, 14-28 Secretory
*Day 14 Ovulation
HSG
’ HSGs are performed on days 7-10 of menstrual cycle, (after menstrual bleeding
complete - i.e. “off the rag”)
“ Contraindications: infection (PID), active bleeding (“rag week’’), pregnancy, and
contrast allergy.
■ Bicornuate vs Septate is tough on HSG - you need MRI or 3D Ultrasound to
evaluate the outer fundal contour.
Salpingits isthmica nodosa
This is a nodular scarring o f the fallopian tubes that
produces an Aunt Minnie Appearance. As trivia, it
usually involves the proximal 2/3 o f the tube. This is
of unknown etiology, but likely post inflammatory /
infectious (i.e. being a woman of questionable moral
standard / “free spirit”). It’s strongly associated with
infertility and ectopic pregnancy and that is likely
the question.
uterin avm
These can be congenital or acquired, with acquired types being way more
common. They can be serious business and you can totally bleed to death from them. The
typical ways to acquire them include: previous dilation and curettage, therapeutic abortion,
caesarean section, or just multiple pregnancies. Doppler ultrasound is going to show:
serpiginous and/or tubular anechoic structures within the myometrium with high velocity
color Doppler flow.
Intrauterine Adhesions (Ashermans)
This is scarring in the uterus, that occurs
secondary to injury: prior dilation and curettage, surgery, pregnancy, or infection (classic GU
TB). This is typically shown on HSG, with either (a) non filling o f the uterus, or (b) multiple
irregular linear filling defects (lacunar pattern), with inability to appropriately distend
the endometrial canal. MRI would show a bunch of T2 dark bands. Clinically, this results in
infertility.
endometritis
This is in the spectrum o f P1D. You often see it 2-5 days after delivery,
especially in women with prolonged labor or premature rupture. You are going to have fluid
and a thickened endometrial cavity. You can have gas in the cavity (not specific in a
postpartum women). It can progress to pyometrium, which is when you have expansion with
pus.
Pelvic Floor
overview
This anatomy is complicated - buncha facial bands “ligaments” muscles etc… created a
“sling” which keeps all this stuff from falling out the bottom. The best way to think about the pelvic sling o f a
female is to group it into 3 functional compartments: Anterior compartment (bladder and urethra), Middle
compartment (vagina, cervix, uterus, and adnexa), and Posterior compartment (anus and rectum). This anatomy
is incredibly complex - but a few o f these vocab terms could make easy questions:
Pelvic Floor
endoplevic fascia
Buncha ligaments / fascia (pubocervical fascia, rectovaginal fascia, cardinal ligaments, etc..) most o f which have vaginal or cervix in the name. Main support for the anterior & middle compartments.
Pelvic Floor
levator ani
This is the main muscular component o f the pelvic floor composed o f the puborectalis, pubococcygeus, and iliococcygeus. This muscle groups constant contraction maintains the pelvic floor height.
Pelvic Floor
urogenital diaphragm
This is the most caudal or superficial musculofascial structure. It does not have a marketable sex toy name (unlike Levator Ani). This thing usually finds it way into multiple choice exams as the anatomic landmark used in the classification o f urethral injury - as discussed in the GU chapter.
Pelvic Floor
relaxation
Pelvic floor relaxation has two components (pelvic floor descent and widening) that can be graded during maximal strain on sag MR1: • Hiatal enlargement (H line) — less than 6cm - measurement o f widening • Pelvic floor descent (M line) - less than 2cm - measurement o f descent Wider H or longer M = Worse. Organs hanging out = worse.
Pelvic Floor
pcl
(pubococcygeal line) = drawn from
inferior margin o f the symphysis pubis to
the junction between the first and second
coccygeal elements.
Pelvic Floor
h line
drawn from the inferior margin
o f the symphysis pubis to the posterior
aspect o f the puborectalis muscle sling.
Pelvic Floor
m line
shortest distance between the
posterior aspect o f the puborectalis
muscle sling and the PCL
Pelvic Floor
anterior compartment
Cystocele - Bladder Descent > 1 cm below the pubococcygeal line.
Urethral hypermobility - what you say if the urethra is rotated horizontally. This changes the treatment f rom , retropubic urethropexy (for normal stress incontinence) to a pubovaginal sling.
Risk Factors: Squeezing a bunch of kids out o f your vagina - can rupture o f the pubocervical fascia
Pelvic Floor
middle compartment
Uterine prolapse - Decent o f the cervix or posterior vaginal fornix < 1 cm above the pubococcygeal line.
A big turd can prop up the uterus - so it is best to measure them with an empty rectum (post defecation phase).
Axial images could show the vagina lose its normal “H” shape - hanging low like the sleeve o f a w izard (or the tongue o f a tired dog).
Risk Factor: Hysterectomy
Pelvic Floor
posterior compartment
Rectocele - Abnormal rectal bulging (typically anteriorly).
Due to weakening o f the rectovaginal fascia.
The describe them by how far they bulge relative to the anal canal.
Risk Factors: Vaginal surgery. Hysterectomy, Chronic Constipation, Being Old as Dirt.
Pelvic Floor
acial image of the ischioanal space
(Triangular o f fat lateral and caudally to the
levator ani - could show a loss o f the normal “H shaped” vagina or direct defects /
asymmetric thinning in the muscular sling. Having said that - for the purpose o f multiple
choice - this anatomy is usually demonstrating an anal fistula in the setting o f Crohns.
Pelvic floor
mri protocol
Steady State - T2 - 3 planes Dynamic State - Rapid T2 with Fat Sat, Sag Plane Only —performed during Valsalva, Kegel, and/or taking a shit (seriously)
Fibroids (Uterine Leiomyoma):
overview
These benign smooth muscle tumors are the most common
uterine mass. They are more common in women of African ancestry. They like estrogen and are most
common in reproductive age (rare in prepubertal females). Because of this estrogen relationship
they tend to grow rapidly during pregnancy, and involute with menopause. Their location is
classically described as submucosal (least common), intramural (most common), or subserosal.
Fibroids (Uterine Leiomyoma):
typical appearance
The general rule is they can look like anything. Having said that, they are
usually hypoechoic on ultrasound, often with peripheral blood flow and shadowing in the so called
“Venetian Blind” pattern. On CT, they often have peripheral calcifications (“popcorn” as seen on
plain film). On MRI, T1 dark (to intermediate), T2 dark, and variable enhancement. The fibroids
with higher T2 signal are said to respond better to IR treatment. A variant subtype is the
lipoleiomyoma, which is fat containing.
Fibroids (Uterine Leiomyoma):
hyaline
Most common type
T1: dark
T2: drak
T1+C: homogenous
Fibroids (Uterine Leiomyoma):
hypercellular
Densely packed smooth muscle (without much connective tissue). Respond well to embolization
T1: dark
T2: bright
T1+C: homognous
Fibroids (Uterine Leiomyoma):
lipoleiomyoma
rare fate containing subtype (maybe the result of degenration) this thing will be hyperechoic on us. will look like a fatty uterine mass on Ct. Will drop signal on fat sat sequences
T1: bright (dark if fat sat)
T2: bright
T1+C: maybe rim enhancement
Fibroids (Uterine Leiomyoma):
degeneration
4 types of degeneration are generally described. What they have in common is a lack of / paucity of enhancement (fibroids normally enhance avidly). The process of degeneration (basically a fibroid stroke) can cause severe pain as well as fever and/or leukocytosis.
Fibroid degeneration
hyaline
Most common type. The fibroid outgrows its blood supply, and you end up getting the accumulation of proteinaceous tissue.
T1: variable (usually dark)
T2: heterogenous (usually dark)
T1+C: none
fibroid degernation
red (carneous)
This one occurs during pregnancy - caused by venous thrombosis. The classic imaging finding is a peripheral rim o fT l high signal.
