GU Flashcards

Question

Syndrome/Association medullary

Answer 1

sickle cell trai

Answer 2

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.

Answer 3

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.

Answer 4

Out of all the renal masses - lymphoma is the most likely to preserve the normal reniform shape.

Answer 5

Lymphoma is the most common metastatic tumor to invade / infiltrate the kidneys

Answer 6

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.

Answer 7

(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.

Answer 8

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:

Answer 9

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.

Answer 10

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.

Answer 11

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?

Answer 12

RCC is typically COLDER than surrounding renal parenchyma on PET, Oncocytoma is typically HOTTER than surrounding renal parenchyma on PET,

Answer 13

A syndrome associated with bilateral oncocytomas is Birt hogg dube (they also get chromophobe RCC).

Answer 14

“Non-communicating, fluid-filled locules, surrounded by thick fibrous capsule.” By definition these things arecharacterized by the absence of a solid component or necrosis.

Answer 15

“protrudes into the renal pelvis.” The question is likely the bimodal occurrence (4 year old boys, and 40 year old women).

Answer 16

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.”

Answer 17

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.”

Answer 18

``` It is bordered anterior by the anterior pararenal space (black arrows) and posterior by the transversalis fascia (white arrows). ```

Answer 19

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.

Answer 20

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.

Answer 21

~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.

Answer 22

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.

Answer 23

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.

Answer 24

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.

Answer 25

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...

Answer 26

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).

Answer 27

Most Common Cause = Over-Anticoagulation (high PT/INR) 2nd Most Common Cause = Rupture / Leaking Aorta 3rd Most Common Cause = Bleeding RCC or AML

Answer 28

Lymphoma Rf fibrosis erheim chester

Answer 29

can displace the aorta forward, and be sen above the renal arteries. tends to push things rather than tether and obstruct

Answer 30

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

Answer 31

huge zebra. gamesmanship would be to show you plain films of legs with bilateral symmetric sclerosis of the metaphysis (sparing the epiphysis)

Answer 32

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)

Answer 33

Basically, if the mass is greater than 70 HU and homogenous, it’s benign (hemorrhagic or proteinaceous cyst) 99.9% of the time.

Answer 34

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.

Answer 35

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.

Answer 36

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.

Answer 37

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).

Answer 38

The cysts will regress after renal transplant.

Answer 39

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

Answer 40

ADPKD Cysts in Liver Kidneys are BIG VHL Cysts in Pancreas Acquired (Uremic) Kidneys are small

Answer 41

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).

Answer 42

* 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)

Answer 43

Lipid poor aml hemorrhagic cyst papillary subtype RCC

Answer 44

• 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.

Answer 45

These will likely be T1 bright

Answer 46

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).

Answer 47

this is the situation where you have multiple tiny cysts forming in utcro from some type of insult.

Answer 48

* "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

Answer 49

In hydronephrosis, the cystic spaces are seen to communicate. In difficult cases renal scintigraphy can be useful. MCDK will show no excretory function.

Answer 50

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.

Answer 51

* Acute ureteral obstruction * Acute pyelonephritis * Medullary sponge kidney * Acute renal vein thrombosis * Radiation nephritis * Acutely following renal contusion * Hypotension (bilateral) * Infantile polycystic kidney (bilateral)

Answer 52

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.

Answer 53

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.

Answer 54

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.

Answer 55

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

Answer 56

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.

Answer 57

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)

Answer 58

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.

Answer 59

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. ”

Answer 60

50% of sickle cell patients develop | papillary necrosis

Answer 61

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.

Answer 62

``` 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.

Answer 63

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

Answer 64

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).

Answer 65

BIG and BRIGHT kidney in HIV positive patient who is clinically in nephrotic syndrome (massive proteinura).

Answer 66

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.

Answer 67

via biopsy o f the big bright kidney.

Answer 68

n HIV patients can result in punctate (primarily cortical) | calcifications.

Answer 69

• 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.

Answer 70

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.

Answer 71

* 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.

Answer 72

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.

Answer 73

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.