T1: peirpheral rim of bright t1
T2: variable
T1+C: none
Fibroid degeneration
myxoid degeneration
uncommon
T1: dark
T2: bright
T1+C: minimal
Fibroids degenration
cystic
uncommon
T1: dark
T2: bright
T1+C: none
Uterine Leiomyosarcoma
The risk o f malignant transformation to a leiomyosarcoma is super low (0.1%). These look like a fibroid, but rapidly enlarge. Areas of necrosis are often seen.
adenomyosis
imaging
Ultrasound is less specific with findings including a heterogeneous uterus (hyperechoic adenomyosis, with hypoechoic muscular hypertrophy), or just enlargement of the posterior wall.
MRI is the way better test with the most classic feature being thickening of the junctional zone of the uterus to more than 12 mm (normal is < 5 mm). The thickening can be either focal or diffuse. Additionally, the findings o f small high T2 signal regions corresponding to regions o f cystic change is a classic finding.
Thick Endometrium
overview
Remember the stripe is measured without including any fluid in the canal. Focal or generalized thickening in post menopausal women greater than 5mm should get sampled. Premenopausal endometriums can get very thick - up to 20mm can be normal.
Thick Endometrium
trivia
- Estrogen secreting tumors - Granulosa Cell tumors o f the ovary will thicken the endometrium.
- Hereditary Non-Polyposis Colon Cancer (HNPCC) - have a 30-50x increased risk of endometrial cancer
Thick Endometrium
tamoxifen changes
This is a SERM (acts like estrogen in the pelvis, blocks the
estrogen effects on the breast). It’s used for breast cancer, but increases the risk of
endometrial cancer. It will cause subendometrial cysts, and the development of
endometrial polyps (30%). Normally, post menopausal endometrial tissue shouldn’t be
thicker than 4mm, but on Tamoxifen the endometrium is often thick (some papers say the
mean is 12 mm at 5 years). When do you biopsy? Clear guidelines on this are illusive (if
forced to guess I’d pick 8 or 10 mm). The only thing that seems consistent is that routine
screening is NOT advised. If you are wondering if a polyp is hiding you can get a
sonohysterogram (ultrasound after instillation o f saline).
Thick Endometrium
endometrial fluid
In premenopausal women this is a common finding. In
postmenopausal women it means either cervical stenosis or an obstructing mass (usually
cervical stenosis).
Postmenopausal Bleeding:
Is it from atrophy or cancer?
- Endometrium less than 5 mm = Probably Atrophy
* Endometrium > 4-5 mm = Maybe cancer and gets a biopsy
Endometrial Cancer
workup
First step is going to be an ultrasound. If the endometrium is too thick (most people say 4- 5mm) then it gets a biopsy. Almost always this will be stage 1 disease, and no further imaging will be done. If there is concern that it’s more than stage 1 - that is when you would get MRI (CT is shit for the uterus and would never be the right answer).
• First Step Postmenopausal Bleeder = Ultrasound
• Too Thick ? = Biopsy
• Extent of Disease = MRI
Endometrial Cancer
appearance on MRI
- T1 Iso
- T2 Mildly Hyper
- Tl+C Homogenous, but less enhancement compared to adjacent myometrium ( it’s dark).
- DWI Will show restricted dijfusion. This sequence is good fo r “Drop mets ” into the vagina, and fo r lymph node detection.
Endometrial Cancer
critical stage
(most testable stage) - Stage I to Stage 2
• Stage 2 disease is defined as cervical stroma invasion. This is supposedly high risk for lymph node mets.
• The diagnostic key is the post contrast imaging (obtained 2-3 mins after injection). If the cervical mucosa enhances normally, you have excluded stromal invasion.
• Stage 2 is probably going to change management by adding pre-op radiation to the cervix, plus a change from TAH to radical hysterectomy (obviously this varies from center to center).
Endometrial Cancer
stage 1 mri
T1+C: Normal Dark Cervical Stroma (star).
Enhancement of the Cervical Mucosa (arrows) Excludes Invasion.
Endometrial Cancer
stage 2 mri
T1+C: Tumor Invasion o f the Cervix
Endometrial Cancer
possible trivia
- Moving from stage 1A (<50% myometrium) to stage 1B (>50% o f the myometrium) also increases the risk o f lymph node disease.
- Some sites will do lymph node sample at stage 1 A, and radical lymph node dissection at stage IB.
Endometrial Cancer
possible trivia
- Moving from stage 1A (<50% myometrium) to stage 1B (>50% o f the myometrium) also increases the risk o f lymph node disease.
- Some sites will do lymph node sample at stage 1 A, and radical lymph node dissection at stage IB.
Cervical Cancer
overview
It’s usually squamous cell, related to HPV (like 90%). The big thing to know is parametrial
invasion (stage lib). Stage Ila or below is treated with surgery. Once you have parametrial
invasion (stage lib), or involvement o f the lower 1/3 o f the vagina it’s gonna get chemo/
radiation. In other words, management changes so that is the most likely test question.
Cervical Cancer
staging pearls
Stage 11A: Spread beyond the cervix, but NO parametrial invasion, Surgery
Stage 11B: Parametrial involvement but NOT extension to pelvic side wall., Chemo/ Radiation
Cervical Cancer
what is the parametrium
he
p aram etrium is a fib ro u s b an d that
sepa ra tes the su prava g in a l ce rv ix from
the bladder. It e x te n d s between the
layers of the bro ad ligament.
Cervical Cancer
why is the parametrium important
The uterine
a rtery runs inside the parametrium,
hen ce the need for ch em o - o n ce
in va de d .
Cervical Cancer
how do you tell if the parametrium is invaded
Normally the ce rv ix has a T2 d a rk ring. That
thing should be intact. If the tum o r goes throug h th a t thing, you g otta call it invaded.
Cervical Cancer
how do you tell if the parametrium is invaded
Normally the ce rv ix has a T2 d a rk ring. That
thing should be intact. If the tum o r goes throug h th a t thing, you g otta call it invaded.
Solid Vaginal Masses
overview
An uninvited solid vaginal mass is usually a bad thing. It can be secondary (cervical or
uterine carcinoma protruding into the vagina), or primary such as a clear cell adenocarcinoma
or rhabdomyosarcoma.
Solid Vaginal Masses:
leiomyoma
Rare in the vagina, but can occur (most commonly in the anterior wall).
Solid Vaginal Masses:
SCC
The most common cancer of the vagina (85%). This is associated with HPV. This is just like the cervix.
Solid Vaginal Masses:
clear cell adenocarcinoma
This is the zebra cancer seen in women whose mothers took
DES (a synthetic estrogen thought to prevent miscarriage). That plus “T-Shaped Uterus” is
probably all you need to know.
Solid Vaginal Masses:
vaginal rhabdomyosarcoma
This is the most common tumor o f the vagina in children.
There is a bimodal age distribution in ages (2-6, and 14-18). They usually come off the
anterior wall near the cervix. It can occur in the uterus, but typically invades it secondarily.
Think about this when you see a solid T2 bright enhancing mass in the vagina / lower uterus
in a child.
Solid Vaginal Masses:
met trivia
- A met to the vagina in the anterior wall upper 1/3 is “always ” (90%) upper genital tract.
- A met to the vagina in the posterior wall lower 1/3 is “always ” (90%) from the Gl tract.
Cystic Vaginal I Cervical Masses
nabothian cysts
These are usually on the cervix and you see them all the time. They are
the result o f inflammation causing epithelium plugging o f mucous glands.
Cystic Vaginal I Cervical Masses
gartner ducst cysts
These are the result o f incomplete regression of the Wolffian ducts.
They are classically located along the anterior lateral wall of the upper vagina. If they are
located at the level o f the urethra, that can cause mass effect on the urethra (and
symptoms).
Cystic Vaginal I Cervical Masses
bartholin cysts
These are the result o f obstruction o f the Bartholin glands (mucinsecreting
glands from the urogenital sinus). They are found below the pubic symphysis
(helps distinguish them from Gartner duct).
Cystic Vaginal I Cervical Masses
skene gland cysts
Cysts in these periurethral glands, can cause recurrent UTIs and urethral obstruction.
Cystic Vaginal I Cervical Masses
highest to lowest
nabothina
gartner duct (anter lateral upper vagina
skene gland anterior
bartholin below near the butthole
O V A R Y / A D N E X A
overview
Before we begin, a few general tips
(1) never biopsy or recommend biopsy o f an ovary,
(2) on CT if you can’t find the ovary, follow the gonadal vein, and
(3) hemorrhage in a cystic mass usually means it’s benign.
A quick note on ovarian size; ovarian volume can be considered normal up until 15 ml (some say 20 ml). The post menopausal ovary should NOT be larger than 6 cc.
Let’s ta lk about ovulation
Follicles seen during the early menstrual cycle are typically small (< 5 mm in diameter). By day 10 of the cycle, there is usually one follicle that has emerged as the dominant follicle. By mid cycle, this dominant follicle has gotten pretty big (around 20 mm).
The size isn’t surprising because it contains a mature ovum. The LH surge causes the dominant follicle to rupture, releasing the egg. The follicle then regresses in size, forming a Corpus Luteum. A small amount of fluid can be seen in the cul-de-sac. Occasionally, a
follicle bleeds and re-expands (hemorrhagic cyst) - more on this later.
Let’s ta lk about ovulation
Follicles seen during the early menstrual cycle are typically small (< 5 mm in diameter). By day 10 of the cycle, there is usually one follicle that has emerged as the dominant follicle. By mid cycle, this dominant follicle has gotten pretty big (around 20 mm).
The size isn’t surprising because it contains a mature ovum. The LH surge causes the dominant follicle to rupture, releasing the egg. The follicle then regresses in size, forming a Corpus Luteum. A small amount of fluid can be seen in the cul-de-sac. Occasionally, a
follicle bleeds and re-expands (hemorrhagic cyst) - more on this later.
Meaningless Vocab (High Yield) Premenopausal Ovarian Cyst
< 1 cm = Follicle
1-2 cm = Dominant Follicle
> 3 cm = Cyst
Cumulus Oophorus
This is a piece of anatomy trivia. It is a collection of
cells in a mature dominant follicle that protrudes into the
follicular cavity, and signals imminent ovulation (its
absence means nothing).
Fertility Meds
Medications such as a Clomiphene Citrate (Clomid), force the maturation of multiple
bilateral ovarian cysts. It is not uncommon for the ovaries of women taking this drug
to have multiple follicles measuring more than 20 mm in diameter by mid cycle.
Theca Lutein Cysts
overview
this is a type of functional
cyst (more on that below), related to overstimulation
from b-HCG. What you see are large cysts (~ 2-3 cm)
and the ovary has a typical multilocular cystic “spokewheel”
appearance.
Theca Lutein Cysts
think about 3 things
- Multifetal pregnancy,
- Gestational trophoblastic disease (moles),
- Ovarian Hyperstimulation syndrome.
Ovarian Hyperstimulation Syndrome
This is a complication associated with fertility
therapy (occurs in like 5%). They will show you the ovaries with theca lutein cysts, then ascites,
and pleural effusions. They may also have pericardial effusions. Complications include increased
risk for ovarian torsion (big ovaries) and hypovolemic shock.
Paraovarian (Paratubal) Cyst =
Cyst that is in the adnexa but not within the ovary. Instead
these things are located adjacent to the ovary or tube. If the cyst is simple (not septated or nodular) and
clearly not ovarian they will not need followup — is doesn’t matter how big it is, as they have incredibly
low rate of malignancy.
TLDR
simple paravoaran cysts do no require follow up
ovary
premenstrual
- The ovaries o f a pediatric patient stay small until around age 8-9.
- Ovaries may contain small follicles.
ovary
premenopausa
• A piece o f trivia; premenopausal ovaries may be HOT on PET
(depending on the menstrual cycle).
• This is why you do a PET in the first week o f the menstrual cycle.
ovar
postmenopausal
( > one year after menses stops):
• Considered abnormal if it exceeds the upper limit of normal, or is twice the size of the other ovary (even if no mass is present).
• Small cysts (< 3 cm) are seen in around 20% o f post menopausal women.
• In general, postmenopausal ovaries are atrophic, lack follicles, and can be difficult to find with ultrasound.
• The ovarian volume will decrease from around 8cc at age 40, to around 1 cc at age 70.
• The maximum ovarian volume in a post menopausal woman is 6 ml.
• Unlike premenopausal ovaries, post menopausal ovaries should NOT be hot on PET.
Incidental Simple Appearing Ovarian Cyst
-Shown on CT
PreMenopausal: < 3 cm = Call it Normal Follicle PreMenopausal: > 3 cm = Get an US PostMenopausal: < 1cm = Call it Normal Cyst PostMenopausal: > 1cm = Get an US
Incidental Simple Appearing Ovarian Cyst
-Shown on US
PrcMenopausal:
< 7 cm = No Follow Up
PreMenopausal: > 7 cm = Follow Up (3 months)
PostMenopausal: < 5 cm = No Follow Up
PostMenopausal: > 5 cm = Follow Up (3 months)
Cyst is not simple (irregular septations, papillary
Droiections. or solid elements) =
gyn consult
Ovary
sinister six
Physiologic and functioning follicles Corpora lutea Hemorrhagic cysts Endometriomas Benign cystic teratomas (dermoids) Polycystic ovaries
Functioning Ovarian Cysts
Functioning cysts (follicles) are affected by the menstrual cycle (as I detailed eloquently above). These cysts are benign and usually 25 mm or less in diameter. They will usually change / disappear in 6 weeks. If a cyst persists and either does not change or increases in size, it is considered a nonfunctioning cyst (not under hormonal control). Simple cysts that are > 7 cm in size may need further evaluation with MR (or surgical evaluation). Just because it’s hard to evaluate them completely on US when they are that big, and you risk torsion with a cyst that size.
Corpus Luteum
The normal corpus luteum arises from a dominant follicle (as I detailed eloquently above). These things can be large (up to 5-6 cm) with a variable appearance (solid
hypoechoic, anechoic, thin-walled, thick walled, cyst with debris). The most common appearance is solid and hypoechoic with a “ring of fire” (intense peripheral blood flow).
Endometrioma
overview
This targets young women during their reproductive years and can cause chronic pelvic painnassociated with menstruation. The traditional clinical history of endometriosis is the triad of infertility, dysmenorrhea, and dyspareunia.
Endometrioma
classic appearance
The classic appearance is rounded mass with homogeneous low level internal echoes and increased through transmission (seen in 95% of cases). Fluid-fluid levels and internal septations can also be seen. It can look a lot like a hemorrhagic cyst (sometimes).
Endometrioma
general rule
As a general rule, the more unusual or varied the echogenicity and the more ovoid or irregular the shape, the more likely the mass is an endometrioma. Additionally, and of more practical value, they are not going to change on follow up (hemorrhagic cysts are). In about 30% of cases you can get small echogenic foci adhering to the walls (this helps make the endometrioma diagnosis more likely). Obviously, you want to differentiate this from a true wall nodule.