Answer 74

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.`

Answer 75

``` 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.

Answer 76

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.

Answer 77

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.

Answer 78

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).

Answer 79

htn post biopsy lithotripsy or trauma

Answer 80

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.

Answer 81

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.

Answer 82

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).

Answer 83

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.

Answer 84

can be seen where a region o f hypodensity / poor enhancement on early phases becomes relatively hyperdense on delayed imaging.

Answer 85

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.

Answer 86

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).

Answer 87

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”).

Answer 88

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.

Answer 89

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).

Answer 90

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).

Answer 91

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).

Answer 92

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

Answer 93

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)

Answer 94

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)

Answer 95

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

Answer 96

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.

Answer 97

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.

Answer 98

is an immediate failure of the graft - and you rarely see this imaged. It is basically a dead on arrival transplant.

Answer 99

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.

Answer 100

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.

Answer 101

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.

Answer 102

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.

Answer 103

US RI elevated mechanism antibody cell mediated timing first week mag3-flow crap mag3 uptake crap/delayd mag3 making piss crap slow progressive excretion

Answer 104

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

Answer 105

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

Answer 106

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

Answer 107

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.

Answer 108

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.”

Answer 109

* 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

Answer 110

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.

Answer 111

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.

Answer 112

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.

Answer 113

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.

Answer 114

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.

Answer 115

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)

Answer 116

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

Answer 117

av fistula pseudoaneurysm traumatic hematoma

Answer 118

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

Answer 119

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

Answer 120

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...

Answer 121

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.

Answer 122

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.

Answer 123

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.

Answer 124

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.

Answer 125

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.

Answer 126

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.

Answer 127

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.

Answer 128

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.

Answer 129

thinsk segmental artery injury

Answer 130

think devascularized kidney

Answer 131

thingk renal vein injury/thrombosis

Answer 132

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).

Answer 133

Stones tend to lodge in 3 spots: UPJ, UVJ, pelvic brim.

Answer 134

Wall calcifications should make you think about two things: (1) TB, (2) Schistosomiasis (worms).

Answer 135

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.

Answer 136

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.

Answer 137

( “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.

Answer 138

premalignant

Answer 139

not premalignant

Answer 140

Not premalignant and usually gets better with antibiotics

Answer 141

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.

Answer 142

is considered premalignant and the | cancer is squamous cell.

Answer 143

associated with squamous cell carcinoma NOT transitional cell

Answer 144

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).

Answer 145

* 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

Answer 146

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.

Answer 147

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.

Answer 148

Retroperitoneal Adenopathy Aortic Aneurysm Psoas Hypertrophy (proximal ureter)

Answer 149

Retroperitoneal Fibrosis Retrocaval Ureter (right side) ``` Pelvic Lipomatosis Psoas Hypertrophy (distal ureter) ```

Answer 150

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%

Answer 151

* Smoking * Azo Dye * Cyclophosphamide * Aristolochic acid (Balkan Nephropathy - see below) * Horseshoe Kidney * Stones * Ureteral Pseudodiverticulosis * Hereditary Non-Polyposis Colon Cancer (type 2)

Answer 152

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).

Answer 153

This is much less common than TCC (in the US anyway). The major predisposing factor is schistosomiasis (they both start with an “S”).

Answer 154

Mets to the ureters are rare but can occur (GI, Prostate, Renal, Breast). They typically infiltrate the periureteral soft tissues and demonstrate transmural involvement.

Answer 155

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.

Answer 156

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.

Answer 157

younger 30-40 smooth/oblong mobile

Answer 158

older 60-70 irregular fixed

Answer 159

This is a malformation triad which occurs in males. Classically shown on a babygram with a kid shaped like a pear (big wide belly).

Answer 160

• Deficiency of abdominal musculature • Hydroureteronephrosis • Cryptorchidism (bladder distention interferes with descent o f testes)

Answer 161

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.

Answer 162

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.

Answer 163

“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.

Answer 164

“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.

Answer 165

GROSS hematuria confers a 4x greater risk than microscopic hematuria. If the question header specifically indicates “GROSS” hematuria - think bladder cancer first.

Answer 166

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.

Answer 167

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.

Answer 168

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.

Answer 169

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).

Answer 170

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.

Answer 171

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.

Answer 172

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.”

Answer 173

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.

Answer 174

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

Answer 175

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.

Answer 176

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.

Answer 177

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).

Answer 178

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

Answer 179

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.

Answer 180

* 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.

Answer 181

* 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.

Answer 182

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.

Answer 183

Used for people with long segment distal ureter injury / disease

Answer 184

CT I VP or Plain Film IVP (with contrast filling the bladder). The “hitched” side has an upward projection towards the psoasmuscle.

Answer 185

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.

Answer 186

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.

Answer 187

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.

Answer 188

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).

Answer 189

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.

Answer 190

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.

Answer 191

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.

Answer 192

This is more o f a sign than a pathology Think two things (1) pelvic lipomatosis, and (2) hematoma.

Answer 193

* Colovesicial Fistula = Diverticular Disease * Ileovesical Fistula = Crohns * Rectovesical Fistula = Neoplasm or Trauma

Answer 194

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).

Answer 195

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.

Answer 196

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.

Answer 197

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.

Answer 198

• 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.

Answer 199

“Next Step” RUG.

Answer 200

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.

Answer 201

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.

Answer 202

stretched posterior urethra is intact and normal on rug

Answer 203

membraouns urethra tear posterior above an intact ug diaphragm extraperitoneal contrast is present no perineum contrast (intact ug diaphrag prevents this) associated with incontinence

Answer 204

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

Answer 205

bladder base injury extending into prostatic urethra posterior associated with incontinence

Answer 206

bulbous uretha "anterior" anterior straddle injury

Answer 207

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

Answer 208

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

Answer 209

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.

Answer 210

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.

Answer 211

This may occur post radiation, and is classically described with brachytherapy (occurs in 1% of patients).

Answer 212

In a man, this is almost always the result of long term foley placement.

Answer 213

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 ).

Answer 214

Cancer in a urethral diverticulum is nearly ALWAYS adenocarcinoma (rather than squamous cell).

Answer 215

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

Answer 216

The buzzword is “saddle-bag” configuration, which supposedly is how you tell it from the urethra.

Answer 217

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%).

Answer 218

Enhances equal to cortex on CM Phase Overall Most Common in Gen Pop Von Hippel-Lindau

Answer 219

Enhances less than cortex on CM Phase Hereditary Papillary Renal Carcinoma Transplant Kidney

Answer 220

birt hogg dube

Answer 221

sickle cell trait

Answer 222

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

Answer 223

* 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

Answer 224

- “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.

Answer 225