What is the most sensitive
imaging feature on MR1 for the
diagnosis of malignancy in an
endometrioma ?
an enhancing mural nodule
complications of endometriosis
The complications of endometriosis (bowel obstruction, infertility, etc…) are due to a fibrotic
reaction associated with the implant. The most common location for solid endometriosis is the
uterosacral ligaments.
do endometriomas ever become cancer
About 1% of endometriomas undergo malignant transformation (usually endometrioid or clear cell carcinoma). How do you tell which one is which??? Malignancy is very rare in endometriomas smaller than 6 cm. They usually have to be
bigger than 9 cm. Additionally, the majority of women with carcinoma in an endometrioma are
older than 45 years. So risk factors for turning into cancer: (a) older than 45, (b) bigger than
6-9 cm.
endometrioima with pregnancy
There is a thing called a “decidualized
endometrioma. ” This is a vocab word used to describe a
solid nodule with blood flow in an endometrioma of a
pregnant girl. Obviously this is still gonna get followed up
- but is a mimic of malignancy. The thing never to forget
is that if the patient is NOT pregnant and you see a solid
nodule with blood flow - that is malignant degeneration -
period - no hesitation, next question.
endometrioma on mri
Will be T1 bright (from the
blood). Fat saturation will not suppress the signal
(showing you it’s not a teratoma). Will be T2 dark! (from
iron in the endometrioma). The shading sign is a buzzword
for endometriomas on MR imaging. On T2 you should
look for “shading.” The shading sign describes T2
shortening (getting dark) of a lesion that is T1 bright.
THIS v.v THAT: Corpus Luteum VS Ectopic Pregnancy
overview
They both can have that “ring of fire” appearance, but please don’t be an idiot about this. Most ectopic pregnancies occur in the tube (the corpus luteum is an ovarian structure). If you are really lucky, a “hint” is that the corpus luteum should move with the ovary, where an ectopic will move separate from the ovary (you can push the ectopic away from it). Also, the tubal ring of an ectopic pregnancy is usually more echogenic when compared to the ovarian parenchyma. Whereas, the wall of the corpus luteum is usually less echogenic. A specific (but not sensitive) finding in ectopic pregnancy is a RI of <0.4 or >0.7.
THIS v.v THAT: Corpus Luteum VS Ectopic Pregnancy
ectopic
RI <0.4 or >0.7
thick echogenic rim
moves separate from the ovary
THIS v.v THAT: Corpus Luteum VS Ectopic Pregnancy
corpus luteum
RI 0.4-0.7
thin echogenic rim
moves with the ovary
ovarian
Hemorrhagic Cysts: overview
As mentioned on prior pages, sometimes a ruptured follicle bleeds internally and reexpands.
The result is a homogenous mass with enhanced through transmission (tumor
w o n ’t do that) with a very similar look to an endometrioma. A lacy “fishnet appearance”
is sometimes seen and is considered classic. Doppler flow will be absent. The traditional
way to tell the difference between a hemorrhagic cyst vs endometrioma, is that the
hemorrhagic cyst will go away in 1-2 menstrual cycles (so repeat in 6-12 weeks).
ovarian
Hemorrhagic Cysts: on mri
Will be T1 bright (from the blood). Fat saturation will not suppress the signal (showing you it’s not a teratoma). The lesion should NOT enhance.
ovarian
Hemorrhagic Cysts: in old ladies
Postmenopausal women may occasionally ovulate, so
you don’t necessarily need to freak out (follow up in 6-12 weeks). Now, late
postmenopausal women should NEVER have a hemorrhagic cyst and if you are shown
something that looks like a hemorrhagic cyst in a 70 year old - it’s cancer till proven
otherwise.
THIS vs THAT: E n d om e triom a vs H em o r rh a g ic C ys t
endometrioma - THIS vs THAT: E n d om e triom a vs H em o r rh a g ic C ys t
hemorrhagic cyst - lacy fishnet appearance
Dermoid
overview
These things typically occur in young women (20s-30s), and are the most common ovarian neoplasm in patients younger than 20. The “Tip of the Iceberg Sign” is a classic buzzword and refers to absorption of most of the US beam at the top of the mass. The typical ultrasound appearance is that of a cystic mass, with a hyperechoic solid mural nodule, (Rokitansky nodule or dermoid plug). Septations arc seen in about 10%.
Dermoid
on mri
Will be bright on T1 (from the fat). There will be fat suppression (not true of hemorrhagic cysts, and endometriomas).
Dermoid
cancer?
About l% of dermoids can undergo malignant transformation (almost always to squamous cell CA). Again, risk factors are size (usually larger than 10cm), and age (usually older than 50).
Dermoid
cancer subtypes
Endometrioma Clear Cell
Dermoid Squamous
Dermoid
gamesmanship
Gross Fat containing ovarian mass on CT
Dermoid
gamesmanship 2
The Old Tooth Trick - shown on plain film, CT, or even as susceptibility (dark stuff) on MR. Remember Dermoids are basically teratomas, and teratomas grow all kinds of gross shit including teeth, hair, finger nails etc… The tooth is obviously the classic one.
Dermoid
gamesmanship 3
“Dot -dash” pattern has been described for hair within a cyst.
Polycystic Ovarian Syndrome
—Typically an overweight girl with infertility, acne, and a pencil mustache (not a full Ron Swanson)
The imaging criteria is:
Ten or more peripheral simple cysts (typically small < 5 mm)
• Usually Characteristic ‘string-of-pearls’ appearance.
Ovaries are typically enlarged (> 10 cc), although in 30% of patients the ovaries have a normal volume
OVARIAN C A N C E R
overview
Ovarian cancers often present as complex cystic and solid masses. They are typically intraovarian
(most extra-ovarian masses are benign). The role o f imaging is not to come down
hard on histology (although the exam may ask this of you), but instead to distinguish benign
from malignant and let the surgeon handle it from there.
OVARIAN C A N C E R
think cancer if
- Unilateral (or bilateral) complex cystic adnexal masses with thick ( > 3 mm) septations, and papillary projections (nodule with blood flow).
- Solid adnexal masses with variable necrosis
OVARIAN C A N C E R
knee jerks
- Multiple thin or thick septations = Call the Surgeon
*Nodule with Flow = Call the Surgeon - Solid Nodules Without Flow =
o Get an MR to make sure it’s not a dermoid plug,
o If it’s not a dermoid, then call the surgeon
Serous Ovarian I Cystadenocarcinoma I Cystadenoma
Serous tumors are the most common type of ovarian malignancy. About 60% of serous tumors are benign, and about 15% are considered borderline (the rest are malignant). They favor women o f childbearing age, with the malignant ones tending to occur in older women. They typically are unilocular with few septations. They are frequently bilateral (especially when malignant). Papillary projections are a common finding, and are suggestive of malignancy. If you see ascites, they have mets (70% have peritoneal involvement at the time o f diagnosis).
Mucinous O v a rian C y s tad e n o c a rc in om a
Often a large mass. They are typically multi-loculated (although septa are often thin). Papillary projections are less common than with serous tumors. You can see low level echos (from mucin). These dudes can get Pseudomyxoma peritonei with scalloping along solid organs. Smoking is a known risk factor (especially for mucinous types).
THIS vs THAT: Serous vs Mucinous
serous
Unilocular (fewer septations)
Papillary Projections Common
THIS vs THAT: Serous vs Mucinous
mucinous
Multi-locular (more septations)
Papillary Projections Less Common
E n dome trio id O v a rian C an c e r
overview
This is the second most common ovarian cancer (serous number one, mucinous number three). These things are bilateral about 15% o f the time.
E n dome trio id O v a rian C an c e r
what to know
- 25% o f women will have concomitant endometrial cancer, with the endometrial cancer as the primary (ovary is met).
- Endometriomas can turn into endometrioid cancer
- 15% are bilateral
Gamesmanship:
Ovarian Mass + Endometrial Thickening
This is a way to show both Endometrioid CA (which often has both ovarian and endometrial CA), and Granulosa-Theca Cell Tumor (which produce estrogen - and cause endometrial hyperplasia)
B.F.M’s - for Adults
ovary
(1) Ovarian Masses - Mucinous and Serous
(2) Desmoids - Remember Gardner Syndrome
(3) Sarcomas
Fibroma I Fibrothecoma
The ovarian fibroma is a benign ovarian tumor, most commonly seen in middle aged women.