``` - Think this when you see Calcifications - Favors the Trigone and Lateral Walls - Association with Schistosomiasis - Association with Chronic Suprapubic Catheter / Urinary Status ```

Answer 226

- Midline Location is Classic - Association with Urachal Remnant - Association with Bladder Exstrophy

Answer 227

adenocarcinoma

Answer 228

TCC (90%) | think about it loike a bladder ca

Answer 229

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.

Answer 230

The shape of the uterus changes - becoming more tube-like, with the cervix and uterus the same size.

Answer 231

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.

Answer 232

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.

Answer 233

The XO kids. Besides often having aortic coarctations, and horseshoe kidneys they will have a pre-puberty uterus and streaky ovaries.

Answer 234

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.

Answer 235

uterus fallopian tubes upper 2/3 of vagina

Answer 236

vas deferans seminal vesicles epididymis

Answer 237

prostate lower / of vagina

Answer 238

failure to form (unilateral kidney and unicarnuate uterus) failure to fuse (tuerus diedelphys or bicornuate) failure to cleave septate uterus

Answer 239

(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

Answer 240

uterus | cervical

Answer 241

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.

Answer 242

llnicornuate + Communicating Cavitary Rudimentary Horn univrouate + non communicating cavitary horn unicornuate + noncavitary rudimentary horn isolated unicornuate (most common)q

Answer 243

``` 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. ```

Answer 244

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.

Answer 245

``` 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.” ```

Answer 246

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.

Answer 247

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.

Answer 248

• “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

Answer 249

• 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

Answer 250

0-7 “Rag Week,” 7-14 Proliferative, 14-28 Secretory | *Day 14 Ovulation

Answer 251

' 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.

Answer 252

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.

Answer 253

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.

Answer 254

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.

Answer 255

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.