The fibrothecoma / thecoma spectrum has similar histology. It’s very similar to a fibroid. On
ultrasound it’s going to be hypoechoic and solid. On MRI it’s going to be T1 and T2 dark, with
a band of T2 dark signal around the tumor on all planes. Calcifications are rare.
Meigs syndrome
This is the triad of ascites, pleural effusion, and a benign ovarian tumor (most commonly fibroma).
Fibromatosis
This is a zebra. You have tumor-like enlargement of the
ovaries due to ovarian fibrosis. It typically hits girls around the age of 25.
It’s associated with omental fibrosis and sclerosing peritonitis. You are
going to get dark T1 and T2 signal. The buzzword for that T2 signal is
“black garland sign. ” The condition is benign, and sometimes managed
with surgical removal of the ovaries.
Brenner Tumor
Epithelial tumor of the ovary seen in women in their 50s-70s. It’s fibrous
and T2 dark. Unlike Fibromas, calcifications are common (80%). They are also sometimes
referred to as “Ovarian Transitional Cell Carcinoma ” for the purpose of fucking with you.
Struma Ovarii
These things are actually a subtype of ovarian teratoma. On imaging you are looking for a
multilocular, predominantly cystic mass with an INTENSELY enhancing solid component. On
MRI - the give away is very low T2 signal in the “cystic” areas which is actually the thick
colloid. These tumors contain THYROID TISSUE, and even though it’s very rare (like 5%), I
would expect that the question stem will lead you to this diagnosis by telling you the patient is
hyperthyroid or in a thyroid storm.
Metastatic Disease to the Ovary
Around 10% of malignant ovarian tumors are mets. The primary is most commonly from
colon, gastric, breast, lung, and contralateral ovary. The most common look is bilateral solid
tumors.
Krukenburg tumor
T h is is a metastatic tumor to the ovaries from the GI tract (usually stomach).
Ovarian Torsion
overview
Rotation of the ovarian vascular pedicle (partial or complete) can result in obstruction to venous outflow and arterial inflow. Torsion is typically associated with a cyst or tumor (anything that makes it heavy, so it flops over on itself).
Critical Point = The most constant finding in ovarian torsion is a large ovary.
Ovarian Torsion
feaatures
Unilateral enlarged ovary (greater than 4 cm) Mass on the ovary Peripheral Cysts Free Fluid Lack of arterial or venous flow
Ovarian Torsion
the ovary is not the testicle
The ovary has a dual blood supply. Just because you have flow, does
NOT mean there isn’t a torsion. You can torse and de-torse. In other words, big ovary + pain =
torsion. Clinical correlation recommended.
Hydrosalpinx
buzzword 1
Thin (or thick in chronic states) elongated tubular structure in the pelvis.
Hydrosalpinx
buzzword 2
The buzzword is “cogwheel appearance,” referring to the normal longitudinal folds of a
fallopian tube becoming thickened. Another buzzword is “string sign” referring to the
incomplete septae. The “waist sign” describes a tubular mass with indentations of its opposing walls
(this is suppose to help differentiate hydrosalpinx from an ovarian mass).
Hydrosalpinx
causes
There are a variety of causes, the most common is being a skank, infidel, or free spirit (PID).
Additional causes include endometriosis, tubal cancer, post hysterectomy (without salpingectomy /
oophorectomy), and tubal ligation. Rare and late complication is tubal torsion.
Pelvic Inflammatory Disease (PID)
overview
Infection or inflammation of the upper female genital tract. It’s usually secondary to the cultural
behaviors of trollops and strumpets (collectors of Gonorrhea / Chlamydia). As a hint, the question
writer could describe the patient as “sexually disreputable. ” The question could also describe the
patient as recently appearing as a guest on the Maury Show (the “Not the Father!” show — google if
unfamiliar, it could be on the exam).
Pelvic Inflammatory Disease (PID)
us
see a Hydrosalpinx. The margin of the uterus may become ill defined
(“indefinite uterus” - is a buzzword). Later on you can end up with tubo-ovarian abscess or pelvic
abscess. You can even get bowel or urinary tract inflammatory changes.
Paraovarian Cyst
This is a congenital remnant that arises from the Wolffian duct. They are more common than you
think with some texts claiming these account for 10-20% of adnexal masses. They are classically
round or oval, simple in appearance, and do NOT distort the adjacent ovary (key finding). They
can indent the ovary and mimic an exophytic cyst, but a good sonographer can use the transducer to
separate the two structures.
Ovarian Vein Thrombophlebitis
This is seen most commonly in postpartum women, often presenting with acute pelvic pain and
fever. For whatever reason, 80% of the time it’s on the right. It’s most likely to be shown on CT
(could be ultrasound) with a tubular structure with an enhancing wall and low-attenuation thrombus
in the expected location of the ovarian vein. A dreaded sequela is pulmonary embolus.
Peritoneal Inclusion Cyst
overview
This is an inflammatory cyst of the peritoneal cavity that occurs when adhesions envelop an ovary.
Adhesions can be thought of as diseased peritoneum. Whereas the normal peritoneum can absorb
fluid, adhesions cannot. So, you end up with normal secretions from an active ovary confined by
adhesions and resulting in an expanding pelvic mass. The classic history is patient with prior pelvic
surgery (they have to tell you that, to clue you in on the presence of adhesions), now with pain.
They could get tricky and say history of PID or endometriosis (some kind of inflammatory process to
piss off the peritoneum). In that case, it is likely they would show an ultrasound (or MR) with a
complex fluid collection occupying pelvic recesses and containing the ovary. It’s not uncommon to
have septations, loculations, and particulate matter within the contained fluid.
Peritoneal Inclusion Cyst
key features
- Lack of walls. “Passive shape” that conforms to and is defined by surrounding structures.
- Entrapment of an ovary. Ovary will be either in the collection, or at the periphery.
Peritoneal Inclusion Cyst
classic vignette
A woman of reproductive age with a history of endometriosis, pelvic surgery, and
pelvic inflammatory disease. Accompanied by images (most likely ultrasound, less likely CT or MR)
or a fluid-filled mass that conforms to the shape of the pelvis and surrounds an ovary.
Gestational Trophoblastic Disease
Think about this with marked elevation of B-hCG. They will actually trend betas for tumor
activity. Apparently, elevated B-hCG makes you vomit - so hyperemesis is often part of the
given history. Other pieces of trivia is that moles are more common in ages over 40, and prior
moles makes you more likely to get another mole.
Hydatidiform mole
complete more overview
(classic mole) (70%): This one involves the entire placenta. There will be no
fetus. The worthless trivia is that the karyotype is diploid. A total zebra scenario is that you
have a normal fetus, with a complete mole twin pregnancy (if you see that in the wild, write it
up). The pathogenesis is fertilization of an egg that has lost its chromosomes (46XX).
Hydatidiform mole
complete moel first trimeter
Classically shows the uterus to be filled with an echogenic, solid, highly vascular mass, often described as “snowstorm” in appearance.
Hydatidiform mole
complete mole tsecond trimester
Vesicles that make up the mole enlarge into individual cysts (2-30 mm) and produce your “bunch of grapes” appearance.
Hydatidiform mole
partial mole
overview
This one involves only a portion of the placenta. You do have a fetus, but
it’s all jacked up (triploid in karyotype). The pathogenesis is fertilization of an ovum by two
sperm (69XXY). Mercifully, it’s lethal to the fetus.
Hydatidiform mole
partial mole us
The placenta will be enlarged, and have areas of multiple, diffuse anechoic lesions. You may see fetal parts.
theca lutein cysts in molar pregnancy
Remember I mentioned that Theca Lutein cysts are seen in molar pregnancies.