Answer 256

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:

Answer 257

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.

Answer 258

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.

Answer 259

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.

Answer 260

``` 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. ```

Answer 261

(pubococcygeal line) = drawn from inferior margin o f the symphysis pubis to the junction between the first and second coccygeal elements.

Answer 262

drawn from the inferior margin o f the symphysis pubis to the posterior aspect o f the puborectalis muscle sling.

Answer 263

shortest distance between the posterior aspect o f the puborectalis muscle sling and the PCL

Answer 264

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

Answer 265

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

Answer 266

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.

Answer 267

(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.

Answer 268

``` 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) ```

Answer 269

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.

Answer 270

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.

Answer 271

Most common type T1: dark T2: drak T1+C: homogenous

Answer 272

Densely packed smooth muscle (without much connective tissue). Respond well to embolization T1: dark T2: bright T1+C: homognous

Answer 273

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

Answer 274

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.

Answer 275

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

Answer 276

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

Answer 277

uncommon T1: dark T2: bright T1+C: minimal

Answer 278

uncommon T1: dark T2: bright T1+C: none

Answer 279

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.

Answer 280

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.

Answer 281

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.

Answer 282

* 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

Answer 283

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).

Answer 284

In premenopausal women this is a common finding. In postmenopausal women it means either cervical stenosis or an obstructing mass (usually cervical stenosis).

Answer 285

* Endometrium less than 5 mm = Probably Atrophy | * Endometrium > 4-5 mm = Maybe cancer and gets a biopsy

Answer 286

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

Answer 287

* 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.

Answer 288

(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).

Answer 289

T1+C: Normal Dark Cervical Stroma (star). | Enhancement of the Cervical Mucosa (arrows) Excludes Invasion.

Answer 290

T1+C: Tumor Invasion o f the Cervix

Answer 291

* 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.

Answer 292

* 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.

Answer 293

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.

Answer 294

Stage 11A: Spread beyond the cervix, but NO parametrial invasion, Surgery Stage 11B: Parametrial involvement but NOT extension to pelvic side wall., Chemo/ Radiation

Answer 295

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.

Answer 296

The uterine a rtery runs inside the parametrium, hen ce the need for ch em o - o n ce in va de d .

Answer 297

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.

Answer 298

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.

Answer 299

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.

Answer 300

Rare in the vagina, but can occur (most commonly in the anterior wall).

Answer 301

The most common cancer of the vagina (85%). This is associated with HPV. This is just like the cervix.

Answer 302

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.

Answer 303

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.

Answer 304

* 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.

Answer 305

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.

Answer 306

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).

Answer 307

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).

Answer 308

Cysts in these periurethral glands, can cause recurrent UTIs and urethral obstruction.

Answer 309

nabothina gartner duct (anter lateral upper vagina skene gland anterior bartholin below near the butthole

Answer 310

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.

Answer 311

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.

Answer 312

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.

Answer 313

< 1 cm = Follicle 1-2 cm = Dominant Follicle > 3 cm = Cyst

Answer 314

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).

Answer 315

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.

Answer 316

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.

Answer 317

* Multifetal pregnancy, * Gestational trophoblastic disease (moles), * Ovarian Hyperstimulation syndrome.

Answer 318

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.

Answer 319

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.

Answer 320

simple paravoaran cysts do no require follow up

Answer 321

* The ovaries o f a pediatric patient stay small until around age 8-9. * Ovaries may contain small follicles.

Answer 322

• 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.

Answer 323

( > 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.

Answer 324

``` PreMenopausal: < 3 cm = Call it Normal Follicle PreMenopausal: > 3 cm = Get an US PostMenopausal: < 1cm = Call it Normal Cyst PostMenopausal: > 1cm = Get an US ```

Answer 325

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)

Answer 326

gyn consult

Answer 327

``` Physiologic and functioning follicles Corpora lutea Hemorrhagic cysts Endometriomas Benign cystic teratomas (dermoids) Polycystic ovaries ```