Theca Lutein Cyst Trivia: Most commonly bilateral and seen in the second trimester
Invasive Mole
This refers to invasion of molar tissue into the myometrium. You typically see it after the
treatment of a hydatidiform mole (about 10% of cases). US may show echogenic tissue in the
myometrium. However, MRI is way better at demonstrating muscle invasive. MRI is going to
demonstrate focal myometrial masses, dilated vessels, and areas of hemorrhage and necrosis.
Choriocarcinoma
(the guacamole has gone bad)
This is a very aggressive malignancy that forms only trophoblasts (no villous structure). The
typical attacking pattern of choriocarcinoma is to spread locally (into the myometrium and
parametrium) then to spread hematogenous to any site in the body. It’s very vascular and bleeds
like stink. The classic clinical scenario is serum p-hCG levels that rise in the 8 to 10 weeks
following evacuation of molar pregnancy. On ultrasound, choriocarcinoma (at any site) results in
a highly echogenic solid mass. Treatment = methotrexate.
Fractured Penis
overview
This is one of the most tragic situations that can occur in medicine.
There are several potential mechanisms of injury. Anecdotally, it seems to be most common
in older men participating in extra-marital relations with strippers named “Whisper.” There
is at least one article stating “impotence” is protective - which makes sense if you think
about the pathophysiology.
Fractured Penis
key trivia
Defined by fracture of the corpus
cavernosum and its surrounding sheath, the tunica
albuginea (black line outlining the dong bone).
Fractured Penis
cartooned t1
Interruption of the black line (tunica albuginea) - arrow.
It’s helpful to look for hemorrhage (Tl bright) in the
corpus cavernosum (the primary stabilizing stmt of this
battering ram).
Fractured Penis
stigmata
Stigmata of this injury can include a sub optimal angulation (Peyronie disease) from fibrous scar formation.
Prostate anatomy
overview
Anatomists like to use “zones” to describe locations, and it actually helps with pathology. The anterior fibromuscular gland is dark on T1 and
T2. The central and transitional zones (together called the “centralgland”) are brighter than the anterior muscular zone, but less bright than the peripheral zone on T2. In other words the peripheral zone is the most T2 bright.
Prostate anatomy
adenocarcinoma
• Peripheral Zone: 70%
*Transition Zone: 20%
• Central Zone: 10%
Prostate anatomy
dark stuf
Central Gland
this is where BPH nodules live
Prostate anatomy
bright stuff
Peripheral Zone
this is where cancer lives
MRI findings for prostate cancer
Cance r is d a rk on T2 (background is h ig h ), restricts on
diffusion (low on ADC), and enhances early and washes out (type 3 curve - just like a breast
cancer).
Prostate cancer mets
Bone scan is the money for prostate mets (vertebral body mets).
prostate cancer trivia
PSA can be useful when considering risk of bone mets. There is at least 1 paper that says a PSA < 20 has a high predictive value in mling OUT skeletal mets. In other words, PSA tends to be high when disease is aggressive enough to go to the bones.
prostate cancer staging
The main thing to know is stage II vs stage III, as extra capsular extension is the most important factor governing treatment.
Prostate cancer addt staging
Seminal vesicles (T3b) and the nerve bundle are also right behind the prostate and can get invaded (urologists love to hear about that).
prostate cancer stage II
Confined by capsule (T2)
Abutment o f the capsule
without bulging
prostate cancer stage III
Extension through capsule (T3a)
Bulging o f the capsule,
or frank extension through it
PSA, Gleason Score, and PI-RADS
key concept
Prostate Cancer is a lot like Breast Cancer - in that it is
very common and often a “benign” entity (1 in 6 men will be diagnosed
with prostate cancer , 3% will die o f it). There are tons and tons of
elderly people with low grade prostate CA and breast cancers (DCIS)
that will never even know they have it unless somebody does a biopsy
on them… or worse performs screening on them. Which brings us to
the PSA. When family medicine doctors starting doing PSA checks on
everybody suddenly there was this enormous spike in the incidence o f
prostate cancer. Suddenly everyone has cancer (I blame the liberal
media).
PSA, Gleason Score, and PI-RADS
who dies of prostate cancer
There are 3 factors - Gleason Scores
8-10, Advanced Clinical Stage (mets), and PSA > 20. People with
Gleason scores less than 6, PSA < 10, and staging < 2a (less than half
the lobe) are unlikely to die o f the prostate cancer.
PSA, Gleason Score, and PI-RADS
managmeent
It is gonna depend a lot on who you ask. Most people will add hormone therapy around stage
2B (more than half the lobe) but it is complicated.
PSA, Gleason Score, and PI-RADS
PSA
This is an antigen produced by the normal prostate and incorporated into the ejaculate (from the window
to the wall), for the purpose of dissolving cervical mucus e tc … It also leaks out into the blood in small amounts
in normal men and in larger amounts when the prostate is abnormal (cancer, infected, riding a bicycle, sticking
stuff up your ass that don’t belong up your ass, and benign hypertrophy). Family Medicine docs will screen
people starting at 50. Some numbers to have a vague familiarity with include: Normal < 4. Low Risk Category
< 10. High Risk Category > 20. After prostatectomy normal is zero, if it rises to 0.2 think recurrence. After
radiation anything over 2.0 is concerning for recurrence (although it’s a little more complicated than that). PSA
< 20 = bone mets unlikely.
Gleason
There is a “grade” a “ score” and a “group” - you better fucking believe the distinction is fair game..
• Gleason Grade: This refers to the histological patterns in the sample “ 1” is normal, “5” is very very not normal. 2-4 are in the middle.
• Gleason Score: This is the sum of the two most common “grades.” The more common pattern is always first. So “A” 3+5 = 8, and “B” 5+3 = 8. “B” has more of 5 than “A” and is therefore worse off. Total scores less than 6 aren’t usually reported.
• Gleason Group: This uses pattern scores to reflect the actual risk. This removes the confusion over one 7 being worse than another 7. For example 3+4 is grade 2, and 4+3 is grade 3. Grade is 1-5
PIRADS overview
Scores are calculated by using data from DWI, T 2, and Enhancement. Tumor in the Transition zone is determined primarily from T2 (t for t). Peripheral zone is determined primarily from DWI.
PIRADS DWI
1 normal 2 linear/wedge 3 vague patch > 4 if enhancing 4 focal <1.5 5 focal >1.5cm
PIRADS T2
1 normal nodules - full capsule
2 atyupical nodule - no capsule > goes to three if focal restricted dwi
3 heterogenous, blurry margins > 4 if restricted dwi >1.5cm
4 lowe signal <1.5
5 lowe signal >1.5 with extracapsular ect
PSA, Gleason Score, and PI-RADS
clincally signigicant cancer
Gleason Score > 7
Cancer Volume > 0.5cc
Extension through the Capsule (loss o f normal T2 signal in the seminal vesicle, bulging of the capsule / frank invasion through it, loss o f fat between prostate and rectum, neurovascular bundle asymmetry).
Benign prostatic hyperplasia (BPH):
overview
Obviously this is super common, and makes old men pee a lot. Volume o f 30cc is one definition. Most commonly involves the transitional zone (cancer is rare in the transitional zone - 10%). The central gland enlarges with age. The median lobe component is the one that hypertrophies and sticks up into the bladder. It can cause outlet obstruction, bladder wall thickening (detrusor hypertrophy), and development of bladder diverticulum.
Benign prostatic hyperplasia (BPH):
buzzwork
The IVP buzzword is “J shaped”, “Fishhook”, or “Hockey stick” shaped ureter - as the distal ureter curves around the enlarged prostate.