Answer 328

``` 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. ```

Answer 329

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).

Answer 330

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.

Answer 331

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).

Answer 332

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.

Answer 333

an enhancing mural nodule

Answer 334

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.

Answer 335

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.

Answer 336

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.

Answer 337

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.

Answer 338

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.

Answer 339

RI <0.4 or >0.7 thick echogenic rim moves separate from the ovary

Answer 340

RI 0.4-0.7 thin echogenic rim moves with the ovary

Answer 341

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).

Answer 342

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.

Answer 343

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.

Answer 344

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

Answer 345

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%.

Answer 346

Will be bright on T1 (from the fat). There will be fat suppression (not true of hemorrhagic cysts, and endometriomas).

Answer 347

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).

Answer 348

Endometrioma Clear Cell | Dermoid Squamous

Answer 349

Gross Fat containing ovarian mass on CT

Answer 350

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.

Answer 351

“Dot -dash” pattern has been described for hair within a cyst.

Answer 352

—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

Answer 353

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.

Answer 354

* 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

Answer 355

* 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

Answer 356

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).

Answer 357

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).

Answer 358

Unilocular (fewer septations) | Papillary Projections Common

Answer 359

Multi-locular (more septations) | Papillary Projections Less Common

Answer 360

This is the second most common ovarian cancer (serous number one, mucinous number three). These things are bilateral about 15% o f the time.

Answer 361

* 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

Answer 362

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)

Answer 363

(1) Ovarian Masses - Mucinous and Serous (2) Desmoids - Remember Gardner Syndrome (3) Sarcomas

Answer 364

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.

Answer 365

This is the triad of ascites, pleural effusion, and a benign ovarian tumor (most commonly fibroma).

Answer 366

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.

Answer 367

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.

Answer 368

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.

Answer 369

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.

Answer 370

T h is is a metastatic tumor to the ovaries from the GI tract (usually stomach).

Answer 371

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.

Answer 372

``` Unilateral enlarged ovary (greater than 4 cm) Mass on the ovary Peripheral Cysts Free Fluid Lack of arterial or venous flow ```

Answer 373

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.

Answer 374

Thin (or thick in chronic states) elongated tubular structure in the pelvis.

Answer 375

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).

Answer 376

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.

Answer 377

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).

Answer 378

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.

Answer 379

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.

Answer 380

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.

Answer 381

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.

Answer 382

* 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.

Answer 383

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.

Answer 384

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.

Answer 385

(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).

Answer 386

Classically shows the uterus to be filled with an echogenic, solid, highly vascular mass, often described as “snowstorm” in appearance.

Answer 387

Vesicles that make up the mole enlarge into individual cysts (2-30 mm) and produce your “bunch of grapes” appearance.

Answer 388

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.

Answer 389

The placenta will be enlarged, and have areas of multiple, diffuse anechoic lesions. You may see fetal parts.

Answer 390

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

Answer 391

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.

Answer 392

(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.

Answer 393

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.

Answer 394

Defined by fracture of the corpus cavernosum and its surrounding sheath, the tunica albuginea (black line outlining the dong bone).

Answer 395

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).

Answer 396

Stigmata of this injury can include a sub optimal angulation (Peyronie disease) from fibrous scar formation.

Answer 397

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.

Answer 398

• Peripheral Zone: 70% *Transition Zone: 20% • Central Zone: 10%

Answer 399

Central Gland | this is where BPH nodules live

Answer 400

Peripheral Zone | this is where cancer lives

Answer 401

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).

Answer 402

Bone scan is the money for prostate mets (vertebral body mets).

Answer 403

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.

Answer 404

``` The main thing to know is stage II vs stage III, as extra capsular extension is the most important factor governing treatment. ```

Answer 405

Seminal vesicles (T3b) and the nerve bundle are also right behind the prostate and can get invaded (urologists love to hear about that).

Answer 406

Confined by capsule (T2) Abutment o f the capsule without bulging

Answer 407

Extension through capsule (T3a) Bulging o f the capsule, or frank extension through it

Answer 408

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).

Answer 409

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.

Answer 410

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.

Answer 411

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.

Answer 412

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

Answer 413

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.

Answer 414

``` 1 normal 2 linear/wedge 3 vague patch > 4 if enhancing 4 focal <1.5 5 focal >1.5cm ```

Answer 415

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

Answer 416

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).

Answer 417

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.