Benign prostatic hyperplasia (BPH):
mri
In the Transitional Zone
(Central Gland)
T2 Heterogenous
Can Restrict Diffusion
May enhance and washout
Prostate post biopsy changes
Classically T1 bright stuff in the gland. It’s subacute blood
Prostate mr summary
peripheral tumor
T2 dark
adc dark
enhancement early enhancement and washout
Prostate mr summary
peripheral zone hermorrhage
t2 dark (sometimes t1 bright)
adc dark
enhancement none
Prostate mr summary
central gland/transitional zone tumor
t2 dark (charcoal)
adc dark
early enhancement and early washout
Prostate mr summary
bph
T2 dark (welldefined)
adc dark
can enhance
midline male pelvic cysts
prostatic utricle
mullerian duct cyst
ejaculatory duct cyst
lateral male pelvic cyst
seminal vesicle cyst
diverticulosis of the ampulla of vas deferns
Seminal Vesicle Cyst
overview
The classic look is a unilateral cyst that is lateral to the prostate. If they get large they can look midline, but if they show you a large one you won’t be able to tell it from a utricle cyst. They can be congenital or acquired.
Seminal Vesicle Cyst
congenital trivia
- Associated with renal agenesis
- Associated with vas deferens agenesis
- Associated with ectopic ureter insertion
- Associated with polycystic kidney disease
Seminal Vesicle Cyst
acquired trivia
- Obstruction often from prostatic hypertrophy, or chronic infection/scarring
- Classic history is prior prostate surgery
Prostatic Utricle Cyst
overview
This represents a focal dilation in the prostatic urethra (remnant of the Mullerian duct) - as such they communicate with the urethra and can cause “dribbling” (both on and off the basketball court).
The tendency towards superinfection is also explained by the
communication with the urethra.
Prostatic Utricle Cyst
assocations
Hvpospadias is the most common associated condition which makes sense given the relationship with the urethra.
• Other Associations: Prune Belly Syndrome, Downs, Unilateral Renal Agenesis. and my personal favorite - the Imperforate Anus
Prostatic Utricle Cyst
sneaky
A sneaky trick would be to show it on a RUG, where a prostate utricle cyst would look like a focal out-pouching from the prostatic urethra.
Mullerian duct cyst male
this represents a failed regerssion of the caudal ends of the mullerian ducst (male equivalent oft he vagina/cervix)
does not communicat eiwth the urethra and does not have the same assocaitons as utricle cyst
this vs that
utricle cyst
Pear Shaped and Usually Smaller
Will NOT extend above the base o f the prostate
Communicates with the Urethra (JJtricle), therefore could opacify on a RUG
this vs that
mullerian cyst
Tear Drop Shaped
Will extend above the base o f the prostate
Does NOT communicate with the Urethra, should not opacify on a RUG
Prostate Abscess
This can cause a thick walled, scptated, heterogenous, cystic lesion
anywhere in the prostate. It is usually bacterial (E. coli). When chronic it can have a more “swiss
cheese” appearance referred to as “cavitary prostatitis.” Usually this is imaged via transrectal
ultrasound - because it gives you (the urologist) the option to do an image guided drain.
Testicular Torsion
overview
Results from the testis and spermatic cord twisting within the serosal space leading to ischemia. If it was 1950 you’d call in your nuclear medicine tech for scintigraphy. Now you just get a Doppler ultrasound.
Testicular Torsion
grey scale
The grey scale findings are fairly straight forward. The testicle is going to be darker (hypo-echoic) and asymmetrically enlarged - at least in the chronic setting. If it’s chronic then it will shrink up.
Testicular Torsion
doppler
The doppler findings are somewhat complex. The most obviously / basic look would be to show you absent arterial flow. This would be the equivalent of an underhand slow pitch. The curve ball would be to show you preserved arterial flow BUT with increased resistance and a decreased diastolic flow (or reversed diastolic flow).
That is correct my friends. Arterial flow does NOT need not be absent for torsion to be present (depending on the duration and severity). This leads the way for some seriously fuckery if the test writer wants to be an asshole.
The best way to think about it is like this: Testicle = Brain.
Just like the brain requires continuous diastolic flow (the thing is never off), so does the testicle.
So when you look at the waveform for a rule out torsion case you need to remember that torsion has three possible patterns
Testicular Torsion
waveform patters
1 - Classic Absence of Arterial Flow
2 - High resistance Arterial Flow (with decreased or reversed diastolic flow)
3 - Monophasic Arterial Waveform (loss of the normal dicrotic notch)
Testicular Torsion
stuffery
We are talking about testicular
artery wave forms here. The normal
cremasteric artery will not have diastolic flow
(think about that think as the artery to a
muscle) - it’s normally high resistance.
Testicular Torsion
cause
The “bell-clapper deformity,” which describes an abnormal high attachment of the tunical vaginalis, increases mobility and predisposes to torsion. It is usually a bilateral finding, so the contralateral side also gets an orchiopexy.
Testicular Torsion
viability
The viability is related to the degree of torsion (how many spins), and how long it has been spun. As a general rule, the surgeons try and get them in the OR before 6 hours.
High Flow States I Hyperemia:
Two things worth thinking about in this scenario: (1) Epididymo-orchitis (2) Detorsion.
The distinction between these two will be the clinical scenario. Orchitis is painful. Detorsion is pain free.
Epididymitis
overview
Inflammation o f the epididymis, and the most common cause of acute onset scrotal pain in adults. In high-school / college age men (likely sexually active men) the typical cause is chlamydia or gonorrhea. In married men (not likely to be sexually active) it is more likely to be e-coli, due to a urinary tract source. The epididymal head is the most affected. Increased size and hyperemia are your ultrasound findings. You can have infection o f the epididymis alone or infection o f the epididymis and testicle (isolated orchitis is rare).
Epididymitis
spread
Tail ► Body ► Head
Epididymitis
gamesmanship
Could be asked as “where is the most common location” ? = Tail (because in most cases it starts there).
Orchitis
overview
Typically progresses from epididymitis (isolated basically only occurs from mumps). It looks like asymmetric hyperemia.
Orchitis
typical
(1) Epididymitis ► (2) Epididymitis + Orchitis
Orchitis
mumps
straight to orchitis
Orchitis
impending infarct
The swelling o f the testicle can become so severe that it compromises venous flow. In this case you will see loss of diastolic flow (or reversal) - similar to the atypical torsion patterns. This is reported as a sign of “impending infarct.”
Testicular Trauma
overview
The big distinction is rupture vs fracture. Surgical intervention is required if there is testicular rupture. Intratesticular fracture, and hematomas (small) do not get surgery.
Testicular Trauma
rupture
Disrupted tunica albuginea, heterogenous testicle, poorly defined testicular outline
Testicular Trauma
fracture
Intact tunica albuginea, linear hypoechoic band across the parenchyma o f the testicle, well defined testicular outline.
Epidermoid Cyst
This is a benign mass of the testicle (no malignant potential), with an Aunt Minnie “onion skin” look, - alternating hypoechoic and hyperechoic rings. It’s relatively non-vascular relative to the rest of the testicle.
Tubular Ectasia of the Rete Testis
This is a common benign finding, resulting from obliteration (complete or partial) o f the efferent ducts. It’s usually bilateral - and in older men. The location of the cystic dilation is next to the mediastinum testis. Think about this as a normal variant. It requires no follow up or further evaluation.
Calcified Vas Deferens
You see this all the time in bad diabetics.
This can be shown on plain film or CT.
Testicular cancer
overview
In general, hypoechoic solid intratesticular masses should be thought of as cancer until
proven otherwise. Doppler flow can be helpful only when it is absent (can suggest hematoma - in the right clinical setting). If it’s extratesticular and cystic, it’s probably benign. The step 1 trivia is that cryptorchidism increases the risk of cancer (in both testicles), and is not reduced by orchiopexy. Most testicular tumors met via the lymphatics (retroperitoneal nodes at the level o f the renal hilum). The testable exception is choriocarcinoma, which mets via the blood. Most testicular cancers are germ cell subtypes (95%) - with seminomas making up about half o f those.
testicular cancer
risk factors
Cryptorchidism (for both testicles), Gonadal Dysgenesis, Klinefelters, Trauma, Orchitis, and testicular microlithiasis (maybe).
Testicular Microlithiasis
This appears as multiple small echogenic foci within the testes. Testicular microlithiasis is usually an incidental finding in scrotal US examinations performed for unrelated reasons. It might have a relationship with Germ Cell Tumors (controversial). Follow-up in 6 months, then yearly is probably the recommendation - although this recommendation is controversial.
Seminoma
This is the most common testicular tumor, and has the best prognosis as they are very radiosensitive. They are much more common (9x) in white people. The classic age is around 25. It usually looks like a homogenous hypoechoic round mass, which classically replaces the entire testicle. On MR1 they are usually homogeneously T2 dark (nonseminomatousnGCTs are often higher in signal).
Non-Seminomatous Germ Cell Tumors
Basically this is not a seminoma. We are
talking about mixed germ cell tumors, teratomas, yolk sac tumors, and choriocarcinoma. They typically occur at a young age relative to seminomas (think teenager). They are more heterogeneous and have larger calcifications.
Testicular Lymphoma
Just be aware that lymphoma can “hide” in the testes because of the
blood testes barrier. Immunosuppressed patients are at increased risk for developing extranodal/
testicular lymphoma. Almost all testicular lymphomas are non-hodgkin B-cell subtypes. On US, the
normal homogeneous echogenic testicular tissue is replaced focally or diffusely with hypoechoic
vascular lymphomatous tissue.
Testicular Lymphoma
buzzword
Multiple hypoechoic masses of the testicle
Burned-Out Testicular Tumor
If you see large, dense calcifications with shadowing in the testicle of an old man this is probably what you should be thinking. The idea is that you’ve had
spontaneous regression of a germ cell testicular neoplasm, that is now calcified. An important pearl is that there can still be viable tumor in there. Management is somewhat controversial and unlikely to be asked (most people pull them out).
Testicular cancer staging pearl
Testicular mets should spread to the para-aortic, aortic, caval region (N1-N3). It’s an embryology thing.
If you have mets to the pelvic, external iliac, and inguinal nodes - this is considered “nonregional” i.e. Ml disease. The exception is some kind of inguinal or scrotum surgery was done before the cancer manifested - but I wouldn’t expect them to get that fancy on the test. Just remember inguinal / pelvic nodes are non-regional and a higher stage (Ml).
High Yield Tes ticle Tumor Trivia
Seminoma is the most common and has the best prognosis (it melts with radiation)
Multiple hypoechoic masses = Lymphoma
Homogenous and Microcalcifications = Seminoma
Cystic Elements and Macrocalcifications = Mixed Germ Cell Tumor / Teratoma
Most testicular tumors met via the lymphatics (choriocarcinoma mets via the blood and tends to bleed like stink)
Gynecomastia can be seen with Sertoli Leydig Tumors
Sertoli Cell Tumors are also seen with Peutz-Jeghers
test tumor
elefated beta hcg
seminoma
choriocarcinoma (non s)
test tumor
elevated aft
mixed germ cell (non s)
yolk sac (non s)
Male infertility
obstructive
Congenital bilateral absence o f the vas deferens (seen in Cystic Fibrosis), ejaculatory duct obstruction, prostatic cysts. Think about associated renal anomalies (Zinner Syndrome).
male infertility
nonobstructive
Varicocele, Cryptorchidism, Anabolic Steroid Use, Erectile Dysfunction and “The Liberal Media.”
Varicocele
This is the most common correctable cause of infertility. They can be unilateral or bilateral. Unilateral is much more common on the left. Isolated right sided should make you think retroperitoneal process compressing the right gonadal vein.
Cryptorchidism
overview
Undescended testes. The testicle is usually found in the inguinal canal. The testicle has an increased risk o f cancer (actually they both will - which is weird). It’s most commonly seen in premature kids (20%).
Cryptorchidism
major complications
- Malignant degeneration - o f both the undescended and contralateral testicle
- Infertility
- Torsion
- Bowel Incarceration - related to the association o f indirect inguinal hernia
Cryptorchidism
gamesmanship
A good distractor would be “orchitis.” It’s a pathology that involves the balls, so it’s not totally far fetched. Obviously they can get IV orchitis… but not at a higher rate. It’s not a reported association - so don’t fall for that.
Zebras and Syndromes Associated With Male Infertility:
pit adenom making prolactin
kallman syndrom (cant smell and infertile)
klinefelter sydrome (tall gynecomastia and infertile)
zinner syndrome (renal agenesis ipsilateral seminal vesicle cyst)
transgender vocab
Transgender: Gender self identity does not match their genetic / sex assigned identity at birth. The alternative is a “Cisgender ” - A man who identifies as a man (XY) or a woman who identifies as a woman (XX). Gender and sexual orientation are different things. Sexual Orientation is the emotion / sexual attraction to others. Transgender people are not necessarily homosexual. Gender self identity is different than who you want to fuck.
Transgender Man
A female (XX) who identifies as the masculine (male) gender
Transgender Woman
A male (XY) who identifies as the feminine (female) gender
top and bottom surgeries
Slang for breast & genital procedures (gender-affirming surgery)
vaginoplasty
Procedure to create a functional and cosmetically acceptable neovagina.
penoscrotal inversion
The most common procedure with the lowest complication rate. It
involves orchiectomy and “penile disassembly” in a method similar to the induction ceremony of
the feared Unsullied Army. The skin from the disassembled parts is inverted / folded back to
create a tunnel. The clitoris is constructed using the native penile neurovascular anatomy.
intestinal interposition
Second line strategy which involves using a segment of bowel (usually
rectosigmoid colon) to create a neovagina by coloperineal anastomosis. They do this because
there uhhh - how best to say this — is “insufficient tissue” from the penis to make the tunnel.
phalloplasty
Procedure to create a functional and cosmetically acceptable neopenis. Standing
urination is a typical metric of success. Several months prior to constructing the neopenis - these
patients typically undergo hysterectomy (+/- oophorectomy).
Vaginectomy and urethroplasty are performed using vascularized vaginal mucosa to
try and elongate the urethra. Skin flaps often fail - but the “RFFF” or radial flap procedure is
probably the most common. Most of these skin grafts use a “tube in tube” strategy. I can’t believe
the details would be on the exam - but you can imagine they roll the skin and subcutaneous fat up
to make something that looks like a dick. Maybe not the most impressive of dicks - but a dick
none the less. Hey… you know what they say, it’s not the size of the dog in the fight - it’s the
size of the fight in the dog. Not sure if this expression applies to a surgically created neo-phallus
but I’m trying to be positive.
metoidoplasty
An alternate technique to phalloplasty - which has a lower complication rate.
The downside is the length of the created neopenis is usually not enough to have sex, but they can
still pee standing up (a major metric to success of the procedure). This technique is performed by
first using hormones to hypertrophy the clitoris (like a female body builder). Then the urethra is
lengthened (by dividing various ligaments) and anastomosed to the clitoris, which serves as the
glans. Labia minora is gonna be the source for skin to construct the shaft.
testicular prostheses/scrotoplasty
Generally made of silicone (high density on CT) and placed
around 6 month post phalloplasty. Just like the those dick pumps you sometimes see in diabetics -
a hydraulic pump apparatus can be placed - that thing will have tubing and be more water density.
testicular prostheses/scrotoplasty
complications
Older technique didn’t resect the vagina - these patients were prone to fistula
between the neourethra and native vagina. DVT / PE is a post op risk if the patient is taking hormone
therapy. Bleeding, infection, urinary complication (urethral stenosis etc) all can occur - as one
might expect.
other transgender surgeries
that could come up on the exam include breast implants, and the various neck
surgeries to make a dude look less like a dude (thyroid chondroplasty / tracheal shave) and sound
less like a dude (glottoplasty, cricothyroid approximation).