Answer 418

The IVP buzzword is “J shaped”, “Fishhook”, or “Hockey stick” shaped ureter - as the distal ureter curves around the enlarged prostate.

Answer 419

In the Transitional Zone (Central Gland) T2 Heterogenous Can Restrict Diffusion May enhance and washout

Answer 420

Classically T1 bright stuff in the gland. It’s subacute blood

Answer 421

T2 dark adc dark enhancement early enhancement and washout

Answer 422

t2 dark (sometimes t1 bright) adc dark enhancement none

Answer 423

t2 dark (charcoal) adc dark early enhancement and early washout

Answer 424

T2 dark (welldefined) adc dark can enhance

Answer 425

prostatic utricle mullerian duct cyst ejaculatory duct cyst

Answer 426

seminal vesicle cyst diverticulosis of the ampulla of vas deferns

Answer 427

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.

Answer 428

* Associated with renal agenesis * Associated with vas deferens agenesis * Associated with ectopic ureter insertion * Associated with polycystic kidney disease

Answer 429

* Obstruction often from prostatic hypertrophy, or chronic infection/scarring * Classic history is prior prostate surgery

Answer 430

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.

Answer 431

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

Answer 432

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.

Answer 433

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

Answer 434

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

Answer 435

Tear Drop Shaped Will extend above the base o f the prostate Does NOT communicate with the Urethra, should not opacify on a RUG

Answer 436

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.

Answer 437

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.

Answer 438

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.

Answer 439

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

Answer 440

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)

Answer 441

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.

Answer 442

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.

Answer 443

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.

Answer 444

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.

Answer 445

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).

Answer 446

Tail ► Body ► Head

Answer 447

Could be asked as “where is the most common location” ? = Tail (because in most cases it starts there).

Answer 448

Typically progresses from epididymitis (isolated basically only occurs from mumps). It looks like asymmetric hyperemia.

Answer 449

(1) Epididymitis ► (2) Epididymitis + Orchitis

Answer 450

straight to orchitis

Answer 451

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.”

Answer 452

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.

Answer 453

Disrupted tunica albuginea, heterogenous testicle, poorly defined testicular outline

Answer 454

Intact tunica albuginea, linear hypoechoic band across the parenchyma o f the testicle, well defined testicular outline.

Answer 455

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.

Answer 456

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.

Answer 457

You see this all the time in bad diabetics. | This can be shown on plain film or CT.

Answer 458

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.

Answer 459

Cryptorchidism (for both testicles), Gonadal Dysgenesis, Klinefelters, Trauma, Orchitis, and testicular microlithiasis (maybe).

Answer 460

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.

Answer 461

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).

Answer 462

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.

Answer 463

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.

Answer 464

Multiple hypoechoic masses of the testicle

Answer 465

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).

Answer 466

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).

Answer 467

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

Answer 468

seminoma choriocarcinoma (non s)

Answer 469

mixed germ cell (non s) yolk sac (non s)

Answer 470

Congenital bilateral absence o f the vas deferens (seen in Cystic Fibrosis), ejaculatory duct obstruction, prostatic cysts. Think about associated renal anomalies (Zinner Syndrome).

Answer 471

Varicocele, Cryptorchidism, Anabolic Steroid Use, Erectile Dysfunction and “The Liberal Media.”

Answer 472

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.

Answer 473

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%).

Answer 474

* Malignant degeneration - o f both the undescended and contralateral testicle * Infertility * Torsion * Bowel Incarceration - related to the association o f indirect inguinal hernia

Answer 475

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.

Answer 476

pit adenom making prolactin kallman syndrom (cant smell and infertile) klinefelter sydrome (tall gynecomastia and infertile) zinner syndrome (renal agenesis ipsilateral seminal vesicle cyst)

Answer 477

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.

Answer 478

A female (XX) who identifies as the masculine (male) gender

Answer 479

A male (XY) who identifies as the feminine (female) gender

Answer 480

Slang for breast & genital procedures (gender-affirming surgery)

Answer 481

Procedure to create a functional and cosmetically acceptable neovagina.

Answer 482

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.

Answer 483

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.

Answer 484

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.

Answer 485

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.

Answer 486

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.

Answer 487

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.

Answer 488

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).

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